Core Concepts in Pharmacology 4th Edition

Brief Contents
Unit I Unit IV
Basic Concepts in Pharmacology 1 The Immune System 361
Chapter 1 Introduction to Pharmacology: Chapter 24 Drugs for Inflammation and Fever 362
Drug Regulation and Approval 2 Chapter 25 Drugs for Immune System
Chapter 2 Drug Classes, Schedules, and Modulation 373
Categories 12 Chapter 26 Drugs for Bacterial Infections 387
Chapter 3 Methods of Drug Administration 20 Chapter 27 Drugs for Fungal, Viral, and
Chapter 4 What Happens After a Drug Has Parasitic Diseases 412
Been Administered 41 Chapter 28 Drugs for Neoplasia 430
Chapter 5 The Nursing Process
in Pharmacology 51
Unit V
Chapter 6 The Role of Complementary and The Respiratory and Digestive
Alternative Therapies in
Pharmacology 59
Systems 453
Chapter 7 Substance Abuse 69 Chapter 29 Drugs for Respiratory Disorders 454
Chapter 30 Drugs for Gastrointestinal
Disorders 476
Unit II
Chapter 31 Vitamins, Minerals, and Nutritional
The Nervous System 85 Supplements 496
Chapter 8 Drugs Affecting Functions of the
Autonomic Nervous System 86 Unit VI
Chapter 9 Drugs for Anxiety and Insomnia 105 The Endocrine and Reproductive
Chapter 10 Drugs for Emotional, Mood, Systems 509
and Behavioral Disorders 122
Chapter 32 Drugs for Endocrine Disorders 510
Chapter 11 Drugs for Psychoses 142
Chapter 33 Drugs for Diabetes Mellitus 528
Chapter 12 Drugs for Degenerative Diseases
and Muscles 157 Chapter 34 Drugs for Disorders and Conditions
of the Reproductive System 542
Chapter 13 Drugs for Seizures 180
Chapter 14 Drugs for Pain Management 197
Unit VII
Chapter 15 Drugs for Anesthesia 217
The Skeletal System,
Integumentary System, and
Unit III Eyes and Ears 563
The Cardiovascular and Chapter 35 Drugs for Bone and Joint Disorders 564
Urinary Systems 233
Chapter 36 Drugs for Skin Disorders 582
Chapter 16 Drugs for Lipid Disorders 234 Chapter 37 Drugs for Eye and Ear Disorders 598
Chapter 17 Diuretics and Drugs for Electrolyte

and Acid–Base Disorders 248 Appendix A References 611
Chapter 18 Drugs for Hypertension 265 Appendix B Brief Answers to NCLEX-PN®

and Case Study Questions 621
Chapter 19 Drugs for Heart Failure 287
Appendix C Calculating Dosages 624
Chapter 20 Drugs for Angina Pectoris,
INDEX 626
Myocardial Infarction, and Stroke 301
GUIDE TO SPECIAL FEATURES 657
Chapter 21 Drugs for Shock and Anaphylaxis 319
*Appendix D (Complete Answers and Rationales for NCLEX-PN®
Chapter 22 Drugs for Dysrhythmias 331
Review and Case Study Questions) and the Glossary appear on the
Chapter 23 Drugs for Coagulation Disorders 346 textbook’s website.
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Brief Contents
Unit I Chapter 21 Drugs for Shock and Anaphylaxis 319
Basic Concepts in Pharmacology 1 Chapter 22 Drugs for Dysrhythmias 331

Chapter 23 Drugs for Coagulation Disorders 346
Chapter 1 Introduction to Pharmacology:
Drug Regulation and Approval 2
Chapter 2 Drug Classes, Schedules, and Unit IV
Categories 12 The Immune System 361
Chapter 3 Methods of Drug Administration 20
Chapter 24 Drugs for Inflammation and Fever 362
Chapter 4 What Happens After a Drug Has
Been Administered 41 Chapter 25 Drugs for Immune System
Modulation 373
Chapter 5 The Nursing Process
in Pharmacology 51 Chapter 26 Drugs for Bacterial Infections 387
Chapter 6 The Role of Complementary and Chapter 27 Drugs for Fungal, Viral, and
Alternative Therapies in Parasitic Diseases 412
Pharmacology 59 Chapter 28 Drugs for Neoplasia 430
Chapter 7 Substance Abuse 69
Unit V
Unit II The Respiratory and Digestive
The Nervous System 85 Systems 453
Chapter 8 Drugs Affecting Functions of the Chapter 29 Drugs for Respiratory Disorders 454
Autonomic Nervous System 86 Chapter 30 Drugs for Gastrointestinal
Chapter 9 Drugs for Anxiety and Insomnia 105 Disorders 476
Chapter 10 Drugs for Emotional, Mood, Chapter 31 Vitamins, Minerals, and Nutritional
and Behavioral Disorders 122 Supplements 496

Chapter 12 Drugs for Degenerative Diseases Unit VI
and Muscles 157
The Endocrine and Reproductive
Systems 509
Chapter 34 Drugs for Disorders and Conditions
Unit III of the Reproductive System 542
The Cardiovascular and
Urinary Systems 233
Unit VII
Chapter 16 Drugs for Lipid Disorders 234
Chapter 17 Diuretics and Drugs for Electrolyte Integumentary System, and
and Acid–Base Disorders 248
Eyes and Ears 563
Chapter 18 Drugs for Hypertension 265
Chapter 19 Drugs for Heart Failure 287 Chapter 35 Drugs for Bone and Joint Disorders 564
Chapter 20 Drugs for Angina Pectoris, Chapter 36 Drugs for Skin Disorders 582
Myocardial Infarction, and Stroke 301 Chapter 37 Drugs for Eye and Ear Disorders 598
iii
iv Brief Contents
Appendix A References 611 INDEX 626

Appendix B Brief Answers toNCLEX-PN® GUIDE TO SPECIAL FEATURES 657
and Case Study Questions 621
*Appendix D (Complete Answers and Rationales for

NCLEX-PN® Review and Case Study Questions) and
the Glossary appear on the textbook’s website.
CORE Concepts iN
Pharmacology
fourth Edition
Leland Norman Holland, Jr., PhD

Program Manager
Hillsborough Community College, Brandon Campus, Tampa, Florida
Michael Patrick Adams, PhD, RT(R)

Professor, Anatomy and Physiology
Saint Petersburg College, Saint Petersburg, Florida
Formerly Dean, Health Professions
Pasco-Hernando Community College, New Port Richey, Florida
Jeanine Lynn Brice, RN, MSN

Nursing Tutor
Saint Petersburg College, Saint Petersburg, Florida
Formerly Professor of Nursing
Pasco-Hernando Community College, New Port Richey, Florida
Boston Columbus Indianapolis New York San Francisco Upper Saddle River
Amsterdam Cape Town Dubai London Madrid Milan Munich Paris Montréal Toronto
Delhi Mexico City São Paulo Sydney Hong Kong Seoul Singapore Taipei Tokyo
Library of Congress Cataloging-in-Publication Data
Holland, Leland Norman.

Core concepts in pharmacology / Leland Norman Holland, Jr., Michael Patrick Adams, Jeanine Brice. — Fourth edition.
p. ; cm.
Includes bibliographical references and index.
ISBN-13: 978-0-13-344981-5
ISBN-10: 0-13-344981-5
I. Adams, Michael, (date) author. II. Brice, Jeanine, author. III. Title.
[DNLM: 1. Pharmacological Phenomena. 2. Drug Therapy. QV 37]
RM301.14
615'.1—dc23 2013042150
Publisher: Julie Levin Alexander

Assistant to the Publisher: Regina Bruno
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Notice: The authors and the publisher of this volume have taken care to make certain that the doses of drugs and schedules
of treatment are correct and compatible with the standards generally accepted at the time of publication. Nevertheless, as new
information becomes available, changes in treatment and in the use of drugs become necessary. The reader is advised to care-
fully consult the instruction and information material included in the package insert of each drug or therapeutic agent before
administration. This advice is especially important when using, administering, or recommending new and infrequently used
drugs. The authors and publisher disclaim all responsibility for any liability, loss, injury, or damage incurred as a consequence,
directly or indirectly, of the use and application of any of the contents of this volume.
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Pearson® is a registered trademark of Pearson plc.
10 9 8 7 6 5 4 3 2 1
ISBN 10: 0-13-344981-5
ISBN 13: 978-0-13-3449815
Preface
Pharmacology is one of the most challenging subjects for prototypes and introduces them in detail. Drug Prototype
those embarking on careers in the health sciences. By its boxes showcase these important medications.
very nature, pharmacology is an interdisciplinary subject,
borrowing concepts from a wide variety of the natural and Focused Nursing Content
applied sciences. Prediction of drug action, the ultimate goal
in the study of pharmacology, requires a thorough knowl- This text provides focused nursing content, allowing stu-
edge of anatomy, physiology, chemistry, and pathology dents quick access to essential content for safe, effective
as well as of the social sciences of psychology and sociology. drug therapy. Nursing Process Focus charts provide a
It is the interdisciplinary nature of pharmacology that succinct, easy-to-read view of the most commonly pre-
makes the subject difficult to learn, but fascinating to study. scribed drug classes. Need-to-know nursing actions are
This text presents pharmacology from an interdisci- presented in a format that reflects the “flow” of the Nursing
plinary perspective. The text draws upon core concepts of Process: nursing assessment, potential nursing diagnoses,
anatomy, physiology, and pathology to make drug therapy planning, interventions (including patient education and
understandable. The text does not assume that the student discharge planning), and evaluation. Rationales for inter-
comes to the course with a strong background in the natu- ventions are included in parentheses. The Nursing Process
ral or applied sciences. Instead, the prerequisite science Focus charts clearly identify what nursing actions are
knowledge necessary for understanding drug therapy is most important.
reviewed in each chapter that presents the core concepts
in pharmacology.
New to this Edition
Organization ■ 2 New Chapters! Because of the expansion in pharma-
cologic development in immune modulation and dia-
The authors use numbered core concepts, a concise means betes management, these topics are presented in new
of communicating to the student the most important phar- chapters.
macologic information. These core concepts are stated at the ■ Updated and Revised! All drugs updated and prototypes
beginning of each chapter, so that the student can get an over- adjusted to reflect modern drug usage.
view of what is to be learned. They are repeated at the end of ■ Updated and Revised! Safety Alert features throughout
the chapter, with a brief summary of each important concept. the text call attention to medication errors and The Joint
Commission safety guidelines.
Disease and Body System Approach ■ Drug Prototype boxes include both therapeutic and phar-
macological drug classifications.
Core Concepts in Pharmacology is organized according
■ Added! Black Box Warnings for the drugs designated as
to body systems and diseases. The framework places the
drugs in the context of how they are used therapeutically. special risk.
This makes it easy for the student to locate all relevant
■ Updated and Revised! End of chapter NCLEX-PN® ques-
anatomy, physiology, pathology, and pharmacology in the tions completely revised. Full rationales and NCLEX
same chapter in which the drugs are discussed. tagging are provided in an online appendix.
■ Updated! Glossary provided with definitions of all key
terms.
Prototype Approach to Drug Therapy ■ Addition of off-label uses of drugs and adverse effects to
The vast number of drugs taught in a pharmacology course drug tables as appropriate.
is staggering. To facilitate learning, this text highlights one ■ Completely Revised! The Nursing Process Focus charts
or two most representative drugs in each classification as reflecting current nursing practice.
vii
viii Preface
Design and Features
Focus on Core Information

C
“Where am I? What
happened? I really hurt.” h
a
Mr. Joshua Hanks
P
T
E
The numbered Core Concepts identify ideas R
and provide an overview of the chapter.

drugs for shock and anaphylaxis
21
CORE CONCEPTS
21.1 Shock is a syndrome characterized by the collapse of 21.4 Vasoconstrictors are administered during shock to
the circulatory system. raise and maintain blood pressure.
21.2 The initial treatment of shock includes basic life 21.5 Inotropic drugs are useful in reversing the decreased
184 Chapter 13 Drugs for Seizures support and identification of the underlying cause. cardiac output that occurs during shock.
21.3 Intravenous (IV) infusions are given to replace fluids 21.6 Anaphylaxis is a type of shock caused by a hyper-
lost during shock. response of body defense mechanisms.
Special Epileptic Syndromes DRUg SNaPShOT

The Drug
Special Snapshot
epileptic provides
seizures include an at-a-glance
the febrile seizures list
of infancy, reflex of and other forms of myo-
epilepsies, The following drugs are discussed in this chapter:
theclonic
drugepilepsies. Myoclonic epilepsies often go along with other neurologic abnormalities or progressively
classes
debilitating symptoms.
and related drug prototypes covered DRUg ClaSSES
Fluid replacement
DRUg PROTOTyPES
normal serum albumin (Albuminar,
drugs Plasbumin, others) 323
febrile = fever in each chapter.
Febrile seizures typically cause tonic-clonic motor activity lasting for one to two minutes, with rapid Vasoconstrictors norepinephrine (Levophed) 326
return of consciousness. These occur together with a rapid rise in body temperature and usually occur only Inotropic drugs dopamine (Dopastat, Intropin) 326
once during any given illness. Febrile seizures are most likely to occur within the three-month to five-year- Drug for anaphylaxis epinephrine (Adrenalin) 327
old age group. 352 Chapter 23 Drugs for Coagulation Disorders
myo = muscle Myoclonic seizures are characterized by large, jerking body movements. Major muscle groups con- lEaRNINg OUTCOmES
clonic = repetitive jerking tract quickly, and patients appear unsteady and clumsy. They may fall from a sitting position or drop After reading this chapter, the student should be able to:
To avoid serious adverse effects, drug therapy with coagulation modifier drugs is individualized to
motions whatever they are holding. Infantile spasms are an example of a type of generalized, myoclonic seizure and 1. Compare and contrast the different 4. Compare
each patient and mustand be contrast
carefullythe use
monitored. For 6. For each
heparin, theofactivated
the classes in the Drug
partial thromboplastin time
types of shock. (apTT) testof is blood products,
used to monitorcolloids, andof anticoagulation.
the extent Snapshot, identifyvalues
Baseline representative
of aPTT range from 25 to
are distinguished by short-lasting muscle spasms in the trunk and extremities. Such spasms are often not 2. Relate the symptoms of shock to
their physiologic causes.
crystalloids in the pharmacotherapy
40 seconds. of
During
shock.
drugs and explain their mechanisms
heparin therapy, the aPTT is maintained
of
at 1.5
drug
to 2 primary
action,
times theactions,
baseline level. If the aPTT
and
rises above 80 seconds, the heparin dosage should be reduced. During the first few days of heparin therapy,
identified as seizures by parents or healthcare providers because the movements are much like the normal 3. Explain the initial treatment of aPTT
a 5. Identify the indications for the use of
is measured every fourand
to six hours to
important adverse
avoid abnormal bleeding.
effects.
vasoconstrictors inotropic drugs.
infantile startle reflex. patient with shock.
Oral anticoagulants
status = state of status epilepticus is a medical emergency caused by the repeated occurrence of seizures. This state kEy TERmS The most frequently prescribed oral anticoagulant is warfarin (Coumadin). Often, patients begin anticoagu-
epilepticus = seizure activity could result with any type of seizure, but usually generalized tonic-clonic seizures are observed. When
Key Terms anaphylactic (ann-ah-fuh-Lak-tick) lation therapy with heparin 323
and are switched to warfarin whendrug
their(eye-noh-trow-pik)
condition stabilizes.
325When transition-
with page
generalized tonic-clonic seizuresnumbers help students
are long and continuous, hypoxia may develop. Continuous muscle con-
shock 320
antigen (ann-tuh-jen) 326
colloids
ing, the two
(ko-loyds)
drugs are(kris-tuh-loyds)
crystalloids
of therapyhypovolemic
administered concurrently
before it achieves
323
inotropic
for two to threeshock
neurogenic
optimum anticoagulationseptic
effects.
days(nyoor-oh-Jen-ik)
because warfarin320
takes several days
shock (high-poh- shock (sep-tik) 320
hypo = lowered
glycemia = blood sugar level
review
tractionsimportant vocabulary
also lead to hypoglycemia, terms.
acidosis, and hypothermia (due to increased metabolic needs, lactic cardiogenic shock (kar-dee-oh-Jen-ik) 320Warfarin inhibits two
voh-Leem-ik) 320 enzymes involved in the shock
formation
320 of activated vitamin K, which is required
for the synthesis of several clotting factor. Warfarin inhibits the synthesis of new clotting factors but does
acid production, and heat loss during muscle movement). Carbon dioxide retention also leads to acidosis. not affect clotting factors that are already circulating in the blood. The result is slowed clot formation and
thermia = body temperature If not treated, status epilepticus can cause brain damage, and ultimately, death. Medical treatment involves increased bleeding time.
Oral alternatives to warfarin include pentoxifylline, rivaroxaban, and apixaban. Although not a true
acid = hydrogen ion the IV administration of antiseizure medications. During seizure activity, steps must be taken to make sure anticoagulant, pentoxifylline (Trental) reduces the viscosity of red blood cells and increases their flex-
ibility. It is given to increase the microcirculation in patients with intermittent claudication. In 2011,
accumulation (reduced pH; that the airway remains open. Life Span Fact rivaroxaban (Xarelto) became the first anticoagulant available by the oral route to directly inhibit Factor
e.g., lactic acid) Bleeding complications are X in the clotting cascade. Rivaroxaban is indicated for the prophylaxis of DVT in patients undergoing
osis = condition of
Concept Review 13.1
more likely to occur in older
adults. Prescribed doses of
anticoagulants are generally
Concept Reviews are questions placed
knee or hip replacement surgery and to reduce the risk of stroke and systemic embolism in patients with
atrial fibrillation. In 2013, apixaban (Eliquis) was approved as an oral medication to reduce the incidence
of stroke and pulmonary embolism in patients with atrial fibrillation. Patients with artial fibrillation are at
■ What is epilepsy? What is the difference between a seizure and a convulsion? Name and
lower for older patients, and
this group receives more fre-
quent assessments and labora-
strategically throughout the chapter to
increased risk for thrombus formation.
The laboratory test used during therapy with the oral anticoagulants is prothrombin time (pT).
identify signs of the more common types of seizures. tory testing to avoid serious
complications. stimulate student comprehension and
Although the normal range for PT is 12 to 15 seconds, this value becomes prolonged with anticoagu-
lant treatment. Daily PT tests may be conducted at the start of pharmacotherapy to ensure optimum
dose levels. The frequency of PT tests is decreased to weekly or monthly as therapy progresses and
retention as they read.
the patient’s condition stabilizes. Because the method of performing PT tests varies from labora-
tory to laboratory, clotting time is sometimes reported as an international normalized ratio (inr),
effective seizure management involves strict adherence to safe drug which is the PT multiplied by a correction factor. Recommended post-treatment INR values range
from 2 to 4.
CORE CONCEPT 13.4 therapy.
The choice of drug for antiseizure pharmacotherapy depends on the patient’s signs, previous medical his-
tory, and associated pathologies. Once a medication is selected, the patient is placed on a low initial dose.
Drug Prototype: Heparin
Prototype Approach
The amount is gradually increased until seizure control is achieved or until drug adverse effects prevent
additional increases in dose. Serum drug levels may be obtained to assist the healthcare provider in deter-
Therapeutic Class: anticoagulant Pharmacologic Class: Indirect thrombin inhibitor
actions and Uses: Heparin is a natural substance found in The patient may experience serious and even life-threatening
mining the most effective drug concentration. If seizure activity continues, a different medication is added
The prototype approachwhile the introduces theisone orreduced.
two most Becauserepresentative
the lining of blood vessels. Its normal function is to prevent thrombosis. Although the half-life of heparin is short, it may
excessive clotting within blood vessels. When given as a drug, take a week after the drug is discontinued for platelets to
in small-dose increments dose of the first drug slowly seizures are likely to heparin provides immediate anticoagulant activity. The binding completely recover.
drugs
occur ifin each classification
antiseizure in detail.
drugs are abruptly withdrawn, Drug Prototype
the medication boxesover
is usually discontinued highlight
a period of of heparin to a substance called antithrombin III results in an
inactivation of some of the clotting factors and an inhibition
Oral anticoagulants, including warfarin, increase the action
of heparin. Ibuprofen, ASA, and other drugs that inhibit platelet
6 to 12 weeks. of thrombin activity. Heparin must be given either subcutane- aggregation may induce bleeding. Nicotine, digoxin, tetracy-
theseAntiseizure
important drugsdrugs. Thisare
with indications edition
shown inincludes
Table 13.1 ◆.both Some of therapeutic
the antiseizure drugsandoffer ad- ishourimmediate,
ously or through IV infusion. The onset of action for IV heparin
whereas subcutaneous heparin may take up to an
for maximum therapeutic effect.
clines, or antihistamines may inhibit anticoagulation. Herbal
supplements that may affect coagulation, such as ginger, garlic,
green tea, feverfew, or ginkgo, should be avoided because they
vantages over others. Owing to the limited induction of drug-metabolizing enzymes, the pharmacokinetic
pharmacologic drug classifications.
profiles of the more recently approved antiseizure drugs seem to be less complicated. In addition, the more
adverse effects and interactions: Abnormal bleeding is
common during heparin therapy. If aPTT becomes prolonged
may increase the risk of bleeding.
or toxicity is observed, stopping the heparin infusion will result

recently approved antiseizure drugs are generally better tolerated. in loss of anticoagulant activity within hours. If serious BLaCk Box warninG:
hemorrhage occurs, a specific blocker, protamine sulfate,
One issue of antiseizure drug therapy relates to recent warnings issued by the Food and Drug Ad- may be administered to neutralize the anticoagulant activity
Epidural or spinal hematomas may occur when heparin or
LMWHs are used in patients receiving spinal anesthesia or
The new Black
ministration
192 Chapter 13 DrugsBox
(FDA). In for
2008, Warning
the FDA analyzed
Seizures element
reports from identifies extremely
clinical studies involving patients taking a of heparin. Protamine sulfate has
and is also a blocker of the LMWHs.
an onset time of five minutes lumbar puncture. Because these can result in long-term or
permanent paralysis, frequent monitoring for neurologic
neur(o) = nerve variety of antiseizure medications. Epilepsy, bipolar disorder, psychoses, migraines, and neuropathic pain Heparin-induced thrombocytopenia (HIT) is a serious com-
adverse drug reactions studied associated with use of a emerging
particular
impairment is essential.
plication that occurs in up to 30% of patients taking the drug.
path = disease were among the disorders mainly because these were conditions as disorders successfully
drug.
treated with antiseizure-type medications. Currently all of these disorders are successfully
medications. Based on pharmacologic mechanisms, which of the drug examples do not treated with
antiseizure medications as covered in Unitfit2.into
conveniently Although
only oneantiseizure medications
drug class? Which of were
theoriginally
drugs controldesigneda wide range
to help people who have epilepsy, of seizure thetypes?
nerve-calming
Which ofqualities
the drugs ofhave
thesetherapeutic
drugs have applications
helped patients otherwith
than seizure
management?
migraines and nerve pain (neuralgia). Indeed, the usefulness of antiseizure drugs has extended beyond
pain management and actually helped calm patients with behavioral and mood disturbances: attention-
deficit hyperactivity disorder (ADHD), borderline personality disorder, and post-traumatic stress disorder
(PTSD). Antiseizure drugs have even helped patients with schizophrenia. In a warning issued by the FDA,
TaBlE 13.4 succinimides
however, healthcare providers have been admonished to balance carefully the clinical need for antiseizure
Drug
drugs against the risk for Route and adult Dose
suicidality among patientsRemarks taking these drugs. Patients and caregivers are encour-
Drug tables provide the most important
aged to pay close
ethosuximide PO; 250
attention
(Zarontin) tomg bid, increased
changes in moodeveryandFornot
absence seizures,
to make myoclonic
changes seizures, and akinetic
in antiseizure regimen epilepsy; may cause
without information for each drug in a user-friendly
4–7 days (max:
consulting with their healthcare 1.5 g/day)
provider. nausea, anorexia, abdominal pain, vomiting, gum overgrowth, blood disorders,
behavioral changes, rash (Stevens–Johnson syndrome)
Additional drawbacks include the fact that AED use may impact early child development. In 2013, a format. Drugs profiled within that chapter
methsuximide (Celontin)whose
study of children PO;mothers
300 mg/day,
every 4–7
tookmay
daysnot
(max:
AEDs while For
increase
1.2 g/day
absence indicated
pregnant
in mixed
seizures; may
types of
anbeincreased
used in combination
seizure activity;
with other
risk of early
may causewhose
dizziness,
anticonvulsants
develop-
drowsiness,
are also identified with a Prototype icon .
ment issues. These children were able to interact socially compared to children mothers didblurred
in divided doses) vision, increased risk for suicidal thoughts, fetal toxicity
not take AEDs. Language and motor skills of the children were also impacted. Some children developed
Drug Prototype: Ethosuximide (Zarontin)

Therapeutic Class: antiseizure drug Pharmacologic Class: Succinimide, low-threshold calcium channel
blocking drug
actions and Uses: Ethosuximide is a drug of choice for absence of psychiatric illness. CNS effects include dizziness, headache,
(petit mal) seizures. It depresses the activity of neurons in the lethargy, fatigue, ataxia, sleep pattern disturbances, attention
motor cortex by elevating the neuronal threshold. It is usually difficulty, and hiccups. Bone marrow suppression and blood
ineffective against psychomotor or tonic-clonic seizures; how- dyscrasias are possible, as is systemic lupus erythematosus.
ever, it may be given in combination with other medications Other reactions include gingival hypertrophy and tongue
that better treat these conditions. It is available in tablet and swelling. Common adverse effects are abdominal distress and
flavored syrup formulations. weight loss.
Drug interactions include ethosuximide, which increases
Preface ix
Highlights key Information for safe, Effective Nursing Care

Core Concept 11.5 153
NURSING PROCESS FOCUS patients receiving atypical antipsychotic therapy

aSSESSmENT POTENTIal NURSINg DIagNOSES
Prior to administration: ■ Risk for Injury related to adverse effects of drug therapy, and thought
■ Obtain a complete health history including cardiovascular, renal and liver processes
Nursing Process Focus charts provide a succinct,

conditions, allergies, drug history, and possible drug interactions. ■ Ineffective Therapeutic Regimen Management related to
■ Acquire baseline vital signs and ECG, laboratory blood levels (CBC, noncompliance with medication regimen, presence of adverse effects,
chemistry, drug screening, renal and liver function studies) and urine and need for long-term medication use
specimens for laboratory analysis.
easy-to-read view of the most important nursing
■ Anxiety related to symptoms of psychosis
■ Determine neurological status. (altered thought processes, hallucina- ■ Noncompliance related to length of time before drug reaches
tions, level of consciousness [LOC], mental status, and identification of therapeutic levels, desire to use alcohol or illegal drugs
recent mood and behavior patterns).
actions for the commonly prescribed drug classes.
■ Deficient Knowledge related to a lack of information about disease
■ Identify patient support system(s). process and drug therapy
PlaNNINg: PaTIENT gOalS aND EXPECTED OUTCOmES

The patient will:
■ Experience therapeutic effects (reduction of psychotic symptoms).
Need-to-know nursing actions are presented in the
■ Be free from or experience minimal adverse effects from drug therapy.
■ Verbalize an understanding of the drug’s use, adverse effects and required precautions. charts; they also include patient education
■ Adhere to recommended treatment regimen.
Core Concept 9.9 1 1 9
ImPlEmENTaTION and discharge planning.
Interventions and (Rationales) Patient Education/Discharge Planning
■ Administer medication correctly and evaluate the patient’s knowledge Instruct the patient:
Although structurally unrelated to other drugs
of proper administration. (Ensuring proper administration helps ■ Not used toany
to take treat
otherinsomnia,
medication or eszopiclone (Lunesta)
herbal therapies unless approved has prop-
erties similar to those of zolpidem (Ambien). Eszopiclone’s
to avoid unnecessary adverse effects and interactions with other
medications while determining effectiveness.)
longer elimination half-life, about twice as
by the healthcare provider.
■ That it may take up to six weeks for full therapeutic effects to be seen.
■
long as that of zolpidem, may give it an advantage
Monitor RBC and WBC counts. (Agranulocytosis [WBCs below 3,500]
in maintaining sleep and decreasing early-morning
Instruct the patient to:
awakening.
can Eeszopiclone
be a life-threatening adverse effect ofisthese
more likely which
medications, to cause■ daytime sedation.
Keep appointments for laboratory testing.
may also suppress bone marrow and lower infection-fighting ability.) ■ Report any sore throat, signs of infection, fatigue without apparent
Zaleplon (Sonata) may be useful for people who desire to fall asleep but need to awake early in the
cause, or bruising to the healthcare provider.
■ morning. It is sometimes used for travel purposes
Observe for adverse effects. (These drugs may affect blood pressure, ■ Instruct the patient to advertised
and has been by pharmaceutical companies
report any adverse effects such as drowsiness,
forrate,
heart thisandpurpose.
other autonomic functions.) dizziness, depression, anxiety, tachycardia, hypotension, nausea/
vomiting, excessive salivation, changes in urinary frequency or ur-
Ramelteon is a melatonin receptor drug, whichgency, hasincontinence,
been shown weightto speed
gain, musclethe
painonset of sleep.
or weakness, It has a rel-
rash, and
atively short onset of action (30 minutes), and its duration is comparable
fever to the healthcare provider. to the noncontrolled release form
■ of zolpidem.
Monitor The adverse
for anticholinergic FDAeffects.indications for remelteon
(These medications may or zolpidem
Instruct are
the patient to: not limited to short-term use because they
cause mouth dryness, constipation, or urinary retention.) ■ Increase dietary fiber, fluids, and exercise to prevent constipation.
do not appear to produce dependence or tolerance to dose.
■ Relieve symptoms of dry mouth with sugar-free hard candy or chew-
Drugs included in Table 9.5 without dosing information are diphenhydramine
ing gum and frequent drinks of water.
(Nytol and
■ Immediately notify the healthcare provider if urinary retention occurs.
Sominex)
and doxylamine (Unisom). These are OTC sleepPossible aids.catheter
Antihistamines
placement may be also produce drowsiness and are
necessary.
■ beneficial
Monitor in calming
for therapeutic patients.
effects, e.g., decrease of They
psychoticoffer the advantage
symptoms. of not
Instruct the patient to: causing dependence, although their use is
(Decreased symptoms indicate an effective dose and type of ■ Notice increases or decreases of symptoms of psychosis, including
often limited by anticholinergic adverse effects. Diphenhydramine
medication.) is apatterns,
hallucinations, abnormal sleep common component
social withdrawal, of antihista-
delusions,
mine combinations available OTC for allergic rhinitis and cough and for allergic reactions in general (see
or paranoia.
■ Contact the healthcare provider if symptoms do not decrease194 over a Chapter 13 Drugs for Seizures
Chapter 25). six-week period.
■ Monitor for alcohol or illegal drug use. (Used concurrently, these will ■ Instruct the patient to avoid alcohol or illegal drug use. Refer the
cause increased CNS depression. The patient may decide to use alcohol patient to AA, NA, or other support group as appropriate.
Concept Review 9.5
or illegal drugs as a means of coping with symptoms of psychosis and
may stop taking the drug.)
■ Monitor caffeine use. (Use of caffeine-containing substances inhibits
Instruct the patient about:
PaTIENTS NEED TO kNOw
■ What are the major drug classes used to
the effects of antipsychotics.) ■ treat GAD, panic disorder, and anxiety symptoms
Common caffeine-containing products.
caused by fearful, recurrent, and traumatic life events?
■ Acceptable substitutes, including decaffeinated coffee and tea, and
Patients taking antiseizure medications need to know the following:
caffeine-free soda.
■ Name popular drugs used to treat symptoms of anxiety and insomnia. In general
■ Monitor for smoking. (Heavy smoking may decrease blood levels of the ■ Instruct the patient to stop or decrease smoking. Refer to smoking
drug.) cessation programs if indicated. 1. Never abruptly stop taking antiseizure medication; doing so can cause seizures to return.
Core Concept 13.3 18 3
2. Avoid alcohol and other CNS depressants because they can increase sedation.
■ Monitor older adult patients closely. (Older patients may be more ■ Instruct older adult patients on ways to counteract anticholinergic
sensitive to anticholinergic adverse effects.) effects of the medication while taking into account any other existing
medical problems. 3. Antiseizure medications may cause drowsiness; avoid driving and the use of machinery
EvalUaTION OF OUTCOmE CRITERIa that could lead to injury.
PaTIENTS NEED TO kNOw
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Table 11.4 for 4. It may require several dosage adjustments over many months to find the dosage that
a list of drugs to which these nursing actions apply. allows performance of normal daily activities while controlling seizures.
Patients taking anxiolytics and CNS depressants need to know the following:
5. It is important to keep laboratory appointments because many antiseizure medications
1. Stimulants such as coffee, tea, and chocolate should be avoided because they coun-
pre-eclampsia and eclampsia are and
teract anxiolytics severe hypertensive
sedatives disorders
and increase the symptoms of pregnancy, characterized by sei-
of anxiety.
require blood testing to ensure that the drug is at a safe and effective level in the blood.
6. Consult a healthcare provider before trying to become pregnant; some antiseizure
zures, coma, and perinatal mortality. Eclampsia is likely to occur from around the 20th week of gestation
2. Exercise, progressive muscle relaxation, and slow, deep breathing can assist with anx-
iety relief.
to are not safe to use during pregnancy.
medications
7. Report excess fatigue, drowsiness, agitation, confusion, or suicidal thoughts to a health-
at least one week following3.delivery of the
Alcohol, antihistamines, baby. Roughly
and other one-fourth
CNS depressants can increaseof
thepatients with
effects of anxio-
lytics. They should be avoided to decrease the risk of accidental depressant overdose
eclampsia experience
care provider.
seizures within 72 hours postpartum.

and death. Regarding hydantoins post =and after
Related medications
4. Anxiolytics can cause drowsiness. Until effects of these drugs have been established, partum adverse = delivery
Seizures can have a significant
The nursing student
assistance impact
with needs
getting onofthe
out to quality
bedlearn
and drivinghow of
maylife.
to They
teach
be needed and may
drug cause
operation of serious injury if8. they
Report the following effects to a healthcare provider: gum overgrowth (gingival
hyperplasia) or skin rash, tremors, weight gain, diarrhea, irregular menses, dizziness,
machinery should be avoided.
occur when a person is driving
administration a vehicle
5. Anxiolytics to
or
and patients
performing
and
sedatives should
a dangerous
families.
be stored
activity.
To tohelp
in a secure place
Without
the inges-
avoid accidental
successful pharmaco-nausea, or oversedation.
9. Hydantoins and related medications interact with many other drugs; do not add any other
therapy, epilepsy can severely tionlimit participation
by children and animals. in school, employment, or social activities and can affect prescription, over-the-counter (OTC) drugs, or herbal supplements until a healthcare
student,6. each drug
Avoid abrupt chapter contains
discontinuation concise
of medication because Patients
withdrawal symptoms may provider is consulted. Do not consume alcohol while taking these medications.
self-esteem. Chronic depression may
occur after accompany
long-term use. poorly controlled seizures. Important considerations in Succinimides
Need to
7. Know
health care include identifying boxes
Report any significant
patients that
changes
atmedications help
in moodstudents
risk forwithout to the healthcare
seizures, teach patients
provider.
documenting
Regarding
8. Do not take any OTC first consulting the healthcare the pattern and type of seizure
provider. 10. Report the following adverse effects to a healthcare provider: hiccups or epigastric pain
and families
activity, and implementing 9. safety
Smoking about drug
precautions.
and nicotine information
dependence are increasedand
In collaboration administration.
with
in patients withthe patient,
anxiety disorders.the healthcare provider,
with ethosuximide (Zarontin), drowsiness, or increased bleeding time.
Thus, it is believed that smoking and pharmacotherapy for anxiety-related disorders
pharmacist, and all healthcarearestaffcounterare instrumental
effective. Quitting smoking incanachieving
reduce anxiety.positive therapeutic outcomes. Through
a combination of pharmacotherapy, patient–family support, and education, effective seizure control can be
achieved in the majority of patients. ChaPTER REvIEw
Safety Alerts highlight potential
SaFETy alERT
epileptic seizures are typically identified as partial, generalized, medication errors and The Joint Commission
or special
Interpreting Physician Orders CORE CONCEPTS SUmmaRy
epileptic syndromes.
It is extremely important for nurses to know their patients’ needs and to clarify with the Safety Guidelines.
CORE CONCEPT 13.3
physician any medication order that is difficult to interpret or is questionable. For exam-
ple, an error could be made if an order to discontinue “SSRI,” intended to mean13.1 “sliding although some types of seizures involve convul- 13.3 epileptic seizures are typically identified as partial,
scale regular insulin,” is misinterpreted as an order to discontinue the “selective serotonin sions, other seizures do not. generalized, or special epileptic syndromes.
reuptake inhibitor.”
Seizure symptoms vary depending on the areas of the brain affected by the abnormal electrical activity. Epilepsy is any disorder characterized by recurrent Epilepsies are identified using the International Clas-
These symptoms range from muscle twitching or slight tremor (shaking) of a limb to sudden, violent shak- Life Span Fact seizures. Seizures are abnormal and uncontrolled neu-
ronal brain discharges. Convulsions are uncontrolled
sification of Epileptic Seizures nomenclature, as partial
(focal), generalized, or special epileptic syndromes.
ing and total loss of consciousness. Staring into space, altered vision, and difficult speech are other behav- muscle contractions that accompany some major sei-
zures. Drugs used to treat epilepsy are oftenOnset
Partial seizures are further described as simple or com-
referredof epilepsy isseizures.
plex most Generalized
com- seizures are described as ab-
iors a person may exhibit during a seizure. It is important to determine the cause of recurrent seizures in to as antiseizure drugs or antiepileptic drugsmon
(AEDs),
among thesence seizures, atonic
youngest and seizures, or tonic-clonic seizures.
rather than anticonvulsants. Special epileptic syndromes include febrile seizures,
order to plan for appropriate treatment options. oldest age groups. About
myoclonic 50%and status epilepticus.
seizures,
Methods of classifying epilepsy have changed over time. For example, the13.2 termsmanygrand
causes mal andactivity
of seizure petitare known;of achildren
few have a generalized
Life replaced
mal epilepsy have been Span Facts provide
by more important
descriptive pediatric
and detailed and
categorization.
are not.
Epilepsies are typically
A seizure is considered a symptom of epilepsy rather
13.4 effective seizure management involves strict ad-
epilepsy syndrome compared
herence to safe drug therapy.
identified using theolder adult considerations

International Classification of for drug therapy,
Epileptic Seizures.so
Example nomenclatures are
than a disorder itself. In partial with
some cases, the exact about 20%The
cause of choice
adults. The for epilepsy pharmacotherapy
of drug
of seizures is not known; however, there are incidence
many of epilepsy
dependsinon older
the type of seizures the patient is experi-
students understand variations in nursing care and
(less used term focal), generalized, and special epileptic syndromes. Types of partial or generalized sei-
known causes. Seizures are the most common neu- encing, the patient’s previous medical history, diag-
rologic problem. Through a combination ofadults
pharma- is greaternostic
thanstudies,
among and the pathologic processes causing
zures may be recognized based ondue
drug actions symptoms
to age. observed during a seizure episode. Some symptoms are hard the general population,
cotherapy, patient–family support, and education, the seizures.per-
In most cases, a single drug can effec-
to notice and reflect the simple nature of neuronal misfiring in specific areas of the brain;
patients.
otherscontrol
effective seizure are can
morebe achievedhaps because of tively
by most the control
greater seizures. In some patients, two antisei-
zure medications may be necessary. When discussing
complex. prevalence of mild strokes
and cardiac arrest in this age
group.
Partial Seizures
partial (focal) seizures involve a limited portion of the brain. Abnormal electrical activity starts on one
side and travels only a short distance before it stops. The area where the abnormal electrical activity starts
is known as the abnormal focus (plural, foci).
Simple partial seizures have an onset from a small, limited focus. Patients may feel disoriented for a
while, and they may hear and see things that are not there. Some patients smell and taste things that are not
present, or have an upset stomach. Others may become emotional and experience a sense of joy, sorrow, or
grief. The arms, legs, or face may twitch.
Complex partial seizures (formerly known as psychomotor or temporal lobe seizures) have sensory, psycho = mind
motor, or autonomic symptoms with some degree of altered or impaired consciousness. Total loss of con- motor = motion or movement
sciousness may not occur during a complex partial seizure, but a period of brief confusion and somnolence
Drug Prototype: Diazepam (Valium)
Therapeutic Class: antiseizure drug, sedative-hypnotic, anxiolytic, anesthetic adjunct, skeletal muscle
relaxant (centrally acting) Pharmacologic Class: Benzodiazepine, gaB receptor drug
actions and Uses: Diazepam binds to GABA receptors located combined sedation effects. Other drug interactions include
throughout the CNS. It produces its effects by suppressing neu- cimetidine, oral contraceptives, valproic acid, and metopro-
ronal activity in the limbic system and subsequent impulses that lol, which potentiate diazepam’s action, and levodopa and
might be transmitted to the reticular activating system. Effects barbiturates, which decrease diazepam’s action. Diazepam
of this drug are suppression of abnormal neuronal foci that may increases the levels of phenytoin in the bloodstream and may
cause seizures, calming without strong sedation, and skeletal cause phenytoin toxicity. When given IV, hypotension, mus-
muscle relaxation. When used orally, maximum therapeutic ef- cular weakness, tachycardia, and respiratory depression are
fects may take from one to two weeks. Tolerance may develop common. Because of tolerance and dependency, use of diaz-
after about four weeks. When given IV, effects occur within min- epam is reserved for short-term seizure control or for status
utes, and its anticonvulsant effects last for about 20 minutes. epilepticus.
Diazepam should be used with caution with herbal supple-
adverse effects and interactions: Diazepam should not be ments, such as kava and chamomile, which may cause an in-
x Preface
taken with alcohol or other CNS depressants because of creased effect.
Cam ThERaPy
The ketogenic Diet for Epilepsy
The ketogenic diet may be used when seizures cannot be controlled through pharmaco- CAM (Complementary and Alternative
therapy or when there are unacceptable adverse effects to medications. Before antiepileptic
drugs were developed, this diet was a primary treatment for epilepsy. Medicine) Therapy boxes present popular
The ketogenic diet is a strict diet that is high in fat and low in carbohydrates and protein. It
limits water intake and carefully controls caloric intake. Each meal has the same ketogenic ratio herbal or dietary supplements that may be
of 4 g of fat to 1 g of protein and carbohydrate. Extra fat is usually given in the form of cream.
Research suggests that the diet produces a high success rate for certain patients. The diet considered along with conventional drugs.
appears to be equally effective for every seizure type. The most frequently reported adverse
effects include vomiting, fatigue, constipation, diarrhea, and hunger. Kidney stones, acidosis,
and slower growth rates are possible risks. Those interested in trying the diet must consult
with their healthcare provider; this is not a do-it-yourself diet and may be harmful if not
monitored carefully by skilled professionals. 182 Chapter 13 Drugs for Seizures
Fast Facts epilepsy

■ Over two million Americans have epilepsy.
■ One of every 100 teenagers has epilepsy.
The Fast Facts feature puts the disease ■ Of the U.S. population, 10% will have seizures within their lifetime.
Most people with seizures are younger than 45 years of age.
in a social and economic perspective.
■
■ Epilepsy is not a mental illness and children with epilepsy have IQ scores equivalent to those of
children without the disorder.
■ Famous people who had epilepsy include Julius Caesar, Alexander the Great, Napoleon, Vincent
van Gogh, Charles Dickens, Joan of Arc, and Socrates.
■ Among adult alcoholics receiving treatment for withdrawal, over half will experience seizures
within six hours upon arriving for treatment.
Drugs described in this chapter are generally referred to as antiseizure drugs rather than
anticonvulsants. Recognizing also that antiseizure drugs are commonly called antiepileptic drugs (AEDs),
the term antiseizure in this chapter applies to the treatment of all seizure-related symptoms, including signs
of epilepsy.
End-of-Chapter Review Resources CORE CONCEPT 13.2 many causes of seizure activity are known; a few are not.
A seizure is considered symptomatic of an underlying disorder, rather than a disease in itself. Triggers
include exposure to strobe or flickering lights or the occurrence of small fluid and electrolyte imbalances.
Patients appear to have a lower tolerance to environmental triggers, and seizures often occur when patients
are sleep deprived.
Student practical and vocational nurses from around the country told us that they start their chapter There are many different causes of seizure activity. In some cases, the cause of seizure activity may
be clear, but not in all situations. Seizures represent the most common serious neurologic problem affecting
reading from the end of the chapter. So, to ensure students’
idio =
pathic =
success in the classroom, on the NCLEX- one’s unknown arising
abnormal state
children, with an overall incidence approaching 2% for febrile seizures and 1% for idiopathic epilepsy.
Certain medications for mood disorders, psychoses, and local anesthesia may cause seizures when given
®
PN exam, and in the workplace, we put dynamite review resources at the end of each chapter. in high doses, possibly because of increased levels of stimulatory neurotransmitters or toxicity. Seizures
may also occur from drug abuse, as with cocaine, or during withdrawal from alcohol or sedative–hypnotic
Chapter Review 17 7
drugs.
Seizures may present as an acute situation, or they may occur on a chronic basis. Seizures resulting
ChaPTER REvIEw from an acute complication are generally not recurrent after the situation has been resolved. On the other
hand, if a brain abnormality exists following an acute complication, recurrent seizures are likely. The fol-
CORE CONCEPTS SUmmaRy
Core Concepts Summaries repeat the
lowing are known causes of seizures:
12.1 medications are unable to cure most degenerative

diseases of the Cns.
178
acetylcholine levels increase and produce a greater ef-
fect on the receptor. This treatment improves function
Chapter
■
important points at the end of the chapter
Infectious diseases Acute infections such as meningitis and encephalitis can cause inflamma-
tion in the brain.
in 12 Drugsoffor Degenerative Diseases and Muscles
and provide a asbrief summary.

Degenerative diseases of the CNS include Alzheimer’s activities daily living, behavior, and cognition.
disease, multiple sclerosis, and Parkinson’s disease.
The cause of most neurologic degenerative disorders
12.6 symptoms of multiple sclerosis result from demy- ■ Trauma Physical trauma such direct blows to the skull may increase intracranial pressure;
elination ofwith
in combination Cnsmedications
nerve fibers. that reduce pain and 12.12 some drugs for spasticity provide relief by act-
is unknown. With the exception of Parkinson’s dis-
ease, drug therapy provides only minimal benefit.
increase rangesclerosis
Multiple of motion. These
is an include centrally
autoimmune disorderact-of the ing directly on muscle tissue, interfering with the chemical trauma such as the presence of toxic substances or the ingestion of poisons may cause
ing drugs
CNS. (affecting
Antibodiesthe brain destroy
and/or spinal
myelincord) that
12.2 parkinson’s disease is progressive, with the occur- haveandthespinal
potentialcord,
slowly
to disrupting
cause sedation and alter
the ability
in the
of reflex
brain
nerves to
release of calcium ions.
Direct-acting drugs produce an antispasmodic effect
brain injury.
rence of full symptoms taking many years. activity.
conduct electrical impulses. Over time, debilitating at the level of the neuromuscular junction. Drugs af-
symptoms appear, including
Parkinson’s disease, or parkinsonism, is a degenera- 12.11 effective treatment for spasticity includes both fatigue, heat sensitivity, fect either calcium release from the muscle, or they ■ Metabolic disorders Changes in fluid and electrolytes such as hypoglycemia, hyponatremia,
pain, muscle cramps and spasms, impaired ability to interfere with the release of acetylcholine.
tive disorder caused by death of neurons that produce
the brain neurotransmitter dopamine. Dopamine-
physical
thinktherapy
and reason, andbalance
medications.
and coordination problems, and water intoxication may cause seizures by altering electrical impulse transmission at the
Spasticity
and bowel is aandcondition in which certain muscle
bladder symptoms. 12.13 neuromuscular blocking drugs block the effect of
producing neurons in the substantia nigra supply cellular level.
Review Questions serve as a post-test for the
nerve signals to the corpus striatum. When dopamine groups remain in a state of contraction. Symptoms acetylcholine at the receptor.
12.7associated
drugs for withmultiple
spasticity sclerosis
include reduce
pain, immune
exaggeratedattacks
Neuromuscular blocking drugs are classified as non-
is depleted, symptoms of parkinsonism, including
tremors, muscle rigidity, bradykinesia (slow move- deepintendon
fixed
the brain
joints.
and treat
reflexes,
Medications
muscle unfavorable
aloneMS areare
symptoms.
spasms, scissoring,
notreducing
adequatethe
and
in im-
depolarizing blockers and depolarizing blockers. Both ■ Vascular diseases Changes in oxygenation such as those caused by respiratory hypoxia and
ment), and postural instability, occur. These symp- Two strategies for treating drugs bind to acetylcholine receptors, relaxing muscles
carbon monoxide poisoning, and changes in perfusion such as those caused by hypotension,
chapter and prepare students for the NCLEX-PN®.
toms are the same EPS effects caused by prolonged reducing
munethe complications
response of spasticity.
and relieving the symptoms. The by slightly different mechanisms and durations of action.
most treatable form of MS is relapsing-remitting
antipsychotic drug treatment.
MS (RRMS), in which unpredictable relapses occur. cerebral vascular accidents, shock, and cardiac dysrhythmias may be causes.
12.3 antiparkinson drugs act on the brain to restore the Drug treatments include immune system modulating
balance between dopamine and acetylcholine.
Balance, posture, muscle tone, and involuntary mus-
REvIEwdrugs, QUESTIONS
immunosuppressants, and miscellaneous drugs
used for treatment of MS symptoms such as inflam-
■
Tests include additional practice in calculating the
Pediatric disorders Rapid increase in body temperature may result in a febrile seizure.
cle movement depend on the proper balance between The followingmation, pain, fatigue, memory loss, and progressive
questions are written in NCLEX-PN® style. An- 5. The patient with Alzheimer’s disease has been started on ■ Neoplastic disease Tumors, especially rapidly growing ones, may occupy space, increase
correct dosage.
weakness.
the neurotransmitter dopamine (inhibitory) and ace- swer these questions to assess your knowledge of the chapter rivastigmine (Exelon). The nurse will evaluate the patient for:
tylcholine (stimulatory) in the corpus striatum. Drug material, and go back and review any material that is not clear
therapy for parkinsonism focuses on restoring dopa- to you. 12.8 muscle spasms are caused by injury, overmedica- 1. Liver toxicity intracranial pressure, and damage brain tissue by disrupting blood flow.
tion, hypocalcemia, and debilitating neurologic 2. Weight loss Chapter Review 179
mine function (dopaminergic drugs) and blocking
the effect of acetylcholine overactivity (cholinergic 1. The patient disorders.
taking levodopa is taught that he must wait at 3. Renal failure An important topic when discussing epilepsy and seizure treatment is birth control. Because several
blockers). Muscle
least one hour before spasms, or involuntary
or after eating foods high in: contractions of a 4. EPS
1. Vitamin Cmuscle or group of muscles, occur for many
A patient is being seen in the emergency room after an
9. reasons,
6. A patient had a surgical procedure in which antiseizure drugs decrease the effectiveness of oral contraceptives, additional barrier methods of birth con-
10. A patient with a spinal cord injury is still suffering from
12.4 patients with alzheimer’s disease experience including overmedication with antipsychotic automobile
drugs, accident. She complains that her lower back hurts. succinylcho-
muscle spasms. The physician has prescribed dantrolene to
a dramatic loss of ability to perform tasks that
2. Carbohydrates
3. Folic acidepilepsy, hypocalcemia, pain, and After an
incapacitating neu-
line (Anectine)
examination wasthe
and x-ray, used to relax
patient the muscles.
is given a diagno- The nurse
helptak- trol should be practiced to avoid unintended pregnancy. Prior to pregnancy and considering the serious
control the spasms. The nurse informs the patient that he
ing care of this patient would monitor the patient for: should report which of the following possible adverse effect(s)
require acetylcholine as the Cns neurotransmitter. sis of muscle
are strain, with associated spasms, and is placed on
4. Protein rologic disorders. Two types of muscle cyclobenzaprine spasms
1. Hypothermia
(Flexeril) to help relax the muscles. In edu- if they should occur: nature of epilepsy, patients should consult with their healthcare provider to determine the most appropriate
Alzheimer’s disease (AD) is a devastating, progres- tonic spasms and clonic spasms.
cating 2. Complaints
wasthe patient of muscle pain the nurse informs
about the cyclobenzaprine,
sive, degenerative disease characterized by impaired 2. A patient in the early stages of Alzheimer’s disease
12.9
memory, confusion or disorientation, inability to rec- started muscle spasms
on donepezil (Aricept)may a few beweeks
treated with
ago. her that:
Shenonpharma-
calls 3. High
the (Select sodium
all that apply.)levels (hypernatremia)
1. Excessive salivation
2. Excessive urination
plan of action for seizure control.
cologic or
ognize family or friends, aggressive behavior, depres- nurse at the doctor’s pharmacologic
office and states that therapies.
she has been 1. expe-
It can cause4. drowsiness.
Low levels of potassium (hypokalemia) 3. Muscle weakness If patients become pregnant, extreme caution is necessary. Most antiseizure drugs are pregnancy cat-
sion, psychoses, and anxiety. AD is responsible for riencing what she abelieves
After thorough to be adverse
medical effects
exam, of the2. drug.
nonpharmacologic
If taken with7. alcohol,
A patientadditional
is givendrowsiness
a prescription mayforoccur. 4. Insomnia
carisoprodol (Soma),
70% of all dementia. Although the cause of AD is Which of thetherapies followingsuch effects could the patient
as immobilization, be or
heat experienc-
cold,
3. It hydro-
is only intended
350 mg, po,for short-term
three timesuse (2–3
a day. Theweeks).
pharmacy provides a bottle egory D. Some antiseizure drugs may cause folate deficiency, a condition correlated with fetal neural tube
unknown, structural brain damage and a dramatic loss ing? (Select all that apply.)
therapy, ultrasound, supervised exercises, 3. massage,
It can causeof headaches.
350 mg tablets. If the patient follows the directions, how
of ability to perform tasks that require acetycholine as 1. Sleepinessand manipulation may be used along with medica- many milligrams will the patient take in one day? defects. Vitamin supplements may be necessary.
the neurotransmitter have been documented. 2. Nausea tions. Medications include analgesics, anti-inflam- 1. 900 mg
3. Diarrhea matory drugs, and centrally acting skeletal muscle
CaSE STUDy 2. 1,115 mg QUESTIONS
12.5 alzheimer’s disease is treated with acetylcholines-
4. Tinnitus relaxants. 3. 1,050 mg
terase inhibitors.
Only a few drugs for AD have been approved. Most 3. 12.10 many musclelevodopa
When administering relaxants to atreat muscle
patient Parkin- by 4. 1,015Remember
with spasms mg
Mr. Wingate, the patient in- 2. After being started on the immune system modulator,
drugs act by intensifying the effect of acetylcholine son’s disease,inhibiting upper motor
the nurse understands thatneuron activity, causing 8. An troduced
this drug: interferonatisthe beginning
prescribed forofa the chap-
patient Mr.The
with MS. Wingate asks the nurse about this class of medications.
at the cholinergic receptor. Acetylcholine is naturally 1. Increases sedation,
cholinergic orstimulation
altering simple withinreflexes.
the brain ter? Now
nurse includes readofthe
which theremainder
followingofpoints
the case The nurse responds by saying: (Select all that apply.)
when educating
degraded in the synapse by the enzyme acetylcho- 2. Restores Skeletal muscleand
acetylcholine relaxants
blockstreat local spasms
dopamine withinresulting
the study.
the patient Based
about drugon the information you have
therapy? 1. “These drugs slow down the destruction of the neuron
linesterase. When acetylcholinesterase is inhibited, brain from muscular injury and may be prescribed alone or learned in this chapter, answer the ques-
1. Report flu-like symptoms to the healthcare provider. caused by MS.”
3. Restores dopamine function and blocks acetylcholine tions that follow
2. Expect urine to be orange. . 2. “These drugs have very few adverse effects.”
within the brain 3. Report 3. “There are no precautions when taking this type of drug
Mr.theRobert
development
Wingate, of adiarrhea.
35-year-old man
4. Destroys dopamine receptors within the brain 4. The symptoms willpersistent
get better pain
over in
a period of a year. with other drugs.”
with MS, has his right
hip and comes in for treatment. He ex- 4. “Adverse effects can include fever, chills, and muscle
4. The patient with Parkinson’s disease is placed on haloper-
idol (Haldol) because of agitation and has started experiencing plains that he has been taking enteric-coated aspirin for sev- aches.”
EPS. Which of the following drugs would the nurse anticipate eral weeks. He explains that he has been experiencing severe
3. In evaluating the effectiveness of Mr. Wingate’s
being ordered? headaches. He has also been experiencing muscle twitches antispasmodic therapy, the nurse would expect that the
1. Levodopa–carbidopa drugs (multiple, rapidly repeating contractions) in his right ham- medication would:
2. Risperidone (Risperdal) string. The muscle twitches have not been severe, but he is
concerned that they may be related to his condition. Lately, 1. Improve Mr. Wingate’s symptoms for the long term.
3. Benztropine (Cogentin) 2. Improve Mr. Wingate’s symptoms for the short term.
4. Cyclobenzaprine (Flexeril) he has been experiencing quite a bit of fatigue, and his vision
is sometimes “blurry.” Laboratory values show slight hypo- 3. Make Mr. Wingate’s symptoms worse.
calcemia. The patient explains that he hasn’t had any trouble 4. Cause Mr. Wingate to be sedated.
with his diet. No abnormalities in bone structure or peripheral 4. If Mr. Wingate’s condition and symptoms were to
inflammatory symptoms are observed on examination. progress significantly, the nurse would expect to administer
which of the following drugs?
1. The nurse caring for Mr. Wingate just received a medica-
tion order to administer an immune system modulator. Which 1. Selegiline (Eldepryl, Zelapar)
of the following medications might the nurse administer? 2. Gabapentin (Neurontin)
3. Mitoxantrone (Novantrone)
1. Amantadine (Symmetrel) 4. Donepezil (ARICEPT)
2. Interferon beta-1b (Betaseron)
3. Memantine (Namenda)
4. Gabapentin (Neurontin)
Case Study Questions NOTE: Answers to the Review and Case Study Questions appear in Appendix B. The complete rationales and answers are located on the
textbook’s website.
Pearson Nursing Student Resources Find additional review materials at nursing.pearsonhighered.com.

help the student apply
pharmacology and
nursing care to a specific
client scenario.
Acknowledgments
We are grateful to all the educators who reviewed the manuscript of this text. Their insights, sug-
gestions, and eye for detail helped us prepare a more relevant and useful book, one that focuses
on the essential components of learning in the field of pharmacology. In particular, we would
like to thank Jeanine Brice, RN, MSN, who reviewed and contributed to all nursing material
including Nursing Process Focus Charts, Safety Alerts, Patients Need to Know, and all of the
end-of-chapter questions. Your nursing experience, expertise, and dedication to the profession is
evident in these materials.
Textbook Reviewers Kevin Dahlstedt, BA, MSN, RN Marlene Lazarus, DNP

Western Nebraska Community College Camden County College
Michaelann Allen, MA Ed, CMA Alliance, NE Blackwood, NJ
North Seattle Community College
Seattle, WA David Flint, MEd, BSHS, EMT, WEMT, Jo Ann Lindemann, MSN, RN
EMT-I Dickinson State University
Kevin Barnard, MS, CCEMT-P, NREMT-P, College of Technology Dickinson, ND
EMSI Idaho State University
Cuyahoga Community College Pocatello, ID Nelda New, PhD, APN, FNP-BC, ANP-BC,
Cleveland, OH CNE
Michele Gerwick, PhD, RN University of Central Arkansas
Carole Berube, MA, MSN, BSN, RN Indiana University of Pennsylvania Conway, AR
Bristol Community College Indiana, PA
Fall River, MA Diana Rangaves, PharmD, RPh
Bonita Gregg, MS Ed, RN Santa Rosa Junior College
Ann Boeglin, MSN, RN Community College of Allegheny County Santa Rosa, CA
Vincennes University Jasper Campus West Mifflin, PA
Jasper, IN Tara Sadler, RN, BSN
Nancy Kennedy, MSN, RN South Arkansas Community College
Charlene Chapman, BSN, RN Ulster BOCES Career and Technical Center El Dorado, AR
Pennsylvania Institute of Technology Port Ewen, NY
Media, PA Lori Wahlberg, RN, MSN
Sharyn Ketcham, AAS, BS, MBA, MHSA, Anoka Technical College
Darlene Clark, MS, RN RMA Anoka, MN
Penn State University Phoenix College
University Park, PA Phoenix, AZ
xi
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About the Authors
Leland Norman Holland, Jr., PhD (Norm), over 20 years ago, started
out like many scientists, planning for a career in basic science research.
Quickly he was drawn to the field of teaching in higher medical education,
where he has spent most of his career since that time. Among the areas where
he has been particularly effective are preparatory programs in nursing, medi-
cine, dentistry, pharmacy, and allied health. Dr. Holland is both an affiliate
and a supporter of nursing education nationwide. He brings to the profession
a depth of knowledge in biology, chemistry, and medically related subjects
such as microbiology, biological chemistry, and pharmacology. Dr. Holland’s
doctoral degree is in Medical Pharmacology. He is very much dedicated to the
success of students and their preparation for work-life readiness. He contin-
ues to motivate students in the lifelong pursuit of learning.
I would like to acknowledge the willful encouragement of Farrell and
Norma Jean Stalcup. I dedicate this book to my beloved wife, Karen, and my
three wonderful children, Alexandria Noelle, my double-deuce daughter; Caleb
Jaymes, my number one son; and Joshua Nathaniel, my number three “O”!
—LNH
Michael Patrick Adams, PhD, RT(R), is an accomplished educator,

author, and national speaker. The National Institute for Staff and Organiza-
tional Development in Austin, Texas, named Dr. Adams a Master Teacher. He
has published two other textbooks with Pearson Publishing: Pharmacology
for Nurses: A Pathophysiologic Approach and Pharmacology: Connections to
Nursing Practice.
Dr. Adams obtained his master’s degree in Pharmacology from Michigan
State University and his Doctorate in Education at the University of South
Florida. Dr. Adams was on the faculty of Lansing Community College and
was Dean of Health Professions at Pasco-Hernando Community College for
over 15 years. He is currently Professor of Anatomy and Physiology at Saint
Petersburg College.
I dedicate this book to nursing educators, who contribute every day to
making the world a better and more caring place.
—MPA
Jeanine L. Brice, RN, MSN, has been a nurse for over 26 years, initially
graduating from the registered nursing program at Charles County Community
College and continuing her nursing education, receiving a BS from the Uni-
versity of Maryland and an MSN from Bowie State University, specializing
in nursing education and community health practice. Her clinical experience
includes acute medical-surgical care, obstetrics, neonatology, and pediatric
public health.
Ms. Brice has been involved in nursing/technical health education for
over 23 years, formerly holding the positions of Professor of Nursing, As-
sistant Dean of Nursing Programs, and Coordinator of Technical Health Pro-
grams at Pasco-Hernando Community College. She currently is employed at
St. Petersburg College tutoring nursing and allied health students.
I dedicate this book to my parents, William and Helen Davis, whom I had
the privilege to care for during their final days . . . and to all those who will
need the care of a nurse. May the information contained in this book help them
receive competent and compassionate nursing care.
—JLB
xiii
Contents
Unit I
Basic Concepts in Pharmacology 1
Chapter 1 Introduction to Pharmacology: Drug Regulation

and Approval 2
Preclinical Investigation 7
Clinical Investigation 7
Submission of an NDA with Review 8
Postmarketing Studies 8
Chapter 2 Drug Classes, Schedules, and Categories 12
Chapter 3 Methods of Drug Administration 20

Tablets and Capsules 27
Sublingual and Buccal Drug Administration 27
Nasogastric and Gastrostomy Drug Administration 28
Transdermal Delivery System 29
Ophthalmic Administration 29
Otic Administration 31
Nasal Administration 31
Vaginal Administration 31
Rectal Administration 32
Intradermal and Subcutaneous Administration 33
Intramuscular Administration 36
Intravenous Administration 37
Chapter 4 What Happens After a Drug Has Been Administered 41
Chapter 5 the nursing process IN PHARMACOLOGY 51
Chapter 6 The Role of Complementary and Alternative Therapies

in Pharmacology 59
Herbal Products 61
Specialty Supplements 65
Chapter 7 Substance Abuse 69

Sedatives and Sedative-Hypnotics 74
Benzodiazepines 74
Opioids 75
Ethyl Alcohol 75
xv
xvi Contents
Unit II
The Nervous System 85
Chapter 8 Drugs Affecting Functions of the Autonomic

Nervous System 86
Drug Prototype Bethanechol (Urecholine) 93
Nursing Process FOCUS Patients Receiving Direct- and Indirect-Acting
Cholinergic Drug Therapy 93
Drug Prototype Atropine (Atro-Pen) 95
Nursing Process FOCUS Patients Receiving Cholinergic Blocker
(Anticholinergic) Therapy 96
Drug Prototype Phenylephrine (Neo-Synephrine) 98
Nursing Process FOCUS Patients Receiving Adrenergic Drug Therapy 98
Drug Prototype Prazosin (Minipress) 100
Nursing Process FOCUS Patients Receiving Adrenergic Blocker Therapy 101
Chapter 9 Drugs for Anxiety and Insomnia 105

Anxiety 106
Insomnia 109
Drug Prototype Escitalopram (Lexapro) 113
Nursing Process FOCUS Patients Receiving Antianxiety Therapy 115
Drug Prototype Lorazepam (Ativan) 116
Drug Prototype Zolpidem (Ambien, Edluar, Others) 118
Chapter 10 Drugs for Emotional, Mood, and Behavioral

Disorders 122
Depression 123
Tricyclic Antidepressants 125
Selective Serotonin Reuptake Inhibitors 128
Atypical Antidepressants 129
Drug Prototype Imipramine (Tofranil) 129
Nursing Process FOCUS Patients Receiving Antidepressant Therapy 130
Monoamine Oxidase Inhibitors 132
Drug Prototype Sertraline (Zoloft) 133
Drug Prototype Phenelzine (Nardil) 133
Bipolar Disorder 133
Attention Deficit Hyperactivity Disorder 136
CNS Stimulants 137
Non-CNS Stimulants 137
Drug Prototype Methylphenidate (Ritalin) 137

Schizophrenia 143
Conventional (First Generation) Antipsychotics 146
Drug Prototype Chlorpromazine 147
Phenothiazines and Phenothiazine-Like Drugs 147
Contents xvii
Nonphenothiazine Drugs 148

Drug Prototype Haloperidol (Haldol) 149
Nursing Process FOCUS Patients Receiving Phenothiazines and
Nonphenothiazine Therapy 149
Atypical (Second Generation) Antipsychotics 151
Drug Prototype Risperidone (Risperdal) 152
Nursing Process FOCUS Patients Receiving Atypical Antipsychotic
Therapy 153
Dopamine System Stabilizers (Third-Generation Antipsychotics) 154
Chapter 12 Drugs for Degenerative Diseases and Muscles 157

Parkinson’s Disease 159
Dopaminergic Drugs 160
Drug Prototype Levodopa, Carbidopa, and Entacapone (Stalevo) 163
Cholinergic Blockers (Anticholinergics) 163
Drug Prototype Benztropine (Cogentin) 164
Alzheimer’s Disease 164
Acetylcholinesterase Inhibitors 165
Other Drugs That Slow Progression of AD 165
Drugs That Treat Behavioral Symptoms of AD 166
Drug Prototype Donepezil (Aricept) 167
Multiple Sclerosis 167
Muscle Spasms 169
Drug Prototype Cyclobenzaprine (Amrix, Flexeril) 171
Spasticity 171
Nursing Process FOCUS Patients Receiving Drugs for Muscle Spasms
or Spasticity 172
Drug Prototype Dantrolene (Dantrium) 175

Seizures 181
Partial Seizures 183
Generalized Seizures 183
Special Epileptic Syndromes 184
Drug Prototype Phenobarbital (Luminal) 188
Drug Prototype Diazepam (Valium) 188
Drug Prototype Phenytoin (Dilantin) 190
Drug Prototype Valproic Acid (Depakene, Depakote) 191
Drug Prototype Ethosuximide (Zarontin) 192
Nursing Process FOCUS Patients Receiving Antiseizure Drug Therapy 192

Acute or Chronic Pain 198
Opioid Analgesics for Severe Pain 203
Opioid Agonists 203
Drug Prototype Morphine (Astramorph PF, Duramorph, Others) 203
xviii Contents
Opioid Antagonists 205

Drug Prototype Naloxone (Narcan) 205
Opioids with Mixed Agonist–Antagonist Effects 206
Nursing Process FOCUS Patients Receiving Opioids 206
Nonopioid Analgesics for Moderate Pain 208
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) 208
Drug Prototype Aspirin (Acetylsalicylic Acid, ASA) 208
Centrally Acting Drugs 210
Tension Headaches and Migraine 210
Triptans 211
Ergot Alkaloids 211
Other Antimigraine and Tension Headache Drugs 213
Drug Prototype Sumatriptan (Imitrex) 213

Local Anesthesia 218
Esters 222
Amides 222
Drug Prototype Lidocaine (Xylocaine) 222
Nursing Process FOCUS Patients Receiving Local Anesthesia 223
General Anesthesia 224
Drug Prototype Nitrous Oxide 225
Drug Prototype Isoflurane (Forane) 225
Gases 226
Volatile Liquids 226
Intravenous Anesthetics 226
Drug Prototype Propofol (Diprivan) 227
Adjuncts to Anesthesia 227
Drug Prototype Succinylcholine (Anectine) 228
Unit III
The Cardiovascular and Urinary Systems 233
Chapter 16 Drugs for Lipid Disorders 234

Drug Prototype Atorvastatin (Lipitor) 240
Drug Prototype Cholestyramine (Questran) 240
Nursing Process FOCUS Patients Receiving Drug Therapy with HMG-CoA
Reductase Inhibitors (Statins) 241
Drug Prototype Gemfibrozil (Lopid) 244
Chapter 17 Diuretics and Drugs for Electrolyte and Acid–Base

Disorders 248
Drug Prototype Furosemide (Lasix) 254
Drug Prototype Hydrochlorothiazide (Microzide) 255
Drug Prototype Spironolactone (Aldactone) 256
Contents xix
Nursing Process FOCUS Patients Receiving Diuretic Therapy 257

Sodium Imbalances 259
Potassium Imbalances 259
Drug Prototype Potassium Chloride (KCl) 260
Drug Prototype Sodium Bicarbonate (NaHCO3 ) 261
Chapter 18 Drugs for Hypertension 265

Nursing Process FOCUS Patients Receiving ACE Inhibitor Therapy 276
Drug Prototype Enalapril (Vasotec) 277
Drug Prototype Nifedipine (Adalat CC, Procardia XL) 279
Nursing Process FOCUS Patients Receiving Calcium Channel Blocker
Therapy 279
Drug Prototype Doxazosin (Cardura) 282
Drug Prototype Hydralazine (Apresoline) 283
Chapter 19 Drugs for Heart Failure 287

Drug Prototype Lisinopril (Prinivil, Zestril) 292
Drug Prototype Digoxin (Lanoxin, Lanoxicaps) 295
Drug Prototype Carvedilol (Coreg) 296
Drug Prototype Milrinone (Primacor) 297
Chapter 20 Drugs for Angina Pectoris, Myocardial Infarction,

and Stroke 301
Angina Pectoris 302
Drug Prototype Nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, Others) 307
Nursing Process FOCUS Patients Receiving Organic Nitrate Therapy 308
Drug Prototype Atenolol (Tenormin) 309
Drug Prototype Diltiazem (Cardizem, Cartia XT, Dilacor XR, Others) 309
Myocardial Infarction 310
Drug Prototype Reteplase (Retavase) 312
Beta-Adrenergic Blockers 312
Antiplatelet and Anticoagulant Drugs 312
Nursing Process FOCUS Patients Receiving Thrombolytic Therapy 313
Angiotensin-Converting Enzyme (ACE) Inhibitors 313
Pain Management 313
Stroke 314
Chapter 21 Drugs for Shock and Anaphylaxis 319

Shock 320
Blood Products 322
Colloids 323
Crystalloids 323
Drug Prototype Normal Serum Albumin (Albuminar, Plasbumin, Others) 323
Nursing Process FOCUS Patients Receiving Intravenous Fluid Therapy 324
Drug Prototype Norepinephrine (Levophed) 326
Drug Prototype Dopamine (Dopastat, Intropin) 326
xx Contents
Anaphylaxis 326
Drug Prototype Epinephrine (Adrenalin) 327
Chapter 22 Drugs for Dysrhythmias 331

Nursing Process FOCUS Patients Receiving Antidysrhythmic Drugs 336
Drug Prototype Procainamide 339
Drug Prototype Propranolol (Inderal, InnoPran XL) 340
Drug Prototype Amiodarone (Cordarone) 341
Drug Prototype Verapamil (Calan, Isoptin SR, Others) 342
Chapter 23 Drugs for Coagulation Disorders 346

Parenteral Anticoagulants 350
Oral Anticoagulants 352
Drug Prototype Heparin 352
Drug Prototype Warfarin (Coumadin) 353
Nursing Process FOCUS Patients Receiving Anticoagulant
and Antiplatelet Therapy 353
Drug Prototype Clopidogrel (Plavix) 356
Drug Prototype Alteplase (Activase) 357
Drug Prototype Aminocaproic Acid (Amicar) 358
Unit IV
The Immune System 361
Chapter 24 Drugs for Inflammation and Fever 362

Inflammation 363
Drug Prototype Naproxen (Naprosyn) and Naproxen Sodium
(Aleve, Anaprox) 366
Nursing Process FOCUS Patients Receiving NSAID Therapy 367
Drug Prototype Prednisone 369
Fever 369
Drug Prototype Acetaminophen (Tylenol) 369
Chapter 25 Drugs for Immune System Modulation 373

Immunostimulants 376
Drug Prototype Hepatitis B Vaccine (Energix-B, Recombivax HB) 378
Drug Prototype Interferon alfa-2b (Intron-A) 380
Drug Prototype Cyclosporine (Gengraf, Neoral, Sandimmune) 382
Nursing Process FOCUS Patients Receiving Immunosuppressants 382
Chapter 26 Drugs for Bacterial Infections 387

Drug Prototype Penicillin G Sodium/Potassium 395
Drug Prototype Cefotaxime (Claforan) 396
Drug Prototype Tetracycline (Sumycin, Others) 397
Drug Prototype Erythromycin (E-Mycin, Erythrocin) 398
Contents xxi
Drug Prototype Gentamicin (Garamycin) 400

Drug Prototype Ciprofloxacin (Cipro) 401
Drug Prototype Trimethoprim–Sulfamethoxazole (Bactrim, Septra) 402
Drug Prototype Vancomycin (Vancocin) 403
Nursing Process FOCUS Patients Receiving Antibacterial Therapy 404
Tuberculosis 406
Drug Prototype Isoniazid (INH, Nydrazid) 406
Nursing Process FOCUS Patients Receiving Antitubercular Drugs 407
Chapter 27 Drugs for Fungal, Viral, and Parasitic Diseases 412

Antifungal Drugs 413
Drug Prototype Amphotericin B (AmBisome, Fungizone, Others) 416
Drug Prototype Nystatin (Mycostatin, Nystop, Others) 416
Nursing Process FOCUS Patients Receiving Superficial Antifungal
Therapy 417
Antiviral Drugs 417
Drug Prototype Zidovudine (AZT, Retrovir) 421
Nursing Process FOCUS Patients Receiving Pharmacotherapy for HIV-
AIDS 422
Treatment of Herpesvirus Infection 423
Treatment of Influenza Virus Infection 424
Drug Prototype Acyclovir (Zovirax) 425
Treatment of Viral Hepatitis Infection 425
Antiparasitic Drugs 425
Drug Prototype Metronidazole (Flagyl) 427
Chapter 28 Drugs for Neoplasia 430

Drug Prototype Cyclophosphamide (Cytoxan) 438
Drug Prototype Methotrexate (Rheumatrex, Trexall) 440
Drug Prototype Doxorubicin (Adriamycin) 441
Drug Prototype Vincristine (Oncovin) 443
Drug Prototype Tamoxifen 444
Drug Prototype Epoetin Alfa (Epogen, Procrit) 446
Nursing Process FOCUS Patients Receiving Antineoplastic Therapy 447
Unit V
The Respiratory and Digestive Systems 453
Chapter 29 Drugs for Respiratory Disorders 454

Upper Respiratory Tract 455
Lower Respiratory Tract 455
Allergic Rhinitis 458
Drug Prototype Diphenhydramine (Benadryl, Others) 460
Nursing Process FOCUS Patients Receiving Antihistamine Therapy 461
Drug Prototype Fluticasone (Flonase, Veramyst) 463
xxii Contents
Drug Prototype Oxymetazoline (Afrin, Others) 464

Asthma 465
Nursing Process FOCUS Patients Receiving Bronchodilators 469
Drug Prototype Cromolyn (Intal) 471
Chronic Obstructive Pulmonary Disease 471
Chapter 30 Drugs for Gastrointestinal Disorders 476

Peptic Ulcer Disease 479
Drug Prototype Omeprazole (Prilosec) 483
Drug Prototype Ranitidine (Zantac) 483
Nursing Process FOCUS Patients Receiving Drug Therapy for Peptic
Ulcer Disease 484
Constipation 486
Drug Prototype Psyllium Mucilloid (Metamucil, Others) 487
Nursing Process FOCUS Patients Receiving Laxative Therapy 487
Diarrhea 488
Drug Prototype Diphenoxylate with Atropine (Lomotil) 488
Nausea and Vomiting 489
Drug Prototype Ondansetron (Zofran, Zuplenz) 490
Weight Loss 491
Pancreatic Enzymes 492
Chapter 31 Vitamins, Minerals, and Nutritional Supplements 496

Drug Prototype Cyanocobalamin (Crystamine, Others) 499
Drug Prototype Ferrous Sulfate (Feosol, Feostat, Others) 501
Nursing Process FOCUS Patients Receiving Iron Supplements 503
Unit VI
The Endocrine and Reproductive Systems 509

Hypothalamic and Pituitary Disorders 514
Drug Prototype Desmopressin (DDAVP) 514
Thyroid Disorders 516
Drug Prototype Levothyroxine (Levothroid, Synthroid, Others) 518
Drug Prototype Propylthiouracil (PTU) 519
NURSING PROCESS FOCUS Patients Receiving Thyroid Hormone Replacement 519
Adrenal Disorders 520
Drug Prototype Hydrocortisone (Cortef, Hydrocortone, Others) 522
Nursing Process FOCUS Patients Receiving Systemic Corticosteroid
Therapy 523

Type 1 Diabetes Mellitus 529
Drug Prototype Regular Insulin (Humulin R, Novolin R) 532
Contents xxiii
Nursing Process FOCUS Patients Receiving Insulin Therapy 533

Type 2 Diabetes Mellitus 534
Drug Prototype Metformin (Fortamet, Glucophage, Glumetza, Others) 537
Nursing Process FOCUS Patients Receiving Pharmacotherapy for Type 2
Diabetes 538
Chapter 34 Drugs for Disorders and Conditions

of the Reproductive System 542
Oral Contraceptives 546
Drug Prototype Estradiol with Norethindrone (Ortho-Novum, Others) 547
Nursing Process FOCUS Patients Receiving Oral Contraceptive Therapy 548
Menopause 549
Uterine Abnormalities 549
Drug Prototype Estrogen, conjugated (Cenestin, Enjuvia, Premarin) 551
Drug Prototype Medroxyprogesterone (Depo-Provera,
Depo-SubQ-Provera, Provera) 552
Labor and Breastfeeding 552
Drug Prototype Oxytocin (Pitocin) 553
Hypogonadism 554
Drug Prototype Testosterone 554
Erectile Dysfunction 555
Drug Prototype Sildenafil (Viagra) 556
Benign Prostatic Hyperplasia 557
Drug Prototype Finasteride (Proscar) 558
Unit VII
The Skeletal System, Integumentary System,
and Eyes and Ears 563
Chapter 35 Drugs for Bone and Joint Disorders 564

Hypocalcemia 565
Osteomalacia and Rickets 566
Drug Prototype Calcium salts 569
Drug Prototype Calcitriol (Calcijex, Rocaltrol) 569
Osteoporosis 569
Selective Estrogen-Receptor Modulators 570
Drug Prototype Raloxifene (Evista) 571
Calcitonin 572
Bisphosphonates 572
Drug Prototype Alendronate (Fosamax) 572
Nursing Process FOCUS Patients Receiving Pharmacotherapy for
Osteoporosis 572
Paget’s Disease 573
Osteoarthritis 574
Rheumatoid Arthritis 575
xxiv Contents
Drug Prototype Hydroxychloroquine (Plaquenil) 575

Gout 576
Drug Prototype Allopurinol (Lopurin, Zyloprim) 578
Chapter 36 Drugs for Skin Disorders 582

Skin Parasites 586
Drug Prototype Permethrin (Acticin, Elimite, Nix) 587
Nursing Process FOCUS Patients Receiving Pharmacotherapy for Lice or Mite
Infestation 588
Sunburn and Minor Skin Irritation 588
Drug Prototype Benzocaine (Americaine, Anbesol, Others) 589
Acne And Rosacea 589
Drug Prototype Tretinoin (Avita, Retin-A, Others) 591
Dermatitis and Eczema 591
Psoriasis 593
Chapter 37 Drugs for Eye and Ear Disorders 598

Glaucoma 600
Drug Prototype Latanoprost (Xalatan) 601
Prostaglandins 602
Direct- and Indirect-Acting Cholinergics (Miotic Drugs) 602
Nonselective Sympathomimetics (Mydriatic Drugs) 602
Beta Adrenergic Blockers 603
Alpha2-Adrenergic Drugs 603
Carbonic Anhydrase Inhibitors 603
Drug Prototype Timolol (Betimol, Timoptic, Others) 604
Osmotic Diuretics 604
Nursing Process FOCUS Patients Receiving Pharmacotherapy for
Glaucoma 604
Eye Examinations and Minor Eye Conditions 605
Ear Conditions 606
Appendix A References 611
Appendix B Brief Answers to NCLEX-PN® and Case Study Questions 621
Index 626
Guide to Special Features 657
*Appendix D (Complete Answers and Rationales for NCLEX-PN® Review and Case Study
Questions) and the Glossary appear on the textbook’s website.
U N I T
1
Basic Concepts
in Pharmacology
Unit Contents
Chapter 1 Introduction to Pharmacology: Drug Regulation and Approval / 2
Chapter 2 Drug Classes, Schedules, and Categories / 12
Chapter 3 Methods of Drug Administration / 20
Chapter 4 What Happens After a Drug Has Been Administered / 41
Chapter 5 The Nursing Process in Pharmacology / 51
Chapter 6 The Role of Complementary and Alternative Therapies

in Pharmacology / 59
Chapter 7 Substance Abuse / 69
c
h
a
p
t
e
r
1 Introduction to Pharmacology:
Drug Regulation and Approval
Core Concepts
1.1
Pharmacology is an expansive and challenging topic. 1.7
U.S. drug standards have become increasingly
1.2
For healthcare providers, the fields of pharmacology complex.
and therapeutics are connected. 1.8
There are four stages of approval for therapeutic
1.3
Agents may be classified as traditional drugs, and biologic drugs.
biologics, and natural alternatives. 1.9
Governmental agencies face the dual challenge of
1.4
Drugs are available by prescription or over the increasing the speed of drug approval while still
counter (OTC). ensuring the safety of new drugs.
1.5
Pharmaceutics is the science of pharmacy. 1.10 Healthcare providers must be prepared to
deal with the threat of biological and chemical
1.6
Drug regulations were created to protect the public attack.
from drug misuse.
Learning Outcomes
After reading this chapter, the student should be able to:
1. Explain the interdisciplinary 6. Identify the advantages and 10. Discuss the roles and responsibilities
nature of pharmacology and give disadvantages of prescription and of branches within the FDA in
examples of subject area expertise OTC drugs. overseeing traditional therapeutic
needed to master the discipline. 7. Distinguish between pharmaceutics drugs, biologics, and natural
2. Identify professions in which and pharmacology. alternative therapies.
knowledge of pharmacology is 8. Discuss the history of U.S. 11. Identify four stages of approval
important. standards, acts, and organizations for therapeutic and biologic
3. Explain how the disciplines of leading to the requirement that drugs.
therapeutics and pharmacology are drug safety must be proven before 12. Discuss current challenges facing
interconnected. marketing. the FDA in approving new drugs
4. Distinguish between therapeutic 9. Discuss the role of the United States for market.
drugs and agents such as foods, Food and Drug Administration 13. Discuss the challenges facing
household products, and cosmetics. (FDA) in determining the safety of healthcare providers in view of
5. Compare and contrast traditional drugs and whether they may be modern-day bioterrorist threats.
drugs, biologics, and natural used for therapy.
alternative therapies.
Core Concept 1.2 3
Key Terms
biologics (beye-oh-LOJ-iks) 4 natural alternative therapies 4 pharmacopoeia
black box warnings 6 off-label use 9 (far-mah-KOH-pee-ah) 5
clinical pharmacology 7 pathophysiology pharmacotherapeutics
(PATH-oh-fiz-ee-OL-oh-jee) 3 (far-mah-koh-THER-ah-PEW-tiks) 3
complementary and alternative medicine
(CAM) therapies 4 pharmaceutics (far-mah-SOO-tiks) 5 pharmacy (FAR-mah-see) 5
formularies (FOR-mew-LEH-reez) 5 pharmacology (far-mah-KOL-oh-jee) 3 therapeutics (ther-ah-PEW-tiks) 3
M ore drugs are being administered to consumers than ever before. Because of the number of new
drugs available for therapy, some experts are concerned that patients might be harmed if drugs
are not thoroughly tested. The purpose of this chapter is to introduce the subject of pharmacol-
ogy and to emphasize the role of the government in ensuring that drugs and natural alternatives are safe
and effective for public use. It addresses the role that drug therapy has in fighting disease as governmental
regulators, consumers, and healthcare professionals face new challenges in the years ahead. Drugs are the
most powerful weapon we have against diseases and worldwide epidemics.
In addition, bioterrorist threats have led to widespread governmental changes in emergency prepared-
ness planning. This chapter briefly introduces the role of pharmacology in the prevention and treatment of
diseases or conditions that might develop due to global biological, chemical, or nuclear threats.
Pharmacology is an expansive and challenging topic. Core Concept 1.1

The word pharmacology is derived from two Greek words: pharmakon, which means “medicine,” and pharmaco 5 medicine
logos, which means “study.” Thus, pharmacology is defined as “the study of medicine.” ology 5 the study of
Healthcare providers practice the discipline of pharmacology to study how drugs improve the health
of the human body. If applied properly, drugs can dramatically improve patients’ quality of life. If applied
improperly, the consequences of drug action can be devastating.
The subject of pharmacology is an expansive topic ranging from a study of how drugs enter and travel
throughout the body to the actual responses they produce. To learn the discipline well, students must mas-
ter concepts from several interrelated areas, including anatomy, physiology, microbiology, chemistry, and
pathophysiology (study of disease and functional changes that occur as a result of disease). The useful patho 5 disease
application of drugs depends on knowledge from at least these areas. physio 5 the nature of
Currently there are more than 10,000 brand and generic varieties of drugs available with many dif- ology 5 the study of
ferent names, interactions, adverse effects, and complicated mechanisms of action. Keeping up with the
numbers of drugs is a huge challenge. Many drugs may be prescribed for more than one disease, and most
produce multiple effects in the body. Further complicating the study of pharmacology is the fact that drugs
may cause different responses depending on factors such as gender, age, health status, body mass, and
genetics.
For healthcare providers, the fields of pharmacology

and therapeutics are connected. Core Concept 1.2
It is obvious that a thorough knowledge of pharmacology is important to those health professionals who
prescribe drugs on a daily basis. This group includes physicians, physician’s assistants, dentists, and ad-
vanced nurse practitioners. Depending on state law, members of other groups may also be permitted to pre-
scribe medications. In this textbook, the group of professions that is allowed to prescribe drugs is referred
to as healthcare practitioners.
A second group of professions includes nursing, allied health, and community service employees.
These occupations have in common direct contact with patients or healthcare practitioners. Nurses and
some other allied health workers are directly involved with drug administration as well as with issues re-
lated to drug education, management, and/or enforcement of drug laws. In this text, these professionals are
referred to as healthcare providers.
Some healthcare providers, such as nurses, may administer drugs on a daily basis, whereas others
may administer drugs occasionally. A strong knowledge of pharmacology is necessary to properly educate
and advise patients regarding their healthcare needs. This knowledge is also essential to communicate ef-
fectively with healthcare practitioners, who rely heavily on nurses and allied health professionals to gather
medical data from their patients and to follow up on results of therapy.
For healthcare providers studying pharmacology, it usually becomes apparent that the fields of phar-
macology and therapeutics are connected. Therapeutics is the branch of medicine concerned with the
treatment of disease and suffering. Pharmacotherapeutics is the use of medicine to treat disease.
4 Chapter 1 Introduction to Pharmacology: Drug Regulation and Approval
Agents may be classified as traditional drugs, biologics,

Core Concept 1.3 and natural alternatives.
Drugs are chemicals that produce biologic responses within the body. From this perspective, drugs may be
considered a part of the body’s normal activities, from the essential gases that people breathe to the foods
that they eat. Yet it is necessary to separate drugs from substances such as foods, household products, and
cosmetics. Many agents, including antiperspirants, sunscreens, toothpastes, and shampoos, might alter the
body’s normal activities, but they are not considered to be medically therapeutic, as drugs taken for a medi-
cal disorder would be.
Therapeutic drugs are sometimes classified on the basis of how they are produced, either chemically
or naturally. Most traditional drugs are chemically produced or synthesized in a laboratory. Biologics are
agents naturally produced in animal cells, in microorganisms, or by the body itself. Natural alternative
therapies are herbs, natural extracts, vitamins, minerals, or dietary supplements. Table 1.1 ◆ shows a sum-
mary of characteristics associated with traditional drug therapies, biologics, and natural alternative thera-
pies. Although drugs may be described in many ways, this text limits its focus to agents used for therapy in
a clinical or home setting. Traditional drugs and drug classes are discussed more thoroughly in Chapter 2.
Natural alternatives are discussed more thoroughly in Chapter 6. In addition, most chapters include a fea-
ture called Natural Alternatives that highlights a specific herbal therapy or dietary supplement.
When studying the various approaches for therapy, the healthcare provider may encounter the cat-
egory of treatment called complementary and alternative medicine (CAM) therapies. In addition to
the herbs, vitamins, or supplements just described, CAM therapies include manipulative and body-based
practices such as physical therapy, occupational therapy approaches, massage, biofeedback, hypnosis, and
acupuncture. Although these and other approaches are successful in treating disease or a medical condition,
traditional therapeutic drugs, biologics, and natural alternative therapies remain the primary focus of this
textbook.
Core Concept 1.4 Drugs are available by prescription or over the counter (OTC).
Legal drugs are obtained either with a prescription or by purchasing them over the counter. There are dif-
ferences between the two methods of dispensing. To obtain prescription drugs, patients must get a physi-
cian’s order authorizing them to receive the drugs. The advantages to this are numerous. Practitioners have
an opportunity to examine their patients and determine a specific diagnosis. Practitioners can maximize
therapy by ordering the proper drug for their patients’ conditions and controlling the specific amount and
frequency of the drug to be dispensed. Healthcare providers may give instructions on how to use the drug
properly and what adverse effects to expect.
A drug’s safety is related to its effectiveness. The difference between its usual effective dose and a
dose that produces severe adverse effects is called its margin of safety. When drugs have been used over
long periods and demonstrate wide margins of safety—that is, they are very safe and effective—regulators
sometimes change them from being prescription drugs to being OTC drugs. Unlike prescription drugs,
OTC drugs do not require an order from a healthcare practitioner.
Patients may treat themselves safely if they carefully follow instructions included with these OTC
drugs. If patients do not follow these guidelines, OTC drugs can have serious adverse effects.
Patients prefer to take OTC medications for many reasons. OTC drugs can be obtained more easily
than prescription drugs. They do not have to make an appointment with a physician, which saves time
Table 1.1 Characteristics of Traditional Therapeutic Drugs, Biologics, and Natural

Alternative Therapies
Traditional Drug Therapies ■ Chemically produced in a laboratory
■ Routinely used by healthcare providers
Biologics ■ Naturally produced by the body itself, in animal cells, or in
microorganisms
■ Include hormones and vaccines
■ Routinely used by healthcare providers
Natural Alternative Therapies ■ Naturally produced
■ Include herbs, extracts, vitamins, minerals, or dietary
supplements
■ Sometimes used, depending on healthcare provider
Core Concept 1.7 5
and money. Without training, however, choosing the proper medication for a specific problem may be
difficult. OTC drugs may react with foods, herbal products, and prescription or other OTC drugs. Pa-
tients may not be aware that some medications can impair their ability to function safely. Self-treatment
is sometimes ineffective, and the potential for injury is much greater if the disease is allowed to progress
without proper treatment.
Pharmaceutics is the science of pharmacy. core concept 1.5

Pharmaceutics is the science of pharmacy (the preparation and dispensing of drugs) and is a very im-
portant part of pharmacotherapy. The general public often confuses pharmaceutics with pharmacology,
or they recognize the root pharm and assume that pharmacology is the same as pharmacy. Correctly put,
pharmaceutics is the science of pharmacy, and it involves dispensing a drug to a patient after he or she
has been examined by a licensed healthcare practitioner. Pharmacists are the experts who catalogue signs,
symptoms, adverse effects, and drug interactions. They often act as drug advisors to patients, making sure
that they receive the proper medication and educating them about undesirable symptoms or interactions.
Concept Review 1.1

■ Explain the meaning of this statement: “Pharmacotherapy involves the science of thera-
peutics and pharmaceutics.”
Drug regulations were created to protect the public from drug misuse. core concept 1.6
For many years, there were no standards or guidelines to protect the public from drug misuse. Patients
could not be assured that available medicines were not a form of quackery. The archives of drug regulatory
agencies are filled with examples of early medicines, such as rattlesnake oil for rheumatism. It became
quite clear that drug regulations were needed to protect the public.
The first standards commonly used by pharmacists were early formularies, or lists of drugs and drug
recipes. In 1820, the first comprehensive publication of drug standards, called the U.S. Pharmacopoeia
(USP), was established. (See the timeline in Figure 1.1 ■.) A pharmacopoeia is a medical reference sum-
mary indicating standards of drug purity and strength and directions for synthesis. In 1852, a national
professional society of pharmacists—the American Pharmaceutical Association (APhA)—was founded.
From 1852 until 1975, two major sources maintained drug standards in the United States: the USP and
the APhA’s National Formulary (NF). All drug substances and products were covered in the USP; the
NF focused on pharmaceutical ingredients. In 1975, the two organizations merged and created a single
publication named the U.S. Pharmacopoeia-National Formulary (USP-NF). Official updates for the USP-
NF are published regularly. Today, the USP label can be found on some medication containers verifying
the exact ingredients found within the container, as shown in Figure 1.2 ■. Although there is a lot of good
information on the label of a drug container, newer labeling guidelines are being proposed in an effort to
promote patient safety and to reduce drug misuse.
In the early 1900s, to protect the public, the government began to develop and enforce tougher drug
legislation. In 1902, the Biologics Control Act was passed to standardize the quality of serums and other
blood-related products. The Pure Food and Drug Act of 1906 gave the government power to control the
labeling of medicines. In 1912, the Sherley Amendment prohibited the sale of drugs labeled with false
therapeutic claims intended to cheat the consumer. In 1938, Congress passed the Food, Drug, and Cosmetic
Act. This was the first law preventing the marketing of drugs that had not been thoroughly tested prior to
marketing. According to the provisions of this law, drug companies were required to prove the safety and
efficacy (i.e., effectiveness) of any drug before it could be sold within the United States.
U.S. drug standards have become increasingly complex. core concept 1.7
Much has changed in the regulation of drugs since 1938. In 1988, the FDA was officially established as
an agency of the U.S. Department of Health and Human Services. Today, the Center for Drug Evaluation
and Research (CDER), a branch of the FDA, has powerful control over whether prescription drugs and
OTC drugs may be used for therapy. The CDER states its mission as “facilitating the availability of safe
effective drugs, keeping unsafe or ineffective drugs off the market, improving the health of Americans, and
providing clear, easily understandable drug information for safe and effective use.” Any pharmaceutical
laboratory, whether private, public, or academic, must obtain FDA approval before marketing any drug.
Another branch of the FDA, the Center for Biologics Evaluation and Research (CBER), regulates the use
of biologics, including serums, vaccines, and products found in the bloodstream. In 1997, the FDA created
boxed warnings to regulate drugs with “special problems.” At the time no precedent had been established
Figure 1.1
TIMELINE REGULATORY ACTS, STANDARDS, AND ORGANIZATIONS
1820 A group of healthcare providers established the first comprehensive publication of drug standards called the
U.S. Pharmacopoeia (USP).
1852 A group of pharmacists founded a national professional society called the American Pharmaceutical Association (APhA).
The APhA then established the National Formulary (NF), a standardized publication focusing on pharmaceutical
ingredients. The USP continued to catalogue all drug-related substances and products.
1862 This was the beginning of the Federal Bureau of Chemistry, established under the administration of President Lincoln.
Over the years and with added duties, it gradually became the Food and Drug Administration (FDA).
1902 Congress passed the Biologics Control Act to control the quality of serums and other blood-related products.
1906 The Pure Food and Drug Act gave the government power to control the labeling of medicines.
1912 The Sherley Amendment made medicines safer by prohibiting the sale of drugs labeled with false therapeutic claims.
1938 Congress passed the Food, Drug, and Cosmetic Act. It was the first law preventing the marketing of drugs not
thoroughly tested. This law now provides for the requirement that drug companies must submit a New Drug
Application (NDA) to the FDA prior to marketing a new drug.
1944 Congress passed the Public Health Service Act, covering many health issues, including biologic products and the
control of communicable diseases.
1975 The U.S. Pharmacopoeia and National Formulary announced their union. The USP-NF became a single standardized
publication.
1986 Congress passed the Childhood Vaccine Act. It authorized the FDA to acquire information about patients taking
vaccines, to recall biologics, and to recommend civil penalties if guidelines regarding biologic use were not followed.
1988 The FDA was officially established as an agency of the U.S. Department of Health and Human Services.
1992 Congress passed the Prescription Drug User Fee Act. It required that nongeneric drug and biologic manufacturers pay
fees to be used for improvements in the drug review process.
1994 Congress passed the Dietary Supplement Health and Education Act that requires clear labeling of dietary supplements.
This act gives the FDA the power to remove supplements that cause a significant risk to the public.
1997 The FDA Drug Modernization Act reauthorized the Prescription Drug User Fee Act. This act represented the largest
reform effort of the drug review process since 1938.
2002 The Bioterrorism Act implemented guidelines for registration of selected toxins that could pose a threat to human,
animal, or plant safety and health.
2007 The FDA Amendments Act reviewed, expanded, and reaffirmed legislation to allow for additional comprehensive
reviews of new drugs and medical products. This extended the reforms imposed from 1997. The FDA’s Critical Path
Initiative was a part of this reform.
2011 Provisions of the Health Care Reform law allowed the FDA to approve generic versions of biologic drugs. Additional
drug rebates and benefits were provided to the American public. The FDA Food Safety Modernization Act represents
the largest reform effort of food safety review since 1938.
2012 Renewal of the Prescription Drug User Fee Act.
Historical timeline of regulatory acts, standards, and organizations.
to monitor drugs with a potential for causing death or serious injury. Black box warnings, named after the
black label appearing around drug safety information on package inserts, eventually became one of the pri-
mary alerts for identifying extreme adverse drug reactions discovered during and after review. The health-
care provider must be increasingly mindful about the level of precaution necessary to promote safety,
including medication verification and special alerts. Because of their importance, black box warnings are
included for all prototype drugs in this text.
Core Concept 1.8 7
Figure 1.2
Each mL contains atropine sulfate 400 mcg (0.4 Inactive ingredients: antifoam AF
EXP
LOT emulsion, flavors, purified water,
mg), sodium chloride 9 mg and benzyl alcohol 0.015 sodium hydroxide or hydrochloric
mL in Water for Injection. pH 3.0-6.5; Sulfuric acid 237 mL acid to adjust pH, sorbitol solution,
added, if needed, for pH adjustment. and tragacanth. Sorbic acid 0.1%
ORAL SUSPENSION added as preservative.
Injection, USP USUAL DOSAGE: See accompanying
POISON circular. Keep container tightly
10 X 20 ,mL Multiple Dose Vials 25 mg per 5 mL closed. Protect from freezing.
FOR SC, IM OR IV USE Usual Dose: See package insert. SHAKE WELL BEFORE USING
Store at controlled room temperature 15°-30°C Store below 30°C (86°F).
Alcohol 1%
400 mcg/mL (59°-86° F).
Avoid temperatures above
Practice Label
50°C (122°F).
(0.4 mg/mL) Caution: Federal law prohibits dispensing without
prescription. Rx only
Practice Label
PL Product Code
Pharmaceuticals 237 mL | No. 3376
2210-43 B-32210 N
00063 37666 2
PL 3
For educational purposes only Pharmaceuticals 9108705

Lot Exp.
Some drug labels show the USP symbol; others do not.
The FDA also oversees administration of herbal products and dietary supplements, but the Center
for Food Safety and Applied Nutrition (CFSAN) regulates use of these substances. Herbal products and Life Span Fact
dietary supplements are regulated by the Dietary Supplement Health and Education Act of 1994. This act One historical achievement
does not provide the same degree of protection as the Food, Drug, and Cosmetic Act of 1938. For example, involving biologics is the 1986
herbal and dietary supplements can be marketed without prior approval from the FDA; however, all pack- Childhood Vaccine Act. This act
age inserts and information are monitored once products have gone to market. The Dietary Supplement authorized the FDA to acquire
Health and Education Act is discussed in more detail in Chapter 6. information about patients tak-
ing vaccines, to recall biologics,
In 1998, the National Center for Complementary and Alternative Medicine (NCCAM) was established
and to recommend civil penal-
as the federal government’s lead agency for scientific research and information about CAM therapies. Its ties if guidelines regarding
mission has been to define “the usefulness and safety of complementary and alternative medicine inter- biologics were not followed.
ventions and their roles in improving health and health care.” Among several areas of focus, this agency
has supported research and serves as a resource for healthcare providers in establishing which alternative
therapies are safe and effective.
There are four stages of approval for therapeutic and biologic drugs. core concept 1.8
The amount of time spent in the review and approval process for both prescription and OTC drugs depends
on several checkpoints in a well-developed and organized plan. Most therapeutic drugs and biologics are re-
viewed in four stages, which are summarized in Figure 1.3 ■. These stages are (1) preclinical investigation,
(2) clinical investigation, (3) submission of a new drug application (NDA) with review, and (4) postmarketing
studies.
Preclinical Investigation
Preclinical investigation involves basic science research. Scientists perform many tests on cells grown in
the laboratory (a process called culture) or on animals to examine the effectiveness of a range of drug doses
and to look for any adverse effects. Laboratory tests on cells and animals are important because they assist
in predicting whether drugs will cause harm in humans. Because laboratory tests do not always reflect the
way a human responds, preclinical investigation results are always inconclusive.
Clinical Investigation
Clinical investigation, the second stage of drug approval, takes place in three different phases, termed clini-
cal phase trials. This is the longest part of the drug approval process and involves clinical pharmacology,
an area of medicine devoted to the evaluation of drugs used for human benefit. During these phases, clini-
cal pharmacologists, researchers, and healthcare providers examine data from volunteers and large groups
of selected patients with certain diseases. Both scientists and healthcare providers establish drug doses and
try to identify adverse effects. Clinical investigators address concerns such as whether the drug worsens
other medical conditions, interacts unsafely with existing medications patients are taking, or affects one
type of patient more than others.
Clinical Phase Trials. Clinical phase trials are essential because responses among patients vary. If a
drug appears to be effective without causing serious adverse effects, approval for marketing may be accel-
erated, or the drug may be used for treatment immediately in special cases with careful monitoring. If the
Figure 1.3
Preclinical Clinical Postmarketing
Investigation Investigation NDA Review Studies
(Stage 1) (Stage 2) (Stage 3) (Stage 4)
Range: 1–3 Range: 2–10 years Range: 2 months–7 years

years Average: 5 years Average: 24 months
Average: 18
months
Adverse
Reaction
Clinical Phase I Trials
Initial Reporting
Synthesis
Surveys/
Clinical Phase II Trials
Sampling/
Testing
Animal
Testing
Clinical Phase III Trials
Short Term Inspections
Long Term
30-Day FDA Time NDA NDA

Safety Review Industry Time Submitted Approved
The approval of a new drug is a four-stage process: (1) preclinical investigation, (2) clinical investigation, (3) NDA
submission and review, and (4) postmarketing studies. Within the second stage (clinical investigation), three phases of
trials are conducted over two to ten years. Postmarketing studies, also called postmarketing surveillance, continue in
large patient groups during the fourth stage of drug development.
drug shows promise but some minor problems are noted, the approval process is delayed until concerns are
addressed. In any case, an NDA must be submitted before a drug is allowed to proceed to the next stage of
the approval process.
Submission of an NDA with Review

A review of the NDA is the third stage of drug approval. During this stage, clinical phase III trials and
animal testing may continue, depending on the results obtained from preclinical testing. If the NDA is ap-
proved, the process continues to the final stage. If the NDA is rejected, the process stops until concerns are
addressed.
Postmarketing Studies
Postmarketing surveillance is the fourth stage of the drug approval process. It takes place after clinical
trials and the NDA review process have been completed. Testing in humans is continued to check for any
new harmful effects in larger and more diverse populations. Some adverse effects take longer to appear and
are not identified until a drug is used by large numbers of patients.
Examples of this process have been approval of the COX-2 selective nonsteroidal anti-inflammatory
drugs (NSAIDs), which were evaluated by the FDA during 2004 and 2005. Manufacturers of valdecoxib
(Bextra), celecoxib (Celebrex), and rofecoxib (Vioxx) were originally asked to revise their labeling owing
to emerging concerns that some NSAIDs exhibited extreme cardiovascular and gastrointestinal risks. In
September 2004, manufacturers of rofecoxib voluntarily withdrew their product from the market due to
safety concerns of heart attack and stroke. In April 2005, the FDA asked the manufacturers of valdecoxib
to remove their product from the market due to similar concerns. Celecoxib has remained on the market,
but the FDA announced that they would continue to analyze reports of COX-2 inhibitors to determine
safety profiles and patient impact.
Core Concept 1.10 9
The FDA holds annual public meetings to hear comments from patients and professional and phar-
maceutical organizations about the effectiveness and safety of new drug therapies. If the FDA discovers a
serious problem, it will require that a drug be withdrawn from the market and its use discontinued.
Governmental agencies face the dual challenge of increasing the speed

of drug approval while still ensuring the safety of new drugs. core concept 1.9
The public once criticized the FDA and other regulatory agencies for being too slow in bringing new,
potentially lifesaving drugs to the consumer. In the early 1990s, organized consumer groups and drug
manufacturers pressured governmental officials to speed up the drug review process. Reasons for delays in
the FDA drug approval process were outdated guidelines, poor communication, and agency understaffing.
In 1992, FDA officials, members of Congress, and representatives from pharmaceutical companies
negotiated the Prescription Drug User Fee Act on a five-year trial basis. This act required drug and biologic
manufacturers to pay substantial application fees at the time of an NDA to fund the approval process. This
act requires that the FDA meet certain benchmarks, mostly related to speeding up the NDA process. With
this extra income, the FDA hired more employees and restructured its organization to handle the greater
number of drug applications more efficiently. Restructuring was a resounding success. From 1992 to 1996,
the FDA approved double the number of drugs while cutting some review times by as much as half. In
1997, the FDA Modernization Act was passed, reauthorizing the Prescription Drug User Fee Act. It al-
lowed drug companies to give healthcare providers information about FDA-unapproved uses of certain
drugs. For example, sometimes drugs are approved to treat one condition, but not others; however, health-
care practitioners may discover that the drug is useful in treating a different problem. When such a benefit
is found frequently, a drug company is allowed to share accurate information with other physicians about
the drug’s “unapproved” but effective use in treating another condition. When a drug is being prescribed
for a condition for which it is not FDA-approved, it said to be an off-label use.
One concern now is that drugs are being developed at a faster rate than risks can be assessed. This is
especially true for those drugs targeted to treat certain cancers. Officials have continued to call for patients,
pharmacists, allied health workers, nurses, physicians, hospitals, and pharmaceutical companies to work
together to minimize risks. Because of the higher numbers of drugs being approved for therapy, the poten-
tial for adverse drug–drug and drug–herbal interactions is greater than ever before.
Concept Review 1.2

■ Can you recall the major U.S. acts, standards, and organizations leading up to the present
time? When was the FDA established? What current U.S. laws regulate how drugs are ap-
proved for marketing?
Healthcare providers must be prepared to deal with the threat

of biological and chemical attack. core concept 1.10
Prior to the September 11, 2001, terrorist attacks in the United States, concern about epidemic diseases
mainly focused on the possible spread of traditional infectious diseases such as influenza, tuberculosis,
cholera, and human immunodeficiency virus (HIV). Healthcare providers were also concerned about wide-
spread food poisoning and sexually transmitted diseases other than HIV. Uncommon diseases such as
anthrax produced fewer fatalities, so less attention was given to them.
Now, however, the healthcare community is more aware of the possibility of bioterrorism—the inten- bio 5 living organisms
tional use of infectious biological agents, chemical substances, or radiation to cause widespread harm or ill- terrorism 5 to induce fear
ness. Such federal agencies as the Centers for Disease Control and Prevention (CDC) and the U.S. Department
of Defense have increased efforts to inform, educate, and prepare the public for disease outbreaks caused by
bioterrorism. In 2002, the U.S. Department of Homeland Security was organized to provide additional security
and defense for the United States in a terrorist attack. The department also prioritized the important issue of
citizen preparedness, educating families how best to prepare for natural emergencies and disasters.
Among the goals of a bioterrorist are to create widespread public panic and cause as many casualties
as possible. The list of agents that can be used for this purpose is long. Some of these agents are easily
obtainable and require little or no specialized knowledge to spread. The most worrisome threats are:
■ Acutely infectious diseases such as anthrax, smallpox, plague, and hemorrhagic viruses
■ Incapacitating chemicals such as nerve gas, cyanide, and chlorinated agents
■ Nuclear and radiation emergencies
One can easily imagine what devastation would be caused if laboratories and healthcare professionals were
not able to identify, isolate, and treat widespread diseases caused by bioterrorism. The following chapters
contain important information related to bioterrorism. Chapter 26 reviews the topic of antibiotics for the
treatment of anthrax. The treatment of chemical nerve warfare agents is discussed in Chapter 8. Chapter 32
includes a discussion of the treatment of radiation exposure.
Chapter Review
Core Concepts Summary
1.1 Pharmacology is an expansive and challenging the Food and Drug Administration and publications,
topic. such as the U.S. Pharmacopoeia-National Formulary.
Pharmacology, the study of medicine, is a subject de-
1.7 U.S. drug standards have become increasingly
voted to proper drug treatment and health of the hu-
complex.
man body. It is an expansive topic utilizing concepts
from human biology, pathophysiology, and chemistry. The Food and Drug Administration (FDA), a branch
of the U.S. Department of Health and Human Ser-
1.2 For healthcare providers, the fields of pharmacol- vices, is the primary agency regulating drug safety.
ogy and therapeutics are connected. Three branches of the FDA control policies regarding
Therapeutics is the science associated with the treat- drug therapies: the Center for Drug Evaluation and
ment of suffering and the prevention of disease. Phar- Research (CDER), the Center for Biologics Evalua-
macotherapeutics is the useful application of drugs for tion and Research (CBER), and the Center for Food
the purpose of fighting disease. The study of phar- Safety and Applied Nutrition (CFSAN). Black box
macology is important to health professionals from warnings are a recent development enacted by the
many different fields. FDA. The National Center for Complementary and
Alternative Medicine (NCCAM) is a newer agency
1.3 Agents may be classified as traditional drugs, bio- established for scientific research and information
logics, and natural alternatives. about alternative therapies.
Drugs are chemical agents used to treat disease by
1.8 There are four stages of approval for therapeutic
producing biological responses within the body.
and biologic drugs.
Therapeutic drugs are classified as substances pro-
duced chemically or naturally. Biologics are natural Drug approval occurs in four stages: preclinical in-
agents produced by animal cells or microorganisms. vestigation, clinical investigation, submission of a
Alternative therapies include natural herbs, plant new drug application (NDA) with review, and post-
extracts, or dietary supplements. marketing studies. Clinical phase trials must be com-
pleted before drugs are approved for public use.
1.4 Drugs are available by prescription or over the
counter (OTC). 1.9 Governmental agencies face the dual challenge of
There are two major methods of dispensing drugs. increasing the speed of drug approval while still
Prescription drugs require a physician’s order; OTC ensuring the safety of new drugs.
drugs do not. There are advantages and disadvantages FDA officials, members of Congress, and pharmaceuti-
to both dispensing methods. cal company representatives negotiated the Prescription
Drug User Fee Act and FDA Modernization Act. These
1.5 Pharmaceutics is the science of pharmacy. acts have sped up the approval process and require drug
Pharmaceutics involves the successful dispensation of and biologic manufacturers to provide yearly prod-
drugs for therapeutic purposes. Dispensing medication uct user fees. The concern now is that drugs are being
safely is a major challenge for healthcare providers approved at a rate faster than risks can be assessed.
and patients.
1.10 Healthcare providers must be prepared to deal
1.6 Drug regulations were created to protect the with the threat of biological and chemical attack.
public from drug misuse. Drugs are among the most powerful weapons to com-
The first drug laws were acts created by Congress to bat bioterrorism. Federal agencies have taken an ac-
protect patients from wrongful therapeutic claims. tive role in educating and preparing the public and
These and other standards form the basis of modern the healthcare community about disease outbreaks
drug regulation agencies and organizations, such as caused by bioterrorism.
Chapter Review 11
Review Questions
The following questions are written 5. Dispensing of drugs to patients after they have been
in NCLEX-PN ® style. A nswer these e xamined by a licensed healthcare provider is:
questions to assess your knowledge of 1. Pharmacology
the chapter material, and go back and 2. Pharmaceutics
review any material that is not clear to 3. Therapeutics
you. 4. Health care
6. The act that prevents the marketing of drugs that have not
1. Pathophysiology is defined as the study of: been thoroughly tested is the:
1. How drugs enter and travel throughout the body and the 1. Pure Food and Drug Act (1906)
responses they produce 2. Food, Drug, and Cosmetic Act (1938)
2. How drugs improve the health of the human body 3. Prescription Drug User Fee Act (1992)
3. Drugs and how they elicit different responses 4. FDA Modernization Act (1997)
4. Diseases and functional changes occurring as a result of disease
7. The longest part of the drug approval process is typically:
2. Biologics are:
1. Preclinical investigation
1. Produced in nature and include herbs, natural extracts, 2. Clinical investigation
vitamins, and minerals 3. NDA submission and review
2. Chemically produced in a laboratory 4. Postmarketing studies
3. Naturally produced in animal cells, microorganisms, or by
the body itself 8. The legislation responsible for cutting new drug applica-
4. Not used routinely by physicians tion review times as much as 50% is the:
1. Pure Food and Drug Act
3. Healthcare providers, such as Licensed Practical Nurses
2. Sherley Amendment
(LPN) and Licensed Vocational Nurses (LVN), are directly
3. Public Health Services Act
involved with drug administration and all of the following
4. Prescription Drug User Fee Act
activities except:
1. Prescribing medications 9. Black box warnings are:
2. Educating patients about their medications 1. Used to inform the consumer about general medication
3. Enforcing drug laws information
4. Helping patients with medication management 2. A list of ingredients within the medication
3. Located on the drug container label
4. What precautions should patients be aware of when
4. The primary alert for notifying consumers of potential
taking OTC drugs? (Select all that apply.)
extreme adverse drug effects
1. Self-treatment is sometimes ineffective.
2. OTC drugs may react with foods, herbal products, and 10. Which of the following is considered a bioterrorist threat?
prescription or other OTC drugs. (Select all that apply.)
3. The potential for further injury or disease is not a consider- 1. Anthrax contamination
ation when taking OTC medications. 2. Incapacitating chemicals
4. Instructions included with the medications should be read 3. Radiation exposure
and followed as directed. 4. Viruses that cause the common cold
NOTE: Answers to the Review Questions appear in Appendix B. The complete rationales and answers are located on the textbook’s
website.

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2 Drug Classes, Schedules, and Categories
Core Concepts
2.1
Drugs may be organized by their therapeutic and 2.4
Drugs with a potential for abuse are categorized
pharmacologic classifications. into schedules.
2.2
Drugs have more than one name. 2.5
In order to assess fetal risks, all prescription drugs
2.3
The differences between brand name drugs and are classified according to safety in pregnancy
their generic equivalents include price, formulations, categories.
and, most importantly, bioavailability.
Learning Outcomes
1. Discuss the basis for placing 5. Explain why generic drug role of the U.S. Drug Enforcement
drugs into therapeutic and names are preferred to other Administration (DEA) in controlling
pharmacologic classes. drug names. drug abuse and misuse.
2. Explain the prototype approach to 6. Discuss why drugs are sometimes 9. Identify the five drug schedules
drug classification. placed on a restrictive list and why and provide examples of drugs at
3. Describe what is meant by a drug’s this is sometimes controversial. each level.
mechanism of action. 7. Explain the meaning of the term 10. Identify the five pregnancy
4. Distinguish between a drug’s controlled substance. categories and explain what each
chemical name, generic name, and 8. Explain the U.S. Controlled category represents.
trade name. Substances Act of 1970 and the
Key Terms
bioavailability generic name (je-NARE-ik) 14 scheduled drugs 16
(BEYE-oh-ah-VALE-ah-BILL-ih-TEE) 15 mechanism of action 13 teratogen (tare-AT-oh-jen) 17
chemical name 14 pharmacologic classification therapeutic classification
combination drugs 15 (FAR-mah-koh-LOJ-ik) 13 (ther-ah-PEW-tik) 13
controlled substance 16 prototype drug (PRO-toh-type) 13 trade name 14
Core Concept 2.1 13
T here are many ways that drugs can be classified, from a strict chemical group name to a trade name
provided by the manufacturer. Because of the large number of drugs available, healthcare providers
and consumers must have a system for identifying drugs and determining the limitations of their
use. This chapter covers the methods by which drugs may be organized—by therapeutic or pharmacologic
classification. This chapter also discusses drug schedules and pregnancy categories.
Drugs may be organized by their therapeutic

and pharmacologic classifications. core concept 2.1
Medications may be classified in two major ways. Drugs may be organized by therapeutic usefulness. This
is referred to as a therapeutic classification. Drugs may also be categorized by mechanism of action or
how they work pharmacologically. This is referred to as a pharmacologic classification. Both methods are
widely used in studying pharmacology, even though healthcare providers often do not make the distinction
when the primary purpose of drug therapy is to improve the health of their patients.
Table 2.1 ◆ shows the method of therapeutic classification, using cardiac care as the example. The
cardiovascular system is concerned with the proper functioning of the heart and blood vessels. Different
types of drugs affect specific cardiovascular functions. Some drugs influence blood clotting, whereas oth-
ers lower blood cholesterol or prevent the onset of stroke. Drugs may be used to lower blood pressure, treat
heart failure, correct abnormal heart rhythm, alleviate chest pain, and treat or prevent circulatory shock.
Drugs that affect cardiac disorders may be placed in numerous therapeutic classes. Drugs that influence
blood clotting are called anticoagulants; those that lower blood cholesterol are called antihyperlipidemics,
and those that lower blood pressure are called antihypertensives.
A therapeutic classification need not be complicated. For example, it is appropriate to classify a medi-
cation simply as “a drug used for stroke” or “a drug used for shock.” The key to therapeutic classification is
to state clearly what a particular drug does clinically. A few additional examples of therapeutic classifica-
tion are antiemetics (to prevent vomiting or emesis), antacids (to reduce GI acid), anti-inflammatory drugs
(to reduce inflammation), and antibiotics (to fight infective microorganisms).
Pharmacologic classification addresses how the medication produces its effects within the body. This
method most directly applies to the foundational areas of science study including principles of cellular and
molecular biology.
Table 2.2 ◆ shows various types of pharmacologic classifications using high blood pressure
(hypertension) as an example. A diuretic is a class of drug used to treat hypertension by lowering plasma
volume. Lowering plasma volume is the mechanism of action by which diuretics work. Calcium channel
blockers treat hypertension by limiting the force of heart contractions. Other drugs, such as angiotensin-
converting enzyme inhibitors, block components of the hormonal network called the renin-angiotensin
pathway, thereby reducing hypertension. Notice that each example describes how hypertension may be
controlled. Thus, the drug’s pharmacologic classification is more specific than its therapeutic classification
and requires application of human biochemical and physiological principles.
Before studying a particular drug’s mechanism of action, it is recommended that students first become
comfortable with the broad drug classes and then gradually move to more specific examples. Prototype
drugs are an excellent place to start. A prototype drug is the well-understood drug model to which other
medications in a pharmacologic class are compared. By learning the prototype drug, students may then pre-
dict the actions and adverse effects of other drugs in the same class. For example, by knowing the effects of
penicillin V, students can apply this knowledge to the other drugs in the penicillin antibiotic class. Students
should be aware, however, that in many cases the original drug prototype is not the most widely used
T a b l e 2 . 1 Organizing Drugs by Therapeutic Classification

Therapeutic Focus
Cardiac care: Drugs affecting cardiovascular function
Therapeutic Usefulness Therapeutic Classification*
influencing blood clotting anticoagulant
lowering blood cholesterol antihyperlipidemic
lowering blood pressure antihypertensive
treating abnormal heartbeat antidysrhythmic
treating chest pain (angina) antianginal drug
*Note: Although the names of some therapeutic categories may sound complicated, drug terminology will
become more familiar as you begin to study drugs and drug classes. When studying this topic, always refer to a
medical dictionary and reference drug guide.
14 Chapter 2 Drug Classes, Schedules, and Categories
T a b l e 2 . 2 Organizing Drugs by Pharmacologic Classification

Focusing on Physiological Action
Therapy for high blood pressure may be achieved by:
Mechanism of Action Pharmacologic Classification
lowering plasma volume diuretic
blocking heart calcium channels calcium channel blocker
blocking hormonal activity angiotensin-converting enzyme inhibitor
blocking stress-related activity adrenergic blocker (drug that inhibits actions
of the sympathetic nervous system)
dilating peripheral blood vessels vasodilator
drug in its class. As new drugs are developed, features such as antibiotic resistance, fewer side effects, or
a more precise site of action might be factors that sway healthcare providers away from using the older
drugs. Therefore, to master the subject of pharmacology, it is essential not only to be familiar with the
drug prototypes but also to keep up with newer and more popular drugs. For all prototype drugs featured in
this book, both therapeutic and pharmacologic classifications are provided to help students organize drug
information.
Concept Review 2.1

■ What is the difference between a therapeutic classification and a pharmacologic classification?
What is a prototype drug, and how is the prototype drug similar to and d
ifferent from other
drugs within the same pharmacologic or therapeutic class?
core concept 2.2 Drugs have more than one name.
A major challenge when studying pharmacology is learning thousands of drug names. Adding to this dif-
ficulty is the fact that most drugs have multiple names. The three basic types of drug names are chemical,
generic, and trade.
A chemical name is assigned using standard nomenclature established by the International Union of
Pure and Applied Chemistry (IUPAC). A drug has only one chemical name, which is helpful in predicting
its physical and chemical properties. Although chemical names convey a clear and concise meaning about
the nature of a drug, they are often very complicated and difficult to pronounce and remember. For example,
the chemical name of diazepam is 7-chloro-1, 3-ciphydro-1-methyl-5-phenyl-2H-1, 4-benzodiazepin-2-one.
In only a few cases, usually when the name is brief and easily remembered, are chemical names com-
monly used. Examples of brief (and therefore useful) chemical names include lithium carbonate, calcium
gluconate, and sodium chloride.
More practically, drugs are sometimes classified by a portion of their chemical structure, known as the
chemical group name. Examples are antibiotic drugs, such as the fluoroquinolones and beta-lactam medi-
cations. Other common examples include the phenothiazines, thiazides, and benzodiazepines. Although
names like these may seem complicated at first, familiarity with chemical group names will grow, and the
nomenclature will become more manageable as students become more proficient and communicate with
fellow healthcare providers.
The generic name of a drug is assigned by the U.S. Adopted Name Council. With few exceptions,
generic names are less complicated and easier to remember than chemical names. Many organizations,
including the FDA, the U.S. Pharmacopoeia, and the World Health Organization, routinely describe a med-
ication by its generic name. Because there is only one generic name for each drug, healthcare providers
routinely use this name, and pharmacology students generally must memorize it.
A drug’s trade name is assigned by the company marketing the drug. The name is usually selected for
marketability, and it is usually easy to remember. The trade name is also called the proprietary, product,
or brand name. The term proprietary relates to ownership. In the United States, a drug developer is given
exclusive rights to name and market a drug for 17 years after a new drug application (NDA) is submitted
to the Food and Drug Administration (FDA). Because it takes several years before a drug can be approved,
the amount of time spent in approval is subtracted from the 17 years. For example, if it takes seven years
for a drug to be approved, competing companies will not be allowed to market a generic equivalent drug for
another 10 years. The rationale for this is that the developing company must be allowed sufficient time to
recoup the millions of dollars spent in research and the time needed to develop the new drug. After 17 years,
Core Concept 2.3 15
T a b l e 2 . 3 Trade Name Products Containing Popular Generic Substances

Generic Substances Trade Names
aspirin Acuprin, Anacin, Aspergum, Bayer, Bufferin, Ecotrin, Empirin,
Magnaprin, Miniprin, Ridiprin, Sloprin, Uni-Buff, Uni-Tren, Zorprin
diphenhydramine Aler-Dryl, Allergia-C, Benadryl, Compoz Nighttime Sleep Aid,
Diphedryl, Diphenadryl, Hydramine, Nytol, Pardryl, PediaCare
Children’s Allergy, Sominex, Unisom
ibuprofen Advil, Dolgesic, Genpril, Haltran, IB Pro, Midol, Motrin, Nuprin, Rufen,
Tab-Profen, Ultraprin
competing companies may sell a generic equivalent drug, using a different trade name, which the FDA
must approve.
Trade names may be a challenge because of the dozens of product names containing similar ingre-
dients. In addition, some combination drugs contain more than one active generic ingredient, making
it difficult to match one generic name with one product name. As an example, refer to Table 2.3 ◆ and
consider the drug diphenhydramine (generic name), also called Benadryl (one of many trade names).
Diphenhydramine is an antihistamine. Low doses of diphenhydramine can be purchased over the counter;
higher doses require a prescription. When looking for diphenhydramine, healthcare providers may find it
listed under many trade names, such as Allerdryl and Compoz. Diphenhydramine may be provided alone
or in combination with other active ingredients. Ibuprofen and aspirin are also examples of drugs with
many different trade names. The rule of thumb is that a formulation’s active ingredients are listed in the
ingredients by their generic names. The generic name is usually written in lowercase, whereas the trade
name is capitalized.
Concept Review 2.2

■ What are the differences between a chemical, a generic, and a trade name? Which name
is most often used to describe the active ingredients within a drug product?
The differences between brand name drugs and their generic

equivalents include price, formulations, and, most importantly,
bioavailability. core concept 2.3
Usually generic drugs are less expensive than brand name drugs. The reason is that a pharmaceutical com-
pany determines the price of a proprietary drug during its 17 years of exclusive rights to that new drug.
Because there is no competition, the price can be kept quite high. The pharmaceutical company that devel-
oped a drug can sometimes use legal tactics to extend its exclusive rights to a drug, earning the company
hundreds of millions of dollars per year in profits for a popular medicine. Once the exclusive rights end,
competing companies market the generic drug for less money, and consumer savings may be considerable.
In some states, pharmacists may routinely substitute a generic drug when the prescription calls for a brand
name. In other states, the pharmacist must dispense drugs directly as written by the healthcare practitioner
or obtain approval before providing a generic substitute.
The companies that market brand name drugs often aggressively oppose laws that might restrict the
routine use of their products. They claim that significant differences exist between a trade name drug and
its generic equivalent, and that switching to the generic drug may be harmful to the patient. Patient advo-
cates, on the other hand, argue that generic substitutions should always be permitted because of the cost
savings.
Are there real differences between a brand name drug and its generic equivalent? Despite the fact that
the dosages may be identical, drug formulations are not always the same. The two drugs may have different
inert ingredients or be processed differently. For example, in a tablet form, the active ingredients may be
more tightly compressed in one of the preparations than in another, and this might affect how well the body
can use the drug.
The key to comparing brand name drugs and their generic equivalents lies in measuring the bioavail-
ability of the two preparations. Bioavailability is the physiologic ability of the drug to reach its target cells bio 5 in the living organism
and produce its effect (Figure 2.1 ■). Anything that affects absorption of a drug or its distribution to the availability 5 free to activate
cellular targets
target cells will certainly affect drug action. Measuring how long a drug takes to exert its effect gives phar-
macologists a crude measure of bioavailability. For example, if a patient is in circulatory shock and it takes
a generic drug five minutes longer than the brand name drug to produce its effect, that difference would
Figure 2.1
Drug
Portal Liver
vein
Absorption Bioavailability (To tissues)
Gut
wall
Metabolism
To feces
A drug’s bioavailability will depend on the dosage form and how much will actually reach the target location.
be significant. However, if a generic medication for arthritis pain relief takes 45 minutes to act, compared
with the brand name drug that takes 40 minutes, it probably does not matter which drug is prescribed.
In some cases, pharmacists must inform or notify patients of substitutions of generics for brand names.
Pharmaceutical companies and some healthcare providers have supported disclosure of substitution, claim-
bio 5 in the living organism ing that generic drugs—even those that have small differences in bioavailability and b ioequivalence or
equivalence 5 same impact same impact in the body—could adversely affect outcomes in patients with critical conditions or illnesses.
Some states have compiled a negative formulary, a list of trade name drugs that pharmacists may not dis-
pense as generic drugs. These drugs must only be dispensed exactly as written on the prescription, using
the trade name drug the physician prescribed. However, laws frequently change: In many instances, the
efforts of consumer advocacy groups have led to changes in or elimination of negative formulary lists.
core concept 2.4 Drugs with a potential for abuse are categorized into schedules.
Some drugs are frequently abused or have a high potential for becoming addictive. Technically, addiction
refers to the overwhelming feeling that drives someone to use a drug repeatedly. Dependence is a related
term, often defined as a physiologic or psychological need for a substance. Physical dependence refers
to an altered physical condition caused by the nervous system adapting to repeated drug use. In this case,
when the drug is no longer available, the individual experiences physical signs of discomfort known as
withdrawal. In contrast, when an individual is psychologically dependent, there are few signs of physi-
cal discomfort when the drug is withdrawn; however, the individual feels an intense compelling desire to
continue drug use. These concepts are discussed in detail in Chapter 7.
Drugs that cause dependency are restricted to use in situations of medical necessity, that is, if they
are allowed at all. According to law, drugs that have a significant potential for abuse are placed into five
categories called schedules. These scheduled drugs are classified according to their potential for abuse:
Schedule I drugs have the highest potential for abuse, and Schedule V drugs have the lowest. Schedule I
drugs have little or no therapeutic value or are intended for research purposes only. Drugs in the other four
schedules may be dispensed only in cases when therapeutic value has been determined. Schedule V is the
only category in which some drugs may be dispensed without a prescription because the quantities of the
controlled drug are so low that the possibility of causing dependence is extremely remote. Table 2.4 ◆
shows the five drug schedules with examples. However, not all drugs with an abuse potential are regulated
or placed into schedules. Tobacco, alcohol, and caffeine are significant examples.
In the United States, a controlled substance is a drug restricted by the Controlled Substances Act
of 1970 and later revisions. The Controlled Substances Act is also called the Comprehensive Drug Abuse
Prevention and Control Act. This act has several implications for the drugs in the controlled substances
schedules. Hospitals and pharmacies must register with the Drug Enforcement Administration (DEA) and
use their assigned registration numbers to purchase scheduled drugs. They must maintain complete records
of all quantities purchased and sold. Drugs with higher abuse potential have more restrictions. For exam-
ple, in the hospital a special drug order form must be used to obtain Schedule II drugs, and orders must be
written and signed by the healthcare providers. Telephone orders to a pharmacy are not permitted. Refills
for Schedule II drugs are not permitted; patients must visit their healthcare providers first. Those convicted
of unlawful manufacturing, distributing, and dispensing of controlled substances face severe penalties.
Core Concept 2.5 17
T a b l e 2 . 4 Drug Schedule and Examples

Drug Abuse Physical Psychological
Schedule Potential Dependence Dependence Examples
I Highest High High heroin, lysergic acid diethylamide (LSD), peyote, methaqualone, and
3,4-methylenedioxymethamphetamine (“ecstasy”)
II High High High hydromorphone, methadone, meperidine, oxycodone, and fentanyl;
amphetamine, methamphetamine, methylphenidate, cocaine,
amobarbital, glutethimide, and pentobarbital
III Moderate Moderate High combination products containing less than 15 mg of hydrocodone
per dosage unit, products containing not more than 90 mg of
codeine per dosage unit, buprenorphine products, benzphetamine,
phendimetrazine, ketamine, and anabolic steroids
IV Lower Lower Lower alprazolam, clonazepam, clorazepate, diazepam, lorazepam,
midazolam, temazepam, and triazolam
V Lowest Lowest Lowest cough preparations containing not more than 200 mg of codeine per
100 mL or per 100 g
The DEA authorizes healthcare providers to prescribe controlled substances. The federal legislation that gives the DEA the right to control drugs
of abuse (and thus affects which drugs can be prescribed or not) is the Controlled Substances Act. See the Drug Enforcement Agency website.
In order to assess fetal risks, all prescription drugs are classified

according to safety in pregnancy categories. core concept 2.5
A major concern of expectant parents is whether a drug will harm their developing baby. Any substance
that will harm a developing fetus or embryo is referred to as a teratogen. Pregnant patients should never terato 5 severe deformity
take any prescribed, illegal, or OTC drug or any herbal or dietary supplement without the advice of their gen 5 something that
produces
healthcare providers.
To protect the fetus from the teratogenic effects of prescription drugs, the FDA has implemented
a category system for classifying drugs based on how safe they are for the mother and the developing
baby. According to this system, drugs are placed into one of five pregnancy categories, labeled as A, B,
C, D, and X. These labels appear within package inserts and identify levels of risk to women and/or the
fetus. The levels are based on degrees to which a drug has been proven to cause birth defects in laboratory
animals or in human beings. These categories are summarized in Table 2.5 ◆.
Consumers sometimes question whether the testing of laboratory animals is an effective way to predict
harm to a developing human fetus or embryo. Results from animal testing are not always transferable to the
human body. In fact, results from animal experimentation often vary from species to species. For this reason,
consumers should always be cautious, even when there is reasonable assurance that a drug is extremely safe.
T a b l e 2 . 5 Categories of Safety in Pregnancy

Safety Category Explanation Examples
A Lowest Risk Studies HAVE NOT shown a risk to women or to the fetus. ferrous fumarate (Ferranol), levothyroxine (Synthroid),
potassium chloride (KCl), potassium gluconate (Kaon
Tablets), prenatal multivitamins, thyroglobulin (Proloid)
B ANIMAL studies HAVE NOT shown a risk to the fetus or, if amoxicillin (Amoxil), fluoxetine (Prozac), insulin (Humulin R),
they have, studies in women have not confirmed this risk. loperamide (Imodium), penicillins, ranitidine (Zantac)
C ANIMAL studies HAVE shown a risk to the fetus, but con- acyclovir (Zovirax), amitryptiline (Elavil), furosemide
trolled studies have not been performed in women. (Lasix), hydrochlorothiazide (HydroURIL), iron dextran (K
FeRON), mineral oil (Fleet Mineral Oil), senna (Senokot)
D Use of this drug category MAY cause harm to the fetus, but ACE inhibitors, alcohol, cortisone acetate (Cortistan),
it may provide benefit to the mother in a life-threatening nonsteroidal anti-inflammatory drugs in the third
situation or when a safer therapy is not available. trimester, tetracyclines
X Highest Risk Studies HAVE shown a significant risk to women and to castor oil (Purge), isotretinoin, methotrexate, most oral
the fetus. contraceptives, norethindrone (Norlutin), oxymetholone
(Anadrol), progesterone (oral forms), statins, warfarin
(Coumadin)
Chapter Review
2.1 Drugs may be organized by their therapeutic and does not object. When generic drugs are substituted,
pharmacologic classifications. differences in bioavailability may affect the safety
Two common ways to classify drugs are by therapeu- and effectiveness of drug therapy.
tic classification and pharmacologic classification.
2.4 Drugs with a potential for abuse are categorized
Therapeutic classes are based on a drug’s clinical
into schedules.
usefulness. Pharmacologic classes are based on a
drug’s mechanism of action. Prototype drugs are Drugs that have the potential for abuse or
used to compare drugs within the same classification. dependency are placed into one of five schedules,
Knowing about prototype drugs can help students Schedule I is the most restrictive category. S
chedule
understand other, similar drugs. V is the least restrictive category. The U.S. Drug
Enforcement Administration (DEA) handles drug
2.2 Drugs have more than one name. misuse.
Drugs may be described by a chemical, generic, or
2.5 In order to assess fetal risks, all prescription drugs
trade name. There are advantages and disadvantages
are classified according to safety in pregnancy
to each naming method.
categories.
2.3 The differences between brand name drugs and In the United States, all drugs are placed into one of
their generic equivalents include price, formula- five pregnancy categories: A, B, C, D, and X. Drugs
tions, and, most importantly, bioavailability. in category A are the safest; those in category X are
In most states, generic drugs may be substituted for the most harmful.
brand name products if the prescribing practitioner
Review Questions
The following questions are written in 4. Which of the following statements is correct?
NCLEX-PN® style. Answer these ques- 1. Because chemical drug names are often complicated and
tions to assess your knowledge of the difficult to remember or pronounce, the chemical structure
chapter material, and go back and review of a drug is rarely considered in pharmacotherapy.
any material that is not clear to you. 2. Matching one active ingredient with one trade name prod-
uct is not a particularly challenging job for the healthcare
provider.
1. Which of the following types of drug classification 3. When referring to a drug, the generic name is usu-
f ocuses on what a drug does clinically? ally capitalized, whereas the trade name is written in
1. Therapeutic lowercase.
2. Pharmacologic 4. The drug trade name is sometimes called the proprietary
3. Chemical name, suggesting ownership.
4. All of the above
2. How a medication produces its effects in the body is referred 5. When examining the question, “Are there real differences
to as a drug’s: between brand name drugs and their generic equivalents?” the
1. Therapeutic usefulness answer that emerges from reading this chapter is:
2. Mechanism of action 1. Drug formulations for brand name drugs are the same as
3. Model for other drugs combating similar diseases their generic equivalents.
4. Clinical focus 2. Brand name drugs are always more tightly compressed
than generic drugs.
3. In which of the following categories does a drug have
3. Generic drugs are always best because they generally cost
only one name?
less.
1. Chemical name 4. Brand name drugs are sometimes preferred because
2. Generic name of differences in bioavailability compared to generic
3. Trade name equivalents.
4. Both 1 and 2
Chapter Review 19
6. Which of the following are true statements about a nega- 3. Restrict the use of all drugs that have an abuse potential.
tive formulary list of trade name drugs? (Select all that apply.) 4. Allow patients to obtain Schedule II drug refills without
1. It is a list of trade name drugs that cannot be substituted visiting their healthcare provider first.
with generic drugs. 9. The drug schedule that allows therapeutic use of a drug
2. It is consistent throughout the United States. with a prescription but contains drugs with relatively lower
3. The drugs on the list must be dispensed by the pharmacist abuse and dependency potential than other scheduled drugs is:
using the drug’s trade name as written on the prescription.
4. It was formed because of concern over the bioavailability 1. Schedule II
of generic drugs and possible adverse effects on patient 2. Schedule III
outcomes. 3. Schedule IV
4. Schedule V
7. An altered physical condition caused by the nervous sys-
tem adapting to repeated drug use is: 10. When preparing to administer medications to pregnant
p atients, nurses should know that their patients:
1. Addiction
2. Physical dependence 1. Are not at risk if they take drugs placed into pregnancy
3. Psychological dependence safety category X
4. Withdrawal 2. Can take herbal or dietary supplements without fear of
teratogenic effects to their developing baby
8. The Controlled Substances Act of 1970 and later revi- 3. Are relatively safe if they take medications within pregnancy
sions enable the DEA to do which of the following? safety category B
1. Introduce drugs into the marketplace. 4. Should never take drugs classified as pregnancy safety
2. Restrict the use of drugs that have a significant potential category D
for abuse.
website.

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3 Methods of Drug Administration
Core Concepts
3.1
A major goal in pharmacotherapy is to limit the 3.6
Certain protocols and techniques are common to all
number and severity of adverse drug events. methods of drug administration.
3.2
The rights of drug administration form the basis of 3.7
Enteral drugs are given orally or via nasogastric or
proper drug delivery. gastrostomy tubes.
3.3
Successful pharmacotherapy depends on patient 3.8
Topical drugs are applied locally to the skin and
compliance. associated membranes.
3.4
Healthcare providers use accepted abbreviations 3.9
Parenteral administration refers to dispensing
to communicate the directions and times for drug medications by routes other than oral or topical.
administration.
3.5
Three systems of measurement are used in pharma-
cology: metric, apothecary, and household.
Learning Outcomes
1. Discuss drug administration as a 4. Give specific examples of how the 7. Explain the proper methods to
component of safe and effective healthcare provider can increase administer enteral, topical, and
health care. patient compliance in taking parenteral drugs.
2. Describe the roles and medications. 8. Compare and contrast the
responsibilities of nurses, nursing 5. Interpret abbreviations used in drug advantages and disadvantages of
assistants, therapists, and technicians administration practices. each route of drug administration.
regarding drug administration. 6. Compare and contrast the three
3. Explain how the six rights of drug systems of measurement used in
administration affect patient safety. pharmacology.
Key Terms
adverse drug events 21 compliance (kom-PLY-ans) 22 intramuscular (IM) route
adverse effects 21 contraindications (IN-trah-musk-u-lar) 36
allergic reaction 22 (CON-trah-EN-deh-KAY-shuns) 21 intravenous (IV) route
enteral route (EN-tur-ul) 27 (IN-trah-VEE-nus) 37
anaphylaxis (ANN-ah-fah-LAX-iss) 22
enteric-coated (in-TARE-ik) 27 metric system 24
apothecary system
(ah-POTH-eh-kare-ee) 25 household systems 25 orally disintegrating tablets (ODTs) 27
astringent effect (ah-STRIN-jent) 31 intradermal (ID) route parenteral route (pah-REN-tur-ul) 32
buccal route (BUCK-ahl) 27 (IN-trah-DERM-ul) 33 prn order 23
Core Concept 3.1 21
routine orders 24 STAT order 23 three checks of drug

single order 23 subcutaneous (SC or SQ) route administration 22
six rights of drug (sub-kew-TAY-nee-us) 33 topical route (TOP-ik-ul) 28
administration 22 sublingual (SL) route (sub-LIN-gwal) 27 transdermal (trans-DER-mul) 29
standing order 24 sustained-release 27 transmucosal (trans-mew-KOH-sul) 31
D rug administration is an important part of providing comprehensive care to the patient. During
drug administration, members of the healthcare team collaborate closely with pharmacists, physi-
cians, their patients, and each other to ensure the safe delivery of prescribed medications. The pur-
pose of this chapter is to introduce the roles and responsibilities of nurses and other healthcare providers, to
define the practice of secure and effective distribution of medications, and to provide a basic overview of
the major routes of drug administration.
A major goal in pharmacotherapy is to limit the number and severity

of adverse drug events. Core Concept 3.1
Whether administering drugs, supervising drug use, or providing assistance, the healthcare provider is ex-
pected to be familiar with the general principles of drug delivery. The large number of different drugs and
the potential consequences of medication errors make this an enormous task.
The main responsibilities of the nurse include knowledge and understanding of the following:
■ What drug is ordered
■ Name (generic and trade) and drug classification
■ Intended or proposed use
■ Expected therapeutic effects on the body
■ Situations under which drugs should not be used, or contraindications contra 5 opposing
indications 5 useful applications
■ Special considerations (e.g., the effects of age, weight, body fat distribution, and individual
pathophysiological states on pharmacotherapeutic response)
■ Unwanted nontherapeutic effects, adverse effects (or side effects) adverse 5 negative
effects 5 drug responses
■ Why the medication has been prescribed for this particular patient
■ How the medication is supplied by the pharmacy
■ How the medication should be administered, including dosage ranges
■ What nursing process considerations related to the medication apply to this patient
Nursing assistants, therapists, and technicians work closely with nurses to provide care to the patients.
Members of the health support staff who do not administer medications but who have an equally important
role in providing care to the patients have a slightly different list of tasks than nurses. These tasks provide
opportunities to monitor patients and make sure no unusual reactions or undesirable effects result from the
medication. Tasks include:
■ Monitoring blood pressure, pulse rate, and respiration rate
■ Changing soiled or wet clothing, wraps, or bandages
■ Dressing wounds, giving massages, and caring for the skin’s surface
■ Preparing food trays or helping to feed patients
■ Observing patients and reporting significant symptoms, reactions, or changes in medical condition
■ Reporting strange behaviors or habits in patients
■ Helping transport patients
■ Monitoring special equipment
Before any drug is administered, healthcare staff must obtain, process, and communicate important in-
formation to one another about the patient’s medical history, physical assessment, disease processes, learn-
ing needs, and capabilities. They must consider growth and developmental factors and remember that many
variables can influence how a patient responds to medications. Understanding these variables can increase
the success of pharmacotherapy. A major goal of pharmacotherapy is to limit the number and severity of
adverse drug events. Many adverse effects are preventable. By applying their experience and knowledge
of pharmacotherapeutics to clinical practice, healthcare providers can avoid many serious adverse drug
22 Chapter 3 Methods of Drug Administration
reactions. Some adverse events, however, are not preventable. It is vital that the healthcare team is prepared
to recognize and respond to potentially damaging medication effects. Allergic and anaphylactic reactions are
particularly serious effects that must be carefully monitored and prevented, when possible.
An allergic reaction is an acquired hyper-response of body defenses to a foreign substance
(allergen). Signs of allergic reactions vary in severity and include skin rash with or without itching, edema,
nausea, diarrhea, runny nose, or reddened eyes with tearing. On discovering that a patient is allergic to a
product, it is the nurse’s responsibility to first alert the charge nurse and patient’s physician of the reaction in
case it is necessary to give the patient medications to reverse the reaction. Next the nurse should document
the allergy in the medical record and apply labels to the chart and medication administration record so that
all healthcare personnel will be aware of the allergy. An agency-approved allergy bracelet should be placed
on the patient. The pharmacist should also be told so that the medication can be checked for cross-sensitivity
with other pharmacologic products. The pharmacotherapy of allergic reactions is covered in Chapter 25.
Anaphylaxis is a severe type of allergic reaction in which massive amounts of histamine and other
chemical mediators of inflammation are released throughout the body. It can lead to life-threatening shock.
Symptoms of anaphylaxis are severe shortness of breath, a sudden drop in blood pressure, and tachycar-
dia. These symptoms require immediate attention. The pharmacotherapy of anaphylaxis is covered in
Chapter 21.
Core Concept 3.2 The rights of drug administration form the basis of proper drug delivery.
The traditional six rights of drug administration form the operational basis for the safe delivery of medi-
cations and are recognized by such organizations as the Institute for Safe Medication Practices (ISMP).
The six rights are simple and practical guidelines for nurses to use during drug preparation, delivery, and
administration. The six rights are as follows:
■ Right patient
■ Right medication
■ Right dose
■ Right route of administration
■ Right time of delivery
■ Right documentation
Additional rights have been added over the years, depending on particular academic curricula or
agency policies. Additions to the original six rights include the right to refuse medication, the right to re-
ceive drug education, and the right preparation.
The three checks of drug administration that nurses use with the six rights help to ensure patient
safety and drug effectiveness. Traditionally these checks include the following:
■ Checking the drug with the medication administration record (MAR) or medication informa-
tion system when removing it from the medication drawer, refrigerator, or controlled substance
locker
■ Checking the drug when preparing it, pouring it, taking it out of the unit dose container, or con-
necting the IV tubing to the bag
■ Checking the drug before administering it to the patient
Despite the use of these checks and rights to provide safe drug delivery, errors still occur, and some of them
are fatal. Although the nurse is accountable for preparing and administering medications, many individuals—in-
cluding physicians, pharmacists, and other healthcare providers—are also responsible for safe drug practices.
Core Concept 3.3 Successful pharmacotherapy depends on patient compliance.
Patient adherence or compliance is another major factor affecting the success of pharmacotherapy. Compliance
means taking a medication in the way it was prescribed by the practitioner or, in the case of over-the-counter
(OTC) drugs, following the instructions on the label. Patient noncompliance can include not taking the medication
at all, taking it at the wrong time, or taking it in the wrong way.
Even when healthcare providers conscientiously use all the principles of effective drug administra-
tion, patients may not agree that the prescribed drug regimen is worthwhile. Before administering the drug,
the nurse should use the nursing process to develop a personalized care plan that will allow the patient to be
an active participant in his or her care. Support staff can help ensure that the care plan works. It is impor-
tant to remember that a responsible, well-informed adult always has the legal option to refuse any medica-
tion. This right allows the patient to accept or reject the pharmacotherapy based on accurate information
presented in a way the patient can understand.
Core Concept 3.4 23
Fast Facts Potentially Fatal Drug Reactions
Toxic Epidermal Necrolysis (TEN)

■ Skin sloughing of 30% or more of the body (caused by skin cell breakdown)
■ Severe and deadly allergic reaction caused by a drug
■ Occurs when the liver fails to properly break down a drug, which then cannot be excreted
normally
■ Risk of death decreased if the drug is quickly withdrawn and supportive care is maintained
Stevens-Johnson Syndrome (SJS)

■ Skin sloughing of 10% of the body
■ Generalized blister-like lesions following within a few days
■ Usually signaled initially by nonspecific upper respiratory infection (URI) with chills, fever, and
malaise
In the plan of care, it is important to address information that the patient must know about the pre-
scribed medications. This includes the name of the drug; why it was ordered; its expected actions; its
possible side effects; and its potential interactions with other medications, foods, herbal supplements, or
alcohol. Patients need to be reminded that they have an active role in ensuring the effectiveness and safety
of their medications.
Many factors influence whether patients comply with pharmacotherapy. The drug may be too Life Span Fact
expensive or may not be approved by the patient’s health insurance plan. Patients sometimes forget doses
of medications, especially when they must be taken three or four times per day. Patients often stop using Many older adults take at least
drugs that have annoying side effects or that affect lifestyle. Adverse effects such as headache, dizziness, three different drugs each day,
nausea, diarrhea, or impotence often cause noncompliance. Patients sometimes self-adjust their doses. with some taking as many as
Some patients believe that if one tablet is good, two must be better. Others believe that they will become eight or more. This leads to
poor compliance among older
dependent on the medication if it is taken as prescribed, and so they take only half the required dose. patients. Noncompliance can
Patients usually do not want to admit or report noncompliance to the nurse because they are embarrassed be even greater for elderly
or fear being reprimanded. Because there are many reasons for noncompliance, the nurse must carefully patients with dementia or
question patients about their medications. When pharmacotherapy fails to produce the expected outcomes, Alzheimer’s disease.
noncompliance should be considered as a possible reason.
Healthcare providers use accepted abbreviations to communicate

the directions and times for drug administration. Core Concept 3.4
Table 3.1 ◆ lists common abbreviations that are used to give directions about drug administration. A STAT
order refers to a medication that should be given immediately and only once. This order is often used with
emergency medications that are needed for life-threatening situations. The physician normally notifies the
nurse of any STAT order, so it can be obtained from the pharmacy and administered immediately.
A single order is for a drug that is to be given only once and at a specific time. An example is a
preoperative order. A prn order is administered as required by the patient’s condition. The nurse makes
the judgment, based on patient assessment, as to when the medication should be administered. Orders
Fast Facts Grapefruit Juice and Drug Interactions

■ Grapefruit juice may not be safe for people who take certain medications.
■ Chemicals in grapefruit juice lower the activity of specific enzymes in the intestinal tract that nor-
mally break down medications. This allows a larger amount of medication to reach the bloodstream,
resulting in increased drug activity.
■ Drugs that may be affected by grapefruit juice include certain sedative-hypnotic drugs, antibiotics,
drugs that lower blood cholesterol, some antihistamines, and antifungal agents.
■ Grapefruit juice should be consumed at least two hours before or five hours after taking a medica-
tion that may interact with it.
■ Some drinks that are flavored with fruit juice could contain grapefruit juice, even if grapefruit is not
part of the name of the drink. Check the ingredients label.
Table 3.1 Drug Administration Abbreviations*

Abbreviation Meaning Abbreviation Meaning
ac before meals prn when needed/necessary
ad lib as desired/as directed q every
AM Morning qh every hour
ASAP as soon as possible qid four times per day
bid twice per day q2h every 2 hours (even)
cap capsule q4h every 4 hours (even)
/d per day q6h every 6 hours (even)
gtt drop q8h every 8 hours (even)
h or hr hour q12h every 12 hours
hs hour of sleep/bedtime Rx take
no number SL sublingual
pc after meals; after eating STAT immediately; at once
PM afternoon tab tablet
PO by mouth tid three times per day
*Many more abbreviations could be listed. The Joint Commission (formerly JCAHO) recommends that some previ-
ously used abbreviations be spelled out to avoid medication errors: Use “daily” (not qd); use “nightly” (not qhs);
use “every other day” (not qod). For additional information, see The Joint Commission’s official “Do Not Use
List”.
not written as single, STAT or prn are called routine orders. These are usually carried out within two
hours of the time the order is written by the physician, but the exact timing is defined by each facility.
A standing order is written in advance of a situation and should be carried out under specific circum-
stances. An example of a standing order is a set of postoperative prn prescriptions that are written for all
patients who have undergone a specific surgical procedure. A common standing order for patients who
have had a tonsillectomy is “Tylenol elixir 325 mg PO q6h prn sore throat.” Because of the legal impli-
cations of putting all patients into a single treatment category, standing orders are no longer permitted in
some facilities.
Agency policies dictate that drug orders be reviewed by the attending physician within specific time
frames, usually at least every seven days. Prescriptions for narcotics and other scheduled drugs are often
automatically stopped after 72 hours, unless specifically reordered by the physician. Automatic stop orders
do not generally apply when the number of doses, or an exact period of time, is specified.
Some medications must be taken at specific times. If a drug causes stomach upset, it is usually ad-
ministered with meals to prevent epigastric pain, nausea, or vomiting. Other medications should be admin-
istered between meals because food interferes with absorption. Some CNS drugs and antihypertensives
are best administered at bedtime, because they may cause drowsiness. Others, such as sildenafil (Viagra),
should be taken 30 to 60 minutes prior to intended sexual intercourse to achieve an erection. The nurse
must pay careful attention when educating patients about when and how to take their medications to in-
crease compliance and therapeutic success.
Once medications are administered, the nurse must correctly document that the medications have been
given to the patient. Depending on the facility, documentation is done on the computer using a special
program for medication administration or on a paper copy of the MAR. Either way, it is necessary that the
drug name, dosage, time administered, and any assessments data be documented. For computer documen-
tation, the identification of the nurse administering the medication is done when he or she logs on using
an assigned password. On the paper copy of the MAR, the nurse must initial and sign his or her name. If
a medication is refused or not given as ordered, this fact (along with the reasons) must be recorded on the
appropriate form within the medical record.
Three systems of measurement are used in pharmacology:

Core Concept 3.5 metric, apothecary, and household.
Dosages are labeled and dispensed according to their weight or volume. The most common system of drug
measurement uses the metric system. The volume of a drug is expressed in terms of a liter (L) or a millili-
ter (mL). The abbreviation “cc” for cubic centimeter, a measurement of volume that is equivalent to 1 mL
Core Concept 3.6 25
Table 3.2 Metric, Apothecary, and Household Approximate Measurement Equivalents

Metric Apothecary Household
1 mL 15–16 minims 15–16 drops
4–5 mL (cc) 1 fluid dram 1 teaspoon or 60 drops
15 mL 4 fluid drams 1 tablespoon or 3–4 teaspoons
30 mL 8 fluid drams or 1 fluid ounce 2 tablespoons
240 mL 8 fluid ounces (1/2 pint) 1 glass or cup
500 mL 1 pint 2 glasses or 2 cups
1L 32 fluid ounces or 1 quart 4 glasses or 4 cups or 1 quart
1 mg 1/60 grain —
60–65 mg 1 grain —
300–325 mg 5 grains —
1g 15–16 grains —
1 kg — 2.2 pounds
To convert grains to grams: Divide grains by 15 or 16.
To convert grams to grains: Multiply grams by 15 or 16.
To convert minims to milliliters: Divide minims by 15 or 16.
of fluid, is no longer recommended for use in medicine. The metric weight of a drug is stated in terms of
kilograms (kg), grams (g), milligrams (mg), or micrograms (mcg). At one time, the abbreviation “µg” was
used for micrograms, but this is no longer recommended. It is now recommended that “micrograms” and
other small unusual measurements be spelled out.
The apothecary system and household systems are older systems of measurement. Although most
physicians and pharmacies use the metric system, these older systems may still be seen. Until the metric
system totally replaces the other systems, the healthcare provider must recognize dosages based on all
three systems of measurement. Approximate equivalents among metric, apothecary, and household units of
volume and weight are listed in Table 3.2 ◆.
Because Americans are familiar with the teaspoon, tablespoon, and cup, it is important for the nurse
to be able to convert between the household and metric systems of measurement. In the hospital, a glass
of fluid is measured in milliliters—an 8-ounce glass of water is recorded as 240 mL. If a patient being
discharged is ordered to drink 2400 mL of fluid per day, the nurse may instruct the patient to drink ten
8-ounce glasses or 10 cups of fluid per day. Likewise, when a child is to be given a drug that is adminis-
tered in elixir form, the nurse should explain that 5 mL of the drug is the same as one teaspoon. The nurse
should encourage the use of accurate medical dosing devices at home, such as oral dosing syringes, oral
droppers, cylindrical spoons, and medication cups. These are preferred over the traditional household mea-
suring spoon because they are more accurate. Eating utensils that are commonly referred to as teaspoons or
tablespoons often do not hold the volume that their names imply.
Certain protocols and techniques are common to all methods

of drug administration. Core Concept 3.6
The three general routes of drug administration are enteral, topical, and parenteral, with subcategories enteral 5 ingestion
among each general route. Each route has both advantages and disadvantages. Although some drugs are topical 5 surface
formulated to be given by several routes, others are made to be given by only one route. Pharmacokinetic parenteral 5 equivalent to
ingestion (as, for example,
considerations, such as how the route of administration affects drug absorption and distribution, are dis- by intravenous route)
cussed in Chapter 4. Certain protocols and techniques are common to all methods of drug administration.
The student should refer to the drug administration guidelines in the following list before reading about
specific routes of administration in Table 3.3 ◆.
■ Review the medication order and check for drug allergies.
■ Wash hands and put on gloves, if indicated.
■ Use aseptic technique when preparing and administering medications.
■ Identify the patient by asking the person to state his or her full name (or by asking the parent or
guardian if the patient is confused), checking the patient’s identification band, and comparing
this information with the MAR.
■ Ask the patient about known allergies, and check to see if he or she is wearing an allergy
identification band.
■ Ensure that the proper equipment and supplies, such as water and cups, are available at the
bedside.
■ Tell the patient what drug you are administering, the purpose of the drug, and how you will
give it.
■ Position the patient for the appropriate route of administration.
■ If the drug is prepackaged as a unit dose, remove it from the packaging at the bedside.
■ Unless specifically instructed to do so in the orders, do not leave drugs at the patient’s bedside.
■ Document the medication administration and any important patient responses on the MAR.
Table 3.3 Enteral Drug Administration

Drug Form Administration Guidelines
A. Tablet, capsule, or liquid 1. Assist the patient into a sitting position.
2. Check to be sure that the patient is alert and can swallow.
3. Place tablets or capsules into a medication cup.
4. If the medication is liquid, shake the bottle to mix the agent, and measure the dose into the cup
at eye level.
5. Hand the patient the medication cup.
6. Offer a glass of water to facilitate swallowing the medication. Milk or juice may be offered (if not
contraindicated).
7. Remain with the patient until all medication is swallowed.
B. Sublingual 1. Check that the patient is alert and can hold the medication under the tongue.
2. Instruct the patient not to chew or swallow the tablet, or move it around with the tongue.
3. Instruct the patient to allow the tablet to dissolve completely before swallowing saliva.
4. Place the sublingual tablet under the patient’s tongue.
5. Remain with the patient to make sure that all of the medication has dissolved.
6. Offer the patient a glass of water.
C. Buccal 1. Check that the patient is alert and can hold the medication between the gums and the cheek.
2. Instruct the patient to allow the tablet to dissolve completely before swallowing saliva.
3. Instruct the patient not to chew or swallow the tablet or move it around with the tongue.
4. Place the buccal tablet between the gum line and the cheek.
5. Remain with the patient to be sure that all of the medication has dissolved.
6. Offer the patient a glass of water.
D. Nasogastric and gastrostomy 1. Administer liquid forms of the medication when possible to avoid clogging the tube.
2. If the medication is solid, crush it into a fine powder and mix it thoroughly with at least 30 mL of warm
water until dissolved. Undissolved medications may clog the tube.
3. Turn off the feeding tube, if applicable.
4. Verify tube placement. Verification can be done by testing the pH of stomach contents, by injecting
10–30 mL of air and listening with a stethoscope over the stomach area, or (the most reliable way) by
x-ray.
5. Attach a syringe (30 or 60 mL) with plunger. Aspirate the patient’s stomach contents and measure the
volume. This is termed the gastric residual volume. If it is greater than 100 mL (for an adult), check the
facility’s policy.
6. Attach the syringe without plunger. Return the residual contents by allowing it to flow back into the
tube via gravity. Flush the tube with about 10 mL (two teaspoons) of tap water. Amount of water may
vary according to institutional policy or healthcare provider’s order.
7. Pour the medication into the syringe barrel, also allowing it to flow into the tube by gravity. Give each
medication separately, flushing between each with water.
8. Keep the head of the bed elevated at 45° angle for one hour to prevent aspiration.
9. Reestablish continual feeding, as scheduled.
Core Concept 3.7 27
Enteral drugs are given orally or via nasogastric

or gastrostomy tubes. Core Concept 3.7
The enteral route includes drugs given orally and those administered through nasogastric (NG) or gas-
trostomy tubes. Oral drug administration (abbreviated PO, which refers to the Latin per os, meaning “by
mouth”) is the most common, most convenient, and usually the least costly of all routes. It is also consid-
ered the safest route because the skin’s protective barrier is not broken. In cases of overdose, medications
remaining in the stomach can be retrieved by causing vomiting. Oral preparations are available in tablet,
capsule, caplet, and liquid forms. Medications administered by the enteral route take advantage of the large
absorptive surfaces of the oral mucosa, stomach, or small intestine.
Tablets and Capsules

Tablets and capsules are the most common forms of drugs. Patients prefer tablets or capsules over other
forms because they are easy to use. In some cases, tablets may be scored so they can easily be broken if the Life Span Fact
dose needs to be made smaller for a specific patient. Orally disintegrating tablets (ODTs) are a newer For children and elderly pa-
type of drug formulation that allows for quick dissolving and absorption of medications in the mouth or tients, as well as those who
cheek. This approach is especially beneficial to patients who have difficulty swallowing (e.g., pediatric and may have trouble swallowing,
geriatric patients) and for noncompliant patients (e.g., patients with psychiatric disorders). the nurse can sometimes crush
The nurse should always check the manufacturer’s instructions for administering the medication to tablets or open capsules and
be sure that crushing or opening is allowed. Some tablets and capsules should not be crushed or opened sprinkle the drug over food
or mix it with juice to make it
because their ingredients are inactivated by doing so. Other medications can severely irritate the stomach easier to swallow and to hide
mucosa and cause nausea or vomiting. Occasionally, drugs should not be crushed because they irritate the its taste.
oral mucosa, are extremely bitter, or contain dyes that stain the teeth. Most drug guides provide lists of
drugs that may not be crushed. Guidelines for administering tablets or capsules are given in Table 3.3A.
The strongly acidic contents in the stomach can destroy some medications. To overcome this problem,
tablets may have a hard, waxy coating that protects the medicine from acidity. These enteric-coated tablets are
designed to dissolve in the alkaline environment of the small intestine. It is important that the nurse not crush
enteric-coated tablets because the medication would then be directly exposed to the stomach environment.
Studies have clearly shown that patients are less compliant when they must take more than one dose
of medicine per day, particularly if the number is three doses or more. With this in mind, pharmacologists
have tried to design new drugs that need to be administered only once or twice daily. Sustained-release
tablets or capsules are designed to dissolve very slowly. They release medication over a longer time, which
increases the drug’s duration of action (or length of time the medication works). Also called extended-
release (ER), long-acting (LA), or slow-release (SR) medications, these forms allow convenient once or
twice daily dosing. These sustained-release medications must not be crushed or opened.
Giving medications by the oral route has some disadvantages. The patient must be conscious and able to
swallow properly. In addition, children and some adults do not like to swallow large tablets and capsules or
take oral medications that are distasteful. Certain types of drugs, including proteins, are inactivated by diges-
tive enzymes in the stomach and small intestine. Medications absorbed from the stomach and small intestine
first travel to the liver, where they may be inactivated before they ever reach their target organs. This process,
called first-pass metabolism, is discussed in Chapter 4. The significant variation in the motility of the GI tract
among patients and in the tract’s ability to absorb medications can create differences in bioavailability.
Sublingual and Buccal Drug Administration

For sublingual and buccal administration, the patient does not swallow the tablet but instead keeps it in the
mouth until it dissolves. The mucosa of the oral cavity contains a rich blood supply that provides an excel-
lent absorptive surface for certain drugs. Medications given by this route are not destroyed by digestive
enzymes nor do they undergo first-pass metabolism in the liver.
For the sublingual (SL) route, the medication is placed under the tongue and allowed to dissolve slowly.
The rich blood supply under the tongue results in a rapid onset of drug action. Sublingual dosage forms are
most often formulated as rapidly disintegrating tablets or as soft gelatin capsules filled with liquid drug.
When multiple drugs have been ordered, the sublingual preparations should be administered after the
oral medications have been swallowed. The patient should be instructed not to move the drug with the tongue,
nor to eat or drink anything until the medication has completely dissolved. The sublingual mucosa is not suit-
able for extended-release formulations because it is a relatively small area and is constantly being bathed by
saliva. Table 3.3B and Figure 3.1a ■ present important points about sublingual drug administration.
To administer by the buccal route, the tablet, capsule, lozenge, or troche is placed in the oral cavity
between the gum and the cheek. The patient must be instructed not to touch the medication with the tongue,
because it could get moved to the sublingual area where it would be more rapidly absorbed or to the back
of the throat where it could be swallowed. Medications are absorbed more slowly from the buccal mucosa
than from the sublingual area. The buccal route is preferred over the sublingual route for sustained-release
delivery because of its greater mucosal surface area. Drugs formulated for buccal administration generally do
not cause irritation and are small enough to not cause discomfort to the patient. Table 3.3C and Figure 3.1b ■
provide important guidelines for buccal drug administration.
Figure 3.1
(a) Sublingual (under
the tongue) drug
administration;
(b) buccal (between the
gums and cheek) drug
administration.
(a) (b)
Nasogastric and Gastrostomy Drug Administration

Patients with a nasogastric (NG) tube or enteral feeding system such as a gastrostomy (G) tube may have
their medications administered through these devices. The soft, flexible NG tube is inserted by way of the
nasopharynx or oropharynx, with the tip lying in the stomach. A G tube is surgically placed directly into the
patient’s stomach. Generally, the NG tube is used for short-term treatment, whereas the G tube is inserted
for patients who require long-term care. Drugs administered through these tubes are usually in liquid form.
Although solid drugs can be crushed or dissolved, they tend to clog the tubes. Sustained-release drugs should
not be crushed and administered through NG or G tubes. Drugs administered by this route are exposed to the
same physiologic processes as those given orally. If a drug is ordered to be given through either tube, and the
drug should not be crushed, the nurse will need to contact the healthcare practitioner for an appropriate re-
placement medication. Table 3.3D gives important guidelines for administering drugs through NG or G tubes.
Topical drugs are applied locally to the skin

Core Concept 3.8 and associated membranes.
The topical route involves applying drugs locally to the skin or the membranous linings of the eye, ear,
nose, respiratory tract, urinary tract, vagina, and rectum. These applications include the following:
■ Dermatologic preparations These drugs are applied to the skin using formulations that include
creams, lotions, gels, powders, and sprays. The skin is the most common topical route.
■ Instillations and irrigations These drugs are applied into body cavities or orifices, including
the eyes, ears, nose, urinary bladder, rectum, and vagina.
■ Inhalations Inhalers, nebulizers, or positive-pressure breathing apparatuses are used to apply
drugs to the respiratory tract. The most common indication for inhaled drugs is bronchoconstric-
tion due to bronchitis or asthma. Many illegal, abused drugs are taken by this route because it
provides a very rapid onset of drug action.
Drugs can be applied topically to produce a local or a systemic effect. Many drugs are applied topi-
cally to produce a local effect. For example, antibiotics may be applied to the skin to treat skin infections.
Antineoplastic agents may be infused into the urinary bladder via catheter to treat tumors of the bladder
mucosa. Corticosteroids are sprayed into the nostrils to reduce inflammation of the nasal mucosa due to
allergic rhinitis. Local, topical delivery of these drugs produces fewer side effects than oral or parenteral
delivery of the same drugs. When these drugs are given topically, they are absorbed very slowly, and only
small amounts reach the general circulation.
Other drugs are given topically to ensure slow release and absorption of the drug in the general circu-
lation. These agents are given for their systemic (system-wide) effects. For example, a nitroglycerin patch
is not applied to the skin to treat a local skin condition, but to treat the systemic condition of coronary
artery disease. Likewise, prochlorperazine (Compazine) suppositories are inserted rectally not to treat a
disease of the rectum but to alleviate nausea. The distinction between topical drugs given for local effects
Core Concept 3.8 29
and those given for systemic effects is an important one for the nurse to know. In the case of local drugs,
absorption is undesirable and may cause side effects. For systemic drugs, absorption is necessary for the Life Span Fact
therapeutic action of the drug. With either type of topical agent, drugs should not be applied to abraded or Although the procedure for
denuded skin, unless the directions so indicate. administering ophthalmic
drugs is the same with a child
as with an adult, it is advisable
Transdermal Delivery System to enlist the help of an adult
Transdermal patches are an effective means of delivering certain medications. Examples include nitro- caregiver. In some cases, the
glycerin for angina pectoris and scopolamine (Transderm-Scop) for motion sickness. Although transdermal infant or toddler may need to
be immobilized, with the arms
patches contain a specific amount of drug, the rate of delivery and the actual dose received may vary. Patches
wrapped to prevent acciden-
are changed on a regular basis, using a site rotation routine, which should be documented in the MAR. Before tal injury to the eye during
applying a transdermal patch, the nurse should verify that the previous patch has been removed and disposed administration. For the young
off appropriately. Drugs to be administered by this route avoid the first-pass effect in the liver and bypass child, demonstrating the pro-
digestive enzymes.Table 3.4A ◆ and Figure 3.2 ■ illustrate the major points of transdermal drug delivery. cedure using a doll helps gain
the child’s cooperation and
decreases the level of anxiety.
Ophthalmic Administration
The ophthalmic route is used to treat local conditions of the eye and surrounding structures. Common
indications include excessive dryness, infections, glaucoma, and dilation of the pupil during eye examina-
tions. Ophthalmic drugs are available in the form of eye irrigations, drops, ointments, and medicated disks.
Figure 3.3 ■ and Table 3.4B give guidelines for adult administration.
Figure 3.2
(a) (b)
Transdermal patch administration: Put on gloves before handling the patch and read the manufacturer’s directions.
Label the patch with the date and time, and your initials. Remove any previous medication or patch, and cleanse the
area. (a) Remove the protective coating from the patch and (b) apply the patch immediately to clean, dry, hairless skin.
Figure 3.3
Ophthalmic drug ad-
ministration: Instilling
eye drops into the
lower conjunctival sac.
Table 3.4 Topical Drug Administration

A. Transdermal 1. Obtain the transdermal patch and read the manufacturer’s guidelines. The application site and frequency of changing
differ according to medication.
2. Put on gloves before handling the patch to avoid absorbing any medication.
3. Label the patch with the date, time, and your initials.
4. Remove the previous medication or patch, and cleanse the area.
5. If using a transdermal ointment, apply the ordered amount of medication in an even line directly on the premeasured
paper that accompanies the medication tube.
6. Press the patch or apply the medicated paper to clean, dry, and hairless skin.
7. Rotate the sites to prevent skin irritation.
B. Ophthalmic 1. Instruct the patient to lie supine or sit with the head slightly tilted back.
2. With your nondominant hand, pull the patient’s lower lid down gently to expose the conjunctival sac, creating a pocket.
3. Ask the patient to look upward.
4. Hold the eyedropper 1/4 to 1/8 inch above the conjunctival sac. Do not hold the dropper over the patient’s eye because
this may stimulate the blink reflex.
5. Instill the prescribed number of drops into the center of the pocket. Avoid touching the eye or conjunctival sac with the
tip of the eyedropper.
6. If applying ointment, follow steps 1–3, then apply a thin line of ointment evenly along the inner edge of the lower lid
margin, from inner to outer canthus.
7. Instruct the patient to gently close the eye. Apply gentle pressure with your finger to the nasolacrimal duct at the
inner canthus for one to two minutes to avoid overflow drainage into the nose and throat. This minimizes the risk of
absorption into the systemic circulation.
8. With a tissue, remove the excess medication from around the patient’s eye.
9. Replace the dropper. Do not rinse the eyedropper.
C. Otic 1. Instruct the patient to lie on his or her side or to sit with the head tilted so that the affected ear is facing up.
2. If necessary, use a clean washcloth to clean the pinna of the ear and the meatus to prevent any discharge from being
washed into the ear canal during the instillation of the drops.
3. Hold the dropper 1/4 inch above the ear canal, and instill the prescribed number of drops into the side of the ear canal,
allowing the drops to flow downward. Avoid placing the drops directly on the tympanic membrane.
4. Gently apply intermittent pressure to the tragus of the ear three or four times.
5. Instruct the patient to remain on his or her side for up to 10 minutes to prevent loss of medication.
6. If cotton ball is ordered, follow steps 1–2, then presoak with medication and insert it into the outermost part of ear
canal.
7. Wipe off any solution that may have dripped from the ear canal with a tissue.
D. Nasal drops 1. Ask the patient to blow his or her nose to clear the nasal passages. Have the patient lie supine.
2. Draw up the correct volume of drug into the dropper.
3. Instruct the patient to open and breathe through the mouth.
4. Hold the tip of the dropper just above the patient’s nostril, and without touching the nose with the dropper, direct the
solution laterally toward the midline of the superior concha of the ethmoid bone—not at the base of the nasal cavity,
where it will run down the throat and into the eustachian tube.
5. Ask the patient to remain in this position for five minutes.
6. Discard any remaining solution that is in the dropper.
E. Vaginal 1. Instruct the patient to assume a dorsal recumbent position with her knees bent and separated.
2. Put on gloves; open the suppository and lubricate the rounded end of the suppository and the gloved forefinger of your
dominant hand with a water-soluble lubricant.
3. Expose the vaginal orifice by separating the labia with your nondominant hand.
4. Insert the rounded end of the suppository about 8–10 cm along the posterior wall of the vagina, or as far as it will pass.
5. If using a cream, jelly, or foam, gently insert the applicator 5 cm along the posterior vaginal wall and slowly push the
plunger until empty. Remove the applicator and place on a paper towel.
6. Ask the patient to lower her legs and remain lying in the dorsal recumbent position for five to ten minutes following
insertion. Offer the patient a perineal pad.
Core Concept 3.8 31
Table 3.4 Topical Drug Administration (continued )

F. Rectal 1. Instruct the patient to lie on the left side (Sims’ position).
suppositories
2. Put on gloves; open the suppository and lubricate the rounded end.
3. Lubricate the gloved forefinger of your dominant hand with water-soluble lubricant.
4. Inform the patient when the suppository is to be inserted; instruct the patient to take slow, deep breaths and deeply
exhale during insertion to relax the anal sphincter.
5. Gently insert the lubricated end of the suppository into the rectum, beyond the anal-rectal ridge to ensure retention.
6. Instruct the patient to remain in the Sims’ position or lie supine to prevent expulsion of the suppository.
7. Instruct the patient to retain the suppository for at least 30 minutes to allow absorption, unless the suppository is
administered to stimulate defecation.
Otic Administration
The otic route is used to treat local conditions of the ear, including infections and soft blockages of the
auditory canal. Otic medications include eardrops and irrigations, which are usually ordered for cleaning.
Figure 3.4 ■ and Table 3.4C present key points in administering otic medications.
Nasal Administration
The nasal route, a transmucosal method of drug delivery, is used for both local and systemic drug ad-
ministration. The nasal mucosa provides an excellent absorptive surface for certain medications. Advan- Life Span Fact
tages of this route include ease of use and avoidance of the first-pass effect in the liver and the digestive Administration of otic drugs
enzymes. Nasal spray formulations of corticosteroids have revolutionized the treatment of allergic rhinitis to infants and young children
because the medication is very safe when administered by this route. must be performed carefully
Although the nasal mucosa provides an excellent surface for drug delivery, there is the potential for to avoid injury to sensitive
damage to the cilia within the nasal cavity, and mucosal irritation is common. In addition, unpredictable structures of the ear. Otic
drops should be at room tem-
mucous secretion in some individuals may affect drug absorption from this site.
perature before adding them
Drops or sprays are often used for their local astringent effect, which is to shrink swollen to the ear. When giving otic
mucous membranes or to loosen secretions and facilitate drainage. This brings immediate relief drugs to young children, gen-
from the nasal congestion caused by the common cold. The nose also provides the route to reach the tly pull the pinna down and
nasal sinuses and the eustachian tube. Proper positioning of the patient prior to giving nose drops back. When giving otic drugs
for sinus disorders depends on which sinuses are being treated. The same holds true for treatment to older children and adults,
gently pull the pinna down
of the eustachian tube. Table 3.4D and Figure 3.5 ■ illustrate important facts related to nasal drug
and forward.
administration.
Vaginal Administration
The vaginal route is used to deliver medications for treating local infections and to relieve vaginal pain and
itching. Vaginal medications are inserted as suppositories, creams, jellies, or foams. It is important that the
Figure 3.4
Otic drug administration:

Instilling eardrops.
Source: Andy Crawford/Dorling
Kindersley
Figure 3.5
Nasal drug
administration.
Figure 3.6
Vaginal drug adminis-

tration: (a) instilling a
vaginal suppository;
(b) using an applicator
to instill a vaginal cream.
(a) (b)
nurse explains the purpose of treatment and provides privacy for the patient. Before inserting vaginal drugs,
the nurse should instruct the patient to empty her bladder. This lessens both discomfort during treatment and
the possibility of irritating or injuring the vaginal lining. The patient should be offered a perineal pad follow-
ing administration. Table 3.4E and Figure 3.6 ■ provide guidelines regarding vaginal drug administration.
Rectal Administration
The rectal route may be used for either local or systemic drug administration. It is a safe and effective means of
delivering drugs to patients who are comatose or who are experiencing nausea and vomiting. Rectal drugs are
normally in suppository form, although a few laxatives and diagnostic agents are given via enema. Although
absorption is slower than by other routes, it is steady and reliable as long as the medication can be retained by
the patient. Venous blood from the lower rectum is not transported by way of the liver. Therefore, the first-pass
effect is avoided, as are the digestive enzymes of the upper GI tract. Table 3.4F gives details about rectal drug
administration.
Parenteral administration refers to dispensing medications

Core Concept 3.9 by routes other than oral or topical.
The parenteral route delivers drugs via a needle into the skin layers, subcutaneous tissue, muscles,
or veins, with the needle inserted at different degrees, depending on the type of injection, as shown in
Figure 3.7 ■. More advanced parenteral delivery includes administration into arteries, body cavities (such
as intrathecal), and organs (such as intracardiac). Parenteral drug administration is much more invasive
Core Concept 3.9 33
(meaning that the delivery method “invades” the barrier that the skin provides to protect the body) than
topical or enteral administration. Because of the possibility of introducing pathogenic microbes directly
into the blood or body tissues, aseptic techniques must be strictly used. The nurse is expected to identify
and use appropriate materials for parenteral drug delivery, including specialized equipment and techniques
involved in the preparation and administration of injectable products. The nurse must know the correct
anatomical locations for parenteral administration and safety procedures regarding hazardous equipment
disposal.
Figure 3.7
10°–15°
45°
Epidermis
Epidermis
Dermis
Dermis
Subcutaneous Subcutaneous
tissue tissue
Muscle Muscle
(a) (b)
90°
Epidermis
Dermis
Subcutaneous
tissue
Muscle
(c)
Parenteral drug administration: Gloves are worn at all times. (a) Intradermal administration is into the dermis at a
10–15° angle. See Figure 3.8. (b) Subcutaneous administration is into the subcutaneous tissue at a 45° angle. See
Figure 3.9. (c) During intramuscular administration, a drug is injected into the muscle at a 90° angle. See Figure 3.10.
Intravenous drug administration (not shown here) is given directly into the bloodstream.
Intradermal and Subcutaneous Administration

Injection into the skin delivers drugs to the blood vessels that supply the layers of the skin. Drugs may be
injected either intradermally or subcutaneously. The major difference between these methods is the depth
of injection, which is controlled by the angle of needle placement (see Figure 3.7). An advantage of both
methods is that they offer a means of administering drugs to patients who are unable to take them orally.
Drugs administered by these routes also avoid the first-pass effect in the liver and the digestive enzymes.
Disadvantages are that only small volumes can be administered, and injections can cause pain and swelling
at the injection site.
An intradermal (ID) route injection is administered into the dermis layer of the skin. Because the
dermis contains more blood vessels than the deeper subcutaneous layer, drugs are more easily absorbed.
This route is usually used for allergy and disease screening or for local anesthetic delivery prior to venous
cannulation. Only very small volumes of drug, usually 0.1 to 0.2 mL, can be given by ID injections. The
usual sites for ID injections are the nonhairy skin surfaces of the upper back, over the scapulae, the high
upper chest, and the anterior forearm. Guidelines for intradermal injections are given in Table 3.5A ◆ and
Figure 3.8 ■.
A subcutaneous (SC or SQ) route injection is delivered to the deepest layers of the skin. Insulin,
heparin, vitamins, some vaccines, and other medications are given in this area because the sites are
easy to reach and provide rapid absorption. Body sites that are ideal for subcutaneous injections include
the following:
■ Posterior upper arm (above the triceps muscle)
■ Middle two thirds of the anterior thigh area
■ Subscapular areas of the upper back

■ Upper dorsogluteal and ventrogluteal areas
■ Abdominal areas, above the iliac crest and below the diaphragm, 2 inches out from
the umbilicus
Subcutaneous doses are small in volume, usually ranging from 0.5 to 1 mL, and are given at a 45°
(normal weight patient) to 90° angle (obese patient). The needle size varies with the patient’s quantity
of body fat but is usually 1/2 to 5/8 inch. The needle length is usually one-half the size of a pinched skin
fold that can be grasped between the thumb and forefinger. Insulin is administered using a special syringe
that has “unit” markings made specifically for insulin. Tuberculin syringes (TB) are 1 mL syringes and
are typically used when administering other medications less than 1 mL. Note that tuberculin syringes
and insulin syringes are not interchangeable and should not be substituted for each other. It is important
to rotate injection sites in an orderly and documented manner, to promote absorption, minimize tissue
damage, and alleviate discomfort. For insulin, rotation should be within an anatomical area that promotes
reliable absorption and maintains consistent blood glucose levels.
Table 3.5 Parenteral Drug Administration

A. Intradermal route 1. Prepare the medication in a tuberculin or 1 mL syringe, using a 25–27 gauge, 3/8–5/8 inch needle.
2. Put on gloves and cleanse the injection site with an antiseptic swab, using a circular motion. Allow
the site to air dry.
3. With the thumb and index finger of your nondominant hand, spread the patient’s skin taut.
4. Insert the needle, with the bevel facing upward, at a 10°–15° angle.
5. Advance the needle until the entire bevel is under the skin; do not aspirate.
6. Slowly inject the medication to form a small wheal or bleb (small raised area).
7. Withdraw the needle quickly, and pat the site gently with a sterile 2 × 2 gauze pad. Do not
massage the area.
8. Instruct the patient not to rub or scratch the area.
B. Subcutaneous route 1. Prepare the medication in a 1–3 mL syringe using a 23–25 gauge, 1/2–5/8 inch needle. For hepa-
rin, the recommended needle is 3/8 inch and 25–26 gauge.
2. Choose the site, avoiding bony areas, major nerves, and blood vessels. For heparin, check your
facility’s policy for the preferred injection sites.
3. Check the previous rotation sites and select a new area for injection.
4. Put on gloves and cleanse the injection site with an antiseptic swab using a circular motion.
5. Allow the site to air dry.
6. Pinch/lift the skin between the thumb and index finger of your nondominant hand.
7. Insert the needle at 45° or 90° angle, depending on the patient’s body size and the length of the
needle you are using: 90° angle for obese patients; 45° angle for average-weight patients.
8. Check facility policy on aspiration of subcutaneous injections. If policy allows, aspirate by gently
pulling back on the plunger. If blood appears, withdraw the needle, discard the syringe, and pre-
pare a new injection. Do not aspirate heparin, low molecular weight heparin, or insulin.
9. Inject the medication slowly.
10. Remove the needle quickly. Gently massage the site with an antiseptic swab. Do not massage the
site after injecting heparin or low molecular weight heparin because tissue damage may occur.
C. Intramuscular route: 1. Prepare the medication using a 20–23 gauge, 1.5 inch needle. (Needle size may vary depending on
ventrogluteal site the site and patient size.)
2. Put on gloves and cleanse the injection site with an antiseptic swab using a circular motion. Allow
the site to air dry.
3. Locate the site by placing your hand with the heel on the greater trochanter and your thumb point-
ing toward the umbilicus. Point to the anterior iliac spine with your index finger, spreading your
middle finger to point toward the iliac crest (forming a V). Injection of medication is given within
the V-shaped area between the index and third finger.
4. Insert the needle with a smooth, dart-like movement at a 90° angle within the V-shaped area.
5. Aspirate and observe for blood. If blood appears, withdraw the needle, discard the syringe, and
prepare a new injection.
6. Inject the medication slowly and with smooth, even pressure on the plunger.
7. Remove the needle quickly.
8. Apply pressure to the site with a dry, sterile 2 × 2 gauze and gently massage to promote absorp-
tion of the medication into the muscle.
Core Concept 3.9 35
Table 3.5 Parenteral Drug Administration (continued )

D. Intravenous route 1. To add a drug to an IV fluid container:
a. Verify the order and compatibility of the drug with the IV fluid.
b. Prepare the medication in a 5–20 mL syringe using a 1–1.5 inch, 19–21 gauge needle.
c. Put on your gloves and assess the injection site for signs of inflammation or extravasation (ooz-
ing of tissue).
d. Locate the medication port on the IV fluid container and cleanse it with an antiseptic swab.
e. Carefully insert the needle or access device into the port and inject the medication.
f. Withdraw the needle and mix the solution by rotating the container end to end.
g. Hang the container and check the infusion rate.
2. To administer an IV bolus (IV push) using an existing IV line or IV lock (reseal):
a. Verify the order and compatibility of the drug with the IV fluid.
b. Determine the correct rate of infusion.
c. Determine if IV fluids are infusing at the proper rate (IV line) and that the IV site is adequate.
d. Prepare the drug in a syringe with a 19–21 gauge needle.
e. Put on your gloves and assess the IV insertion site for signs of inflammation or extravasation
(oozing of fluid within the tissue).
f. Select an injection port on the tubing that is closest to the insertion site (IV line).
g. Cleanse the tubing or lock port with an antiseptic swab and insert the needle into the port.
h. If administering medication through an existing IV line, occlude the tubing by pinching it just
above the injection port.
i. Slowly inject the medication over the designated time (which is not usually faster than 1 mL/
min, unless otherwise specified).
j. Withdraw the syringe. Release the tubing and ensure the proper IV infusion if using an existing
IV line.
k. If using an IV lock, check your facility’s policy for use of saline flush before and after injecting
medications.
Figure 3.8
Intradermal drug
administration: The
needle is inserted, bevel
up, at 10–15° angle.
When performing subcutaneous injections, it is usually not necessary to aspirate prior to the injec-
tion. It depends on what is being injected and the patient’s anatomy. Aspiration might prevent inadvertent
administration into a vein or artery in a thin person. Heparin and low molecular weight heparin, such as
enoxaparin (Lovenox) should never be aspirated because of the drug’s anticoagulant properties. Aspiration
can cause bleeding, bruising and possible damage to the surrounding tissue. Massage after injection is also
not recommended for the same reasons. Table 3.5B and Figure 3.9 ■ include important information regard-
ing subcutaneous drug administration.
Intramuscular Administration
An intramuscular (IM) route injection delivers medication into specific muscles. Because muscle tissue
has a rich blood supply, medication moves quickly into blood vessels to produce a more rapid onset of
action than with oral, ID, or SC administration. The anatomical structure of muscle permits this tissue to
receive a larger volume of medication than the subcutaneous region. An adult with well-developed muscles
can safely tolerate up to 5 mL of medication in a large muscle, although only 2 to 3 mL is recommended.
The deltoid and triceps muscles should receive a maximum of 1 mL.
A major consideration for the nurse regarding IM drug administration is the selection of an appropri-
ate injection site. Injection sites must be located away from bones, large blood vessels, and nerves. Both
the size and length of the needle are determined by body size and muscle mass, the type of drug to be ad-
ministered, the amount of adipose (fat) tissue overlying the muscle, and the age of the patient. Information
regarding IM injections is given in Table 3.5C and Figure 3.10 ■. The four common sites for IM injections
are as follows:
■ Ventrogluteal site This area provides the greatest thickness of gluteal muscles, contains no
Life Span Fact large blood vessels or nerves, is sealed off by bone, and contains less fat than the buttock area,
The vastus lateralis is the site
thus eliminating the need to determine the depth of subcutaneous fat.
of choice for IM injections in ■ Deltoid site Used in well-developed teens and adults for volumes of medication not to exceed
pediatric patients. 1 mL.
■ Dorsogluteal site Used for adults and for children who have been walking for at least six
months. The site is safe as long as the nurse appropriately locates the injection landmarks to
avoid puncture or irritation of the sciatic nerve and blood vessels.
■ Vastus lateralis site Usually thick and well developed in both adults and children, the middle
third of the muscle is the site for IM injections.
Figure 3.9
Subcutaneous drug
administration: Skin is
pinched, and depend-
ing on amount of
subcutaneous tissue,
needle is inserted at a
45° or 90° angle.
Core Concept 3.9 37
Figure 3.10
Intramuscular drug
administration: Skin is
spread taut between
thumb and forefinger
and the needle is in-
serted at a 90° angle.
Intravenous Administration
The intravenous (IV) route enables administration of medications and fluids directly into the bloodstream
and allows their immediate availability for use by the body. The IV route is used when a very rapid onset
of action is desired. Like other parenteral routes, IV medications bypass the enzymes of the digestive sys-
tem and the first-pass effect of the liver. The three basic types of IV administration are as follows:
■ Large-volume infusion This type of infusion is used for fluid maintenance, replacement,
or supplementation. Compatible drugs may be mixed into a large-volume IV container with
fluids such as normal saline or Ringer’s lactate. Table 3.5D and Figure 3.11 ■ illustrate this
technique.
■ Intermittent infusion A small amount of IV solution is “piggy-backed” (added) to the primary
large-volume infusion. This type of infusion, also illustrated in Figure 3.11, is used to give
additional medications, such as antibiotics or analgesics over a short time.
■ IV bolus (push) administration A concentrated single dose of medication is delivered directly to the
circulation via syringe. Bolus injections may be given through an intermittent injection port or by di-
rect IV push. Details on the bolus administration technique are given in Table 3.5D and Figure 3.12 ■.
Although the IV route provides the fastest onset of drug action, it is also the most dangerous. Once
injected, the medication cannot be retrieved. If the drug solution or the needle is contaminated, pathogens
have a direct route to the bloodstream and body tissues. Patients who are receiving IV injections must be
closely monitored for adverse reactions. Some adverse reactions occur immediately after injection; others
may take hours or days to appear. Antidotes for drugs that can cause potentially dangerous or fatal reac-
tions must always be readily available. Several types of needleless IV systems are also available and have
been shown to greatly reduce the chance of needlestick injuries among healthcare professionals.
Safety Alert
Medication Administration Error–Mistaken Patient Identity
It is the responsibility of the nurse to check the patient’s identification band, ask the patient
to state name and date of birth, and verify that these pieces of information match those
listed on the patient’s medication administration record (MAR). Consider the evening nurse
who entered Ms. Brown’s room to administer medications. Ms. Brown was already in bed and
asleep. The nurse gently shook her and said, “I have your 10 p.m. medication, Ms. Brown.” Al-
though the patient responded, she was not fully awake. She took the medication and quickly
returned to sleep. Upon leaving, however, the nurse noticed the room number and realized
that medication had just been given to Ms. Crown in the room next to Ms. Brown. This situ-
ation could have been avoided if the nurse had checked the ID band, asked the patient for
identification information, and cross-checked the data against the MAR.
Figure 3.11
Administration of
intravenous fluids: A
large volume IV infusion
bag with intermittent
infusion bag “piggy-
backed” into primary
tubing.
Figure 3.12
Injecting a medication
by IV push.
Chapter Review 39
Patients Need To Know
Patients need to know the following:
1. Always ask the healthcare provider or pharmacist which medications may be taken
with food and water to reduce nausea and stomach irritation.
2. Do not crush, cut, or administer enteric-coated tablets with alkaline substances, such as
antacids.
3. Establish a routine for taking medications by selecting a familiar time of the day, usu-
ally on the hour. Special organizers can be obtained to properly store medicines accord-
ing to times, days, and dosages.
4. Follow the dosing times exactly. If a medication is missed, do not try to “catch up” on
the next scheduled dose. If remembered soon after the scheduled time, it is appropri-
ate to take the medicine. Otherwise, wait until the next scheduled dose. An exception
would be if the next dose is not scheduled until the next day. For answers to specific
questions, consult a healthcare provider.
5. Store medications in a safe, dry place. Discard them if they become old or outdated.
6. Use the measuring device provided by the drug manufacturer to take medications. Do
not rely on kitchen utensils to judge the exact recommended dose.
Chapter Review
3.1 A major goal in pharmacotherapy is to limit the There are established orders and time schedules by
number and severity of adverse drug events. which medications are routinely administered. The
Healthcare staff must be familiar with the general prin- single order (such as a preoperative order) is for a
ciples of drug delivery. The nurse must have a com- drug that is to be given only once and at a specific
prehensive knowledge of the actions and side effects time. A prn order is administered as required by the
of drugs before they are administered to limit the num- patient’s condition. Orders not written as single,
ber and severity of adverse drugs events. Allergic and STAT, or prn are called routine orders. A standing
anaphylactic reactions are serious effects that must be order is written in advance of a situation and is to be
carefully monitored and prevented, when possible. carried out under specific circumstances. Document-
ing drug administration and reporting side effects are
3.2 The rights of drug administration form the basis important responsibilities of the nurse.
of proper drug delivery.
3.5 Three systems of measurement are used in phar-
The six rights and three checks are guidelines to safe macology: metric, apothecary, and household.
drug administration, which involves a collaborative
Healthcare professionals must recognize dosages
effort among nurses, physicians, and other healthcare
based on all three systems of measurement: the met-
professionals. The six rights are right patient, right
ric, apothecary, and household systems. The nurse
medication, right dose, right route of administration,
must be able to convert between household and met-
right time of delivery, and right documentation. The
ric systems of measurement.
three checks are checking the MAR, checking the
drug during preparation, and checking the drug be- 3.6 Certain protocols and techniques are common to
fore administering it to the patient. all methods of drug administration.
The student should understand drug administra-
3.3 Successful pharmacotherapy depends on patient tion guidelines before proceeding to a study of spe-
compliance. cific drug administration routes. The three general
Pharmacologic compliance requires patients to routes of drug administration are enteral, topical, and
understand and personally accept the value of the parenteral.
prescribed drug regimen. Understanding the reasons
for noncompliance can help the healthcare team 3.7 Enteral drugs are given orally or via nasogastric
increase pharmacotherapeutic success. or gastrostomy tubes.
Drugs administered via the enteral route are given
3.4 Healthcare providers use accepted abbreviations orally or through nasogastric (NG) or gastrostomy
to communicate the directions and times for drug (G) tubes. The enteral route is the most effective way
administration. to administer drugs.
3.8 Topical drugs are applied locally to the skin and 3.9 Parenteral administration refers to dispensing
associated membranes. medications by routes other than oral or topical.
Topical drugs are applied locally to the skin or mem- Parenteral administration is the dispensing of medica-
branous linings of the eye, ear, nose, respiratory tract, tions via a needle, usually into the skin layers (ID), sub-
urinary tract, vagina, and rectum. cutaneous tissue (SC or SQ), muscles (IM), or veins (IV).
Review Questions
The following questions are written 6. The nurse checks the label three times during the course
in NCLEX-PN® style. Answer these of administering a medication: while getting the medication
questions to assess your knowledge out of the container or drawer, before placing it into the medi-
of the chapter material, and go back cation cup, and before administering the medication or when
and review any material that is not placing the stock bottle back on the shelf. Of the “six rights of
clear to you. drug administration,” this nurse is checking for the right:
1. A nurse enters the patient’s room with medication along with 1. Medication
a stethoscope, a fairly large-looking syringe, and container of wa- 2. Documentation
ter. In the course of administering the medication, the nurse will 3. Patient
use all of these items. From your understanding of drug adminis- 4. Time of delivery
tration, which of the following routes will the nurse likely use? 7. When administering medications, the nurse’s main re-
1. Transdermal sponsibilities are to know and understand: (Select all that
2. Intravenous (parenteral) apply.)
3. Nasogastric (enteral) 1. The medication being ordered
4. Rectal 2. The intended use of the medication
2. The nurse will not crush the extended-release medica- 3. Any special considerations, such as the patient’s age or
tions ordered for his or her patient because: pathophysiological state
4. Any possible side/adverse effects the medication may cause
1. They are very distasteful, and this reduces patient
compliance. 8. Which information is not listed in the medication admin-
2. Crushing alters the rate of absorption and medication istration record (MAR)?
delivery. 1. Date of medication administration
3. Multiple drug pieces cause obstructive symptoms. 2. Route of drug administration
4. Crushed oral medications have reduced bioavailability. 3. Dose of medication
3. The reason why it is necessary to aspirate during an IM 4. Drug classification
injection is to: 9. The doctor ordered 5 mL of an oral decongestant twice a
1. Avoid placement of the needle into a blood vessel. day for one of his or her pediatric patients. When teaching the
2. Produce an air pocket for better drug distribution. mother of the patient about how much medication to give, the
3. Avoid nerve puncture. nurse tells her that 5 mL is equal to:
4. Remove air from the syringe. 1. Two (2) teaspoons
4. Which of the following routes of drug administration has
2. One (1) tablespoon
the fastest onset of action? 3. 1/4 of a cup
4. One (1) teaspoon
1. Transdermal
2. Intramuscular 10. The abbreviation “qod” was read in a patient’s chart by a
3. Intravenous nursing student. The student knows that:
4. Ophthalmic 1. This abbreviation should not be used. Instead write out
5. After checking the doctor’s orders, the nurse notes that the
“every other day.”
medication is to be given immediately. This type of order is a: 2. This abbreviation means “every hour.”
3. The abbreviation should not be used. Instead, write out
1. STAT order “nightly.”
2. Single order 4. This abbreviation means “four times per day.”
3. prn order
4. Standing order
website.

C
H
A
P
T
E
R
What Happens After a Drug

Has Been Administered 4
Core Concepts
4.1 Pharmacokinetics focuses on what the body does to 4.6
The rate of elimination and half-life characteristics
the drugs. influence drug responsiveness.
4.2
Absorption is the first step in drug transport. 4.7
Pharmacodynamics focuses on what the drugs do
4.3
Distribution refers to how drugs are transported to the body.
throughout the body. 4.8
Drugs activate specific receptors to produce
4.4
Metabolism is a process whereby drugs are made a response.
less or more active. 4.9
Potency and efficacy are terms often used to
4.5
Excretion processes remove drugs from the body. describe the success of drug therapy.
Learning Outcomes
1. Identify the four major processes of patients, and explain the 10. Explain how rate of elimination and
pharmacokinetics. significance of this difference to plasma half-life (t1/2) are related to
2. Discuss the factors affecting drug the success of drug therapy. the duration of drug action.
absorption. 7. Explain how intermediate 11. Discuss how successful
3. Describe how plasma proteins products of drug metabolism may pharmacotherapy depends on
affect drug distribution. produce more intense responses principles of pharmacodynamics.
than the original drug. 12. Explain the significance of the
4. Explain the significance of the
blood-brain barrier, blood-placental 8. Identify the major processes by receptor theory.
barrier, and blood-testicular barrier which drugs are eliminated from 13. Describe how “blockers” of drug
to drug therapy. the body. action work.
5. Explain the importance of the 9. Explain the importance of 14. Compare and contrast the
first-pass effect. enterohepatic recirculation to therapeutic terms potency and
drug therapy. efficacy.
6. Describe how metabolic enzymes
differ in younger and in older
Key Terms
absorption (ab-SORP-shun) 43 efficacy (EFF-ik-ah-see) 47 minimum effective concentration 45
agonists (AG-on-ists) 47 enterohepatic recirculation onset of drug action 45
antagonists (an-TAG-oh-nists) 47 (EN-ter-oh-HEE-pah-tik) 44 peak plasma level 46
biotransformation excretion (eks-KREE-shun) 44 pharmacodynamics
(BEYE-oh-trans-for-MAY-shun) 43 first-pass effect 43 (FAR-mah-koh-deye-NAM-iks) 46
distribution (dis-tree-BU-shun) 43 half-life (t1/2) 45 pharmacokinetics
duration of drug action 46 metabolism (meh-TAHB-oh-liz-ehm) 43 (FAR-mah-koh-kee-NET-iks) 42
42 Chapter 4 What Happens After a Drug Has Been Administered
potency (POH-ten-see) 47 receptor theory 47 therapeutic (THARE-ah-PEW-tick)

prodrugs 43 termination of drug range 45
receptor (ree-SEP-tor) 47 action 46 toxic concentration 45
D rugs do not affect all patients the same way. Whether a drug achieves or falls short of achieving
a therapeutic response is an important concern to patients and healthcare providers. Within a
population, a dose of medication may produce a dramatic response in one patient while having no
effect in another.
Many factors determine a drug’s response. Patients sometimes take medications under conditions that
interfere with drug activity. This interference is called a drug interaction. Food–drug interactions may oc-
cur when patients take their medication with food or beverages. Patients often take more than one medica-
tion at the same time. After drugs have been absorbed, the effectiveness of drug therapy may be altered by
drug–drug interactions in the bloodstream.
To understand the impact that drug interactions have on drug safety and effectiveness, one must un-
derstand concepts from two important areas: pharmacokinetics and pharmacodynamics.
core concept 4.1 Pharmacokinetics focuses on what the body does to the drugs.
pharmaco 5 drug related As the root words indicate, pharmacokinetics focuses on four processes: absorption, distribution,
kinetics 5 movement metabolism, and excretion, as shown in Figure 4.1 ■. A thorough knowledge of pharmacokinetics en-
ables the healthcare provider to understand the therapeutic effects of a drug, as well as to predict potential
adverse effects of drug therapy.
F i g u re 4 . 1
Drugs Drugs
Stomach
Absorption
Distribution Kidney
Bl o
od
Excretion
str
Small intestine
ea
m
Absorption
Urine
Large intestine
Liver Metabolism
Excretion
Feces
The four processes of pharmacokinetics (drug movement) are absorption, metabolism, distribution, and excretion.
Core Concept 4.4 43
Absorption is the first step in drug transport. core concept 4.2
Absorption is the first step in how the body handles a drug. Absorption is a process involving the move-
ment of a substance from its site of administration across one or more body membranes. A drug may be
absorbed locally and produce a biologic effect at a remote site. Absorption may occur across the skin and
associated mucous membranes, or drugs may move across membranes that line blood vessels. Ultimately,
most drugs move across many membranes to reach their target cells. Many basic science textbooks cover
the ways that foods and drugs are absorbed, including passive transport and energy-requiring transport
processes. The presence of food in the digestive tract slows the absorption of drugs administered orally.
Distribution refers to how drugs are transported throughout the body. core concept 4.3
Distribution is the process by which drugs are transported after they have been absorbed or administered
directly into the bloodstream. Between the site of drug administration and the target tissue, many factors
affect drug movement. One important example is the binding that occurs between drugs and other sub-
stances, such as plasma proteins, already present in the bloodstream. When a drug binds with a plasma
protein such as albumin, the drug is held by the plasma protein in the bloodstream, where it is unable to
reach its target cells. Often, a second drug will interfere with this binding by displacing the first drug from
the plasma protein. In this case, the first drug’s activity is intensified. The term bioavailability is often used
to describe how much of a drug will be available after administration to produce a biological effect.
Even if a drug is not bound by plasma proteins, it still may not be able to reach all body tissues. Three
important organs contain anatomic barriers that prevent some drugs from gaining access. These are the
brain, the placenta, and the testes. Even though these organs have a larger blood supply compared to most
other organs in the body, their cellular barriers only allow fat-soluble substances to cross. These special
barriers are called the blood-brain barrier, blood-placental barrier, and blood-testicular barrier.
Some drugs are able to cross the blood-brain barrier without difficulty. These include antianxiety
drugs, sedatives (sleep-inducing), and psychoactive (or mind-altering) drugs. Other medications, such as
many antibiotics and anticancer medications, are absorbed easily in the intestinal tract but do not easily
cross into the brain.
The blood-placental barrier serves an important protective function because it regulates which sub-
stances pass from the mother’s bloodstream to the fetus. However, many potentially damaging agents such
as cocaine and alcohol, and even some prescription or OTC medications, are not prevented from crossing
this barrier. This is an extremely important issue. All food items and therapeutic drugs should be evaluated
to assess their adverse effects on pregnant women and their unborn children, as discussed in Chapter 2. In
males, the blood-testicular barrier prevents many drugs from reaching the testes, making it difficult to treat
testicular disorders.
Metabolism is a process whereby drugs are made less or more active. core concept 4.4
Metabolism is the next step in pharmacokinetics. It is often described as the total of all chemical reac-
tions in the body. Metabolism occurs in almost every cell and organ—including the intestinal tract and
kidneys—but the liver is the primary site. The individual chemical reactions of metabolism are called
biotransformation reactions: They are the chemical conversion of drugs from one form to another that bio 5 biologic
may result in increased or decreased activity. Metabolism is important to drug therapy because these chem- transformation 5 changing
ical reactions deactivate most drugs. For this reason, patients with liver disease usually receive much lower process
doses than normal because their liver is unable to metabolize the drug to a safe, active form.
Certain drugs called prodrugs require metabolism to make them active. In these cases, as the drug is pro 5 before
broken down by chemical reactions of metabolism, the products formed by the breakdown produce a more drug 5 medication form
intense response than does the original drug. An example of such a prodrug is sulfasalazine (Azulfidine),
which is not active in its original form taken orally. Azulfidine is taken for the condition of ulcerative coli-
tis. It is broken down by bacteria in the colon into two products that become active. Such cases of prodrugs
are infrequent. Usually, metabolism is affected by the use of other drugs or the presence of other diseases.
An important mechanism that affects metabolism and drug action is the first-pass effect. Substances
absorbed across the intestinal wall enter blood vessels known as the hepatic portal circulation, which car-
ries blood directly to the liver (Figure 4.2 ■). Drugs administered orally are absorbed into the hepatic portal
circulation and are taken directly to the liver for metabolism. The liver may then metabolize the drug to a
less active form before it is distributed to the rest of the body and target organs. In some cases, this first-
pass effect can inactivate more than 90% of an orally administered drug before it can reach the general
circulation.
Many patients differ in how efficiently their metabolic enzymes work to metabolize drugs. Age,
kidney and liver disease, genetics, and other factors can dramatically affect metabolism. Some patients
metabolize drugs very slowly, others very quickly.
F i g u re 4 . 2
e To heart and
systemic circulation
Stomach
d Inactive drug metabolites
Liver First-pass
c metabolism
a Absorption Small intestine
b Hepatic portal
circulation
Portal vein
First-pass effect: Drugs given orally are absorbed (a) through the intestinal wall and enter the hepatic portal circula-
tion (b). Absorbed drugs are taken directly to the liver (c) for metabolism (d) before reaching the heart and circulating
throughout the rest of the body (e).
core concept 4.5 Excretion processes remove drugs from the body.
The last step of pharmacokinetics is excretion. Most substances that enter the body are removed by urina-
tion, exhalation, defecation, and/or sweating. Drugs are normally removed from the body by the kidneys,
the respiratory tract, bile, or glandular activity.
The main organ of excretion is the kidney. The major role of the kidneys is to remove all nonnatural
and harmful agents in the bloodstream while maintaining a balance of other natural substances. Most drugs
are excreted by the kidneys. Therefore, kidney damage can significantly prolong drug action and is a com-
mon cause of adverse reactions. Drugs that affect the kidney and its filtration processes are presented in
Chapter 17.
Drugs that are easily changed into gaseous form are especially suited for excretion by the respiratory
system. The rate of respiratory excretion is dependent on the many factors that affect gas exchange, includ-
ing diffusion, gas solubility, and blood flow. The greater the blood flow into lung capillaries, the greater
the excretion. In contrast to other methods of excretion, the lungs excrete most drugs in their original un-
metabolized form.
Some drugs are excreted through bile. However, most components of bile are circulated back to the
liver by a process known as enterohepatic recirculation, as shown in Figure 4.3 ■. Recirculating drugs
are then metabolized by the liver and excreted by the kidneys. The fraction of drug that is not recirculated
continues on its way to the feces. Because of recirculation, elimination of drugs through bile may continue
Life Span Fact for several weeks after therapy has stopped, resulting in prolonged drug action.
Glands (other than the breast glands) that produce body fluids, such as saliva and sweat are less ef-
In general, metabolic enzyme
fective at excreting drugs. Most of the substances that are secreted in saliva and perspiration, such as urea
activity is reduced in very
young and in elderly patients. or other waste products, are natural products. However, the breast glands can secrete any drug capable of
Therefore, pediatric and geri- crossing these membranes. Therefore, a breastfeeding mother should always check with her healthcare
atric patients are usually more provider before taking any prescription drug, over-the counter (OTC) drug, or natural alternative therapy.
sensitive to medications than
are other patients. Drug doses
to the youngest and oldest Concept Review 4.1
age groups are often reduced
to compensate for these ■ What does the term pharmacokinetics mean? Describe the four major parts of
differences. pharmacokinetics?
Core Concept 4.6 45
F i g u re 4 . 3
Liver
Bile transported from the

liver to the small intestine
by way of the gallbladder
Gallbladder
Bile salts absorbed and circulated

back to the liver by way of the
capillaries of the digestive tract Stomach
and hepatic portal vein
Small intestine
To large
Absor ption intestine
B l o o d s tr e a m
In the process of enterohepatic recirculation, bile is circulated back to the liver, where contained drugs are metabolized
and then excreted by the kidneys. Elimination of drugs through the bile may result in prolonged drug action.
The rate of elimination and half-life characteristics influence drug

responsiveness. core concept 4.6
Elimination, which is another term for excretion, is often measured so that dosages of drugs can be deter-
mined more accurately. The term rate of elimination refers to the amount of drug removed per unit of time
from the body by normal physiologic processes. The rate of elimination is helpful in determining how long
a particular drug will remain in the bloodstream, and is thus an indicator of how long a drug will produce
its effect.
The half-life (t1/2) of a drug is a related measurement used to ensure that maximum therapeutic
dosages are administered. Half-life is the length of time required for a drug’s concentration in the plasma
(i.e., in circulation) to decrease by one half. It is an indicator of how long a drug will produce its effect in
the body. The larger the half-life value, the longer it takes for a drug to be eliminated. Some drugs have a
half-life of just a few minutes, whereas others have a half-life of several hours or days. A drug with a half-
life of 10 hours will take longer to be eliminated from the body than a drug with a half-life of five hours.
Drugs with longer half-lives may be given less frequently—for example, once per day.
When a patient has a renal or hepatic disease, the plasma half-life of a drug increases. This reflects the
important relationship of half-life to metabolism and excretion.
Several important pharmacokinetic principles can be illustrated by measuring the serum level of
a drug following a single-dose administration. These pharmacokinetic values are shown graphically in
F igure 4.4 ■ . This figure demonstrates two plasma drug levels. First is the minimum effective
c oncentration, the amount of drug required to produce a therapeutic effect. Second is the toxic
concentration, the level of drug that will result in serious adverse effects. The plasma drug concentra-
tion between the minimum effective concentration and the toxic concentration is called the therapeu-
tic range of the drug. The onset of drug action represents the amount of time it takes to produce a
therapeutic effect after drug administration. Factors that affect drug onset may be many, depending on
F i g u re 4 . 4
14
Toxic
concentration
12
Plasma drug concentration (mcg/mL)

Peak plasma level
10
Therapeutic
range
8
on
Ex
pti
cre
6
or
t
ion
s
Duration of action Minimum
Ab effective
4 Onset Termi- concentration
of nation
action of
2
action
0
2 4 6 8 10 12
Time (hours)
Single-dose drug administration: pharmacokinetic values for this drug are as follows: onset of action 5 two hours; dura-
tion of action 5 six hours; termination of action 5 eight hours after administration; peak plasma concentration 5
10 mcg/mL; time to peak drug effect 5 five hours; t1/2 5 four hours.
numerous pharmacokinetic variables. As the drug is absorbed and then begins to circulate throughout
the body, the level of medication reaches its peak. The peak plasma level occurs when the medication
has reached its highest concentration in the bloodstream. Depending on accessibility of medications to
their targets, peak drug levels are not necessarily associated with optimal therapeutic effects. Multiple
doses of medication may be necessary to reach therapeutic drug levels. Duration of drug action is the
amount of time it takes for a drug to maintain its desired effect. Termination of drug action is when the
drug effect stops.
Concept Review 4.2

■ Why are rate of elimination and half-life (t1/2) important to the healthcare provider?
core concept 4.7 Pharmacodynamics focuses on what the drugs do to the body.
As discussed already, many variables influence the effectiveness of drug therapy, such as rate of admin-
istration, frequency of drug dosing, and changing medical condition. Some of these factors are listed in
Table 4.1 ◆.
Successful pharmacotherapy depends on these variables as well as how effectively the body r esponds
to drugs at specific target locations. This leads to another important core area of p harmacology: the field
of pharmacodynamics. The field of pharmacodynamics is complex and requires extensive knowledge of
pharmaco 5 drug related human physiology and biochemistry. Pharmacodynamics deals with the mechanisms of drug action, or
dynamics 5 powerful how the drug exerts its effects. As the root words suggest, drugs have a powerful influence on body pro-
change cesses. The remaining part of this chapter is devoted to a few basic pharmacodynamic principles.
Table 4.1 Factors That Influence the Effectiveness of Drug Therapy

Concentration (dose) of administered drug Metabolic rate (lower in children and elderly patients)
Frequency of drug dosing Genetics
Food–drug interactions Excretion rate (rate of elimination)
Drug–drug interactions Half-life (t1/2) of administered drug
Absorption rate (refer to Core Concept 4.1) Changing medical condition (liver or kidney disease)
Core Concept 4.9 47
F i g u re 4 . 5
Agonist
dy
ral bo Anta
Natu tance gon
ist
sub s (b) (c)
(a)
Action Action
Action inhibited or
blocked
Cellular receptors: (a) A neurotransmitter or hormone binds to the receptor. A drug is a close “mimic” of the
neurotransmitter or hormone and initiates a response by binding to the same receptor site. (b) An agonist is a drug
that facilitates the pharmacologic response. (c) An antagonist is a drug that temporarily blocks or depresses the
pharmacologic response.
Drugs activate specific receptors to produce a response. core concept 4.8
Successful pharmacotherapy is based on the principle that in order to treat a disorder, a drug must interact
with specific receptors in its target tissue. The receptor theory is a classic theory referring to the cellular recept 5 receiving
mechanism by which most drugs can change body processes. A receptor is any structural component of a or 5 entity
cell to which a drug binds in a dose-related manner. Receptors can be located on the plasma membrane or
in the cytoplasm or nucleus of the cell. The drug or natural body substance attaches to its receptor much
like a thumb drive to a computer docking port (Figure 4.5 ■). Some drug actions are not linked to a recep-
tor, but are connected directly with cell function, such as changing the membrane excitability or stability of
a nerve or muscle cell.
The terms agonist and antagonist are often used to describe drug action at the receptor level. Agonists ant 5 against
are drugs capable of binding with receptors and causing a cellular response; these are facilitators of cel- agonist 5 activator
lular action. When they are present in the bloodstream, agonists cause the tissue to respond, resulting in a
therapeutic action. Antagonists are drugs that inhibit or block the responses of agonists. Antagonists are therapeu 5 healing
called blockers. treatment
tic 5 pertaining to
Potency and efficacy are terms often used to describe the success
of drug therapy. core concept 4.9
Potency refers to a drug’s strength at a certain concentration or dose. As shown in Figure 4.6 ■, dose- potency 5 power quality
response curves are used to compare potencies of different drugs. If drug A has a higher potency than drug
B, it means that drug A will produce a more intense effect than drug B if both drugs are given at the same
dose (Figure 4.6a). A higher potency also means that a much smaller dose of the medication will be needed
to produce the same effect as another drug, as shown by the shift to the left of the dose-response curve for
drug A in Figure 4.6a.
Another core concept is efficacy. Efficacy refers to the ability of a drug to produce a more intense efficacy 5 effectiveness
response as its concentration is increased. As an example, consider Figure 4.6b. If the doses of two simi-
larly acting drugs (A and B) are increased, they will both produce a more intense effect, but drug B will
have a maximum intensity that is lower than drug A. The drug reaching a lower maximum intensity
compared to another drug is said to have a lower efficacy.
In pharmacotherapeutics, it is generally more important to have a drug with higher efficacy than one
with higher potency. For example, at recommended doses ibuprofen (200 mg) and aspirin (650 mg) are
equally effective at relieving headache; thus, they have the same efficacy. The fact that ibuprofen relieves
pain at a lower dose indicates that this agent is more potent than aspirin. If the patient is experiencing
severe pain, however, neither aspirin nor ibuprofen has sufficient efficacy to bring relief. In this instance,
morphine has a greater efficacy than aspirin or ibuprofen and can effectively treat this type of pain. In this
example, the average dose is unimportant to the patient, but efficacy—the ability of the pain medication to
bring essential relief—is crucial.
F i g u re 4 . 6
100
Drug A Drug B
(% of maximum response)
Intensity of drug response
75
50 higher POTENCY lower
25
Dotted line indicates the
same dose for both drugs
0
(a) 10 100 1,000 10,000
Log dose
Drug A higher
100
(% of maximum response)
Intensity of drug response
75
Drug B
50 EFFICACY
25
lower
0
(b) 10 100 1,000 10,000
Log dose
Potency and efficacy: (a) drug A has a higher potency than drug B; (b) drug A has a higher efficacy than drug B.
Concept Review 4.3

■ What does the term pharmacodynamics mean? Identify the importance of receptors, ago-
nists, and antagonists in influencing drug action. What is the difference between a drug’s
potency and its efficacy?
Chapter Review
4.1 Pharmacokinetics focuses on what the body does 4.2 Absorption is the first step in drug transport.
to the drugs. Absorption is the first step in pharmacokinetics. It
Pharmacokinetics is an area of pharmacology dealing involves movement of a drug from its site of admin-
with how drugs move throughout the body. There are istration across body membranes. Drugs cross many
four components of drug transport: absorption, distri- membranes before reaching target organs. Drug ab-
bution, metabolism, and excretion. sorption is affected by many factors.
Chapter Review 49
4.3 Distribution refers to how drugs are transported 4.6 The rate of elimination and half-life characteristics
throughout the body. influence drug responsiveness.
Distribution begins after absorption and continues The elimination rate of a drug is defined as the amount
until drug action. Drugs bound to plasma proteins of drug removed from the body by normal physiologic
may be isolated in the plasma and prevented from processes per unit of time. Plasma half-life is the
reaching their target cells. The blood-brain barrier, amount of time it takes for the body to remove half of
blood-placental barrier, and blood-testicular barrier the drug from the general circulation. These and other
all represent areas in the body where drug distribution important factors affect the duration of drug action.
may be limited.
4.7 Pharmacodynamics focuses on what the drugs do
4.4 Metabolism is a process whereby drugs are made to the body.
less or more active. Pharmacodynamics is an area of pharmacology con-
Metabolic processes take place in the liver, and to a cerned with how drugs produce responses within the
lesser extent, in organs such as the kidney and cells body. Successful drug therapy depends on the effec-
of the gastrointestinal tract. The first-pass effect is tiveness of these responses.
an important phenomenon. Many drugs absorbed
across intestinal membranes are routed directly to the 4.8 Drugs activate specific receptors to produce a
liver. Metabolic liver enzymes are usually less active response.
in younger and in older patients; therefore, drug ef- Generally, the response of a drug begins when the agent
fects will most likely be greater in these age groups. encounters the receptor of its target cell. The receptor
Prodrugs are agents converted to a more active form theory states that most responses in the body are caused
when they are metabolically changed. by interactions of drugs with specific receptors. Recep-
tors may be located on the plasma membrane, or they
4.5 Excretion processes remove drugs from the body. may be found in the cytoplasm or nucleus of the cell.
The kidneys, lungs, sweat glands, mammary glands,
and gallbladder are the major structures involved in 4.9 Potency and efficacy are terms often used to
eliminating drugs from the body. The main organ in- describe the success of drug therapy.
volved with excretion is the kidney. Enterohepatic re- Potency relates to the concentration or amount of
circulation is a unique type of mechanism responsible drug required to produce a maximum response.
for recirculating bile back into the bloodstream from Efficacy refers to how great the maximal response of
the gastrointestinal tract. a drug will be.
Review Questions
The following questions are written 3. “You will need to speak to your physician about this.”
in NCLEX-PN® style. Answer these 4. “The first dose of the medication is blocked by deactiva-
questions to assess your knowledge tion and the second dose is metabolized by the body.”
of the chapter material, and go back
and review any material that is not 3. The nursing student learns that which of the following
clear to you. principles are true about how medications work? (Select all
that apply.)
1. Patients with liver disorders would most likely have prob- 1. For a drug to be effective, it must be potent.
lems with which pharmacokinetic phase? 2. For drug efficacy to occur, a lower dose must be ad-
1. Absorption ministered.
2. Distribution 3. Antagonists bind to receptors and produce responses to
3. Metabolism block agonists.
4. Excretion 4. The agonist-receptor interaction causes a cellular response,
resulting in a therapeutic action.
2. The patient asks the nurse why he or she must take his or
her medication twice a day instead of just once. The nurse’s 4. The nurse is administering a drug that binds with a receptor
best response would be: to produce a therapeutic response. This type of drug is called a(n):
1. “Taking it once a day is fine as long as it is taken at the 1. Antagonist
same time every day.” 2. Facilitator
2. “Taking the medication twice a day ensures that maximum 3. Agonist
concentrations are maintained within the body.” 4. Blocker
5. If a patient takes a medication on a full stomach, the nurse 8. When orally administered drugs are extensively metabo-
is aware that the medication will be: lized by the liver, with only part of the drug dose reaching tar-
1. Absorbed more rapidly get organs, this is known as:
2. Absorbed more slowly 1. Half-life
3. Neutralized by gastric enzymes 2. Potency
4. Activated by gastric enzymes 3. First-pass effect
4. Rate of elimination
6. When planning care for a patient, the nurse takes into con-
sideration which of the following factors that could directly 9. A patient asks the nurse how the body will “get rid of all
influence the effectiveness of drugs that will be given? (Select the drugs” she is taking. The nurse responds by saying: (Select
all that apply.) all that apply.)
1. Drug–drug interactions 1. “Drugs are normally removed from the body by the kidneys.”
2. Food–drug interactions 2. “Some drugs are removed from the body through some
3. Route of administration glands.”
4. Time of administration within the day 3. “Some drugs can be more effectively excreted through the
sweat glands.”
7. An antibiotic has been ordered for the patient with a brain 4. “Some drugs are changed into a gaseous form and are
abscess. The nurse understands that: excreted by the lungs.”
1. There are no antibiotics effective to treat brain abscesses
because they cannot cross the blood-brain barrier. 10. An elderly patient has reduced metabolic activity. The
2. Only fat-soluble substances will pass the blood-brain bar- nurse may expect to see what change in the dosage of a drug
rier so the antibiotic will need to be fat-soluble. given to this patient?
3. The half-life of the antibiotic will be decreased when cross- 1. Increase the medication dosage.
ing the blood-brain barrier. 2. Increase the number of times the patient has to take the
4. The intestinal tract will prevent absorption from occurring. medication.
3. Decrease the medication dosage.
4. Reduce the number of times the patient has to take the
medication.
website.

C
H
A
P
T
E
R
The Nursing Process

in Pharmacology 5
Core Concepts
5.1
The first step of the nursing process is the assess- 5.4
The implementation phase puts the plan of care into
ment phase. action.
5.2
Nursing diagnoses are based on the data gathered 5.5
In the evaluation phase, the nurse obtains data
in the assessment phase. to determine if the goal or outcome has been
5.3 In the planning phase, the nurse creates an indi- achieved.
vidualized plan of care for a patient based on the
identified nursing diagnoses and etiologies.
Learning Outcomes
1. Describe the five steps of the nursing 3. Explain how nursing diagnoses can 5. Identify pharmacology applications
process. be used to improve medication included in the implementation
2. Identify how the assessment phase administration. phase of the nursing process.
of the nursing process can be used to 4. Describe the steps in the 6. Explain the importance of
gather data pertinent to medication planning phase of the nursing the evaluation phase in the
administration. process. nursing process as applied to
pharmacotherapy.
Key Terms
assessment phase 52 goal 54 nursing process 51
etiologies (e-tee-OL-o-gees) 53 implementation phase 55 outcome 54
evaluation criteria 54 interventions 53 planning phase 53
evaluation phase 56 nursing diagnosis 53
T he nursing process, a systematic method of problem solving, forms the foundation of all nursing practice. The use of the nursing
process is particularly essential during medication administration. By using the steps of the nursing process, the nurse can ensure that
the interdisciplinary practice of pharmacology results in safe, effective, and individualized medication administration and outcomes
for all patients under their care.
The nursing process is an ongoing activity involving five distinct phases: assessment, diagnosis, planning, implementation, and evalua-
tion. The nursing process is cyclical and each phase is related to all the others; they are not separate entities but overlap. The licensed practi-
cal nurse (LPN) or licensed vocational nurse (LVN) contributes to each phase of the process under the direction of the registered nurse (RN).
In this chapter, each phase is briefly reviewed, and each phase’s use in pharmacology is emphasized. A summary of the phases is shown in
Figure 5.1 ■.
52 Chapter 5 The Nursing Process in Pharmacology
Core Concept 5.1 The first step of the nursing process is the assessment phase.
The assessment phase of the nursing process is the systematic collection, organization, validation, and
documentation of patient data. The assessment phase serves two purposes. The first is to gather data that
will enable the nurse to identify current patient health challenges and problems that the patient is at particu-
lar risk for developing. These data will eventually be used to identify appropriate nursing diagnoses and to
develop a plan of care.
The second purpose of the assessment phase is to gather initial baseline data on the patient that will
be compared to subsequent data during the evaluation phase of the nursing process. These comparisons
will indicate to what extent the treatment goals have been achieved. When applying the nursing process to
pharmacology, baseline data are necessary for the nurse to be able to evaluate therapeutic drug effects and
adverse drug effects. For example, a common adverse effect of many antibiotics is the risk for allergic reac-
tion, often identified by skin rash. To determine whether the rash is due to a medication, the nurse must first
assess that a rash was not present prior to initiating drug therapy. As another example, if a patient is exhibit-
ing elevated liver enzymes during hospitalization, the nurse will use baseline assessment data to determine
whether the patient had this condition on admission, or whether it is a sign of a recent adverse drug reaction.
Data collected in the assessment phase come from many sources. These include the patient, caregivers,
medical records, and other healthcare professionals. Subjective data include what the patient says or perceives,
such as pain, anxiety, or nausea. Whenever possible, the subjective data are verified by objective data that are
gathered through physical examination, medical history, laboratory tests, and other diagnostic sources.
Assessment must always include a comprehensive health history that includes the patient’s use of
prescription drugs, over-the-counter (OTC) agents, dietary supplements, and herbal products. The nurse
should inquire about tobacco and alcohol use as well as past or current history of drug abuse because these
may influence treatment outcomes. Any allergic or unusual reactions to drugs should be documented, in-
cluding serious adverse drug reactions that may have occurred to close family members.
Figure 5.1
The five overlapping

phases of the nursing
process. Each phase de- ASSESSING
pends on the accuracy • Collect data
of the other phases. ASSESSING • Organize data
Each phase involves • Validate data
• Document data
critical thinking. The nursing process is cyclical; that is,
Source: Berman, A., & Snyder, S. its components follow a logical
(2012). Kozier & Erb’s funda- sequence, but more than one
mentals of nursing: Concepts, component may be involved at
process, and practice (9th ed.). DIAGNOSING
one time. At the end of the
Upper Saddle River, NJ: Pearson
first cycle, care may be DIAGNOSING • Analyze data
Education. • Identify health problems,
terminated if goals are
risks, and strengths
achieved, or the cycle
• Formulate diagnostic
may continue with statements
reassessment, or the
plan of care may be
modified.
PLANNING
PLANNING • Prioritize problems/diagnoses
• Formulate goals/desired outcomes
• Select nursing interventions
• Write nursing interventions
IMPLEMENTING IMPLEMENTING
• Reassess the client
• Determine the nurse’s need for assistance
• Implement the nursing interventions
• Supervise delegated care
• Document nursing activities
EVALUATING
EVALUATING
• Collect data related to outcomes
• Compare data with outcomes
• Relate nursing actions to client goals/outcomes
• Draw conclusions about problem status
• Continue, modify, or terminate the client’s care plan
Core Concept 5.3 53
The initial health history gathered during the assessment phase is used to determine whether the pa-
tient has a contraindication that would present a risk for drug therapy. For example, the nurse may discover
during assessment that the patient is pregnant and should not receive isotretinoin (Accutane) for her acne
because it is a pregnancy category X drug. The nurse may discover that the patient has a history of allergy
to penicillin, and therefore, should not be prescribed ampicillin due to the potential for cross-allergy. A
thorough assessment is the best way to prevent adverse drug effects.
Concept Review 5.1

■ What types of assessments would be important for the nurse to perform on patients who
will be required to self-administer their medications at home?
Nursing diagnoses are based on the data gathered

in the assessment phase. Core Concept 5.2
During the diagnosis phase of the nursing process, the nurse analyzes assessment data, identifies health
problems, and formulates diagnostic statements. A nursing diagnosis is a clinical judgment of a pa- dia 5 through or complete
tient’s response to an actual or potential health problem, a problem that is within the nurse’s scope of gnosis 5 knowledge
practice to address. It is the responsibility of the RN to identify the appropriate diagnosis and develop a
plan of care. The LPN/LVN contributes to this phase by collecting data and collaborating with the RN.
Nursing diagnoses differ from medical diagnoses, which are determined by physicians. Whereas
the medical diagnosis remains constant during a patient’s hospital stay, nursing diagnoses are in con-
stant flux as the patient responds to treatments. Nursing diagnoses address changes in the patient’s
condition—for example, alterations in mobility, nutritional intake, urinary elimination, knowledge,
ability for self-care, and risk for injury. These nursing diagnoses are used to set goals and plan care.
Nursing diagnoses are often stated as a problem, or the risk for a problem, followed by a “related to”
clause that identifies the etiologies, or those conditions that have caused or contributed to the problem. By etio 5 cause
altering one or more of these etiologies, nurses are able to effect improvements in the diagnosed problem. This ology 5 study of
is accomplished by planning and implementing interventions, which are actions that the nurse takes to achieve
patient goals. The nurse chooses interventions that are patient focused and target the etiologies of the problem.
The North American Nursing Diagnosis Association (NANDA) has developed standard wording, known as
the nursing diagnosis, for identifying actual and potential patient health problems. For example, a nursing diag-
nosis may be, “Activity Intolerance related to acute knee pain.” The nurse designs interventions to address the
etiology (acute knee pain) that may include the administration of pain medications, heat, or ice packs.
Nursing diagnoses are prioritized by their level of importance and immediacy to the patient’s clinical
condition. For example, alterations in breathing would likely take precedence over the potential for skin
breakdown. A primary nursing role is to enable patients to become active participants in their own care.
Patients need to vocalize, to the extent possible, their priorities for care, which should be considered by the
nurse when diagnoses are prioritized. By including patients when identifying needs, the nurse encourages
them to take a more active role in working toward meeting the identified goals.
When applied to pharmacotherapy, the diagnosis phase of the nursing process addresses three main
areas of concern:
■ Promoting therapeutic drug effects
■ Minimizing adverse drug effects and toxicity
■ Maximizing the ability of the patient for self-care, including the knowledge, skills, and re-
sources necessary for safe and effective drug administration
The teaching of patients is one of the basic roles of nursing, and careful attention to drug teaching can
promote therapeutic outcomes as well as minimize adverse effects. Examples of nursing diagnoses that
intimately involve drug teaching include Deficient Knowledge related to a lack of information about new
drug therapy and Noncompliance related to not taking the prescribed medication. The teaching of patients
is discussed further in the planning phase. See Table 5.1 ◆ for selected nursing diagnoses for pharmaco-
therapy. For a complete list, the student should refer to a nursing fundamentals textbook.
In the planning phase, the nurse creates an individualized plan of care for
a patient based on the identified nursing diagnoses and etiologies. Core Concept 5.3
After a nursing diagnosis has been established, the nurse begins to plan ways to assist the patient to es-
tablish an optimum level of wellness. In the planning phase of the nursing process, the nurse prioritizes
diagnoses, formulates desired goals, and selects nursing interventions.
Table 5.1 Common Nursing Diagnoses in Pharmacotherapy

Acute Confusion related to substance abuse
Risk for Confusion related to drug effects
Impaired Comfort related to drug effects
Deficient Fluid Volume related to drug effects
Excess Fluid Volume related to drug effects
Noncompliance related to lack of knowledge of drug therapy
Risk for Infection related to adverse drug effects
Risk for Injury related to adverse drug effects
Insomnia related to drug effects
Imbalanced Nutrition: Less than body requirements related to drug-induced nausea
Ineffective Health Maintenance related to drug therapy regimen
Activity Intolerance related to drug effects
Deficient Knowledge related to a lack of information about new drug therapy
*Other nursing diagnosis may be applicable depending on patient assessment and type of medication being used.
Source: NANDA International Nursing Diagnosis: Definitions and Classifications 2012–2014, Wiley-Blackwell (2011)
There are two main steps of the planning phase. The first step is to identify the desired goal, or outcome,
to be achieved, and the specific evaluation criteria that will be used to determine if that goal has been met.
The outcome may be a short-term or long-term goal, should include the time frame whenever possible, and
must be realistic for the patient to achieve. The evaluation criteria should be specific and measurable. These
criteria are often indicated by the abbreviation AEB (as evidenced by). The outcome should directly address
the problem identified in the nursing diagnosis. For example, if the nursing diagnosis is Risk for Dysfunc-
tional Gastrointestinal Motility related to opioid analgesic use, a goal might be: the absence of altered bowel
elimination, AEB regular bowel evacuation, absence of difficulty passing stool, and absence of abdominal
bloating or discomfort. Notice how this plan includes a clear goal as well as specific evaluation criteria.
The second step of the planning phase is to develop a list of interventions. The interventions are spe-
cific nursing actions designed to help move the patient toward the established goal.
When planning interventions the nurse should consider the specific health problem and etiologies,
current practice guidelines, acceptability to the patient, and the nurse’s own capabilities. In addition, the
chosen nursing interventions should be safe and appropriate for the patient’s age, health, and condition;
congruent with the patient’s values, beliefs, and culture; and appropriate to the other ordered therapies. The
choice of nursing interventions will also depend on what is realistic and practical to the situation in terms
of equipment availability, financial status of the patient, and available resources, including staff, agency,
family, or community resources.
With respect to pharmacotherapy, the planning phase involves two main issues: drug administration
and patient teaching. For the first issue, the nurse must plan how and when to administer the drug. For oral
medications, does it need to be given with food or on an empty stomach? Is it more effective if adminis-
tered at a certain time of day? Can it be crushed or split? For all medications, the nurse will plan interven-
tions to enhance therapeutic outcomes and minimize or prevent adverse drug effects.
When planning patient drug teaching, the projected length of pharmacotherapy influences the amount
and type of teaching provided by the nurse. Is the drug to be given for a short time during an acute care
hospitalization, or is pharmacotherapy going to be long term and self-administered following discharge? If
a drug is to be given short term, the patient should be told the name of the drug and its basic actions, why
the patient is receiving it, and some of the drug’s most common and major adverse effects, including any
that should be promptly reported to the nurse or healthcare provider.
For drugs that will be taken after discharge, patient teaching should be comprehensive and be pro-
vided both orally and in writing. This teaching should include the drug name (both generic and trade), the
drug class and its major effects, why the drug is being prescribed, the therapeutic effects and when they
should occur, how and when to take the drug, the common and major adverse effects and which ones
should be reported to the prescriber, the types of follow-up monitoring needed, potential drug interac-
tions, the duration of drug therapy, the activities to avoid while taking the drug, and what to do if a dose
is missed or forgotten. Table 5.2 ◆ gives tips for effective patient teaching that can be used for patients of
all ages.
Core Concept 5.4 55
Table 5.2 Teaching Throughout the Life Span

Patient teaching is an essential component of the nursing process. To be effective, oral and written teaching
must be age appropriate. The following are some tips for effective teaching.
Children
■ Use family-centered approaches when providing drug teaching for children and adolescents.
■ Engage young children and toddlers by using interactive strategies.
■ Use simple, nonthreatening language.
■ Provide a developmentally appropriate environment when teaching adolescents.
■ Encourage problem solving to help adolescents make effective choices.
Adults
■ Adult learners are independent; the nurse should facilitate learning.
■ Adults learn best when the topic is of immediate value, and when new material is connected to previous
experiences.
■ Adults vary widely in their learning styles and preferences; teaching and learning is enhanced when
patient learning styles are considered.
■ Consider the literacy level of learners. It is recommended that written materials be on a fifth-grade
reading level.
■ Employ multiple methods of delivering information; a combination of verbal and written material
is best.
Older Adults
■ Plan several short learning sessions; repeat and review material covered; time needed for learning often
increases with age.
■ Relate new learning to the patient’s real-life experiences.
■ Provide printed material, videos, and/or pictures and diagrams that the patient can refer to at a
later time.
■ Modify teaching methods to sensory-perceptual deficits or cognitive decline. Ensure that the
patient has the necessary aids (glasses, magnifying glass, hearing aid) to maximize the learning
experience.
■ Offer opportunities for practice of psychomotor skills related to administering medications.
The implementation phase puts the plan of care into action. Core Concept 5.4
The implementation phase is when the nurse applies the knowledge, skills, and principles of nursing care
to help move the patient toward the desired goal and optimal wellness. Implementation involves action
on the part of the nurse or patient: administering a drug, providing patient teaching, and initiating actions
identified by the nursing diagnoses and plan of care. The implementation phase should be designed to
maximize therapeutic drug responses and prevent adverse reactions.
It must be remembered that implementation of the plan of care is subject to modification based on
the patient’s evolving condition. In implementing pharmacotherapy, an important decision that the nurse
must make is whether it is appropriate to administer the drug at the planned time. To make this decision,
the nurse needs to understand the drug’s therapeutic and adverse effects well enough to know the circum-
stances under which it is appropriate, or not appropriate, to give the drug. After assessing a current vital
sign, a laboratory result, a new health problem, or a physical assessment finding, it may be appropriate for
the nurse to delay administration of an ordered drug until the prescriber can be contacted. For example,
if the patient’s current serum potassium level is below the normal range, and the nurse has an order to
administer furosemide (Lasix), it would be an error for the nurse to administer the drug. Carrying out the
order would cause serum potassium to fall, which could trigger cardiac dysrhythmias. Likewise, a patient
who has a scheduled dose of morphine for pain relief but currently has a respiratory rate of less than eight
should not receive the drug because it may cause respiratory failure.
As pharmacotherapy progresses, the nurse must be aware of circumstances that might require
modification of the implementation phase. The patient may develop new symptoms that contraindicate
the use of the drug being administered. For example, the patient may begin to show signs of a devel-
oping rash, changes in blood pressure, or alterations in mental status that call for discontinuation of
the drug until the prescriber can be contacted. These examples help illustrate the cyclic nature of the
Figure 5.2
Teaching patients about

drugs and their effects
is an important step in
the nursing process.
Source: Science Photo Library
nursing process: the importance of continuous assessment and the revision of the planning and imple-
mentation phases.
Implementation also includes patient teaching (Figure 5.2 ■). Table 5.2 gives tips for effective patient
teaching that can be used for patients of all ages. Patient drug teaching should start with what the patient
already knows about a drug and build from there. The specific topics to include in this teaching are devel-
oped in the planning phase. When preparing to carry out the teaching, other factors that the nurse should
consider are the patient’s readiness to learn and whether or not it is an appropriate time for teaching. Pa-
tients who are in pain, sleepy, anxious, or distracted are less likely to understand instructions. Drug teach-
ing should be tailored to the patient’s developmental level, learning capacity, and preferred learning style.
Patients may prefer that a family member or caregiver be present during the teaching. This is especially
important for patients with limited English proficiency, pediatric patients, older adults with cognitive defi-
cits, and patients with mental illnesses who may be incapable of safe self-administration. Patient teaching
is sometimes a collaborative effort, requiring coordination with other medical disciplines as part of the ses-
sions. Often a registered dietician, physical therapist, or diabetes educator collaborates in the patient teach-
ing. When teaching, sufficient time must always be allotted to address any areas of concern for the patient.
Finally, documentation is an essential part of the implementation phase. This includes a thorough
reporting of the interventions carried out, the drugs that were given (or withheld), the teaching that took
place, and the patient’s responses to the interventions.
In the evaluation phase, the nurse obtains data to determine

Core Concept 5.5 if the goal or outcome has been achieved.
The evaluation phase compares the patient’s current health status with the established outcome to deter-
mine if the plan of care is appropriate or if it needs revision. Essentially, the evaluation phase is used to
determine if the goal or outcome has been met. If it has been met, the plan of care was appropriate. If the
goal was partially met, the nurse may determine that the interventions may need to be continued for a lon-
ger time or otherwise modified to better resolve the health problem.
As it relates to pharmacotherapy, evaluation is used to determine whether the therapeutic effects of
the drug have been achieved as well as whether adverse effects have been prevented or kept to acceptable
levels. For example, if a drug is given for symptoms of pain, has the pain subsided? If an antibiotic is given
for an infection, have the signs of that infection improved? If the evaluation data show no improvement in
health status over the baseline data, the interventions will likely need to be revised, drug doses may need to
be adjusted, more time may be needed to achieve a therapeutic drug response, or a different or additional
drug may be needed. The data gathered during the evaluation phase becomes part of the assessment data
and continues the cycle of nursing process as outcomes and interventions are revised. The evaluation data
needs to be documented in the patient’s record to ensure proper communication of the patient’s response to
the nursing interventions.
In an outpatient setting, lack of drug response determined during the evaluation phase may be caused
by patient nonadherence to the drug regimen. During the assessment phase, the nurse must determine if the
patient is taking the drug as prescribed. If nonadherence is discovered, the nurse must plan and implement
Chapter Review 57
strategies for increasing adherence, which includes identifying reasons for the nonadherence. Additional
patient teaching is critical to obtain maximum patient adherence to the drug regimen: The nurse must help Life Span Fact
the patient to value pharmacotherapy as important to the improvement of the patient’s health. When evaluating the suc-
cess of drug therapy in older
adults, the healthcare provider
Concept Review 5.2 should understand that nonad-
herence may be due to physi-
■ What strategies might the nurse implement to improve adherence to drug therapy for a cal or other limitations in. The
geriatric patient? inability to open childproof
containers or to read the in-
structions on the label are pos-
sible causes of nonadherence.
Older adults may be depend-
ing on caregivers to pick up or
administer their medications
CAM Therapy on a regular basis. In many
cases, simply forgetting to take
Medication Errors and Dietary Supplements a medication is a cause of lack
of drug effect. The healthcare
Some herbal and dietary supplements have powerful effects on the body that can influence the
provider should assist older
outcomes of prescription drug therapy. In some cases, OTC supplements can enhance the ef-
patients in overcoming these
fects of prescription drugs, whereas in other instances supplements may cancel the therapeutic
limitations so that pharmaco-
effects of medications. For example, many patients with heart disease take garlic supplements
therapy can be optimized.
in addition to warfarin (Coumadin) to prevent clots from forming. Because garlic and warfarin
are both anticoagulants, taking them together could cause excessive bleeding. As another ex-
ample, high doses of calcium supplements can cancel the beneficial antihypertensive effects of
drugs, such as nifedipine (Procardia), a calcium channel blocker.
Chapter Review
5.1 The first step of the nursing process is the assess- the evaluation criteria that will be used to determine
ment phase. whether or not the goal has been achieved. The sec-
Assessment is the careful, systematic collection of ond step is the formulation of nursing interventions
patient data. During this phase, the nurse gathers data to be used to help move the patient toward the estab-
that identify patient health challenges. lished goal.
5.4 The implementation phase puts the plan of care

5.2 Nursing diagnoses are based on the data gathered
into action.
in the assessment phase.
When applied to pharmacology, the implementation
Nursing diagnoses are clinical judgments based on
phase involves administering the drug and provid-
a patient’s response to actual or potential patient
ing patient drug teaching that maximizes therapeutic
problems; they include the etiologies of the health
effects and minimizes side effects.
problem. These etiologies are factors that can be ad-
dressed by nursing interventions to address the health 5.5 In the evaluation phase, the nurse obtains data
challenges of the patient. to determine if the goal or outcome has been
achieved.
5.3 In the planning phase, the nurse creates an indi- By comparing the evaluation data to baseline data,
vidualized plan of care for a patient based on the the nurse is able to determine whether or not the es-
identified nursing diagnoses and etiologies. tablished goal was met. Evaluation data are used to
The first step of the planning phase is identifica- develop revised goals, plans, or interventions that will
tion of a goal or outcome for the patient, including better resolve the health challenges of the patient.
Review Questions
The following questions are writ- 6. The second phase of the nursing process involves ana-
ten in NCLEX-PN® style. Answer lyzing data and identifying health problems, such as Activity
these questions to assess your Intolerance related to pain. This phase is known as:
knowledge of the chapter mate- 1. Assessment
rial, and go back and review any 2. Implementation
material that is not clear to you. 3. Nursing diagnosis
1. The nurse reviews a patient record for drug allergies, current 4. Planning
medications, and disease states that could affect drug responses. 7. The nursing process, as it relates to pharmacology, can
These actions are part of which phase of the nursing process? best be described as a:
1. Assessment 1. Way of determining whether a patient should use a cane or
2. Planning crutches when walking
3. Implementation 2. Method of documentation that nurses use in their daily
4. Evaluation practice
2. The implementation phase of the nursing process involves 3. Problem-solving method that encourages nurses to rely
which two main activities related to pharmacology? solely on their textbook knowledge of a patient’s condition
1. Developing and performing nursing interventions before determining a course of action
2. Providing and evaluating patient teaching 4. Systematic approach to problem solving that ensures the
3. Administering drugs and providing patient education safe and effective administration of medication
4. Assessing and evaluating adverse drug effects 8. The role of the LPN/LVN is to:
3. Which of the following would be most important for the 1. Work independently of the RN and other healthcare pro-
nurse in the evaluation phase of the nursing process? viders when establishing a plan of care for a patient.
1. Patient satisfaction with drug therapy 2. Assist the physician in establishing a patient’s plan of care.
2. Evidence of therapeutic drug effects 3. Contribute to each phase of the process under the direction
3. Development of minor adverse drug effects of the RN.
4. The possibility of noncompliance with drug therapy 4. Rely completely on the RN to utilize the nursing process
when caring for patients.
4. Which of the following is appropriate information to
gather in the assessment phase of the nursing process? (Select 9. A male patient has just been diagnosed with diabetes mel-
all that apply.) litus. The interdisciplinary team, including the LPN/LVN, is in
the process of developing a schedule of teaching sessions with
1. Drug allergies him on subjects such as glucose monitoring, insulin injections
2. Therapeutic response to the drug and signs of hypoglycemia. What phase of the nursing process
3. History of renal or hepatic disease does this represent?
4. Baseline physical assessment data
1. Assessment
5. Ms. Smith is complaining of pain in her lower back. After 2. Planning
asking Ms. Smith about her pain level, the nurse prepared the 3. Implementation
pain medication as ordered and is about to administer it to her. 4. Evaluation
What phase of the nursing process is the nurse using?
10. The nursing diagnosis statement is Insomnia related to
1. Assessment anxiety as manifested by difficulty falling and staying asleep.
2. Planning The etiology of the problem is:
3. Implementation
4. Evaluation 1. Insomnia
2. Anxiety
3. Difficulty falling asleep
4. Difficulty staying asleep
website.

C
H
A
P
T
E
R
The Role of Complementary and

Alternative Therapies
in Pharmacology 6
Core Concepts
6.1
Complementary and alternative therapies are used 6.4
Herbs can have significant pharmacologic actions
by a large number of people to prevent and treat and can interact with conventional drugs.
disease. 6.5
Specialty supplements are nonherbal products that
6.2
Natural products from plants have been used as are widely used to promote wellness.
medicines for thousands of years. 6.6
Herbal products and specialty are not regulated in
6.3
Herbal products are standardized with respect to the same manner as prescription medications.
a specific active ingredient.
Learning Outcomes
1. Identify specific types of the types of formulations made from 6. Explain why it is important to
complementary and alternative these parts. standardize herbal products based
therapies that are used by patients 4. Describe legislation that governs on specific active ingredients.
to promote wellness. the use of herbal and dietary 7. Discuss the role of the healthcare
2. Discuss the reasons why herbal supplements. provider in teaching patients about
products and dietary supplements 5. Describe drug interactions and complementary and alternative
have steadily increased in popularity. adverse effects that may be caused therapies.
3. Identify the parts of an herb that by herbal and dietary supplements.
may contain active ingredients and
Key Terms
complementary and alternative medicine Dietary Supplement and Nonprescription herb 61
(CAM) 60 Drug Consumer Protection Act 67 specialty supplements 65
dietary supplements 66 Dietary Supplement Health and Educa-
tion Act (DSHEA) of 1994 66
60 Chapter 6 The Role of Complementary and Alternative Therapies in Pharmacology
C omplementary and alternative therapies represent a multibillion dollar industry. Sales of dietary
supplements alone exceed $26 billion annually, with over 200 million consumers using them. Con-
sumers have turned to these treatments for a wide variety of reasons. Many people have the impres-
sion that natural substances have more healing power than synthetic medications. The ready availability of
over-the-counter (OTC) herbal supplements and specialty supplements at a reasonable cost, combined with
effective marketing strategies, has convinced many people to try them. This chapter examines the role of
herbal and specialty supplements in the prevention and treatment of disease.
Complementary and alternative therapies are used by a large number

Core Concept 6.1 of people to prevent and treat disease.
Complementary and alternative medicine (CAM) comprises an extremely diverse set of therapies and
healing systems that are considered to be outside of mainstream health care. CAM systems have the fol-
lowing common characteristics:
■ Focus on treating the individual
■ Consider the health of the whole person
■ Emphasize the integration of mind and body
■ Promote disease prevention, self-care, and self-healing
■ Recognize the role of spirituality in health and healing
Because of its popularity, the scientific community has focused considerable attention on determining
the effectiveness or lack of effectiveness of CAM. Although some research into these alternative systems
has been conducted, few CAM therapies have been subjected to rigorous clinical and scientific study. It is
likely that some of these therapies will become mainstream treatments, whereas others will be found inef-
fective. The line between what is defined as an alternative therapy and what is considered mainstream is
constantly changing. Increasing numbers of healthcare providers now recommend CAM therapies to their
patients. Table 6.1 ◆ describes some of these therapies.
Table 6.1 Complementary and Alternative Therapies

Healing Method Examples
Biologic therapies Herbal therapies
Nutritional supplements
Special diets
Alternate healthcare systems Naturopathy
Homeopathy
Chiropractic
Native American medicine (e.g., sweat lodges, medicine wheel)
Chinese traditional medicine (e.g., acupuncture, Chinese herbs)
Manual healing Massage
Physical therapy
Pressure-point therapies
Mind–body interventions Yoga
Meditation
Hypnotherapy
Guided imagery
Biofeedback
Movement-oriented therapies (e.g., music, dance)
Spiritual Shamanism
Faith and prayer
Core Concept 6.2 61
Fast Facts Alternative Therapies in America
One of the largest studies of Americans’ use of complementary therapies conducted by the National
Center for Complementary and Alternative Medicine (NCCAM) surveyed over 23,000 people (Barnes,
Bloom, & Nahin, 2008). Findings of this study included the following:
■ Thirty-eight percent of adults and about 12% of children are currently using CAM.
■ Women and those with higher educational levels are most likely to use CAM.
■ The most frequent conditions treated with CAM are back pain (17%), head or chest cold (10%), joint
pain/arthritis (5%), neck pain (5%), and anxiety or depression (5%).
■ People are more likely to use CAM when they are unable to afford conventional health care.
Healthcare providers have long known the value of CAM therapies in preventing and treating disease.
For example, prayer, meditation, massage, and yoga have been used for centuries to treat both body and
mind. From a therapeutic perspective, much of the value of CAM therapies is their ability to reduce the
need for medications. If a patient can find anxiety relief through massage or biofeedback therapy, for ex-
ample, the use of antianxiety drugs may be reduced or eliminated. Reduction of drug dose leads to fewer
adverse effects and better compliance with drug therapy. This chapter focuses on two CAM therapies:
herbs and specialty supplements.
Concept Review 6.1

■ How does the healing philosophy of complementary and alternative medicine differ from
that of conventional mainstream medicine?
Herbal Products
The number of people seeking herbal alternatives to conventional medical therapies has steadily increased
over the past three decades. Many herbs are extensively used by patients as supplements to traditional
pharmacotherapy.
Natural products from plants have been used as medicines

for thousands of years. Core Concept 6.2
Technically, an herb is a plant that lacks woody stems or bark. Over time, the term herb has come to re-
fer to any plant product with a useful application, either as a food enhancer (such as a flavoring) or as a
medicine.
The use of herbs in the treatment of disease has been recorded for thousands of years. One of the earli-
est recorded uses of plant products was a prescription for garlic in 3000 b.c. Eastern and Western medicine
have recorded thousands of herbs and herb combinations claimed to have therapeutic value. Some of the
most popular herbs and their primary uses are shown in Table 6.2 ◆.
The public’s interest in herbal medicine began to decline when the pharmaceutical industry was born
in the late 1800s. Drugs could be standardized and produced more cheaply than natural herbal products. In
the early 1900s, regulatory agencies required that medicines be safe and effective. The focus of health care
shifted to treating specific diseases, rather than promoting wellness and holistic care. Information about
most herbal and alternative therapies was no longer taught in medical schools; these healing techniques
were criticized as being unscientific relics of the past.
Beginning in the 1970s and continuing to the present day, herbal medicine has experienced a remark-
able comeback. The majority of adult Americans are either currently taking herbal products on a regular
basis or have taken them in the past. This increase in popularity has been due to a number of factors, in-
cluding increased availability of herbal products, aggressive marketing by the herbal industry, increased
attention to natural alternatives, and renewed interest in preventive medicine. The gradual aging of the
population has led to more patients seeking therapeutic alternatives for chronic conditions such as pain,
arthritis, prostate difficulties, and the need for hormone replacement. In addition, the high cost of prescrip-
tion medicines has driven many people to seek less expensive alternatives.
Table 6.2 Popular Herbal Products

Common Name Medicinal Part Primary Use(s)
Aloe Leaves Treat skin ailments (topical) and constipation (oral)
Bilberry Berries/leaf Terminate diarrhea, improve and protect vision
Black cohosh Roots Relieve menopause symptoms
Cranberry Berries/juice Prevent urinary tract infection
Echinacea Entire plant Enhance immune system, reduce inflammation
Life Span Fact
Evening primrose Oil extracted from seeds Relieve pain and inflammation
A wide range of dietary sup-
Flaxseed Seeds and oil Reduce blood cholesterol, laxative
plements, such as herbs and
other specialty products, are Garlic Bulbs Reduce blood cholesterol and blood pressure, as an
being used to treat children. anticoagulant
Unfortunately, the use of these
therapies has not been well Ginger Root Relieve GI upset and motion sickness, as an
studied with children. Just as anti-inflammatory
with conventional medicine, Ginkgo biloba Leaves and seeds Improve memory, reduce dizziness
children may react differently
than adults to herbal and Ginseng Root Relieve stress, enhance immune system, decrease
other CAM therapies. The fatigue
healthcare provider should as-
sess for the use of supplements Horny goat weed Leaves and roots Enhance sexual function
in all pediatric patients. It is Milk thistle Seeds As an antitoxin to protect against liver disease
important to ensure that care-
givers know the importance Red yeast rice extract Dried in capsules Reduce blood cholesterol
of an accurate diagnosis from
a licensed healthcare provider
Saw palmetto Ripe fruit/berries Relieve urinary problems related to prostate
and that supplements or other
enlargement
CAM products should not Soy Beans Source of protein, vitamins, and minerals; relieve
replace or delay conventional menopausal symptoms; prevent cardiovascular
medical care. In addition, disease; as an anticancer agent
caregivers should be taught to
store all herbs/dietary supple- St. John’s wort Flowers, leaves, stems Reduce depression, reduce anxiety, as an
ments away from children, use anti-inflammatory
only as directed, and report
Valerian Roots Relieve stress, promote sleep
any side effects to the child’s
healthcare provider.
Herbal products are standardized with respect to a specific

Core Concept 6.3 active ingredient.
The active ingredients in an herbal product may be present in only one specific part of the plant or in all
parts. For example, the active chemicals in saw palmetto are in the berries. For ginger and black cohosh,
the roots are used for their healing properties.
Most modern drugs contain only one active ingredient. This chemical is standardized and accurately
measured so that the amount of drug received by the patient is precisely known. It is a common miscon-
ception that herbal products also contain one active ingredient, which can be extracted and delivered to
patients in exact amounts, like drugs. Herbs, however, may contain dozens of active chemicals, many of
which have not yet been isolated, studied, or even identified. It is possible that some of these substances
work together synergistically and may not have the same activity if isolated. Furthermore, the strength of
an herbal preparation often varies from batch to batch depending on where the herb was grown and how it
was collected, prepared, and stored.
To achieve consistency in the strength or “dose” of an herbal product, scientists have attempted
to standardize herbal products. Standardization allows the consumer to compare products and know
the strength of the herb. Some of these standardizations are shown in Table 6.3 ◆. Until science can
better characterize these substances, however, it is best to view the active ingredient of an herb as
being the entire herb. An example of standardization—the ingredients of ginkgo biloba—is shown in
Figure 6.1 ■.
The two basic formulations of herbal products are solid and liquid. Solid products include pills, tablets,
and capsules made from dried herbs. Other solid products are salves and ointments that are administered
topically. Liquid formulations are made by extracting the active chemicals from the plant and include teas,
infusions, tinctures, and extracts. Some formulations of ginkgo biloba, one of the most popular herbals, are
illustrated in Figure 6.2 ■.
Core Concept 6.4 63
Table 6.3 Standardization of Selected Herb Extracts

Herb Standardization Percent
Black cohosh Triterpene glycosides 2.5
Echinacea Echinacosides 4
Ginger Pungent compounds (gingerols) Greater than 10
Ginkgo leaf Flavonglycosides 24–25
Lactones 6
Ginseng root Ginseosides 5–15
Milk thisle root Silymarin 80
St. John’s wort Hypericins 0.3–0.5
Hyperforin 3–5
Saw palmetto Fatty acids and sterols 80–90
Figure 6.1
Ginkgo Biloba label.

GINKGO BILOBA Supplement Facts
Serving Size: 1 capsule
The label indicates the
product is standardized
Dietary Supplement to percent flavonglyco-
Amount Per Serving
Natures
sides and percent ter-
Ginkgo biloba leaf 175 mg* penes, active substances
Standardized to: that are found in the
Herbal
24% Flavonglycosides ginkgo leaf. Also note
6% Terpene lactones the health claims on the
*Daily value not established. label, which have not
Harvest
been evaluated by the
Recommended Dose: 1 capsule FDA.
per day with a meal as a food
supplement.
† May support memory
200 Capsules and concentration †This statement has not been evaluated by the Food
175 mg † May help to maintain and Drug Administration. This product is not intended
to diagnose, treat, cure or prevent any disease.
circulation
Herbs can have significant pharmacologic actions and can

interact with conventional drugs. Core Concept 6.4
A key concept to remember when dealing with alternative therapies is that natural does not always mean
better or safe. There is no question that some herbs contain active chemicals as powerful as, and per-
haps more effective than, currently approved medications. Thousands of years of experience, combined
with current scientific research, have shown that some of these herbal remedies have therapeutic actions.
Because a substance comes from a natural product, however, does not make it either safe or effective.
For example, poison ivy is natural, but it certainly is not safe or therapeutic. Natural products may not
offer an improvement over conventional therapy in treating certain disorders and, indeed, may be of no
value whatsoever. Most importantly, a patient who substitutes an unproven alternative therapy for an
established, effective medical treatment may delay healing, suffer harmful effects, and endanger his or
her health.
Some herbal products contain ingredients that may interact with prescription drugs. For example, pa-
tients taking medications with potentially serious adverse effects, such as insulin, warfarin (Coumadin), or
digoxin (Lanoxin), should be warned never to take any dietary supplement without first discussing their
needs with their nurse practitioner or physician. Pregnant or lactating women should not take herbal products
Figure 6.2
Three different ginkgo

formulations: tablets,
tea bags, and liquid
extract.
Table 6.4 Selected Herb–Drug Interactions

Common Name Interacts With Comments
Echinacea Amiodarone, anabolic steroids, ketoconazole, Possible increased hepatotoxicity
methotrexate
Garlic Aspirin and other NSAIDs, warfarin Increased bleeding risk
(Coumadin)
Insulin, oral hypoglycemic agents Additive hypoglycemic effects
Ginger Aspirin and other NSAIDs, heparin, warfarin Increased bleeding risk
Ginkgo biloba Anticonvulsants Possible decreased anticonvulsant
effectiveness
Aspirin and NSAIDs Increased bleeding potential
Heparin and warfarin (Coumadin) Increased bleeding potential
Tricyclic antidepressants Possible decreased seizure
threshold
Ginseng CNS depressants Increased sedation
Digoxin (Lanoxin) Increased toxicity
Diuretics Possible weakened diuretic effects
Insulin and oral hypoglycemic agents Increased hypoglycemic effects
Warfarin Decreased anticoagulant effects
St. John’s wort CNS depressants and opiates Increased sedation
Cyclosporine (Sandimmune) Possible decreased cyclosporine
levels
Oral contraceptives Decreased drug effectiveness
Selective serotonin reuptake inhibitors Possible serotonin syndrome
(SSRIs), tricyclic antidepressants (headache, dizziness, sweating,
agitation)
Warfarin (Coumadin) Decreased anticoagulant effects
Valerian Barbiturates, benzodiazepines, and other Increased sedation
CNS depressants
without the approval of their healthcare provider. The health professional should also remember that the
potential for any drug interaction increases in older adults, especially those with hepatic or renal impairment.
Although the true extent of herb–drug interactions is largely unknown, some of the documented interactions
are shown in Table 6.4 ◆.
Another warning that must be heeded with natural products is to beware of allergic reactions. Most
herbal products contain a mixture of ingredients, and it is not unusual to find dozens of different chemicals
in teas and infusions made from the flowers, leaves, or roots of a plant. Patients who have known allergies
to certain foods or medicines should seek medical advice before taking an herbal product. It is always wise
to take the smallest amount possible—less than the recommended dose—when starting herbal therapy to
see if allergies or other adverse effects occur.
Core Concept 6.6 65
Healthcare providers have an obligation to seek the latest medical information on herbal products be-
cause there is a good possibility that their patients are using them to supplement traditional medicines. Patients
should be advised to be skeptical of claims on the labels of dietary supplements and to seek their health infor-
mation from reputable sources. Healthcare providers should never condemn patients’ use of alternative thera-
pies, but instead be supportive and seek to understand their goals for taking the supplements. The healthcare
provider should teach patients the appropriate role of alternative therapies in the treatment of their disorders
and discuss which treatments or combination of treatments will best meet their health goals.
Specialty Supplements
Specialty supplements are nonherbal dietary supplements that can come from either plant or animal
sources. Like herbal therapies, they are available OTC and are widely used by patients to enhance wellness.
Specialty supplements are nonherbal products that are widely used to

promote wellness. Core Concept 6.5
The actions of specialty supplements are more specific than those of herbal products, and they are generally
targeted for one or a small number of conditions. Popular specialty supplements are listed in Table 6.5 ◆
In general, specialty supplements have a legitimate rationale for their use. For example, chondroi-
tin and glucosamine are natural substances in the body necessary for cartilage growth and maintenance.
Amino acids are natural building blocks of muscle protein. Fish oils contain omega fatty acids that have
been shown to reduce the risk of heart disease in certain patients.
Unfortunately, the link between most specialty supplements and their benefits is unclear. In some
cases, the body already has sufficient quantities of the substance; therefore, taking additional amounts may
be of no benefit. In other cases, the supplement is marketed for conditions for which it has no proven effect
(See Figure 6.3 ■). The good news is that these substances, when taken in amounts stated on the label, are
generally not harmful. The bad news, however, is that they can give patients false hopes of an easy cure for
a chronic condition such as heart disease or the pain of arthritis. As with herbal products, the healthcare pro-
vider should advise patients to be skeptical about the health claims regarding the use of these supplements.
Concept Review 6.2

■ Explain the differences between an herbal product and a specialty supplement.
Herbal products and specialty supplements are not regulated in the same
manner as prescription medications. Core Concept 6.6
Since the passage of the Food, Drug, and Cosmetic Act of 1935, Americans have come to expect that all
prescription and OTC drugs have passed rigid standards of safety prior to being marketed. Furthermore, it
Table 6.5 Popular Specialty Supplements

Name Common Uses
Amino acids Build protein, muscle strength, and endurance
Carnitine Enhance energy and sports performance, heart health,
memory, immune function, and male fertility
Coenzyme Q10 Treat heart disease, as an antioxidant
Dehydroepiandrosterone (DHEA) Boost immune functions and memory
Fish oil Reduce blood cholesterol, enhance brain function, increase
visual acuity (due to presence of omega-3 fatty acids)
Glucosamine and chondroitin Treat arthritis and other joint problems
Lactobacillus acidophilus Maintain intestinal health
Melatonin Restore normal sleep patterns
Methyl sulfonyl methane (MSM) Reduce allergic reactions to pollen and foods, relieve pain
and inflammation of arthritis and similar conditions
Selenium Reduce the risk of certain types of cancer
Vitamin C Prevent colds
Figure 6.3
L-carnitine is a popular
dietary supplement.
Notice the marketing
targeted to improve (a)
athletic performance
and (b) weight loss,
neither of which have
been supported by the
scientific literature.
L-Carnitine
100% Natural
(a) (b)
is assumed that the effectiveness of these drugs has been tested, and that they truly provide the therapeutic
benefits claimed by the manufacturer. Indeed, most people would be outraged if they found out that the
drug they purchased for pain relief or to cure an infectious disease was totally ineffective. Unfortunately,
herbal products and specialty supplements are regulated by a far less restrictive law, the Dietary Supple-
ment Health and Education Act (DSHEA) of 1994, than are drugs.
The DSHEA exempts dietary supplements from the Food, Drug, and Cosmetic Act, the legislation that
regulates prescription drugs. Dietary supplements are defined as products intended to enhance or supple-
ment the diet. They are not approved as drugs by the Food and Drug Administration (FDA). The DSHEA
requires these products to be clearly labeled as dietary supplements. Figure 6.1 shows the label for ginkgo
biloba clearly stating that the supplement is not approved by the FDA to treat any medical condition.
One strength of the legislation is that it gives the FDA the power to remove from the market any
product that poses a “significant or unreasonable” risk to the public. The FDA used this legislative author-
ity when the dietary supplement ephedra was removed from the market because of reported serious side
effects in some patients. However, it took seven years from the time the FDA first warned consumers of the
dangers of ephedra until it was removed from the market.
Unfortunately, the DSHEA has significant weaknesses that allow a lack of standardization in the
dietary supplement industry and less protection of the consumer. These flaws include:
■ Dietary supplements do not have to be tested by the manufacturer prior to marketing.
■ The effectiveness of a dietary supplement does not have to be demonstrated by the
manufacturer.
■ The manufacturer does not have to prove the safety of the dietary supplement. It is the govern-
ment’s job to prove that the dietary supplement is unsafe and to take the necessary steps to
remove it from the market.
■ The label of a dietary supplement must clearly state that the product is not intended to diagnose,
treat, cure, or prevent any disease. However, claims about a product’s effect on body structure
and function are allowed, including the following:
■ Helps promote healthy immune systems
■ Reduces anxiety and stress
■ Helps to maintain cardiovascular function
■ May reduce pain and inflammation
■ The DSHEA does not regulate the accuracy of the label; the product may or may not contain the
product listed in the amounts claimed.
Chapter Review 67
Several steps have been taken to address the lack of purity and mislabeling of herbal and di-
etary supplements. In an attempt to protect consumers, Congress passed the Dietary Supplement and
Nonprescription Drug Consumer Protection Act, which took effect in 2007. Companies marketing
herbal and dietary supplements are now required to include contact information (address and phone
number) on the product labels for consumers to use in reporting adverse events. Companies must notify
the FDA of a “serious adverse event,” which is defined as any adverse reaction resulting in death, a
life-threatening experience, inpatient hospitalization, a persistent or significant disability, or a birth
defect. Companies must notify the FDA of any serious adverse event reports within 15 days of receiv-
ing such reports.
Also in 2007, the FDA announced a final rule that requires the manufacturers of dietary supplements
to evaluate the identity, purity, potency, and composition of their products. The labels must accurately re-
flect what is in the product, which must be free of contaminants such as pesticides, toxins, glass, or heavy
metals.
Concept Review 6.3

■ How does the federal regulation of an herb by the DSHEA differ from the federal regula-
tion of a prescription drug?
Chapter Review
6.1 Complementary and alternative therapies are used 6.4 Herbs can have significant pharmacologic actions
by a large number of people to prevent and treat and can interact with conventional drugs.
disease. Just because a substance comes from a natural prod-
Complementary and alternative medicine (CAM) is uct does not make it safe or effective. Although herbal
a set of therapies and healing systems used by many supplements may have therapeutic applications, they
patients for disease prevention and self-healing. may not be the best product for treating the disease
Complementary therapies offer nonpharmacologic and may interact with prescription medicines.
alternatives to promote health and healing. They fo-
cus on the holistic treatment of each patient, integrate 6.5 Specialty supplements are nonherbal products
mind and body, and are often used in conjunction that are widely used to promote wellness.
with conventional medical therapies.
Specialty supplements include nonherbal therapies
6.2 Natural products from plants have been used as that are used to enhance a specific aspect of well-
medicines for thousands of years. ness. These products usually have a rational basis for
therapy, although their benefits have not been conclu-
Thousands of herbal therapies are recorded in Eastern
sively proven.
and Western history. The popularity of alternative
herbal remedies has steadily increased in recent
years. 6.6 Herbal products and specialty supplements are
not regulated in the same manner as prescription
6.3 Herbal products are standardized with respect to a medications.
specific active ingredient. The DSHEA loosely regulates herbal and dietary sup-
Herbal products are marketed in a number of differ- plements. Dietary supplements and herbal products
ent formulations, some consisting of standardized ex- can be marketed without any proof that they are safe
tracts of specific chemicals, others containing whole or effective. The Dietary Supplement and Nonpre-
herbs. Unlike drugs, herbs contain a large number of scription Drug Consumer Protection Act of 2007 re-
chemicals that may act in a coordinated manner to quired manufacturers to evaluate the purity, potency,
produce a therapeutic effect. The active ingredients and composition of their products. Labels must accu-
may be in the flowers, leaves, stems, or roots of an rately reflect what is in the product, which must be
herb. free of contaminants.
Review Questions
The following questions are written in 3. CAM therapies could interact with prescription and OTC
NCLEX-PN ® style. Answer these ques- medications.
tions to assess your knowledge of the 4. Most CAM therapies are totally ineffective.
chapter material, and go back and re-
view any material that is not clear 6. The nurse understands that specialty supplements are
to you. used:
1. For a diverse range of disease conditions
1. The patient is to be started on warfarin (Coumadin) ther- 2. For treatment of a targeted condition
apy. It is important for the nurse to check for the use of which 3. When prescriptive medications are no longer effective
herbs? (Select all that apply.) 4. When the body no longer makes sufficient quantities of the
1. Ginseng substance
2. Ginger
3. St. John’s wort 7. The Dietary Supplement Health and Education Act
4. Valerian (DHSEA) is responsible for:
1. Strict herbal product testing
2. Patients often use herbal therapies for which of the fol- 2. Ensuring that herbal products are labeled as “dietary
lowing reasons? supplements”
1. To prevent overuse of prescription medications 3. Sending the herbal product to the FDA for evaluation
2. To increase feelings of wellness and promote holistic 4. Ensuring safety of the product
treatment
3. Because herbal therapies are much more regulated than 8. The patient is admitted with digoxin (Lanoxin) toxicity.
prescription drugs The nurse checks for the use of which of the following herbal
4. Because herbal therapies are so much safer than man-made products?
drugs 1. St. John’s wort
2. Valerian
3. It is important that nurses ensure that their patients re- 3. Fish oil
ceive education regarding herbal products because: 4. Ginseng
1. Herbal products are approved under strict FDA regulations.
2. Labeling is not always reliable and herbal products should 9. The patient requests information on alternative treatments
be used with caution. for her arthritis. The nurse provides the patient information on
3. There are so few side effects, and they can be purchased which of the following supplements?
without a prescription. 1. Garlic and soy
4. The manufacturer has repeatedly demonstrated effectiveness. 2. Fish oil
3. Chondroitin and glucosamine
4. An example of a specialty supplement is: 4. DHEA
1. Lactobacillus acidophilus
2. Ginseng 10. Which of the following herbal products is commonly
3. Garlic used to enhance the immune system?
4. Ginkgo biloba 1. Soy
2. Saw palmetto
5. It is important for the nurse to collect information from 3. Cranberry
the patient about the use of complementary and alternative 4. Echinacea
medicine (CAM) because:
1. Patients must be warned that most CAM therapies are
dangerous.
2. Additional treatment may not be needed.
website.

C
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T
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Substance Abuse
7
Core Concepts
7.1
Abused substances belong to many different 7.6
Central nervous system (CNS) depressants decrease
chemical classes. the activity of the central nervous system.
7.2
Addiction depends on multiple, complex, and 7.7
Marijuana produces little physical dependence or
interacting variables. tolerance.
7.3
Substance dependence is classified as physical 7.8
Hallucinogens cause an altered state of thought and
dependence or psychological dependence. perception similar to that found in dreams.
7.4
Withdrawal results when an abused substance is no 7.9
CNS stimulants increase the activity of the central
longer available. nervous system.
7.5 Tolerance occurs when higher and higher doses 7.10 Nicotine is powerful and highly addictive.
of a drug are needed to achieve the initial 7.11 Healthcare providers strive to remain free from
response. impairment due to alcohol and drug addiction.
Learning Outcomes
1. Discuss the underlying causes of 4. Explain the significance of drug 6. List the reasons why healthcare
addiction. tolerance to pharmacotherapy. providers may have problems with
2. Compare and contrast psychological 5. Explain the major characteristics of alcohol or substance abuse.
and physical dependence. abuse, dependence, and tolerance 7. Identify the signs of substance
3. Compare and contrast classic and resulting from alcohol, nicotine, abuse exhibited by the healthcare
conditioned withdrawal. marijuana, hallucinogens, CNS provider.
stimulants, sedatives, and opioids.
Key Terms
addiction (ah-DIK-shun) 71 designer drugs substance abuse 70
alcohol intoxication (AL-ku-hol in-tak-su- (de-ZEYE-ner drugs) 70 substance dependence 72
KA-shun) 75 narcolepsy (NAR-koh-lep-see) 78 tetrahydrocannabinol (THC) (TEH-trah-
analgesics (AN-ahl-GEE-siks) 70 opioids (OH-pee-oyds) 72 HEYE-droh-cah-NAB-in-ol) 76
attention deficit disorder (ADD) 78 physical dependence tolerance (TOL-er-ans) 73
attention deficit-hyperactivity disorder (FI-zi-kul dee-PEN-dens) 72 withdrawal syndrome (with-DRAW-ul
(ADHD) 78 psychedelics (seye-keh-DEL-iks) 76 SIN-drom) 72
club drugs 70 psychological dependence
cross-tolerance (krause TOL-er-ans) 73 (seye-koh-LOJ-i-kul dee-PEN-dens) 72
70 Chapter 7 Substance Abuse
S
ubstance abuse is the self-administration of a drug in a way that one’s culture or society views
as abnormal and not acceptable. Throughout history, individuals have consumed both natural and
prescription drugs to increase physical or mental performance, cause a relaxed feeling, change a
psychological state, or simply fit in with the crowd. Substance abuse has a tremendous economic, social,
and public health impact on society.
Core Concept 7.1 Abused substances belong to many different chemical classes.
Substances from a wide variety of chemical classes are abused and can be taken by many different routes.
Abused substances have in common an ability to affect the nervous system, particularly the brain. Some
agents, such as opium, marijuana, cocaine, nicotine, caffeine, and alcohol, are obtained from natural
sources. Others agents are synthetic or designer drugs that are created in illegal laboratories solely for
making money in illegal drug trafficking. Club drugs are substances taken at dance clubs, all-night parties,
and raves.
Although the public often connects substance abuse with illegal drugs, this is not necessarily the
case: Alcohol and nicotine are the two most commonly abused drugs. Legal prescription medications such
as oxycodone (OxyContin), methamphetamine, and alprazolam (Xanax) have become frequent drugs of
abuse. Volatile inhalants, found in common household products such as aerosols and paint thinners, are
often abused. Aerosols will make a user high with the practice of “huffing.” Marijuana is the most frequently
an 5 without abused illegal drug nationwide. Other frequently abused substances include analgesics or pain-reducing
algesics 5 causing pain drugs, sedatives, hallucinogens like lysergic acid diethylamide (LSD), and club drugs such as Ecstasy and
flunitrazepam (Rohypnol), a powerful benzodiazepine depressant.
sedatives 5 causing sedation Several drugs once used therapeutically are now illegal because of their high potential for abuse.
hallucinogens 5 causing Cocaine was once widely used as a local anesthetic, but today all cocaine purchased and used in the pri-
hallucinations vate sector is illegal. LSD is now illegal, although in the 1940s and 1950s it was used in psychotherapy.
Phencyclidine (PCP) was popular in the early 1960s as an anesthetic but was taken off the market in 1965
because patients reported hallucinations, delusions, and anxiety after recovering from anesthesia. Many of
the amphetamines, once prescribed for bronchodilation, were stopped in the 1980s after psychotic episodes
were reported. Some commonly abused substances are summarized in Table 7.1 ◆.
Fast Facts Substance Abuse in the United States

■ Over 28 million Americans have used illicit drugs at least once.
■ Over 25% of high school students use an illegal drug monthly.
■ An estimated 2.4 million Americans have used heroin during their lives.
■ About one in five Americans has lived with an alcoholic while growing up. Children of alcoholic
parents are four times more likely to become alcoholics than children of nonalcoholic parents.
■ Alcohol is an important factor in 68% of manslaughters, 54% of murders, 48% of robberies, and
44% of burglaries.
■ Among youth between the ages of 12 and 17, approximately 7.2 million have drunken alcohol at
least once. Girls are as likely as boys to drink alcohol.
■ Barbiturate overdose is a factor in almost one-third of all drug-related deaths.
■ Thirty-six percent of 10th graders and 46% of 12th graders have reported using marijuana and
hashish.
■ Almost 8% of high school seniors have reported using cocaine.
■ Two million Americans have used cocaine on a monthly basis; about 567,000 have used crack
cocaine.
■ Approximately 70% of the cocaine entering the United States comes from Colombia and passes
through south Florida.
■ Sixteen percent of 8th graders and 11% of 12th graders have reported using volatile inhalants.
■ Thirty percent of all Americans are cigarette smokers, including 25% who are between the ages of
12 and 25.
■ Forty-three percent of 10th graders and 54% of 12th graders have reported smoking cigarettes.
Eight percent of 12th graders consume half a pack or more each day.
■ Eight percent of 12th graders have reported using Ecstasy (MDMA).
■ LSD is one of the most potent drugs known, with only 25–150 mcg constituting a dose. Almost 9%
of 12th graders have reported using LSD.
Core Concept 7.2 71
Table 7.1 Commonly Abused Substances

Natural Substances Medications
Legal Substances Without Prescription
Ethyl alcohol Drinking alcohol OTC drugs
Aerosol inhalants Solvents, varnishes
Caffeine Coffee OTC drugs
Nicotine Tobacco Smoking cessation drugs
Legal Substances with Prescription
Barbiturates Sedatives; CNS depressants
Benzodiazepines Sedatives; CNS depressants
Dextromethorphan (DMX) OTC cough suppressants
Opioid Analgesics Pain therapy
Ketamine Anesthetic
Gamma hydroxybutyrate (GHB) Anesthetic
Amphetamines, methamphetamines, and methylphenidate (Ritalin) CNS stimulants
Anabolic steroids Weight or muscle gain products
Illegal Substances or Discontinued in Traditional Therapies
Opioids Opium Heroin
Cannabinoids (THC)* Marijuana Glaucoma therapy
LSD Rye/grain fungus Psychiatric therapy
Psilocybin Mushrooms
Mescaline Peyote
Phencyclidine (PCP)* Anesthetic
Cocaine Coca plant Local anesthetic
Club Drugs with No Medicinal Use—Designer Drugs
MDA*
MMDA* (Ecstasy)
DOM* (STP)
*Chemical names are complicated and extensive; see Core Concepts 7.7 and 7.8 for more information.
Addiction depends on multiple, complex, and interacting variables. Core Concept 7.2
Addiction, the progressive and chronic abuse of a substance, is an overwhelming feeling that drives some- addict 5 given over
one to use a drug repeatedly despite serious health and social consequences. It is impossible to predict
accurately whether a person will become an addict. Scientists have used psychological profiles and inves-
tigated genetic links in an attempt to predict a person’s addictive tendency, but no firm connections have
been found. Addiction depends on multiple, complex, and interacting variables. These variables fall into
the following categories:
■ Agent or drug factors Cost, availability, dose, method of administration (e.g., oral, IV, inhala-
tion), speed of onset/duration of effect, and length of drug use
■ User factors Genetic factors (e.g., metabolic enzymes, natural tolerance), tendency toward
risk-taking behavior, prior experiences with drugs, disease that may require a scheduled drug
■ Environmental factors Social/community norms (behavior accepted within a community), role
models, peer influences, educational opportunities
Addiction may begin with a real need for pharmacotherapy. For example, narcotic analgesics may be
prescribed for pain, or sedatives for a sleep disorder. A favorable experience of pain relief or being able to
fall asleep may cause a patient to want to repeat these positive experiences.
It is a common misunderstanding, even among some health professionals, that the therapeutic
use of scheduled drugs creates large numbers of patients with addiction. In fact, prescription drugs
rarely cause addiction when used as prescribed. The risk of addiction for prescription medications
is mostly a function of the dose and the length of therapy. For this reason, medications having a
potential for abuse are usually prescribed at the lowest effective dose for the shortest time necessary
to treat the medical problems (see Chapter 14 for more information on pain management). As men-
tioned in Chapters 1 and 2, numerous laws have been passed in an attempt to limit drug abuse and
addiction.
Substance dependence is classified as physical dependence

Core Concept 7.3 or psychological dependence.
Whether a substance is addictive relates to how easily an individual can stop taking it repeatedly. When a
person has an overwhelming desire to take a drug and cannot stop, it is referred to as substance dependence.
Substance dependence is classified into two categories: physical dependence and psychological
dependence.
Physical dependence is an altered physical condition caused by the nervous system adapting to re-
peated substance use. Over time, the body’s cells are tricked into believing that it is normal for the substance
to continually be present. With physical dependence, uncomfortable symptoms, known as withdrawal
syndrome, occur when the agent is stopped. Opioids, such as morphine and heroin, may produce physical
dependence rather quickly with repeated doses, particularly when taken intravenously. Alcohol, sedatives,
some stimulants, and nicotine are other examples of substances that may easily produce physical depen-
dence with repeated use.
In contrast to physical dependence, psychological dependence causes no apparent signs of physical
discomfort after the agent is stopped. The person, however, will have an intense craving and will display an
overwhelming desire to continue using the substance even if there are obvious negative economic, physi-
cal, or social consequences. The intense craving may be associated with the individual’s home environ-
ment or social contacts. Strong psychological cravings for a substance may continue for months or even
re 5 again years and is often responsible for relapse (return to the original drug-seeking behavior) during substance
lapse 5 fall back abuse therapy. Psychological dependence usually occurs only after relatively high doses of the substance
have been used for a long time, such as with marijuana and antianxiety drugs. However, psychological
dependence may develop quickly, perhaps after only one use, as with crack cocaine—a potent, inexpensive
form of the drug.
Withdrawal results when an abused substance

Core Concept 7.4 is no longer available.
Once an individual becomes physically dependent and the substance is stopped, withdrawal syndrome
will occur. Symptoms of withdrawal syndrome may be severe for patients who are physically dependent
on alcohol and sedatives. Helping a patient withdraw from these agents is best done in a substance abuse
treatment facility. Examples of withdrawal syndromes related to different abused substances are listed in
Table 7.2 ◆.
Prescription drugs may be used to reduce the severity of withdrawal symptoms. For example, alcohol
withdrawal can be treated with a benzodiazepine such as diazepam (Valium), and opioid withdrawal might
be treated with methadone. Other drugs used in the treatment of opioid dependence include buprenorphine
(Subutex) and naloxone. These are discussed in Chapter 14. Symptoms of nicotine withdrawal may be
relieved by nicotine replacement therapy (NRT) in the form of patches or chewing gum and the use of bu-
propion (Wellbutrin). No specific pharmacologic treatments are indicated for withdrawal from CNS stimu-
lants, hallucinogens, marijuana, or inhalants.
With chronic substance abuse, patients will often associate their conditions and surroundings—
including social contacts with other users—with use of the drug. Users tend to return to drug-seeking
behavior when they interact with other substance abusers. Counselors often encourage patients to stop
associating with past social contacts or having relationships with other substance abusers to lessen the
possibility of relapse. With the assistance of self-help groups such as Alcoholics Anonymous, some pa-
tients are able to move to a drug-free lifestyle by making friends with new people who are drug free and
alcohol free.
Core Concept 7.5 73
Table 7.2 Selected Drugs of Abuse, Withdrawal Symptoms, and Characteristics

Drug Physiological and Psychological Effects Signs of Toxicity
Alcohol Tremors, fatigue, anxiety, abdominal cramping, halluci- Extreme somnolence, severe CNS depression, dimin-
nations, confusion, seizures, delirium ished reflexes, respiratory depression
Barbiturates Insomnia, anxiety, weakness, abdominal cremps, tremor, Severe CNS depression, tremor, diaphoresis,
anorexia, seizures, skin hypersensitivity reactions, hal- vomiting, cyanosis, tachycardia, Cheyne–Stokes
lucinations, delirium respirations
Benzodiazepines Insomnia, restlessness, abdominal pain, nausea, sen- Somnolence, confusion, diminished reflexes,
sitivity to light and sound, headache, fatigue, muscle coma
twitches
Cocaine and amphetamines Mental depression, anxiety, extreme fatigue, hunger Dysrhythmias, lethargy, skin pallor, psychosis
Hallucinogens Rarely observed; dependent on specific drug Panic reactions, confusion, blurred vision, increase
in blood pressure, psychotic-like state
Marijuana Irritability, restlessness, insomnia, tremor, chills, weight Euphoria, paranoia, panic reactions, hallucinations,
loss psychotic-like state
Nicotine Irritability, anxiety, restlessness, headaches, increased Heart palpitations, tachyarrhythmias, confusion,
appetite, insomnia, inability to concentrate, decrease in depression, seizures
heart rate and blood pressure
Opioids Excessive sweating, restlessness, dilated pupils, agita- Respiratory depression, cyanosis, extreme somno-
tion, goose bumps, tremor, violent yawning, increased lence, coma
heart rate and blood pressure, nausea/vomiting,
abdominal cramps and pain, muscle spasms with kicking
movements, weight loss
Tolerance occurs when higher and higher doses of a drug are needed
to achieve the initial response. Core Concept 7.5
Tolerance is a biological condition that occurs when the body adapts to a substance after it is repeatedly
administered. Over time, higher doses of the agent are needed to produce the initial effect. For example,
at the start of pharmacotherapy, a patient may find that 2 mg of a sedative is effective for causing sleep.
After taking the medication for several months, the patient notices that it takes 4 mg or perhaps 6 mg to fall
asleep. Development of drug tolerance is common for substances that affect the nervous system. Tolerance
should be thought of as a natural consequence of continued drug use and not be considered evidence of ad-
diction or substance abuse.
Tolerance does not develop at the same rate for all actions of a drug. For example, patients
usually develop tolerance to the nausea and vomiting produced by narcotic analgesics after only a
few doses. Tolerance to the mood-altering effects of these drugs and to their ability to reduce pain
develops more slowly but eventually may be complete. Tolerance never develops to these drugs’
ability to constrict the pupils. Patients will often put up with annoying side effects of drugs, such
as the sleepiness caused by antihistamines, if they know that tolerance to these effects will develop
quickly.
Once tolerance develops to one substance, it often also occurs with use of closely related drugs. This
reaction is known as cross-tolerance. For example, a heroin addict will be tolerant to the analgesic effects
of other opioids such as morphine or meperidine. Patients who have developed tolerance to alcohol will
show tolerance to other CNS depressants such as barbiturates, benzodiazepines, and some general anes-
thetics. This is important to know because doses of related medications may need to be adjusted so that the
patient receives maximum therapeutic benefit.
The terms immunity and resistance are often confused with tolerance. These terms more correctly
refer to the immune system and infections, and they should not be used to mean tolerance. For example,
microorganisms become resistant to the effects of an antibiotic; they do not become tolerant. Patients be-
come tolerant to the effects of pain relievers; they do not become resistant. Therefore, it is incorrect to say
that patients are immune to drug therapy.
cam TherapY
Milk Thistle for Liver Damage
Milk thistle is a plant found growing in the Mediterranean region that has been used as an
herbal medicine for centuries. The active ingredient in the milk thistle plant (Silybum mari-
anum), silymarin, has been thought to protect the liver against injury. Some studies have
indeed shown that silymarin is able to neutralize the effects of alcohol and actually stimulate
liver regrowth. It acts as an antioxidant and free-radical scavenger. It is typically taken for
liver cirrhosis, chronic hepatitis, and gallbladder disorders. The herb has few side effects other
than mild diarrhea, bloating, and upset stomach.
Anti-inflammatory and anticarcinogenic properties of milk thistle have also been docu-
mented. Milk thistle has been claimed to reduce the growth of cancer cells, but this has not
been confirmed by controlled research studies. The nurse should urge patients to report the
use of this herb to their healthcare provider.
Concept Review 7.1

■ What is the difference between physical dependence and psychological dependence?
How do patients know when they are physically dependent on a substance?
Central nervous system (CNS) depressants decrease the activity

Core Concept 7.6 of the central nervous system.
depressant 5 dispirited CNS depressants form a group of drugs that cause patients to feel sedated or relaxed. Drugs in this group
or lowered feeling include barbiturates, nonbarbiturate sedative-hypnotics, benzodiazepines, alcohol, and opioids. Although
the majority of these substances are legal, they are controlled because of their abuse potential.
Sedatives and Sedative-Hypnotics

tranquilizer 5 causing Sedatives, sometimes referred to as tranquilizers, are prescribed mostly for sleep disorders and some forms
a tranquil state of epilepsy. The two primary classes of sedatives are the barbiturates and the nonbarbiturate sedative-
hypnotics. See Chapter 9 for discussion of their historic use in treating sleep disorders and Chapter 13 for
their use in treating epilepsy. Their actions, indications, safety profiles, and addictive potential are gener-
ally the same. Physical dependence, psychological dependence, and tolerance develop when these agents
are taken for long periods at high doses. Patients sometimes abuse these drugs by taking more doses than
prescribed, sharing their medication with friends, or selling their medication. These drugs are frequently
combined with other drugs of abuse such as CNS stimulants or alcohol. People with addiction often alter-
nate between amphetamines, which keep them awake for several days, and barbiturates, which help them to
relax and fall asleep. Methamphetamine, for example, is an amphetamine-like stimulant drug (Core Concept
7.9). It has the ability to keep someone awake and produce many of the signs that counter sleep such as an
elevated breathing rate and heart rate, and increased blood pressure.
Many sedatives have a long duration of action. Effects may last an entire day, depending on the specific
drug. Patients may appear dull or apathetic, with slurred speech and lack of motor coordination. High doses
of these drugs suppress the respiratory centers in the brain, and the user may stop breathing or enter a coma.
Death may result from overdose. Withdrawal symptoms from these drugs may also be life threatening.
One drug of interest is gamma hydroxybutyric acid (GHB). GHB is approved by the Food and Drug
Administration (FDA) as sodium oxybate (Xyrem) to treat patients with narcolepsy. Recreational users
eu 5 healthy or well often abuse GHB by consuming this drug in high doses. Although used to produce a euphoric (pleasure)
phoric 5 bearing state, overdose of this drug can cause severe respiratory depression, seizures, and coma. Thus, its depres-
sant effects warrant close attention in the nonbarbiturate sedative-hypnotic category.
Benzodiazepines
Benzodiazepines are another group of CNS depressants that have a potential for abuse. They are one of the
most widely prescribed classes of drugs and have largely replaced the barbiturates for certain disorders.
anxio 5 anxiety/restlessness Their primary indication is anxiety; thus, they are called anxiolytic drugs (see Chapter 9). They are also
lytic 5 destruction used for short-term treatment of seizures (see Chapter 13) and as muscle relaxants (see Chapter 12). Com-
mon benzodiazepines include alprazolam (Xanax), clonazepam (Klonopin), diazepam (Valium), temaze-
pam (Restoril), triazolam (Halcion), and midazolam (Versed). Flunitrazepam (Rohypnol) is not approved
amnestic 5 loss of memory by the FDA for any medical condition, but it is a club drug noted for its amnestic properties. Users will
often feel carefree, without worry, and can even be subject to assault.
Core Concept 7.6 75
Although benzodiazepines are one of the most frequently prescribed drug classes, benzodiazepine abuse
has various presentations. Those individuals who do abuse benzodiazepines may appear detached, sleepy, or
disoriented. Death due to overdose is rare, even with high doses, unless benzodiazepines are used in combi-
nation with other CNS depressants. Abusers may combine these agents with alcohol, cocaine, or heroin to
increase their drug experience. If combined with other agents, death due to overdose is very likely. Benzodi-
azepine withdrawal syndrome by itself is less severe than barbiturate withdrawal or alcohol withdrawal.
Opioids
Opioids are prescribed for severe pain, persistent cough, and diarrhea. The opioid class includes opium,
morphine, and codeine, which are processed from natural substances found in the unripe seeds of the
poppy plant, and synthetic drugs, such as hydromorphone (Dilaudid), oxycodone (OxyContin), fentanyl
(Duragesic, Sublimaze), methadone (Dolophine), and heroin. The therapeutic effects of the opioids are
discussed in detail in Chapter 14.
The effects of oral opioids begin within 30 minutes and may last over a day. Parenteral forms pro-
duce immediate effects, including the brief, intense rush of euphoria sought by heroin addicts. Individuals
experience a range of CNS effects, from extreme pleasure to slowed body activities and extreme sedation.
Signs include constricted pupils, an increase in the ability to withstand pain, and respiratory depression.
Addiction to opioids can occur rapidly, and withdrawal can produce intense symptoms. Although
extremely unpleasant, withdrawal from opioids is not necessarily life threatening. Methadone is a narcotic
sometimes used to treat opioid addiction. Although methadone has addictive properties of its own, it does
not produce the same degree of euphoria as other opioids, and its effects are longer lasting. Heroin addicts
may be switched to methadone to prevent unpleasant withdrawal symptoms. Because methadone is taken
orally, the serious risks associated with intravenous drug use, such as hepatitis and AIDS, are eliminated.
Patients sometimes remain on methadone maintenance for their lifetimes. Withdrawal from methadone is
more prolonged than from heroin or morphine, but the symptoms are less intense.
Ethyl Alcohol
Ethyl alcohol, commonly known as alcohol, is one of the most widely abused drugs. Alcohol is a legal sub-
stance for adults and is available as beer, wine, and liquor. The economic, social, and health consequences
of alcohol abuse are staggering. In contrast to the many negative consequences associated with long-term
abuse of alcohol, drinking small quantities of alcohol on a daily basis has been found to reduce the risk of
stroke and heart attack.
Alcohol is classified as a CNS depressant, because it slows the actions of the region of the brain re-
sponsible for alertness and wakefulness. Alcohol easily crosses the blood–brain barrier, and its effects can
be noticed within 5 to 30 minutes. Effects of alcohol are directly related to the amount consumed within
a certain time frame and include relaxation, sedation, memory impairment, loss of motor coordination,
reduced judgment, and decreased inhibition. Alcohol intoxication occurs when muscle coordination is lost
and mental function is affected. It results in a characteristic odor to the breath and increased blood flow in
certain areas of the skin, causing a flushed face, pink cheeks, or red nose. Although these symptoms are
easily recognized, the nurse must be aware that other substances and disorders may cause similar effects.
For example, many antianxiety agents, sedatives, and antidepressants can cause drowsiness, memory dif-
ficulties, and loss of motor coordination. Certain mouthwashes, medicines, and other substances containing
alcohol can give the breath an “alcoholic” smell.
The presence of food in the stomach will slow the absorption of alcohol, thus delaying the onset of
drug action. Metabolism, or detoxification of alcohol by the liver, occurs at a slow, constant rate, which
is not affected by the presence of food. The average rate is about 15 mL per hour—equal to one alcoholic
beverage per hour. If consumed at a higher rate, alcohol will accumulate in the blood and produce greater
effects on the brain. An overdose of alcohol produces vomiting, severe hypotension, respiratory failure,
and coma. Death due to alcohol poisoning is common.
Chronic alcohol consumption produces both psychological and physiological dependence and results
in a large number of adverse health effects. The organ most affected by chronic alcohol abuse is the liver.
Alcoholism is a common cause of cirrhosis, a harmful and often fatal failure of the liver to perform its vital cirrh 5 orange/yellow
functions. Liver failure causes abnormalities in blood clotting and nutritional deficiencies and sensitizes osis 5 condition
the patient to the effects of all medications metabolized by the liver.
Alcohol withdrawal syndrome is severe and may be life threatening. The use of antiseizure medica-
tions for treating severe alcohol withdrawal symptoms is discussed in Chapter 13. Long-term treatment
for alcohol abuse includes behavioral counseling and participation in self-help groups such as Alcohol-
ics Anonymous. Disulfiram (Antabuse) may be given to discourage relapses. Disulfiram inhibits ac-
etaldehyde dehydrogenase, the enzyme that metabolizes alcohol. If alcohol is consumed while taking
disulfiram, the patient becomes violently ill within 5 to 10 minutes, with headache, shortness of breath,
nausea/vomiting, and other unpleasant symptoms. Disulfiram is only effective in highly motivated pa-
tients, because the success of pharmacotherapy is entirely dependent on patient compliance. Alcohol sensi-
tivity can continue for up to two weeks after disulfiram has been discontinued. As a pregnancy category X
drug, disulfiram should never be taken during pregnancy.
In addition to disulfiram, acamprosate calcium (Campral, Forest) is an FDA-approved drug for main-
taining alcohol abstinence in patients with alcohol dependence. Additional studies comparing the therapeu-
tic benefit of disulfiram with acamprosate are needed. Adverse reactions to acamprosate include diarrhea,
flatulence, and nausea. The drug is not recommended for patients who have impaired kidney functioning.
Concept Review 7.2

■ Compare the potential to cause coma or death of barbiturates and benzodiazepines.
Core Concept 7.7 Marijuana produces little physical dependence or tolerance.
Cannabinoids are substances obtained from the hemp plant Cannabis sativa, which grows in tropical cli-
mates. Cannabinoid agents are usually smoked and include marijuana, hashish, and hash oil. Although
more than 61 cannabinoid chemicals have been identified, the ingredient responsible for most of the psy-
choactive properties is delta-9-tetrahydrocannabinol (THC).
Marijuana (street names “grass,” “pot,” “weed,” “reefer,” or “dope”) is a natural product obtained
from C. sativa. It is the most commonly used illegal drug in the United States even though it has been
legalized on a limited basis in some states. Use of marijuana slows motor activity, decreases coordination,
para 5 beside and causes disconnected thoughts, paranoia, and euphoria. It increases thirst and craving for food, particu-
noia 5 mind larly chocolate and other candies. One hallmark symptom of marijuana use is red or bloodshot eyes, caused
by dilation of blood vessels. THC also accumulates in the gonads.
When inhaled, marijuana produces effects that occur within minutes and last up to 24 hours. Because
marijuana smoke is inhaled more deeply and held within the lungs for a longer time than cigarette smoke,
marijuana smoke introduces four times more tar into the lungs than tobacco smoke. Smoking marijuana on
a daily basis may increase the risk of lung cancer and other respiratory disorders. Chronic use is associated
with lack of motivation and loss of productivity.
Unlike many abused substances, marijuana produces little physical dependence or tolerance. With-
drawal symptoms are mild, if they are experienced at all. Metabolites of THC, however, remain in the
body for months to years, allowing laboratory specialists to determine easily whether someone has used
marijuana. For several days after use, THC can also be detected in the urine. Despite numerous attempts by
scientists and clinicians to demonstrate therapeutic applications for marijuana, results have been controver-
sial and the medical value of the drug remains to be proven.
Concept Review 7.3

■ Name three legal substances that are both used in traditional therapies and frequently
abused. Are these substances natural or synthetic? Compare ethyl alcohol and marijuana
in terms of common use.
Hallucinogens cause an altered state of thought and perception

Core Concept 7.8 similar to that found in dreams.
Hallucinogens consist of an assorted class of chemicals that have in common the ability to produce an
altered, dreamlike state of consciousness. Sometimes called psychedelics, the prototype substance for this
class is LSD. All hallucinogens are Schedule I drugs and have no medical use.
For nearly all drugs of abuse, predictable symptoms occur in every user. Effects from hallucinogens,
however, are highly variable and depend on the mood and expectations of the user and the surrounding en-
vironment in which the substance is used. Two patients taking the same agent will report completely differ-
ent symptoms, and the same patient may report different symptoms with each use. Users who take LSD or
psilocybin (Figure 7.1 ■) may experience symptoms such as laughter, visions, religious revelations, or deep
personal insights. Common occurrences are hallucinations and afterimages (images that are projected onto
people as they move). Users also report unusually bright lights and vivid colors. Some users hear voices;
others report smells. Many experience a profound sense of truth and deep thoughts. Unpleasant experiences
can be terrifying and may include anxiety, panic attacks, confusion, severe depression, or paranoia.
LSD (street names “acid,” “the beast,” “blotter acid,” “California sunshine”) is made from a fungus
that grows on rye and other grains. LSD is almost always used in an oral form. It can be manufactured in
capsules, tablets, or liquids. A common and inexpensive method for distributing LSD is to place drops of
the drug on small pieces of paper that often contain images of cartoon characters or graphics related to the
drug culture. After drying, the paper containing the LSD is swallowed to produce the drug’s effects.
Core Concept 7.8 77
Figure 7.1
Comparison of psilocybin and LSD. Psilocybin is derived from a mushroom, shown in (a); an LSD “blot” is shown in (b).
Source: (left) Janine Wiedel Photolibrary/Alamy, (right) Joe Bird/Alamy
LSD is distributed throughout the body immediately after use. Effects are experienced within an hour
and may last 6 to 12 hours. It affects the central and autonomic nervous systems, increasing blood pressure,
elevating body temperature, dilating pupils, and increasing heart rate. Repeated use may cause memory
loss and inability to reason. In extreme cases, patients may develop psychoses. One unusual adverse effect
is flashbacks, in which the user experiences the effects of the drug again—sometimes weeks, months, or
years after the drug was initially taken. Although users may experience tolerance, they have little or no
dependence with hallucinogens.
Other hallucinogenic drugs that are abused include the following:
■ Mescaline found in the peyote cactus of Mexico and Central America (Figure 7.2 ■)
■ MDMA (3,4-methylenedioxymethamphetamine, “XTC,” or “Ecstasy”) an amphetamine
originally created for research purposes but now extremely popular as a drug of abuse
■ DOM (2,5 dimethoxy-4-methylamphetamine, “STP”) a recreational drug often linked with
rave parties
■ MDA (3,4-methylenedioxyamphetamine) called the “love drug” because of a belief that it
enhances sexual desires
■ PCP (chemical name phenylcyclohexylpiperadine; also called phencyclidine; street name
“angel dust”) produces a trancelike state that may last for days and results in severe brain
damage; used as an animal tranquilizer
■ Ketamine (“date rape” drug or “special K”) produces unconsciousness and amnesia;
primary legal use is as an anesthetic
Figure 7.2
Mescaline is derived
from the peyote plant
(shown in photo).
Source: Konig/Jacana/Photo
Researchers, Inc.
Concept Review 7.4

■ In examining and interviewing a patient, how could you determine whether he or she is
under the influence of marijuana or hallucinogens?
Core Concept 7.9 CNS stimulants increase the activity of the central nervous system.
stimulant 5 arousing feelings Stimulants include a varied family of drugs with the ability to increase the activity of the CNS. Some are
available by prescription for use in the treatment of narcolepsy (a sleep disorder in which people fall asleep
narco 5 numbness or stupor unexpectedly), obesity, and attention deficit disorder (ADD) or attention deficit hyperactivity disorder
lepsy 5 seizure (ADHD). As drugs of abuse, CNS stimulants are taken to produce a sense of exhilaration, improve mental
and physical performance, reduce appetite, prolong wakefulness, or simply “get high.” Stimulants include
amphetamines, cocaine, methylphenidate, and caffeine.
CNS stimulants have effects similar to the neurotransmitter norepinephrine, which is discussed in
Chapter 8. Norepinephrine activates neurons in a part of the brain that affects awareness and wakefulness,
called the reticular formation (see Chapter 9 for an in-depth discussion). High doses of amphetamines give
the user a feeling of self-confidence, euphoria, alertness, and empowerment. Long-term use, however, of-
ten causes feelings of restlessness, anxiety, and fits of rage, especially when the user is coming down from
a drug high.
Most CNS stimulants affect cardiovascular and respiratory activities, raising blood pressure and in-
creasing respiration rate. Other symptoms include dilated pupils, sweating, and tremors. Overdoses of
some stimulants lead to seizures and cardiac arrest.
Amphetamines and dextroamphetamines were once widely prescribed for depression, obesity, drows-
iness, and congestion. In the 1960s, the healthcare profession realized that the risk for amphetamine depen-
dence outweighed the drug’s therapeutic usefulness. Because of the development of safer medications, the
current therapeutic uses of these drugs are extremely limited. Most substance abusers get these agents from
illegal laboratories, which can easily produce amphetamines and make tremendous profits.
Dextroamphetamine (Dexedrine) may be used to treat narcolepsy and for short-term weight loss when
all other attempts to lose weight have been exhausted. Adderall (formulation of dextroamphetamine and
amphetamine) is used to treat narcolepsy and ADHD.
Methamphetamine (street name “ice” or “crank”) is often used as a recreational drug for those who
like the “rush” that it provides. It is usually administered in powder or crystal form, but it also may be
smoked. Methamphetamine is a Schedule II drug marketed under the trade name Desoxyn, although most
abusers obtain it from illegal methamphetamine laboratories. A drug related to methamphetamine, called
methcathinone (street name “cat”), is made illegally and snorted, taken orally, or injected intravenously.
Methcathinone is a Schedule I agent.
Methylphenidate (Ritalin) is a CNS stimulant (Schedule II drug) that is widely prescribed for children
diagnosed with ADD/ADHD (see Chapter 10). Ritalin has a calming effect on children who are inatten-
tive or hyperactive. It stimulates the alertness center in the brain and allows the child to focus on tasks for
longer periods. Lisdexamfetamine (Vyvanse) is another amphetamine-like substance used to treat ADHD.
In adults and teens, Ritalin and Vyvanse usually produce the same effects as cocaine and amphetamines
and are sometimes abused by adolescents and adults seeking euphoria. The tablets are crushed and used
intranasally or dissolved in liquid and injected intravenously. Ritalin is also sometimes mixed with heroin
(street name “speedball”).
Cocaine is a natural substance obtained from the leaves of the coca plant, which grows in the Andes
Mountain region of South America. The plant has been used by Andean cultures since 2500 b.c. Natives of
this region chew the coca leaves or make teas of the dried leaves. Because it is taken orally, its absorption
is slow, and the leaves contain only 1% cocaine, so users do not have the ill effects caused by chemically
pure extracts from the plant. In the Andean culture, the use of coca leaves is not considered substance
abuse because it is part of that society’s culture.
Cocaine is a Schedule II drug that produces actions similar to those of the amphetamines,
although its effects are usually more rapid and intense. It is the second most commonly abused
illegal drug in the United States. Routes of administration include snorting, smoking, and injecting.
In smaller doses, cocaine produces feelings of intense euphoria, a decrease in hunger, analgesia, delu-
sions of physical strength, and increased sensory perception. Larger doses will magnify these effects
and also cause rapid heartbeat, sweating, dilation of the pupils, and elevated body temperature. After
euphoria diminishes, the user often feels irritable, depressed, and distrustful and usually has insom-
nia. Some users report the sensation that insects are crawling under their skin. Users who snort co-
caine develop a chronic runny nose, a crusty redness around the nostrils, and deterioration of the nasal
cartilage. Overdose can cause dysrhythmias, convulsions, stroke, or death due to respiratory arrest.
The withdrawal syndrome for amphetamines and cocaine is much less intense than that from alcohol
or barbiturates.
Table 7.3 Caffeine Content of Common Drugs, Foods, and Beverages

Serving Size Caffeine (mg)
OTC DRUGS
NoDoz, maximum strength; Vivarin 1 tablet 200
Excedrin 2 tablets 130
NoDoz, regular strength 1 tablet 100
Anacin (also available in caffeine-free formulation) 2 tablets 64
Coffees
Coffee, brewed and instant 8 ounces 95–135
Coffee, decaffeinated 8 ounces 5
Teas
Tea, leaf or bag 8 ounces 50
Tea, green 8 ounces 30
Tea, instant 8 ounces 15
Soft Drinks
Mountain Dew 12 ounces 55.5
Diet Coke 12 ounces 46.5
Coca-Cola Classic 12 ounces 34.5
Pepsi-Cola 12 ounces 37.5
Chocolates and Candies
Hershey’s Special Dark chocolate bar 1 bar (1.5 ounces) 31
Hershey Bar (milk chocolate) 1 bar (1.5 ounces) 10
Cocoa or hot chocolate 8 ounces 85
Caffeine is a natural substance found in the seeds, leaves, or fruits of more than 63 plant species
throughout the world. Significant amounts of caffeine are consumed in chocolate, coffee, tea, and soft
drinks (Table 7.3 ◆). Sometimes caffeine is added to over-the-counter (OTC) pain relievers to help re-
lieve migraines and other conditions. Caffeine travels to almost all parts of the body after ingestion, and
several hours are needed for the body to metabolize and eliminate the drug. Caffeine has a pronounced
diuretic effect.
Caffeine is considered a CNS stimulant because it produces increased mental alertness, restlessness,
nervousness, irritability, and insomnia. The physical effects of caffeine include bronchodilation, increased
blood pressure, increased production of stomach acid, and changes in blood glucose levels. Repeated use
of caffeine may result in physical dependence and tolerance.
Concept Review 7.5

■ Identify three groups of stimulants discussed in this section, and give examples for each
group. Identify the major systems in the body affected by these stimulants.
Nicotine is powerful and highly addictive. Core Concept 7.10
Nicotine is sometimes considered a CNS stimulant because of its ability to increase alertness. However,
its actions and long-term consequences place it into a class by itself. Nicotine is unique among abused
substances in that it is legal, strongly addictive, and highly carcinogenic. Furthermore, use of tobacco can
cause harmful effects from secondhand smoke to those in the immediate area of the smoker. Patients often
do not consider tobacco use to be substance abuse.
The most common method by which nicotine enters the body is through the inhalation of cigarette,
pipe, or cigar smoke. Tobacco smoke contains more than 1,000 chemicals, many of which are carcinogens.
The primary addictive substance in cigarette smoke is nicotine. Effects of inhaled nicotine may last from
30 minutes to several hours.
Nicotine affects many body systems, including the nervous, cardiovascular, and endocrine systems.
Nicotine stimulates the CNS directly, causing increased alertness and ability to focus, feelings of relax-
ation, and lightheadedness. The cardiovascular effects of nicotine include accelerated heart rate and in-
creased blood pressure, caused by activation of nicotinic receptors located within the autonomic nervous
system (see Chapter 8). These cardiovascular effects can be serious in patients taking oral contraceptives.
The risk of a fatal heart attack is five times greater in smokers than in nonsmokers. Muscular tremors may
occur with moderate doses of nicotine, and convulsions may result from very high doses. Nicotine affects
the endocrine system by increasing the basal metabolic rate leading to weight loss. Nicotine also reduces
appetite. Chronic use may lead to bronchitis, emphysema, and lung cancer.
Both psychological and physical dependence occur relatively quickly with nicotine. Once started on
tobacco, patients tend to continue their drug use for many years, despite overwhelming medical evidence
that their quality of life may be adversely affected and their life span shortened. Discontinuation results
in agitation, weight gain, anxiety, headache, and an extreme craving for the drug. Although NRT (such
as patches or gum), buproprion (Zyban, Wellbutrin), and varenicline tartrate (Chantix) assist patients in
dealing with the unpleasant withdrawal symptoms, users often relapse because of stress, weight gain, and
unpleasant symptoms.
Healthcare providers strive to remain free from impairment

Core Concept 7.11 due to alcohol and drug addiction.
Healthcare providers play a key role in the identification, prevention, and treatment of substance abuse.
Abusers are often reluctant to report their drug use, for fear of embarrassment or being arrested. Healthcare
staff must be knowledgeable about the signs of substance abuse and withdrawal symptoms, and develop a
keen sense of perception during interaction with their patients. A trusting healthcare provider–patient re-
lationship is essential in helping patients deal with their dependence. By using therapeutic communication
skills and by demonstrating a nonjudgmental, empathetic attitude, the healthcare team can build a trusting
relationship with people that need medical assistance.
Impairment due to substance abuse is not only a behavioral or societal problem, but also a con-
cern for the healthcare provider. Most nurses, for example, report that they have routinely encountered
coworkers with perceived alcohol or substance abuse problems. Generally among nurses and other
healthcare staff, alcohol is the most commonly abused legal substance; prescription drugs are abused
secondly. Critical care nurses are especially likely to abuse stimulants and substances like marijuana or
anxiolytic medications.
Reasons for these problems seem to be increasing tension due to the demands of the healthcare
profession in general; social environments among medical professionals that promote self-reliance and
independence; difficulty sleeping, in particular among workers with rotating shifts; and overall fatigue.
Warning signs of substance abuse are overworking habits (e.g., arriving early and staying late for many
days on end), high performance followed by deteriorating performance, isolation from other working
staff, and frequent excuses (unexplained or complicated variables related to the worker’s professional or
social life).
Obvious signs may be frequent mood swings, irritability, or tearful outbursts followed by depres-
sion. Signs of substance abuse may be smell of alcohol on the breath covered up by mints or mouthwash,
frequent absence from the unit to visit the restroom, or patients complaining of not receiving medications.
Patients may complain about feeling pain despite having received seemingly adequate or repeated dosing
of medication.
There are organizations that focus chiefly on addiction and the nursing profession as well as psy-
chiatric disorders among nurses and other healthcare workers. The focus need not be just on disciplin-
ary action but also on monitoring and support services. Agencies have adopted alternative disciplinary
and peer assistance programs to make sure that both patients and healthcare providers receive proper
assistance.
Chapter Review 81
Patients Need to Know

Patients taking medications with abuse potential need to know the following regarding:
Alcohol
1. Limit alcoholic beverage intake to two drinks per day for men or one drink per day for
women.
2. Avoid alcohol use entirely if liver disease, gastric reflux, peptic ulcers, or pregnancy
exists.
3. Check with your healthcare provider when combining alcohol and medications (pre-
scription or over the counter). Alcohol is considered a CNS depressant, so never combine
it with other CNS depressants.
4. Consuming more than one alcoholic drink per hour will usually result in blood alcohol
levels above the legal limit for operating a vehicle.
CNS Stimulants
5. Avoid sources of caffeine such as OTC drugs with caffeine, chocolate, coffee, and tea if
taking methylphenidate.
6. Always take methylphenidate (Ritalin) at least six hours prior to sleep to avoid insomnia.
CNS Depressants
7. Never take more CNS depressant medication than prescribed. If the prescribed dose is
not providing sufficient relief, a healthcare provider should be notified due to the
possibility of a developed tolerance.
8. Never combine CNS depressants (including alcohol) unless advised to do so by a
Tobacco
9. Nicotine is a major contributor to cancer, heart disease and stroke.
10. Secondhand smoke is dangerous, particularly to children and pregnant women.
11. If using NRT, discontinue smoking immediately and follow the instruction sheet
provided with the NRT of choice.
Chapter Review
7.1 Abused substances belong to many different chem- Dependence is an overwhelming need to take a drug
ical classes. on a continual basis. When physical dependence ex-
Some abused substances, such as alcohol and nico- ists, the patient exhibits signs of withdrawal after the
tine, are available without a prescription. Others, such drug is discontinued. Psychological dependence is an
as barbiturates, benzodiazepines, and most opioids, intense craving for the drug.
have legitimate medical uses. Still others, such as
LSD and heroin, are illegal, having no current medi- 7.4 Withdrawal results when an abused substance
cal applications. is no longer available.
When an abused drug is discontinued, patients may
7.2 Addiction depends on multiple, complex, and experience uncomfortable physical symptoms known
interacting variables. as withdrawal syndrome. Symptoms vary depending
on the specific drug of abuse and range from mild to
Addiction is an overwhelming feeling that causes
life threatening.
someone to continue taking drugs. Although ideas
about addiction have changed over the years, 7.5 Tolerance occurs when higher and higher doses of
healthcare providers now recognize addiction as a drug are needed to achieve the initial response.
being related to drug, genetic, and environmental Tolerance occurs over time when patients adapt to con-
factors. tinued drug use and require higher doses to produce
the same effect. Cross-tolerance or tolerance resulting
7.3 Substance dependence is classified as physical from prior exposure to a related drug also results in
dependence or psychological dependence. higher doses needed to produce the same effect.
7.6 Central nervous system (CNS) depressants de- Amphetamines, methylphenidate, cocaine, and caf-
crease the activity of the central nervous system. feine increase alertness by stimulating the central
Substances that make patients feel relaxed and sleepy, nervous system. Some substances are available by
and work by generally slowing neuronal activity in prescription and are used for narcolepsy, obesity,
the brain, include sedatives, opioids, and ethyl alco- and attention deficit disorder. Caffeine is available in
hol. Examples of sedatives are barbiturates and ben- many consumer products, including chocolate, cof-
zodiazepines. Because of their abuse potential, many fee, tea, soft drinks, and coffee ice cream. Cocaine
of these substances are controlled. Ethyl alcohol is a is among the most commonly abused substances in
legal substance. America.
7.7 Marijuana produces little physical dependence or 7.10 Nicotine is powerful and highly addictive.
tolerance. Nicotine is a unique, legal, carcinogenic, and highly
Despite legalization in some states, the most com- addictive substance. The most common method of
monly abused illegal substance nationwide is mari- entry into the body is by inhalation of cigarette, pipe,
juana. Marijuana produces less physical dependence or cigar smoke. Important effects of inhaled nicotine
than most other drugs and produces less tolerance. The include stimulation of the CNS and increased cardio-
medical value of this drug remains controversial and vascular effects.
unproven. The risks of using this substance are lung
cancer, respiratory problems, and lack of motivation. 7.11 Healthcare providers strive to remain free from
impairment due to alcohol and drug addiction.
7.8 Hallucinogens cause an altered state of thought Reasons why healthcare providers have problems
and perception similar to that found in dreams. with alcohol or drug abuse seem to be related to
Hallucinogens, also called psychedelics, have the demands in the health profession, including self-
ability to produce altered states of consciousness reliant social and professional environments, rotat-
and dreams. They include LSD, mescaline, MDMA ing working shifts, and fatigue. Signs of impairment
(Ecstasy), DOM (STP), MDA (love drug), and are frequent mood swings, irritability or depressive
ketamine (an anesthetic). symptoms, smell of alcohol on the breath, frequent
absences from the unit, and patients not receiving
7.9 CNS stimulants increase the activity of the central proper medications. Support groups and organiza-
nervous system. tions assist with these related issues.
Review Questions
The following questions are written in 3. The patient requires a higher dose of the substance to pro-
NCLEX-PN® style. Answer these ques- duce the initial effect. The nurse recognizes this as:
tions to assess your knowledge of the 1. Toxicity
chapter material, and go back and review 2. Resistance
any material that is not clear to you. 3. Immunity
4. Tolerance
4. The patient has developed an opioid addiction. The nurse
anticipates that which of the following medications will be
1. The two most commonly abused drugs are: used for opioid withdrawal?
1. Methylphenidate (Ritalin) and meperidine (Demerol) 1. Methadone
2. Lysergic acid diethylamide (LSD) and phencyclidine (PCP) 2. Heroin
3. Alcohol and nicotine 3. Diazepam (Valium)
4. Opioids and inhalants 4. Alprazolam (Xanax)
2. A patient has been admitted to the emergency room with a 5. The nurse understands that which of the following
diagnosis of cocaine overdose. The nurse monitors the patient for: s ubstances produces little physical dependence or tolerance?
1. Irritability, restlessness, and abdominal cramping 1. Heroin
2. Dysrhythmias, convulsions, and stroke 2. Marijuana
3. Insomnia, hallucinations, and tremors 3. Alcohol
4. Delirium, extreme fatigue, hunger, and headaches 4. Cocaine
Chapter Review 83
6. The nurse recognizes that methylphenidate (Ritalin) is 3. Increased pain threshold and hallucinations
classified as a: 4. Increased blood pressure and respirations
1. Schedule I drug 9. Physical dependence differs from psychological depen-
2. Schedule II drug dence in that with physical dependence:
3. Schedule III drug
4. Schedule IV drug 1. There is an intense craving for the drug.
2. There is an overwhelming need to take the drug.
7. The nurse checks the patient and finds the following: in- 3. The patient exhibits signs of withdrawal after the drug is
creased heart rate, dilated pupils, elevated body temperature, discontinued.
and sweating. The nurse suspects: 4. Higher doses are required to produce the initial effect of
1. Marijuana use the drug.
2. Heroin use
3. Cocaine use 10. The nurse educates the patient on disulfiram (Antabuse),
4. Amphetamine use explaining that:
1. Only small amounts of alcohol may be ingested while on
8. Which of the following would the nurse find when moni- this drug.
toring the patient for use of barbiturates? 2. If alcohol is ingested, the patient may experience shortness
1. Drowiness, lack of muscle coordination, decreased of breath, nausea and vomiting, and headache.
respirations 3. It is safe for use in pregnancy.
2. Euphoria and irritability 4. It enhances alcohol metabolism within the body.
website.

U n i t
2
The Nervous System
Unit Contents
Chapter 8 Drugs Affecting Functions of the Autonomic Nervous System / 86
Chapter 9 Drugs for Anxiety and Insomnia / 105
Chapter 10 Drugs for Emotional, Mood, and Behavioral Disorders / 122
Chapter 11 Drugs for Psychoses / 142
Chapter 12 Drugs for Degenerative Diseases and Muscles / 157
Chapter 13 Drugs for Seizures / 180
Chapter 14 Drugs for Pain Management / 197
Chapter 15 Drugs for Anesthesia / 217

c
“I thought this was going to
h be a simple procedure. But
a after 4 days in bed, now I
p can’t even urinate.”
t Mrs. Martha Wheaton
e
r
8 Drugs Affecting Functions of

the Autonomic Nervous System
Core Concepts
8.1
The nervous system has two major divisions: central 8.6
Cholinergic drugs have few therapeutic uses because
and peripheral. of their numerous adverse effects.
8.2
The autonomic nervous system (a subdivision of the 8.7
Cholinergic blockers are mainly used to dry
PNS) has sympathetic and parasympathetic branches. secretions and to treat asthma.
8.3
Synapses are common sites of drug action. 8.8
Adrenergic drugs are primarily used for their effects
8.4
Norepinephrine and acetylcholine are the two on the heart, bronchial tree, and nasal passages.
primary neurotransmitters in the autonomic nervous 8.9
Adrenergic blockers are primarily used to treat
system. hypertension and are the most widely prescribed
8.5
Autonomic drugs are classified according to the class of autonomic drugs.
receptors that they stimulate or block.
Drug Snapshot
The following drugs are discussed in this chapter:
Drug Classes Drug Prototypes
Cholinergic drugs bethanechol
(Urecholine) 93
Cholinergic blockers atropine (Atro-Pen) 95
Adrenergic drugs phenylephrine
(Neo-Synephrine) 98
Adrenergic blockers prazosin (Minipress) 100
Learning Outcomes
1. Identify the two primary divisions of 4. Describe the three parts of a synapse. 7. Compare and contrast the types
the nervous system. 5. Identify the neurotransmitters of effects that occur when a drug
2. Identify the three primary functions important to the autonomic stimulates alpha- and beta-receptors.
of the nervous system. nervous system and the associated 8. For each of the classes in the Drug
3. Compare and contrast the nerves. Snapshot, identify representative
actions of the sympathetic and drugs and explain their mechanisms
6. Compare and contrast nicotinic and
parasympathetic nervous systems. of drug action, primary actions, and
muscarinic receptors.
important adverse effects.
Core Concept 8.2 87
Key Terms
acetylcholine (Ach) (ah-SEET-ul-KOH- cholinergic drugs 91 parasympathomimetics (PAIR-ah-SIM-
leen) 88 epinephrine (EH-pin-NEF-rin) 90 path-oh-mah-MET-iks) 91
adrenergic (add-rah-NUR-jik) 90 ganglia (GANG-lee-ah) 90 sympathetic nervous system (SIM-pah-
adrenergic blockers 91 THET-ik) 87
muscarinic (MUS-kah-RIN-ik) 90
adrenergic drugs 91 sympatholytics (SIM-path-oh-LIT-iks) 91
nicotinic (NIK-oh-TIN-ik) 90
alpha-receptor 90 sympathomimetics (sim-path-oh-mih-
norepinephrine (NE) (nor-EH-pin-NEF-
met-iks) 91
anticholinergics 91 rin) 88
beta-receptor 90 parasympathetic nervous system
cholinergic (kol-in-UR-jik) 90 (PAIR-ah-SIM-pah-THET-ik) 87
cholinergic blockers 91
N europharmacology represents one of the largest, most complicated, and least understood branches
of pharmacology. Nervous system medications are used to treat a vast and diverse variety of
conditions, including pain, anxiety, depression, schizophrenia, insomnia, and seizures. Through
their effects on nerves, medications are also used to treat disorders common to the other organ systems.
Examples include abnormalities in heart rate and rhythm, high blood pressure, pressure within the eyeball,
asthma, and congestion.
Traditionally, the study of neuropharmacology begins with the autonomic nervous system. A firm
grasp of autonomic pharmacology is necessary to understand and treat disorders of the affected organ
systems. The remaining chapters in this unit are devoted to the specific treatment of nervous system
conditions.
Core Concept 8.1 The nervous system has two major divisions: central and peripheral.
The nervous system is divided into the central nervous system (CNS) and the peripheral nervous system
(PNS). The CNS is made up of the brain and spinal cord. The PNS consists of all nervous tissue outside of
the CNS. The basic functions of the nervous system are to:
■ Recognize changes in the internal and external environments
■ Process and integrate these environmental changes
■ React to the environmental changes with a series of actions or responses
Figure 8.1 ■ shows the basic divisions of the PNS. Nerves in the PNS either recognize changes to the
environment (sensory subdivision) or respond to these changes by moving muscles or secreting chemicals
soma 5 body (motor subdivision). The somatic nervous system consists of nerves that provide voluntary control over
skeletal muscle. Nerves of the autonomic nervous system, on the other hand, exert involuntary control over
auto 5 self
nom 5 regulation smooth muscle, cardiac muscle, and glands. Organs and tissues regulated by nerves from the autonomic
ic 5 relating to nervous system include the heart, digestive tract, respiratory tract, reproductive tracts, arteries, salivary
glands, and portions of the eye.
The autonomic nervous system (a subdivision of the PNS) has sympathetic

Core Concept 8.2 and parasympathetic branches.
The autonomic nervous system has two branches called the sympathetic nervous system and the
parasympathetic nervous system. Almost all organs and glands receive nerves from both branches of the
autonomic nervous system.
The sympathetic nervous system is activated under conditions of stress and results in a set of
reactions called the fight-or-flight response. The parasympathetic nervous system is activated under
nonstressful c onditions and results in reactions called the rest-and-digest response. Most of the reactions
of the sympathetic branch are opposite to those of the parasympathetic branch. For example, activation of
sympathetic nerves increases heart rate, whereas activation of parasympathetic nerves decreases heart rate.
The major actions of the two branches are shown in Figure 8.2 ■. It is essential to learn these actions early
in the study of pharmacology because knowledge of autonomic effects is used to predict the actions and
adverse effects of many drugs.
88 Chapter 8 Drugs Affecting Functions of the Autonomic Nervous System
Figure 8.1
The Nervous System
Central Nervous System (CNS) Peripheral Nervous System (PNS)
CNS Body
Brain Spinal Cord Motor Neurons Sensory Neurons

• Receives and processes • Conducts signals to and Sensory Organs
sensory information from the brain CNS
• Initiates responses • Controls reflex activities CNS
Muscles Glands
• Stores memories
• Generates thoughts
and emotions
Somatic Nervous System Autonomic Nervous System

• Controls voluntary • Controls involuntary responses
movements
Sympathetic Division Parasympathetic Division

“fight or flight” “rest and digest”
Functional divisions of the nervous system.
Concept Review 8.1

■ How would a person who is engaging in stressful or energetic activity benefit from the
sympathetic effects of bronchodilation, slowed GI motility, and pupil dilation?
Core Concept 8.3 Synapses are common sites of drug action.
The basic functional unit of the nervous system is the nerve cell or neuron. For information to be trans-
mitted throughout the nervous system, neurons must communicate with each other and with muscles and
glands. A nerve impulse travels along a neuron to an area at the end of the neuron called a synapse. The
synapse contains a space called the synaptic cleft, which must be crossed in order for impulses to reach the
pre = before next neuron. The neuron generating the original impulse is called the presynaptic neuron. The nerve on
post = after the other side of the synapse, waiting to receive the impulse, is called the postsynaptic neuron. This basic
synaptic = relating to the
structure is shown in Figure 8.3 ■.
synapse
Chemicals called neurotransmitters allow nerve impulses to cross the synaptic cleft. Neurotransmitters are
released into the synaptic cleft when a nerve impulse reaches the end of a presynaptic neuron. The neurotrans-
mitter travels across the synaptic cleft to reach receptors on the postsynaptic neuron, which then regenerates the
impulse. Many different types of neurotransmitters are located throughout the nervous system, each related to
distinct functions. Many drugs are identical to or have the same general structure as neurotransmitters. Drugs
alter autonomic function by either blocking or enhancing the activity of these neurotransmitters.
Norepinephrine and acetylcholine are the two primary neurotransmitters

Core Concept 8.4 in the autonomic nervous system.
The two primary neurotransmitters of the autonomic nervous system are norepinephrine (NE) and
acetylcholine (Ach). In the sympathetic nervous system, NE is released at the junction of the postsynaptic
neuron and the organ or gland to be acted upon. For example, sympathetic nerves in the heart release NE
onto cardiac muscle stimulating the heart to contract faster and with greater force. Sympathetic nerves also
release NE onto the smooth muscle lining of the digestive tract, and its action is to slow contractions, or
Core Concept 8.4 89
Figure 8.2
PARASYMPATHETIC SYMPATHETIC
DIVISION DIVISION
“rest and digest” “fight or flight”
constricts dilates pupil

pupil
stimulates inhibits
salivation salivation
cranial
slows nerves accelerates
heart heart
cervical
nerves
constricts dilates
bronchioles bronchioles
stimulates thoracic inhibits

digestion nerves digestion
stimulates stimulates
gallbladder release of
glucose
lumbar
nerves
secretes
epinephrine and
norepinephrine
sacral
nerves
contracts relaxes
bladder bladder
stimulates inhibits sex

sex organs organs
Effects of the sympathetic and parasympathetic nervous systems. Source: Krogh, David. Biology: a guide
to the natural world, 5th ed, 2011, Pearson Education. Reprinted and electronically reproduced by permission of Pearson
Education, Inc., Upper Saddle River, NJ.
Figure 8.3
Preganglionic neuron Postganglionic neuron
Ganglionic
Ventral spinal cord synapse
Target tissue
Basic structure of the autonomic pathway.

adren 5 adrenal gland motility. Sympathetic nerves are sometimes called adrenergic. This term comes from the word adrenaline,
(adrenaline) which is a chemical in the body closely related to NE. Adrenaline from the adrenal glands is the same
chemical structure as epinephrine. Epinephrine and NE are both released under conditions of extreme
stress.
The physiology of Ach is more complicated because it is released in several locations. When released
at the ends of parasympathetic neurons, it produces effects opposite of NE, such as slowing the activity of
the heart and increasing the motility of the digestive tract. Ach is also the neurotransmitter released at the
ganglia 5 nerve knots end of all presynaptic neurons at sites called ganglia, which are collections of neuron cell bodies located
outside of the spinal cord. In addition, Ach is also a neurotransmitter of sympathetic neurons that activate
sweat glands; this is a unique case in which Ach is associated with sympathetic rather than parasympathetic
cholin 5 acetylcholine activity. Neurons that release Ach are called cholinergic. The sites of Ach and NE action are shown in
erg 5 work Figure 8.4 ■.
ic 5 relating to Because Ach can stimulate receptors both at the ganglia and at the organ level, different names
are assigned to these receptors. Ach receptors in the ganglia and in skeletal muscle are called nicotinic
receptors, named after nicotine, the chemical found in tobacco products. Ach receptors at the end of
postsynaptic neurons in the parasympathetic nervous system are called muscarinic receptors, named after
an extract of the mushroom Amanita muscaria. Nicotinic and muscarinic receptors are shown in Figure 8.4.
NE receptors are of two basic subtypes: alpha (A)-receptors and beta (B)-receptors. Alpha and
beta are Greek letters commonly used in naming chemical and scientific compounds. These receptors are
further subdivided into beta1, beta2, beta3, alpha1, and alpha2. Drugs may be selective and affect only one
type of NE receptor, or they may affect all receptors. The type of response depends on the specific type
of receptor that is activated. Drugs may also affect one type of receptor at low doses and begin to affect
other receptors when the dose is increased. Table 8.1 ◆ shows a list of receptors and expected autonomic
adipose 5 fat responses when receptors are activated.
Figure 8.4
(a) Sympathetic pathway

Cholinergic receptor Adrenergic
(nicotinic) receptor ( or )
Ach
NE
Cholinergic Adrenergic
preganglionic postganglionic
Spinal cord neuron neuron
Ganglia Target tissue
(b) Parasympathetic pathway
Cholinergic receptor Cholinergic receptor

(nicotinic) (muscarinic)
Ach
Cholinergic Cholinergic
preganglionic postganglionic
Spinal cord neuron neuron Ach
Ganglia
Target tissue
Ach = Acetylcholine
NE = Norepinephrine
Norepinephrine (NE) receptors are adrenergic receptors (a and b) in the sympathetic pathway. Acetylcholine (Ach)
receptors in the ganglia and skeletal muscles (not shown here) are called nicotinic. Ach receptors at the ends of
postganglionic neurons in the parasympathetic pathway are called muscarinic.
Core Concept 8.5 91
Table 8.1 Types of Autonomic Receptors

Neurotransmitter Receptor Primary Locations Responses
Acetylcholine Muscarinic Parasympathetic target: organs Stimulation of smooth
(cholinergic) other than the heart muscle contractions and
gland secretions
Heart Decrease in heart rate
and force of contraction
Nicotinic Cell bodies of postganglionic Stimulation of smooth
neurons (sympathetic and muscle contractions and
parasympathetic pathways) gland secretions
Norepinephrine Alpha1 All sympathetic target organs Constriction of blood

(adrenergic) except the heart vessels, dilation of pupils
Alpha2 Presynaptic adrenergic neuron Inhibition of norepineph-
terminals rine release
Beta1 Heart and kidneys Increase in heart rate
and force of contraction;
release of renin
Beta2 All sympathetic target organs Inhibition of smooth
except the heart muscle contractions
Beta3 Adipose tissue Breakdown of fat
Bladder Suppress emptying of
bladder
Autonomic drugs are classified according to the receptors that they

stimulate or block. Core Concept 8.5
Because they can block or activate either the sympathetic or parasympathetic nervous system, autonomic
drugs are classified based on one of four possible actions:
1.
Activation of the sympathetic nervous system. These drugs are called sympathomimetics or sympatho 5 sympathetic
adrenergic drugs. They produce the classic symptoms of the fight-or-flight response. parasympatho 5
parasympathetic
2.
Activation of the parasympathetic nervous system. These drugs are called cholinergic drugs mimetic 5 to mimic
or parasympathomimetics and produce the classic symptoms of the rest-and-digest response. lytic 5 to undo
3.
Inhibition of the sympathetic nervous system. These drugs are called adrenergic blockers or
sympatholytics and produce actions opposite to those of the sympathomimetics.
4.
Inhibition of the parasympathetic nervous system. These drugs are called anticholinergics or
cholinergic blockers and produce actions opposite to those of the parasympathomimetics.
Students beginning their study of pharmacology often have difficulty understanding the terminology
and actions of autonomic drugs. It is only necessary to learn one group well because the others are logical
extensions of the first. If the fight-or-flight symptoms of the adrenergic drugs are learned, the actions of the
other three groups can be remembered as being either the same or opposite. For example, both the adren-
ergic drugs and the cholinergic blockers increase heart rate and dilate the pupils. The other two groups, the
cholinergic drugs and the adrenergic blockers, have the opposite effects of slowing heart rate and constrict-
ing the pupils. Mastering the actions and terminology of autonomic drugs early in the study of pharmacol-
ogy will reap rewards later in the course when these drugs are applied to various systems. See Table 8.2 ◆
for a quick review of the autonomic drug classes.
Table 8.2 Review of Autonomic Drug Classes

Stimulation Inhibition
Parasympathetic Cholinergic drugs Cholinergic blockers
Nervous System (parasympathomimetics) (anticholinergics)
Sympathetic Nervous Adrenergic drugs Adrenergic blockers
System (sympathomimetics) (sympatholytics)
Cholinergic drugs have few therapeutic uses because of their numerous

Core Concept 8.6 adverse effects.
Remember the term cholinergic refers to neurons having Ach as the neurotransmitter. Cholinergic drugs or
parasympathomimetics mimic actions of the parasympathetic nervous system. These drugs are associated
with rest-and-digest responses. Because of their high potential for serious adverse effects, direct-acting
cholinergic drugs are used only in a clinical setting. For instance, in ophthalmology, they are used to re-
duce intraocular pressure in patients with glaucoma (see Chapter 37). Others are used after anesthesia to
stimulate the smooth muscles of the bowel or urinary tract. Potential adverse effects are increased saliva-
tion, sweating, abdominal cramps, and hypotension.
Indirect-acting cholinergic drugs, or drugs that inhibit the important enzyme acetylcholines-
terase, have the same effects and adverse effects as direct-acting drugs including increased gland
activity, sweating, increased muscle activity, and lowered heart rate. Acetylcholinesterase inhibi-
tors facilitate the effects of the natural neurotransmitter Ach. Therefore, neostigmine (Prostigmin)
and physostigmine (Antilirium) can induce actions in the body associated with rest and digestion.
(Refer back to Figure 8.2.)
Several drugs in this class are used for their effects on Ach receptors in skeletal muscle rather
than for their parasympathetic action. For example, myasthenia gravis is an autoimmune disorder char-
acterized by destruction of cholinergic receptors found on the membranes of skeletal muscle tissue.
Administration of pyridostigmine (Mestinon), neostigmine (Prostigmin), and other drugs (Table 8.3 ◆)
will stimulate skeletal muscle contraction and diagnose or temporarily help to restore the severe mus-
cle weakness found in this disease. Because several drugs useful in treating Alzheimer’s disease are
structurally similar to myasthenia drugs, the table includes drugs such as donepezil (Aricept), galan-
tamine (Razadyne), rivastigmine (Exelon), and tacrine (Cognex). These drugs increase the amount of
Ach binding to receptors located within the brain (see Chapter 12). Thus, cholinergic drugs may have
effects in both the PNS and CNS.
Nerve agents (see Chapter 1) such as sarin and organophosphate insecticides are chemicals that in-
hibit acetylcholinesterase enzyme in the synaptic cleft throughout the entire nervous system. These agents
can cause widespread and toxic parasympathomimetic effects. Symptoms are severe salivation, increased
sweating, muscle twitching, involuntary urination and defecation, confusion, convulsions, and death. In an
emergency, if nerve agents are released, Mark I injector kits containing the anticholinergic drug atropine or
related medications are used to counteract toxic effects. Atropine blocks the attachment of Ach to receptor
sites and prevents overstimulation caused by harmful nerve agents. In instances where too much anticho-
linergic activity occurs, as with atropine overdose or ingestion of poisonous substances, physostigmine
(Antilirium) can be used as an antidote to counter overall adverse effects resulting from intense cholinergic
blockade.
Table 8.3 Cholinergic Drugs (Parasympathomimetics)

Type Drug Primary Uses
Direct acting bethanechol (Urecholine) Stimulation of urination
cevimeline HCl (Evoxac) Treatment of dry mouth
pilocarpine (Isopto Carpine, Ocusert, Salagen) Glaucoma, treatment of dry mouth
Indirect acting (inhibitors of ambenonium (Mytelase) Myasthenia gravis
cholinesterase enzyme) donepezil (Aricept) (see page 167 for the Drug Prototype box) Alzheimer’s disease
edrophonium (Tensilon) Diagnosis of myasthenia gravis
galantamine (Razadyne) Alzheimer’s disease
neostigmine (Prostigmin) Myasthenia gravis
physostigmine (Antilirium) Cholinergic-blocking toxicity
pyridostigmine (Mestinon, Regonol) Myasthenia gravis
rivastigmine (Exelon) Alzheimer’s disease
tacrine (Cognex) Alzheimer’s disease
Core Concept 8.6 93
Drug Prototype: Bethanechol (Urecholine)

Therapeutic Class: Urinary retention (incomplete bladder emptying) treatment
Pharmacologic Class: Cholinergic receptor drug, parasympathomimetic
Actions and Uses: Bethanechol is a direct-acting sweating, abdominal cramping, and hypotension that can
parasympathomimetic that interacts with Ach receptors to lead to fainting. It should not be given to patients with sus-
cause actions typical of parasympathetic stimulation. It affects pected urinary or intestinal obstruction or those with active
mostly the digestive and urinary tracts, where it stimulates asthma.
smooth muscle contraction. These actions are particularly useful Do not use with ambenonium, neostigmine, and other
in stimulating the return of normal gastrointestinal (GI) and cholinergic drugs; mecamylamine (blocker of Ach at the
urinary tract function following general anesthesia. ganglia) may cause abdominal symptoms and hypotension.
Procainamide, quinidine, atropine, and epinephrine reduce the
Adverse Effects and Interactions: The adverse effects of effects of bethanechol.
bethanechol are parasympathetic actions: increased salivation,
Nursing Process Focus Patients Receiving Direct- and Indirect-Acting Cholinergic Drug Therapy
Assessment Potential Nursing Diagnoses
Prior to administration: ■ Urinary Incontinence related to the adverse effects of direct-acting

■ Obtain a complete health history including cardiovascular, respiratory, drugs
GI, urinary, vision and neuromuscular conditions, allergies, and drug ■ Impaired Urinary Elimination related to adverse effects of direct-acting
history for possible drug interactions. drugs
■ Acquire the results of a complete physical examination including vital ■ Impaired Physical Mobility related to adverse effects of indirect-acting
signs, height, weight, bowel sounds, ability to urinate, mental status, drugs
muscle strength, chewing ability, and signs such as ptosis and diplopia. ■ Deficient Knowledge related to a lack of information about drug
■ Evaluate laboratory blood findings: CBC, chemistry, renal and liver therapy
function studies. ■ Risk for Injury related to adverse effects of drug therapy
■ Noncompliance related to adverse effects of drug therapy
Planning: Patient Goals and Expected Outcomes
The patient will:

■ Experience therapeutic effects: direct acting (an increase in bowel and bladder function and tone; regain normal pattern of elimination).
■ Experience therapeutic effects: indirect acting (a decrease in myasthenia gravis symptoms such as muscle weakness, ptosis, and diplopia).
■ Verbalize an understanding of the drug’s use, adverse effects, and required precautions.
Implementation
All Cholinergic drugs
■ Monitor for therapeutic effects dependent on the reason drug is be- ■ Encourage patient and caregivers to practice support measures to max-
ing given. (Improvement in mental status, urinary output and muscle imize therapeutic effects, e.g., adequate rest periods and assistance
strength indicates effectiveness of drug therapy.) with ADLs.
■ Monitor for adverse effects and notify healthcare provider if pulse ■ Instruct the patient to immediately report any of the following symp-
drops below 60 beats per minute or blood pressure is below approved toms to their healthcare provider: nausea, vomiting, diarrhea, rash,
parameters. (These drugs may decrease heart rate and BP, which may jaundice, change in color of stool, feeling faint, tremors, or changes in
indicate cholinergic crisis that requires atropine.) behavior.
■ Monitor liver enzymes at the start of therapy and weekly for six ■ Instruct the patient to adhere to laboratory testing regimen for serum
weeks. (Drugs may cause liver toxicity.) blood level tests of liver enzymes as directed.
continued . . .
NURSING PROCESS FOCUS (continued)
■ Administer medication correctly and evaluate the patient’s knowledge Instruct the patient to:
of proper administration. (Proper administration helps to prevent ■ Take the drug as directed on regular schedule to maintain serum levels
complications.) and control symptoms.
■ Not chew or crush sustained-release tablets.
■ Take oral cholinergic drugs on an empty stomach to lessen incidence of
nausea and vomiting and to increase absorption.
Direct Acting
■ Monitor intake and output ratio. Palpate the abdomen for bladder ■ Advise the patient to be near bathroom facilities after taking these
distention. (Frequent monitoring will detect early signs of thera- drugs.
peutic or adverse effects. Drug onset of action is within 60 minutes,
stimulating the smooth muscle of the bladder to contract and causing
urination.)
■ Provide for eye comfort such as adequately lighted areas and continue Advise the patient:
to monitor vision. (A cholinergic effect may cause blurred vision and ■ That blurred vision is a possible adverse effect and to take appropriate
difficulty seeing in low light.) safety precautions.
■ Not to drive or engage in potentially hazardous activities until the
drug’s effects are known.
■ Help patients to rise from a lying to sitting or standing position until ■ Instruct the patient to avoid abrupt position changes and to avoid pro-
drug effects are determined. (Cholinergic drugs may cause orthostatic longed standing in one place.
hypotension.)
Indirect Acting
■ Monitor neuromuscular status including muscle strength, ptosis, diplo- ■ Instruct patients to report to their healthcare provider any difficulty
pia, and chewing. (Improvement demonstrates therapeutic effects.) with vision or swallowing.
■ Schedule the medication around mealtimes. Check drug reference ma- ■ Instruct the patient about the appropriate time to take medications.
terial on administration with or without food. (Some drugs should be
taken with food and others on an empty stomach.)
■ Schedule activities to avoid fatigue. (Excess fatigue can lead to cholin- Instruct the patient to:
ergic crisis.) ■ Plan activities according to muscle strength and fatigue.
■ Take frequent rest periods to avoid fatigue.
■ Monitor for muscle weakness after dose is given. (Depending on time Instruct the patient to:
of onset, it may indicate cholinergic crisis—overdose—OR myasthenic ■ Report any severe muscle weakness that occurs 1 hour after adminis-
crisis—underdose.) tration of medication.
■ Report any muscle weakness that occurs three or more hours after
medication administration because this is a major symptom of myas-
thenic crisis.
Evaluation of Outcome Criteria
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Table 8.3 for a
list of drugs to which these nursing actions apply.
Cholinergic blockers are mainly used to dry secretions and to treat

Core Concept 8.7 asthma.
Cholinergic blockers are drugs that have actions opposite those of the parasympathetic branch. They mimic
the fight-or-flight response. Although the term anticholinergic is commonly used, a better term for this
class of drugs would be muscarinic blockers, which more accurately describes blockade of the muscarinic
receptor. Most therapeutic uses of the cholinergic blockers relate to their autonomic actions: dilation of
pupils, increase in heart rate, drying of secretions, and dilation of the bronchi. Cholinergic blockers have
been widely used in medicine for many disorders. A relatively high incidence of adverse effects and the
development of safer, and sometimes more effective, medications has limited the current use of cholinergic
blockers. For example, cholinergic blockers were once drugs of choice in treating peptic ulcers, but they
have been replaced by proton-pump inhibitors and H2-receptor blockers (see Chapter 30). Two important
Core Concept 8.7 95
Table 8.4 Cholinergic-Blocking Drugs (Anticholinergics)

Drug Primary Uses
atropine (Atro-Pen) Poisoning with anticholinesterase agents; to increase heart rate, dilate pupils
benztropine (Cogentin) (see page 164 for the Drug Parkinson’s disease, neuroleptic side effects
Prototype box)
cyclopentolate (Cyclogyl) Dilation of pupils
dicyclomine (Bentyl, others) Irritable bowel syndrome
fesoterodine (Toviaz) Prevention of urgent, frequent, or uncontrolled urination
glycopyrrolate (Cuvposa, Robinul) Production of a dry field prior to anesthesia, reduced salivation,
peptic ulcers
ipratropium (Atrovent) Asthma
methscopolamine (Pamine) Motion sickness, ulcers
oxybutynin (Ditropan, Oxytrol) Incontinence
propantheline (Pro-Banthine) Irritable bowel syndrome, peptic ulcer
scopolamine (Hyoscine, Transderm-Scop) Motion sickness, irritable bowel syndrome, adjunct to anesthesia
tiotropium (Spiriva) Asthma
tolterodine (Detrol) Overactive bladder with symptoms of urge urinary incontinence, urgency, and
frequency
trihexyphenidyl Parkinson’s disease
tropicamide (Mydriacyl, Tropicacyl) Mydriasis and cycloplegia for diagnostic procedures
incontinence 5 not
controlled (usually
adverse effects that limit their usefulness include tachycardia (fast heart rate) and the tendency to cause digestive or urinary)
urinary retention in men with prostate disorders. mydriasis 5 prolonged
Some of the cholinergic blockers are used for their effects in the CNS, rather than their autonomic ac- pupil dilation
tions. Scopolamine (Hyoscine, Transderm-Scop) is used to produce sedation and prevent motion sickness cycloplegia 5 ciliary
(see Chapter 6); benztropine (Cogentin) and trihexyphenidyl (Artane) are prescribed to reduce the muscu- eye muscle paralysis
lar tremor and rigidity associated with Parkinson’s disease (see Chapter 12). tachy 5 rapid
Some of the more common cholinergic blockers and their primary uses are listed in Table 8.4 ◆. cardia 5 heart beat
Drug Prototype: Atropine (Atro-Pen)

Therapeutic Class: Antidote for anticholinestrase poisoning, antidysrhythmic, mydriatic (pupil dilating drug)
Pharmacologic Class: Anticholinergic, cholinergic receptor blocker
Actions and Uses: Atropine is a natural product found in the Adverse Effects and Interactions: The adverse effects of atro-
deadly nightshade plant, or Atropa belladonna. By blocking pine limit its therapeutic usefulness. Adverse effects include
Ach (muscarinic) receptors, atropine causes symptoms of dry mouth, constipation, urinary retention, and an increased
the fight-or-flight response, such as increased heart rate, heart rate. Atropine is usually contraindicated in patients with
bronchodilation, decreased motility in the GI tract, mydriasis (pupil glaucoma because the drug may increase pressure within the
dilation), and decreased secretions from glands. Throughout his- eyeball.
tory, atropine has been used for a variety of purposes, although Use of amantadine, antihistamines, tricyclic antidepres-
its use has declined because of the development of safer, more sants, quinidine, disopyramide, and procainamide can increase
effective medications. Atropine is used to treat hypermotility dis- the anticholinergic effects of atropine. Use with levodopa may
eases of the GI tract such as irritable bowel syndrome, to suppress decrease the effects of the latter. The antipsychotic effects of
secretions during surgical procedures, to increase the heart rate in phenothiazines are generally decreased.
patients with a slow heart beat bradycardia), to dilate the pupil
during eye examinations, and to cause bronchodilation in patients
with asthma. Atropine is an antidote for poisoning with nerve gas
agents and organophosphate insecticides.
Nursing Process Focus Patients Receiving Cholinergic Blocker (Anticholinergic) Therapy
Prior to administration: ■ Deficient Knowledge related to a lack of information about drug

■ Obtain a complete health history including cardiovascular, respiratory, therapy
vision and neurological conditions, allergies, and drug history for pos- ■ Decreased Cardiac Output related to adverse effects of drug
sible drug interactions. therapy
■ Evaluate laboratory blood findings: CBC, chemistry, renal and liver ■ Risk for Imbalanced Body Temperature related to inhibited sweat
function studies. gland secretions
■ Acquire the results of a complete physical examination including heart ■ Impaired Oral Mucous Membranes related to decrease in exocrine
rate/rhythm, blood pressure, temperature, weight, bowel sounds, and secretions
elimination patterns. ■ Constipation related to adverse effect of drug therapy
■ Urinary Retention related to adverse effects of drug therapy
■ Risk for Injury related to neurological effects of medication
The patient will:

■ Experience therapeutic effects (a decrease in symptoms for which the medication is prescribed).
Implementation
■ Closely monitor heart function and notify healthcare provider if BP ■ Instruct the patient to monitor vital signs, ensuring proper use of
or pulse exceeds established parameters or dysrhythmias develop. home equipment.
(Anticholinergic drugs stimulate heart rate, increasing the chance for
dysrhythmias.)
■ Observe for adverse effects such as drowsiness, blurred vision, tachy- Instruct the patient to:
cardia, dry mouth, constipation, urinary hesitancy/retention, and ■ Immediately report adverse effects such as palpitations shortness of
decreased sweating. (Adverse effects are the result of the block- breath or drowsiness to their healthcare provider.
age of muscarinic receptors; can also be caused by an overdose of ■ Avoid driving and hazardous activities until effects of drugs are
medication.) known.
■ Provide comfort measures. For dry mucous membranes, apply lubricant Instruct the patient to:
to moisten lips and oral mucosa, and assist in rinsing mouth. Use artifi- ■ Use oral rinses, sugarless gum or candy, and frequent oral hygiene to
cial tears for dry eyes, as needed. (Adverse effects of drug therapy can help relieve dry mouth.
include dry mucous membranes and photosensitivity.) ■ Avoid alcohol-containing mouthwashes that can further dry
oral tissue.
■ Wear sunglasses to decrease sensitivity to bright light.
■ Minimize exposure to heat or cold and strenuous exercise. (Cholinergic ■ Advise the patient to limit activity outside when the temperature is
blockers can inhibit sweat gland secretions due to direct blockade of hot. Strenuous activity in a hot environment may cause heat stroke.
the muscarinic receptors on the sweat glands. Sweating is necessary
for patients to cool down, so this inhibition of sweating can increase
their risk for hyperthermia.)
■ Monitor intake and output ratio. Palpate the abdomen for bladder ■ Instruct the patient to notify the healthcare provider if difficulty in
distention. (Cholinergic blockers can cause urinary retention.) voiding occurs.
■ Monitor patients routinely for abdominal distention and auscultate ■ Advise the patient to increase fluid intake and add bulk to the diet, if
for bowel sounds. (Cholinergic blockers may decrease tone and constipation becomes a problem.
motility of the intestinal tract.)
Core Concept 8.8 97
Adrenergic drugs are primarily used for their effects on the heart,
bronchial tree, and nasal passages. Core Concept 8.8
Adrenergic drugs, or sympathomimetics, have actions similar to those produced by activation of the sympa-
thetic nervous system (the fight-or-flight response). Again, remember that the term adrenergic refers to neu-
rons having adrenaline-like substances in the nerve terminal. The adrenergic drugs produce many of the same
symptoms as the cholinergic blockers. However, because the sympathetic nervous system activates alpha- and
beta-receptors, the actions of the adrenergics are more specific and have wider therapeutic applications.
Although most effects of adrenergics are predictable based on their autonomic actions, their primary effects
depend on which adrenergic receptors are stimulated. Drugs such as phenylephrine (Neo-Synephrine) stimulate
alpha1-receptors and are often used to dry nasal secretions. Because beta1-receptors are predominant in the heart,
beta1-drugs such as dobutamine (Dobutrex) are used to stimulate the heart rate and increase its strength of contrac-
tion. Beta2-drugs such as albuterol (Proventil) cause bronchodilation and are useful in the treatment of asthma.
Some adrenergic drugs are nonselective, stimulating more than one type of adrenergic receptor. For
example, epinephrine stimulates all types of adrenergic receptors and is used for cardiac arrest and asthma.
Pseudoephedrine (Sudafed and others) stimulates both alpha1- and beta2-receptors and is used orally as
a nasal decongestant. Isoproterenol (Isuprel) stimulates both beta1- and beta2-receptors and is used to in-
nonselective = not
crease the rate, force, and conduction speed of the heart and, occasionally, to treat asthma. The nonselec-
specifically directed
tive drugs generally cause a wider variety of adverse effects all over the body.
Some of the more commonly used adrenergic drugs are shown in Table 8.5 ◆. Most drugs in this hyper = elevated
class are presented in other chapters of this book. For prototypes of drugs in this class, see epinephrine tension = blood pressure
(Adrenalin) and norepinephrine (Levophed) in Chapter 22, oxymetazoline (Afrin, others) in Chapter 17, anaphylactic = itchy rash,
and salmeterol (Serevent) in Chapter 28. low blood pressure, swollen
throat
obstructive = narrowed
Concept Review 8.2 pulmonary = lung passage
■ Why do the adrenergic drugs produce many of the same symptoms as the cholinergic dys = abnormal
blockers? rhythmias = heart rhythms
Table 8.5 Adrenergic Drugs (Sympathomimetics)

Drug Primary Receptor Subtype Primary Uses
albuterol (Proventil, Ventolin, VoSpire) Beta2 Asthma
clonidine (Catapres) Alpha2 in CNS Hypertension
dobutamine (Dobutrex) Beta1 Cardiac stimulant
dopamine (Intropin) (see page 326 for the Drug Alpha1 and beta1 Shock
Prototype box)
epinephrine (Adrenalin, others) (see page 327 for the Alpha and beta Cardiac arrest, asthma; anaphylactic and
Drug Prototype box) allergic reactions
formoterol (Foradil, Performist) Beta2 Asthma, chronic obstructive pulmonary
disease (COPD)
isoproterenol (Isuprel) Beta1 and beta2 Asthma, dysrhythmias, heart failure
metaproterenol Beta2 Asthma
methyldopa (Aldomet) Alpha2 in CNS Hypertension
midodrine (ProAmatine) Alpha Hypertension
mirabegron (Myrbetriq) Beta3 Urinary incontinence
norepinephrine (Levophed) (see page 326 for the Drug Alpha and beta1 Shock
Prototype box)
oxymetazoline (Afrin and others) (see page 464 for Alpha Nasal congestion
the Drug Prototype box)
phenylephrine (Neo-Synephrine) Alpha Maintain BP, nasal congestion
pseudoephedrine (Sudafed and others) Alpha and beta Nasal congestion
salmeterol (Serevent) Beta2 Asthma
terbutaline Beta2 Asthma
Drug Prototype: Phenylephrine (Neo-Synephrine)

Therapeutic Class: Nasal decongestant, mydriatic agent, antihypotensive
Pharmacologic Class: Adrenergic drug, alpha1-adrenergic drug
Actions and Uses: Phenylephrine is a selective alpha- congestion (see Chapter 37). Ophthalmic preparations can
adrenergic drug that is available in several formulations, cause narrow-angle glaucoma because of their mydriatic effect.
including intranasal, ophthalmic, IM, SC, and IV. All of its High doses can cause reflex bradycardia due to the elevation of
actions and indications result from sympathetic stimulation. blood pressure caused by stimulation of alpha1-receptors. When
When applied intranasally by spray or drops, it reduces nasal given parenterally, the drug should be used with caution in pa-
congestion by constricting small blood vessels in the nasal tients with advanced coronary artery disease or hypertension.
mucosa. Applied topically to the eye during ophthalmic ex- Anxiety, restlessness, and tremor may occur due to the drug’s
aminations, phenylephrine can dilate the pupil without caus- stimulatory effect on the CNS. Patients with hyperthyroidism
ing significant paralysis of the eye muscles (cycloplegia). The may experience a severe increase in basal metabolic rate, result-
parenteral administration of phenylephrine can reverse acute ing in increased blood pressure and tachycardia. Drug interac-
hypotension caused by spinal anesthesia or vascular shock. tions may occur with monoamine oxidase (MAO) inhibitors,
Because it lacks beta-adrenergic activity, it produces relatively causing a hypertensive crisis. Increased effects may also occur
few cardiac adverse effects at therapeutic doses. Its longer with tricyclic antidepressants. This drug is incompatible with
duration of activity and lack of significant cardiac effects iron preparations (ferric salts).
gives phenylephrine some advantages over epinephrine or
norepinephrine in treating acute hypotension.
Black Box Warning:
Adverse Effects and Interactions: When used topically or Severe reactions, including death, may occur with IV
intranasally, adverse effects are uncommon. Prolonged infusion even when appropriate dilution is used to avoid
intranasal use can cause burning of the mucosa and rebound rapid diffusion. Therefore, restrict IV use for situations in
which other routes are not feasible.
Nursing Process Focus Patients Receiving Adrenergic Drug Therapy

vision and liver conditions, allergies, and drug history for possible drug ■ Decreased Cardiac Output related to bradycardia (disorder)
interactions ■ Ineffective Cardiopulmonary Tissue Perfusion related to
■ Obtain data regarding treatment of nasal congestion and current bronchoconstriction (disorder)
status of nasal mucosa for changes such as excoriation or bleeding ■ Risk for Injury related to adverse effects of drug therapy
■ Acquire the results of a complete physical examination including vital ■ Ineffective Breathing Pattern related to nasal congestion
signs, height, weight, cardiac and urinary output. ■ Disturbed Sleep Pattern related to adrenergic stimulation and
■ Evaluate laboratory blood findings: CBC, chemistry, renal and liver drug-induced excitation
function studies.
The patient will:

■ Experience therapeutic effects (a decrease in symptoms for which the drug is being given).
■ Demonstrate proper nasal/ophthalmic medication instillation technique.
Implementation
of proper administration. If drug is being administered IV, closely ■ Use the drug as prescribed and not “double up” on doses.
monitor IV insertion sites for extravasation and use an infusion pump ■ Take the medication early in the day to avoid insomnia.
to deliver medication. Use a tuberculin syringe when administering SC ■ Keep drug on hand for emergencies if using rescue inhalers or epi-
doses that are extremely small. For metered-dose inhalation, shake the nephrine kits; notify healthcare provider immediately after use.
container well, and wait at least two minutes between medications.
Instill only the prescribed number of drops when using ophthalmic
solutions.
continued . . .
Core Concept 8.9 99
■ Monitor the patient for adverse effects. (Adverse effects of adrenergic Instruct the patient to:
drugs may be serious and limit therapy.) ■ Immediately report shortness of breath, palpitations, dizziness, chest/
arm pain or pressure, or other angina-like symptoms to the healthcare
provider.
■ Consult the healthcare provider before attempting to use adrenergic
drugs to treat nasal congestion or eye irritation.
■ Monitor blood pressure, pulse, and temperature to ensure proper use
of home equipment.
■ Monitor breathing patterns and observe for shortness of breath Instruct the patient:
and/or audible wheezing. Provide supportive nursing measures ■ To immediately report any difficulty breathing.
such as proper positioning for patients with dyspnea. (Monitoring ■ With a history of asthma to consult a healthcare provider before using
provides information about effects of medication. Patients over-the-counter (OTC) drugs to treat nasal stuffiness.
with respiratory problems should consult their healthcare
provider to ensure the correct medication is being used for
their condition.)
■ Observe the patient’s responsiveness to light. (Some adrenergic drugs ■ Instruct patients using ophthalmic adrenergic drugs that transient
cause photosensitivity by affecting the pupillary light accommodation/ stinging and blurred vision on instillation is normal. Headache and/or
response.) brow pain may also occur.
■ Provide eye comfort by reducing exposure to direct bright light in the ■ Instruct the patient to avoid driving and other activities requiring
environment; shield the eyes with a rolled washcloth or eye bandages visual acuity until blurring subsides.
for severe photosensitivity. (Adrenergic drugs can cause mydriasis and
sensitivity to light.)
■ For patients receiving nasal adrenergic drugs, observe the nasal cav- Instruct the patient to:
ity. Monitor for rhinorrhea and epistaxis. (Vasoconstriction may cause ■ Observe the nasal cavity for signs of excoriation or bleeding before
transient stinging, excessive dryness, or bleeding.) instilling nasal spray or drops; review procedure for safe instillation of
nasal sprays or eyedrops.
■ Limit usage of OTC adrenergic drugs; inform the patient about
rebound nasal congestion.
Adrenergic blockers are primarily used to treat hypertension and are the
most widely prescribed class of autonomic drugs. Core Concept 8.9
Adrenergic blockers inhibit the actions of the sympathetic nervous system. These drugs produce many of
the same responses as the cholinergic drugs, but they are more widely used. Because the sympathetic ner-
vous system has alpha- and beta-receptors, the actions of adrenergic blockers are specific and have wide
therapeutic applications. In fact, they are the most widely prescribed class of autonomic drugs. Many of the
adrenergic blockers are shown in Table 8.6 ◆.
Alpha-adrenergic blockers, or simply alpha blockers, are primarily used for their effects on
vascular smooth muscle. By relaxing vascular smooth muscle in small arteries, alpha1 blockers such
as doxazosin (Cardura) cause vasodilation, which results in decreased blood pressure (hypotensive vaso = smooth muscle (blood
vessel)
effect). Their primary use is in the treatment of hypertension, either alone or in combination with
dilation = enlargement of
other drugs. diameter
Some drugs in this class selectively block beta1-receptors. Because beta1-receptors are only present in
the heart, the effects of drugs such as atenolol (Tenormin) are often called cardioselective. By slowing the hypo = lowered
tensive = blood pressure
heart rate, they lower blood pressure, which is their primary use.
Some beta blockers, such as propranolol (Inderal, InnoPran XL), are nonselective, blocking both beta1- cardio = the heart
and beta2-receptors. The nonselective beta blockers are used to treat hypertension, angina, and cardiac selective = directed (toward)
rhythm abnormalities. Their nonselective actions generally result in more adverse effects than the selec- nonselective = not
tive beta blockers. Prototypes of adrenergic blockers can be found for doxazosin (Cardura) in Chapter 18, specifically
directed
carvedilol (Coreg) in Chapter 19, propranolol (Inderal, InnoPran XL) in Chapter 22, and atenolol (Tenor-
min) in Chapter 20. angina = chest pain
Concept Review 8.3

benign 5 gentle ■ Both cholinergic drugs and adrenergic blockers produce similar actions. Why are adren-
prostatic 5 prostate-related ergic blockers used to treat hypertension, but cholinergic drugs are not used for this
hyperplasia 5 enlargement purpose?
Table 8.6 Adrenergic-Blocking Drugs (Sympatholytics)

Drug Primary Receptor Subtype Primary Uses
acebutolol (Sectral) Beta1 Hypertension, dysrhythmias, angina
alfuzosin (UroXatral) Alpha1 Benign prostatic hyperplasia (BPH)
atenolol (Tenormin) (see page 309 for the Drug Beta1 Hypertension, angina
Prototype box)
carteolol (Cartrol) Beta1 and beta2 Hypertension, glaucoma
carvedilol (Coreg) (see page 296 for the Drug Alpha1, beta1, and beta2 Hypertension, heart failure
Prototype box)
doxazosin (Cardura) (see page 282 for the Drug Alpha1 Hypertension
Prototype Box)
esmolol (Brevibloc) Beta1 Hypertension, dysrhythmias
metoprolol (Lopressor, Toprol) Beta1 Hypertension
nadolol (Corgard) Beta1 and beta2 Hypertension
phentolamine (Regitine) Alpha Severe hypertension
prazosin (Minipress) Alpha1 Hypertension
propranolol (Inderal, Innopran XL) (see page 340 Beta1 and beta2 Hypertension, dysrhythmias, heart
for the Drug Prototype box) failure
silodosin (Rapaflo) Alpha1 BPH
sotalol (Betapace) Beta1 and beta2 Dysrhythmias
tamsulosin (Flomax) Alpha1 BPH
terazosin (Hytrin) Alpha1 Hypertension
timolol (Blocadren, Timoptic) (see page 604 Beta1 and beta2 Hypertension, angina, glaucoma
for the Drug Prototype box)
Drug Prototype: Prazosin (Minipress)

Therapeutic Class: Antihypertensive Pharmacologic Class: Sympatholytic, alpha1-adrenergic blocker
Actions and Uses: Prazosin is a selective alpha1-adrenergic Adverse Effects and Interactions: Like other alpha blockers,
blocker that competes with NE at its receptors on vascular prazosin has a tendency to cause orthostatic hypotension due
smooth muscle in arterioles and veins. Its major action is a rapid to alpha1-inhibition in vascular smooth muscle. In rare cases,
decrease in peripheral resistance that reduces blood pressure. this hypotension can be so severe as to cause unconscious-
It has little effect on cardiac output or heart rate, and it causes ness about 30 minutes after the first dose. This is called the
less reflex tachycardia than some other drugs in this class. first-dose phenomenon. To avoid this situation, the first dose
Tolerance to its antihypertensive effect may occur. Its most should be very low and given at bedtime. Dizziness, drowsiness,
common use is in combination with other drugs, such as beta or lightheadedness may occur as a result of decreased blood
blockers or diuretics, in the pharmacotherapy of hypertension. flow to the brain due to the drug’s hypotensive action. Reflex
Prazosin has a short half-life and is often taken two or three tachycardia may occur due to the rapid falls in blood pressure.
times per day. The alpha blockade may also result in nasal congestion or
inhibition of ejaculation.
Drug interactions include increased hypotensive effects
with concurrent use of antihypertensives and diuretics.
Nursing Process Focus Patients Receiving Adrenergic Blocker Therapy

■ Obtain a complete health history including neurological, liver, GI and therapy
GU conditions; allergies; and drug history for possible drug interactions. ■ Risk for Injury related to dizziness, syncope
■ Acquire the results of a complete physical examination including vital ■ Impaired Urinary Elimination (frequency) related to adverse effects of
signs, height, weight. For BPH (obtain urinary pattern and output). drug therapy
■ Evaluate laboratory blood findings: CBC, chemistry, renal and liver ■ Risk for Sexual Dysfunction related to adverse effects of drug
function studies. therapy
The patient will:

■ Experience therapeutic effects (a decrease in blood pressure or ease of urination).
■ Verbalize an understanding of the drug’s use, adverse effects and required precautions.
Implementation
■ In patients with prostatic hypertrophy, monitor for urinary hesitancy/ ■ Instruct the patient to report increased difficulty with urination to a
feeling of incomplete bladder emptying, and interrupted urinary healthcare provider.
stream.
■ Monitor for syncope. (Alpha-adrenergic blockers produce first-dose Instruct the patient to:
syncope phenomenon and may cause loss of consciousness.) ■ Take this medication at bedtime, and to take the first dose
immediately before getting into bed.
■ Avoid abrupt changes in position; warn the patient about first-dose
phenomenon and reassure that this effect diminishes with continued
therapy.
■ Take vital signs and notify healthcare provider if pulse or blood pres- Instruct the patient:
sure drops below approved parameters. Monitor for dizziness, drowsi- ■ To monitor vital signs, especially blood pressure, ensuring proper use
ness, or lightheadedness. (These drugs can cause severe hypotension. of home equipment.
Dizziness is a sign of decreased blood flow to the brain due to the ■ Regarding the normotensive range of blood pressure; instruct the
drug’s hypotensive action.) patient to consult the nurse regarding “reportable” blood pressure
readings.
■ To rise from lying to sitting or standing slowly to avoid dizziness.
■ To report dizziness or syncope that persists beyond the first dose, as
well as paresthesias and other neurologic changes.
■ Monitor level of consciousness and mood. (Adrenergic blockers can ■ Instruct the patient to immediately report any feelings of depression.
exacerbate existing mental depression.) ■ Interview the patient regarding suicide potential; obtain a “no-self
harm” verbal contract from the patient.
■ Observe for adverse effects that may include blurred vision, tinnitus, Inform the patient:
epistaxis, and edema. ■ That nasal congestion may be an adverse effect.
■ To report any adverse reactions to the healthcare provider.
■ About the potential danger of concomitant use of OTC nasal
decongestants.
■ Monitor liver function. (These drugs increase the risk for liver toxicity.) Instruct the patient:
■ To adhere to a regular schedule of laboratory testing for liver function
as ordered by the healthcare provider.
■ To report signs and symptoms of liver toxicity: nausea, vomiting,
diarrhea, rash, jaundice, abdominal pain, tenderness or distention, or
change in color of stool.
■ About importance of ongoing medication compliance and
follow-up.

Patients treated with autonomic medications need to know the following:
In General
1.
Do not take any OTC cold, cough, or sinus drugs without seeking medical advice because
these likely contain autonomic drugs.
2. Report any palpitations, shortness of breath, chest pain, or large changes in blood pres-
sure immediately to a healthcare provider. Some of the most significant adverse effects of
autonomic drugs relate to the cardiovascular system.
3. Notify a healthcare provider before taking autonomic drugs if the following conditions
are present: thyroid disease, diabetes mellitus, dysrhythmias, or hypertension. Such
medications have the potential to cause serious adverse effects in individuals with these
conditions.
4. Move slowly when changing from a supine to an upright position to avoid dizziness and
perhaps fainting. Many of the autonomic medications affect blood pressure.
5. Notify a healthcare provider if any significant change in bowel habits or abdominal
cramping/constipation occurs after taking autonomic drugs.
6. Inform a healthcare provider before taking cholinergic blockers (anticholinergics) if uri-
nating difficulty is present or if the diagnosis of benign prostatic hyperplasia (BPH) has
been made.
7. Chew gum or suck on hard candies if dry mouth is experienced when taking autonomic
drugs. Proper oral hygiene is important to avoid dental caries.
Regarding Adrenergic Blockers

8. Do not discontinue the use of beta blockers abruptly because doing so can result in chest
pain or rebound hypertension.
9. Alpha blockers can sometimes cause impotence as an adverse effect. If there are
difficulties with ejaculation, notify a healthcare provider so that other drug options can
be explored.
Chapter Review
8.1 The nervous system has two major divisions: synaptic cleft. Neurotransmitters cross this synaptic
central and peripheral. cleft to regenerate the nerve impulse.
The central nervous system consists of the brain and
8.4 Norepinephrine and acetylcholine are the two
spinal cord. The peripheral nervous system consists
p rimary neurotransmitters in the autonomic
of a sensory portion and a motor portion. Outgoing
nervous system.
motor signals are characterized as voluntary (somatic)
or involuntary (autonomic). Norepinephrine is the neurotransmitter at the organ
level in the sympathetic nervous system. Norepi-
8.2 The autonomic nervous system (a subdivision of nephrine receptors may be alpha or beta subtypes.
the PNS) has sympathetic and parasympathetic Acetylcholine is the neurotransmitter at the end of all
branches. presynaptic nerves (ganglia), at sweat glands, and in
Stimulation of sympathetic nerves causes symp- skeletal muscle. Acetylcholine receptors may be nic-
toms of the fight-or-flight response. Stimulation of otinic or muscarinic.
parasympathetic nerves induces the rest-and-digest
8.5 Autonomic drugs are classified according to the
response. With few exceptions, the actions of the two
receptors that they stimulate or block.
divisions oppose each other.
Adrenergic drugs stimulate sympathetic nerves, and
8.3 Synapses are common sites of drug action. cholinergic drugs primarily stimulate parasympa-
Synapses consist of a presynaptic nerve and a post- thetic nerves. Adrenergic blockers inhibit the sympa-
synaptic nerve with a space between them called the thetic division, whereas cholinergic blockers mostly
inhibit the parasympathetic branch.
Chapter Review 103
8.6 Cholinergic drugs have few therapeutic uses be- 8.8 Adrenergic drugs are primarily used for their effects
cause of their numerous adverse effects. on the heart, bronchial tree, and nasal passages.
Cholinergic drugs are used to treat glaucoma and Adrenergic drugs may stimulate one or several sub-
to stimulate the urinary or digestive tracts fol- types of adrenergic receptors. Uses include increasing
lowing general anesthesia. Toxic nerve agents are the heart rate, dilating the bronchi, and drying excess
cholinergic drugs, producing harmful effects in the secretions caused by colds.
body.
8.9 Adrenergic blockers are primarily used to treat
8.7 Cholinergic blockers are mainly used to dry secre- hypertension and are the most widely prescribed
tions and to treat asthma. class of autonomic drugs.
The use of cholinergic blockers has declined due Adrenergic blockers are the most commonly pre-
to their numerous adverse effects. They are used scribed autonomic medications. They may be
to dry secretions, dilate the bronchi, and dilate the selective for only one receptor subtype, such as the
pupils. beta1-blockers, or inhibit several subtypes. Hyperten-
sion is their primary indication.
Review Questions
The following questions are written in NCLEX-PN® style. An- 3. Increased blood pressure
swer these questions to assess your knowledge of the chapter 4. Vasoconstriction
material, and go back and review any material that is not clear
to you. 6. While obtaining a patient’s medication history, the patient
tells the nurse, “I’m on metoprolol (Lopressor).” The nurse
1. While assisting the RN with the development of a plan of knows that this drug is a(n):
care for a patient with glaucoma, the LPN recognizes that which 1. Alpha blocker
of the following drugs would be contraindicated for the patient? 2. Beta blocker
1. Pilocarpine (Carpine) 3. Cholinergic
2. Betaxolol HCl (Betoptic) 4. Cholinergic blocker
3. Timolol (Timoptic)
4. Atropine 7. Prior to administering atenolol (Tenormin), the nurse
assesses:
2. The nurse is aware that the patient diagnosed with glau- 1. Respirations and blood pressure
coma would most likely be prescribed which of the following 2. Respirations and heart rate
drugs? 3. Heart rate and blood pressure
1. Adrenergic drugs 4. Temperature and blood pressure
2. Cholinergic drugs
3. Adrenergic blockers 8. The healthcare practitioner orders metaproterenol 20 mg,
4. Cholinergic blockers by mouth three times a day. The pharmacy sends metaproter-
enol sulfate syrup, 10 mg/5 mL. The nurse will administer
3. The nurse informs the patient that rebound congestion ________ per day.
can occur with long-term use of this adrenergic drug: 1. 20 mL
1. Albuterol (Proventil) 2. 60 mL
2. Neostigmine (Prostigmin) 3. 30 mL
3. Salmeterol (Serevent) 4. 40 mL
4. Phenylephrine (Neo-Synephrine)
9. A patient has been prescribed phenylephrine to help re-
4. The patient is diagnosed with urinary bladder urgency lieve nasal congestion. The nurse informs her that prolonged
and incontinence. According to the physician’s orders, the use of this drug can cause:
nurse administers which of the following cholinergic blockers 1. Decreased heart rate
for this condition? 2. Decreased blood pressure
1. Dicyclomine (Bentyl) 3. Drowsiness
2. Ipratropium (Atrovent) 4. Rebound congestion
3. Oxybutynin (Ditropan)
4. Scopolamine (Transderm-Scop) 10. The nurse suspects that the cholinergic blocker the pa-
tient is taking is causing which one of the following adverse
5. A patient is told that he is being given an alpha1-adrenergic effects?
blocker. When he asks what this drug does, the nurse tells him 1. Diaphoresis
that alpha-adrenergic blockers cause: (Select all that apply.) 2. Confusion
1. Vasodilation 3. Dry mouth
2. Decreased blood pressure 4. Increased urination
Case Study Questions
Remember Mrs. Wheaton, the patient 2. The nurse is reviewing information about bethanechol
introduced at the beginning of the with Mrs. Wheaton. What information does the nurse provide?
chapter? Now read the remainder of (Select all that apply.)
the case study. Based on the informa- 1. No adverse effects are significant to report when taking
tion you have learned in this chapter, this medication.
answer the questions that follow. 2. The patient should avoid abrupt position changes.
Mrs. Martha Wheaton, an 80-year-old woman, has been hav- 3. Salivation and sweating may increase.
ing problems with nonobstructive urinary retention following 4. The patient should be near a bathroom after taking this
surgery, a retropubic urethral suspension. She required a Foley medication.
catheter for four days but was unable to void after removal of A couple of months later, Mrs. Wheaton has been diag-
the catheter. The physician ordered bethanechol (Urecholine) nosed with severe hypertension and is prescribed prazosin
for Mrs. Wheaton. (Minipress).
1. Mrs. Wheaton asks the nurse why the physician ordered
bethanechol. The nurse explains that: 3. The nurse informs Mrs. Wheaton that prazosin is a type of:
1. It causes the kidneys to produce more urine, which in- 1. Cholinergic drug
creases the pressure within the bladder, forcing her to 2. Cholinergic blocker
urinate. 3. Adrenergic drug
2. It inhibits smooth muscle contractions, causing the bladder 4. Adrenergic blocker
to relax. 4. Mrs. Wheaton asks the nurse if there are any precautions
3. It stimulates smooth muscle contractions, causing the blad- she should know about. The nurse informs her that alpha-
der to function normally. adrenergic blockers may cause: (Select all that apply.)
4. It decreases the amount of urine produced in the kidneys so
as not to put as much pressure on the bladder. 1. Dizziness when changing positions
2. Possible increased heart rate
3. Nasal congestion
4. Nausea
Note: Answers to the Review and Case Study Questions appear in Appendix B. The complete rationales and answers are located on the

C
“I’m so nervous all the time;
I can’t even care for my h
children. All I can think of is a
that terrible accident.” p
Ms. Cynthia Reynolds t
e
r
Drugs for Anxiety

and Insomnia 9
Core Concepts
9.1
Anxiety disorders fall into categories of generalized 9.6
When taken properly, antidepressants reduce symp-
anxiety, panic disorder, and anxiety due to fearful, toms of panic and anxiety.
recurrent, and traumatic life events. 9.7
Benzodiazepines are useful for the short-term treat-
9.2
Regions of the cerebral cortex, diencephalon, ment of anxiety and insomnia.
and brain stem are responsible for anxiety and 9.8
Barbiturates depress CNS function and cause
wakefulness. drowsiness.
9.3
Anxiety is managed with both pharmacologic and 9.9
Additional drugs provide therapy for anxiety-related
nonpharmacologic strategies. symptoms and sleep disorders.
9.4
An inability to sleep is linked with anxiety.
9.5
Anxiety and insomnia are treated with many types
of central nervous system (CNS) drugs.
Drug Snapshot
Antidepressants escitalopram
(Lexapro) 113
Benzodiazepines lorazepam (Ativan) 116
Barbiturates
Nonbenzodiazepine, zolpidem (Ambien) 118
Nonbarbiturate CNS Drugs
Learning Outcomes
1. Identify the major categories of 3. Identify the four categories of CNS 5. Categorize drugs used for anxiety and
anxiety disorders. drugs used to treat anxiety and sleep insomnia based on their classification
2. Discuss factors contributing disorders. and mechanism of action.
to anxiety and explain some 4. Explain the pharmacologic 6. For each of the classes listed in the
nonpharmacologic therapies used to management of anxiety and Drug Snapshot, identify representative
cope with this disorder. insomnia. drugs and explain their mechanisms
of drug action, primary actions, and
106 Chapter 9 Drugs for Anxiety and Insomnia
Key Terms
antidepressants CNS depressants (dee-PRESS-ahnts) 110 rebound insomnia 110
(AN-tee-dee-PRESS-ahnts) 110 generalized anxiety disorder (GAD) 106 reticular activating system (RAS) 107
anxiety 106 insomnia (in-SOM-nee-uh) 109 reticular formation (re-TIK-u-lurr) 107
anxiolytics (ANG-zee-oh-LIT-iks) 109 limbic system (LIM-bik) 107 sedative-hypnotic (SED-ah-tiv
barbiturates (bar-bi-CHUR-ates) 116 obsessive–compulsive disorder (OCD) 106 hip-NOT-ik) 111
benzodiazepines (ben-zo-di-AZ-eh- panic disorder 106 sedatives (SED-ah-tivs) 111
peenz) 113 phobias (FO-bee-ahs) 106 social anxiety disorder 106
black box warning 111 posttraumatic stress disorder (PTSD) 106
P atients experience nervousness and tension more often than any other symptoms. Seeking relief
from these symptoms, patients often turn to a variety of pharmacologic and alternative therapies.
Most healthcare providers agree that even though drugs do not cure the underlying problem, they
can provide short-term help to calm patients who are experiencing acute anxiety or who have simple sleep
disorders. This chapter discusses drugs that treat anxiety, cause sedation, or help patients sleep.
Anxiety
According to the International Classification of Diseases, 10th edition (ICD-10), anxiety is a state of
“apprehension, tension, or uneasiness that stems from the anticipation of danger, the source of which is
largely unknown or unrecognized.” Anxious individuals can often identify at least some factors that bring on
their symptoms. Most people state that their feelings of anxiety are disproportionate to any factual dangers.
Anxiety disorders fall into categories of generalized anxiety,

phobia 5 fear
Core Concept 9.1 panic disorder, and anxiety due to fearful, recurrent,
and traumatic life events.
The anxiety experienced by people faced with a stressful environment or situations is called situational
anxiety. To a certain degree, situational anxiety is beneficial because it motivates people to accomplish
tasks in a prompt manner—if for no other reason than to end the source of nervousness. Situational stress
may be intense, but many people often learn to cope with this kind of stress without seeking conventional
medical intervention.
Generalized anxiety disorder (GAD) is difficult-to-control, excessive anxiety that lasts six months or
more. It occurs in response to a variety of life events or activities, and it interferes with normal, day-to-day
functions. It is by far the most common type of stress disorder routinely observed by healthcare providers.
Symptoms include restlessness, fatigue, muscle tension, nervousness, inability to focus or concentrate, an
overwhelming sense of dread, and sleep disturbances. Autonomic signs of sympathetic nervous system acti-
vation involve sweating, blood pressure elevation, heart palpitations, varying degrees of respiratory change,
and dry mouth. Parasympathetic responses may involve abdominal cramping, diarrhea, and urinary urgency.
Additional motor symptoms experienced by the patient may include increased reflexes and numbness and
tingling of the extremities. Females are slightly more likely to experience GAD, and its prevalence is highest
in those ages 20 to 35.
A second category of anxiety, called panic disorder, is characterized by intense feelings of immedi-
ate apprehension, fearfulness, terror, or impending doom, accompanied by increased autonomic nervous
system activity. Although panic attacks usually last less than 10 minutes, patients may describe them as
seemingly endless. As many as 5% of the population will experience one or more panic attacks during their
lifetimes, and women are affected about twice as often as men.
phobia 5 fear Other categories of anxiety disorders include phobias, OCD, and PTSD. Phobias are fearful feelings
attached to specific objects or situations. Attacks may occur when a person feels trapped, embarrassed,
or unable to escape. Fear of crowds is termed social anxiety disorder, or social phobia. Performers may
experience feelings of dread, nervousness, or apprehension termed performance anxiety. Some anxiety
is normal when a person faces a crowd or performs for a crowd, but extreme fear is not normal. Phobias
compel a patient to avoid the fearful stimulus entirely, to the point that his or her behavior is unnatural.
Obsessive–compulsive disorder (OCD) involves recurrent, intrusive thoughts or repetitive behaviors that
interfere with normal activities or relationships. Common examples include fear of exposure to germs and
repetitive hand washing. Posttraumatic stress disorder (PTSD) is a type of extreme situational anxiety
Fast Facts Anxiety Disorders
■ Millions of Americans experience anxiety every year.

■ Other illnesses commonly coexist with anxiety, including depression, eating disorders, and substance
abuse.
■ The top five causes of anxiety affecting people between the ages of 18 and 54 are:
■ Phobias
■ About 9% of the U.S. population has some type of specific phobia.
■ Specific phobias usually begin in childhood and last for many years.
■ Over 15 million Americans have social phobia.
■ Over 1.8 million Americans have agoraphobia, an intense fear of crowds.
■ Posttraumatic stress disorder (PTSD)
■ More than 3% of the U.S. population has PTSD.
■ PTSD can develop at any age, although the average age of onset is 24 years old.
■ Generalized anxiety disorder (GAD)
■ About 3% of the U.S. population is diagnosed with GAD in a given year.
■ Generalized anxiety symptoms usually begin in an individual’s early 30s.

■ Panic Disorder
■ About 3% of the U.S. population has panic disorder.
■ The average age of onset is 24 years old.

■ Obsessive–compulsive disorder (OCD)
■ One percent of the U.S. population has OCD.
■ Almost 51% of OCD cases is classified as severe.
■ The first symptoms of OCD usually begin in the late teenage years (average age 19 years old).
■ For details, see the National Institutes of Mental Health website.
that develops in response to reexperiencing a previous life event. Traumatic life events such as war, physi-
cal or sexual abuse, natural disasters, or homicidal situations may lead to a sense of helplessness and reex-
periencing of the traumatic event. The terrorist attacks on September 11, 2001, and Hurricanes Katrina and
Sandy are examples of situations that triggered PTSD around the turn of the millennium through the cen-
tury’s first decade. Economic changes, global recession, and unemployment have been largely responsible
for much persistent anxiety. People who experience lingering traumatic life events are at risk for develop-
ing signs and symptoms of PTSD.
Regions of the cerebral cortex, diencephalon, and brain stem are

responsible for anxiety and wakefulness. Core Concept 9.2
The emotional areas of the brain responsible for anxiety and restlessness are mostly the limbic system,
hypothalamus, and the reticular activating system (Table 9.1 ◆). The limbic system is an area of the cere-
bral cortex responsible for emotional expression, learning, and memory. Signals routed through the limbic
system connect with the hypothalamus, an area of the brain referred to as the diencephalon. Emotional
states associated with this connection include anxiety, fear, anger, aggression, remorse, depression, eupho-
ria, and changes in appetite and sexual drive.
The hypothalamus is an important center that triggers unconscious responses to extreme stress, such
as increased blood pressure, elevated breathing rate, and dilated pupils. These are responses associated
with the fight-or-flight response of the autonomic nervous system (see Chapter 8). The endocrine functions
of the hypothalamus are discussed in Chapter 32.
The hypothalamus also connects with the reticular formation, a network of neurons found along
the entire length of the brainstem. Stimulation of the reticular formation causes increased alertness and
arousal; inhibition causes drowsiness and sleep.
The larger area in which the reticular formation is found is called the reticular activating system
(RAS). The RAS controls sleeping and wakefulness and performs an alerting function for the cerebral
cortex. It also helps a person focus attention on individual tasks by transmitting information to higher brain
centers. The RAS is the neural mechanism thought to be responsible for emotions such as anxiety and fear.
It is also the mechanism associated with restlessness and an interrupted sleeping pattern.
Table 9.1 Areas of the Brain Responsible for Anxiety and Restlessness
Major Brain Region Specific Brain Region Role in Anxiety Symptoms
Cerebrum Basal nuclei Responsible for emotional expression,
fear, dread, learning, and memory
Limbic system
Diencephalon Thalamus Triggers unconscious responses to
extreme stress (fight-or-flight response)
Hypothalamus
Epithalamus
Brainstem Midbrain Responsible for overall level of heightened
awareness
Pons
Medulla oblongata
Reticular formation
Cerebellum
Cingulate gyrus
(limbic lobe)
Reticular formation
Hypothalamus
Parahippocampal
gyrus (limbic lobe)
Shaded areas and labels represent brain regions that have a specific role in anxiety symptoms.
Anxiety is managed with both pharmacologic and nonpharmacologic

Core Concept 9.3 strategies.
Although stress itself may be incapacitating, it is often only a symptom of an underlying disorder. Uncov-
ering and addressing the cause of the anxiety is more productive than merely treating the symptoms with
medications. Patients should be encouraged to explore and develop nonpharmacologic coping strategies to
deal with the underlying causes. Such strategies may include behavioral therapy, biofeedback techniques,
meditation, and other complementary and alternative therapies. One model for anxiety management is
shown in Figure 9.1 ■.
Figure 9.1
This model shows how
Stressful events stressful events can
lead to anxiety.
Nonpharmacologic
Change the way coping strategies often
Short-term
you think help to eliminate short-
anxiety
term anxiety, whereas
medication may be
Eliminate needed if anxiety and
the cause related symptoms
begin to occur on a
Fearful
longer basis.
feelings
Changing
mental
Medication
condition
Increased activity
Lack of sleep
Unusual
behavior
Anxiety and related Normal

symptoms on a behavior
longer basis
When anxiety becomes severe enough to significantly interfere with daily activities of life,
p harmacotherapy is indicated. In most types of stress, anxiolytics, or drugs having the ability to relieve anx- anxio 5 anxiety
iety, are quite effective. These include medications in a number of therapeutic categories, involving drugs lytic 5 to dissolve away; break
for depression (see Chapter 10) and seizures (see Chapter 13). Anxiolytics provide treatment for GAD,
panic disorder, phobias, PTSD, and OCD.
Concept Review 9.1

■ What does the term anxiolytic mean? What disorders do anxiolytic drugs treat?
Insomnia
Insomnia is a condition characterized by a patient’s inability to fall asleep or remain asleep. Pharmacotherapy in 5 not (without)
may be needed if the sleeplessness interferes with normal daily activities. somnia 5 sleep
An inability to sleep is linked with anxiety. Core Concept 9.4
Why is it that we need sleep? During an average lifetime, about 33% of our time is spent sleeping or trying
to sleep. Insufficient sleep is associated with increased workplace and driving accidents. Although it is well
established that sleep is essential for wellness, scientists are unsure of its function or how much is needed.
Following are some theories:
■ Inactivity during sleep gives the body time to repair itself.
■ Sleep is a function that evolved as a protective mechanism. Throughout history, nighttime was
the safest time of day, so deep rest (sleep) occurred during those hours.
■ Sleep deals with “electrical” charging and discharging of the brain. The brain needs time for
processing and filing new information collected throughout the day. When this is done without
interference from the environment, these vast amounts of data can later be retrieved through
memory.
Fast Facts Insomnia

■ One-third of the world’s population has trouble sleeping during part of the year.
■ Insomnia is more common in women than in men.
■ Patients older than 65 years old sleep less than patients in any other age group.
■ Only about 70% of people with insomnia ever report this problem to their healthcare provider.
■ People buy over-the-counter (OTC) sleep medications and combination drugs with sleep additives
more than any other drug category. Trade name products include Advil P.M., Excedrin P.M., Nytol,
Equate Nighttime Sleep-Aid, Sominex, Compoz, Tylenol P.M., and Unisom.
■ As a natural alternative for sleep, some people take melatonin, kava kava, or valerian.
The acts of sleeping and waking are synchronized with many different bodily functions. Body tem-
perature, blood pressure, hormone levels, and respiration fluctuate cyclically throughout the 24-hour day.
When this cycle is impaired, pharmacologic or other interventions may be needed to readjust it. Increased
levels of the neurotransmitter serotonin help initiate the various processes of sleep.
Insomnia, or sleeplessness, is a disorder associated with anxiety. There are several major types of
insomnia. Short-term or behavioral insomnia may be attributed to stress caused by a hectic lifestyle or
the inability to resolve day-to-day conflicts within the home or workplace. Worries about work, mar-
riage, children, and health are common reasons for short-term sleep loss. When stress interrupts normal
sleeping patterns, patients cannot sleep because their minds are too active. Long-term insomnia may be
caused by more intense emotional and mood-related illnesses such as depression, manic disorders, or
chronic pain.
Foods or beverages containing stimulants such as caffeine may interrupt sleep. Patients may also find
Life Span Fact that using tobacco products makes them restless and edgy. Alcohol, although often enabling a person to
fall asleep, may produce vivid dreams and frequent awakening that prevent restful sleep. Eating a large
Older adults are more likely
meal—especially one high in protein and fat—close to bedtime may interfere with sleep because metabo-
to experience medication-
related sleep problems. For the
lism increases to digest the food. Certain medications cause CNS stimulation, and these should not be
first night or two, drugs may taken immediately before bedtime. Stressful conditions—for example, too much light, an uncomfortable
seem to help the insomnia of room temperature (especially one that is too warm), snoring, sleep apnea, and recurring nightmares—also
an elderly patient, but as the interfere with sleep.
medication accumulates in the Nonpharmacologic means of relieving insomnia are usually tried before drug therapy, because long-
system, it produces general-
term use of sleep medications will likely worsen insomnia and may cause physical or psychological de-
ized brain dysfunction. The
agitated patient may then be
pendence. Some patients experience a phenomenon called rebound insomnia. This effect occurs when a
mistakenly overdosed with sedative drug is stopped abruptly or when it has been taken for a long time and drug dependence occurs.
higher doses of medication. Alcohol abuse can also cause rebound insomnia.
Concept Review 9.2

■ Why might a patient not be able to enjoy normal sleep? Why is long-term drug therapy
for lack of sleep not a good idea?
Anxiety and insomnia are treated with many types of central nervous
Core Concept 9.5 system (CNS) drugs.
CNS drugs are used to alter brain activity in patients with anxiety or sleep disorders. These medica-
tions are grouped into four major classes: (1) antidepressants, (2) benzodiazepines, (3) barbiturates, and
(4) nonbarbiturate and nonbenzodiazepine CNS drugs.
anti 5 against Antidepressants have an ability to enhance mood by altering the levels of two important neurotrans-
depressant 5 depressed mitters in the brain—norepinephrine and serotonin. By restoring the balance of these neurotransmitters,
neuronal function antidepressants can reduce the symptoms associated with depression, panic, obsessive–compulsive be-
havior, and phobia. Antidepressants used to treat anxiety and insomnia include selective serotonin reup-
take inhibitors (SSRIs), atypical antidepressants (such as serotonin–norepinephrine reuptake inhibitors
(SNRIs)), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs). Use of the latter
two types of drugs has declined in recent years. The mechanisms of action and important considerations of
these drugs are covered in Chapter 10.
Another approach to relieving anxiety is the use of CNS depressants that slow neuronal activity
in the brain. These drugs range from those that relax, to those that sedate, to those that cause sleep and
anesthesia. Coma and death are the end stages of CNS depression. Some drug classes can produce the full
range of CNS depression from relaxation to full anesthesia, whereas others are less effective across this
range. Medications that depress the CNS are sometimes called sedatives because of their ability to sedate
or relax a patient. At higher doses, many of the same drugs can cause sleep and therefore are called hyp-
notics. The term sedative-hypnotic is often used to describe a drug with the ability to produce a calming sedative 5 calming
effect at lower doses and sleep at higher doses. Tranquilizer is an older term used to describe a drug that hypnotic 5 sleep-inducing
produces a soothing or tranquil feeling. tranquilizer 5 drug that
CNS depressants used for anxiety and sleep disorders are categorized into two major classes: benzo- soothes or makes you
diazepines and barbiturates. An additional category consists of miscellaneous drugs chemically unrelated tranquil
to the other drug groups. These have additional therapeutic usefulness in the treatment of anxiety-related
symptoms and insomnia:
■ Buspirone (BuSpar), a mild sedative
■ Valproate (Depakote), an antiseizure medication
■ Atenolol (Tenormin) and propranolol (Inderal, InnoPran XL), beta blockers to reduce stress
■ Eszopiclone (Lunesta), zolpidem (Ambien), and zaleplon (Sonata), sleep disorder medications
that directly activate benzodiazepine receptors in the brain
■ Ramelteon (Rozerem), medication that activates melatonin receptors in the brain
■ Diphenhydramine (Nytol and Sominex) and doxylamine (Unisom), OTC antihistamine sleep
aids that cause drowsiness
As discussed in Chapter 7, long-term use of many CNS depressants can lead to physical or psy-
chological dependence. The withdrawal syndrome for some CNS depressants can cause life-threatening
neurologic reactions, including fever, psychosis, and seizures. Other withdrawal symptoms include
increased heart rate and lowered blood pressure; loss of appetite; muscle cramps; impaired memory,
concentration, and orientation; abnormal sounds in the ears and blurred vision; and insomnia, agitation,
anxiety, and panic. Noticeable withdrawal symptoms typically last two to four weeks. Subtle ones can
last months.
Concept Review 9.3

■ Describe what each of the following terms means in relation to anxiety and alertness:
CNS depressants, sedatives, hypnotics, sedative-hypnotics, and tranquilizers.
When taken properly, antidepressants reduce symptoms of panic

and anxiety. Core Concept 9.6
In the 1960s, antidepressants were mainly used for the treatment of depression or depression that occurred
with anxiety. Today, antidepressants are used not only to treat major depressive disorder termed clinical
depression (see Chapter 10) but also to treat symptoms of anxiety associated with panic disorder, OCD, so-
cial phobia, and PTSD. Because many of the features observed in patients with depressive disorder overlap
with anxiety disorders, methods of intervention are often the same.
For most patients, panic symptoms come in two stages. The first stage is called anticipatory anxi-
ety, when the patient begins to think about an upcoming challenge and starts to feel dread. The second
stage is when physical symptoms such as shortness of breath, rapid heart rate, and muscle tension be-
gin. Many of the stressful symptoms are associated with activation of the autonomic nervous system.
The strategy in treating panic attacks is to help the patient face the fear and suppress symptoms during
one or both of these stages. Drugs can lessen the negative thoughts associated with anticipating the
panic, thereby reducing the stress. Drugs also decrease neuronal activity and suppress functions of the
autonomic nervous system, helping the patient to remain calm. The patient can then use self-help skills
to control behavior.
Antidepressants are often used to reduce persistent symptoms of panic and anxiety. These medica-
tions are summarized in Table 9.2 ◆. SSRIs and atypical antidepressants not only treat panic symptoms but
also treat symptoms of PTSD, OCD, and phobias. Off-label uses are included. SSRIs and SNRIs produce
fewer major adverse effects than the TCAs or MAOIs.
As with all CNS drugs, precautions must be taken to make sure that medications are effective. B ecause
of adverse reactions, some patients might find antidepressant treatment unacceptable. In 2004, the Food
and Drug Administration issued an advisory warning (black box warning) pointing out the potential warn-
ing signs of suicide in adults and children at the beginning of antidepressant therapy and when doses are
changed. In the course of treatment, it is possible that several signs that are the focus of anxiety therapy—
for example, irritability, panic attacks, agitation, insomnia, and hostility—may emerge. See Chapter 10
Table 9.2 Antidepressants for Anxiety Disorders

Drug Route and Adult Dose Clinical Uses
Selective Serotonin Reuptake Inhibitors (SSRIs)
citalopram (Celexa) PO; start at 20 mg/day, may increase to 40 Depression
mg/day if needed
escitalopram (Lexapro) PO; 10 mg/day, may increase to 20 mg/day if Depression, GAD, social anxiety
needed after 1 week
fluoxetine (Prozac) 20 mg/day in a.m., may increase by 20 mg/day Depression, social anxiety, OCD
at weekly intervals (max: 80 mg/day); 20 mg/
day in a.m.; when stable may switch to 90 mg
sustained-release capsule every week (max:
90 mg/week)
fluvoxamine (Luvox) PO; start with 50 mg/day, may increase slowly up Depression, social anxiety, OCD
to 300 mg/day given at bedtime or divided two
times/day
paroxetine (Paxil) PO; 20–60 mg/day Depression, GAD, social anxiety, panic
disorder, OCD, PTSD
sertraline (Zoloft) (see page 133 for the PO; begin with 50 mg/day, gradually increase Depression, social anxiety, panic disorder,
Drug Prototype box) every few weeks according to response (max: OCD, PTSD
200 mg)
Atypical Antidepressants
bupropion (Wellbutrin, Zyban) PO; 75–100 mg tid (greater than 450 mg/day Depression
increases risk for adverse reactions)
duloxetine (Cymbalta) PO; 40–60 mg/day in one or two divided doses Depression, GAD, neuropathic pain, chronic
fatigue syndrome, stress urinary continence,
fibromyalgia
mirtazapine (Remeron) PO; 15 mg/day in a single dose at bedtime; may Depression
increase every
1–2 weeks (max: 45 mg/day)
trazodone (Oleptro) PO; 150 mg/day in divided doses, may increase Depression, GAD
by 50 mg/day every 3–4 days (max: 400–600
mg/day)
venlafaxine (Effexor) Start with 37.5 mg sustained release every day Depression, social anxiety, GAD, neuropathic
and increase to 75–225 mg sustained release pain, migraines
per day
Tricyclic Antidepressants (TCAs)
amitriptyline (Elavil) PO; 75–100 mg/day, may gradually increase to Depression
150–300 mg/day (use lower doses in outpatients)
clomipramine (Anafranil) PO; 75–100 mg/day in divided doses OCD, depression
desipramine (Norpramin) PO; 75–100 mg/day at bedtime or in divided Depression
doses, may gradually increase to 150–300 mg/day
(use lower doses in older adults)
doxepin (Silenor) PO; 30–150 mg/day at bedtime or in divided Depression
doses, may gradually increase to 300 mg/day
(use lower doses in older adults)
imipramine (Tofranil) (see page 129 for PO; 75–100 mg/day in divided doses (max: 300 Depression, GAD
the Drug Prototype box ) mg/day)
nortriptyline (Aventyl, Pamelor) PO; 25 mg three times/day or four times/day, Depression
gradually increased to 100–150 mg/day
trimipramine (Surmontil) PO; 75–100 mg/day (max: 300 mg/day) in Depression
divided doses
Monoamine Oxidase Inhibitors (MAOIs)
phenelzine (Nardil) (see page 133 for the PO; 15 mg three times/day, rapidly increase to at Depression
Drug Prototype box least 60 mg/day, may need up to 90 mg/day
tranylcypromine (Parnate) PO; 30 mg/day in two divided doses (20 mg in Depression
a.m., 10 mg in p.m.), may increase by 10 mg/day
at 3-week intervals (max: 60 mg/day)
Drug Prototype: Escitalopram (Lexapro)

Therapeutic Class: Antidepressant; anxiolytic
Pharmacologic Class: Selective serotonin reuptake inhibitor (SSRI)
Actions and Uses: Escitalopram is a selective serotonin reup- plasma levels of metoprolol and cimetidine. Concurrent use of
take inhibitor (SSRI). Selective inhibition of serotonin reuptake alcohol and other CNS depressants may enhance CNS depressant
results in antidepressant activity without adverse autonomic effects; patients should avoid alcohol when taking this drug.
effects such as increased heart rate or hypertension. This medi- Use caution with herbal supplements such as St. John’s wort,
cation is indicated for generalized anxiety and depression. Off- which may cause serotonin syndrome and increase the effects of
label uses include the treatment of panic disorders. escitalopram.
Adverse Effects and Interactions: Serious reactions include diz-

ziness, nausea, insomnia, somnolence, confusion, and seizures if
taken in overdose. MAOIs should be avoided due to serotonin Black Box Warning:
syndrome, marked by autonomic hyperactivity, hyperthermia, Antidepressants increase the risk of suicidal thinking and
rigidity, diaphoresis, and neuroleptic malignant syndrome. Com- behavior in children, adolescents, and young adults with
bination with MAOIs could result in hypertensive crisis, hyper- major depressive disorder and other psychiatric disorders.
thermia, and autonomic instability. Escitalopram will increase
for more detailed primary actions and adverse effects of these drugs. Following is a brief introduction to hyper 5 elevated
important considerations for each type of antidepressant: thermia 5 temperature
dia 5 across (through pores)
■ SSRIs These drugs are safer than the other classes of antidepressants and result in fewer phoresis 5 to carry (implying
o ccurrences of unfavorable sympathomimetic effects and anticholinergic effects (see Chapter 8). sweat)
Because serotonin is thought to play a role in mood, these medications have received more at-
tention in recent years. SSRIs can cause weight gain and sexual dysfunction. Excessive doses of neuro 5 nerve
leptic 5 locked (seized up)
these medications can cause confusion, anxiety, restlessness, hypertension, tremors, sweating,
fever, blurred vision, constipation, and muscle incoordination. Serotonin syndrome is a poten- malignant 5 aggressive harm
tially life-threatening drug reaction when taking too-high doses of SSRIs. Patients taking these syndrome 5 abnormal
characteristic
drugs should avoid alcohol. SSRIs are often the preferred drugs for anxiety.
■ Atypical antidepressants These are chemically unrelated to the other antidepressants. Their
adverse effects are generally similar to those of SSRIs. SNRIs inhibit the reuptake of both se-
rotonin and norepinephrine; therefore, these drugs are included here. Atypical antidepressants
were the first effective alternatives to TCAs because of their more tolerable adverse effects.
Common adverse effects are headache, insomnia, nervousness, dry mouth, dizziness, weight
loss, sexual dysfunction, and chills.
■ TCAs These are not recommended in patients with a history of heart attack, heart block, or
abnormal heart rhythm. Patients often have annoying anticholinergic effects (see Chapter 8).
Most TCAs are pregnancy category C or D. These drugs should not be used with alcohol or other
CNS depressants. Patients with asthma, gastrointestinal disorders, alcoholism, schizophrenia,
or bipolar disorder should use these drugs with extreme caution.
■ MAOIs Patients should strictly avoid foods containing tyramine (a form of the amino acid
tyrosine) and caffeine. MAOIs intensify the effects of insulin and other diabetes drugs. Common
adverse effects include orthostatic hypotension, hypertension crisis, headache, and diarrhea.
MAOIs are prescribed less often due to food interactions and serious adverse effects. Serotonin
syndrome is a potentially life-threatening drug reaction when taking too-high doses of MAOIs.
Benzodiazepines are useful for the short-term treatment of anxiety

and insomnia. Core Concept 9.7
The benzodiazepines are one of the most widely prescribed drug classes. The root word benzo refers benzo 5 aromatic or ring
to an aromatic compound, one having a carbon ring structure attached to different atoms or to another structure
carbon ring. Two nitrogen atoms incorporated into the ring structure are the reason for the diazepine di 5 two
azepine 5 nitrogen containing
portion of the name.
The benzodiazepines are used for panic disorder, generalized anxiety, phobias, and insomnia
(Table 9.3 ◆). Since the introduction of the first benzodiazepines—chlordiazepoxide (Librium) and diazepam
(Valium)—in the 1960s, the class has become one of the most widely prescribed in medicine. Although
newer benzodiazepines are available, all have the same actions and adverse effects. They differ primarily in
their onset and duration of action. Some, such as the induction drug midazolam (Versed), have a rapid onset
Table 9.3 Benzodiazepines for Anxiety and Insomnia

Drug Route and Adult Dose Related Clinical Uses
Anxiety
alprazolam (Xanax) For panic: PO; 1–2 mg three times/day GAD, phobias, social anxiety, panic disorder
For anxiety: PO; 0.25–0.5 mg three times/day
chlordiazepoxide (Librium) Mild anxiety: PO; 5–10 mg three or four times/day Phobias, alcohol withdrawal
Severe anxiety: PO; 20–25 mg three or four times/day
clonazepam (Klonopin) PO; 1–2 mg/day in divided doses Phobias, social anxiety, seizures, panic
(max: 4 mg/day) disorder
clorazepate (Tranxene) PO; 15 mg/day at bedtime (max: 4 mg/day) Alcohol withdrawal, seizures
diazepam (Valium) (see page 188 PO; 2–10 mg two times/day Alcohol withdrawal, seizures, muscle spasms,
for the Drug Prototype box) induction of anesthesia
lorazepam (Ativan) For anxiety: PO; 2–6 mg/day in divided doses (max: 10 Panic disorder, phobias, alcohol withdrawal,
mg/day) seizures, induction of anesthesia
oxazepam (Serax) PO; 10–30 mg three or four times/day Phobias, alcohol withdrawal
Insomnia
estazolam PO; 1 mg at bedtime, may increase to 2 mg if necessary Insomnia: 15–60 min onset and medium
duration
flurazepam (Dalmane) PO; 15–30 mg at bedtime Insomnia: 30–60 min onset and long
duration
quazepam (Doral) PO; 7.5–15 mg at bedtime Insomnia: 20–45 min onset and long
duration
temazepam (Restoril) PO; 7.5–30 mg at bedtime Insomnia: 45–60 min onset and medium
duration
triazolam (Halcion) PO; 0.125–0.25 mg at bedtime Insomnia: 15–30 min onset and short
(max: 0.5 mg/day) duration
time of 15 to 30 minutes; others, such as oxazepam (Serax), take 2 to 3 hours to reach peak blood levels.
In cases in which the benzodiazepines are used for insomnia therapy, this is important because time of
onset translates to time until sleep for the patient. Duration of action translates to time of anticipated sleep
or drowsiness. The benzodiazepines are categorized as Schedule IV drugs, although they produce consider-
ably less physical dependence and result in less tolerance than the barbiturates.
These drugs intensify the effect of gamma-aminobutyric acid (GABA), which is a natural inhibitory
neurotransmitter found throughout the brain. Most are metabolized in the liver to active metabolites and
excreted primarily in urine. Death with routine use of benzodiazepines is unlikely, unless the benzodiaz-
epines are taken in combination with other CNS depressants, or the patient suffers from sleep apnea.
Most benzodiazepines are given orally. Those that can be given parenterally, such as diazepam
(Valium) and lorazepam (Ativan), should be monitored carefully because of their rapid onset of CNS
effects and possible respiratory depression. Also, some benzodiazepines may be inappropriate for patients
who have an existing diagnosis such as substance abuse.

Because of their greater safety, the benzodiazepines are primarily used for the short-term treatment of
insomnia caused by anxiety. Benzodiazepines shorten the length of time it takes to fall asleep and r educe
the frequency of interrupted sleep. Although most benzodiazepines increase total sleep time, some reduce
Stage IV sleep, and some affect REM sleep. In general, the benzodiazepines used to treat short-term
insomnia are different from those used to treat GAD (see Table 9.3).
Benzodiazepines have a number of other important indications. Diazepam (Valium) is featured as
a prototype drug in Chapter 13 for its use in treating seizure disorders. Other uses include treatment of
alcohol withdrawal symptoms (see Chapter 7), central muscle relaxation (see Chapter 12), and as induction
drugs in general anesthesia (see Chapter 15).
Nursing Process Focus Patients Receiving Antianxiety Therapy
Prior to administration: ■ Acute Confusion related to adverse effects of drug therapy

■ Obtain a complete health history including cardiovascular, neurologi- ■ Deficient Knowledge related to a lack of information about adminis-
cal, and renal and liver conditions; allergies, drug history, likelihood of tration and adverse effects of drug therapy
drug dependency, and possible drug interactions. ■ Ineffective Coping related to anxiety and/or drug dependence
■ Identify factors that precipitate anxiety or insomnia and actions that ■ Risk for Injury related to sedative effect of drug
have been previously tried to decrease symptoms. ■ Insomnia related to anxiety or adverse effects of drug therapy
■ Acquire baseline vital signs and neurological status including level of
consciousness (LOC) and stress/coping patterns.
■ Evaluate laboratory blood findings: renal and liver function studies.
PLANNING: Patient Goals and Expected Outcomes
The patient will:

■ Experience therapeutic effects (an increase in psychological comfort, normal sleep patterns).
■ Be free from or experience minimal adverse effects from drug therapy (absence of physical and behavioral manifestations of anxiety).
Implementation
■ Monitor vital signs. Observe respiratory patterns, especially during Instruct the patient:
sleep, for evidence of apnea or shallow breathing. (Benzodiazepines ■ To consult a healthcare provider before taking this drug if snoring is a
can reduce the respiratory drive in susceptible patients.) problem (snoring may indicate an obstruction in the upper respiratory
tract, resulting in hypoxia).
■ Regarding methods to monitor vital signs at home, especially
respirations.
■ Monitor neurologic status, especially level of consciousness. (Confusion ■ Instruct the patient to report extreme lethargy, slurred speech, disori-
or lack of response may indicate overmedication.) entation, or ataxia to the healthcare provider.
■ Ensure patient safety (i.e., nurses call light within reach). (Drug may Instruct the patient to:
cause excessive drowsiness.) ■ Not drive or perform hazardous activities until the effects of the drug
are known.
■ Request assistance when getting out of bed and walking until the
effect of the medication is known.
■ Monitor the patient’s intake of stimulants, including caffeine (in Instruct the patient to:
beverages such as coffee, tea, cola, and other soft drinks and in OTC ■ Avoid drinking or eating drinks or food with caffeine, especially before
analgesics such as Excedrin), nicotine from tobacco products, and any bedtime.
drugs such as alcohol that produce drowsiness. (These products can ■ Avoid taking alcohol or OTC sleep-inducing antihistamines such as
reduce or enhance the drug’s effectiveness.) diphenhydramine.
■ Consult a healthcare provider before self-medicating with any OTC
preparation.
■ Monitor effect and emotional status. (Drug may increase risk of men- Instruct the patient to:
tal depression, especially in patients with suicidal tendencies.) ■ Report significant mood changes, especially depression.
■ Avoid consuming alcohol or taking other CNS depressants while on
benzodiazepines because these increase depressant effect.
of proper administration. Avoid abrupt discontinuation of therapy. ■ To take the drug exactly as prescribed. Discontinuation of medication
(Withdrawal symptoms, including rebound anxiety and sleeplessness, must be done gradually.
are possible with abrupt discontinuation after long-term use.) ■ To keep all follow-up appointments as directed by the healthcare
provider to monitor response to medication.
■ About nonpharmacologic methods for reestablishing sleep regimen.
Evaluate effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Tables 9.2 (SSRIs)
and 9.3 for a list of drugs to which these nursing actions apply.
Drug Prototype: Lorazepam (Ativan)

Therapeutic Class: Sedative-hypnotic, anxiolytic, anesthetic adjunct
Pharmacologic Class: Benzodiazepine, GABA receptor drug
Actions and Uses: Lorazepam is a benzodiazepine that acts by Lorazepam interacts with multiple drugs; for example,
increasing the effects of GABA, an inhibitory neurotransmitter c oncurrent use of CNS depressants, including alcohol, increases
in the CNS. It is one of the most potent benzodiazepines. It has sedation effects and the risk of respiratory depression and
an extended half-life of 10 to 20 hours that allows for once or death. Lorazepam may contribute to digoxin toxicity by
twice a day oral dosing. In addition to its use as an anxiolytic, increasing the serum digoxin level. Symptoms include visual
lorazepam is used as a preanesthetic medication to provide changes, nausea, vomiting, dizziness, and confusion.
sedation and for the management of status epilepticus. Lorazepam should be used with caution with herbal
supplements. For example, sedation-producing herbs such as
Adverse Effects and Interactions: The most common adverse kava, valerian, chamomil, or hops may have an additive effect
effects of lorazepam are drowsiness and sedation, which may with medication. Stimulant herbs such as gotu-kola and ma
decrease with time. When given in higher doses or by the huang may reduce the drug’s effectiveness.
intravenous (IV) route, more severe effects may be observed,
such as amnesia, weakness, disorientation, ataxia, sleep
disturbance, blood pressure changes, blurred vision, double
vision, nausea, and vomiting.
Core Concept 9.8 Barbiturates depress CNS function and cause drowsiness.
barbiturate 5 barbituric acid Barbiturates are drugs derived from barbituric acid. Until the discovery of the benzodiazepines, barbiturates
compound were used extensively for anxiety and insomnia treatment (Table 9.4 ◆). Although barbiturates are still indi-
cated for several conditions, they are rarely, if ever, prescribed for treating anxiety or insomnia because of their
significant adverse effects and the availability of more effective medications. The risk of psychological and
physical dependence is high—several are Schedule II drugs. The withdrawal syndrome from barbiturates is ex-
tremely severe and can be fatal. Overdose results in profound respiratory depression, hypotension, and shock.
People have used barbiturates to commit suicide, and death due to overdose is not uncommon.
Barbiturates are capable of depressing CNS function at all levels. Like benzodiazepines, barbiturates
act by binding to GABA receptor–chloride channel molecules, intensifying the effect of GABA throughout
the brain. At low doses, they reduce anxiety and cause drowsiness. At moderate doses, they inhibit seizure
activity (see Chapter 10) and promote sleep, probably by inhibiting brain impulses traveling through the
limbic system and the RAS. At higher doses, some barbiturates can produce anesthesia (see Chapter 15).
Table 9.4 Barbiturates for Sedation and Insomnia

Drug Route and Adult Dose
SHORT ACTING
pentobarbital (Nembutal) Sedative: PO; 20–30 mg two or three times/day
Hypnotic: PO; 120–200 mg
secobarbital (Seconal) Sedative: PO; 100–300 mg/day in three divided doses
Hypnotic: PO; 100–200 mg
INTERMEDIATE ACTING
amobarbital (Amytal) Sedative: PO; 30–50 mg two or three times/day
Hypnotic: PO; 65–200 mg (max: 500 mg)
butabarbital (Butisol) Sedative: PO; 15–30 mg three or four times/day
Hypnotic: PO; 50–100 mg at bedtime
Long Acting
mephobarbital (Mebaral) Sedative: PO; 32–100 mg three times/day
phenobarbital (Luminal) (see page 188 for the Sedative: PO; 30–120 mg/day
Drug Prototype box)
When taken for prolonged periods, barbiturates stimulate the microsomal enzymes in the liver that
metabolize medications. Thus, barbiturates can stimulate their own metabolism as well as that of hundreds
of other drugs that use these enzymes for their breakdown. With repeated use, tolerance develops to the
sedative effects of these drugs, and cross-tolerance to other CNS depressants such as the opioids. Tolerance
does not develop, however, to the respiratory depressant effects.
Concept Review 9.4

■ Identify the major drug classes used for sedation and insomnia. Why are CNS depressants
especially dangerous if administered in high doses?
Additional drugs provide therapy for anxiety-related symptoms and

sleep disorders. Core Concept 9.9
The final group of CNS drugs used for anxiety and sleep disorders consists of miscellaneous drugs that are
chemically unrelated to either benzodiazepines or barbiturates. These include the antiseizure medication val-
proate (Depakote) and the beta blockers atenolol (Tenormin) and propranolol (Inderal). Drugs used mainly
for insomnia therapy include eszopiclone (Lunesta), zaleplon (Sonata), and zolpidem (Ambien). Buspirone
(BuSpar) and zolpidem (Ambien) are commonly prescribed for their anxiolytic effects. Zolpidem (Ambien),
ramelteon (Rozerem), and eszopiclone (Lunesta) are used primarily for their hypnotic effects. Dexmedetomi-
dine (Precedex) is primarily used as an adjunctive medication during short surgical procedures (Table 9.5 ◆).
Table 9.5 Nonbenzodiazepine, Nonbarbiturate CNS Drugs for Anxiety and Insomnia
Drug Route and Adult Dose Clinical Uses
Anxiety Therapy
Sedatives
buspirone (BuSpar) PO; 7.5–15 mg in divided doses, may GAD, OCD
increase by 5 mg/day every 2–3 days if
needed (max: 60 mg/day)
dexmedetomidine (Precedex) IV; loading dose 1 mcg/kg over 10 min; Adjunctive medication during surgery,
maintenance dose 0.2–0.7 mcg/kg/hr induction in anesthesia
Antiseizure Medication
valproate/valproic acid (Depakene, Depakote) For mania: PO; 250 mg three times/day Panic disorder, seizures, smoking, bipolar
(max: 60 mg/kg/day) disorder, prevention of migraines
Beta Blockers
atenolol (Tenormin) (see page 309 for the PO; 25–100 mg once/day Performance anxiety, social anxiety
Drug Prototype box)
propranolol (Inderal, InnoPran XL) (see page For trembling: PO; 40 mg two times/day Performance anxiety, social anxiety
340 for the Drug Prototype box) (max: up to 320 mg/day)
Drug Route and Adult Dose Onset and Duration

INSOMNIA THERAPY
Nonbenzodiazepines
eszopiclone (Lunesta) PO; 1–2 mg at bedtime; depending on the 60 min onset and medium duration
age, clinical response, and tolerance of the
patient
zaleplon (Sonata) PO; 10 mg at bedtime (max: 20 mg at 15–30 min onset and short duration
bedtime)
zolpidem (Ambien, Edular, others) PO; 5–10 mg at bedtime 30 min onset and short (medium CR) duration
Melatonin Receptor Drug
ramelteon (Rozerem) PO; 8 mg at bedtime 30 min onset and short duration
Antihistamines
diphenhydramine (Nytol and Sominex) OTC medication 60–180 min onset and long duration
doxylamine (Unisom) OTC medication 60–120 min onset and long duration
The mechanism of action for buspirone (BuSpar) is unclear but appears to be related to D 2 dopamine
receptors in the brain. The drug has profound effects on presynaptic dopamine receptors and a high attrac-
cognitive 5 thinking, tion for serotonin receptors. Buspirone is less likely than benzodiazepines to affect cognitive and motor
remembering, and performance and rarely interacts with other CNS depressants. Common adverse effects include dizziness,
reasoning headache, and drowsiness. Dependence and withdrawal problems are less of a concern with buspirone.
motor 5 producing motion Therapy may take several weeks to achieve optimal results.
or action The antiseizure medication valproate/valproic acid (Depakene, Depakote) is an important drug used
to treat a variety of seizure types. Common uses include treatment for all partial and generalized seizures
(see Chapter 13), the control of symptoms in patients with bipolar disorder (see Chapter 10), and to prevent
migraine headaches (see Chapter 14). For these reasons, valproic acid is listed as one medication that might
be helpful in reducing anxiety symptoms among patients predisposed to panic disorders, mood swings, or
intense headaches. Adverse gastrointestinal effects such as nausea and vomiting are common. Rare life-
threatening hepatotoxicity and pancreatitis are a concern.
Beta blockers were covered in Chapter 8 and are covered more thoroughly as they pertain to manage-
ment of hypertension (see Chapter 18), angina (see Chapter 20), and cardiac dysrhythmias (see Chapter
22). Sweating, heart palpitations, and shaking are expected signs of situational, social, and performance
anxiety. Low doses of beta blockers reduce symptoms connected with panic, tension, and excitement.
Zolpidem (Ambien) is a Schedule IV controlled substance limited to the short-term treatment of insom-
nia. It is highly specific to the GABA receptor and produces muscle relaxation (see Chapter 12) and antisei-
zure effects (see Chapter 13) only at doses much higher than hypnotic doses. As with other CNS depressants,
zolpidem should be used cautiously in patients with respiratory impairment, in elderly persons, and in con-
junction with other CNS depressants. Lower dosages may be necessary. In 2011, the FDA issued a statement
saying that sleeping pills containing the drug zolpiden were dosed too high, especially for women, related to
incidences of car crashes and accidents. Ambien has been shown to decrease sleep latency for up to 35 days in
controlled clinical studies. Also, because of the rapid onset of this drug (within 30 minutes), zolpidem should
be taken just prior to expected sleep. Adverse reactions are usually minimal (mild nausea, dizziness, diarrhea,
daytime drowsiness). Rebound insomnia may occur when the drug is discontinued.
Drug Prototype: Zolpidem (Ambien, Edluar, others)

Therapeutic Class: Sedative-hypnotic
Pharmacologic Class: Nonbenzodiazepine, nonbarbiturate CNS depressant,
GABA receptor drug
Actions and Uses: Although it is a nonbenzo- Adverse Effects and Interactions: Adverse
diazepine, zolpidem acts in a similar fashion effects include daytime sedation, confusion,
to facilitate GABA-mediated CNS depression amnesia, dizziness, depression, nausea, and
in the brain. The only indication for zolpidem vomiting. The drug should be used with caution
is short-term insomnia management (two to in depressed patients or those with a potential
six weeks). It is available in immediate release, for suicide ideation.
extended release, orally disintegrating tablet, Drug interactions with zolpidem include an
and spray forms. Zolpidem is pregnancy increase in sedation when used concurrently with
category B (immediate release) or C (extended other CNS depressants, including alcohol. When
release). taken with food, absorption is slowed signifi-
cantly and the onset of action may be delayed.
CAM Therapy
Valerian for Anxiety and Insomnia
Valerian (Valeriana officinalis) is a perennial plant that grows in Europe, Asia, and North America.
Valerian has several substances in its roots that affect the CNS; the exact active chemical has
yet to be identified. This herb has been used to treat nervousness, anxiety, and insomnia for
thousands of years and is one of the most widely used herbal CNS depressants. The herb ap-
pears to have effects similar to benzodiazepines such as diazepam (Valium). The major side
effects of valerian are extensions of its therapeutic effects: drowsiness and decreased alertness.
Valerian should not be combined with alcohol or other drugs that cause sedation or drowsi-
ness because excessive drowsiness may occur.
Although structurally unrelated to other drugs used to treat insomnia, eszopiclone (Lunesta) has prop-
erties similar to those of zolpidem (Ambien). Eszopiclone’s longer elimination half-life, about twice as
long as that of zolpidem, may give it an advantage in maintaining sleep and decreasing early-morning
awakening. Eeszopiclone is more likely to cause daytime sedation.
Zaleplon (Sonata) may be useful for people who desire to fall asleep but need to awake early in the
morning. It is sometimes used for travel purposes and has been advertised by pharmaceutical companies
for this purpose.
Ramelteon is a melatonin receptor drug, which has been shown to speed the onset of sleep. It has a rel-
atively short onset of action (30 minutes), and its duration is comparable to the noncontrolled release form
of zolpidem. The FDA indications for remelteon or zolpidem are not limited to short-term use because they
do not appear to produce dependence or tolerance to dose.
Drugs included in Table 9.5 without dosing information are diphenhydramine (Nytol and Sominex)
and doxylamine (Unisom). These are OTC sleep aids. Antihistamines also produce drowsiness and are
beneficial in calming patients. They offer the advantage of not causing dependence, although their use is
often limited by anticholinergic adverse effects. Diphenhydramine is a common component of antihista-
mine combinations available OTC for allergic rhinitis and cough and for allergic reactions in general (see
Chapter 25).
Concept Review 9.5

■ What are the major drug classes used to treat GAD, panic disorder, and anxiety symptoms
caused by fearful, recurrent, and traumatic life events?
■ Name popular drugs used to treat symptoms of anxiety and insomnia.

Patients taking anxiolytics and CNS depressants need to know the following:
1. Stimulants such as coffee, tea, and chocolate should be avoided because they coun-
teract anxiolytics and sedatives and increase the symptoms of anxiety.
2. Exercise, progressive muscle relaxation, and slow, deep breathing can assist with anx-
iety relief.
3. Alcohol, antihistamines, and other CNS depressants can increase the effects of anxio-
lytics. They should be avoided to decrease the risk of accidental depressant overdose
and death.
4. Anxiolytics can cause drowsiness. Until effects of these drugs have been established,
assistance with getting out of bed and driving may be needed and operation of
machinery should be avoided.
5. Anxiolytics and sedatives should be stored in a secure place to avoid accidental inges-
tion by children and animals.
6. Avoid abrupt discontinuation of medication because withdrawal symptoms may
occur after long-term use.
7. Report any significant changes in mood to the healthcare provider.
8. Do not take any OTC medications without first consulting the healthcare provider.
9. Smoking and nicotine dependence are increased in patients with anxiety d isorders.
Thus, it is believed that smoking and pharmacotherapy for anxiety-related disorders
are counter effective. Quitting smoking can reduce anxiety.
Safety Alert
Interpreting Physician Orders
It is extremely important for nurses to know their patients’ needs and to clarify with the
physician any medication order that is difficult to interpret or is questionable. For exam-
ple, an error could be made if an order to discontinue “SSRI,” intended to mean “sliding
scale r egular insulin,” is misinterpreted as an order to discontinue the “selective serotonin
reuptake inhibitor.”
Chapter Review
9.1 Anxiety disorders fall into categories of general- barbiturates, and other drugs. These drugs suppress
ized anxiety, panic disorder, and anxiety due to impulses traveling through the limbic and reticular
fearful, recurrent, and traumatic life events. activating systems, thereby reducing symptoms of
There are at least five major types of anxiety disor- stress, producing drowsiness, and promoting sleep.
ders: generalized anxiety, panic disorder, phobias,
9.6 When taken properly, antidepressants reduce
obsessive–compulsive disorder, and posttraumatic
symptoms of panic and anxiety.
stress disorder.
Several classes of antidepressants treat panic and
9.2 Regions of the cerebral cortex, diencephalon, anxiety symptoms: tricyclic antidepressants (TCAs),
and brain stem are responsible for anxiety and monoamine oxidase inhibitors (MAOIs), selective se-
wakefulness. rotonin reuptake inhibitors (SSRIs), and atypical anti
The limbic system and the reticular activating system depressants. The new SSRIs are preferred because
control anxiety and wakefulness. Neural signals pass- they produce fewer sympathomimetic and anticholin-
ing between these two brain regions and the cerebral ergic effects.
cortex are responsible for anxiety, fear, restlessness,
9.7 Benzodiazepines are useful for the short-term
and an interrupted sleep pattern.
treatment of anxiety and insomnia.
9.3 Anxiety is managed with both pharmacologic and Benzodiazepines are commonly prescribed for
nonpharmacologic strategies. insomnia. Several drugs are used; in general, they dif-
Patients should be encouraged to explore and develop fer from the ones used to treat anxiety. Onset and dura-
coping strategies for dealing with stress. In cases tion of action help determine therapeutic application.
when anxiety becomes too severe, anxiolytics are an
9.8 Barbiturates depress CNS function and cause
effective treatment.
drowsiness.
9.4 An inability to sleep is linked with anxiety. Barbiturates are rarely, if ever, prescribed for insom-
There are many reasons why a patient might experi- nia. The primary role of this class of drugs is sedation.
ence sleeplessness. Stress is one factor in short-term They depress CNS function by binding to GABA
insomnia. Others include caffeine, nicotine, room receptors and causing drowsiness.
temperature, light, snoring, and sleep apnea. In long-
9.9 Additional drugs provide therapy for anxiety-
term insomnia, psychological and physiological fac-
related symptoms and sleep disorders.
tors may be involved.
Miscellaneous drugs provide relief from anxiety and
9.5 Anxiety and insomnia are treated with many types anxiety-related symptoms. These include CNS de-
of central nervous system (CNS) drugs. pressants, antiseizure medications, and beta blockers.
Antidepressants treat stress and related symptoms Additional drugs employed for insomnia therapy in-
by altering levels of norepinephrine and serotonin in volve nonbenzodiazepines, melatonin receptor drugs,
the brain. Sedatives, sedative-hypnotics, and CNS de- and antihistamines. Antihistamines are often found in
pressants are terms used to describe benzodiazepines, OTC medications.
Review Questions
The following questions are written in NCLEX-PN® style. Answer 2. Your patient was started on buspirone (BuSpar) for his
these questions to assess your knowledge of the chapter material, anxiety disorder three days ago. The patient now calls the phy-
and go back and review any material that is not clear to you. sician’s office stating that it “just isn’t working.” The nurse’s
best response would be:
1. After eight months of use, the patient abruptly discontin-
ues his zaleplon (Sonata). The patient is now complaining of 1. “BuSpar should give you immediate relief. I will notify the
anxiety and inability to sleep. The nurse suspects: physician that this medication is not effective.”
2. “It may take several weeks for BuSpar to be fully effective.”
1. A panic disorder 3. “You may need an increased dose of BuSpar for it to work.”
2. Long-term insomnia 4. “You will need additional medications to ease your anxiety.”
3. Behavioral insomnia
4. Rebound insomnia
Chapter Review 121
3. The hospitalized patient is sleeping at the time the next 7. Anixety and insomnia are treated with: (Select all that
sedative is ordered. The nurse should: apply.)
1. Wake the patient and administer the next dose of sedative. 1. Benzodiazepines
2. Notify the physician. 2. Antidepressants
3. Hold the dose and document the reason. 3. Antipsychotics
4. Hold this dose and administer it with the next dose. 4. Barbiturates
4. The nurse informs the patient on zolpidem (Ambien) 8. It is important to ensure the patient knows to avoid
that it: ______, which can increase the effects of sedatives.
1. Will take a week for the medication to be effective 1. Nicotine
2. May be taken two to three hours before bedtime 2. Alcohol
3. Should be taken just prior to going to bed 3. Chocolate
4. Must be used long term to be effective 4. Tea
5. The patient has been taking barbiturates for the last few 9. Which of the following is used in the treatment of gener-
months for difficulty sleeping. The nurse’s main concern for alized anxiety disorder (GAD)?
the patient who suddenly stops taking the barbiturate would be: 1. Alprazolam (Xanax)
1. Respiratory depression 2. Estazolam
2. Severe withdrawal 3. Clonazepam (Klonopin)
3. Hypotension 4. Lorazepam (Ativan)
4. Shock
10. The nurse monitors the patient taking lorazepam (Ativan)
6. Which of the following nursing interventions would be for which of the following adverse effects?
most appropriate for a patient who has just been administered 1. Ataxia
a sedative? 2. Euphoria
1. Orient to surroundings. 3. Astigmatism
2. Assess for respiratory dysfunction. 4. Tachypnea
3. Shut off the lights and close the door.
4. Make sure the call light is within the patient’s reach.
Remember Ms. Reynolds, the patient 1. There are a couple of SSRIs indicated for the signs and
introduced at the beginning of the symptoms of PTSD. The nurse would expect Ms. Reynolds to
chapter? Now read the remainder of take:
the case study. Based on the informa- 1. Celexa
tion you have learned in this chapter, 2. Lexapro
answer the questions that follow. 3. Prozac
Ms. Cynthia Reynolds is a 34-year-old interior designer who 4. Paxil
witnessed and was nearly involved in a fatal car accident on her
2. While taking the SSRI, Ms. Reynolds is monitored for:
way to a patient’s house about 6 months ago. Since that time she
has been having dreams about the accident, and during the day 1. Diarrhea
she often thinks about the events and the injured people she saw. 2. Hypotension
She is fearful of driving and does all she can to avoid leaving 3. Hallucinations
her home-based office. When she hears a siren, she feels immedi- 4. Weight gain
ate anxiety and terror. After seeing a physician, Ms. Reynolds is
diagnosed with Post Traumatic Stress Disorder (PTSD) and was
given an SSRI to help relieve her anxiety.
NOTE: Answers to the Review and Case Study Questions appear in Appendix B. The complete rationales and answers are located on the

C
“I hate my job. And my
H family is constantly nagging
A me about sleeping too much
P and eating too little. I don’t
know what’s wrong with me.”
T
Mrs. Rachel Coxilean
E
R
10 Drugs for Emotional, Mood, and

Behavioral Disorders
Core Concepts
10.1 People suffer from depression for many reasons. 10.5 Mood stabilization in patients with bipolar disorder
10.2 For best results, treatment of severe depression is accomplished with lithium and other drugs.
requires both medication and psychotherapy. 10.6 Attention deficit hyperactivity disorder (ADHD)
10.3 Antidepressants enhance mood by boosting the presents challenges for children and adults.
actions of neurotransmitters, including norepineph- 10.7 Central nervous system (CNS) stimulants have been
rine, dopamine, and serotonin. the main course of treatment for ADHD.
10.4 Patients with bipolar disorder may experience emo-
tions ranging from depression to extreme agitation.
Drug Snapshot
Drug Classes Drug Prototypes Drug Classes Drug Prototypes
Antidepressants Drugs for Bipolar Disorder
Tricyclic antidepressants (TCAs) imipramine (Tofranil) 129 Mood stabilizers
Selective serotonin reuptake sertraline (Zoloft) 133 Antiseizure drugs
inhibitors (SSRIs)
Atypical antipsychotic drugs
Atypical antidepressants
Drugs for Attention Deficit–Hyperactivity Disorder (ADHD)
Monoamine oxidase phenelzine (Nardil) 133
inhibitors (MAOIs) CNS stimulants methylphenidate
(Ritalin) 137
Nonstimulant drugs for ADHD
Learning Outcomes
1. Identify the general categories depression, bipolar disorder, and based on their classes and drug
of mood disorders and their attention deficit–hyperactivity actions.
symptoms. disorder (ADHD). 6. For each of the classes listed
2. Explain the causes of major 4. Identify symptoms of ADHD. in the Drug Snapshot, identify
depressive disorder. 5. Categorize drugs used for mood, representative drugs and explain their
3. Discuss the pharmacologic emotional, and behavioral disorders mechanisms of drug action, primary
management of patients with actions, and important adverse effects.
Key Terms
antidepressants (AN-tee-dee-PRESS- dysthymic disorder (dis-THIGH-mick) 124 selective serotonin reuptake inhibitors
ahnts) 125 major depressive disorder 123 (SSRIs) (sir-eh-TO-nin) 128
antipsychotic drugs 135 monoamine oxidase inhibitors (MAOIs) serotonin–norepinephrine reuptake
attention deficit disorder (ADD) 137 (mon-oh-AHM-een OK-se-daze) 132 inhibitors (SNRIs) 129
attention deficit–hyperactivity disorder mood stabilizers 134 serotonin syndrome (SES) 129
(ADHD) 136 postpartum depression 124 situational depression 124
bipolar disorder (bi-PO-ler) 133 psychotic depression 124 tricyclic antidepressants (TCAs)
clinical depression 123 (treye-SICK-lick) 125
seasonal affective disorder (SAD) 124
depression (dee-PRESS-shun) 123
I nappropriate or unusually intense emotions are among the leading causes of mental health disorders.
Although mood changes are a normal part of life, when those changes become severe and impair func-
tioning within the family, work environment, or interpersonal relationships, an individual may be diag-
nosed as having a mood disorder. The two major categories of mood disorders are depression and bipolar
disorder. A third behavioral disorder, ADHD, is also included in this chapter.
Depression
Depression is an emotional disorder characterized by many symptoms, some of which are depressed mood,
lack of energy, sleep disturbances, abnormal eating patterns, and feelings of despair, guilt, and misery
(Table 10.1).
People suffer from depression for many reasons. Core Concept 10.1
In some cases, depression may be situational or reactive, meaning that it results from challenging circum-
stances such as severe physical illness, loss of a job, death of a loved one, divorce, or financial difficulties
coupled with inadequate psychosocial support. In other cases, the depression may be biological or physi-
ological in origin, associated with dysfunction of neurologic processes associated with an imbalance of
neurotransmitters. Family history of depression increases the risk of biological depression.
Among the most common forms of mental illness, major depressive disorder or clinical depression
is estimated to affect 5% to 10% of adults in the United States. The American Psychiatric Association’s
Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), describes the following
Table 10.1 Situational and Biological Causes of Depression

Situational Causes of Depression
■ Unpleasant life circumstances—grief from a lost loved one, divorce, loss of or dissatisfaction with a job,
financial difficulty, excessive stress or responsibilities
■ Negative thinking patterns—an environment that is likely to cause an individual to feel as if any attempts
to escape or correct a situation are hopeless; poor self-image or lack of support from family or friends
■ Substance abuse—substances that produce unpleasant adverse effects or withdrawal symptoms, such as
opiates, alcohol, or other CNS depressants
■ Medication intended for therapeutic use—unfavorable adverse effects from medication intended to treat
a medical disorder (e.g., some antihypertensive drugs and oral contraceptives)
Biological Causes of Depression
■ Genetic—history of depression in one’s family
■ Hormonal changes in the body—fluctuations of reproductive or metabolic hormones
■ Neurobiological dysfunction—chemical disturbances in the brain; usually related to abnormal functioning
or release of neurotransmitters (e.g., dopamine, norepinephrine, serotonin, or melatonin)
■ Symptoms from a second disorder—almost any debilitating disorder, including head trauma, dementia,
brain stroke or tumors, chronic pain, or thyroid dysfunction
124 Chapter 10 Drugs for Emotional, Mood, and Behavioral Disorders
criteria for diagnosis of a major depressive disorder: a depressed affect plus at least five of the following
symptoms lasting for a minimum of two weeks:
■ Difficulty sleeping or sleeping too much
■ Extremely tired; without energy
■ Abnormal eating patterns (eating too much or not enough)
■ Vague physical symptoms (gastrointestinal [GI] pain, joint/muscle pain, or headaches)
■ Inability to concentrate or make decisions
■ Feelings of despair, guilt, and misery; lack of self-worth
■ Obsessed with death (expressing a wish to die or to commit suicide)
■ Avoiding psychosocial and interpersonal interactions
■ Lack of interest in personal appearance or sex
■ Delusions or hallucinations
The majority of depressed patients are not found in psychiatric hospitals but in mainstream society. For
proper diagnosis and treatment to occur, recognition of depression is often a collaborative effort among health-
care providers. For example, it might be the pharmacist who recognizes that a customer is depressed when the
customer buys natural or over-the-counter (OTC) remedies to control anxiety symptoms or to induce sleep.
Depression due to situational depression may be the result of circumstances in a person’s life.
dys 5 ill Dysthymic disorder is a condition characterized by less severe depressive symptoms of an unknown ori-
thymic 5 mind gin that may prevent a person from feeling well or functioning normally. The process from recognizing
depression to properly diagnosing and treating patients should be a collective attempt among healthcare
meno = monthly
pause = stop providers. All staff members should be alert for signs and symptoms of depression in patients they treat.
Some women experience intense mood shifts associated with hormonal changes during the menstrual
post 5 after cycle, pregnancy, childbirth, and menopause. For example, up to 80% of women experience postpartum
partum 5 delivery depression during the first several weeks after the birth of their baby. Many women face additional stresses such
as responsibilities both at work and home, single parenthood, and caring for children and aging parents. If mood
is severely depressed and persists long enough, many women will likely benefit from medical treatment.
peri 5 around Because of the possible consequences of perinatal mood disorders, some state agencies mandate that
natal 5 birth all new mothers receive information about mood shifts prior to their discharge after giving birth. Health-
care providers in obstetrician’s offices, pediatric outpatient settings, and family medicine centers are en-
couraged to conduct routine screening for symptoms of perinatal mood disorders.
During the dark winter months, some patients experience a type of depression known as seasonal
Life Span Fact affective disorder (SAD). This type of depression is associated with a reduced release of the brain neuro-
hormone melatonin. Exposing patients on a regular basis to specific wavelengths of light may relieve SAD
Depression is the most com- depression and prevent future episodes.
mon mental health disorder of
Psychotic depression is another condition characterized by the expression of mood shifts and unusual
elderly patients, encompassing
a variety of physical, emo- behaviors. Intense behaviors include hallucinations, combativeness, and disorganized speech patterns. For
tional, cognitive, and social patients with psychosis and for patients with extreme mood swings, unusual behaviors are often treatable
considerations. with antipsychotic drugs (see Chapter 11).
For best results, treatment of severe depression requires both

Core Concept 10.2 medication and psychotherapy.
The first step to treating depression is a complete health assessment. Drugs such as corticosteroids, levodopa,
and oral contraceptives can cause symptoms of depression, and the healthcare provider should rule out this
possibility. Medical and neurologic disorders, ranging from vitamin B deficiencies to thyroid gland disorders
to early Alzheimer’s disease, can mimic depression. Once physical causes for depression are ruled out, a psy-
chological evaluation may be performed by a psychiatrist or psychologist to confirm the diagnosis.
During the health assessment, inquiries should be made about alcohol and drug use, and whether the
patient has had thoughts about death or suicide. In addition, because depression is sometimes associated
with heredity, the health history should include questions about whether other family members have had a
depressive illness and, if treated, what therapies they received and which of them were effective.
After healthcare providers assess for symptoms of depression, it is necessary to determine the course
of treatment. In general, severe depressive illness, particularly that which recurs, requires treatment with
both medication and psychotherapy to achieve the best response. Counseling therapies help patients gain
insight into and resolve their problems through verbal interaction with the therapist. Behavioral therapies
help patients learn how to obtain more satisfaction and rewards through their own actions and how to un-
learn the behavioral patterns that contribute to or result from their depression.
Two short-term psychotherapies that are helpful for some forms of depression are interpersonal
and cognitive-behavioral therapies. Interpersonal therapy focuses on the patient’s disturbed personal
relationships that both cause and worsen the depression. Cognitive-behavioral therapy helps the patient
change the negative styles of thought and behavior that are often associated with depression. Psychody-
namic therapies, often postponed until the depressive symptoms are significantly improved, focus on re-
solving the patient’s internal conflicts.
In patients with serious and life-threatening mood disorders that are unresponsive to pharmacother-
apy, electroconvulsive therapy (ECT) has been the traditional treatment. Although ECT has been found to
be safe, there may be serious complications related both to the anesthesia that is used and to the potential
seizure activity caused by ECT. Studies suggest that repetitive transcranial magnetic stimulation (rTMS) trans 5 across
may improve mood in major depressive disorder. In contrast to ECT, it has minimal effects on memory, cranial 5 head
does not require general anesthesia, and produces its effects without a generalized seizure.
Even with the best professional care, the patient with depression may take a long time to recover. Indi-
viduals with major depression may have multiple bouts of the illness over the course of their lifetime. This
can take its toll on the patient’s family, friends, and other caregivers who may sometimes feel exhausted,
frustrated, and even depressed themselves. They may experience episodes of anger toward the depressed
loved one, only to subsequently suffer reactions of guilt about being angry. Such feelings can be distress-
ing, and the caregiver may not know where to turn for help. It is often the healthcare provider who is best
able to assist the family members of a person suffering from depression.
Antidepressants enhance mood by boosting the actions of neurotransmit-

ters, including norepinephrine, dopamine, and serotonin. Core Concept 10.3
Antidepressants are medications that combat depression by enhancing mood. Depression is thought to
be associated with an imbalance of neurotransmitters in certain regions of the brain. Although medication
does not completely restore these chemical imbalances, it does help to reduce depressive symptoms while
the patient develops effective means of coping. Remember that antidepressants are often used off-label to
treat a greater variety of symptoms, including anxiety and restlessness (see Chapter 9); so, many areas of
the CNS are potentially targeted by this drug class. Antidepressants may also be used in pain management.
Antidepressants work by increasing the action of specific neurotransmitters in the brain, mainly nor-
epinephrine, dopamine, and serotonin (chemical name, 5-hydroxytryptamine [5-HT]). There are two major
ways in which most antidepressants work: (1) by blocking the enzymatic breakdown of norepinephrine
and dopamine, and (2) by slowing the reuptake of serotonin and/or norepinephrine. The primary classes of
antidepressant drugs, also shown in Table 10.2 ◆, are as follows:
■ Tricyclic antidepressants (TCAs)
■ Selective serotonin reuptake inhibitors (SSRIs)
■ Atypical antidepressants
■ Monoamine oxidase inhibitors (MAOIs)
Concept Review 10.1

■ What are the major causes of depression? Identify symptoms of major depressive disor-
der. What is the name used to describe drugs that treat depression?
Tricyclic Antidepressants
Tricyclic antidepressants (TCAs) are drugs named for their three-ring chemical structure. They were the tri 5 three
mainstay of depression pharmacotherapy from the early 1960s until the 1980s and are still used. cyclic 5 rings
TCAs act by inhibiting the reuptake of both norepinephrine and serotonin into presynaptic nerve ter- pre 5 before
minals, as shown in Figure 10.1 ■. TCAs are used mainly for major depressive disorder and occasionally post 5 after
for situational depression. Clomipramine (Anafranil) is approved for treatment of obsessive–compulsive synaptic 5 the synapse
disorder, and other TCAs are sometimes used as off-label treatments for panic attacks (see Chapter 9). One
use for TCAs, not related to psychopharmacology, is to treat childhood enuresis (bed-wetting). The mecha- enuresis 5 urination
nism for this is not completely understood. One idea is that since TCAs have anticholinergic effects, they
ortho 5 standing up
decrease bladder tone and therefore allow more time for the bladder to fill. static 5 still
Although TCAs treat depressive symptoms, they have some unpleasant and serious adverse effects. hypo 5 reduced
The most common adverse effect is orthostatic hypotension (feeling dizzy when changing to an upright or tension 5 blood pressure
standing position), which occurs due to vasoconstriction of blood vessels. Sedation is a frequently reported
complaint at the beginning of therapy, but patients usually become tolerant to this effect after several weeks Life Span Fact
of treatment. Most TCAs have a long half-life, which increases the risk of adverse effects for patients with
delayed excretion. Anticholinergic effects, such as dry mouth, constipation, urinary retention, blurred vi- TCAs can cause heart block
and other adverse cardiac ef-
sion, and tachycardia, are common (see Chapter 8). Significant drug interactions can occur with CNS defects. They must be used cau-
pressants, sympathomimetics, anticholinergics, and MAOIs. Since the discovery of newer antidepressants, tiously in older adults or those
TCAs are less frequently used as first-line drugs in the treatment of anxiety mixed with depression. with cardiac disease.
Table 10.2 Antidepressants

Drug Route and Adult Dose Remarks
Tricyclic Antidepressants (TCAs)
amitriptyline (Elavil) Adult: PO; 75–100 mg/day (may gradually increase For biological depression; inhibits gastric acid secretion by
to 150–300 mg/day); geriatric: PO; 10–25 mg at blocking histamine-2 receptors in the body
bedtime (may gradually increase to 25–150 mg/day)
amoxapine (Asendin) Adult: PO; begin with 100 mg/day, may increase on For situational and biological depression; not associated
day 3 to 300 mg/day; geriatric: PO; 25 mg at bed- with cardiotoxicity; mild sedative
time, may increase every 3–7 days to 50–150 mg/
day (max: 300 mg/day)
clomipramine (Anafranil) PO; 75–300 mg/day in divided doses For depression accompanying obsessive–compulsive disorder
desipramine (Norpramin) PO; 75–100 mg/day, may increase to 150–300 mg/day Active metabolite of imipramine
doxepin (Sinequan) PO; 30–150 mg/day at bedtime, may gradually in- For depression accompanying anxiety or alcohol dependence
crease to 300 mg/day
imipramine (Tofranil) PO; 75–100 mg/day (max: 300 mg/day) For biological depression or alcohol or cocaine dependence;
may cause cardiac dysfunction and abnormal blood cell
count; available IM; may control bed-wetting in children
maprotiline (Ludiomil) Mild to moderate depression: PO; start at 75 mg/ For a broad range of depression from mild to severe
day and gradually increase every 2 weeks to 150
mg/day; severe depression: PO; start at 100–150
mg/day and gradually increase to 300 mg/day
nortriptyline (Aventyl, PO; 25 mg tid or qid; may increase to 100–150 For biological depression; interactions similar to imipramine
Pamelor) mg/day
protriptyline (Vivactil) PO; 15–40 mg/day in three to four divided doses For symptoms of depression; few sedative qualities; causes
(max: 60 mg/day) increased heart rate
trimipramine (Surmontil) PO; 75–100 mg/day (max: 300 mg/day) For depression accompanied by a sleep disorder (has strong
sedative effects)
Selective Serotonin Reuptake Inhibitors (SSRIs)
citalopram (Celexa) PO; start at 20 mg/day (max: 40 mg/day) Does not mimic the sympathetic response; has no acetylcho-
line blocking properties
escitalopram (Lexapro) PO; 10 mg daily, may increase to 20 mg after May be used for generalized anxiety disorder
(see page 113 for the Drug 1 week
Prototype box)
fluoxetine (Prozac) PO; 20 mg/day in the a.m. (max: 80 mg/day) May be used for obsessive–compulsive disorder and eating
disorders
fluvoxamine (Luvox) PO; start with 50 mg/day (max: 300 mg/day) May be used for obsessive–compulsive disorder; no severe
adverse cardiovascular effects; fewer acetylcholine blocking
effects
paroxetine (Paxil, Pexeva) Depression: PO; 10–50 mg/day (max: 80 mg/day); May be used for obsessive–compulsive disorder and panic
obsessive–compulsive disorder: PO; 20–60 mg/day; attacks
panic attacks: PO; 40 mg/day
sertraline (Zoloft) Adult: PO; start with 50 mg/day, gradually increase Does not mimic sympathetic response; has no acetylcholine
every few weeks to a range of 50–200 mg; geriat- blocking properties
ric: start with 25 mg/day
vilazodone (Viibryd) Adult: PO; start with 10 mg/day for 7 days; follow For major depression; thought not to cause significant
with 20 mg once daily for an additional 7 days; weight gain or decreased sexual desire
increase to 40 mg once daily
bupropion (Wellbutrin, PO; 75–100 mg tid (greater than 450 mg/day For changing moods, schizoaffective disorders, and as an aid
Zyban) increases risk for adverse reactions) to quit smoking; increased risk for seizures; weaker blocker
of serotonin and norepinephrine uptake
duloxetine (Cymbalta) PO; 40–60 mg/day in one or two divided doses For major depression, generalized anxiety disorder, neuro-
pathic pain, chronic fatigue syndrome, stress urinary conti-
nence, and fibromyalgia
Table 10.2 Antidepressants (continued)

mirtazapine (Remeron) PO; 15 mg/day in a single dose at bedtime, may Potent blocker of 5-HT2 and 5-HT3 receptor subtypes; blocks
increase every 1–2 weeks (max: 45 mg/day) presynaptic alpha2-receptors, enhancing norepinephrine re-
lease; use caution in patients with kidney or liver dysfunction
nefazodone PO; 50–100 mg bid, may increase up to 300–600 Minimal cardiovascular effects; fewer effects in blocking ace-
mg/day tylcholine; less sedation; less sexual dysfunction compared
to other antidepressants
trazodone (Oleptro) PO; 150 mg/day, may increase by 50 mg/day every Increases total sleep time; reduces night awakenings; has
3–4 days. (max: 400–600 mg/day for regular re- anxiolytic effects
lease and 375 mg/day for extended release)
venlafaxine (Effexor) PO; start with 37.5 mg sustained release every day For major depression, situational depression, generalized
and increase to 75–225 mg sustained release per day anxiety disorder, neuropathic pain, and migraines
Monoamine Oxidase Inhibitors (Maois)
isocarboxazid (Marplan) PO; 10–30 mg/day (max: 30 mg/day) May cause peripheral edema and high blood pressure; used
in cases in which other approaches for treatment of depres-
sion are not successful
phenelzine (Nardil) PO; 15 mg tid (max: 90 mg/day) May cause a hypertensive crisis or respiratory depression;
use cautiously in patients with epilepsy or diabetes, or who
are likely to abuse drugs and alcohol
selegiline (Emsam) Transdermal patch; applied to dry, intact skin on the Skin patch used to treat major depressive disorder. It is de-
upper torso, upper thigh, or the outer surface of the signed to deliver medication over a 24-hour period
upper arm once every 24 hours; the recommended
starting dose and target dose is 6 mg/24 hours
tranylcypromine (Parnate) PO; 30 mg/day (give 20 mg in a.m. and 10 mg in For severe depression in cases in which patients have not
p.m.), may increase by 10 mg/day at 3-week inter- responded to other medications
vals up to 60 mg/day
Figure 10.1
TCAs inhibit the reup-

take of both norepi-
1 Neurotransmitters are nephrine and serotonin.
released by presynaptic
neuron
Dopamine is a Dopamine 2 Neurotransmitter binds
chemical precursor to postsynaptic receptor
of NE.
Norepinephrine (NE)
or
Serotonin
2
3 Tricyclic antidepressants
inhibit the reuptake of
NE and serotonin into the
presynaptic terminal; Postsynaptic
thus effects of both receptor for
neurotransmitters are
more dramatic. NE or serotonin
Selective Serotonin Reuptake Inhibitors

Selective serotonin reuptake inhibitors (SSRIs) are drugs that slow the reuptake of serotonin into pre-
synaptic nerve terminals. They have become preferred drugs for the treatment of depression.
In the 1970s, it became increasingly clear that serotonin had a more substantial role in depression than
once thought. Researchers knew that the TCAs altered the sensitivity of serotonin to certain receptors in
the brain, but they did not know how this was connected with depression. Ongoing efforts to find antide-
pressants with fewer adverse effects led to the development of the SSRIs.
Serotonin (also called 5-HT) is a natural neurotransmitter in the CNS and is found in high concentra-
tions in neurons of the hypothalamus, limbic system, medulla oblongata, and spinal cord. Serotonin is
important to several body activities, including the cycling between nonrapid eye movement (NREM) and
rapid eye movement (REM) sleep, pain perception, and emotional states (see Chapter 9). Lack of adequate
serotonin in the CNS can lead to depression. Serotonin is metabolized to a less active substance by an en-
mono 5 one zyme located in presynaptic terminals called monoamine oxidase (MAO). A second enzyme, catecholamine
amine 5 NH2 chemical formula O-methyl transferase (COMT), metabolizes serotonin in the synaptic cleft.
oxidase 5 water-forming The TCAs inhibit the reuptake of both norepinephrine and serotonin into presynaptic nerve terminals.
enzyme (hydrogen reacts
In contrast, the SSRIs are selective for just serotonin. Increased levels of serotonin in the synaptic cleft
with oxygen)
cause complex neurotransmitter changes in presynaptic and postsynaptic neurons in the brain. Presynaptic
catecholamine 5 receptors become less sensitive, whereas postsynaptic receptors become more sensitive. This concept is
sympathomimetic amine illustrated in Figure 10.2 ■.
(dopamine, epinephrine, or
norepinephrine)
SSRIs have approximately the same efficacy at relieving depression as the MAO inhibitors and the
tricyclics. The major advantage of the SSRIs, and the one that makes them first-line drugs, is their greater
O-methyl transferase 5 safety profile. Sympathomimetic effects (increased heart rate and hypertension) and anticholinergic effects
special CH3 transferring
enzyme (O = ortho position
(dry mouth, blurred vision, urinary retention, and constipation) are less common with this drug class. Seda-
[chemical term]) tion is also experienced less frequently and cardiotoxicity is not observed. All drugs in the SSRI class have
equal efficacy and similar side effects. In general, SSRIs elicit a therapeutic response more quickly than
TCAs.
One of the most common adverse effects of SSRIs relates to sexual dysfunction. Up to 70% of both
men and women may experience decreased libido and lack of ability to reach orgasm. In men, delayed
ejaculation and impotence may occur. For patients who are sexually active, these adverse effects may
Figure 10.2
SSRIs selectively inhibit

the reuptake of sero-
Normally:
tonin, causing complex
changes in the presyn- 1 Serotonin released by
aptic and postsynaptic presynaptic neuron.
neurons. 2 Serotonin binds to its
Serotonin postsynaptic receptor.
3 Presynaptic receptors
bind with serotonin
4 Step 3 results in less
serotonin being released.
– 5 When SSRIs are administered:
4
5 If serotonin reuptake
1 is blocked, more
onin serotonin will be available
3 rot in the synaptic space.
Se
Presynaptic 6 The sensitivities of both
serotonin 2
the presynaptic and
receptor postsynaptic receptors
Postsynaptic will then change:
serotonin postsynaptic
receptor receptors will become
more sensitive;
presynaptic receptors
will become less
sensitive.
result in noncompliance with pharmacotherapy. Other common adverse effects of SSRIs include weight
gain, nausea, headache, anxiety, and insomnia.
Serotonin syndrome (SES) is an adverse event that may occur when a patient is taking an SSRI
and an additional medication that affects the metabolism, synthesis, or reuptake of serotonin. The re-
sult is that serotonin accumulates in the body. Symptoms can begin as early as two hours or as late as
several weeks after taking the first dose. SES can be produced by the administration of an SSRI with
an MAOI, a TCA, lithium, or a number of other medications. Symptoms of SES include mental sta-
tus changes (confusion, anxiety, and restlessness), hypertension, tremors, sweating, fever, and lack of
muscular coordination. Conservative treatment is to discontinue the SSRI and provide supportive care.
In severe cases, mechanical ventilation and muscle relaxants may be necessary. If left untreated, death
may occur.
In terms of classification, the atypical antidepressants do not fit conveniently into the other antidepressant a 5 not
drug classes. Thus, “atypical” in this case really refers to the unique chemical structures represented in the typical 5 characteristic
group.
Duloxetine (Cymbalta) and venlafaxine (Effexor), sometimes considered to be in their own sub-
group, are the serotonin–norepinephrine reuptake inhibitors (SNRIs). They specifically inhibit the
reabsorption of serotonin and norepinephrine and elevate mood by increasing the levels of these neu-
rotransmitters in the CNS. In many cases, levels of dopamine are also affected with the SNRIs. In addi-
tion to being approved for the treatment of major depression, duloxetine (Cymbalta) is also approved for
the treatment of generalized anxiety disorder and for neuropathic pain characteristic of fibromyalgia and
diabetic neuropathy. Venlafaxine (Effexor), approved to treat depression and generalized anxiety disor-
der, is available in an intermediate-release form that requires two or three doses a day and an extended-re-
lease (XR) form that allows the patient to take the medication just once a day. Bupropion (Wellbutrin) not
only inhibits the reuptake of serotonin but may also affect the activity of norepinephrine and dopamine.
It should be used with caution in patients with seizure disorders because it lowers the seizure threshold.
Bupropion is marketed as Zyban for use in cessation of smoking. Mirtazapine (Remeron) is used for
depression and blocks presynaptic serotonin and norepinephrine receptors, thereby enhancing release of
these neurotransmitters. Nefazodone is similar to Remeron. It was originally designed to treat depression,
and causes minimal cardiovascular effects, fewer anticholinergic effects, less sedation, and less sexual
dysfunction than the other antidepressants. Trazodone (Oleptro) is often used as a sleep aid, rather than as
an antidepressant. The high levels of trazodone needed for the improvement of depression causes sedation
in many patients.
Drug Prototype: Imipramine (Tofranil)

Therapeutic Class: Antidepressant, treatment of nocturnal enuresis (bed-wetting) in children
Pharmacologic Class: Tricyclic antidepressant (TCA), serotonin and norepinephrine reuptake inhibitor (SNRI)
Actions and Uses: Imipramine blocks the reuptake of serotonin may decrease its antihypertensive effects and increase risk for
and norepinephrine into nerve terminals. It is mainly used for CNS depression. Use of oral contraceptives may increase or de-
major depressive disorder, although it is occasionally used for crease imipramine levels. Disulfiram may lead to delirium and
the treatment of nocturnal enuresis in children. The nurse may tachycardia.
find imipramine prescribed for a number of off-label uses, in- Imipramine should be used with caution with herbal sup-
cluding intractable pain, anxiety disorders, and withdrawal syn- plements, such as evening primrose oil or ginkgo biloba, which
dromes from alcohol and cocaine. may lower the seizure threshold. St. John’s wort used with imip-
ramine may cause serotonin syndrome.
Adverse Effects and Interactions: Adverse effects include seda-
tion, drowsiness, blurred vision, dry mouth, and cardiovascular
symptoms such as dysrhythmias, heart block, and extreme
hypertension. Agents that mimic the action of norepinephrine Black Box Warning:
or serotonin should be avoided because imipramine inhibits Antidepressants can increase the risk of suicidal thinking
their metabolism and may produce toxicity. Some patients and behavior, especially in children, adolescents, and young
may experience photosensitivity. Concurrent use of other CNS adults with major depressive disorder and other psychiatric
depressants, including alcohol, may cause sedation. Cimetidine disorders. This drug is not approved for use in pediatric
(Tagamet) may inhibit the metabolism of imipramine, lead- patients.
ing to increased serum levels and possible toxicity. Clonidine
Nursing Process Focus Patients Receiving Antidepressant Therapy
Prior to drug administration: ■ Ineffective Coping related to inadequate level of confidence in ability
■ Obtain a complete health history including cardiovascular, thyroid, to cope
renal and liver conditions, allergies, drug history, likelihood of drug ■ Risk for Injury related to adverse effects of medications and depressive
dependency, and possible drug interactions. state
■ Evaluate laboratory blood findings: CBC, chemistry, clotting factors, ■ Deficient Knowledge related to a lack of information about drug
glucose, renal and liver function studies. therapy
■ Determine neurologic status, including history of mental previous dis- ■ Noncompliance related to length of time before medication reaches
orders, seizure activity, level of consciousness (LOC), and identification therapeutic levels and adverse effects of drug therapy
of recent mood and behavior patterns. ■ Urinary Retention related to adverse anticholinergic effects of drug
■ Identify factors that may have precipitated the depressive episode and
actions that have been previously tried to decrease symptoms.
The patient will:

■ Experience therapeutic effects (mood elevation and effectively engage in activities of daily living).
Implementation
Interventions and (Rationales) Patient Teaching/Discharge Planning

■ Administer medication correctly and evaluate patient’s knowledge of Instruct the patient to:
proper administration. (Proper administration helps to increase effec- ■ Take exactly as prescribed and use the same manufacturer’s brand,
tiveness of drugs and prevent severe adverse effects). if possible.
■ Take a missed dose as soon as it is noticed but do not take double or
extra doses to catch up.
■ Take with food to decrease GI upset.
■ Not abruptly discontinue taking medication.
■ Practice reliable contraception and notify healthcare provider if preg-
nancy is planned or suspected.
■ Monitor vital signs, especially pulse and blood pressure. Notify health- Instruct the patient to:
care provider if pulse or BP drop below approved parameters. (Tricyclic ■ Report any change in sensorium, particularly impending syncope.
antidepressants may cause orthostatic hypotension.) ■ Avoid abrupt changes in position.
■ Monitor vital signs (especially blood pressure), ensuring proper use of
home equipment.
■ Consult the healthcare provider regarding “reportable” blood pressure
readings (e.g., lower than 80/50 mmHg).
■ Observe for serotonin syndrome in SSRI use: confusion, anxiety, rest- Inform the patient:
lessness, hypertension, tremors, diaphoresis, fever, lack of muscular co- ■ That overdosage may result in serotonin syndrome, which can be life
ordination, and possibly death (usually occurs with concurrent use of threatening.
St. John’s wort or MAOIs). If suspected, discontinue the drug and initi- ■ To seek immediate medical attention for dizziness, headache, tremor,
ate supportive care. Respond according to intensive care unit (ICU)/ nausea/vomiting, anxiety, disorientation, lack of muscle coordination,
emergency department protocols. sweating, and fever.
■ To seek medical attention if an increase in sweating is associated with
nausea, vomiting, or chest pain.
■ Monitor cardiovascular status. Observe for hypertension and signs ■ Instruct the patient to immediately report severe headache, dizziness,
of impending stroke or MI and heart failure (CV symptoms may paresthesias, bradycardia, chest pain, tachycardia, nausea/vomiting, or
be a result of the sympathomimetic effects of MAOI and tricyclic diaphoresis.
antidepressants).
■ Monitor neurologic status. Observe for somnolence and seizures. Instruct the patient to:
(Tricyclic antidepressants may cause somnolence related to CNS depres- ■ Report any significant changes in neurologic status, such as seizures,
sion and may reduce the seizure threshold.) extreme lethargy, slurred speech, disorientation, or ataxia to the
healthcare provider, and to discontinue the drug.
■ Take the dose at bedtime to avoid daytime sedation.
■ Monitor mental and emotional status. Observe for suicidal ideation. Instruct the patient:
(Therapeutic benefits may be delayed. Outpatients should have no ■ To immediately report dysphoria or suicidal impulses
more than a seven-day medication supply.) Also monitor for underly- ■ To commit to a “no-self harm” verbal contract
ing or concomitant psychoses such as schizophrenia or bipolar disor- ■ That it may take a couple of weeks before improvement is noticed,
ders (may trigger manic states). and about one month to achieve full therapeutic effect
continued . . .
■ Monitor sleep–wake cycle. Observe for insomnia and/or daytime som- Instruct the patient to:
nolence. (Sleep disturbances can be an effect of disease processes or ■ Take the drug very early in the morning to promote normal timing of
use of certain antidepressants such as MAOIs.) sleep onset.
■ Avoid driving or potentially hazardous activities until the effects of the
drug are known.
■ Take at bedtime if daytime drowsiness persists.
■ Take in the morning if insomnia persists.
■ Monitor renal status and urinary output. (Medications may cause Instruct the patient to:
urinary retention due to muscle relaxation in the urinary tract. Imipra- ■ Monitor fluid intake and output.
mine is excreted through the kidneys. Fluoxetine is slowly metabolized ■ Notify the healthcare provider of edema, dysuria (hesitancy, pain,
and excreted, increasing the risk of organ damage.) diminished stream), changes in urine quantity or quality (e.g., cloudy,
with sediment).
■ Report fever or flank pain that may be indicative of a urinary tract in-
fection related to urine retention.
■ Use cautiously with elderly or young patients. (Diminished kidney and Instruct the patient that:
liver function related to aging can result in higher serum drug levels ■ Elderly patients may be more prone to adverse effects such as hyper-
and may require lower doses. Children, due to an immature CNS, re- tension and dysrhythmias.
spond paradoxically to CNS-active drugs.) ■ Children on imipramine for nocturnal enuresis may experience mood
alterations.
■ Monitor gastrointestinal status. Observe for abdominal distention. Instruct the patient to:
(Muscarinic blockade reduces tone and motility of intestinal smooth ■ Exercise, drink adequate amounts of fluids, and add dietary fiber to
muscle and may cause paralytic ileus.) promote stool passage.
■ Consult the healthcare provider regarding a bulk laxative or stool soft-
ener if constipation becomes a problem.
■ Continue to monitor laboratory studies, including CBC, clotting fac- Instruct the patient to:
tors, and liver enzymes. Observe for signs and symptoms of liver ■ Report nausea, vomiting, diarrhea, rash, jaundice, epigastric or ab-
toxicity. (Some antidressants may cause liver toxicity or cause gastro- dominal pain, tenderness, or change in color of stool to the healthcare
intestinal bleeding. Antidepressants need to be used cautiously with provider.
patients with a history of liver disease.) ■ Adhere to laboratory testing regimen for blood tests and urinalysis as
directed.
■ Observe for signs of bleeding. (Imipramine may cause blood dyscrasias. ■ Instruct the patient to report excessive bruising, fatigue, pallor, short-
Use with warfarin may increase bleeding time.) ness of breath, frank bleeding, and/or tarry stools to the healthcare
provider.
■ Conduct guaiac testing on stool for occult blood.
■ Monitor for signs of dehydration. (Dehydration may cause lithium ■ Inform the patient about the importance of staying well hydrated.
toxicity.) ■ Instruct the patient to report any nausea, emesis, diarrhea, weakness,
lack of muscle coordination, confusion, lethargy, polyuria, or seizures
(signs of lithium toxicity) to the healthcare provider.
■ Monitor immune/metabolic status. Use with caution in patients with Instruct the patient:
diabetes mellitus or hyperthyroidism. (If given in hyperthyroidism, ■ With diabetes to monitor glucose level daily and to consult the nurse
this drug can cause agranulocytosis. Imipramine may either increase regarding reportable serum glucose levels.
or decrease serum glucose. Fluoxetine may cause initial anorexia and ■ To monitor weight. Possible anorexia and weight loss will diminish
weight loss, but prolonged therapy may result in weight gain of up to with continued therapy.
20 pounds.)
■ Observe for extrapyramidal and anticholinergic effects. In overdosage, Instruct the patient to:
12 hours of anticholinergic activity is followed by CNS depression. Do ■ Immediately report any involuntary muscle movement of the face or
not treat overdosage with quinidine, procainamide, atropine, or bar- upper body (e.g., tongue spasms), fever, anuria, lower abdominal pain,
biturates. (Quinidine and procainamide can increase the possibility of anxiety, hallucinations, psychomotor agitation, visual changes, dry
dysrhythmia; atropine can lead to severe anticholinergic effects; and mouth, and difficulty swallowing to the healthcare provider.
barbiturates can lead to excess sedation.) ■ Relieve dry mouth with (sugar-free) hard candies, by chewing gum,
and by drinking fluids.
■ Avoid alcohol-containing mouthwashes, which can further dry oral
mucous membranes.
■ Monitor visual acuity. Use with caution in narrow-angle glaucoma. Instruct the patient to:
(Imipramine may cause an increase in intraocular pressure. Anticholin- ■ Report any visual changes, headache, or eye pain to the healthcare
ergic effects may produce blurred vision.) provider.
■ Inform an eye care professional of imipramine therapy.
■ Ensure patient safety. (Dizziness caused by postural hypotension in- Instruct the patient to:
creases the risk of fall injuries.) ■ Call for assistance before getting out of bed or attempting to ambu-
late alone.
■ Avoid driving or performing hazardous activities until blood pressure is
stabilized and effects of the drug are known.

Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Table 10.2 for
a list of drugs to which these nursing actions apply.
Monoamine Oxidase Inhibitors

As discussed, the action of norepinephrine at adrenergic synapses is terminated through two means:
(1) reuptake into the presynaptic nerve and (2) enzymatic destruction by the enzyme MAO. By de-
creasing the effectiveness of the enzyme MAO, monoamine oxidase inhibitors (MAOIs) limit the
breakdown of norepinephrine, dopamine, and serotonin in the CNS. This creates higher levels of these
neurotransmitters in the brain to facilitate neurotransmission and to alleviate the symptoms of depres-
sion (Figure 10.3 ■),
In the 1950s, the MAOIs were the first drugs approved to treat depression. They are just as effective
as the TCAs and SSRIs in treating depression. However, because of drug–drug and food–drug interactions,
hepatotoxicity, and the development of safer antidepressants, MAOIs are now reserved for patients who
are not responsive to the other antidepressant classes.
Common adverse effects of the MAOIs include orthostatic hypotension, headache, insomnia, and di-
arrhea. A primary concern is that these agents interact with a large number of foods and other medications,
sometimes with serious effects. A hypertensive crisis can occur when a MAOI is used together with other
antidepressants or sympathomimetic drugs. Combining an MAOI with an SSRI can produce SES. If given
with antihypertensives, the patient can experience excessive hypotension. MAOIs also increase the hypo-
glycemic effects of insulin and oral antidiabetic drugs. Extreme fever is known to occur in patients taking
MAOIs with meperidine (Demerol), dextromethorphan (Pedia Care and others), and TCAs.
A hypertensive crisis can also result from an interaction between MAOIs and foods containing tyra-
mine, a form of the amino acid tyrosine. In fact, tyrosine is a precursor to norepinephrine in the nervous
system. In many respects, tyramine resembles norepinephrine. Tyramine is usually degraded by MAO in
the intestines. If a patient is taking MAOIs, however, tyramine enters the bloodstream in high amounts and
displaces norepinephrine in presynaptic nerve terminals. The result is a sudden increase in norepinephrine,
causing acute hypertension. Symptoms usually occur within minutes of ingesting the food and include
occipital headache, stiff neck, flushing, palpitations, profuse sweating, and nausea. Calcium channel block-
ers may be given as an antidote to reduce blood pressure. Examples of foods containing tyramine include
pre = before smoked or pickled meats, most cheeses, yogurt, soy sauce, yeast, avocados, chocolate, pineapple and alco-
menstrual = menstruation holic beverages.
Figure 10.3
MAOIs inhibit
monoamine oxidase, Normal:
an enzyme that
stops the actions of 1 NE is released.
neurotransmitters 2 NE binds with its receptor.
such as dopamine,
norepinephrine, and 3 The action of NE is terminated
serotonin. Dopamine, by MAO and COMT.
Norepinephrine When MAOIs are administered:
(NE), and Serotonin
4 If MAO is inhibited, NE is not
1 broken down as quickly and
4 produces a more dramatic effect.
MAO
NE
3
2
COMT
Postsynaptic
adrenergic
neuron
MAO = Monoamine oxidase

COMT = Catecholamine
O-methyl transferase
Drug Prototype: sertraline (Zoloft)

Therapeutic Class: Antidepressant Pharmacologic Class: Selective serotonin reuptake inhibitor (SSRI)
Actions and Uses: Sertraline is used for the treatment of depres- due to risk of toxicity and increased blood concentrations lead-
sion, anxiety, obsessive–compulsive disorder, and panic. The ing to increased bleeding. MAOIs may cause neuroleptic malig-
antidepressant and anxiolytic properties of this drug can be at- nant syndrome, extreme hypertension, and serotonin syndrome,
tributed to its ability to inhibit the reuptake of serotonin in the characterized by headache, agitation, dizziness, fever, diarrhea,
brain. Other uses include premenstrual dysphoric disorder, post- sweating, and shivering. Use cautiously with other centrally act-
traumatic stress disorder, and social anxiety disorder. Therapeu- ing drugs to avoid adverse CNS effects. Patients should use cau-
tic actions include enhancement of mood and improvement of tion if taking St. John’s wort or L-tryptophan to avoid serotonin
affect with maximum effects observed after several weeks. syndrome.
Adverse Effects and Interactions: Adverse effects include agita-

tion, insomnia, headache, dizziness, somnolence, and fatigue.
Take extreme precautions in patients with cardiac disease, he- Black Box Warning:
patic impairment, seizure disorders, suicidal ideation, mania, or Antidepressants can increase the risk of suicidal thinking
hypomania. Concomitant use of sertraline and MAOIs or primo- and behavior, especially in children, adolescents, and young
zide is not advised. Antabuse should be avoided because of the adults with major depressive disorder and other psychiatric
alcohol content of the drug concentrate. Highly protein-bound disorders.
medications such as digoxin and warfarin should be avoided
Concept Review 10.2

■ Name the major classes of antidepressants. Name representative drugs within each class,
and describe how each drug works pharmacologically.
Drug Prototype: Phenelzine (Nardil)

Therapeutic Class: Antidepressant Pharmacologic Class: Monoamine oxidase inhibitor (MAOI)
Actions and Uses: Phenelzine produces its effects by irrevers- SSRIs should be avoided, because the combination can cause
ible inhibition of MAO; therefore, it intensifies the effects of temperature elevation and seizures. Opiates, including meperi-
norepinephrine in adrenergic synapses. It is used to manage dine, should be avoided due to increased risk of respiratory fail-
symptoms of depression not responsive to other types of phar- ure or hypertensive crisis.
macotherapy, and it is occasionally used for panic disorder. Drug Phenelzine should be used with caution with herbal sup-
effects may continue for two to three weeks after therapy is plements such as ginseng, which could cause headache, tremors,
discontinued. mania, insomnia, irritability, and visual hallucinations. Concur-
rent use of ephedra could cause hypertensive crisis.
Adverse Effects and Interactions: Common adverse effects are
constipation, dry mouth, orthostatic hypotension, insomnia,
nausea, and loss of appetite. It may increase heart rate and neu- Black Box Warning:
ral activity, leading to delirium, mania, anxiety, and convulsions. Antidepressants can increase the risk of suicidal thinking
Severe hypertension may occur when ingesting foods contain- and behavior, especially in children, adolescents, and young
ing tyramine. Seizures, respiratory depression, circulatory col- adults with major depressive disorder and other psychiatric
lapse, and coma may occur in cases of severe overdose. Many disorders.
other drugs affect the action of phenelzine. Use with TCAs and
Bipolar Disorder
Bipolar disorder is characterized by extreme and opposite moods. Patients may display signs of euphoria bi 5 two
and depression or feelings of excitement and calm. polar 5 extremes
Patients with bipolar disorder may experience emotions ranging from

Core Concept 10.4 depression to extreme agitation.
Once known as manic depression, bipolar disorder is characterized by extreme and opposite moods, such
as euphoria and depression. Although the moods of patients may shift between extremes, usually patients
will remain in one state for awhile, or they may remain in a normal state for prolonged times.
dys 5 difficulty (as in illness) Depressed and slightly depressed or dysphoric signs and symptoms are the same as those described
phoric 5 bearing earlier in this chapter. Patients with bipolar disorder also display signs of mania, an emotional state charac-
mania 5 excessively intense or terized by high psychomotor activity and irritability. Symptoms of mania are shown in the following list;
excited mood these are generally the opposite of depressive symptoms.
■ Insomnia
■ Activity for days without rest and without appearing tired
■ Easy agitation and aggression
■ Feelings of exaggerated confidence
■ Making choices without regard for a long-term plan or consequences of action
■ Attention seeking
■ Unusual interest in sex
■ Drug abuse, including alcohol, cocaine, or sleeping medications
■ Denial that the behavior is a problem
Concept Review 10.3

■ Identify the symptoms of mania. How do manic symptoms generally compare with
depressive symptoms?
Mood stabilization in patients with bipolar disorder is accomplished with

Core Concept 10.5 lithium and other drugs.
Drugs for bipolar disorder are called mood stabilizers because they have the ability to moderate extreme
anti 5 against shifts in emotions between mania and depression. Currently, lithium, antiseizure drugs, and atypical anti-
psychotic 5 psychosis, psychotic drugs are the choices used for mood stabilization in patients with bipolar disorder. Table 10.3 ◆
mental state lists selected drugs used to treat bipolar disorder.
seizure 5 to take hold For years, the traditional treatment of bipolar disorder has been lithium (Eskalith), which was
used as monotherapy or in combination with other drugs. Lithium was approved in the United States
in 1970. With lithium, serum levels must be checked every one to three days when beginning therapy,
and every two to three months thereafter. To ensure therapeutic action, concentrations of lithium in the
blood must remain within the range of 0.6 to 1.5 mEq/L. Close monitoring encourages compliance and
helps to avoid toxicity. Lithium is taken as a salt, so it mixes in the bloodstream like sodium chloride.
CAM TherapY
St. John’s Wort for Depression
One of the most popular herbs in the United States, St. John’s wort (Hypericum perforatum)
grows throughout Asia, Europe, and North America. Its modern use is as an antidepressant. It
gets its name from a legend that red spots once appeared on its leaves on the anniversary of
the beheading of St. John the Baptist. The word wort is a British term for “plant.”
Research suggests that substances found in St. John’s wort selectively inhibit serotonin
reuptake in certain brain neurons. A number of clinical studies suggest that St. John’s wort is
an effective treatment for mild to moderate depression, and that it may be just as effective
as TCAs and SSRIs. Recent analyses also suggest that the herb may be effective for major
depression and that it causes fewer adverse effects than traditional drugs. St. John’s wort
may interact with many medications, including oral contraceptives, warfarin, digoxin, and
cyclosporine. It should not be taken concurrently with antidepressant medications.
St. John’s wort is well tolerated, producing mild adverse effects such as gastrointestinal (GI)
distress, fatigue, and allergic skin reactions. The herb contains compounds that photosensitize
the skin; thus patients should be advised to apply sunscreen or to wear protective clothing
when outdoors.
Table 10.3 Drugs for Bipolar Disorder: Mood Stabilizers

lithium (Eskalith) PO; initial 600 mg tid, maintenance 300 mg tid For treatment of mania and depressive symptoms; must be
(max: 2.4 g/day) used cautiously in epilepsy and in psychosis
Antiseizure Drugs
carbamazepine (Tegretol) PO; 200 mg bid, gradually increased to For treatment of manic depressive and schizoaffective symp-
800–1200 mg/day in three to four divided doses toms; used as antiseizure medication
lamotrigine (Lamictal) PO; 50 mg/day for 2 weeks, then 50 mg bid for Used as antiseizure medication; fatal rash has been reported
2 weeks; may increase gradually up to 300–500 in children less than 16 years old
mg/day in two divided doses (max: 700 mg/day)
valproate/valproic acid PO; 250 mg tid (max: 60 mg/kg/day) For treatment of mania and prevention of migraine headache;
(Depakene, Depakote) (see used as antiseizure medication
page 191 for the Drug
Prototype box)
Atypical antipsychotic drugs
aripiprazole (Abilify) PO; 10–15 mg/day (max: 30 mg/day) For add-on treatment in adults with major depression; for ma-
nia or mixed episodes of bipolar disorder; for schizophrenia;
for irritability associated with autistic disorder in pediatric
patients
asenapine (Saphris) Adult: 10 mg sublingually twice daily (mono- For the acute treatment of mania or mixed episodes associ-
therapy); 5 mg sublingually twice daily (adjunct ated with bipolar disorder in adults; taken alone or with a
to lithium or valproic acid therapy) mood stabilizer (lithium or valproate)
olanzapine (Zyprexa) Adult: PO; start with 5–10 mg/day; may increase For schizophrenia and manic episodes of bipolar disorder
by 2.5–5 mg every week (range 10–15 mg/day;
max: 20 mg/day). Geriatric: PO; start with
5 mg/day
quetiapine (Seroquel) PO; start with 25 mg bid; may increase to a tar- Approved as a once-daily monotherapy for the acute treat-
get dose of 300–400 mg/day in divided doses ment of the depressive episodes associated with bipolar
disorder
risperidone (Risperdal) (see PO; 1–6 mg bid; increase by 2 mg daily to an For symptoms of schizophrenia; for episodes of mania or
page 152 for the Drug Proto- initial target dose of 6 mg/day mixed episodes of bipolar disorder; for behavior problems
type box) such as aggression, self-injury, and sudden mood changes in
teenagers and children with autism
ziprasidone (Geodon) PO; 20 mg bid (max: 80 mg bid) For acute mania or mixed episodes associated with bipolar
disorder; for maintenance treatment of bipolar disorder when
added to lithium or valproate; for schizophrenia
Therefore, conditions in which sodium is lost (e.g., excessive sweating or increased urination which leads
to dehydration) can cause the kidneys to reabsorb the lithium salts back into the blood, producing elevated
serum levels of lithium known as lithium toxicity. Lithium overdose may be treated with hemodialysis
and supportive care.
For the most complete control of bipolar disorder, it is not unusual for other drugs to be used in com-
bination with lithium. During the depressed stage, a TCA or an atypical antidepressant such as bupropion
(Wellbutrin) may be necessary. During manic phases, a benzodiazepine will moderate manic symptoms
(see Chapter 9). In cases of extreme agitation, delusions, or hallucinations, antipsychotic drugs may be
indicated (see Chapter 11). Continued patient compliance is essential to achieving successful pharmaco-
therapy because some patients do not perceive their condition as abnormal.
Today, antiseizure drugs (see Chapter 13) and atypical antipsychotic drugs (see Chapter 11) have
emerged as probably the most effective agents for mood stabilization. For example, valproic acid (De-
pakene, Depakote), carbamazepine (Tegretol), and lamotrigine (Lamictal) are the antiseizure drugs most
often used in the treatment of rapidly cycling and mixed states of bipolar disorder. Several atypical anti-
psychotics are very effective for the treatment of extreme mania. Important antipsychotic drugs for bipolar
disorder are aripiprazole (Abilify), asenapine (Saphris), olanzapine (Zyprexa), quetiapine (Seroquel), ris-
peridone (Risperdal), and ziprasidone (Geodon). Longer term stabilization of extreme and unusual behav-
iors with atypical antipsychotics is covered in Chapter 11. Lithium has remained effective for purely manic
or purely depressive states.
Concept Review 10.4

■ Give the general name of drugs used to treat bipolar disorder. What has been the main
drug used to treat bipolar disorder, and how does it work pharmacologically? What other
drugs treat bipolar disorder?
Attention DeficiT Hyperactivity disorder
A condition characterized by poor attention span, behavior control issues, and/or hyperactivity is called at-
tention deficit hyperactivity disorder (ADHD). Although the condition has most often been diagnosed in
childhood, symptoms of ADHD may extend into adulthood, and an increasing number of adults are being
evaluated for ADHD.
Attention deficit hyperactivity disorder presents challenges for children

Core Concept 10.6 and adults.
ADHD is characterized by developmentally inappropriate behaviors involving difficulty in paying attention

or focusing on tasks. ADHD may be diagnosed when a child’s hyperactive behaviors significantly interfere
with normal play, sleep, or learning activities. Hyperactive children usually have increased motor activity
shown by a tendency to be fidgety and impulsive and to interrupt and talk excessively during their devel-
opmental years; therefore, they may not be able to interact with others appropriately at home or school. In
boys, the activity levels are usually more overt. Girls show less aggression and impulsiveness but may show
more anxiety, mood swings, social withdrawal, and cognitive and language delays. Girls also tend to be
older at the time of diagnosis, so problems and setbacks related to the disorder exist for a longer time before
treatment interventions are undertaken. Symptoms of ADHD are shown in the following list:
■ Easy distractability
■ Failure to receive or follow instructions properly
■ Inability to focus on one task at a time and tendency to jump from one activity to another
■ Difficulty remembering
■ Frequent loss or misplacing of personal items
■ Excessive talking and interrupting other children in a group
■ Inability to sit still when asked repeatedly
■ Impulsiveness
■ Sleep disturbances
Most children with ADHD have associated challenges. Many find it difficult to concentrate on tasks
assigned in school. Even if they are gifted, their grades may suffer because they have difficulty following a
conventional routine; discipline may also be a problem. Teachers are often the first to suggest that a child
should be examined for ADHD and receive medication when behaviors in the classroom escalate to the
point of interfering with learning. A diagnosis is based on psychological and medical evaluations.
Fast Facts ADHD

■ ADHD is the major reason why children are referred for mental health treatment.
■ About 50% of children are also diagnosed with oppositional defiant or conduct disorder.
■ Anxiety disorder is diagnosed in 25% of children.
■ About one-third are also diagnosed with depression.
■ Learning disabilities are present in about 20% of children.
The cause of ADHD is not clear. Evidence suggests that hyperactivity may be related to a deficit or
dysfunction of dopamine, norepinephrine, and serotonin in the reticular activating system of the brain (see
Chapter 9). ADHD was once thought to be caused by sugar, chocolate, high-carbohydrate foods and bever-
ages, and certain food additives, but these have been disproved as causing or aggravating ADHD.
One-third to one-half of children diagnosed with ADHD also experience symptoms of attention dys-
function in their adult years. Symptoms of attention deficit disorder (ADD) in adults appear similar to Life Span Fact
those of mood disorders and include anxiety, mania, restlessness, and depression, which can also cause ADHD affects as many as 5%
difficulties in interpersonal relationships. Attention dysfunction in adults is often linked with poor self- of all children. Most children
esteem, diminished social success, and introverted behaviors. Patients may have mood swings similar to diagnosed with this condition
bipolar disorder. are between the ages of three
and seven years, and boys are
four to eight times more likely
to be diagnosed than girls.
Central nervous system (CNS) stimulants have been the main course of
treatment for ADHD. Core Concept 10.7
Traditional therapies for ADHD include CNS stimulants. Newer therapies have added non-CNS stimulants.
CNS Stimulants
These drugs stimulate specific areas of the CNS that heighten alertness and increase focus. In 2002, a non-
CNS stimulant was first approved to treat ADHD. Agents for treating ADHD are listed in Table 10.4 ◆.
Stimulants reverse many of the symptoms and help patients to focus on tasks. The most widely
prescribed drug for ADHD is methylphenidate (Ritalin). Other less prescribed CNS stimulants include
d- and 1-amphetamine racemic mixtures (Adderall), dextroamphetamine (Dexedrine), or methamphet-
amine (Desoxyn). More recently, extended release forms have been made available: dextroamphetamine
mixture (Adderall XR), dexmethylphenidate (Focalin XR), and slow-releasing methylphenidate (Ritalin,
LA/SR). Lisdexamfetamine (Vyvanse) is a psychostimulant prodrug of phenethylamine and amphetamine.
It is a once-daily prescription medication thought to help increase attention and decrease impulsiveness and
hyperactivity in patients with ADHD.
Patients taking CNS stimulants must be carefully monitored because the drugs may cause paradoxical
hyperactivity. Adverse reactions include insomnia, nervousness, anorexia, and weight loss. Occasionally,
a patient may suffer from dizziness, depression, irritability, nausea, or abdominal pain. These drugs are
Schedule II controlled substances and pregnancy category C.
Non-CNS Stimulants
Non-CNS stimulants are now approved for treatment of ADHD. This is an advantage because they have no
abuse potential. A fairly recent addition (2002) to the treatment of ADHD in children and adults is atomox-
etine (Strattera). Although its exact mechanism is not known, it is classified as a norepinephrine reuptake
inhibitor. Efficacy appears to be equivalent to methylphenidate (Ritalin). Patients on atomoxetine have
demonstrated an improved ability to focus on tasks and reduced hyperactivity. Common adverse effects in-
clude headache, insomnia, upper abdominal pain, decreased appetite, and cough. Unlike methylphenidate,
Drug Prototype: Methylphenidate (Ritalin)

Therapeutic Class: Drug for attention deficit hyperactivity disorder, narcolepsy drug
Pharmacologic Class: Central nervous system stimulant, norepinephrine and dopamine releasing agent
Actions and Uses: Methylphenidate activates the reticular acti- Methylphenidate interacts with many drugs. For example,
vating system, causing heightened alertness in various regions it may decrease the effectiveness of anticonvulsants, antico-
of the brain, particularly those centers associated with focus agulants, and guanethidine. Use with clonidine may increase
and attention. Activation is partially achieved by the release adverse effects. Antihypertensives or other CNS stimulants could
of neurotransmitters such as norepinephrine, dopamine, and increase the vasoconstrictive action of methylphenidate. MAOIs
serotonin. Impulsiveness, hyperactivity, and disruptive behavior may produce hypertensive crisis.
are usually reduced within a few weeks. These changes promote
improved psychosocial interactions and academic performance.
Adverse Effects and Interactions: In a patient with no ADHD,

methylphenidate causes nervousness and insomnia. All patients Black Box Warning:
are at risk for irregular heartbeat, high blood pressure, and liver Methylphenidate is a Schedule II drug with high abuse po-
toxicity. Methylphenidate is a Schedule II drug, indicating its potential. Administration for longer periods of time may lead to
tential to cause dependence when used for extended periods. drug dependence. Misuse may cause sudden death or a seri-
Periodic drug-free “holidays” are recommended to reduce drug ous cardiovascular adverse event.
dependence and to assess the patient’s condition.
Table 10.4 Drugs for Attention Deficit–Hyperactivity Disorder

CNS Stimulants
amphetamine (Adderall, 3–5 years old: PO; 2.5 mg one to two times/day, may increase by May be used for daytime sleep disorder (narco-
Adderall-XR) 2.5 mg at weekly intervals lepsy); high potential for abuse
6 years old: PO; 5 mg daily to bid, may increase by 5 mg at
weekly intervals (max: 40 mg/day);
Adult: 10 mg extended release, once daily (max: 30 mg/day)
dexmethylphenidate 6 years old to adult: PO; 2.5 mg bid, may increase by 2.5–5 mg/ Mild stimulant to the central nervous system;
(Focalin, Focalin-XR) week (max: 20 mg/day); 5 mg/day extended release may increase used to treat ADHD
by 5 mg/week
dextroamphetamine 3–5 years old: PO; 2.5 mg daily to bid, may increase by 2.5 mg at Potent appetite suppressant; should only be
(Dexedrine) weekly intervals; used for short-term treatment of ADHD; safety
6 years old: PO; 5 mg daily to bid, increase by 5 mg at weekly in children less than 3 years old has not been
intervals (max: 40 mg/day) established
lisdexamfetamine 6 years old to adult: PO: 20–70 mg once daily in a.m. (max: 70 Once-daily prescription medication for chil-
(Vyvanse) mg/day); doses vary depending on age dren, teens, and adults with ADHD; prodrug of
dextroamphetamine
methamphetamine 6 years old: PO; 2.5–5 mg daily to bid, may increase by 5 mg at Abuse potential high in adults
(Desoxyn) weekly intervals (max: 20–25 mg/day)
methylphenidate 6 years old: PO; 5–10 mg before breakfast and lunch, with grad- Most widely used drug for patients with ADHD;
(Concerta, Daytrana, ual increase of 5–10 mg/week as needed (max: 60 mg/day) more dramatic effect on attention deficit than
Metadate, Methylin, Adult: PO; 5–20 mg (prompt-release tablets) two to three times for hyperactivity; may be used for daytime sleep
Ritalin, Quillivant XR) daily; may switch to extended release once the maintenance dose disorder (narcolepsy); once-daily extended release
is determined; doses will vary depending on drug formulation liquid form available
Nonstimulants
atomoxetine (Strattera) Children less than 70 kg: PO; start with 0.5 mg/kg/day; may Inhibits reuptake of norepinephrine; safety and
increase after 3 days to target dose of 1.2 mg/kg/day (max dose: efficacy in children less than 6 years old has not
1.4 mg/kg/day or 100 mg) been established
Adult: PO; start with 40 mg in a.m., may increase after 3 days
to target dose of 80 mg/day given either once in the morning,
divided morning, or late afternoon/early evening; may increase to
max of 100 mg/day if needed
clonidine (Kapvay) 6 years old to 17 years old: PO; Start with 0.1 mg/day and gradu- Sometimes prescribed when patients are ex-
ally increase to desired response (max: 0.4 mg/day) tremely aggressive, active, or have difficulty
sleeping; stimulates alpha2-receptors in the brain;
once-daily dosing provided; intermediate-releas-
ing form and extended-release form available
guanfacine (Intuniv) 6 years old to 17 years old: PO; Start with 1 mg/day and gradu- Treats high blood pressure; also used alone or
ally increase to desired response (max: 4 mg/day) together with other medicines to treat attention
deficit hyperactivity disorder (ADHD)
it is not a scheduled drug; thus, parents who are hesitant to place their child on stimulants have a reasonable
alternative.
Clonidine (Kapvay) is sometimes prescribed when patients are extremely aggressive or active
or have difficulty falling asleep. Clonidine improves clinical symptoms of ADHD and is a cen-
trally acting alpha 2-adrenergic drug. The extended release tablet offers the advantage of once-daily
dosing. Blood pressure should be monitored during therapy due to hypotensive effects caused by
clonidine.
Guanfacine (Intuniv) was approved in 2011, for use in combination therapy with stimulants. Because
the drug is a known antihypertensive, blood pressure should always be monitored during therapy. Sedation
is common especially at the initiation of drug therapy.
Concept Review 10.5

■ What are the symptoms experienced by patients with ADHD? Which drug is most often
used in the treatment of these symptoms? What are the common symptoms experienced
by adults with ADD?

Patients taking antidepressants need to know the following:
In General
1. Avoid driving or operating machinery until response to the medication is known. Its
sedating effects can increase the risk for accidental injury.
2. Do not stop taking the medication without consulting your healthcare provider.
3. Antidepressants may take one to four weeks to become fully effective.
Regarding Tricyclics
4.
Tricyclics may increase appetite, cause dizziness upon rapid change of position, and be
sedating. Report dry mouth, constipation, urinary retention, increase in heart rate and
palpitations, or blurred vision if they occur.
5. Avoid the use of alcohol; it increases sedative effects.
Regarding MAOIs
6. MAOIs may cause problems with sleep, agitation, dizziness when rapidly changing po-
sition, and dangerous interactions with other medications. Eating foods high in tyra-
mine can cause a hypertensive crisis. Such foods include aged cheeses, wine, luncheon
meats, and sausages.
7. Report any of the following adverse effects to your healthcare provider: increased
heart rate or lightheadedness when changing positions.
8. Monitor weight; an increase or a decrease may occur.
9. A decrease in sexual interest or performance may occur. If this does, discuss a change
in medication with your healthcare provider.
Regarding SSRIs
10. SSRIs may cause GI upset, dizziness, skin rash, and headache. Report these signs and
symptoms to your healthcare provider.
11. Avoid foods containing large amounts of tryptophan, such as cottage cheese, poultry,
peanuts, and sesame seeds.
12. Do not combine MAOIs and SSRIs. Do not take St. John’s wort with any antidepres-
sant. These combinations, such as confusion, mania, headache, respiratory problems,
kidney failure, and possibly death, can cause serious adverse effects, termed SES.
13. If insomnia is a problem, take the medication in the morning.
14. If nausea is a problem, take the medication with food, unless otherwise instructed.
For Attention Deficit Hyperactivity Disorder (ADHD)
15. Many drugs used for the treatment of ADHD are controlled substances.
16. Dependence may occur due to the high abuse potential of CNS stimulants.
17. CNS stimulants often increase blood pressure. Nonstimulants may reduce blood pres-
sure. Monitor blood pressure closely.
18. Take drugs at least six hours before bedtime to avoid insomnia.
19. Avoid giving drinks containing caffeine to children who are seizure prone and those
with diabetes. (CNS stimulants lower the threshold in patients with seizure disorders
and alter insulin needs in patients with diabetes.)
20. Monitor height and weight in children with prolonged therapy.
21. Take drugs after meals to reduce appetite-suppressive effects.
22. Do not take these medications for the purpose of combating fatigue.
23. Even though atomoxetine (Strattera) is a nonstimulant ADHD medication, it still has
many of the adverse effects of the other ADHD medications.
Chapter Review
10.1 People suffer from depression for many reasons. 10.4 Patients with bipolar disorder may experience emo-
The two major categories of mood disorders are de- tions ranging from depression to extreme agitation.
pression and bipolar disorder. Depression may in- Bipolar disorder is characterized by sometimes extreme
volve both situational and biological causes. The and opposite moods, such as depression and euphoria.
recognition of depression is a collaborative effort During the depressive stages, patients express signs of
among healthcare providers. A third emotional disor- major depression. Patients may then change to signs of
der is attention deficit–hyperactivity disorder. mania or high psychomotor activity and irritability.
10.2 For best results, treatment of severe depression 10.5 Mood stabilization in patients with bipolar disor-
requires both medication and psychotherapy. der is accomplished with lithium and other drugs.
After a health examination is performed to rule Drugs for bipolar disorder are called mood stabilizers.
out physical causes of depression, a psychological Lithium (Eskalith) may be used alone or in combina-
evaluation may be performed. Patients diagnosed tion with other drugs, including antidepressants and
with a major depressive disorder have at least five antianxiety agents. Antiseizure drugs and atypical an-
symptoms of recognized depression. Treatment may tipsychotic drugs have emerged as more effective drug
include medication in addition to a number of other treatments for bipolar disorder. Drugs are selective
approaches, including counseling and behavioral for extreme mania, extreme depression, or cycling of
therapy, short-term psychotherapies, interpersonal mood that occurs between extreme emotional states.
therapy, psychodynamic therapies, and in extreme
cases, electroconvulsive therapy (ECT) and repeti- 10.6 Attention deficit hyperactivity disorder (ADHD)
tive transcranial magnetic stimulation (rTMS). Most presents challenges for children and adults.
therapeutic approaches involve a long-term com- ADHD is a condition characterized by poor attention
mitment from patients, healthcare providers, and span, behavior control issues, and/or hyperactivity.
family. ADHD is normally diagnosed in childhood, although one-
third to one-half of children with symptoms of attention
10.3 Antidepressants enhance mood by boosting the deficit experience them into adulthood. As adults, patients
actions of neurotransmitters, including norepi- with ADD have symptoms similar to mood disorders.
nephrine, dopamine, and serotonin.
Drugs for depression are called antidepressants. The 10.7 Central nervous system (CNS) stimulants have
major classes of antidepressants are tricyclic anti- been the main course of treatment for ADHD.
depressants (TCAs), selective serotonin reuptake The traditional drugs used to treat attention deficit in
inhibitors (SSRIs), atypical antidepressants, and children have been the CNS stimulants. Patients tak-
monoamine oxidase inhibitors (MAOIs). All drug ing CNS stimulants must be carefully monitored to
classes work mainly by increasing the amount of nor- avoid adverse reactions. Recently, non-CNS stimu-
epinephrine, serotonin, and possibly other neurotrans- lants, including the new drug atomoxetine (Strattera),
mitters in the nerve synapse and thereby intensifying have been used as a reasonable alternative to existing
neurotransmitter action and enhancing mood. Schedule II controlled substances.
Review Questions
The following questions are written in NCLEX-PN® style. An- may be possible and plans on having what drug on hand as an
swer these questions to assess your knowledge of the chapter ma- antidote?
terial, and go back and review any material that is not clear to you. 1. Meperidine (Demerol)
1. Patient education for the patient started on an SSRI would 2. Dextromethorphan
include: 3. Calcium channel blockers
4. Carbamazepine (Tegretol)
1. The avoidance of tyramine-containing foods
2. The signs and symptoms of hypertension crisis 3. The nurse informs the patient to remain well hydrated
3. That tremors are a common adverse effect while taking lithium because dehydration can lead to:
4. That sexual dysfunction is one of the most common adverse
1. Lower serum lithium levels
effects
2. Increased effectiveness
2. A patient is taking an MAOI for depression. In planning 3. The need to increase the lithium dosage
care for this patient, the nurse knows that a hypertensive crisis 4. Lithium toxicity
Chapter Review 141
4. The patient on methylphenidate (Ritalin) should be 3. Onions

onitored for:
m 4. Apples
1. Signs of weight loss 8. An older patient has a prescription for sertraline (Zoloft)
2. Hypotension 25 mg/day, PO, to be taken for 1 week and then increased to
3. Renal toxicity 50 mg/day the second week. The pharmacy gives the patient
4. Extreme euphoria 50 mg tablets. How many tablets will the patient take per day
5. Which of the following symptoms would indicate to the during the first week?
nurse that a patient may be at risk for lithium toxicity? 1. One-quarter of the tablet
1. Increased urination and sweating 2. One tablet
2. Dry mouth, vomiting, hypotension 3. Half tablet
3. Constipation, blurred vision, hypertension 4. One and one-half tablets
4. Increased appetite, increased energy, memory loss 9. The nurse is providing education material to a patient just pre-
6. Imipramine (Tofranil) has been ordered in a patient ex- scribed duloxetine (Cymbalta) for depression. The patient states that
periencing depression. The nurse ensures the patient knows he has heard this medication is also used for: (Select all that apply.)
about which of the following? 1. Phobias
1. The use of alcohol is permitted with this drug. 2. Generalized anxiety
2. Avoid standing up too quickly. 3. Neuropathic pain
3. Effectiveness occurs within a few hours 4. Seizures
of administration. 10. A patient asks how most antidepressants work. The nurse
4. If a dose is missed, double up on the next dose. responds by saying that antidepressants improve mood by in-
7. The patient is taking phenelzine (Nardil). The nurse ad- creasing levels of:
vises the patient to avoid eating: 1. Epinephrine and norepinephrine
1. Eggs 2. Reticular formation
2. Aged cheeses 3. Norepinephrine and serotonin
4. GABA and serotonin
Remember Mrs. Coxilean, the patient 2. The physician is thinking of prescribing her phenelzine
introduced at the beginning of the (Nardil). If Mrs. Coxilean were to take this medication, the
chapter? Now read the remainder of nurse would most likely tell her:
the case study. Based on the informa- 1. “Avoid reducing your salt intake. It increases excretion of
tion you have learned in this chapter, this medication.”
answer the questions that follow. 2. “Avoid chocolate and some other foods when taking this
Mrs. Rachel Coxilean, a 32-year-old woman, visits her fam- medication.”
ily doctor and explains that lately she has been experiencing 3. “You can take herbal supplements without any risks.”
frequent headaches, disinterest in eating and sex, and a hard 4. “You can continue to take OTC medication for sleep, but
time “keeping focused.” For the past two years, she has been monitor the frequency.”
taking OTC medication to help her sleep. Two times within the
3. After considering Mrs. Coxilean’s symptoms and noting
past year, she missed work because of extreme fatigue. Mrs. that her lab values were normal, the nurse would expect that
Coxilean does not drink alcohol but admits, “The pressure is she would be started on which medication?
almost overwhelming sometimes.” Mrs. Coxilean is diagnosed
with major depressive disorder. 1. Doxepin (Sinequan)
2. Tranylcypromine (Parnate)
1. During the planning process, it is determined that the 3. Sertraline (Zoloft)
main reason why Mrs. Coxilean would not be treated with 4. Bupropion (Wellbutrin)
mood stabilizers is the lack of:
4. An SSRI was prescribed for Mrs. Coxilean. Which of the fol-
1. Complaints from the patient, suggesting attention deficit lowing effects might still remain a problem? (Select all that apply.)
disorder 1. Headaches
2. Toxicity concerns for this class of drug 2. Loss of appetite
3. Evidence that the patient feels her condition is normal 3. Poor sexual activity
4. Extreme shifts between mania and depression 4. Ability to focus

C
“I don’t need medication.
H What I need is for you to tell
A those FBI and CIA agents to
P stop looking in my windows
every night.”
T
E —Mr. Jeremy Wayne
11 Drugs for Psychoses
Core Concepts
11.1 Most psychoses have no identifiable cause and 11.4 Conventional antipsychotic drugs include the
require long-term drug therapy. phenothiazines, phenothiazine-like drugs, and
11.2 Patients with schizophrenia experience many nonphenothiazines.
different symptoms that may change over time. 11.5 Atypical antipsychotic drugs and dopamine system
11.3 The experience and skills of the healthcare provider stabilizers also address the needs of patients with
are critical to the pharmacologic management of psychoses.
psychoses.
Drug Snapshot
Conventional Antipsychotics
Phenothiazines chlorpromazine 147
Nonphenothiazines haloperidol (Haldol) 149
Atypical Antipsychotics risperidone (Risperdal) 152
Dopamine System Stabilizers (Third-Generation
Antipsychotics)
Learning Outcomes
1. Identify the signs characteristic of 4. Explain the importance of antipsychotic drugs based on their
psychosis. patient drug compliance in the classification and drug action.
2. Compare and contrast the positive pharmacotherapy of schizophrenia. 7. For each of the classes listed
and negative symptoms of 5. Explain the symptoms associated in the Drug Snapshot, identify
schizophrenia. with extrapyramidal adverse effects representative drugs and explain
3. Describe the theories for the cause of antipsychotic drugs. their mechanisms of drug action,
of schizophrenia. 6. Explain the goals of primary actions, and important
pharmacotherapy and categorize adverse effects.
Key Terms
akathisia (ACK-ah-THEE-shea) 148 neuroleptics (noo-roh-LEP-ticks) 146 schizophrenia (SKIT-soh-FREN-ee-uh) 143
extrapyramidal symptoms (EPS) parkinsonism 148 tardive dyskinesia (TAR-div dis-ki-NEE-
(peh-RAM-ed-el) 148 positive symptoms 144 zee-uh) 148
negative symptoms 144 schizoaffective disorder (SKIT-soh-
neuroleptic malignant syndrome (NMS) ah-FEK-tiv) 144
(noo-roh-LEP-tik) 147
S evere mental illness can be incapacitating for the patient and intensely frustrating for family mem-
bers dealing with the patient on a regular basis. Before the 1950s, patients with acute mental dys-
function were institutionalized, often for their entire lives. With the introduction of chlorpromazine
in the 1950s and the development of subsequent drugs, antipsychotic drugs have revolutionized the treat-
ment of mental illness. With proper medical management, patients with serious mental disorders can now
lead normal or near-normal lives as functional members of society.
Most psychoses have no identifiable cause and require long-term drug

therapy. Core Concept 11.1
Patients with psychoses often are unable to distinguish what is real from what is illusion. Because of
this, patients may be viewed as medically and legally incompetent. The following signs are characteristic
of psychosis:
■ Delusions (strong beliefs in something that is false or not based on reality); for example, the
patient may believe that someone is planting thoughts in his or her head.
■ Hallucinations (seeing, hearing, or feeling something that is not there); for example, the patient
may hear voices or see spiders crawling on walls that others around the patient do not hear or
see.
■ Illusions (distorted or misleading perceptions of something that is actually real); for example,
the patient may see a shadow and believe it is really a person.
■ Disorganized behavior For example, the patient may wear clothes in an entirely inappropriate
manner and for no apparent reason, such as dressing up with layers of clothes including a hat,
sunglasses, and several pairs of socks over the hands and feet.
■ Difficulty relating to others For example, the patient may become withdrawn from other
people in the room, showing signs of distress, maybe even turning combative if confronted or
questioned. Behavior may range from total inactivity to extreme agitation.
■ Paranoia For example, the patient may have an extreme suspicion that he or she is being
followed, or that someone is trying to kill him or her.
Psychosis may be classified as acute or chronic. Acute psychotic episodes occur over hours or days,
whereas chronic psychoses develop over months or years. Sometimes a cause may be attributed to the psy-
chosis, such as brain damage, overdoses of certain medications, extreme depression, chronic alcoholism, or
drug addiction. Genetic factors are known to play a role in some psychoses. Unfortunately, the vast major-
ity of psychoses have no identifiable cause.
People with psychosis are usually unable to function in society without long-term drug therapy.
Patients must see their healthcare provider periodically, and medication must be taken for life. Family
members and social support groups are important sources of help for patients who cannot function without
continuous drug therapy.
Schizophrenia
Schizophrenia is a type of psychosis characterized by abnormal thoughts and thought processes, schizo 5 split
disordered communication, withdrawal from other people and the outside environment, and a high risk for phrenia 5 mind
suicide. Several subtypes of schizophrenic disorders are based on clinical presentation.
144 Chapter 11 Drugs for Psychoses
Patients with schizophrenia experience many different symptoms that

Core Concept 11.2 may change over time.
Schizophrenia is the most common psychotic disorder, affecting 1% to 2% of the population. Symptoms
generally begin to appear in early adulthood, with a peak incidence in men 15 to 24 years of age and in
women 25 to 34 years of age. Patients experience a variety of symptoms that may change over time.
When observing patients with schizophrenia, healthcare workers should look for both positive and nega-
tive symptoms. Positive symptoms are those that add on to normal behavior. These include hallucinations,
delusions, and disorganized thoughts or speech. Negative symptoms are those that subtract from normal
behavior. These include lack of interest, motivation, responsiveness, or pleasure in daily activities. Proper
diagnosis of positive and negative symptoms is important for selecting the most appropriate antipsychotic
drug for treatment. The following symptoms may appear quickly or take several months or years to develop:
Positive Symptoms
■ Hallucinations, delusions, or paranoia
■ Strange behavior, such as talking in rambling statements or making up words
■ Strange or irrational actions
■ Changes from stupor to extreme hyperactivity
Negative Symptoms
■ Attitude of indifference toward or detachment from life activities
■ Neglect of personal hygiene, job, and school
■ Noticeable withdrawal from social activities and relationships
■ Changes from extreme hyperactivity to stupor
Concept Review 11.1

■ What are the characteristic signs of schizophrenia? What distinguishes a positive s ymptom
from a negative symptom?
Fast Facts

Psychosis
■ Symptoms of psychosis are often associated with other mental health problems, including substance abuse, depression, and
dementia.
■ More than 3 million Americans have schizophrenia.
■ Patients with psychosis often develop symptoms between the ages of 13 and the early 20s.
■ As many as 50% of homeless people in America have schizophrenia.
■ The probability of developing schizophrenia is 1 in 100 for the general population, 1 in 10 if one parent has the disorder, and 1 in 4
if both parents are schizophrenic.
■ There are a variety of services that help patients and the families of patients with schizophrenia:
■ Case management
■ Psychosocial rehabilitation programs
■ Self-help groups
■ Drop-in centers
■ Housing programs
■ Employment programs
■ “Talk” therapy and counseling
■ Crisis Services
schizo 5 schizophrenia Schizoaffective disorder is a related condition in which the patient exhibits symptoms of both
affective 5 mood s chizophrenia and mood disorder. For example, an acute schizoaffective reaction may include distorted
perceptions, hallucinations, and delusions, followed by extreme depression. Over time, both positive and
negative psychotic symptoms appear.
Many conditions can cause bizarre behavior, and these should be distinguished from schizophrenia.
Chronic use of amphetamines or cocaine can create a paranoid syndrome. Certain complex partial sei-
zures (see Chapter 13) can cause unusual symptoms that are sometimes mistaken for psychoses. Brain
neoplasms, infections, or hemorrhage can also cause bizarre, psychotic-like symptoms.
Figure 11.1
Presynaptic
neuron Striatum
Dopamine
Frontal
cortex Substantia
nigra
a
b
Nucleus Ventral
accumbens tegmental area
Hippocampus
Antipsychotic Dopamine (D2)

medication receptors
blocks dopamine
Postsynaptic
neuron
One theory of schizophrenia is that (a) too much dopamine is produced by neurons within the corpus striatum and
other nuclei of the brain including locations in the frontal cortex and hippocampus. The extra dopamine overexcites the
receptors. (b) Antipsychotic drugs act by attaching to D2 receptors and preventing the extra dopamine from overstimu-
lating the postsynaptic neurons.
The causes of schizophrenia have not been determined, although several theories have been proposed.
There is a definite genetic component to schizophrenia, because many patients suffering from it have
family members who have been afflicted with the same disorder. Another theory suggests that the disorder
is caused by imbalances in neurotransmitters in specific brain areas. This theory suggests the possibility
of overactive dopaminergic pathways found in the basal nuclei, an area of the brain that controls motor
activity. The basal nuclei are responsible for starting and stopping synchronized motor activity, such as leg
and arm motions during walking.
Synchronized motor activity seems to be associated with dopamine D 2-type receptors. The basal
nuclei are particularly rich in D2-type receptors, whereas the cerebrum contains very few. All a ntipsychotic
drugs act by entering dopaminergic synapses and competing with dopamine. By blocking a majority of the
D2-type receptors, antipsychotic drugs reduce the symptoms of schizophrenia (Figure 11.1 ■).
Concept Review 11.2

■ What are the major types of psychoses, and how are they differentiated? How are the
symptoms of schizophrenia reduced?
The experience and skills of the healthcare provider are critical to the
pharmacologic management of psychoses. Core Concept 11.3
The medical management of severe mental illness is extremely challenging. Many patients do not see
their behavior as abnormal and have difficulty understanding the need for medication. If their medication
produces undesirable adverse effects, such as severe muscle twitching or loss of sexual function, patient
compliance diminishes and symptoms of their pretreatment illness quickly return. Agitation, distrust, and
extreme frustration are common, because patients cannot comprehend why others are unable to think and
see the same as they do.
The primary goal of pharmacotherapy for patients with schizophrenia is to reduce psychotic symptoms
to a level that allows the patient to maintain satisfactory social relationships, as well as self-care and keeping
a job. From a pharmacologic perspective, therapy has both a positive and a negative side. Although many
symptoms of psychoses can be managed with current drugs, adverse effects are common and often severe. The
antipsychotic drugs do not cure mental illness, and symptoms remain in remission only as long as the patient
chooses to take the drug. The relapse rate for patients who discontinue their medication is 60% to 80%.
In terms of effectiveness, there is little difference among the various antipsychotic drugs; in other words,
there is no single drug of choice for schizophrenia. Selection of a specific drug is based on clinician experience,
the occurrence of adverse effects, and the needs of the patient. For example, patients with psychosis due to a
extra 5 outside degenerative disease may need an antipsychotic with minimal extrapyramidal adverse effects. (Extrapyramidal
pyramidal 5 brain stem is named after the place in the brainstem where brain impulses exit the brain. These are motor impulses or
pyramids nerve signals that may cause intense skeletal muscle contractions. Hence “extra” impulses or signals outside
of the pyramids (named for the triangular-shaped bulges appearing along the brain stem) should be reduced
for optimal pharmacotherapy in patients who are already susceptible to degenerative-related symptoms. Extra-
pyramidal symptoms are abbreviated “EPS.”) Those who operate machinery need a drug that does not cause
sedation. People, especially men who are sexually active, may want a drug without negative sexual effects.
Erections are very difficult with antipsychotic medications. The experience and skills of the healthcare pro-
vider and mental health professionals are particularly valuable in achieving successful psychiatric pharmaco-
therapy. The patient’s caregiver, when applicable, can be an essential partner in helping the healthcare team
manage severe mental illness along with all of the challenges accompanying antipsychotic drug therapy.
The pharmacotherapy of psychosis has undergone two major “generations.” Aripiprazole (Abilify) is the
one example thought to reduce the risk of hyperglycemia and diabetes with longer-term use; therefore, this drug
is sometimes grouped as a “third generation” antipsychotic. The first generation appeared in the early 1950s when
the original drugs for treating severe mental illnesses were discovered. These drugs include conventional antipsy-
chotics such as chlorpromazine. This essentially ended the era of placing all patients in insane asylums for their
lifetimes. The second-generation or atypical antipsychotic drugs were discovered in the 1970s and 1980s and are
neuro = nervous more frequently prescribed because they produce significantly fewer adverse effects. Because of the common
leptic = state of mind neurologic adverse effects, antipsychotic drugs are sometimes referred to as neuroleptics.
Conventional (first generation)

Antipsychotics
Conventional antipsychotic drugs include the phenothiazines,

Core Concept 11.4 phenothiazine-like drugs, and nonphenothiazines.
Conventional or first-generation antipsychotic drugs were the first category of drugs to be developed. The
conventional antipsychotics include the phenothiazines and phenothiazine-like drugs listed in Table 11.1 ◆.
Within each category, drugs are named by their chemical structure. Both groups have similar actions and
are considered first-generation antipsychotics.
Table 11.1 Conventional Antipsychotics: Phenothiazines

chlorpromazine PO; 25–100 mg tid or qid (max: 1,000 mg/day) Strong sedative properties; controls nausea and vomit-
IM/IV; 25–50 mg (max: 600 mg every 4–6 hours) ing, dementia, and hiccups not treated by any other
means; for agitated patients
fluphenazine PO; 0.5–10 mg/day (max: 20 mg/day) Also for dementia; available in IM or subcutaneous
forms
perphenazine PO; 4–16 mg bid to qid (max: 64 mg/day) Also for dementia and nausea; available in IM and
IV forms
prochlorperazine (Compazine) PO; 0.5–10 mg/day (max: 20 mg/day) Antiemetic drug used to treat nausea and vomiting
thioridazine (Mellaril) PO; 50–100 mg tid (max: 800 mg/day) Strong sedative properties; for moderate to severe
depression and dementia
trifluoperazine PO; 1–2 mg bid (max: 20 mg/day) Also for dementia; use cautiously in patients with
seizure disorders; available in IM form
Drug Prototype: Chlorpromazine

Therapeutic Class: Conventional antipsychotic, schizophrenia agent
Pharmacologic Class: Phenothiazine, D2 dopamine receptor blocker
Actions and Uses: Chlorpromazine provides symptomatic relief taking chlorpromazine and exposed to warmer temperatures
of positive symptoms of schizophrenia and controls manic should be monitored more closely for symptoms of NMS.
symptoms in patients with schizoaffective disorder. Many Chlorpromazine interacts with several drugs. For example,
patients must take chlorpromazine for seven or eight weeks use with sedative medications such as phenobarbital should be
before they experience improvement. Extreme agitation may avoided. Taking chlorpromazine with tricyclic antidepressants
be treated with IM or IV injections, which begin to act within can elevate blood pressure. Use of chlorpromazine with
minutes. Chlorpromazine can also control severe nausea and antiseizure medication can lower the seizure threshold.
vomiting. Use with caution with herbal supplements, such as kava
and St. John’s wort, which may increase the risk and severity of
Adverse Effects and Interactions: Strong blockade of dystonia.
alpha2-adrenergic receptors and weak blockade of cholinergic
receptors explain some of chlorpromazine’s adverse effects.
Common adverse effects are dizziness, drowsiness, and
Black Box Warning:
orthostatic hypotension.
EPS occur mostly in older adult patients, women, and Older adult patients with dementia-related psychosis are
pediatric patients who are dehydrated. Neuroleptic malignant at increased risk for death when taking conventional
syndrome (NMS; described in Table 11.2) may also occur. Patients antipsychotics.
Phenothiazines and Phenothiazine-Like Drugs

The phenothiazines are most effective at treating the positive symptoms of schizophrenia, such as
hallucinations and delusions, and have been the treatment of choice for psychoses for 50 years.
The first effective drug used to treat schizophrenia was the low-potency phenothiazine chlorprom-
azine, approved by the Food and Drug Administration (FDA) in 1954. Other phenothiazines are now
available to treat mental illness. All block the excitement associated with the positive symptoms of schizo-
phrenia, although they differ in their potency and adverse effect profiles. Hallucinations and delusions of-
ten begin to diminish within days. Other symptoms, however, may require as long as seven to eight weeks
of pharmacotherapy to improve. Because of the high rate of recurrence of psychotic episodes, pharmaco-
therapy should be considered long term, usually for the life of the patient. Phenothiazines are thought to act
by preventing both dopamine and serotonin from occupying critical neurologic receptor sites.
Although the phenothiazines once revolutionized treatment of severe mental illness, they exhibit nu-
merous adverse effects that can limit pharmacotherapy. General adverse effects are listed in Table 11.2 ◆.
Table 11.2 Adverse Effects of the Conventional Antipsychotics

Effect Description
Acute dystonia Severe spasms, particularly the back muscles, tongue, and facial muscles;
twitching movements
Akathisia Constant pacing with repetitive, compulsive movements
Anticholinergic effects Dry mouth, tachycardia, blurred vision
Hypotension Particularly severe when moving quickly from a recumbent position to an
upright position
Neuroleptic malignant syndrome Symptoms include high fever, confusion, muscle rigidity, and e levated
serum creatine kinase levels; NMS can be fatal
Parkinsonism Tremor, muscle rigidity, stooped posture, and shuffling gait
Sedation Usually diminishes with continued therapy
Sexual dysfunction Impotence and diminished libido
Tardive dyskinesia Bizarre tongue and face movements such as lip smacking and w ormlike
motions of the tongue; puffing of cheeks, uncontrolled chewing
movements
Anticholinergic effects such as dry mouth, postural hypotension, and urinary retention are common. Ejacu-
lation disorders occur in a high percentage of patients; delay in achieving orgasm (in both men and women)
is a common cause for noncompliance. Menstrual disorders are common. Each phenothiazine has a slightly
different spectrum of adverse effects.
Unlike many other drugs whose primary action is on the central nervous system (CNS) (e.g., am-
phetamines, barbiturates, anxiolytics, alcohol), antipsychotic drugs do not cause physical or psychological
dependence. They also have a wide safety margin between a therapeutic dose and a lethal dose; deaths due
to overdoses of antipsychotic drugs are uncommon.
Extrapyramidal symptoms (EPS) are a particularly serious set of adverse reactions to antipsy-
chotic drugs. EPS include acute dystonia, akathisia, parkinsonism, and tardive dyskinesia. Acute dysto-
nias (see Chapter 12) occur early in the course of pharmacotherapy and involve severe muscle spasms,
particularly of the back, neck, tongue, and face. Akathisia, the most common EPS, is an inability
to rest or relax. The patient paces, has trouble sitting or remaining still, and has difficulty sleeping.
Symptoms of phenothiazine-induced parkinsonism include tremor, muscle rigidity, stooped posture,
brady 5 slow bradykinesia, and a shuffling gait. Parkinsonism results from abnormal neuronal activity in areas of the
kinesia 5 movement corpus striatum and substantia nigra. Long-term use of phenothiazines may lead to tardive dyskinesia,
corpus 5 body which is characterized by unusual tongue and face movements such as lip smacking and wormlike mo-
striatum 5 striped tions of the tongue. If extrapyramidal effects are reported early and the drug is withdrawn or the dosage
is reduced, the adverse effects can be reversible. With higher doses given for prolonged periods, the
substantia 5 substance EPS may become permanent.
nigra 5 black
With the conventional antipsychotics, it is not always possible to control the disabling symptoms of
tardive 5 late schizophrenia without producing some degree of extrapyramidal effects. In these patients, drug therapy
dyskinesia 5 abnormal may be warranted to treat EPS. Concurrent pharmacotherapy with an anticholinergic drug may prevent
movement some of the extrapyramidal signs (see Chapter 12). For acute dystonia, benztropine (Cogentin) may be
given parenterally. Levodopa medications are usually avoided, because of their ability to increase dopa-
mine function and thus antagonize the action of the phenothiazines. Beta-adrenergic blockers and benzodi-
azepines are sometimes given to reduce signs of akathisia.
Nonphenothiazine Drugs
non 5 not having The nonphenothiazine antipsychotic class consists of drugs whose chemical structures are dissimilar to
pheno 5 chemical ring the phenothiazines (Table 11.3 ◆). Introduced shortly after the phenothiazines, the nonphenothi-
structure azines were initially expected to produce fewer adverse effects. Unfortunately, this appears not to
thiazine 5 sulfur and be the case. The spectrum of adverse effects for the nonphenothiazines is identical to that for the
itrogen around four
n
carbon atoms
phenothiazines, although the degree to which a particular effect occurs depends on the specific drug.
In general, the nonphenothiazine drugs cause less sedation and fewer anticholinergic adverse effects
than chlorpromazine but exhibit an equal or even greater incidence of extrapyramidal signs. Concur-
rent therapy with other CNS depressants must be carefully monitored because of the potential addi-
tive effects.
Drugs in the nonphenothiazine class have the same therapeutic effects and effectiveness as the pheno-
thiazines. They are also believed to act by the same mechanism as the phenothiazines—that is, by blocking
postsynaptic D2 dopamine receptors. As a class, they offer no significant advantages over the phenothi-
azines in the treatment of schizophrenia.
Table 11.3 Conventional Antipsychotics: Nonphenothiazines

haloperidol (Haldol) PO; 0.2–5 mg bid or tid For severe psychosis, dementia, and Tourette’s
syndrome; available in IM form
loxapine (Loxitane) PO; start with 20 mg/day and rapidly increase to Also for dementia
60–100 mg/day in divided doses (max: 250 mg/day)
pimozide (Orap) PO; 1–2 mg/day in divided doses; gradually increase For Tourette’s syndrome; use cautiously in patients
every other day to 7–16 mg/day, whichever is less with seizure disorders
(max: 10 mg/day)
thiothixene (Navane) PO; 2 mg tid; may increase up to 15 mg/day (max: Also for dementia; off-label use as an antidepressant
60 mg/day)
Drug Prototype: Haloperidol (Haldol)

Therapeutic Class: Conventional antipsychotic, schizophrenia agent
Pharmacologic Class: Nonphenothiazine, D2 dopamine receptor blocker
Actions and Uses: Haloperidol is classified chemically as a Haloperidol interacts with many drugs. For example, the
butyrophenone. Its primary use is for the management of acute following drugs decrease the effects/absorption of haloperidol:
and chronic psychotic disorders. It may be used to treat patients aluminum- and magnesium-containing antacids, levodopa
with Tourette’s syndrome and children with severe behavior (also increases chances of levodopa toxicity), lithium (increases
problems such as unprovoked aggressiveness and explosive chance of severe neurologic toxicity), phenobarbital, phenytoin
hyperexcitability. It is approximately 50 times more potent than (also increases chances of phenytoin toxicity), rifampin, and
chlorpromazine but has equal efficacy in relieving symptoms beta blockers (may increase blood levels of haloperidol, thus
of schizophrenia. Haldol LA is a long-acting preparation leading to possible toxicity). Haloperidol inhibits the action of
that lasts for approximately three weeks following IM or SC centrally acting antihypertensives.
administration. This is particularly beneficial for patients who Use with caution with herbal supplements such as kava,
are uncooperative or unable to take oral medications. which may increase the effect of haloperidol.
Adverse Effects and Interaction: Haloperidol produces less

sedation and hypotension than chlorpromazine, but the Black Box Warning:
incidence of EPS is high. Older adults are more likely to Older adult patients with dementia-related psychosis are
experience adverse effects and often are prescribed half at increased risk for death when taking conventional
the adult dose until the adverse effects of therapy can be antipsychotics.
determined. Although NMS is rare, it can occur.
Nursing Process Focus Patients Receiving Phenothiazines and Nonphenothiazine Therapy

Prior to administration: ■ Ineffective Therapeutic Regimen Management related to

■ Obtain a complete health history including cardiovascular, renal noncompliance with medication regimen, presence of adverse effects,
and liver conditions, allergies, drug history, and possible drug and need for long-term medication use
interactions. ■ Anxiety related to symptoms of psychosis and adverse effects of drug
■ Acquire baseline vital signs and ECG, laboratory blood levels (CBC, therapy
chemistry, drug screening, renal and liver function studies), and urine ■ Risk for Injury related to adverse effects of drug therapy and thought
specimens for laboratory analysis. processes
■ Determine neurological status. (altered thought processes, level of ■ Noncompliance related to length of time before medication reaches
consciousness (LOC), mental status, and identification of recent mood therapeutic levels and adverse effects of drug therapy
and behavior patterns). ■ Deficient Knowledge related to a lack of information about disease
The patient will:

Implementation

of proper administration. (Ensuring proper administration helps to ■ Not to take any other medication or herbal therapies unless approved
avoid unnecessary adverse effects and interactions with other medica- by the healthcare provider.
tions while determining effectiveness.) ■ That it may take up to eight weeks for full therapeutic effects to be seen.
■ Monitor for therapeutic effects, e.g., decreased psychotic symptoms. Instruct the patient to:
(If the patient continues to exhibit symptoms of psychosis, he or she ■ Notice increases or decreases of symptoms of psychosis, including hallucina-
may not be taking the drug as ordered, may be taking an inadequate tions, abnormal sleep patterns, social withdrawal, delusions, or paranoia.
dose, or may not be affected by the drug; it may need to be discontin- ■ Contact the healthcare provider if no decrease of symptoms occurs
ued and another antipsychotic begun.) over a six-week period.
continued . . .
■ Monitor for adverse effects of medications such as drowsiness, dizzi- Instruct the patient:
ness, lethargy, headaches, blurred vision, skin rash, diaphoresis, nau- ■ Regarding the adverse effects specific to the type of antipsychotic
sea/vomiting, anorexia, diarrhea, anuresis, depression, hypotension, or medication being taken.
hypertension. ■ To report adverse effects to their healthcare provider.
■ Monitor for anticholinergic adverse effects such as orthostatic hypo- Instruct the patient to:
tension, constipation, anorexia, genitourinary problems, respiratory ■ Avoid abrupt changes in position.
changes, and visual disturbances. ■ Not drive or perform hazardous activities until the effects of the drug
are known.
■ Report vision changes.
■ Comply with required laboratory tests.
■ Increase dietary fiber, fluids, and exercise to prevent constipation.
■ Relieve symptoms of dry mouth with sugarless hard candy or gum and
frequent drinks of water.
■ Notify the healthcare provider immediately if urinary retention occurs.
■ Monitor for extrapyramidal effects such as those associated with tar- Instruct the patient to:
dive dyskinesia, dystonia, akathisia, pseudoparkinsonism. (Presence ■ Recognize that extrapyramidal effects such as the development of
of EPS may be sufficient reason for the patient to discontinue the tremors, involuntary repetitive movements, decreased muscle tone,
antipsychotic. Monitor for NMS, which is life threatening and must be or increased restlessness may occur and not to stop taking medication
reported and treated immediately.) until healthcare provider is seen.
■ Immediately seek treatment for elevated temperature, unstable blood
pressure, profuse sweating, dyspnea, muscle rigidity, incontinence.
■ Monitor for weight gain, menstrual irregularities, impotence, and ■ Instruct the patient and caregivers to weigh the patient weekly and to
gynecomastia. (Some antipsychotic drugs may cause weight gain and report a weight gain of two pounds or more per week to the health-
have pituitary effects.) care provider.
■ Instruct the patient to talk to healthcare provider about sexual
concerns.
■ Monitor for alcohol/illegal drug use. (Patient may decide to use alco- ■ Instruct the patient to refrain from alcohol and illegal drug use. Refer
hol or illegal drugs as a means of coping with symptoms of psychosis, the patient to community support groups such as Alcoholics Anony-
so he or she may stop taking the antipsychotic. Concurrent use will mous (AA) or Narcotics Anonymous (NA) as appropriate.
cause increased CNS depressant effect.)
■ Monitor caffeine use. (Use of caffeine-containing substances will ne- Instruct the patient to:
gate effects of antipsychotics.) ■ Avoid caffeine.
■ Recognize common caffeine-containing products and assist in finding
acceptable substitutes, such as decaffeinated coffee and tea, caffeine-
free colas.
■ Continue to monitor vital signs, especially BP and heart rate. Monitor ■ Instruct the patient that dizziness and falls, especially on sudden posi-
for cardiovascular changes, including hypotension, tachycardia, and tion changes, may indicate cardiovascular changes.
electrocardiogram (ECG) changes. (Haloperidol has fewer cardiotoxic ■ Provide information on safety measures such as slowly rising from a
effects than other antipsychotics and may be preferred for patients sitting position.
with existing cardiovascular problems.)
■ Monitor for smoking. (Heavy smoking may decrease metabolism of ■ Instruct the patient to stop or decrease smoking. Refer to smoking ces-
haloperidol, leading to decreased effectiveness.) sation programs, if indicated.
■ Monitor older adult patients closely. (Older adult patients may need Instruct the patient:
lower doses and a more gradual dosage increase. Older adult women ■ To look for unusual reactions such as confusion, depression, and hal-
are at greater risk for developing tardive dyskinesia.) lucinations and for symptoms of tardive dyskinesia, and to report them
immediately.
■ On ways to counteract anticholinergic effects of medication while tak-
ing into account any other existing medical problems.
■ Monitor laboratory results, including CBC, and drug levels. ■ Advise the patient of the necessity of having regular laboratory studies
done.
■ Monitor for use of medication. (All antipsychotics must be taken as ■ Instruct the patient that medication must be continued as ordered,
ordered for therapeutic results to occur.) even if no therapeutic benefits are felt, because it may take several
months for full therapeutic benefits to take effect.
■ Monitor for seizures. (Drug may lower seizure threshold.) ■ Instruct the patient that seizures may occur and review appropriate
safety precautions.
■ Monitor the patient’s environment. (Drug may cause the patient to Instruct the patient to:
perceive a brownish discoloration of objects or experience photo- ■ Wear dark glasses to avoid discomfort from photophobia.
phobia. Drug may also interfere with the ability to regulate body ■ Avoid temperature extremes.
temperature.) ■ Be aware that perception of brownish discoloration of objects may ap-
pear, but that it is not harmful.
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Tables 11.1
and 11.3 for lists of the drugs to which these nursing actions apply.
Atypical (second generation) Antipsychotics

Atypical antipsychotics treat both positive and negative symptoms of schizophrenia. They have become
preferred drugs for treating psychoses.
Atypical antipsychotic drugs and dopamine system stabilizers also address

the needs of patients with psychoses. Core Concept 11.5
The approval of clozapine (Clozaril), the first atypical antipsychotic, marked the first major advance
in the pharmacotherapy of psychoses since the discovery of chlorpromazine decades earlier. Clozapine
and the other drugs in this class are called second generation or atypical, because they have a broader
spectrum of action than the conventional antipsychotics, controlling both the positive and the nega-
tive symptoms of schizophrenia (Table 11.4 ◆). Furthermore, at therapeutic doses they exhibit their
Table 11.4 Atypical Antipsychotic Drugs

aripiprazole (Abilify) PO; 10–15 mg daily (max: 30 mg/day) For schizophrenia; may cause loss of glycemic control
in patients with diabetes. Often considered a “third
generation” antipsychotic
asenapine (Saphris) Sublingual; 5 mg twice daily (max: 10 mg twice daily) For acute management of mania or mixed episodes
associated with bipolar disorder in adults
clozapine (Clozaril) PO; start at 25–50 mg/day and increase to a target For schizophrenia (adults older than 16 years); causes
dose of 50–450 mg/day in 3 days, may increase further neutropenia and agranulocytosis
(max: 900 mg/day)
iloperidone (Fanapt) PO; 12–24 mg/day administered twice daily For schizophrenia (adults older than 16 years)
lurasidone (Latuda) PO; 40 mg once daily (max: 80 mg/day) For schizophrenia; once-a-day oral medication
olanzapine (Zyprexa) PO adult: start with 5–10 mg/day, may increase by Blocks alpha receptors and acetylcholine
2.5–5 mg every week (range 10–15 mg/day, max: 20
mg/day); geriatric: start with 5 mg/day
paliperidone (Invega) PO; 6 mg/day (max: 12 mg/day) For schizophrenia; for the treatment of schizoaffective
disorder in adults and adolescents (12–17 years old)
quetiapine (Seroquel) PO (regular release); start with 25 mg bid, may increase Patients may experience hypotension when changing
to a target dose of 300–400 mg/day in divided doses positions; use cautiously in older adults; also used for
PO (extended release); 300 mg daily may increase to depression
400–800 mg daily (max: 800 mg/day)
risperidone (Risperdal) PO; 1–6 mg bid, increase by 2 mg daily to an initial Off-label use in behavioral disturbances (patients with
target dose of 6 mg/day intellectual and developmental disabilities)
IM 25 mg once every 2 weeks (max: 50 mg)
ziprasidone (Geodon) PO; 20 mg bid (max: 80 mg bid) Off-label use for Tourette’s syndrome; patients may
IM 10–20 mg every 2–4 hours (max: 40 mg/ day) experience hypotension when changing positions
antipsychotic actions without producing the major EPS effects of the conventional drugs. Some atypi-
cal drugs, such as clozapine and risperidone, are especially useful for patients in whom other drugs
have proved unsuccessful. Unfortunately, however, clozapine and other atypical antipsychotics can
neutro 5 neutrophil cause neutropenia (decreased neutrophil count) and agranulocytosis (increased WBCs without gran-
penia 5 deficiency ules; decreased WBCs with granules).
Atypical antipsychotics are thought to act by blocking several receptor types in the brain. Like the
agranulo 5 without
phenothiazines, they block dopamine D2 receptors. However, the atypicals also block serotonin and alpha2-
granules
cytosis 5 greater than adrenergic receptors, which is thought to account for some of their properties. Because the atypical drugs
normal cells are loosely bound to D2 receptors, they produce fewer extrapyramidal adverse effects than the conventional
antipsychotics.
Although there are fewer adverse effects with atypical antipsychotics, adverse effects are still
significant, and patients must be carefully monitored. Most antipsychotics cause weight gain, and
the atypical drugs are associated with obesity and its risk factors. Risperidone (Risperdal) and some
of the other antipsychotic drugs increase prolactin levels, which can lead to menstrual disorders, de-
creased libido, and osteoporosis in women. In men, high prolactin levels can cause lack of libido and
impotence. There is also concern that some atypical drugs alter glucose metabolism, which can lead
to type II diabetes.
Concept Review 11.3

■ What is a neuroleptic drug? What are the two general classes of drugs used to treat
sychoses? How does each drug category generally affect positive and/or negative
p
symptoms of schizophrenia?
Drug Prototype: Risperidone (Risperdal)

Therapeutic Class: Atypical antipsychotic, schizophrenia agent, psychotic depression agent
Pharmacologic Class: Serotonin (5-HT) receptor antagonist, D2 dopamine receptor antagonist (weaker affinity)
Actions and Uses: Therapeutic effects of risperidone include Common adverse effects are extrapyramidal reac-
treatment and prevention of schizophrenia relapse and tions (involuntary shaking of the head, neck, and arms),
expression of bipolar mania symptoms. Risperidone also hyperactivity, fatigue, nausea, dizziness, visual disturbances,
treats symptoms of irritability in children with autism. fever, and orthostatic hypotension. Risperidone may cause
Expected results are a reduction of excitement, paranoia, or weight gain.
negative behaviors associated with psychosis. Effects result Patients taking risperidone should avoid CNS depressants
from blockade of dopamine type 2, serotonin type 2, and such as alcohol, antihistamines, sedative-hypnotics, or opioid
alpha2-adrenergic receptors located within the CNS. For a full analgesics. These can increase some of the adverse effects of
range of effectiveness, the drug is sometimes combined with risperidone. Due to inhibition of liver enzymes, other drugs that
lithium (Eskalith) or valproic acid (Depakene). Risperidone is a increase the adverse effects of risperidone include the selective
long-acting preparation, which, following IM administration, serotonin reuptake inhibitors (SSRIs) such as paroxetine,
releases only a small amount. After a three-week lag, the rest of sertraline, and fluoxetine (Prozac), and antifungal drugs such
the drug releases and lasts for approximately four to six weeks. as fluconazole, itraconazole, and ketoconazole. Risperidone
PO preparations release sooner and have a one- to two-week may interfere with elimination by the kidneys of clozapine, also
onset of action. increasing the risk of adverse reactions.
Kava, valerian, or chamomile may increase risperidone’s
Adverse Effects and Interactions: If elderly patients with CNS depressive effects.
dementia-related psychoses are given risperidone, they are
at an increased risk for heart failure, pneumonia, or sudden
death. Patients with underlying cardiovascular disease may
be especially prone to dysrhythmias and hypotension. Risperi- Black Box Warning:
done should be avoided in patients with a history of seizures, Older adult patients with dementia-related psychosis are
suicidal ideations, or kidney/liver disease. This medication may at increased risk for death when taking conventional
cause hyperglycemia and worsen glucose control in patients antipsychotics.
with diabetes. It is not known whether risperidone passes
into breast milk or if it could harm a nursing baby. Due to its
category C classification, safety in pregnancy has not been
established.
Nursing Process Focus Patients Receiving Atypical Antipsychotic Therapy

Prior to administration: ■ Risk for Injury related to adverse effects of drug therapy, and thought
■ Obtain a complete health history including cardiovascular, renal and liver processes
conditions, allergies, drug history, and possible drug interactions. ■ Ineffective Therapeutic Regimen Management related to
■ Acquire baseline vital signs and ECG, laboratory blood levels (CBC, noncompliance with medication regimen, presence of adverse effects,
chemistry, drug screening, renal and liver function studies) and urine and need for long-term medication use
specimens for laboratory analysis. ■ Anxiety related to symptoms of psychosis
■ Determine neurological status. (altered thought processes, hallucina- ■ Noncompliance related to length of time before drug reaches
tions, level of consciousness [LOC], mental status, and identification of therapeutic levels, desire to use alcohol or illegal drugs
recent mood and behavior patterns). ■ Deficient Knowledge related to a lack of information about disease

The patient will:
Implementation
of proper administration. (Ensuring proper administration helps ■ Not to take any other medication or herbal therapies unless approved
to avoid unnecessary adverse effects and interactions with other by the healthcare provider.
medications while determining effectiveness.) ■ That it may take up to six weeks for full therapeutic effects to be seen.
■ Monitor RBC and WBC counts. (Agranulocytosis [WBCs below 3,500] Instruct the patient to:
can be a life-threatening adverse effect of these medications, which ■ Keep appointments for laboratory testing.
may also suppress bone marrow and lower infection-fighting ability.) ■ Report any sore throat, signs of infection, fatigue without apparent
cause, or bruising to the healthcare provider.
■ Observe for adverse effects. (These drugs may affect blood pressure, ■ Instruct the patient to report any adverse effects such as drowsiness,
heart rate, and other autonomic functions.) dizziness, depression, anxiety, tachycardia, hypotension, nausea/
vomiting, excessive salivation, changes in urinary frequency or ur-
gency, incontinence, weight gain, muscle pain or weakness, rash, and
fever to the healthcare provider.
■ Monitor for anticholinergic adverse effects. (These medications may Instruct the patient to:
cause mouth dryness, constipation, or urinary retention.) ■ Increase dietary fiber, fluids, and exercise to prevent constipation.
■ Relieve symptoms of dry mouth with sugar-free hard candy or chew-
ing gum and frequent drinks of water.
■ Immediately notify the healthcare provider if urinary retention occurs.
Possible catheter placement may be necessary.
■ Monitor for therapeutic effects, e.g., decrease of psychotic symptoms. Instruct the patient to:
(Decreased symptoms indicate an effective dose and type of ■ Notice increases or decreases of symptoms of psychosis, including
medication.) hallucinations, abnormal sleep patterns, social withdrawal, delusions,
or paranoia.
■ Contact the healthcare provider if symptoms do not decrease over a
six-week period.
■ Monitor for alcohol or illegal drug use. (Used concurrently, these will ■ Instruct the patient to avoid alcohol or illegal drug use. Refer the
cause increased CNS depression. The patient may decide to use alcohol patient to AA, NA, or other support group as appropriate.
or illegal drugs as a means of coping with symptoms of psychosis and
may stop taking the drug.)
■ Monitor caffeine use. (Use of caffeine-containing substances inhibits Instruct the patient about:
the effects of antipsychotics.) ■ Common caffeine-containing products.
■ Acceptable substitutes, including decaffeinated coffee and tea, and
caffeine-free soda.
■ Monitor for smoking. (Heavy smoking may decrease blood levels of the ■ Instruct the patient to stop or decrease smoking. Refer to smoking
drug.) cessation programs if indicated.
■ Monitor older adult patients closely. (Older patients may be more ■ Instruct older adult patients on ways to counteract anticholinergic
sensitive to anticholinergic adverse effects.) effects of the medication while taking into account any other existing
medical problems.

Dopamine System Stabilizers

(Third-Generation Antipsychotics)
In 2002, due to side effects caused by conventional and atypical antipsychotic medications, a newer drug
class was developed to better meet the needs of patients with psychoses. This class, sometimes considered
a third-generation class of antipsychotics, consists of dopamine system stabilizers (DSSs) or dopamine
partial agonists. Aripiprazole (Abilify) received FDA approval in 2002 for the treatment of schizophrenia
and schizoaffective disorder. Because aripiprazole controls both the positive and the negative symptoms of
schizophrenia, it is grouped in Table 17.4 with the atypical antipsychotic drugs.
Aripiprazole is generally well tolerated in patients with schizophrenia. In particular, its use seems
to be associated with a lower incidence of EPS than haloperidol and fewer weight-gain issues than other
atypical antipsychotics, for example, olanzapine. Anticholinergic adverse effects are virtually nonexistent.
In fact, the incidence of adverse effects generally compared to the other atypical antipsychotic drugs is
very low. Notable side effects, however, include headache, nausea/vomiting, fever, constipation, and anxi-
ety. Healthcare providers are encouraged to balance the risks and benefits of medications when choosing
an antipsychotic for an individual patient.

Patients being treated for psychoses of the nervous system need to know the following:
1. It is important to report the development of tremors, muscle spasms, involuntary
r epetitive movements, decreased muscle tone, or increased restlessness to the
healthcare provider. These symptoms may indicate serious adverse effects that can
be reversed if medication is changed soon after they start.
2. Consult a healthcare provider if dry mouth, rapid heart rate, constipation, or urinary
retention occurs. An additional medication may be prescribed to relieve these signs
and symptoms.
3. Avoid taking antacids with antipsychotics because they delay or decrease
antipsychotic absorption.
4. Avoid alcohol or other sedatives while taking antipsychotics; it increases the
depressant effects.
5. Extra protection from the sun is necessary; wear a hat and sunscreen.
6. Avoid driving or operating machinery until response to the medication is known. Its
sedating effects can increase the risk for accidental injury.
7. Contact a healthcare provider for guidance if symptoms get worse or are not relieved
by the medication. Do not stop the medication unless directed to do so.
Chapter Review
11.1 Most psychoses have no identifiable cause and 11.2 Patients with schizophrenia experience many
require long-term drug therapy. different symptoms that may change over time.
Psychosis is characterized by delusions, hallucina- Schizophrenia is the most common psychiatric
tions, illusions, disorganized behavior, difficulty disorder; it is characterized by abnormal thoughts,
relating to others, and paranoia. Psychoses may be disordered communication, withdrawal, and suicidal
classified as acute or chronic. Sometimes a cause can risk. Patients with schizophrenia exhibit positive
be found for the psychosis, but the vast majority of (adding) or negative (subtracting) symptoms. Proper
cases have no identifiable cause. Most patients with diagnosis of these symptoms is important for select-
psychoses are not able to function normally in society ing the appropriate antipsychotic drug. The cause of
without long-term drug therapy. schizophrenia has not been determined. Symptoms
Chapter Review 155
seem to be associated with neural dopamine type 2 antipsychotics. With conventional antipsychotics,
(D2) receptors found in the basal nuclei. Schizoaffec- it is not always possible to control extrapyramidal
tive disorders are characterized by symptoms of both symptoms (EPS) which include muscle spasms (dys-
schizophrenia and mood disorder. tonia), inability to sit down (akathisia), and unusual
tongue and facial movements (tardive dyskinesia).
11.3 The experience and skills of the healthcare provider Phenothiazines, phenothiazine-like drugs, and non-
are critical to the pharmacologic management of phenothiazines treat positive signs of schizophrenia,
psychoses. but all have unpleasant adverse effects.
Management of severe mental illness is difficult.
Many patients do not see themselves as abnormal and 11.5 Atypical antipsychotic drugs and dopamine system
have difficulty understanding the need for medica- stabilizers also address the needs of patients with
tion. Although many symptoms of psychosis can be psychoses.
controlled with current drug therapy, adverse effects Atypical antipsychotic drugs treat both positive and
are common and often severe. Skills of the healthcare negative signs of schizophrenia and have become
team are particularly valuable to achieving successful drugs of choice for treating psychoses. Like the phe-
psychiatric drug treatment. nothiazine drugs, atypical drugs block D2 receptors.
Although there are fewer adverse effects with atypi-
11.4 Conventional antipsychotic drugs include the cal drugs, adverse effects are still significant, and pa-
phenothiazines, phenothiazine-like drugs, and tients must be carefully monitored. Dopamine system
nonphenothiazines. stabilizers (DSSs) represent the third-generation class
Antipsychotic drugs are sometimes called neuro- of antipsychotics developed to better meet the needs
leptics. The two basic categories of drugs for psy- of patients with psychoses.
chosis are conventional antipsychotics and atypical
Review Questions
The following questions are written in NCLEX-PN® style. 4. The patient is on thioridazine (Mellaril) and has d
eveloped
A nswer these questions to assess your knowledge of the muscle spasms, difficulty sleeping, and a shuffling gait. The
chapter material, and go back and review any material that is nurse recognizes this as:
not clear to you. 1. Anticholinergic effects
1. While caring for a patient taking an antipsychotic drug, 2. Cholinergic effects
the nurse understands that: 3. Extrapyramidal adverse effects
4. Serotonin syndrome
1. Antipsychotic medications cure mental illnesses.
2. Some adverse effects of antipsychotic drugs can lead to 5. The patient states that he has not taken his antipsychotic
noncompliance. drug for the past two weeks because it was causing sexual
3. Antipsychotic medications are only administered when the dysfunction. The nurse explains that it is important to continue
patient is symptomatic. taking his medication as prescribed because:
4. Antipsychotic drugs improve symptoms within hours of 1. Hypertensive crisis may occur with abrupt withdrawal.
administration. 2. Muscle twitching may occur.
2. Family members of a patient diagnosed with schizo- 3. Noncompliance may bring on parkinsonism.
phrenia are being educated on the adverse effects of pheno- 4. Symptoms of psychosis are likely to return.
thiazines. Which of the following would the nurse include? 6. The nurse understands that when evaluating the effects
(Select all that apply.) of certain antipsychotic medications, neuroleptic malignant
1. The patient may experience a sedative effect that usually syndrome (NMS) is most likely to occur with use of which of
diminishes with continued therapy. the following drug?
2. Severe muscle spasms may occur early in therapy. 1. Chlorpromazine
3. Tardive dyskinesia can occur with long-term therapy. 2. Aripiprazole (Abilify)
4. Medications can be given to help prevent some adverse 3. Risperidone (Risperdal)
effects. 4. Clozapine (Clozaril)
3. Which of the following symptoms does the nurse 7. The nurse understands that haloperidol (Haldol) may be
r ecognize as an anticholinergic effect of chlorpromazine? ordered for which of the following reasons:
1. Hallucinations, illusions, paranoia 1. Seizures
2. Hypertension, polyuria, increased salivation 2. Unprovoked aggressiveness
3. Dry mouth, tachycardia, blurred vision 3. Severe mental depression
4. High fever, confusion, muscle rigidity 4. Alcoholism
8. The nurse monitors the patient taking which of the 10. A patient is taking aripiprazole (Abilify). Which patient
f ollowing drug groups because it can lead to type II diabetes? effects should the nurse observe to determine whether the drug
1. Phenothiazines is having a therapeutic effect?
2. Nonphenothiazines 1. Elevated mood and coping skills
3. Atypical antipsychotics 2. Orthostatic hypotension and sedation
4. All antipsychotics 3. Decreased delusional thinking and hallucinations
4. Improved sleep and dietary habits
9. The nurse is speaking to a patient and his family about
the use of herbal supplements. She warns them about possible
interactions with prescribed medications, specifically combin-
ing herbal supplements with antipsychotic medication. When
asked what herbal supplements are used to treat mental illness,
the nurse suggests:
1. Echinacea
2. St. John’s wort
3. Black cohosh
4. Saw palmetto
Remember Mr. Wayne, the patient 2. Mr. Wayne has been taking risperidone (Risperdal) for
introduced at the beginning of the the past 10 years that he has been experiencing psychotic
chapter? Now read the remainder of episodes. Mr. Wayne is placed back on his medication so the
the case study. Based on the informa- nurse monitors him closely for which of the following adverse
tion you have learned in this chapter, effects: (Select all that apply.)
answer the questions that follow. 1. Hyperactivity
Mr. Jeremy Wayne, age 38, has been diagnosed with a psychosis 2. Spasms (shaking of head/neck)
characterized by the following symptoms: reports of seeing 3. Fatigue
people who are not there, talking about government agents who 4. Fever
are trying to kill him, and communicating with “double agents”
3. According to the doctor’s order, the nurse gives Mr. Wayne
about suspicious behavior. This patient has been in and out of which of the following medications to help reduce the incidence
the hospital for the past four weeks. Mr. Wayne’s family reports of dystonia (spasms)?
difficulty in controlling him because he has not been taking his
medication. Members in the community have seen Mr. Wayne 1. Levodopa (Larodopa)
pacing up and down the highway for several weeks. It becomes 2. Benztropine (Cogentin)
necessary to temporarily confine Mr. Wayne for medical treat- 3. Thioridazine (Mellaril)
ment. He has had this disorder for 15 years and has a strong, 4. Trifluoperazine
supportive family (mother and father). 4. The physician orders the long-acting preparation of
f luphenazine 15 mg SC. The pharmacy supplies fluphenazine
1. The symptoms described for Mr. Wayne are called 25 mg/mL. The nurse administers _______.
__________ symptoms and respond best to treatment with
which class of antipsychotic medication? 1. 0.4 mL
2. 1.4 mL
1. Positive; conventional or typical antipsychotics 3. 0.6 mL
2. Negative; conventional or typical antipsychotics 4. 1.6 mL
3. Positive; atypical antipsychotics
4. Negative; atypical antipsychotics

C
“It’s hard to face the future,
knowing what MS does to H
you.” A
Mr. Robert Wingate P
T
E
R
Drugs for Degenerative Diseases

and Muscles 12
Core Concepts
12.1 Medications are unable to cure most degenerative 12.8 Muscle spasms are caused by injury, overmedication,
diseases of the CNS. hypocalcemia, and debilitating neurologic disorders.
12.2 Parkinson’s disease is progressive, with the 12.9 Muscle spasms may be treated with
occurrence of full symptoms taking many years. nonpharmacologic or pharmacologic therapies.
12.3 Antiparkinson drugs act on the brain to restore the 12.10 Many muscle relaxants treat muscle spasms by
balance between dopamine and acetylcholine. inhibiting upper motor neuron activity, causing
12.4 Patients with Alzheimer’s disease experience a sedation, or altering simple reflexes.
dramatic loss of ability to perform tasks that require 12.11 Effective treatment for spasticity includes both
acetylcholine as the CNS neurotransmitter. physical therapy and medications.
12.5 Alzheimer’s disease is treated with acetylcholinesterase 12.12 Some drugs for spasticity provide relief by acting
inhibitors. directly on muscle tissue, interfering with the release
12.6 Symptoms of multiple sclerosis result from of calcium ions.
demyelination of CNS nerve fibers. 12.13 Neuromuscular blocking drugs block the effect of
12.7 Drugs for multiple sclerosis reduce immune attacks acetylcholine at the receptor.
in the brain and treat unfavorable symptoms.
Drug Snapshot
Drugs for Parkinson’s Disease Drugs for Multiple Sclerosis
Dopaminergic levodopa, carbidopa, Immune system
drugs and entacapone modulating drugs
(Stalevo) 163
Immunosuppressants
Cholinergic blockers benztropine
Drugs for Muscle Spasms
(anticholinergics) (Cogentin) 164
Centrally acting muscle cyclobenzaprine
Drugs for Alzheimer’s Disease
relaxants (Amrix, Flexeril) 171
Acetylcholinesterase donepezil (Aricept) 167
Drugs for Spasticity
inhibitors
Direct-acting dantrolene
Other drugs that slow
antispasmodics (Dantrium) 175
progression of AD
Neuromuscular Blocking Drugs
Drugs that treat behavioral
symptoms of AD Nondepolarizing blockers
Depolarizing blockers
158 Chapter 12 Drugs for Degenerative Diseases and Muscles
Learning Outcomes
1. Identify the most common drugs used in the treatment of 8. Compare and contrast the roles
degenerative diseases of the CNS. degenerative diseases based on their of centrally acting skeletal muscle
2. Describe symptoms of Parkinson’s class and drug action. relaxants and direct-acting
disease, Alzheimer’s disease, multiple 5. Describe the pharmacologic antispasmodics in treating muscle
sclerosis, and spasticity. management of muscle spasms. spasms and spasticity.
3. Explain the neurochemical bases of 6. Discuss nonpharmacologic therapies 9. For each of the classes listed
central degenerative diseases and used to treat muscle spasms and in the Drug Snapshot, identity
muscle spasms. spasticity. representative drugs and explain
their mechanisms of drug action,
4. Explain the goals of 7. Discuss the pharmacology of primary actions, and important
pharmacotherapy and categorize neuromuscular blocking drugs. adverse effects.
Key Terms
acetylcholinesterase (AchE) (AS-ee-til- dementia (dee-MEN-she-ah) 158 neuromuscular blocking drugs (NEWR-oh-
KOH-lin-ES-ter-ays) 165 dystonia (diss-TONE-ee-ah) 172 musc-you-lahr) 175
Alzheimer’s disease (AD) (ALLZ-heye-mers) multiple sclerosis (MS) (skle-ROH-sis) parkinsonism 159
164 167 spasticity (spas-TISS-ih-tee) 172
C entral degenerative diseases and muscle disorders affect a patient’s ability to perform daily
a ctivities and most often lead to immobility. Appropriate body movement depends on in-
tact n eural pathways and proper muscle functioning. Without medical intervention, neuro-
logic disorders can result in major sensory, cognitive, and/or motor problems. Parkinson’s disease,
Alzheimer’s disease (AD), and m ultiple sclerosis (MS) are three common debilitating and progres-
sive neurologic disorders. Although medications are unable to stop or reverse the progressive nature
of these diseases, therapy can often slow down the disorders and offer symptomatic relief. Common
muscle disorders are muscle spasms and spasticity. This chapter focuses on the pharmacotherapy of
neurodegenerative diseases and muscle disorders as well as treatments involving the neuromuscular
junction.
Core Concept 12.1 Medications are unable to cure most degenerative diseases of the CNS.
Degenerative diseases of the central nervous system (CNS) include a variety of disorders with different
causes and outcomes. Some, such as Huntington’s disease, are quite rare, affect younger patients, and are
caused by chromosomal defects. Others, such as AD, affect millions of people, mostly elderly patients,
and have a devastating economic and social impact. Table 12.1 ◆ lists major degenerative diseases of
the CNS.
Table 12.1 Degenerative Diseases of the Central Nervous System

Disease Description
Alzheimer’s disease Progressive loss of brain function characterized by memory loss, confusion, and dementia (a degenerative dis-
order characterized by progressive memory loss, confusion, and inability to think or communicate effectively)
Amyotrophic lateral sclerosis (ALS) Progressive weakness and wasting of muscles caused by destruction of motor neurons
Huntington’s chorea Autosomal dominant genetic disorder resulting in progressive dementia and involuntary, spasmodic move-
ments of limb and facial muscles
Multiple sclerosis (MS) Demyelination of neurons in the central nervous system (CNS) resulting in progressive weakness, visual
disturbances, mood alterations, and cognitive deficits
Parkinson’s disease Progressive loss of dopamine in the CNS causing tremor, muscle rigidity, and abnormal movement and posture
Fast Facts Neurodegenerative Diseases
Parkinson’s Disease
■ Over 1.5 million Americans have Parkinson’s disease.
■ Most patients with Parkinson’s disease are above the age of 50.
■ Greater than 50% of patients with Parkinson’s disease who have difficulty with voluntary movement
are less than 60 years of age.
■ More men than women develop this disorder.
Dementia
■ Of all patients with dementia, 60% to 70% have Alzheimer’s disease.
■ Over 4 million Americans have Alzheimer’s disease.
■ Alzheimer’s disease mainly affects patients over the age of 65.
Multiple Sclerosis
■ About 1.1 million people worldwide have MS.
■ Onset of symptoms typically occurs between ages 15 and 40.
■ Women are affected twice as often as men.
■ MS occurs most often in Caucasian people of northern European origin.
■ MS is about five times more prevalent in temperate climates than in tropical climates.
The cause of most neurologic degenerative diseases is unknown. Most progress from hardly noticeable
signs and symptoms early in the disease to serious neurologic and cognitive deficits. In their early stages,
disorders may be difficult to diagnose. With the exception of Parkinson’s disease, pharmacotherapy
provides only minimal benefit. Currently, medication is unable to cure any of the major neurodegenerative
diseases.
Parkinson’s Disease
Parkinson’s disease is a degenerative disorder of the CNS caused by death of neurons that produce the
brain neurotransmitter dopamine. It is the second most common degenerative disease of the nervous sys-
tem, affecting many Americans. Pharmacotherapy is often successful in reducing some of the distressing
symptoms of this disorder.
Parkinson’s disease is progressive with the occurrence of full symptoms

taking many years. Core Concept 12.2
Parkinson’s disease primarily affects patients older than 50 years of age; however, even teenagers can
develop the disorder. Men are affected slightly more often than women. The disease is progressive. The
appearance of full symptoms often takes many years. The symptoms of Parkinson’s disease, described as
parkinsonism, are summarized as follows:
■ Tremors The hands and head develop a palsy-like motion or shakiness when at rest; pill-rolling
is a common behavior in progressive states, in which patients rub the thumb and forefinger
together as if a pill were between them.
■ Muscle rigidity Stiffness may resemble symptoms of arthritis. Patients often have difficulty
bending over or moving limbs. These symptoms may not be noticeable at first but become more
obvious as the disease progresses.
■ Bradykinesia This is the most noticeable of all symptoms. Patients may have difficulty brady 5 slow
chewing, swallowing, or speaking. Patients with Parkinson’s disease have difficulties initiating kinesia 5 movement
movement and controlling fine muscle movements. Walking often becomes difficult, and
patients shuffle their feet without taking normal strides.
■ Postural instability Patients may be humped over slightly and may easily lose their balance.
Stumbling results in frequent falls and injuries.
affective 5 body emotion ■ Affective flattening Patients often have a “masked face” where there is little facial expression
flattening 5 without or blinking of the eyes.
expression
Although Parkinson’s disease is a progressive neurologic disorder primarily affecting muscle move-
ment, other health problems often develop in these patients, including anxiety, depression, sleep distur-
bances, dementia, and disturbances of the autonomic nervous system (difficulty urinating and performing
sexually). Several theories have been proposed to explain the development of parkinsonism. Because some
patients with Parkinson’s symptoms have a family history of this disorder, a genetic link is highly prob-
able. Numerous environmental toxins, such as carbon monoxide, cyanide, manganese, chlorine, and pes-
ticides, also have been suggested as a cause, but results of studies have not proven the cause–effect link.
Viral infections, head trauma, and stroke have also been proposed as causes of parkinsonism.
Symptoms of parkinsonism develop due to the degeneration and destruction of dopamine-producing
substantia 5 substance neurons found within an area of the brain known as the substantia nigra. When not enough dopamine is
nigra 5 black released, this neurotransmitter cannot make contact with other critical areas of the brain.
The most critical area for dopamine contact is the corpus striatum, an area responsible for controlling
corpus 5 body
striatum 5 striped unconscious muscle movement. Patients with Parkinson’s disease have difficulty initiating and controlling
movements. Balance, posture, muscle tone, and involuntary muscle movements depend on the proper bal-
ance between dopamine (inhibitory) and acetylcholine (stimulatory). Under normal conditions, the inhibi-
tory effects of dopamine and the excitatory effects of acetycholine balance one another to produce smooth
coordinated muscle movement. If dopamine is absent, acetylcholine is able to overstimulate the corpus
striatum. For this reason, drug therapy for parkinsonism focuses not only on restoring dopamine function
but also on blocking the effect of acetylcholine within this sensitive area of the brain.
extra 5 outside Extrapyramidal symptoms (EPS) develop in response to the same neurochemical actions that cause
pyramidal 5 medullary Parkinson’s disease. Recall that antipsychotic drugs act by blocking dopamine receptors. Treatment with
pyramidal tracts some antipsychotic drugs may cause parkinsonism-like symptoms by interfering with the same neural
symptoms 5 involuntary pathway and functions affected by the lack of dopamine. Antiparkinson drugs are sometimes used to treat
motor characteristics
(e.g., EPS)
EPS caused by antipsychotic medications.
EPS may occur suddenly and become a medical emergency. With acute EPS, patients’ muscles may
spasm or lock up. Fever and confusion are other signs or symptoms of this reaction. If acute EPS occur
in a healthcare facility, short-term medical treatment may be provided by administering diphenhydramine
(Benadryl), which is an antihistamine that has acetylcholine-blocking properties. When symptoms are rec-
ognized outside a healthcare facility, the patient should be immediately taken to the emergency depart-
ment. Untreated acute episodes of EPS can be fatal.
Concept Review 12.1

■ Parkinson’s disease primarily affects which body functions? What are the five major
symptoms of this disorder?
Antiparkinson drugs act on the brain to restore the balance between

Core Concept 12.3 dopamine and acetylcholine.
The goal of pharmacotherapy for Parkinson’s disease is to increase the ability of the patient to perform
normal daily activities such as eating, walking, dressing, and bathing. Although pharmacotherapy does not
cure this disorder, it can dramatically reduce symptoms in some patients.
As mentioned, antiparkinson drugs are given to restore the balance of dopamine and acetylcholine
anti 5 against within the corpus striatum of the brain. These drugs include dopaminergic drugs and anticholinergics
cholinergic 5 acetylcholine (cholinergic blockers).
action
Dopaminergic Drugs
dopaminergic 5 dopamine Dopaminergic drugs, shown in Table 12.2 ◆, are used to increase dopamine action within critical areas
action of the corpus striatum. The basic ingredient in many of the preferred drugs for parkinsonism is levodopa,
a dopaminergic substance that has been used more often than any other for this disorder. As shown in
Figure 12.1 ■, levodopa is a precursor (a more basic chemical form) of dopamine. Supplying the nerve
terminals directly with levodopa leads to increased synthesis of dopamine. Levodopa can cross the blood-
brain barrier but dopamine cannot. Therefore, dopamine by itself is not used for therapy. The effectiveness
of levodopa can be enhanced by combining it with carbidopa. This combination, marketed as Parcopa or
Sinemet, makes more levodopa available to enter the CNS. Carbidopa (Lodosyn) alone can also increase
the concentration of dopamine and levodopa in the brain.
Levodopa is chemically similar to some amino acids. Foods high in protein use the same pathways
for the absorption into the bloodstream or brain, and therefore compete with levodopa (with or without
Table 12.2 Dopaminergic Drugs Used for Parkinsonism

amantadine (Symmetrel) PO; 100 mg daily or bid Also for infection with influenza A virus; for
relief of drug-induced EPS; may cause release
of dopamine from nerve terminals
apomorphine SC; 2 mg for the first dose; every few days, Activates dopamine receptors; may improve
doses may be increased by 1 mg (max: 6 mg); ability to walk, talk, and move
if more than 1 week passes between doses,
titration should be restarted at 2 mg
bromocriptine (Parlodel) PO; 1.25–2.5 mg/day up to 100 mg/day in Also for suppression of lactation, female
divided doses infertility, and overproduction of growth
hormone; activates the dopamine receptor
directly
entacapone (Comtan) PO; 200 mg given with levodopa–carbidopa Blocks synaptic enzyme catecholamine
up to 8 times/day O-methyl transferase (COMT) responsible for
metabolizing dopamine
levodopa–carbidopa (Parcopa, Sinemet) PO; 1 tablet containing 10 mg carbidopa/100 Prevents metabolism of levodopa, enhancing
mg levodopa or 25 mg carbidopa/100 mg dopamine action
levodopa tid (max: 6 tablets/day)
levodopa–carbidopa-entacapone PO; 1 tablet containing 10 mg carbidopa/100 Chemical precursor to dopamine combined
(Stalevo) mg levodopa or 25 mg carbidopa/100 mg with a dopamine enhancer and a
levodopa tid (max: 6 tablets/day) catecholamine O-methyl transferase (COMT)
enzyme inhibitor
pramipexole (Mirapex) PO; start with 0.125 mg tid for 1 week, Activates dopamine receptors; also approved
double this dose for the next week, continue to treat restless legs syndrome
to increase by 0.25 mg/dose tid every week
to a target dose of 1.5 mg tid
rasagiline (Azilect) PO; 0.5–1 mg once daily Blocks monoamine oxidase (MAO), the en-
zyme that degrades dopamine within brain
nerve terminals
ropinirole (Requip) PO; start with 0.25 mg tid, may increase by Activates dopamine receptors; approved to
0.25 mg/dose tid every week to a target dose treat restless legs syndrome
of 1 mg tid
rotigotine (Neupro) Transdermal; start at 2 mg/24 hours for Approved to treat early-stage Parkinson’s
patients with early-stage Parkinson’s dis- disease, advanced-stage Parkinson’s disease
ease; may be increased weekly by 2 mg/24 and restless legs syndrome
hours (max: 6 mg/24 hours); patients with
advanced-stage Parkinson’s disease may be
initiated at 4 mg/24 hours (recommended:
8 mg/24 hours); for restless legs syndrome,
start at 1 mg/24 hours (max: 3 mg/24 hours)
selegiline (Eldepryl, Zelapar) PO; 5 mg/dose bid; doses greater than 10 Blocks monoamine oxidase (MAO), the
mg/day are potentially toxic enzyme that degrades dopamine within brain
nerve terminals; also for depression
tolcapone (Tasmar) PO; 100 mg tid (max: 600 mg/day) Blocks synaptic enzyme COMT responsible
for metabolizing dopamine
carbidopa) for absorption. If levodopa is taken with foods high in protein, the effectiveness of the medica- catecholamine 5
tion will be reduced. In addition, levodopa is absorbed in the small intestine, therefore any foods or condi- neurotransmitter group
tions that delay gastric emptying will reduce drug availability. synthesized from dopamine
Other approaches to enhancing dopamine are used in treating parkinsonism. Tolcapone (Tasmar), O-methyl-transferase 5
entacapone (Comtan), rasagiline (Azilect), and selegiline (Eldepryl, Zelapar) inhibit enzymes that nor- degrading enzyme
mally destroy levodopa and dopamine. Rasagiline and selegiline are monoamine oxidase (MAO) inhibi- transferring a methyl (CH3 )
tors. Apomorphine (Apokyn), bromocriptine (Parlodel), pramipexole (Mirapex), and ropinirole (Requip) group (e.g., COMT)
directly activate the dopamine receptor and are called dopamine receptor drugs. Amantadine (Symmetrel), monoamine oxidase
an antiviral agent, causes the release of dopamine from nerve terminals. All these drugs are considered (MAO) 5 catecholamine
adjuncts to the pharmacotherapy of parkinsonism because they are not as effective as levodopa. In terms of degrading enzyme
F i g u re 1 2 . 1
1 Neurons in nigrostriatal pathway are progressively injured.
Dopamine-containing neurons are especially damaged.

Progressive Antipsychotic
Head held degeneration of dopamine-
Basal nuclei:
forward neurons in the and blocking
nigrostriatal drugs can
Caudate Drooping pathway can produce:
nucleus eyelids, open produce:
mouth, drooling
Lenticular
nucleus
Symptoms of Parkinson’s Disease:
Tremor of • Tremors (resting tremors)
hands • Rigid body structure
• Slowness of movement
(bradykinesis)
• Loss of balance
Corpus striatum
“striped body”
Stimulatory
• Basal nuclei
• Internal capsule Cholinergic
Group of structures neuron
forms a stripe.
Slow, shuffling
gait, short Acetycholine
steps
2 Drug therapy tends to help with symptoms. Post

synaptic
Cholinergic neuron
Dopaminergic agents:
receptor
• Precursors to dopamine:
eg: Levodopa (L-Dopa) Dopamine Dopamine
• Dopamine receptor agents: receptor
eg: Ropinirole, Pramipexole
Cholinergic-blocking drugs: Inhibitory Dopaminergic
• Benztropine neuron
Levodopa
Dopamine
Levodopa
Dopamine cannot cross the blood–brain barrier. Levodopa, its precursor, can. Once levodopa crosses the blood–brain
barrier and enters neurons, it is converted into dopamine, which normally inhibits firing of the next neuron. Natural
acetylcholine in the brain stimulates the same postsynaptic neuron. Thus, to restore normal neuronal activity, drug
therapy attempts to either (a) restore dopamine inhibitory action or (b) block acetylcholine (cholinergic) stimulatory
activity.
activities of daily living (ADLs), most levodopa–carbidopa combination drugs are thought to control motor
symptoms better. Pramipexole (Mirapex) and ropinirole (Requip) have proven to be safe and effective for
initial sole therapy and also when combined with levodopa–carbidopa.
Additional drugs that reduce the requirements for levodopa–carbidopa include the catechol-O-methyl
transferase (COMT) inhibitors. Entacapone (Comtan) and tolcapone (Tasmar) are COMT inhibitors.
Like levodopa–carbidopa, these drugs increase concentrations of existing dopamine in nerve terminals
and improve motor fluctuations related to the “wearing-off” effect. Entacapone combined with carbidopa
and levodopa is marketed as Stalevo. Side effects of COMT inhibitors include mental confusion and
hallucinations, nausea and vomiting, cramps, headache, diarrhea, and possible liver damage.
Rotigotine (Neupro) is a new dopamine receptor transdermal patch that can be applied once daily.
In clinical trials (2012), it was shown to effectively treat early Parkinson’s disease as monotherapy and
was even shown to be effective in the treatment of advanced-stage Parkinson’s disease and restless legs
syndrome (RLS). The most common side effects of rotigotine for RLS are application site reactions,
drowsiness, nausea, and headache.
Drug Prototype: Levodopa, Carbidopa, and Entacapone (Stalevo)

Therapeutic Class: Antiparkinson drugs
Pharmacologic Class: Dopamine precursor, dopaminergic drugs
Actions and Uses: Stalevo restores the neurotransmitter vitamin B6 will decrease the effectiveness of levodopa or
dopamine in extrapyramidal areas of the brain, thus relieving levodopa–carbidopa.
some Parkinson’s symptoms. To increase its effect, levodopa is Stalevo interacts with many drugs. For example, tricyclic
combined with two other drugs, carbidopa and entacapone, antidepressants decrease effects of Stalevo, increase postural
which prevent its enzymatic breakdown. Several months may be hypotension, and may increase sympathetic activity, with
needed to achieve maximum therapeutic effects. hypertension and sinus tachycardia. Stalevo cannot be used
if an MAO inhibitor was taken within 14 to 28 days, because
Adverse Effects and Interactions: Side effects of Stalevo concurrent use may precipitate hypertensive crisis. Haloperidol
include uncontrolled and purposeless movements such as taken concurrently may antagonize the therapeutic effects of
extending the fingers and shrugging the shoulders, involuntary Stalevo. Methyldopa may increase toxicity. Antihypertensives
movements, loss of appetite, nausea, and vomiting. Muscle may cause increased hypotensive effects. Antiseizure medication
twitching and spasmodic winking are early signs of toxicity. may decrease the therapeutic effects of Stalevo. Antacids
Orthostatic hypotension is common in some patients. The drug containing magnesium, calcium, or sodium bicarbonate may
should be discontinued gradually, because abrupt withdrawal increase Stalevo absorption, which could lead to toxicity. Kava
can produce acute parkinsonism. Foods high in protein and may worsen the Parkinson’s symptoms.
Cholinergic Blockers (Anticholinergics)

A second approach to changing the balance between dopamine and acetylcholine in the brain is to
give cholinergic blockers, or anticholinergics. By blocking the effect of acetylcholine, anticholinergics
inhibit the overactivity of this neurotransmitter within the corpus striatum. These drugs are listed in
Table 12.3 ◆.
Anticholinergics such as atropine were the first drugs used to treat parkinsonism. The large n umber
of adverse effects has limited the use of these drugs. The anticholinergics now used for parkinsonism
act within the CNS and produce fewer adverse effects. However, they continue to cause unpleasant
autonomic symptoms such as dry mouth, blurred vision, tachycardia, urinary retention, and constipation
(very troublesome). The centrally acting anticholinergics are not as effective as levodopa in relieving
severe symptoms of parkinsonism. They are used early in the courses of the disease when symptoms are
less severe, in patients who cannot tolerate levodopa, and in combination therapy with older antiparkin-
son drugs.
Concept Review 12.2

■ Antiparkinson drugs attempt to restore the balance of which two major CNS neurotrans-
mitters?
Table 12.3 Anticholinergic Drugs Used for Parkinsonism

benztropine (Cogentin) PO; 0.5–1 mg/day, gradually increase as Also used to relieve EPS from neuroleptic drugs; does
needed (max: 6 mg/day) not lighten tardive dyskinesia
biperiden (Akineton) PO; 2 mg daily to qid Blocks acetylcholine receptors; thus, actions associated
with muscarinic blockade are observed (e.g., blurred vi-
sion, dry mouth); available in IM/IV forms.
diphenhydramine (Benadryl) (see PO; 25–50 mg tid or qid (max: 300 mg/day) Also for allergic reactions, motion sickness, sedation,
page 460 for the Drug Prototype and coughing; blocks cholinergic function even though
box) it is an antihistamine; available in IM/IV forms.
trihexyphenidyl (Artane) PO; 1 mg for day 1; double this for day 2; Also used to relieve EPS; off-label use for Huntington’s
then increase by 2 mg every 3–5 days up to chorea and spasmodic torticollis
6–10 mg/day (max: 15 mg/day)
Drug Prototype: Benztropine (Cogentin)

Therapeutic Class: Antiparkinson drug
Pharmacologic Class: Centrally acting cholinergic receptor blocker
Actions and Uses: Benztropine acts by blocking excess Benztropine interacts with many drugs. For example,
cholinergic stimulation of neurons in the corpus striatum. It is benztropine should not be taken with alcohol, tricyclic
used for relief of parkinsonism symptoms and for the treatment antidepressants, MAOIs, phenothiazines, procainamide, or
of EPS brought on by antipsychotic pharmacotherapy. This quinidine because of combined sedative effects. Over-the-
medication suppresses tremors but does not affect tardive counter (OTC) cold medicines and alcohol should be avoided.
dyskinesia. Other drugs that enhance dopamine release or activation of the
dopamine receptor may produce additive effects. Haloperidol
Adverse Effects and Interactions: As expected from its auto- will cause decreased effectiveness.
nomic action, benztropine can cause typical anticholinergic Antihistamines, phenothiazines, tricyclics, disopyramide,
adverse effects such as sedation, dry mouth, constipation, and and quinidine may increase anticholinergic effects, and antidiar-
tachycardia. rheals may decrease absorption.
Alzheimer’s Disease
Alzheimer’s disease (AD) affects memory, thinking, and behavior. It is one of the forms of dementia that
gradually gets worse over time. As many as 50% of people are affected with this disease by the age of
85. The patient generally lives 5 to 10 years following diagnosis; AD is the fourth leading cause of death.
Drugs help slow down the rate at which symptoms become worse.
Dementia is a degenerative disorder characterized by progressive memory loss, confusion, and
inability to think or communicate effectively. Consciousness and perception are usually unaffected.
Although the cause of most dementia is unknown, it is usually associated with cerebral atrophy or other
structural changes within the brain.
Structural damage within the brain of patients with AD has been well documented. Amyloid plaques
and neurofibrillary tangles, found at autopsy, are present in nearly all patients with AD. It is suspected that
these structural changes are caused by chronic inflammatory or oxidative cellular damage to surrounding
neurons. There is a loss in both the number and function of neurons in patients with AD.
Patients with Alzheimer’s disease experience a dramatic loss of ability to

Core Concept 12.4 perform tasks that require acetylcholine as the CNS neurotransmitter.
Patients with AD experience a dramatic loss of ability to perform tasks that require acetylcholine as the
neurotransmitter. Because acetylcholine is a major neurotransmitter within the hippocampus (an area of the
brain responsible for learning and memory) and other parts of the cerebral cortex, neuronal function within
these brain areas is especially affected. Thus, an inability to remember and to recall information is among
the early symptoms of AD. Symptoms of AD include the following:
■ Impaired memory and judgment
■ Confusion or disorientation
■ Inability to recognize family or friends
■ Aggressive behavior
■ Depression
■ Psychoses, including paranoia and delusions
■ Anxiety
Core Concept 12.5 Alzheimer’s disease is treated with acetylcholinesterase inhibitors.
acetylcholinesterase Drugs are used to slow memory loss and other progressive symptoms of dementia. Additional drugs may
(AchE) 5 Ach terminating be given to treat associated symptoms such as depression, anxiety, or psychoses. The acetylcholinesterase
enzyme inhibitors are the most widely used class of drugs for treating AD. Representative drugs used for treatment
inhibitor 5 suppressing factor
of AD are listed in Table 12.4 ◆.
Table 12.4 Drugs Used for Alzheimer’s Disease

donepezil (Aricept) PO; 5–10 mg at bedtime For mild to moderate dementia; may cause nausea,
diarrhea, muscle cramps, and weight loss
galantamine (Razadyne, PO; start with 4 mg bid at least 4 weeks; if toler- For mild to moderate dementia; may cause weight
Reminyl) ated, may increase by 4 mg bid every 4 weeks to loss, dizziness, nausea, vomiting, and hypotension
target a dose of 12 mg bid (max: 8–16 mg bid) when changing positions
memantine (Namenda) PO; starting dose is 5 mg once daily; the dose usu- For moderate to severe dementia; NMDA receptor
ally is increased to 5 mg twice daily, then 5 mg and blocking drug; may cause a serious skin reaction,
10 mg as separate doses daily, and finally 10 mg fatigue, dizziness, headache, confusion, vomiting,
twice daily coughing, constipation, pain, and difficulty in
breathing
rivastigmine (Exelon) PO; start with 1.5 mg bid with food, may increase For mild to moderate dementia; may cause flu-like
by 1.5 mg bid every 2 weeks if tolerated; target symptoms, dizziness, and weight loss
dose is 3–6 mg bid (max: 12 mg bid)
Transdermal; 5 cm2 patch (4.6mg/24 hours), 10 cm2
patch (9.5mg/24 hours)
tacrine (Cognex) PO; 10 mg qid, increase in 40 mg/day increments For mild to moderate dementia; off-label used for
not sooner than every 6 weeks (max: 160 mg/day) severe dementia in patients with HIV infection; may
cause nausea, vomiting, and liver toxicity
Acetylcholinesterase Inhibitors
The Food and Drug Administration (FDA) has approved only a few drugs specifically for AD. The most
effective of these medications acts by intensifying the effect of acetylcholine at the cholinergic receptor,
as shown in Figure 12.2 ■ . Acetylcholine is naturally degraded in the synapse by the enzyme acetylcho-
linesterase (AchE). When AchE is inhibited, acetylcholine levels increase and greatly impact the recep-
tors. As described in Chapter 8, the AchE inhibitors indirectly stimulate the receptors for acetylcholine.
When treating AD, the goal of pharmacotherapy is to improve function in ADLs, behavior, and cogni- ADLs 5 activities of daily living
tion. Although the AchE inhibitors improve functions in all three areas, their effectiveness is limited. These
drugs do not cure AD—they only slow its progression. Therapy is begun as soon as the diagnosis of AD is
established. These drugs are ineffective in treating the severe stages of this disorder, probably because so
many neurons have been damaged. Increasing the levels of acetylcholine is only effective if there are func-
tioning neurons present. Therefore, the AchE inhibitors are often discontinued as the disease progresses
because their therapeutic benefit may not outweigh their expense or the risk of adverse effects. When dis-
continuing therapy, doses of the AchE inhibitors should be lowered gradually.
All AchE inhibitors used to treat AD are equally effective. Their adverse effects are those expected of
drugs that enhance the parasympathetic nervous system (see Chapter 8). These include nausea, vomiting,
and diarrhea. Of the drugs available for AD, tacrine (Cognex) is associated with liver toxicity. Rivastig-
mine (Exelon) is associated with weight loss, a potentially serious adverse effect in some older adults.
Other Drugs That Slow Progression of AD

Although AchE inhibitors are the mainstay of treatment for AD dementia, several other agents have been
investigated for possible benefit in delaying the progression of this disease. Because at least some of the
neuronal changes in AD are caused by oxidative cellular damage, antioxidants such as vitamin E have been
examined. Other drugs purported to prevent or help slow the onset of AD progression have been NSAIDs
and selegiline, an MAO inhibitor.
In 2003, memantine (Namenda) was approved by the FDA for combination treatment of moderate
to severe AD. Its mechanism of action differs from that of the cholinesterase inhibitors. Unlike cholines-
terase inhibitors that address the cholinergic defect in the brains of patients with AD, memantine reduces
the abnormally high levels of glutamate. Glutamate exerts its neural effects through interaction with the
N-methyl-D-aspartate (NMDA) receptor. When bound to the receptor, glutamate causes calcium to enter
neurons, producing an excitatory effect. Too much glutamate in the brain may be responsible for brain cell
death. Memantine, along with cholinesterase inhibitors such as donepezil, may have a protective function
in reducing neuronal calcium overload.
Caprylidene (Axona) is a medical food approved for patients with AD. This food medication is me-
tabolized into ketone bodies, which the brain can use for energy even when its ability to process glucose is
impaired. Brain-imaging scans of older adults and those with AD have revealed an impaired ability to take
up glucose, the brain’s preferred source of energy. Thus, patients with AD may benefit from this type of
therapy.
F i g u re 1 2 . 2
Alzheimer’s medications
work by intensifying the
effect of acetylcholine
at the receptor.
Body of fornix
Mammillary
bodies
Hippocampus
Amygdaloid
bodies
Cholinergic neuron
Pyruvate
Normally:
1 Ach is released. AcetylCoA
+ Acetylcholine
2 Ach binds with
Choline (Ach)
its receptor. 1 Normal role of
acetylcholine
3 The action of
in a vast array
Ach is terminated of brain
by AchE. functions,
4 If AchE is Choline including the
inhibited, Ach is ability to
+ Ach 2
not broken down Acetate speak, move,
4 see, think, and
as quickly and
3 AchE remember
produces a more
dramatic effect.
Cholinergic receptor
AchE = acetylcholinesterase
Neuron with
cholinergic receptor
Drugs That Treat Behavioral Symptoms of AD

Agitation occurs in most patients with AD. This is often accompanied by delusional behavior, paranoia,
hallucinations, or other psychotic symptoms. Atypical antipsychotic drugs such as risperidone (Risperdal)
and olanzapine (Zyprexa) may be used to control these episodes. Conventional antipsychotics such as
haloperidol (Haldol) are occasionally prescribed, although EPS often limit their use.
Although not as common as agitation, anxiety and depression may also occur in patients with AD.
Anxiolytics such as buspirone (BuSpar) or some of the benzodiazepines are used to control excessive
anxiety (see Chapter 9). Mood stabilizers such as sertraline (Zoloft), citalopram (Celexa), or fluoxetine
(Prozac) may be given when major depression interferes with ADLs (see Chapter 10).
Concept Review 12.3

■ Alzheimer’s disease is a dysfunction of which brain neurotransmitters? How do drugs
for Alzheimer’s disease restore neurotransmitter function and improve symptoms of
dementia?
Drug Prototype: Donepezil (Aricept)

Therapeutic Class: Drug for Alzheimer’s disease Pharmacologic Class: Acetylcholinerase inhibitor
Actions and Uses: Donepezil is an AchE inhibitor that improves eadache, and irritability. Musculoskeletal adverse effects
h
memory in cases of mild to moderate Alzheimer’s dementia by include muscle cramps, arthritis, and bone fractures. Generalized
enhancing the effects of acetylcholine in neurons in the cere- adverse effects include headache, fatigue, chest pain, in-
bral cortex that have not yet been damaged. Patients should creased libido, hot flashes, urinary incontinence, dehydration,
receive pharmacotherapy for at least six months prior to assess- and blurred vision. Unlike with tacrine, hepatotoxicity has
ing the maximum benefits of drug therapy. Improvement in not been observed. Patients with bradycardia, hypotension,
memory may be observed as early as one to four weeks follow- asthma, hyperthyroidism, or active peptic ulcer disease should
ing medication. The therapeutic effects of donepezil are often be monitored carefully. Anticholinergics will be less effective.
short-lived, and the degree of improvement is modest at best. Donepezil interacts with several other drugs. For example,
An advantage of donepezil over other drugs in its class is that bethanechol causes a synergistic effect. Phenobarbital, phe-
its long half-life permits it to be given once daily. nytoin, dexamethasone, and rifampin may speed elimination of
donepezil. Quinidine or ketoconazole may inhibit metabolism
Adverse Effects and Interactions: Common adverse effects of donepezil. Because donepezil acts by increasing cholinergic
of donepezil are vomiting, diarrhea, and darkened urine. activity, two parasympathomimetics should not be administered
CNS adverse effects include insomnia, syncope, depression, at the same time.
Cam therapy
Ginkgo biloba for Dementia
The seeds and leaves of Ginkgo biloba have been used in traditional Chinese medicine for
thousands of years. The tree is planted throughout the world, including the United States. In
Western medicine, the focus has been on treating depression and memory loss. In Germany,
an extract of Ginkgo biloba is approved for the treatment of dementia.
Ginkgo has been shown to improve mental functioning and stabilize AD. The mechanism
of action seems to be related to increasing the blood supply to the brain by dilating blood
vessels, decreasing the viscosity of the blood, and modifying the neurotransmitter system.
The exact benefit of ginkgo remains unclear because some studies concluded that cognitive
performance improved, whereas others have shown no improvement in the symptoms or
progress of AD. Ginkgo is considered safe; however, it may increase the risk of bleeding in
patients taking anticoagulants. A review of nine different trials of the effects of ginkgo on
dementia concluded that the supplement was more effective than a placebo (Weinmann,
Roll, Schwartzbach, Vauth & Willich, 2010)
Multiple Sclerosis
Multiple sclerosis (MS) is a disorder characterized by damaged myelin located within the CNS. Antibod- oligo 5 little
ies produced by the patient slowly target and destroy myelin, axonal membranes, and supporting cells of dendro 5 branched
the CNS, for example oligodendrocytes. As axons are destroyed, the ability of nerves to conduct electrical cytes 5 cells
impulses is impaired. Inflammation accompanies damaged tissue, and multiple filamentous plaques called
scleroses 5 thickened or
scleroses are formed. hardened plaques
Symptoms of multiple sclerosis result from demyelination of CNS nerve

fibers. Core Concept 12.6
During the early stages of MS, some damaged axons recover due to partial myelination and the develop-
ment of alternative circuitry, but as antibodies continue to attack neural tissue, further damage and inflam- neurologic 5 pertaining to
mation lead to neuronal death. Patients often have recurrent episodes of neurologic dysfunction, which the nervous system
progress at a fairly rapid rate.
The etiology of MS is unknown. Many clinicians and scientists suspect genetic or microbial factors
due to reports that, in most cases, MS occurs in regions of colder climate. One theory proposes acquired
immunological resistance against pathogenic factors in warmer climates. Microscopic pathogens such as
viruses have been suggested, though there is no strong evidence for this theory.
neuropathic 5 nervous disease Signs and symptoms associated with axonal injury include fatigue, heat sensitivity, neuropathic
pain, spasticity, impaired cognitive ability, disruption of balance and coordination, bowel and bladder
spasticity 5 stiffness of muscle
symptoms, sexual dysfunction, dizziness, vertigo, visual impairment, and slurred speech. Although the
cognitive 5 reasoning ability disease is progressive, the precise course of MS is unpredictable, and each patient experiences a variety of
vertigo 5 confusion and
symptoms depending on the extent and localization of demyelination.
disorientation
Drugs for multiple sclerosis reduce immune attacks in the brain and treat
Core Concept 12.7 unfavorable symptoms.
Like many neurodegenerative disorders, there are no drugs available that can cure MS or reverse the
progressive nature of the disease. Existing drugs are only partially effective and some have serious adverse
effects. Drugs are used in the treatment of MS to either modify the progression of the disease or to manage
symptoms of the disease. Drugs for treating MS are shown in Table 12.5 ◆.
One approach to modify disease progression attempts to reduce inflammation and prevent attacks on
the nervous system. Drugs also address impairment of movement due to demyelination of neurons. Goals
are accomplished through the use of immune system modulating drugs, immunosuppressants, and drugs
that block neuronal potassium channels.
The most treatable form of this disorder is relapsing-remitting MS (RRMS). This condition involves
unpredictable relapses (attacks) during which time new symptoms appear or existing symptoms become
more severe. These symptoms can last for varying periods (days or months), followed by partial or total
remission (recovery). In RRMS, the disease may be inactive for months or years. On average, people with
RRMS have one or two attacks a year.
Immune system modulating drugs (also described later in the text as immunostimulants [see Chapter 25])
are used to treat the underlying causes of MS and to decrease the overall relapse rate. Interferon beta-1a
(Avonex, Rebif) and interferon beta-1b (Betaseron, Extavia) are first-line therapies for slowing the neuronal
damage caused by MS. Although generally well tolerated, the interferons have u nfavorable a dverse effects,
including flu-like symptoms (e.g., headaches, fever, chills, muscle aches), anxiety, discomfort experienced at
the injection site, and liver toxicity. Due to toxicity concerns and additive e ffects, caution should be exercised
when taking these drugs in combination with chemotherapeutic agents or bone marrow-suppressing drugs.
Another first-line drug treatment, glatiramer (Copaxone) is an immunomodulating synthetic protein
that resembles myelin basic protein, an essential part of the nerve’s myelin coating. Because glatiramer
resembles myelin, it is thought to curb the body’s attack on the myelin covering and reduce the creation
Table 12.5 Drugs Used for Multiple Sclerosis

Drug Comments Administered
For Immune Attacks Against the CNS
dalfampridine (Ampyra) Potassium channel blocker to treat walking PO
impairment
dimethyl fumarate (Tecfidera) Myelin oxidative stress reducer PO
fingolimod (Gilenya) Immune system modulator PO
glatiramer (Copaxone) Immune system modulator; myelin protein SC
protectant
interferon beta-1a (Avonex, Rebif) Immune system modulator IM and SC
interferon beta-1b (Betaseron, Extavia) Immune system modulator SC
mitoxantrone (Novantrone) Immunosuppressant drug IV
natalizumab (Tysabri) Immune system modulator IV
teriflunomide (Aubagio) Immune system modulator PO
Drug Comments Symptoms Relieved

For the Relief of MS Symptoms
modafinil (Provigil) Central adrenergic drug Fatigue, memory loss, weakness
amantadine (Symmetrel) Dopaminergic drug Fatigue, memory loss, weakness
gabapentin (Neurontin) Antiseizure drug Anxiety, insomnia, neuropathic pain
methylprednisolone (Solu-Medrol) Corticosteroid medication Myelin swelling and inflammation
of new brain lesions. Glatiramer is available in prefilled syringes that can be kept at room temperature
for several days. However, patients often complain of adverse effects and having to inject themselves.
Adverse effects include redness, pain, swelling, itching, or a lump at the site of injection. Flushing, chest
pain, weakness, infection, pain, nausea, joint pain, anxiety, and muscle stiffness are other common adverse
effects.
Mitoxantrone (Novantrone) is an FDA-drug approved for patients with MS who have not responded
to interferon or glatiramer therapy. Primarily a chemotherapeutic drug, mitoxantrone is substantially more
toxic than the immune system modulating drugs. Toxicity is a concern due to irreversible cardiac injury
and potential harm to a fetus. Notable adverse effects are reversible hair loss, gastrointestinal (GI) discom-
fort (nausea and vomiting), and allergic symptoms (itching, rash, hypotension). Some patients experience a
blue-green tint to their urine, which is harmless.
Approved by the FDA in 2010, fingolimod (Gilenya) is an oral medication used for treating relaps-
ing forms of MS. Its mechanism of action is unknown, although it may work by reducing the number of
circulating lymphocytes, leading to reduced migration of leukocytes into the CNS. White blood cells cause
inflammation and destruction of nerves in patients with MS. Fingolimod decreases the number of MS
flare-ups and slows down the development of physical impairment caused by MS.
In 2010, dalfampridine (Ampyra) tablets were approved by the FDA as the first treatment to address
walking impairment in patients with MS. It exerts an effect through its broad-spectrum potassium channel
blockade and has been shown to increase nerve conduction and improve walking speed. The most bother-
some adverse effect of dalfampridine is increased seizure activity. Because of this concern, this drug is
contraindicated in patients with a prior history of seizures. contraindicated 5 not
Approved in 2012, teriflunomide (Aubagio) is one of the newest immunomodulator therapies for re- advisable
lapsing MS. Teriflunomide is the active metabolite of leflunomide (Arava), a drug previously approved to
treat rheumatoid arthritis. Therapy with teriflunomide must be carefully monitored because the drug can
cause severe liver damage, renal failure, and bone marrow suppression. It is contraindicated in pregnant
patients due to possible teratogenic effects on the fetus. teratogenic 5 causing birth
Miscellaneous drugs used for MS include modafinil (Provigil) and amantadine (Symmetrel) for treat- defects
ing fatigue, memory loss, and progressive weakness symptoms. Modafinil is an alpha1-adrenergic drug
thought to activate receptors that respond to the brain neurotransmitter norepinephrine. This agent in-
creases alertness and energy and improves memory. Gabapentin (Neurontin) is an antiseizure drug used for
treating mood disturbances, including depression and sensitivity to pain (see Chapter 13). Methylpredniso-
lone (Solu-Medrol) and prednisone are steroidal anti-inflammatory agents that are administered for brief
periods when the patient is experiencing acute MS symptoms caused by swelling and inflammation in the
brain. Other medications not found the in the table may be used routinely to help treat fatigue and neuro-
logic symptoms due to MS (i.e., pain and discomfort).
Muscle Spasms
Muscle spasms are involuntary contractions of a muscle or groups of muscles. The muscles tighten, develop
a fixed pattern of resistance, and lose functioning ability.
Muscle spasms are caused by injury, overmedication, hypocalcemia, and

debilitating neurologic disorders. Core Concept 12.8
Muscle spasms are a common condition usually associated with overuse of and local injury to the skeletal hypo 5 lowered
calc 5 calcium
muscle. Other causes of muscle spasms include overmedication with antipsychotic drugs (see Chapter 11), emia 5 blood levels
epilepsy, hypocalcemia, pain, and debilitating neurologic disorders. Patients with muscle spasms may
experience inflammation, edema, and pain at the affected muscle; loss of coordination; and reduced tonic 5 single prolonged
mobility. When a muscle goes into spasm, it freezes in a contracted state. A single, prolonged contraction transient
clonic 5 multiple repetitive
is called a tonic spasm, whereas multiple, rapidly repeated contractions are called clonic spasms. Treatment
transient
of muscle spasms includes use of both nonpharmacologic and pharmacologic therapies. spasms 5 involuntary
contractions
Muscle spasms may be treated with nonpharmacologic or pharmacologic
therapies. Core Concept 12.9
Identifying the etiology of muscle spasms requires a careful history and a physical exam. After a deter- etiology 5 cause or origin
mination has been made, nonpharmacologic therapies are normally used in conjunction with medications.
Nonpharmacologic measures may be immobilization of the affected muscle, application of heat or cold,
hydrotherapy, ultrasound, supervised exercises, massage, or manipulation.
Fast Facts Muscle Spasms
■ More than 12 million people worldwide have muscle spasms.

■ Muscle spasms severe enough to warrant drug therapy are often found in patients who have
had other debilitating disorders, such as neurodegenerative diseases, stroke, injury or cerebral
palsy.
■ Cerebral palsy is usually associated with events that occur before or during birth, but it may be
caused by head trauma or infection during the first few months or years of life.
■ Dystonia affects about 250,000 people in the United States; it is the third most common movement
disorder after Parkinson’s disease and essential tremor.
■ Researchers have recognized multiple forms of inheritable dystonia and identified at least 10 genes
or chromosomal locations responsible for the various manifestations.
Pharmacotherapy for muscle spasms may include combinations of analgesics, anti-inflammatory

drugs, and centrally acting skeletal muscle relaxants. Most skeletal muscle relaxants relieve symptoms of
muscular stiffness and rigidity that result from muscular injury. Drugs also help improve mobility. Thera-
peutic goals are to minimize pain and discomfort, increase range of motion, and improve the patient’s abil-
ity to function independently.
Concept Review 12.4

■ Give several reasons why muscle spasms develop. What is the main goal of therapy for
muscle spasms?
Many muscle relaxants treat muscle spasms by inhibiting upper motor

Core Concept 12.10 neuron activity, causing sedation, or altering simple reflexes.
Antispasmodic drugs relieve symptoms of muscular stiffness and rigidity. They improve mobility in cases
in which patients have restricted movements.
Many antispasmodic drugs treat muscle spasms at the level of the CNS. The exact mechanisms of ac-
tion are not fully known, but it is believed that these drugs affect the brain and/or spinal cord by inhibiting
upper motor neuron activity, causing sedation, or altering simple reflexes.
Skeletal muscle relaxants are used to treat local spasms resulting from muscular injury and may
be prescribed alone or in combination with other medications to reduce pain and increase range of
motion. Commonly used centrally acting medications are baclofen (Lioresal), cyclobenzaprine (Am-
rix, Flexeril), tizanidine (Zanaflex), and benzodiazepines such as diazepam (Valium), clonazepam
(Klonopin), and lorazepam (Ativan) (Table 12.6 ◆). All of the centrally acting drugs can cause
sedation.
Baclofen (Lioresal) is structurally similar to the inhibitory neurotransmitter gamma amino butyric
acid (GABA) and produces its effect by a mechanism that is not fully known. It inhibits neuronal
activity within the brain and possibly the spinal cord. There is some uncertainty about whether the spi-
nal effects of baclofen are associated with GABA. Baclofen may be used to reduce muscle spasms in
patients with MS, cerebral palsy, or spinal cord injury. Common adverse effects of baclofen are drowsi-
ness, dizziness, weakness, and fatigue. Baclofen is often the drug of first choice because of its wide
safety margin.
Tizanidine (Zanaflex) is a centrally acting alpha 2-adrenergic agonist that inhibits motor neurons,
mainly at the spinal cord level. It also affects some neural activity in the brain, patients receiving high
doses report drowsiness. Though uncommon, one adverse effect of tizanidine is hallucinations. The drug’s
most frequent adverse effects are dry mouth, fatigue, dizziness, and sleepiness. Tizanidine is as effective as
baclofen and is considered by some to be the drug of first choice.
As discussed in Chapter 13, benzodiazepines inhibit both sensory and motor neuron activities by en-
hancing the effects of GABA. Common adverse effects include drowsiness and ataxia (loss of coordina-
tetany 5 prolonged tion). Benzodiazepines are usually prescribed for muscle relaxation when baclofen and tizanidine fail to
tightened muscles produce adequate relief.
Table 12.6 Centrally Acting Antispasmodic Drugs

baclofen (Lioresal) PO; 5 mg tid (max: 80 mg/day) May be administered orally or by an implantable
pump, which infuses medication directly into the
subarachnoid space
carisoprodol (Soma) PO; 350 mg tid CNS depressant; does not inhibit motor activity
like other conventional muscle relaxers; muscle
relaxation seems to be related to sedation
chlorzoxazone (Paraflex, Parafon PO; 250–500 mg tid–qid (max: 3 g/day) Depresses nerve transmission in the brain and
Forte) spinal cord, possibly by sedation; not effective for
cerebral palsy
clonazepam (Klonopin) PO; 0.5 mg tid (max: 20 mg/day) Benzodiazepine usually taken in combination with
other drugs; used for the relief of skeletal muscle
spasms; primarily for seizure disorders
cyclobenzaprine (Amrix, PO; 10–20 mg bid–qid (max: 60 mg/day) Short-term relief of muscle spasms associated with
Flexeril) acute musculoskeletal conditions; not for cerebral
palsy or central nervous system diseases
diazepam (Valium) (see page 188 PO; 4–10 mg bid–qid; IM/IV 2–10 mg, repeat Benzodiazepine used for the relief of skeletal
for the Drug Prototype box) if needed in 3–4 hours; IV pump; administer muscle spasms associated with cerebral palsy,
emulsion at 5 mg/min partial paralysis
lorazepam (Ativan) (see page 116 PO; 1–2 mg bid–tid (max: 10 mg/day) Benzodiazepine used for extreme muscle tension
metaxalone (Skelaxin) PO; 800 mg tid–qid for maximum of 10 days For acute musculoskeletal conditions; causes its
effect through sedation
methocarbamol (Robaxin) PO; 1.5 g qid for 2–3 days, then reduce to 1 g qid Adjunct to physical therapy for acute
musculoskeletal disorders and tetany
orphenadrine (Banflex, Myolin, PO; 100 mg bid IM/IV forms available
Norflex)
tizanidine (Zanaflex) PO; 4–8 mg tid–qid (max: 36 mg/day) To relax muscle tone associated with spasticity;
effective at the spinal cord level
Drug Prototype: Cyclobenzaprine (Amrix, Flexeril)

Therapeutic Class: Skeletal muscle relaxant, centrally acting
Pharmacologic Class: Catecholamine reuptake inhibitor
Actions and Uses: Cyclobenzaprine relieves muscle spasms of Adverse Effects and Interactions: Adverse reactions to
local origin without interfering with general muscle function. cyclobenzaprine include drowsiness, blurred vision, dizziness,
This drug acts by depressing motor activity, primarily in the dry mouth, rash, and tachycardia. It should be used with caution
brainstem, with limited effects also occurring in the spinal cord. in patients with myocardial infarction (MI), dysrhythmias, or
It increases circulating levels of norepinephrine, blocking presyn- severe cardiovascular disease. One reaction, although rare, is
aptic uptake. Its mechanism of action is similar to that of tricyclic swelling of the tongue.
antidepressants (see Chapter 10). It causes muscle relaxation in Alcohol, phenothiazines, and other CNS depressants may
acute muscle spasticity, but it is not effective in cases of cerebral cause additive sedation. Cyclobenzaprine should not be used
palsy or diseases of the brain and spinal cord. This medication is within two weeks of an MAOl because hyperpyretic crisis and
meant to provide therapy for only two to three weeks. convulsions may occur.
Spasticity
Spasticity is a condition in which muscle groups remain in a continuous state of contraction, usually as a
result of damage to the CNS. The contracting muscles become stiff with increased muscle tone. Signs and
symptoms may include mild to severe pain, exaggerated deep tendon reflexes, muscle spasms, scissoring
(involuntary crossing of the legs), and fixed joints.
Effective treatment for spasticity includes both physical therapy and

Core Concept 12.11 medications.
spasticity 5 rigidly stiff Spasticity usually results from damage to the motor area of the cerebral cortex, which controls muscle
muscles movement. Etiologies most commonly associated with this condition include neurologic disorders such
dys 5 abnormal as cerebral palsy, severe head injury, spinal cord injury or lesions, and stroke. Dystonia, a chronic
tonia 5 tension neurologic disorder, is characterized by involuntary muscle contraction that forces body parts into ab-
normal, occasionally painful movements or postures. It affects the muscle tone of the arms, legs, trunk,
neck, eyelids, face, or vocal cords. Spasticity, whether short term or long term, can be distressing and
greatly impacts an individual’s quality of life. In addition to causing pain, it also impairs physical
mobility, thereby influencing the person’s ability to perform ADLs and diminishing his or her sense of
independence.
Nursing Process Focus Patients Receiving Drugs for Muscle Spasms or Spasticity
Prior to administration: ■ Pain (acute/chronic) related to muscle spasms

■ Obtain a complete health history including cardiovascular, respiratory, ■ Impaired Physical Mobility related to acute/chronic pain
and neuromuscular conditions, allergies, drug history and possible ■ Risk for Injury related to adverse effects of drug therapy
drug interactions. ■ Deficient Knowledge related to a lack of information about drug
■ Acquire baseline vital signs and ECG. therapy or disease process
■ Evaluate laboratory blood levels: CBC, chemistry, drug screening, renal
and liver function studies.
■ Determine neurologic status; especially LOC and neurological effects
on the motor and respiratory function.
The patient will:

■ Experience therapeutic effects (a decrease in pain, increase in range of motion and reduction of muscle spasms).
Implementation
■ Monitor LOC and vital signs. (Some skeletal muscle relaxants alter the Instruct the patient to:
patient’s LOC. Others within this class may alter blood pressure and ■ Avoid driving and other activities requiring mental alertness until the
heart rate.) effects of the medication are known.
■ Report any significant change in sensorium, such as slurred speech,
confusion, hallucinations, or extreme lethargy.
■ Report palpitations, chest pain, dyspnea, unusual fatigue, weakness,
and visual disturbances.
■ Avoid using other CNS depressants such as alcohol that will intensify
sedation.
■ Monitor pain and provide proper medication. Determine the location, Instruct the patient to:
duration, and precipitating factors of the patient’s pain. (Drugs should ■ Report the development of new sites of muscle pain.
diminish the patient’s pain.) ■ Take medications as ordered.
■ Provide additional pain relief measures such as positional support, Instruct the patient:
gentle massage, and moist heat or ice packs. (Drugs alone may not be ■ That complementary pain interventions such as positioning, gentle
sufficient in providing pain relief.) massage, and the application of heat or cold to the painful area may
be helpful.
■ In relaxation techniques, deep breathing, and meditation methods to
facilitate relaxation and reduce pain.
■ Monitor muscle tone, range of motion, and degree of muscle spasm. Instruct the patient:
(Helps to determine the effectiveness of drug therapy and possible ■ To perform gentle range of motion, only to the point of mild physical
need for changes in drug therapy.) discomfort, throughout the day.
■ That medication may cause a decrease in muscle strength and dosage
may need to be reduced.

■ Monitor for adverse effects such as drowsiness, weakness, fatigue, dry Instruct the patient:
mouth, dizziness, faintness, rash, blurred vision, photosensitivity, rash, ■ To report any adverse effects to healthcare provider.
tachycardia, erratic blood pressure, photosensitivity, and urinary reten- ■ To take medication with food to decrease GI upset.
tion. (These adverse effects may occur with common antispasmodic ■ That frequent mouth rinses, sips of water, and sugarless candy or gum
drugs). may help with dry mouth.
■ To report signs of urinary retention such as a feeling of urinary
bladder fullness, distended abdomen, and discomfort.
■ To use sunscreen and protective clothing when outdoors.
■ Administer medication correctly and evaluate the patient’s knowledge ■ Advise the patient not to abruptly discontinue medication. This action
of proper administration. Do not abruptly stop providing medication may result in withdrawal reactions such as visual hallucinations,
and monitor for withdrawal symptoms. (Abrupt withdrawal of drugs paranoid ideation, and seizures.
such as baclofen may cause serious symptoms.)
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Tables 12.6 and
12.7 for lists of drugs to which these nursing actions apply.
CAM TherapY
Cayenne for Muscular Tension
Cayenne (Capsicum annum), also known as chili pepper, paprika, or red pepper, has been
used as a remedy for muscle tension and associated pain. Applied in a cream base, it is
commonly used to relieve muscle spasms in the shoulder and areas of the arm. Capsaicin,
the active ingredient in cayenne, diminishes the chemical messengers that travel through the
sensory nerves, thereby decreasing the sensation of pain. Its effect accumulates over time, so
creams containing capsaicin need to be applied regularly to be effective. Although no known
medical condition exists that would prevent the use of cayenne, it should never be applied
over broken skin. External use of full-strength cayenne should be limited to no more than
two days, because it may cause skin inflammation, blisters, and ulcers. It also needs to be kept
away from eyes and mucous membranes to avoid burns. Hands must be washed thoroughly
after usage. Commercial OTC creams containing capsaicin are available.
Effective treatment for spasticity includes both physical therapy and medications. Medications alone are not
adequate to reduce the complications of spasticity, but regular and consistent physical therapy exercises have been
shown to be effective in decreasing the severity of symptoms. Types of treatment include muscle stretching to
help prevent contractures, muscle group strengthening exercises, and r epetitive motion exercises for improvement
of accuracy. In extreme cases, surgery for tendon release or to sever the nerve-muscle pathway has been used.
Some drugs for spasticity provide relief by acting directly on muscle

tissue, interfering with the release of calcium ions. Core Concept 12.12
Drugs that are effective in the treatment of spasticity include two centrally acting drugs, baclofen (Lioresal)
and diazepam (Valium), and a direct-acting drug, dantrolene (Dantrium). The direct-acting drugs produce
an antispasmodic effect at the level of the neuromuscular junction, as shown in Figure 12.3 ■.
Dantrolene relieves spasticity by interfering with the release of calcium ions in skeletal muscle. Other
direct-acting drugs include incobotulinumtoxin A (Xeomin), onabotulinumtoxin A (Botox, Dysport), and
rimabotulinumtoxin B (Myobloc). Although these botulinum toxins are generally known for their use in
cosmetic procedures, in some instances they may offer temporary relief of dystonia symptoms.
Botulinum toxin is an unusual drug because in high doses it acts as a poison. Clostridium botulinum
is the bacterium responsible for food poisoning or botulism. At lower doses, however, this drug is safe and
effective as a muscle relaxant. It produces its effect by blocking the release of acetylcholine from choliner-
gic nerve terminals (see Chapter 8). Botulinum can cause extreme weakness, so its use may require the ad-
dition of other therapies to improve muscle strength. To prevent major problems with mobility or posture,
botulinum toxin is often applied to small muscle groups. Sometimes this drug is administered together with
centrally acting oral medications to further increase the functional use of a range of muscle groups.
F i g u re 1 2 . 3
1 Spasticity: Sarcomere contracting 2 Administration of antispasmodics Botulinum toxin (Botox;

Myobloc) blocks release of Ach.
Dependent on calcium release Neuron
Symptoms: Dantrolene (Dantrium) blocks
Axon calcium release within muscle.
• Pain
• Immobility
• Inability to perform ADLs
Direction of
Myofibrils nerve signal Skeletal
Cell body muscle
(effector)
Sarcomere contracting Thick filaments Arrival of Synaptic
(myosin) nerve terminals
impulse
Thin filaments
(actin)
Neuromuscular
Tightened muscles Myosin junction
3 Sarcomere at rest Vesicles

containing
Result of drug therapy:
neurotransmitter
• Reduced pain
molecules
• Mobility
(acetylcholine)
• Greater range of muscle activity
Sarcomere at rest
Synaptic
Neurotransmitter
cleft
receptors
Initiation of new
Relaxed muscles impulse
The use of antispasmodics, which block release of Ach or calcium, can result in reduced pain as well as greater mobility
and range of motion.
Drawbacks to botulinum therapy are its delayed and limited effects. The treatment is mostly effective
blepharospasm 5 within six weeks of administration, and its effects last for only three to six months. Another drawback is
involuntary blinking of the the pain of injecting botulinum directly into the muscle. Local anesthetics are usually given to block this
eyelids pain. Direct-acting antispasmotic drugs are summarized in Table 12.7 ◆.
Table 12.7 Direct-Acting Antispasmodic Drugs

dantrolene (Dantrium) PO; 25 mg daily; increase to 25 mg bid–qid; may Hydantoin-like medication; also for the treatment
increase every 4–7 days up to 100 mg bid–tid of malignant hyperthermia; IV form available
incobotulinumtoxin A (Xeomin) 120 units injected per treatment session directly For treatment of cervical dystonia and involuntary
into target muscle blinking of the eyelids (blepharospasm)
onabotulinumtoxin A (Botox, 25 units injected directly into target muscle (max: Mainly used for cosmetic procedures, this drug
Dysport) 30-day dose should not exceed 200 units) has been used to treat excessive sweating and
wrinkles; relaxes facial muscles around the eye and
forehead
rimabotulinumtoxin B (Myobloc) 2,500–5,000 units/dose injected directly into target May be used in cases of cervical dystonia
muscle; doses should be divided among muscle
groups
Drug Prototype: Dantrolene (Dantrium)

Therapeutic Class: Skeletal muscle relaxant, peripheral-acting
Pharmacologic Class: Skeletal muscle calcium release blocker
Actions and Uses: Dantrolene is often used for spasticity, espe- antihistamines, alcohol, or other CNS depressants. Verapamil
cially for spasms of the head and neck. It directly relaxes muscle and other calcium channel blockers taken with dantrolene in-
spasms by interfering with the release of calcium ions from stor- crease the risk of ventricular fibrillation and cardiovascular col-
age areas inside skeletal muscle cells. It does not affect cardiac lapse. Patients with impaired cardiac or pulmonary function or
or smooth muscle. Dantrolene is especially useful for muscle hepatic disease should not take this drug.
spasms when they occur after spinal cord injury or stroke and
in cases of cerebral palsy, multiple sclerosis, and occasionally for
the treatment of muscle pain after heavy exercise. It is also used
for the treatment of malignant hyperthermia. Black Box Warning:
Dantrolene has a potential for hepatotoxicity. Liver
Adverse Effects and Interactions: Adverse effects include muscle dysfunction may be evidenced by blood chemical enzyme
weakness, drowsiness, dry mouth, dizziness, nausea, diarrhea, levels. The risk of hepatic injury is greater in females over
tachycardia, erratic blood pressure, photosensitivity, and urinary 35 years of age and after 3 months of therapy. Therapy
retention. should be discontinued after 45 days if no observable
Dantrolene interacts with many other drugs. For example, benefit.
it should not be taken with OTC cough preparations and
Quinine sulfate (Quinamm, Quiphile) has been used to treat nocturnal leg cramps, but in 2006 the
FDA issued a warning that quinidine sulfate produces serious adverse effects such as cardiac dysrrhyth-
mias, severe hypersensitivity reactions, and an abnormal platelet count. Labelling of the drug was modified
to restrict the use of quinine sulfate for malaria only and not for leg cramps.
Neuromuscular blocking drugs block the effect of acetylcholine at the

receptor. Core Concept 12.13
Neuromuscular blocking drugs bind to nicotinic receptors located on the surface of skeletal muscle
f ibers. For pharmacotherapy drugs called nicotinic blocking drugs interfere with the binding of nicotin 5 nicotine
acetylcholine, thereby preventing voluntary muscle contraction. Nicotinic blocking drugs are cholinergic ic 5 related to
(see Chapter 8). cholin 5 acetycholine
Neuromuscular blocking drugs are classified into two major categories: nondepolarizing blockers and erg 5 work (action)
depolarizing blockers. Nondepolarizing blockers compete with acetylcholine for the receptor. As long as ic 5 related to
drugs interfere with the binding of acetylcholine, muscles remain relaxed. By a related mechanism, de-
polarizing blockers bind to the acetylcholine receptor and produce a state of continuous depolarization.
Remember that depolarization is the rapid cycling influx of sodium into neurons, propagating the electrical
signal. This action first results in small fasciculations or a time of brief repeated muscle movements, fol- fascicu 5 muscle fascicle
lowed by relaxation of muscle fibers. Relaxation is short-lived until charges across the muscle membrane (bundle)
are restored (repolarization). Importantly, patients treated with neuromuscular blockers are able to feel pain lation 5 movement
even though they cannot react to it. Thus, for surgical procedures, concomitant use of anesthetic agents is
essential (see Chapter 15).
It is important to note that neuromuscular blocking drugs are different from ganglionic blocking drugs ganglion 5 cell bodies
that target the autonomic nervous system. With ganglionic blocking drugs, acetylcholine does indeed bind grouped outside CNS
to nicotinic receptors, but the resulting actions of these drugs are involuntary and do not involve skeletal
muscle (see Chapter 8). Ganglionic blockers dampen parasympathetic tone and produce effects such as
increased heart rate, dry mouth, urinary retention, and reduced GI activity. They also dampen sympathetic
tone, resulting in reduced sweating and less norepinephrine being released from postsynaptic nerve ter-
minals. As an example, mecamylamine (Inversine) is a ganglionic blocker primarily used to treat patients
with essential hypertension (see Chapter 18).
The classic example of a nondepolarizing blocker is tubocurarine. Tubocurarine and related blocking
drugs are used to relax the muscles of patients being prepared for longer surgical procedures (Table 12.8 ◆).
Although not preferred for mechanical ventilation or endotracheal intubation, small doses of these drugs
may be used for intermediate surgical procedures. Concerns of tubocurarine-like treatment include over-
relaxation of muscles. For example, normal breathing activity (involving the diaphragm, glottic, and in-
tercostal muscles) and swallowing activity (involving the neck and certain esophageal muscles) require
skeletal muscle contraction.
Table 12.8 Neuromuscular Blocking Drugs

Drug Duration Administration Route
Nondepolarizing Blockers
atracurium (Tracrium) Long duration IV
cisatracurium (Nimbex) Long duration IV
mivacurium (Mivacron) Shorter duration IV
pipecuronium (Arduan) Longest duration IV
rocuronium (Zemuron) Long duration IV
tubocurarine Longest duration; oldest of the nondepolarizing IV and IM
drugs
vecuronium (Norcuron) Long duration IV
Depolarizing Blockers
succinylcholine (Anectine) (see Shortest duration IV and IM
page 228 for the Drug Prototype
box)
Depolarizing agents are used primarily to relax the muscles of patients receiving e lectroconvulsive
malignant 5 harmful therapy (ECT) (see Chapter 13) and for brief surgical procedures (see Chapter 15). Short surgical
hyper 5 elevated procedures involve mechanical ventilation and endotracheal intubation. Succinylcholine (Anectine) is the
thermia 5 fever
prototype example of a depolarizing blocker. Adverse effects include elevated blood levels of potassium,
post 5 after malignant hyperthermia, and postoperative muscle pain and persistent paralysis in some patients. As a
operative 5 surgery specific antidote for persistent paralysis, patients are often given cholinesterase inhibitors.

Patients being treated for degenerative diseases and disorders of the neuromuscular
system need to know the following:
Regarding Drugs for Parkinson’s Disease or Dementia

1. T ake levodopa–carbidopa at least 30–60 minutes before eating in order to allow the
medication to be absorbed before food can interfere. Do not take with foods that
contain protein, as these foods can decrease drug effectiveness.
2. Be extremely careful about getting up quickly from a seated position. Many dementia
drugs cause dizziness, lightheadedness, blurred vision, and difficulty in concentrating.
3. Do not skip taking the medications, and do not take OTC preparations (especially
medications for colds or pain) without checking with a healthcare provider.
4. Be aware that urine may become a little dark. This is a normal side effect of
dopamine-like drugs.
5. Do not drink alcoholic beverages or take sedatives. Combined effects may be harmful.
6. Be familiar with adverse effects specific for the drugs being taken. Drugs used for
Parkinson’s may produce nausea, dry mouth, and diminished sweating in some cases.
Drugs used for dementia may cause nausea, diarrhea, muscle cramps, weight loss, and
change in urine color.
Regarding Drugs for Muscle Spasms and Spasticity

7. When receiving treatment for problems with mobility, it often takes several weeks for
effectiveness to begin. Follow the advice of a healthcare provider in order to achieve
full therapeutic effect.
8. Most antispasmodic drugs produce adverse effects such as drowsiness and dizziness.
Therefore, avoid CNS depressants and alcohol.
Regarding Neuromuscular Blockers

9. S ome patients react adversely to neuromuscular blockers. Inform the healthcare pro-
vider about any important family history, such as malignant hyperthermia, myasthenia
gravis, cardiovascular disease, and any other unusual problems.
10. Be aware that unpleasant muscle pain may be associated with surgical procedures.
Chapter Review 177
Chapter Review
12.1 Medications are unable to cure most degenerative acetylcholine levels increase and produce a greater ef-
diseases of the CNS. fect on the receptor. This treatment improves function
Degenerative diseases of the CNS include Alzheimer’s in activities of daily living, behavior, and cognition.
disease, multiple sclerosis, and Parkinson’s disease.
12.6 Symptoms of multiple sclerosis result from demy-
The cause of most neurologic degenerative disorders
elination of CNS nerve fibers.
is unknown. With the exception of Parkinson’s dis-
ease, drug therapy provides only minimal benefit. Multiple sclerosis is an autoimmune disorder of the
CNS. Antibodies slowly destroy myelin in the brain
12.2 Parkinson’s disease is progressive, with the occur- and spinal cord, disrupting the ability of nerves to
rence of full symptoms taking many years. conduct electrical impulses. Over time, debilitating
Parkinson’s disease, or parkinsonism, is a degenera- symptoms appear, including fatigue, heat sensitivity,
tive disorder caused by death of neurons that produce pain, muscle cramps and spasms, impaired ability to
the brain neurotransmitter dopamine. Dopamine- think and reason, balance and coordination problems,
producing neurons in the substantia nigra supply and bowel and bladder symptoms.
nerve signals to the corpus striatum. When dopamine
12.7 Drugs for multiple sclerosis reduce immune attacks
is depleted, symptoms of parkinsonism, including
in the brain and treat unfavorable symptoms.
tremors, muscle rigidity, bradykinesia (slow move-
ment), and postural instability, occur. These symp- Two strategies for treating MS are reducing the im-
toms are the same EPS effects caused by prolonged mune response and relieving the symptoms. The
antipsychotic drug treatment. most treatable form of MS is relapsing-remitting
MS (RRMS), in which unpredictable relapses occur.
12.3 Antiparkinson drugs act on the brain to restore the Drug treatments include immune system modulating
balance between dopamine and acetylcholine. drugs, immunosuppressants, and miscellaneous drugs
Balance, posture, muscle tone, and involuntary mus- used for treatment of MS symptoms such as inflam-
cle movement depend on the proper balance between mation, pain, fatigue, memory loss, and progressive
the neurotransmitter dopamine (inhibitory) and ace- weakness.
tylcholine (stimulatory) in the corpus striatum. Drug
therapy for parkinsonism focuses on restoring dopa- 12.8 Muscle spasms are caused by injury, overmedica-
mine function (dopaminergic drugs) and blocking tion, hypocalcemia, and debilitating neurologic
the effect of acetylcholine overactivity (cholinergic disorders.
blockers). Muscle spasms, or involuntary contractions of a
muscle or group of muscles, occur for many reasons,
12.4 Patients with Alzheimer’s disease experience including overmedication with antipsychotic drugs,
a dramatic loss of ability to perform tasks that epilepsy, hypocalcemia, pain, and incapacitating neu-
require acetylcholine as the CNS neurotransmitter. rologic disorders. Two types of muscle spasms are
Alzheimer’s disease (AD) is a devastating, progres- tonic spasms and clonic spasms.
sive, degenerative disease characterized by impaired
memory, confusion or disorientation, inability to rec- 12.9 Muscle spasms may be treated with nonpharma-
ognize family or friends, aggressive behavior, depres- cologic or pharmacologic therapies.
sion, psychoses, and anxiety. AD is responsible for After a thorough medical exam, nonpharmacologic
70% of all dementia. Although the cause of AD is therapies such as immobilization, heat or cold, hydro-
unknown, structural brain damage and a dramatic loss therapy, ultrasound, supervised exercises, massage,
of ability to perform tasks that require acetycholine as and manipulation may be used along with medica-
the neurotransmitter have been documented. tions. Medications include analgesics, anti-inflam-
matory drugs, and centrally acting skeletal muscle
12.5 Alzheimer’s disease is treated with acetylcholines- relaxants.
terase inhibitors.
Only a few drugs for AD have been approved. Most 12.10 Many muscle relaxants treat muscle spasms by
drugs act by intensifying the effect of acetylcholine inhibiting upper motor neuron activity, causing
at the cholinergic receptor. Acetylcholine is naturally sedation, or altering simple reflexes.
degraded in the synapse by the enzyme acetylcho- Skeletal muscle relaxants treat local spasms resulting
linesterase. When acetylcholinesterase is inhibited, from muscular injury and may be prescribed alone or
in combination with medications that reduce pain and 12.12 Some drugs for spasticity provide relief by act-
increase range of motion. These include centrally acting directly on muscle tissue, interfering with the
ing drugs (affecting the brain and/or spinal cord) that release of calcium ions.
have the potential to cause sedation and alter reflex Direct-acting drugs produce an antispasmodic effect
activity. at the level of the neuromuscular junction. Drugs af-
fect either calcium release from the muscle, or they
12.11 Effective treatment for spasticity includes both
interfere with the release of acetylcholine.
physical therapy and medications.
Spasticity is a condition in which certain muscle 12.13 Neuromuscular blocking drugs block the effect of
groups remain in a state of contraction. Symptoms acetylcholine at the receptor.
associated with spasticity include pain, exaggerated Neuromuscular blocking drugs are classified as non-
deep tendon reflexes, muscle spasms, scissoring, and depolarizing blockers and depolarizing blockers. Both
fixed joints. Medications alone are not adequate in drugs bind to acetylcholine receptors, relaxing muscles
reducing the complications of spasticity. by slightly different mechanisms and durations of action.
Review Questions
The following questions are written in NCLEX-PN® style. An- 5. The patient with Alzheimer’s disease has been started on
swer these questions to assess your knowledge of the chapter rivastigmine (Exelon). The nurse will evaluate the patient for:
material, and go back and review any material that is not clear 1. Liver toxicity
to you. 2. Weight loss
1. The patient taking levodopa is taught that he must wait at 3. Renal failure
least one hour before or after eating foods high in: 4. EPS
1. Vitamin C 6. A patient had a surgical procedure in which succinylcho-
2. Carbohydrates line (Anectine) was used to relax the muscles. The nurse tak-
3. Folic acid ing care of this patient would monitor the patient for:
4. Protein 1. Hypothermia
2. A patient in the early stages of Alzheimer’s disease was 2. Complaints of muscle pain
started on donepezil (Aricept) a few weeks ago. She calls the 3. High sodium levels (hypernatremia)
nurse at the doctor’s office and states that she has been expe- 4. Low levels of potassium (hypokalemia)
riencing what she believes to be adverse effects of the drug. 7. A patient is given a prescription for carisoprodol (Soma),
Which of the following effects could the patient be experienc- 350 mg, po, three times a day. The pharmacy provides a bottle
ing? (Select all that apply.) of 350 mg tablets. If the patient follows the directions, how
1. Sleepiness many milligrams will the patient take in one day?
2. Nausea 1. 900 mg
3. Diarrhea 2. 1,115 mg
4. Tinnitus 3. 1,050 mg
3. When administering levodopa to a patient with Parkin- 4. 1,015 mg
son’s disease, the nurse understands that this drug: 8. An interferon is prescribed for a patient with MS. The
1. Increases cholinergic stimulation within the brain nurse includes which of the following points when educating
2. Restores acetylcholine and blocks dopamine within the the patient about drug therapy?
brain 1. Report flu-like symptoms to the healthcare provider.
3. Restores dopamine function and blocks acetylcholine 2. Expect urine to be orange.
within the brain 3. Report the development of diarrhea.
4. Destroys dopamine receptors within the brain 4. The symptoms will get better over a period of a year.
4. The patient with Parkinson’s disease is placed on haloper-
idol (Haldol) because of agitation and has started experiencing
EPS. Which of the following drugs would the nurse anticipate
being ordered?
1. Levodopa–carbidopa drugs
2. Risperidone (Risperdal)
3. Benztropine (Cogentin)
4. Cyclobenzaprine (Flexeril)
Chapter Review 179
9. A patient is being seen in the emergency room after an 10. A patient with a spinal cord injury is still suffering from
automobile accident. She complains that her lower back hurts. muscle spasms. The physician has prescribed dantrolene to
After an examination and x-ray, the patient is given a diagno- help control the spasms. The nurse informs the patient that he
sis of muscle strain, with associated spasms, and is placed on should report which of the following possible adverse effect(s)
cyclobenzaprine (Flexeril) to help relax the muscles. In edu- if they should occur:
cating the patient about the cyclobenzaprine, the nurse informs 1. Excessive salivation
her that: (Select all that apply.) 2. Excessive urination
1. It can cause drowsiness. 3. Muscle weakness
2. If taken with alcohol, additional drowsiness may occur. 4. Insomnia
3. It is only intended for short-term use (2–3 weeks).
3. It can cause headaches.
Remember Mr. Wingate, the patient in- 2. After being started on the immune system modulator,
troduced at the beginning of the chap- Mr. Wingate asks the nurse about this class of medications.
ter? Now read the remainder of the case The nurse responds by saying: (Select all that apply.)
study. Based on the information you have 1. “These drugs slow down the destruction of the neuron
learned in this chapter, answer the ques- caused by MS.”
tions that follow. 2. “These drugs have very few adverse effects.”
Mr. Robert Wingate, a 35-year-old man 3. “There are no precautions when taking this type of drug
with MS, has persistent pain in his right with other drugs.”
hip and comes in for treatment. He ex- 4. “Adverse effects can include fever, chills, and muscle
plains that he has been taking enteric-coated aspirin for sev- aches.”
eral weeks. He explains that he has been experiencing severe
3. In evaluating the effectiveness of Mr. Wingate’s
headaches. He has also been experiencing muscle twitches a ntispasmodic therapy, the nurse would expect that the
(multiple, rapidly repeating contractions) in his right ham- medication would:
string. The muscle twitches have not been severe, but he is
concerned that they may be related to his condition. Lately, 1. Improve Mr. Wingate’s symptoms for the long term.
he has been experiencing quite a bit of fatigue, and his vision 2. Improve Mr. Wingate’s symptoms for the short term.
is sometimes “blurry.” Laboratory values show slight hypo- 3. Make Mr. Wingate’s symptoms worse.
calcemia. The patient explains that he hasn’t had any trouble 4. Cause Mr. Wingate to be sedated.
with his diet. No abnormalities in bone structure or peripheral 4. If Mr. Wingate’s condition and symptoms were to
inflammatory symptoms are observed on examination. p rogress significantly, the nurse would expect to administer
which of the following drugs?
1. The nurse caring for Mr. Wingate just received a medica-
tion order to administer an immune system modulator. Which 1. Selegiline (Eldepryl, Zelapar)
of the following medications might the nurse administer? 2. Gabapentin (Neurontin)
3. Mitoxantrone (Novantrone)
1. Amantadine (Symmetrel) 4. Donepezil (Aricept)
2. Interferon beta-1b (Betaseron)
3. Memantine (Namenda)
4. Gabapentin (Neurontin)

C
“I felt so helpless when I
H found out Destiny’s problem
A was seizures. I’m glad
P there’s a medication that will
help her live a normal life.”
T
Mrs. Kemi Anthonia
E
R
13 Drugs for Seizures
Core Concepts
13.1 Although some types of seizures involve convulsions, 13.5 Antiseizure pharmacotherapy is directed at control-
other seizures do not. ling the movement of electrolytes across neuronal
13.2 Many causes of seizure activity are known; a few membranes or affecting neurotransmitter balance.
are not. 13.6 By increasing the effects of gamma-aminobutyric
13.3 Epileptic seizures are typically identified as partial, acid or GABA in the brain, some drugs reduce a wide
generalized, or special epileptic syndromes. range of seizure types.
13.4 Effective seizure management involves strict 13.7 Hydantoin and related drugs are generally effective
adherence to safe drug therapy. in treating partial seizures and tonic-clonic seizures.
13.8 Succinimides generally treat absence seizures.
Drug Snapshot
Drugs That Potentiate GABA Action Hydantoin and Related Drugs
Barbiturates phenobarbital Hydantoins phenytoin (Dilantin) 190
(Luminal) 188
Phenytoin-like drugs valproic
acid
Benzodiazepines diazepam (Valium) 188 (Depakene) 191
Other GABA-Related Drugs Succinimides ethosuximide

(Zarontin) 192
Learning Outcomes
1. Compare and contrast the terms pharmacotherapy of epilepsy and 7. Explain the mechanisms of action by
epilepsy, seizures, and convulsions. seizures. which barbiturates, benzodiazepines,
2. Recognize possible causes of and miscellaneous drugs control
5. Describe the pharmacologic seizure activity.
seizures. management of epilepsy and acute
seizures. 8. For each of the classes listed in the
3. Relate signs and symptoms to specific
Drug Snapshot, identify representative
types of seizures. 6. Categorize drugs used in the drugs and explain their mechanisms
4. Explain the importance of safety treatment of seizures based on their of drug action, primary actions, and
and patient drug compliance in the classifications. important adverse effects.
Key Terms
action potential (poh-TEN-shial) 189 febrile seizures 182 seizure (SEE-zhurr) 181
convulsions (kon-VULL-shuns) 181 generalized seizures 183 status epilepticus (ep-ih-LEP-tih-kus) 184
eclampsia (ee-KLAMP-see-uh) 183 partial (focal) seizures 183
epilepsy (EPP-ih-lepp-see) 181 pre-eclampsia (pree-ee-KLAMP-see-uh) 183
A s the most common neurologic disorder, epilepsy affects more than 2 million Americans. By
definition, epilepsy is any condition characterized by recurrent seizures. Symptoms of epilepsy
depend on the type of seizure and may include signs such as blackout, fainting spells, sensory
disturbances, jerking body movements, and temporary loss of memory. This chapter examines the drug
therapies used to treat different kinds of seizures and epilepsy.
epilepsy = taking hold or
to seize
Seizures
A seizure is a disturbance of electrical activity in the brain that may affect consciousness, motor activity,
and sensation. Seizures are caused by abnormal or uncontrolled neuronal discharges. Uncontrolled charges
start in one area of the brain and often move to other areas. As a valuable tool in measuring uncontrolled
neuronal activity, the electroencephalogram (EEG) is useful in diagnosing seizure disorders. Figure 13.1 ■
compares normal and abnormal neuronal tracings.
Although some types of seizures involve convulsions, other

seizures do not. Core Concept 13.1
Seizures and convulsions are not interchangeable terms. Convulsions specifically refer to involuntary, vio-
lent spasms of large skeletal muscles of the face, neck, arms, and legs. Although some types of seizures
involve convulsions, other seizures do not. Thus, it may be stated that all convulsions are seizures, but not
all seizures are convulsions.
Figure 13.1
Patient A. Normal
Patient B. Absence seizure
Patient C. Generalized tonic–clonic seizure
Neurons produce tiny impulses when they communicate. These impulses may be detected by an electroencephalogram
(EEG), a device that captures brain-wave activity. Brain waves have characteristic patterns termed alpha, beta, delta,
and theta. Although interpretation of brain waves is a complex art, you can see from these examples that the EEG
tracings of patients B and C are dramatically different from those of patient A, who has no seizures. Alpha waves
are the predominant waveform observed in patients with normal brain activity.
182 Chapter 13 Drugs for Seizures
Fast Facts Epilepsy

■ Over two million Americans have epilepsy.
■ One of every 100 teenagers has epilepsy.
■ Of the U.S. population, 10% will have seizures within their lifetime.
■ Most people with seizures are younger than 45 years of age.
■ Epilepsy is not a mental illness and children with epilepsy have IQ scores equivalent to those of
children without the disorder.
■ Famous people who had epilepsy include Julius Caesar, Alexander the Great, Napoleon, Vincent
van Gogh, Charles Dickens, Joan of Arc, and Socrates.
■ Among adult alcoholics receiving treatment for withdrawal, over half will experience seizures
within six hours upon arriving for treatment.
Drugs described in this chapter are generally referred to as antiseizure drugs rather than
a nticonvulsants. Recognizing also that antiseizure drugs are commonly called antiepileptic drugs (AEDs),
the term antiseizure in this chapter applies to the treatment of all seizure-related symptoms, including signs
of epilepsy.
Core Concept 13.2 Many causes of seizure activity are known; a few are not.
A seizure is considered symptomatic of an underlying disorder, rather than a disease in itself. Triggers
include exposure to strobe or flickering lights or the occurrence of small fluid and electrolyte imbalances.
Patients appear to have a lower tolerance to environmental triggers, and seizures often occur when patients
are sleep deprived.
There are many different causes of seizure activity. In some cases, the cause of seizure activity may
be clear, but not in all situations. Seizures represent the most common serious neurologic problem affecting
idio = one’s unknown arising children, with an overall incidence approaching 2% for febrile seizures and 1% for idiopathic epilepsy.
pathic = abnormal state Certain medications for mood disorders, psychoses, and local anesthesia may cause seizures when given
in high doses, possibly because of increased levels of stimulatory neurotransmitters or toxicity. Seizures
may also occur from drug abuse, as with cocaine, or during withdrawal from alcohol or sedative–hypnotic
drugs.
Seizures may present as an acute situation, or they may occur on a chronic basis. Seizures resulting
from an acute complication are generally not recurrent after the situation has been resolved. On the other
hand, if a brain abnormality exists following an acute complication, recurrent seizures are likely. The fol-
lowing are known causes of seizures:
■ Infectious diseases Acute infections such as meningitis and encephalitis can cause inflamma-
tion in the brain.
■ Trauma Physical trauma such as direct blows to the skull may increase intracranial pressure;
chemical trauma such as the presence of toxic substances or the ingestion of poisons may cause
brain injury.
■ Metabolic disorders Changes in fluid and electrolytes such as hypoglycemia, hyponatremia,
and water intoxication may cause seizures by altering electrical impulse transmission at the
cellular level.
■ Vascular diseases Changes in oxygenation such as those caused by respiratory hypoxia and
carbon monoxide poisoning, and changes in perfusion such as those caused by hypotension,
cerebral vascular accidents, shock, and cardiac dysrhythmias may be causes.
■ Pediatric disorders Rapid increase in body temperature may result in a febrile seizure.
■ Neoplastic disease Tumors, especially rapidly growing ones, may occupy space, increase
intracranial pressure, and damage brain tissue by disrupting blood flow.
An important topic when discussing epilepsy and seizure treatment is birth control. Because several
antiseizure drugs decrease the effectiveness of oral contraceptives, additional barrier methods of birth con-
trol should be practiced to avoid unintended pregnancy. Prior to pregnancy and considering the serious
nature of epilepsy, patients should consult with their healthcare provider to determine the most appropriate
plan of action for seizure control.
If patients become pregnant, extreme caution is necessary. Most antiseizure drugs are pregnancy cat-
egory D. Some antiseizure drugs may cause folate deficiency, a condition correlated with fetal neural tube
defects. Vitamin supplements may be necessary.
Pre-eclampsia and eclampsia are severe hypertensive disorders of pregnancy, characterized by sei-
zures, coma, and perinatal mortality. Eclampsia is likely to occur from around the 20th week of gestation to
at least one week following delivery of the baby. Roughly one-fourth of patients with eclampsia experience
seizures within 72 hours postpartum. post = after
Seizures can have a significant impact on the quality of life. They may cause serious injury if they partum = delivery
occur when a person is driving a vehicle or performing a dangerous activity. Without successful pharmaco-
therapy, epilepsy can severely limit participation in school, employment, or social activities and can affect
self-esteem. Chronic depression may accompany poorly controlled seizures. Important considerations in
health care include identifying patients at risk for seizures, documenting the pattern and type of seizure
activity, and implementing safety precautions. In collaboration with the patient, the healthcare provider,
pharmacist, and all healthcare staff are instrumental in achieving positive therapeutic outcomes. Through
a combination of pharmacotherapy, patient–family support, and education, effective seizure control can be
achieved in the majority of patients.
Epileptic seizures are typically identified as partial, generalized, or special

epileptic syndromes. Core Concept 13.3
Seizure symptoms vary depending on the areas of the brain affected by the abnormal electrical activity.
These symptoms range from muscle twitching or slight tremor (shaking) of a limb to sudden, violent shak- Life Span Fact
ing and total loss of consciousness. Staring into space, altered vision, and difficult speech are other behav- Onset of epilepsy is most com-
iors a person may exhibit during a seizure. It is important to determine the cause of recurrent seizures in mon among the youngest and
order to plan for appropriate treatment options. oldest age groups. About 50%
Methods of classifying epilepsy have changed over time. For example, the terms grand mal and petit of children have a generalized
mal epilepsy have been replaced by more descriptive and detailed categorization. Epilepsies are typically epilepsy syndrome compared
with about 20% of adults. The
identified using the International Classification of Epileptic Seizures. Example nomenclatures are partial
incidence of epilepsy in older
(less used term focal), generalized, and special epileptic syndromes. Types of partial or generalized sei- adults is greater than among
zures may be recognized based on symptoms observed during a seizure episode. Some symptoms are hard the general population, per-
to notice and reflect the simple nature of neuronal misfiring in specific areas of the brain; others are more haps because of the greater
complex. prevalence of mild strokes
and cardiac arrest in this age
group.
Partial Seizures
Partial (focal) seizures involve a limited portion of the brain. Abnormal electrical activity starts on one
side and travels only a short distance before it stops. The area where the abnormal electrical activity starts
is known as the abnormal focus (plural, foci).
Simple partial seizures have an onset from a small, limited focus. Patients may feel disoriented for a
while, and they may hear and see things that are not there. Some patients smell and taste things that are not
present, or have an upset stomach. Others may become emotional and experience a sense of joy, sorrow, or
grief. The arms, legs, or face may twitch.
Complex partial seizures (formerly known as psychomotor or temporal lobe seizures) have sensory, psycho = mind
motor, or autonomic symptoms with some degree of altered or impaired consciousness. Total loss of con- motor = motion or movement
sciousness may not occur during a complex partial seizure, but a period of brief confusion and somnolence somno = sleepiness
may follow the seizure. Such seizures are often preceded by an aura, sometimes described as an unpleasant lence = filled with
odor or taste. Seizures may start with a blank stare, and patients may begin to chew or swallow repetitively.
Some patients fumble with clothing; others try to take off their clothes. Most patients will not pay attention
to verbal commands and will act as if they are having a psychotic episode. After a seizure, patients do not
remember the seizure incident.
Generalized Seizures
As the name suggests, generalized seizures are not localized to one area but travel throughout the entire
brain on both sides. The seizure is thought to originate bilaterally and symmetrically within the brain. bi = two
Absence seizures (formerly known as petit mal seizures) most often occur in children and last only for lateral = sides
a few seconds. Because episodes are short-lived, they are difficult to detect. Absence epilepsy often goes sym = same
unrecognized, or this disorder may be mistaken for daydreaming/signs of attention deficit disorder. Staring metrically = measurement
and temporary loss of responsiveness are the most common signs. There may be slight motor activity with
eyelid fluttering or repetitive jerking motions.
Atonic seizures are sometimes called drop attacks. Patients often stumble and fall for no apparent a = without
reason. Lasting for only a matter of seconds, episodes are very short. tonic = tension
Tonic-clonic seizures (formerly known as grand mal seizures) are the most common type. This ap-
plies to all age groups. Seizures may be preceded by an aura (e.g., spiritual feeling, flash of light, special
noise). Intense muscle contractions indicate the tonic phase. Due to air being forced out of the lungs, a
hoarse cry may occur at the onset of the seizure. Patients may temporarily lose bladder or bowel control. Life Span Fact
Breathing may become shallow and even stop momentarily. The clonic phase is characterized by alternat- Preventing the onset of high
ing contraction and relaxation of muscles. The seizure usually lasts one to two minutes, after which the fever is the best way to control
patient becomes drowsy, disoriented, and sleeps deeply. febrile seizures in children.
Special Epileptic Syndromes

Special epileptic seizures include the febrile seizures of infancy, reflex epilepsies, and other forms of myo-
clonic epilepsies. Myoclonic epilepsies often go along with other neurologic abnormalities or progressively
debilitating symptoms.
febrile = fever Febrile seizures typically cause tonic-clonic motor activity lasting for one to two minutes, with rapid
return of consciousness. These occur together with a rapid rise in body temperature and usually occur only
once during any given illness. Febrile seizures are most likely to occur within the three-month to five-year-
old age group.
myo = muscle Myoclonic seizures are characterized by large, jerking body movements. Major muscle groups con-
clonic = repetitive jerking tract quickly, and patients appear unsteady and clumsy. They may fall from a sitting position or drop
motions whatever they are holding. Infantile spasms are an example of a type of generalized, myoclonic seizure and
are distinguished by short-lasting muscle spasms in the trunk and extremities. Such spasms are often not
identified as seizures by parents or healthcare providers because the movements are much like the normal
infantile startle reflex.
status = state of Status epilepticus is a medical emergency caused by the repeated occurrence of seizures. This state
epilepticus = seizure activity could result with any type of seizure, but usually generalized tonic-clonic seizures are observed. When
generalized tonic-clonic seizures are long and continuous, hypoxia may develop. Continuous muscle con-
hypo = lowered tractions also lead to hypoglycemia, acidosis, and hypothermia (due to increased metabolic needs, lactic
glycemia = blood sugar level acid production, and heat loss during muscle movement). Carbon dioxide retention also leads to acidosis.
thermia = body temperature If not treated, status epilepticus can cause brain damage, and ultimately, death. Medical treatment involves
acid = hydrogen ion the IV administration of antiseizure medications. During seizure activity, steps must be taken to make sure
accumulation (reduced pH; that the airway remains open.
e.g., lactic acid)
osis = condition of
Concept Review 13.1
■ What is epilepsy? What is the difference between a seizure and a convulsion? Name and
identify signs of the more common types of seizures.
Effective seizure management involves strict adherence to safe drug

Core Concept 13.4 therapy.
The choice of drug for antiseizure pharmacotherapy depends on the patient’s signs, previous medical his-
tory, and associated pathologies. Once a medication is selected, the patient is placed on a low initial dose.
The amount is gradually increased until seizure control is achieved or until drug adverse effects prevent
additional increases in dose. Serum drug levels may be obtained to assist the healthcare provider in deter-
mining the most effective drug concentration. If seizure activity continues, a different medication is added
in small-dose increments while the dose of the first drug is slowly reduced. Because seizures are likely to
occur if antiseizure drugs are abruptly withdrawn, the medication is usually discontinued over a period of
6 to 12 weeks.
Antiseizure drugs with indications are shown in Table 13.1 ◆. Some of the antiseizure drugs offer ad-
vantages over others. Owing to the limited induction of drug-metabolizing enzymes, the pharmacokinetic
profiles of the more recently approved antiseizure drugs seem to be less complicated. In addition, the more
recently approved antiseizure drugs are generally better tolerated.
One issue of antiseizure drug therapy relates to recent warnings issued by the Food and Drug Ad-
ministration (FDA). In 2008, the FDA analyzed reports from clinical studies involving patients taking a
neur(o) = nerve variety of antiseizure medications. Epilepsy, bipolar disorder, psychoses, migraines, and neuropathic pain
path = disease were among the disorders studied mainly because these were conditions emerging as disorders successfully
treated with antiseizure-type medications. Currently all of these disorders are successfully treated with
antiseizure medications as covered in Unit 2. Although antiseizure medications were originally designed
to help people who have epilepsy, the nerve-calming qualities of these drugs have helped patients with
migraines and nerve pain (neuralgia). Indeed, the usefulness of antiseizure drugs has extended beyond
pain management and actually helped calm patients with behavioral and mood disturbances: attention-
deficit hyperactivity disorder (ADHD), borderline personality disorder, and post-traumatic stress disorder
(PTSD). Antiseizure drugs have even helped patients with schizophrenia. In a warning issued by the FDA,
however, healthcare providers have been admonished to balance carefully the clinical need for antiseizure
drugs against the risk for suicidality among patients taking these drugs. Patients and caregivers are encour-
aged to pay close attention to changes in mood and not to make changes in antiseizure regimen without
consulting with their healthcare provider.
Additional drawbacks include the fact that AED use may impact early child development. In 2013, a
study of children whose mothers took AEDs while pregnant indicated an increased risk of early develop-
ment issues. These children were not able to interact socially compared to children whose mothers did
not take AEDs. Language and motor skills of the children were also impacted. Some children developed
Table 13.1 Selected Antiseizure Drugs with Indications

Generalized Seizures Special
Drug Partial Seizures Absence Tonic–Clonic Myoclonic
Drugs that Potentiate GABA
diazepam (Valium) ✓ ✓ ✓
gabapentin (Neurontin) ✓
lorazepam (Ativan) ✓
phenobarbital (Luminal) ✓ ✓
pregabalin (Lyrica) ✓
primidone (Mysoline) ✓ ✓
tiagabine (Gabitril) ✓
topiramate (Topamax, Trokendi XR) ✓ ✓ ✓
Hydantoin and Related Drugs
carbamazepine (Tegretol) ✓ ✓
lamotrigine (Lamictal) ✓ ✓ ✓ ✓
levetiracetam (Keppra) ✓
oxcarbazepine (Trileptal, Oxtellar XR) ✓ ✓
phenytoin (Dilantin) ✓ ✓
valproic acid (Depakene) ✓ ✓ ✓ ✓
zonisamide (Zonegran) ✓ ✓ ✓ ✓
Succinimides
ethosuximide (Zarontin) ✓
autistic traits. This study compounds the fact that women who take oral contraceptives and antiseizure
drugs together are at risk for pregnancy (see Chapter 34). This is a relatively well-known idea in health
care. Thus, while many antiseizure drugs have advantages, they may also have disadvantages. A good fact
to remember about all antiseizure drugs is that they can have serious clinical drawbacks if not taken safely.
Many of the antiseizure medications are used in adjunctive therapy. Some drugs have been investi- adjunctive = joined or added
gated for their potential use in monotherapy. In most cases, effective seizure management can be obtained mono = only
using only a single drug. For some patients, two antiseizure medications may be needed, although un- therapy = treatment
wanted adverse effects may appear. Some antiseizure drug combinations may actually increase the inci-
dence of seizures.
After several years of being seizure free, patients may question the need for their medication. In gen-
eral, withdrawal of antiseizure drugs should be attempted only after at least three years of seizure-free
activity and only under close direction from the healthcare provider. Doses of medications are reduced
slowly, one at a time, over a period of several months. If seizures recur during the withdrawal process,
pharmacotherapy is resumed, usually with the original stabilizing drug.
Concept Review 13.2

■ Give the names of antiseizure drugs used for the management of specific seizure types.
Match the drugs with the types of seizures they best control. Which drugs are generally
used for a broader range of seizures?
Antiseizure pharmacotherapy is directed at controlling the movement

of electrolytes across neuronal membranes or affecting
neurotransmitter balance. Core Concept 13.5
In a resting state, neurons are normally surrounded by a higher concentration of sodium ions, calcium
ions, and chloride ions. Potassium ion levels are higher inside the cell. An influx of sodium or calcium
ions into the neuron enhances neuronal activity, whereas an influx of chloride ions suppresses neuronal
activity.
The goal of antiseizure pharmacotherapy is to suppress neuronal activity just enough to prevent abnor-
mal or repetitive firing. To this end, there are three general mechanisms by which antiseizure drugs work:
■ Stimulating an influx of chloride ions, an effect associated with the neurotransmitter gamma-
aminobutyric acid (GABA)
■ Delaying an influx of sodium ions
■ Delaying an influx of calcium ions
Some drugs act by more than one mechanism. This has prompted drug researchers to try to understand
more clearly various drug mechanisms and to develop newer, better-controlled drugs. Recently a fourth
mechanism has been studied: blocking of the primary excitatory neurotransmitter glutamate. Glutamate
works in concert with the cell’s Na+-K+ ATPase pump, which helps to restore ion balances across neuronal
membranes after firing. Any drug that blocks glutamate activity prevents an influx of positive ions into the
cell, so this is consistent with the last two mechanisms.
By increasing the effects of gamma-aminobutyric acid or GABA in the

Core Concept 13.6 brain, some drugs reduce a wide range of seizure types.
Several important antiseizure drugs act by increasing the action of GABA, the primary inhibitory neurotrans-
mitter in the brain. These drugs mimic the effects of GABA by stimulating an influx of chloride ions that inter-
act with the GABA receptor–chloride channel molecule. A model of this receptor is shown in Figure 13.2 ■.
When the receptor is stimulated, chloride ions move into the cell and suppress the firing of neurons.
A number of drugs, called GABA agonists, have been found to activate the GABA receptor. Drugs
may bind directly to the GABA receptor through specific binding sites designated as GABAA or GABAB.
Most antiseizure drugs bind to the GABAA site. Drugs may enhance GABA release, or drugs may block
the reuptake of GABA into nerve cells and other supporting cells in the central nervous system (CNS).
Drugs have also been developed that inhibit GABA degrading enzymes.
Barbiturates, benzodiazepines, and several newer drugs reduce seizure activity by intensifying GABA
action. These drugs are listed in Table 13.2 ◆. The predominant effect of GABA activation is CNS depression.
The antiseizure properties of phenobarbital were discovered in 1912, and this drug is still prescribed
for seizures. As a class, barbiturates generally have a low margin for safety, a high potential for depen-
dence, and may cause significant CNS depression. Phenobarbital, however, is able to suppress abnormal
neuronal discharges without causing profound sedation. It is inexpensive, long acting, and produces a low
incidence of adverse effects. When the drug is given orally, several weeks may be necessary to achieve
optimum effects. Phenobarbital is a preferred drug used in the pharmacotherapy of neonatal seizures.
Other than phenobarbital, mephobarbital is occasionally used for epilepsy treatment. Mephobarbital
(Mebaral) is converted to phenobarbital in the liver and offers no significant advantages over phenobar-
bital. Primidone (Mysoline) has a pharmacologic profile similar to phenobarbital and is among the drugs
used to potentiate GABA action.
Like barbiturates, benzodiazepines and several other drugs intensify the effect of GABA in the
brain. The benzodiazepines bind directly to the GABA receptor, suppressing abnormal neuronal firing.
Figure 13.2
Cl-
GABA Benzodiazepines
Barbiturates
GABA receptor-chloride
channel molecule
Model of the GABA receptor–chloride channel. The chloride selectivity filter allows the channel to open exclusively to
chloride ions when GABA, benzodiazepines, or barbiturates bind to the cellular receptor (shown in green). Some anti-
seizure drugs are similar to the structure of GABA, or they may potentiate GABA indirectly. After the influx of chloride
ions, the net result is inhibition of the neuron’s action potential and suppression of the neuron’s firing rate.
Table 13.2 Antiseizure Drugs That Activate GABA Receptors (GABA Agonists)
Barbiturates
mephobarbital (Mebaral) PO; 400–600 mg/day Rarely used in the management of seizures; converted
to phenobarbital by the liver.
phenobarbital (Luminal) For partial and generalized seizures: PO; 100–300 mg/ For the management of tonic-clonic seizures, partial
day, IV/IM; 200–600 mg up to 20 mg/kg seizures, status epilepticus, and eclampsia; Schedule IV
For status epilepticus: IV; 15–18 mg/kg in single or drug; may cause respiratory depression, agranulocytosis,
divided doses (max: 20 mg/kg) laryngospasm, angioedema (swelling of the dermis).
primidone (Mysoline) PO; 250 mg/day, increased by 250 mg/wk up to a Similar treatment profile to phenobarbital.
maximum of 2 g in two to four divided doses
Benzodiazepines
clonazepam (Klonopin) PO; 1.5 mg/day in three divided doses, increased by For absence seizures and minor motor seizures; also for
0.5–1 mg every three days until seizures are controlled panic disorder; Schedule IV drug; may cause drowsiness
and impaired cognitive and motor performance.
clorazepate (Tranxene) PO; 7.5 mg tid For partial seizures; also for anxiety; Schedule IV drug.
diazepam (Valium) IV push, administer emulsion at 5 mg/min; IM/IV Treatment for status epilepticus; also for anxiety-
5–10 mg (repeat as needed at 10–15 min intervals up to related symptoms and muscle spasms; see Drug Proto-
30 mg; repeat again as needed every two to four hours) type box for adverse effects
lorazepam (Ativan) (see IV; 4 mg injected slowly at 2 mg/min; if inadequate Most potent of the available benzodiazepines; for
page 116 for the Prototype response after 10 min, may repeat once management of status epilepticus; also for nausea and
Drug box) vomiting, preoperative sedation, anxiety, and insomnia;
Schedule IV drug.
OTHER Gaba-Related Drugs
ezogabine (Potiga) PO; start with 100 mg every eight hours; may increase For use along with other medications to control partial
dose at weekly intervals, not to exceed dosage increase onset seizures; often referred to as potassium channel
of 150 mg/day/week. Optimize effective dosage be- openers due to their ability to suppress recurrent neuro-
tween 200 mg three times daily (600 mg per day) to nal activity; may cause psychiatric and nervous system
400 mg three times daily (1,200 mg per day) symptoms: confusion, memory impairment, blurred
vision, balance disorder.
gabapentin (Neurontin) For additional therapy: PO; start with 300 mg on day Chemical structure similar to GABA; speeds up the release
one, 300 mg bid on day two, 300 mg tid on day three, of GABA from brain neurons; used for partial seizures or
continue to increase over one week to a dose of seizures that could become generalized; used in adults to
1,200 mg/day (400 mg tid); may increase to 1,800– treat nerve pain caused by herpes virus or shingles (her-
2,400 mg/day pes zoster), and to treat restless legs syndrome (RLS); may
cause unsteadiness, weight gain, fatigue, dizziness.
pregabalin (Lyrica) PO; start with 150 mg/day; may be increased up to 300 Chemical structure similar to GABA; used in the treat-
mg/day within 1 week, (max: 600 mg/day) ment of partial seizures; used for management of nerve
pain associated with diabetes, nerve pain caused by
herpes virus or shingles (herpes zoster), and fibromyal-
gia; similar adverse effects to gabapentin.
tiagabine (Gabitril) PO; start with 4 mg/day, may increase by 4–8 mg/day Inhibits uptake of GABA into presynaptic neurons,
every week up to 56 mg/day in two to four divided prolonging GABA action; for the treatment of partial
doses seizures; may cause confusion, stuttering; loss of sensa-
tion in the fingertips.
topiramate (Topamax, PO (regular release); start with 50 mg/day, increase by Sugar-like chemical molecule; enhances the action of
Trokendi XR) 50 mg/week to effectiveness (max: 1,600 mg/day) GABA; for partial seizures; useful in trigeminal neu-
PO (extended release); 200–400 mg once daily ralgia; may cause weight loss, numbness and tingling
of the fingers and toes, behavioral issues including
depression, agitation, hostility.
vigabatrin (Sabril) PO; for infantile spasms, begin therapy at 50 mg/kg/day Increases GABA in the CNS; for the treatment of in-
twice daily, increasing total daily dose per instructions to fantile spasms in babies one month to two years old
a maximum of 150 mg/kg/day; for adults with refractory and refractory complex partial seizures in adults; may
complex partial seizures (CPS), initiate therapy at 500 mg cause fatigue, headache, irritability, gastrointestinal
twice daily, increasing total daily dose per instructions. disturbances, inflamed throat, and irritated respiratory
The recommended dose is 1.5 grams twice daily passages.
Benzodiazepines used in treating epilepsy include clonazepam (Klonopin), clorazepate (Tranxene), diaz-
epam (Valium), and lorazepam (Ativan). Parenteral diazepam is used to terminate status epilepticus. Other
short-term indications of benzodiazepines include absence seizures and myoclonic seizures. Because toler-
ance may begin to develop after only a few months of therapy, seizures may recur unless doses are peri-
odically adjusted. Benzodiazepines and other GABA-related drugs are generally not used alone in seizure
pharmacotherapy, but instead used in combination with other antiseizure medications.
Drug Prototype: Phenobarbital (Luminal)

Therapeutic Class: Antiseizure drug, sedative-hypnotic Pharmacologic Class: Barbiturate, GABAA receptor drug
Actions and Uses: Phenobarbital is a long-acting barbiturate include drowsiness, vitamin deficiencies (vitamin D, folate, B9,
used for the management of a variety of seizures. It is also used and B12), and laryngospasms. With overdose, phenobarbital
for insomnia. Phenobarbital should not be used for pain relief, may cause severe respiratory depression, CNS depression, coma,
because it may increase a patient’s sensitivity to pain. and death. Phenobarbital is a pregnancy category D drug.
Phenobarbital acts biochemically in the brain by enhancing Phenobarbital interacts with many other drugs. For ex-
the action of the neurotransmitter GABA, which is responsible for ample, it should not be taken with alcohol or other CNS depres-
suppressing abnormal neuronal discharges that can cause epilepsy. sants. These substances potentiate the action of barbiturates,
increasing the risk of life-threatening respiratory depression or
Adverse Effects and Interactions: Phenobarbital is a Schedule cardiac arrest. Phenobarbital increases the metabolism of many
IV drug that may cause dependence. Common adverse effects other drugs, reducing their effectiveness.
Drug Prototype: Diazepam (Valium)

Therapeutic Class: Antiseizure drug, sedative-hypnotic, anxiolytic, anesthetic adjunct, skeletal muscle
relaxant (centrally acting) Pharmacologic Class: Benzodiazepine, GAB receptor drug
Actions and Uses: Diazepam binds to GABA receptors located combined sedation effects. Other drug interactions include
throughout the CNS. It produces its effects by suppressing neu- cimetidine, oral contraceptives, valproic acid, and metopro-
ronal activity in the limbic system and subsequent impulses that lol, which potentiate diazepam’s action, and levodopa and
might be transmitted to the reticular activating system. Effects barbiturates, which decrease diazepam’s action. Diazepam
of this drug are suppression of abnormal neuronal foci that may increases the levels of phenytoin in the bloodstream and may
cause seizures, calming without strong sedation, and skeletal cause phenytoin toxicity. When given IV, hypotension, mus-
muscle relaxation. When used orally, maximum therapeutic ef- cular weakness, tachycardia, and respiratory depression are
fects may take from one to two weeks. Tolerance may develop common. Because of tolerance and dependency, use of diaz-
after about four weeks. When given IV, effects occur within min- epam is reserved for short-term seizure control or for status
utes, and its anticonvulsant effects last for about 20 minutes. epilepticus.
Diazepam should be used with caution with herbal supple-
Adverse Effects and Interactions: Diazepam should not be ments, such as kava and chamomile, which may cause an in-
taken with alcohol or other CNS depressants because of creased effect.
Cam therapy
The Ketogenic Diet for Epilepsy
The ketogenic diet may be used when seizures cannot be controlled through pharmaco-
therapy or when there are unacceptable adverse effects to medications. Before antiepileptic
drugs were developed, this diet was a primary treatment for epilepsy.
The ketogenic diet is a strict diet that is high in fat and low in carbohydrates and protein. It
limits water intake and carefully controls caloric intake. Each meal has the same ketogenic ratio
of 4 g of fat to 1 g of protein and carbohydrate. Extra fat is usually given in the form of cream.
Research suggests that the diet produces a high success rate for certain patients. The diet
appears to be equally effective for every seizure type. The most frequently reported adverse
effects include vomiting, fatigue, constipation, diarrhea, and hunger. Kidney stones, acidosis,
and slower growth rates are possible risks. Those interested in trying the diet must consult
with their healthcare provider; this is not a do-it-yourself diet and may be harmful if not
monitored carefully by skilled professionals.
Since 2003, some of the GABA-related antiseizure drugs have been used for a variety of other condi- neur = nerve
tions including depression, migraines, and for the management of neuropathic pain associated with diabetic fibro = fiber-related
peripheral neuropathy, postherpetic neuralgia, fibromyalgia, and spinal cord injury. In addition, some my = muscle
algia = pain
antiseizure drugs have been used for the management of anxiety and bipolar disorder symptoms. Two
antiseizure drugs, gabapentin (Neurontin) and pregabalin (Lyrica) stand out as off-label approaches for the post = after
successful management of neuropathic pain and postherpetic neuralgia. Topiramate (Topamax, Trokendi herpet = herpes
XR) may be used in the treatment of trigeminal neuralgia. ic = related
Hydantoin and related drugs are generally effective in treating partial sei-
zures and tonic-clonic seizures. Core Concept 13.7
Hydantoins and related drugs dampen CNS activity by delaying an influx of sodium ions across neuronal
membranes. Sodium movement is the major factor that determines whether a neuron will undergo an ac-
tion potential. Sodium channels guide the movement of sodium ions into the cell. If sodium channels are
temporarily inactivated, neuronal activity will be suppressed. If sodium channels are blocked, neuronal ac-
tivity completely stops, as occurs with local anesthetic drugs (see Chapter 15). With hydantoin and related
drugs, sodium channels are not blocked completely; they are just made to be less sensitive.
Several drugs in this group also affect the threshold of neuronal firing, or they may interfere with
activation of the excitatory neurotransmitter glutamate. These approaches, although not directly connected
with desensitization of sodium channels, result in the same effect (delayed depolarization of the neuron).
Hydantoin and related drugs are listed in Table 13.3 ◆.
The oldest and most commonly prescribed antiseizure medication is phenytoin (Dilantin). Approved in
the 1930s, phenytoin is a broad-spectrum hydantoin drug, useful in treatment of all kinds of epilepsy except
absence seizures. It provides effective seizure suppression without the potential for abuse or extreme seda-
tive effects. Patients vary significantly in their ability to metabolize phenytoin; therefore, dosages are highly
individualized. Because of the very narrow range between therapeutic dose and toxic dose, patients must be
carefully monitored. Hematologic toxicities have been associated with phenytoin drug use: thrombocyto- hematologic =
penia, leukopenia, neutropenia, agranulocytosis, anemias, and other blood disorders have been reported. In blood-related
addition, liver disease, renal dysfunction, and cardiac toxicity are severe potential hazards. Phenytoin and thrombocytopenia =
fosphenytoin (drug converted to phenytoin) are first-line drugs in the treatment of status epilepticus. reduced platelets
Some phenytoin-related drugs are used less frequently; others are more widely used. Most drugs share a
neutropenia = reduced
mechanism similar to the hydantoins, including carbamazepine (Tegretol), oxcarbazepine (Trileptal, Oxtellar),
neutrophils
and valproic acid (Depakene), which is also available as valproate and divalproex sodium. Because carba-
mazepine produces fewer adverse effects than phenytoin or phenobarbital, it is a preferred drug for treating agranulocytosis = elevated
tonic-clonic and partial seizures. Carbamazepine has been approved for the treatment of trigeminal neuralgia, a agranulocytes (reduced
granulocytes)
painful condition of the nerve responsible for facial sensation. Carbamazepine is also used off-label for a vari-
ety of indications, including ADHD, schizophrenia, borderline personality disorder, and PTSD. Oxcarbazepine anemias = red blood cell
is a derivative of carbamazepine, so its treatment profile is similar. Oxcarbazepine is slightly better tolerated, deficiencies
although serious skin and organ hypersensitivity reactions have been noted. Valproic acid is a preferred drug
for absence seizures and is used in combination with other drugs for partial seizures. Valproic acid, carbamaze-
pine, and lamotrigine are used in the treatment of bipolar disorder (see Chapter 10).
Newer approved antiseizure drugs show promise in treatment for a range of disorders, includ-
ing absence seizures, partial seizures, myoclonic seizures, generalized tonic-clonic seizures, and mood
Table 13.3 Hydantoins and Related Drugs

Hydantoins
ethotoin (Peganone) PO; initial dose 1 g/day or less in four to six divided For tonic-clonic and complex partial seizures; prevents the spread
doses with subsequent gradual dosage increases over of seizure activity rather than to abolish the primary focus of
a period of several days. Usual maintenance dosage is seizure discharges; may cause swelling of the lips, tongue and
2–3 g/day throat, mood changes, chest pain, vision problems, fever.
fosphenytoin IV; initial dose 15–20 mg PE/kg at 100–150 mg PE/ Converted to phenytoin in the body; for control of status
(Cerebyx) min followed by 4–6 mg PE/kg/day (PE = phenytoin epilepticus; short-term substitute for oral phenytoin.
equivalents)
phenytoin PO; 15–18 mg/kg or 1 g initial dose, then 300 mg/ For tonic-clonic seizures, complex partial seizures, and seizures
(Dilantin) day in one to three divided doses; may be gradually after head trauma; may cause unsteadiness and moderate
increased 100 mg/week cognitive problems, potential cosmetic issues (abnormal body/
face hair and growth), skin blemishes, blood disorders, bone
marrow suppression
(continued )
Table 13.3 Hydantoins and Related Drugs (continued)

Phenytoin-Like Drugs
carbamazepine PO; 200 mg bid, gradually increased to 800–1,200 mg/ For tonic-clonic and complex partial seizures; useful in tri-
(Tegretol) day in three to four divided doses geminal neuralgia (condition characterized by intense pain
along the angle of the jaw); also for bipolar disorder, ADHD,
schizophrenia, borderline personality disorder, and PTSD; may
cause rash (Stevens–Johnson syndrome), blood disorders, liver
disease, reduced bone health.
felbamate (Felbatol) Partial seizures: PO; start with 1,200 mg/day in three to For use in Lennox-Gastaut syndrome and partial seizures; may
four divided doses; may increase by 600 mg/day every cause anemia and liver toxicity in some patients.
2 weeks (max: 3,600 mg/day)
Lennox-Gastaut syndrome: PO; start at 15 mg/kg/day in
three to four divided doses; may increase 15 mg/kg at
weekly intervals to max of 45 mg/kg/day
lamotrigine (Lamictal) PO; 50 mg/day for 2 weeks, then 50 mg bid for 2 weeks; For partial seizures, generalized tonic-clonic seizures, myo-
may increase gradually up to 300–500 mg/day in two clonic seizures; also for bipolar disorder; may cause dizziness,
divided doses (max: 700 mg/day) fatigue, insomnia.
levetiracetam PO; 500 mg twice daily (max: 3,000 mg total per day) For use in partial seizures; may cause drowsiness, weakness,
(Keppra) susceptibility to infections, nasal problems, nervousness.
oxcarbazepine PO; initiation of monotherapy, 300 mg twice daily, Derivative of carbamazepine with similar treatment profile;
(Trileptal, Oxtellar XR) increase 300 mg/day every third day up to may cause serious skin and organ hypersensitivity reactions in
1,200 mg/day some patients.
rufinamide (Banzel) PO; 400 to 800 mg per day, taken as two equal doses per For the adjunctive treatment of seizures associated with
day. The dose should be increased by 400 to 800 mg every Lennox-Gastaut syndrome in children four years and older and
two days until a maximum of 3,200 mg daily is reached adults.
valproic acid PO/IV; 15 mg/kg/day in divided doses when total daily Broad-spectrum medication; for absence seizures, mixed gen-
(Depakene, dose is greater than 250 mg; increase 5–10 mg every eralized types of seizures; also for bipolar disorder; see Drug
Depakote)** week until seizures are controlled (max: 60 mg/kg/day) Prototype box for adverse effects.
zonisamide PO; 100–400 mg/day Broad-spectrum medication; for partial seizures; it is a sulfon-
(Zonegran) amide, which means that it may cause an allergic reaction in
some patients.
**Other formulations of valproic acid include its salts, valproate, and divalproex sodium.
Drug Prototype: Phenytoin (Dilantin)

Therapeutic Class: Antiseizure drug, antidysrhythmic Pharmacologic Class: Hydantoin, sodium influx
suppressing drug
Actions and Uses: Phenytoin acts by desensitizing sodium chan- and aplastic anemia. It may cause severe skin reactions,
nels in the CNS responsible for neuronal responsivity. Desensiti- such as rashes, including exfoliative dermatitis, and
zation prevents the spread of disruptive electrical charges in the Stevens–Johnson syndrome. Connective tissue reactions
brain that produce seizures. It is effective against most types of include lupus erythematosa, hypertrichosis, hirsutism, and
seizures except absence seizures. Phenytoin has antidysrhyth- gingival hypertrophy.
mic activity similar to lidocaine (Class IB). An off-label use is for Phenytoin interacts with many other drugs, including oral
digoxin-induced dysrhythmias. anticoagulants, glucocorticoids, H2 antagonists, antituberculin
drugs, and food supplements such as folic acid, calcium, and
Adverse Effects and Interactions: Phenytoin may cause dys- vitamin D. It impairs the effectiveness of drugs such as digoxin,
rhythmias such as bradycardia or ventricular fibrillation, se- doxycycline, furosemide, estrogens and oral contraceptives, and
vere hypotension, and hyperglycemia. Severe CNS reactions theophylline. Phenytoin, when combined with tricyclic antide-
include headache, nystagmus, ataxia, confusion and slurred pressants, can trigger seizures.
speech, paradoxical nervousness, twitching, and insomnia. Pe- Phenytoin should be used with caution with herbal supple-
ripheral neuropathy may occur with long-term use. Phenytoin ments such as herbal laxatives (buckthorn, cascara sagrada, and
can cause multiple blood dyscrasias, including agranulocytosis senna), which may increase potassium loss.
Drug Prototype: Valproic Acid (Depakene, Depakote)

Therapeutic Class: Antiseizure drug, bipolar disorder drug, migraine prophylaxis Pharmacologic Class:
Valproate, sodium influx suppressing drug, calcium influx suppressing drug, GABA potentiating drug
Actions and Uses: The mechanism of action of valproic acid is pruritus, photosensitivity, erythema multiforme, and fatal
the same as phenytoin, although effects on GABA and calcium hepatotoxicity.
channels may cause some additional actions. It is useful for a Valproic acid interacts with many drugs. For example, as-
wide range of seizure types, including absence seizures and pirin, cimetidine, chlorpromazine, erythromycin, and felbamate
mixed types of seizures. Other uses include treatment of bipolar may increase valproic acid toxicity. Concomitant warfarin, aspi-
disorder and prevention of migraine headaches. rin, or alcohol use can cause severe bleeding. Alcohol, benzodi-
Valproic acid has several trade names and formulations, azepines, and other CNS depressants potentiate CNS depressant
which sometimes causes confusion when studying this drug. action. Lamotrigine, phenytoin, and rifampin lower valproic
These include the following. acid levels. Valproic acid increases serum phenobarbital and
phenytoin levels. Use of clonazepam concurrently with valproic
■ Valproic acid (Depakene) is the standard form of the drug acid may induce absence seizures.
given by the oral route.
■ Valproate sodium is the sodium salt of valproic acid given
orally or IV (Depacon).
■ Divalproex sodium (Depakote ER) is a sustained release com- Black Box Warning:
bination of valproic acid and its sodium salt. It is given orally May result in fatal hepatic failure, especially in children under
and is available in an enteric-coated form. the age of two years. Nonspecific symptoms often precede
hepatic toxicity: weakness, facial edema, anorexia, and vomit-
Adverse Effects and Interactions: Adverse effects include seda- ing. Liver function tests should be performed prior to treat-
tion, drowsiness, gastrointestinal (GI) upset, and prolonged ment and at specific intervals during the first six months of
bleeding time. Other effects include visual disturbances, muscle treatment. Valproic acid can produce life-threatening pancre-
weakness, tremor, psychomotor agitation, bone marrow sup- atitis and teratogenic effects including spina bifida.
pression, weight gain, abdominal cramps, rash, alopecia,
disorders. The most common adverse effects of the newer antiseizure drugs are drowsiness, dizziness, and
blurred vision. Lamotrigine (Lamictal) has a broad spectrum of antiseizure activity and is FDA approved
for long-term maintenance of bipolar disorder. This drug’s duration of action is greatly affected by other
drugs that inhibit or enhance hepatic metabolizing enzymes. Levetiracetam (Keppra) and zonisamide
(Zonegram) are approved for adjunctive therapy of partial seizures in adults. Among the newer approved
antiseizure drugs, levetiracetam has been generally less reactive than the other antiseizure medications.
Conversely, zonisamide (a sulfonamide) has triggered hypersensitivity reactions in some patients. In ad-
dition, felbamate (Felbatol) has induced potentially harmful reactions, including liver toxicity and aplas-
tic anemia.
In a severe form of epilepsy called Lennox-Gastaut syndrome (LGS), valproic acid (Depakene, Depa-
kote), lamotrigine (Lamictal), felbamate (Felbatol), topiramate (Topamax, Trokendi XR), and rufinamide
(Banzel) are often used for treatment. LGS is characterized by tonic, atonic, atypical absence, and myo-
clonic symptoms. There is usually no single antiseizure medication that will control symptoms of this
particular syndrome.
Succinimides generally treat absence seizures. Core Concept 13.8
Neurotransmitters, hormones, and some medications bind to neuronal membranes, stimulating the entry of
calcium. Without calcium influx, neuronal transmission would not be possible. Succinimides delay entry succin = chemical related to
of calcium into neurons by blocking calcium channels, increasing the electrical threshold of the neuron, succinic acid
and reducing the likelihood of an action potential. By raising the seizure threshold, succinimides keep neu- imide = having an NH
functional group
rons from firing too quickly, thus suppressing abnormal foci. The succinimides are generally effective only
against absence seizures. These drugs are listed in Table 13.4 ◆.
Ethosuximide (Zarontin) is the most commonly prescribed drug in this class. It remains the preferred
drug for absence seizures. It joins the other positive ion suppressing drugs that successfully treat absence
seizures: valproic acid (Depakene, Depakote), lamotrigine (Lamictal), and zonisamide (Zonegran).
Concept Review 13.3

■ Name three general drug classes introduced by the Drug Snapshot feature at the be-
ginning of this chapter. Identify the various stated chemical categories of antiseizure
medications. Based on pharmacologic mechanisms, which of the drug examples do not

conveniently fit into only one drug class? Which of the drugs control a wide range
of seizure types? Which of the drugs have therapeutic applications other than seizure
management?
Table 13.4 Succinimides

ethosuximide (Zarontin) PO; 250 mg bid, increased every For absence seizures, myoclonic seizures, and akinetic epilepsy; may cause
4–7 days (max: 1.5 g/day) nausea, anorexia, abdominal pain, vomiting, gum overgrowth, blood disorders,
behavioral changes, rash (Stevens–Johnson syndrome)
methsuximide (Celontin) PO; 300 mg/day, may increase For absence seizures; may be used in combination with other anticonvulsants
every 4–7 days (max: 1.2 g/day in mixed types of seizure activity; may cause dizziness, drowsiness, blurred
in divided doses) vision, increased risk for suicidal thoughts, fetal toxicity
Drug Prototype: Ethosuximide (Zarontin)

Therapeutic Class: Antiseizure drug Pharmacologic Class: Succinimide, low-threshold calcium channel
blocking drug
Actions and Uses: Ethosuximide is a drug of choice for absence of psychiatric illness. CNS effects include dizziness, headache,
(petit mal) seizures. It depresses the activity of neurons in the lethargy, fatigue, ataxia, sleep pattern disturbances, attention
motor cortex by elevating the neuronal threshold. It is usually difficulty, and hiccups. Bone marrow suppression and blood
ineffective against psychomotor or tonic-clonic seizures; how- dyscrasias are possible, as is systemic lupus erythematosus.
ever, it may be given in combination with other medications Other reactions include gingival hypertrophy and tongue
that better treat these conditions. It is available in tablet and swelling. Common adverse effects are abdominal distress and
flavored syrup formulations. weight loss.
Drug interactions include ethosuximide, which increases
Adverse Effects and Interactions: Ethosuximide may impair phenytoin serum levels. Valproic acid causes ethosuximide
mental and physical abilities. Psychosis or extreme mood swings, serum levels to fluctuate (increase or decrease). Serum
including depression with suicidal intent, can occur. Behav- drug levels should be done periodically to determine drug
ioral changes are more prominent in patients with a history concentration.
Nursing Process Focus Patients Receiving Antiseizure Drug Therapy

Prior to administration: ■ Risk for Injury related to effects of seizure and adverse effects of drug
■ Obtain a complete health history including cardiovascular, renal and therapy
liver conditions, growth and developmental patterns, allergies, drug ■ Noncompliance related to length of time before medication reaches
history, and possible drug interactions. therapeutic levels and adverse effects of drug therapy
■ Evaluate laboratory blood findings: CBC, chemistry, renal and liver ■ Deficient Knowledge related to a lack of information about disease
function studies, and drug screening. process and drug therapy
■ Acquire the results of a complete physical examination including vital ■ Ineffective Therapeutic Regimen Management related to noncompli-
signs, ECG and neurological status (level of consciousness [LOC], ance with medication regimen, presence of adverse effects, and need
mental status and identification of recent seizure activity). for long-term medication use
Planning: Patient Goals and Outcomes

The patient will:
■ Experience therapeutic effects (absence of seizures or a reduction in the number or severity of seizures).
Implementation

■ Monitor neurologic status, especially changes in level of consciousness Instruct the patient to:
and/or mental status. (Sedation may indicate overmedication or an ad- ■ Report any significant change in sensorium, such as slurred speech,
verse effect.) confusion, hallucinations, or lethargy to the healthcare provider.
■ Report any changes in seizure quality or unexpected involuntary
muscle movement such as twitching, tremor, or unusual eye move-
ment to the healthcare provider.
■ Be aware of the risk for suicidality when not following proper medica-
tion regimen.
■ Protect the patient from injury during seizure events until the thera- ■ Instruct the patient to avoid driving and other hazardous activities un-
peutic effects of the drugs are achieved. til the effects of the drug are known.
■ Monitor effectiveness of drug therapy. (Observe for developmental Instruct the patient to:
and neurological changes; may indicate a need for dose adjustment.) ■ Keep a seizure diary to chronicle events during symptoms phase or
during dose adjustment.
■ Take the medication exactly as ordered, including the same manufac-
turer’s drug, each time the prescription is refilled. (Switching brands
may result in alterations in seizure control.)
■ Take a missed dose as soon as remembered, but do not take double
doses. (Doubling doses could result in toxic serum level.)
■ Monitor labs for drug levels: CBC renal and liver function studies. ■ Instruct the patient about the importance of keeping all laboratory
(Many antiseizure medications require blood testing to ensure appointments.
therapeutic levels are achieved/maintained and are used to
determine medication dosages. Some drugs can cause liver
toxicity.)
■ Monitor for adverse effects. Observe for hypersensitivity, nephrotoxic- ■ Instruct the patient to report adverse effects (specific to the drug regi-
ity, and hepatotoxicity. men) immediately to the healthcare provider.
■ Monitor oral health. Observe for signs of gingival hypertrophy, bleed- Instruct the patient to:
ing, or inflammation (phenytoin specific). ■ Use a soft toothbrush and oral rinses as prescribed by a dentist.
■ Avoid mouthwashes containing alcohol.
■ Report changes in oral health, such as excessive bleeding or inflamma-
tion of the gums.
■ Maintain a regular schedule of dental visits.
■ Monitor gastrointestinal status. (Valproic acid is a GI irritant and anti- Instruct the patient to:
coagulant.) Conduct guaiac stool testing for occult blood. (Phenytoin’s ■ Take the drug with food to reduce GI upset.
CNS depressant effects decrease GI motility, producing constipation.) ■ Immediately report any severe or persistent heartburn, upper GI pain,
nausea, or vomiting to the healthcare provider.
■ Increase exercise, fluid intake, and fiber intake to facilitate stool
passage.
■ Monitor nutritional status. (Phenytoin’s action on electrolytes may Instruct the patient:
cause decreased absorption of folic acid, vitamin D, magnesium, and ■ In dietary or drug administration techniques specific to prescribed
calcium. Deficiencies in these vitamins and minerals lead to anemia medications.
and osteoporosis. Valproic acid may cause an increase in appetite ■ To report significant changes in appetite or weight gain.
and weight.)
■ Obtain information and monitor use of other medications. Antiseizure ■ Instruct the patient to report use of any medication to the healthcare
medications should not be used with CNS depressants or alcohol. provider.
■ Inform the patient not to drink alcohol while taking these
medications.
■ Administer medication correctly and evaluate the patient’s knowledge ■ Advise the patient not to discontinue medication abruptly. This action
of proper administration. Do not abruptly stop providing medication may result in status epilepticus.
and monitor for presence of seizures. (Abrupt withdrawal of drugs can
cause seizures to occur.)

Evaluate effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Tables 13.2, 13.3,

Patients taking antiseizure medications need to know the following:
In General
1. Never abruptly stop taking antiseizure medication; doing so can cause seizures to return.
2. Avoid alcohol and other CNS depressants because they can increase sedation.
3. Antiseizure medications may cause drowsiness; avoid driving and the use of machinery
that could lead to injury.
4. It may require several dosage adjustments over many months to find the dosage that
allows performance of normal daily activities while controlling seizures.
5. It is important to keep laboratory appointments because many antiseizure medications
require blood testing to ensure that the drug is at a safe and effective level in the blood.
6. Consult a healthcare provider before trying to become pregnant; some antiseizure
medications are not safe to use during pregnancy.
7. Report excess fatigue, drowsiness, agitation, confusion, or suicidal thoughts to a health-
care provider.
Regarding Hydantoins and Related Medications

8. Report the following adverse effects to a healthcare provider: gum overgrowth (gingival
hyperplasia) or skin rash, tremors, weight gain, diarrhea, irregular menses, dizziness,
nausea, or oversedation.
9. Hydantoins and related medications interact with many other drugs; do not add any other
prescription, over-the-counter (OTC) drugs, or herbal supplements until a healthcare
provider is consulted. Do not consume alcohol while taking these medications.
Regarding Succinimides
10. Report the following adverse effects to a healthcare provider: hiccups or epigastric pain
with ethosuximide (Zarontin), drowsiness, or increased bleeding time.
Chapter Review
13.1 Although some types of seizures involve convul- 13.3 Epileptic seizures are typically identified as partial,
sions, other seizures do not. generalized, or special epileptic syndromes.
Epilepsy is any disorder characterized by recurrent Epilepsies are identified using the International Clas-
seizures. Seizures are abnormal and uncontrolled neu- sification of Epileptic Seizures nomenclature, as partial
ronal brain discharges. Convulsions are uncontrolled (focal), generalized, or special epileptic syndromes.
muscle contractions that accompany some major sei- Partial seizures are further described as simple or com-
zures. Drugs used to treat epilepsy are often referred plex seizures. Generalized seizures are described as ab-
to as antiseizure drugs or antiepileptic drugs (AEDs), sence seizures, atonic seizures, or tonic-clonic seizures.
rather than anticonvulsants. Special epileptic syndromes include febrile seizures,
myoclonic seizures, and status epilepticus.
13.2 Many causes of seizure activity are known; a few
are not. 13.4 Effective seizure management involves strict ad-
A seizure is considered a symptom of epilepsy rather herence to safe drug therapy.
than a disorder itself. In some cases, the exact cause The choice of drug for epilepsy pharmacotherapy
of seizures is not known; however, there are many depends on the type of seizures the patient is experi-
known causes. Seizures are the most common neu- encing, the patient’s previous medical history, diag-
rologic problem. Through a combination of pharma- nostic studies, and the pathologic processes causing
cotherapy, patient–family support, and education, the seizures. In most cases, a single drug can effec-
effective seizure control can be achieved by most tively control seizures. In some patients, two antisei-
patients. zure medications may be necessary. When discussing
Chapter Review 195
antiseizure medications, suicidality, developmental and glia, or inhibit GABA degrading enzymes. Barbi-
issues of children, birth control, and pregnancy are turates, benzodiazepines, and several newer GABA-
important topics for consideration. related drugs reduce seizure activity by potentiating
GABA action.
13.5 Antiseizure pharmacotherapy is directed at con-
trolling the movement of electrolytes across neu- 13.7 Hydantoin and related drugs are generally effec-
ronal membranes or affecting neurotransmitter tive in treating partial seizures and tonic-clonic
balance. seizures.
There are three general mechanisms by which anti- This class of drugs depresses CNS activity by de-
seizure drugs work: stimulating an influx of chloride sensitizing sodium channels and also by affecting
ions (an effect associated with the neurotransmitter the threshold of neuronal firing. Several widely used
GABA), delaying an influx of sodium, and delaying drugs, including phenytoin (Dilantin), carbamaze-
an influx of calcium. Antiseizure drugs are repre- pine (Tegretol), and valproic acid (Depakene), work
sented by these and possibly additional overlapping by this mechanism. Some drugs act by more than
mechanisms: blocking of the excitatory neurotrans- one mechanism. Additional newer antiseizure drugs
mitter, glutamate, and delaying an efflux of potas- have been added to the regimen and may be used
sium ions across neuronal membranes. alone in therapy or as adjunctive drugs.
13.6 By increasing the effects of gamma-aminobutyric 13.8 Succinimides generally treat absence seizures.
acid (GABA) in the brain, some drugs reduce a Succinimides delay entry of calcium into neurons
wide range of seizure types. by blocking calcium channels, increasing the elec-
Some antiseizure drugs mimic the effects of GABA trical threshold, and reducing the likelihood that an
by stimulating an influx of chloride ions. Drugs may action potential will be generated. Ethosuximide
bind directly to the GABA receptor, enhance GABA (Zarontin) is the most commonly prescribed drug in
release, block the reuptake of GABA into nerve cells this class.
Review Questions
The following questions are written in NCLEX-PN® style. An- 3. “It may take up to three years before you are cured.”
swer these questions to assess your knowledge of the chapter 4. “The goal of therapy is to control seizure activity.”
to you. 4. A patient who has had repeated tonic-clonic seizures
is admitted into the hospital. He has had a history of status
1. A young woman with a diagnosed seizure disorder asks epilepticus. In preparation for the possibility that status epi-
the nurse about getting pregnant. In planning her response, lepticus may happen again, the nurse will have which drug
the nurse knows that most antiseizure medications fall under available to terminate this serious type of seizure?
which pregnancy category? 1. Diazepam (Valium)
1. A 2. Gabapentin (Neurontin)
2. B 3. Clorazepate (Tranxene)
3. C 4. Clonazepam (Klonopin)
4. D
5. The nurse is reviewing a patient’s chart and reads
2. The patient on phenytoin (Dilantin) asks why he or she that the patient experienced a generalized seizure involv-
must have his or her labs checked. The nurse’s best response ing alternating contractions and relaxation of the muscles.
would be: The nurse knows that this phase of the seizure is called the
1. “Dilantin can cause blood disorders.” _______ phase.
2. “You will need to ask your doctor.” 1. Absence
3. “We are checking to make sure you are getting enough but 2. Clonic
not too much medication.” 3. Febrile
4. “We must see if you are developing any adverse effects of 4. Myoclonic
the medication.”
6. The nurse teaches the patient that one of the most com-
3. The patient on antiseizure medication wants to know how mon adverse effects of newer antiseizure drugs is:
long he or she must take his or her medication before he or she 1. GI upset
is cured. The nurse’s best response would be: 2. Spasms
1. “You should be totally seizure free in one to three weeks.” 3. Drowsiness
2. “We may need to add additional medications before you 4. Dry mouth
are cured.”
7. A nurse is teaching a patient the importance of taking his 9. The nurse monitors for the occurrence of gingival hy-
or her antiseizure medication, phenobarbital (Luminal), every perplasia for the patient who is taking which antiseizure
day at the same time. She informs the patient not to take more medication?
of this medication than prescribed because this antiseizure 1. Valproic acid (Depakene)
drug may cause: (Select all that apply.) 2. Carbamazepine (Tegretol)
1. Severe respiratory depression 3. Phenytoin (Dilantin)
2. Coma 4. Primidone (Mysoline)
3. Confusion
4. Death 10. The nurse checks a patient’s phenytoin serum levels be-
cause, in addition to taking phenytoin, the patient is also
8. The nurse collects data on a patient taking ethosuximide taking:
(Zarontin) for which of the following possible adverse effects? 1. Ethosuximide (Zarontin)
1. Urinary dysfunction 2. Phenobarbital (Luminal)
2. Gingival hyperplasia 3. Carbamazepine (Tegretol)
3. Tremors 4. Valproic acid (Depakene)
4. Depression
Remember Mrs. Anthonia and 2. Mrs. Anthonia asks the nurse how ethosuximide (Zaron-
her daughter, Destiny, who tin) works to help her daughter’s condition. The nurse replies
were introduced at the be- that ethosuximide will:
ginning of the chapter? Now 1. Enhance the release of a neurotransmitter called GABA,
read the remainder of the case which suppresses the firing of neurons.
study. Based on the informa- 2. Delay the amount of sodium going into the nerves, decreas-
tion you have learned in this ing the ability of nerve impulses to travel.
chapter, answer the questions that follow. 3. Delay the entry of calcium into nerves keeping them from
Mrs. Kemi Anthonia and her nine-year-old daughter, Destiny, firing too quickly.
recently visited the family physician. Mrs. Anthonia was con- 4. Activate the receptors that receive the neurotransmitter
cerned that Destiny’s development might be stunted. Several GABA.
complaints were noted: “Destiny sometimes acts very unusual,
3. The nurse lets Mrs. Anthonia know that Destiny will need
like she is not paying attention . . . on occasion she is unre- to return to clinic to:
sponsive and bats her eyes . . . this sometimes lasts for a few
seconds and everything appears normal again . . . lately she 1. Be reexamined because Destiny’s medication has a high
has been waking up a lot during the night.” After a complete potential for dependence
neurologic exam and set of laboratory tests, the family physi- 2. Be reexamined because Destiny’s medication can cause
cian prescribed ethosuximide (Zarontin) for Destiny to be taken anemia
in gradually increased doses over seven days and then for a 3. Check serum drug levels to determine the most effective
sustained period at the same dose. The physician then sched- drug concentration
uled a return visit to the clinic in seven days. 4. Check to be sure Destiny is OK because her medication has
a low margin of safety
1. The maintenance (sustained) dose of ethosuximide is usu- 4. Which of the following medications, if prescribed for
ally based on 20 mg/kg/day in divided doses. Destiny weighs Destiny as a second medication, would cause ethosuximide
66 pounds. How many kg does Destiny weigh? How many (Zarontin) serum levels to fluctuate?
milligrams will she receive in a day? The nurse calculates the 1. Phenobarbital (Luminal)
medication dosage and determines that Destiny weighs: 2. Diazepam (Valium)
1. 33 kg and will receive 600 mg/day 3. Pregabalin (Lyrica)
2. 30 kg and will receive 660 mg/day 4. Valproic acid (Depakene)
3. 30 kg and will receive 600 mg/day
4. 30 kg and will receive 630 mg/day

C
“I was playing tennis and
it just popped. How many H
more months is this going to A
hurt?” P
Mr. Damian Coidiuf T
E
R
Drugs for Pain Management

14
Core Concepts
14.1 Pain assessment is the first step to pain 14.5 Opioids have multiple therapeutic effects, including
management. relief of severe pain.
14.2 Pain transmission processes allow several major 14.6 Nonsteroidal anti-inflammatory drugs (NSAIDs) are
targets for pharmacologic intervention. the preferred nonopioid analgesics for inflammation
14.3 Nonpharmacologic techniques and adjuvant and less severe pain.
analgesics assist in providing adequate pain relief. 14.7 Migraines can be effectively treated with a variety
14.4 Opioid analgesic medications exert their effects by of drug classes.
interacting with specific receptors.
Drug Snapshot
Opioid Analgesics for Severe Pain Ibuprofen and ibuprofen-like
Opioid agonists morphine (Astramorph PF, drugs
Duramorph, others) 203 Selective COX-2 inhibitors
Opioid antagonists naloxone (Narcan) 205 Centrally acting drugs
Opioids with mixed Antimigraine and Tension Headache Drugs
agonist–antagonist activity
Triptans sumatriptan (Imitrex) 213
Nonopioid Analgesics for Moderate Pain
Ergot alkaloids
Nonsteroidal anti-
Other drugs
inflammatory drugs (NSAIDs)
Aspirin and other salicylates aspirin (acetylsalicylic acid,
ASA) 208
198 Chapter 14 Drugs for Pain Management
Learning Outcomes
1. Relate the importance of 5. Compare and contrast the types 9. Categorize drugs used in the
pain assessment to effective of opioid receptors and their treatment of pain based on their
pharmacotherapy. importance to pharmacology. classifications and mechanisms of
2. Explain the neural mechanism for 6. Explain the role of opioid action.
pain at the level of the spinal cord. antagonists in the diagnosis and 10. For each of the classes listed
3. Explain how pain can be controlled treatment of acute opioid toxicity. in the Drug Snapshot, identify
by inhibiting the release of spinal 7. Describe the long-term treatment of representative drugs and explain
neurotransmitters. opioid dependence. their mechanisms of drug action,
primary actions, and important
4. Describe the role of nonpharmacologic 8. Compare the pharmacotherapeutic adverse effects.
therapies and adjuvant analgesics in approaches of preventing migraines
pain management. to those of aborting migraines.
Key Terms
Aδ fibers 199 cyclooxygenase (cox) (sye-klo-OK- opiates (OH-pee-ahts) 201
adjuvant analgesics (ADD-jeh-vent an- sah-jen-ays) 208 opioid (OH-pee-oyd) 201
ul-JEE-ziks) 201 endogenous opioids (en-DAHJ-en-nuss patient-controlled analgesia (PCA)
analgesics (an-ul-JEE-ziks) 201 O-pee-oyds) 200 (patient-controlled an-ul-JEE-ziah 203
auras (AUR-uhs) 211 migraine (MYE-grayne) 211 prostaglandins (pros-tah-GLAN-dins) 208
bradykinin (bray-dee-KYE-nin) 208 narcotic (nar-KOT-ik) 202 substance P 199
C fibers 199 nociceptor (no-si-SEPP-ter) 198 tension headache 211
P ain is a physiological and emotional experience characterized by unpleasant feelings, u sually

associated with a medical procedure, trauma, or disease. On a basic level, pain has always been
described as a defense mechanism that helps the body avoid a potentially dangerous situation.
Pain is a natural reaction prompting patients to seek medical help. Although the neural and chemical
mechanisms for pain are well characterized, psychological and emotional processes modify pain; anxiety,
fatigue, and depression can increase the perception of pain. Positive attitudes and support from caregivers
can reduce the perception of pain. Patients are more likely to tolerate their pain if they know the source of
the sensation and the course of medical treatment necessary to manage the pain.
Acute or Chronic Pain
The purpose of pain assessment is to guide the appropriate course of medical treatment. Pain can be
characterized as acute or chronic. Acute pain is an intense pain occurring over a brief time, usually from
time of injury until tissue repair. Chronic pain is longer lasting pain that may persist for weeks, months, or
years. Pain lasting longer than six months can interfere with activities of daily living and can contribute to
feelings of helplessness or hopelessness.
Core Concept 14.1 Pain assessment is the first step to pain management.
noci 5 pain or injury The psychological reaction to pain is a subjective experience. The same degree and type of pain may be described
ceptor 5 receiver as excruciating and unbearable by one patient and not even be mentioned by another patient. Several numerical
somatic 5 referring to the body scales and survey instruments are available to help healthcare providers characterize the pain and measure the
progress of drug therapy. Often the healthcare provider will simply ask, “How does your pain feel on a scale of
visceral 5 deeper organ zero to ten, ten being the most intense pain you have ever experienced?” S
uccessful pain management depends on
neur(o) 5 nerve-related an accurate assessment of both the degree of pain and the source of pain experienced by the patient.
algia 5 pain Besides being termed acute or chronic, pain can also be described by its source. Injury to tissues
path(y) 5 damage or disease produces nociceptor pain. This type of pain may be further subdivided into somatic pain, which produces
state sharp, localized sensations in the body, or visceral pain, which produces generalized dull and internal
ic 5 related to throbbing or aching pain. The term nociceptor refers to activation of receptor nerve endings that receive
trigeminal 5 fifth cranial and transmit pain signals to the central nervous system. Neuropathic pain is caused by direct injury to the
nerve (tri 5 three branches; nerves. Whereas nociceptor pain responds quite well to conventional pain relief medications, neuropathic
geminal 5 matching face) pain responds less successfully. Common types of neuropathic pain are shown in Table 14.1 ◆.
Table 14.1 Common Types of Neuropathic Pain

Examples Description
Carpal tunnel syndrome pain due to nerve compression in the wrist, thumb, and fingers
Central pain syndrome general pain caused by damage of nerves in the CNS—that is, due to stroke or
multiple sclerosis
Degenerative disk disease back pain due to damage of nerves entering or exiting the spinal cord
Diabetic neuropathy burning or stabbing pain in the hands and feet of patients suffering from
diabetes
Intractable cancer pain pain due to progressive or metastatic spread of cancer
Phantom limb pain pain occurring in some patients after a limb is amputated
Postherpetic neuralgia pain brought on by herpes and herpes–related viruses or the outbreak of
shingles
Postsurgical pain pain after a surgical procedure
Sciatica leg pain due to compression or irritation of the sciatic nerve
Trigeminal neuralgia shooting pain in the upper neck and jaw
Fast Facts Pain
■ Pain is a common symptom.

■ Approximately 16 million people experience chronic arthritic pain.
■ At least 31 million adults report low back pain, with 19 million people experiencing this on a chronic basis.
■ Currently, 50 million people are fully or partially disabled as a result of pain.
■ Over 50% of adults experience muscle pain each year.
■ Up to 40% of people with cancer report moderate to severe pain.
■ About 28 million Americans suffer from headaches and migraines.
■ Use of drug therapy and other measures controls 95% of migraines.
■ After puberty, women have four to eight times more migraines than men.
■ Before puberty, more boys have migraines than girls.
■ Headaches and migraines appear mostly among people ages 20 to 40.
■ Persons with a family history of headache or migraine have a greater chance of developing these disorders.
Concept Review 14.1

■ What questions would you ask to identify a patient’s type of pain? How would you
istinguish between acute pain and chronic pain? Which is the more difficult type of pain
d
to treat?
Pain transmission processes allow several major targets for p

harmacologic
intervention. Core Concept 14.2
The process of pain transmission begins when nociceptors are stimulated. Nociceptors are free nerve
endings located throughout the entire body. The nerve impulse signaling the pain is sent to the spinal cord
along two types of sensory neurons, called Aδ and C fibers. Aδ fibers are sensory neurons that are thinly
wrapped in myelin, a fatty substance that speeds up nerve transmission and signals sharp, well-defined
pain. C fibers are unmyelinated fibers; thus, they carry nerve impulses more slowly and conduct dull,
poorly localized pain.
Once pain impulses reach the spinal cord, neurotransmitters pass the message along to the next
neuron. Here, a neurotransmitter called substance P is thought to be responsible for continuing the pain
message, although other neurotransmitter candidates have been proposed. Spinal substance P is critical
because it controls whether pain signals will continue to the brain. The activity of substance P may be
affected by other neurotransmitters released from neurons in the central nervous system (CNS). One group
F i g u re 1 4 . 1
Neural pathways for pain.
Opioids (enkephalins) or
Substance P serotonin (5-HT) or
norepinephrine
These inhibit the
release of substance P
Receptor for Receptor for

substance P opioids, serotonin,
or norepinephrine Descending inhibitory
endogenous opioid/
serotonin/norepinephrine
neurons (coming
Ascending down from the brain)
pathway to
the brain
Pain
transmission
Free nerve endings

(nociceptor)
endo 5 within of these neurotransmitters, called endogenous opioids, includes endorphins, dynorphins, and enkephalins.
genous 5 coming from Figure 14.1 ■ shows one point of contact where endogenous opioids modify sensory information at the
level of the spinal cord. If pain impulses reach the brain, many possible actions may occur, ranging from
immediate reaction to the stimulus, persistent aching and suffering, or thoughts of mental depression if the
pain signal is repetitive and long-lasting.
Because pain signals begin at nociceptors located within peripheral body tissues and then proceed
throughout the CNS, there are several targets where medications can work to stop pain transmission. In
general, two major classes of drugs are employed to manage pain: opioid analgesics and nonopioid anal-
gesics such as the nonsteroidal anti-inflammatory drugs (NSAIDs). Opioids act within the CNS, whereas
NSAIDs act at the nociceptor level. There are multiple sites throughout the CNS where centrally acting
drugs can produce their effects, and there are many peripheral targets as well, depending on the approach
of drug therapy.
Concept Review 14.2

■ What is a nociceptor? Consider substance P and endogenous opioids, and describe the
approaches of pain management.
Nonpharmacologic techniques and adjuvant analgesics assist in providing

Core Concept 14.3 adequate pain relief.
Although drugs are quite effective at relieving pain in most patients, they can have significant adverse
effects. For example, at high doses, opioids can cause nausea, constipation, loss of appetite, and profound
somno 5 drowsiness or somnolence, and aspirin can cause gastrointestinal (GI) bleeding.
sleepiness To help patients obtain adequate pain relief, nonpharmacologic techniques are often used as
lence 5 state of an essential form of adjunctive therapy. Rarely will nonpharmacologic techniques be used in place
of pharmacotherapy, but when used together with medication, nonpharmacologic techniques allow
medication doses to be lowered. Lowered doses typically mean fewer drug-related adverse effects. Some
nonpharmacologic techniques employed for reducing pain include the following:
■ Physical therapy
■ Massage
■ Biofeedback therapy
■ Heat or cold packs

■ Meditation or prayer
■ Relaxation therapy
■ Art or music therapy
■ Imagery
■ Chiropractic manipulation
■ Hypnosis
■ Therapeutic touch
■ Transcutaneous electrical nerve stimulation (TENS)
■ Energy therapies such as reiki and qi gong
■ Acupuncture
Nonpharmacologic techniques have an advantage that they can help improve the patient’s mood,
r educe anxiety, and provide the patient with a sense of control. Depending on the technique, nonphar-
macologic strategies often relax muscles, strengthen coping abilities, and generally improve the patient’s
quality of life. There are many determinants of successful therapy depending on the type of pain, its dura-
tion and severity. The success of therapy will also vary from patient to patient and will depend on many
factors including the patient’s age, attitude, tolerance, and level of compliance with overall therapy. The
patient’s coping skills, capabilities, and commitment will play a role in both pain management and recov-
ery. Costs of health care, availability of support from family members, and support from members within
the surrounding community are extremely important.
Patients with challenging or intractable (not easy to relieve) pain may require additional therapy. In in 5 opposite of
this case, adjuvant analgesics or co-analgesics may be used. Antiseizure drugs (Chapter 13) and local an- tractable 5 control
esthetics (Chapter 15) are examples of drug categories approved by the FDA for successful management of
pain. Carbamazepine (Tegretol) is approved for treatment of pain due to trigeminal neuralgia. Valproic acid
(Depakene or Depakote) is approved for the treatment of pain due to migraines. Gabapentin (Neurontin)
is prescribed for the management of postherpetic neuralgia. Pregabalin (Lyrica) is approval for treatment
of fibromyalgia, postherpetic neuralgia, and pain due to peripheral diabetic neuropathy. All of these drugs
were originally developed to treat conditions other than pain, but now have found useful application for
pain that is difficult to manage. Anesthetic nerve blocking drugs are another type of adjuvant analgesic
used for the management of acute and chronic pain, and are administered in a variety of ways for differ-
ent purposes. Lidoderm, for example, is a local anesthetic patch with 5% lidocaine used to reduce pain or
discomfort caused by skin irritations such as sunburn, insect bites, plant resins, minor cuts, scratches, and
burns. It is also used for post-surgical and post-shingles pain (Chapters 15 and 36). Corticosteroids reduce
inflammation and can also control certain types of inflammatory pain (Chapter 24).
Many medications are appropriately used for pain management, even though the FDA has not
specifically approved them for a particular use. Some well-established off-label medications for
pain management are the tricyclic antidepressants (TCAs) (Chapter 10). Examples are amitriptyline
(Elavil), nortriptyline (Aventyl, Pamelor) and imipramine (Tofranil), which have been used to sup-
press a variety of pain impulses characterized as chronic and neuropathic. Neuropathic pain impulses
are even slowed by dysrhythmic drugs when TCAs are not effective. Thus, cardiovascular drugs
have even found a place in pain management. Examples are mexiletine (Mexitil) and flecainide
(Tambocor) (Chapter 22).
Opioid analgesic medications exert their effects by interacting with

specific receptors. Core Concept 14.4
Analgesics are medications used to relieve pain. The two basic categories of analgesics are the opioids an 5 without
(narcotics) and the nonopioids. Terminology for the narcotic analgesics may be confusing. Several of algesia 5 pain
these drugs are obtained from opium, a milky extract from the unripe seeds of the poppy plant, which narc 5 numbness or stupor
contains more than 20 different chemicals having pharmacologic activity. Opium consists of 9% to 14% otic 5 like
morphine and 0.8% to 2.5% codeine. These natural substances are called opiates. In a search for safer
analgesics, chemists have created several dozen synthetic drugs with activity similar to that of the opi-
ates. For example, morphine is a natural narcotic; meperidine is a synthetic narcotic. Opioid is a general opi 5 opium
term referring to any of these substances, natural or synthetic, and is often used interchangeably with the oid 5 shape or form
term opiate. An opioid analgesic is a natural or synthetic morphine-like substance responsible for reduc-
ing moderate to severe pain. Opioids are narcotic substances, meaning that they produce numbness or
stupor-like symptoms.
Narcotic is a general term often used to describe opioid drugs that produce analgesia and CNS
d epression. In common usage, a narcotic analgesic is the same as an opioid, and the terms are often used
interchangeably. In the context of drug enforcement, however, the term narcotic describes a much broader
range of abused illegal drugs such as hallucinogens, heroin, amphetamines, and marijuana. This is an
important fact to remember when discussing use of opioids with members of law enforcement.
Opioids exert their actions by interacting with at least four major types of receptors: mu, kappa,
delta, and an opioid-like receptor called nociceptin or orphanin FQ peptide. For pain management, the mu
receptors and kappa receptors have been the ones traditionally targeted. Delta receptors also have a role in
affective 5 expressive analgesia; they are connected with the emotional and affective components of the pain experience and thus,
have become recent targets for drug development.
Responses produced by activation of mu and kappa receptors are listed in Table 14.2 ◆. Some opioids,
such as morphine, activate both mu and kappa receptors. Opioid blockers such as naloxone (Narcan)
inhibit both the mu and kappa receptors. Other opioids, such as pentazocine (Talwin), exert mixed effects
by a ctivating the kappa receptors but blocking the mu receptors. This is the body’s way of providing
for a diverse set of body responses from one substance. Figure 14.2 ■ illustrates actions resulting from
stimulation of mu and kappa receptors.
Concept Review 14.3

■ Distinguish between the following terms: opioid, opiate, and narcotic. Name four classes
of opioid receptors, and identify those that are connected with analgesia.
Table 14.2 Responses Produced by Activation of Specific Opioid Receptors

Response Mu Receptor Kappa Receptor
Analgesia ✓ ✓
Decreased GI motility ✓ ✓
Euphoria ✓
Miosis (constricted pupils) ✓
Physical dependence ✓
Respiratory depression ✓
Sedation ✓ ✓
F i g u re 1 4 . 2
Opioid receptors. Pure opioid Mixed opioid Mixed opioid Pure opioid
agonist agonist agonist antagonist
Morphine Buprenorphine Pentazocine Naloxone
Codeine Butorphanol
Cell receptors
Mu: Analgesia
Decreased GI motility
Respiratory depression
Sedation
Physical dependence
Kappa:
Analgesia
Decreased GI motility
Sedation
Opioid Analgesics for Severe Pain
Opioids have multiple therapeutic effects, including relief of severe pain. Core Concept 14.5
Opioids are drugs for moderate to severe pain that cannot be controlled with other classes of a nalgesics.
Narcotic opioids bind to opioid receptors and produce multiple responses throughout the body. As p owerful
CNS depressants, opioid narcotics can cause sedation, which may be a therapeutic effect or an adverse
effect, depending on the patient’s disease state. Some patients experience euphoria and intense relaxation,
which are reasons why opiates are sometimes abused. There are many adverse effects, including respira-
tory depression, sedation, nausea, and vomiting. More than 20 different opioids are available as medica-
tions, and they can be classified by similarities in their chemical structures, by their mechanisms of action,
or by their effectiveness. The most useful method is by effectiveness, which places opiates into categories
of high or moderate narcotic activity (Table 14.3 ◆).
Opioid Agonists
Drugs that stimulate a particular opioid receptor are called opioid agonists. Morphine is the prototype opioid ag-
onist used to treat severe pain. It is usually the standard by which the effectiveness of other opioids is compared.
All of the opioid agonists have the potential to cause physical and psychological dependence, as discussed
in Chapter 7. Over the years, healthcare providers have been hesitant to administer the proper amount of opioid
analgesic for fear of causing patient dependence or of producing serious adverse effects, such as sedation or
respiratory depression. Because of this tendency, some patients have not received complete pain relief.
When used according to accepted medical practice, patients can, and indeed should, receive the pain
relief they need without fear of addiction or adverse effects. One method available to accomplish this is
patient-controlled analgesia (PCA). In this instance, patients are allowed to self-medicate with opiate
medication by pressing a button. Safe levels of pain medication are delivered with an infusion pump.
The fentanyl transdermal system (Duragesic patch) is another strong prescription medication used for
the control of moderate to severe chronic pain. The patch enables longer-lasting relief from persistent pain.
Fentanyl (Lazanda) nasal spray is available for quick delivery across nasal mucous membranes. Fentanyl is
also administered as a lozenge (Oralet, Actiq), tablet (Fentora, Onsolis), or via sublingual (Abstral) admin-
istration. These slowly dissolve in the mouth, and drugs are absorbed via the mouth’s mucous membranes.
Drug Prototype: Morphine (Astramorph PF, Duramorph, Others)

Therapeutic Class: Opioid analgesic
Pharmacologic Class: Opioid agonist receptor drug
Actions and Uses: Morphine binds with both mu and kappa anesthetics, sedatives, and antidepressants such as monoamine
receptor sites to produce strong analgesia. It causes euphoria, oxidase inhibitors (MAOIs) and tricyclics, increases the action
constriction of the pupils, and stimulation of cardiac muscle. It of opiates and thereby raises the risk of severe respiratory
is used for relief of serious acute and chronic pain after non- depression and death.
narcotic analgesics have failed, as preanesthetic medication, to Use with caution with herbal supplements, such as
relieve shortness of breath associated with heart failure and yohimbe, which may increase the effect of morphine.
pulmonary edema, and for acute chest pain connected with
myocardial infarction (MI).
Adverse Effects and Interactions: Morphine may cause Black Box Warning:
dysphoria (restlessness, depression, and anxiety), hallucinations, When morphine is administered as an epidural drug, due to
nausea, constipation, dizziness, and an itching sensation. the risk of adverse effects, patients must be observed in a
Overdose may result in severe respiratory depression or fully equipped and staffed environment for at least
cardiac arrest. Tolerance develops to the analgesic, sedative, 24 hours. Morphine administered as extended-release tablets
and euphoric effects of the drug. Cross-tolerance also has an abuse liability similar to other opioid analgesics.
develops between morphine and other opioids such as heroin, Morphine is a Schedule II controlled substance and should
methadone, and meperidine. Physical and psychological be taken properly according to dispensing instructions (i.e.,
dependence develop when high doses are taken for pro- tablets/capsules should be taken whole and not broken,
longed periods. Morphine may intensify or mask the pain of chewed, dissolved, or crushed). Alcohol should be avoided
gallbladder disease due to biliary tract spasms. with morphine products (e.g., Avinza). Failure to follow
Morphine interacts with several drugs. For example, use these warnings could result in fatal respiratory depression.
with CNS depressants, such as alcohol, other opioids, general
Table 14.3 Opioids for Pain Management

Opioid Agonists with High Effectiveness
fentanyl (Actiq, Abstral Duragesic, Fentora, IM; 0.05–0.1 mg Used with anesthesia for surgery and other
Lazanda, Onsolis, Oralet,) Transdermal 25–100 mcg every 72 hours procedures; also available by the buccal and
nasal spray routes.
hydromorphone (Dilaudid, Exalgo) PO; 1–4 mg every 4–6 hours prn Also for cough; available in IM, IV,
subcutaneous, and rectal forms.
levorphanol (Levo-Dromoran) PO; 2–3 mg tid to qid prn Also available in subcutaneous form.
meperidine (Demerol) PO; 50–150 mg every 3–4 hours prn For preoperative medication or obstetric
analgesia; available in IM, IV, and
subcutaneous forms.
methadone (Dolophine) PO; 2.5–10 mg every 3–4 hours prn For detoxification treatment of opioid
dependency; available in IM and IV forms.
morphine (Astramorph PF, Duramorph, PO; 10–30 mg every 4 hours prn Available in IM, IV, subcutaneous,
others) intrathecal, epidural, and rectal forms.
oxymorphone (Opana) Subcutaneous/IM; 1–1.5 mg every 4–6 hours Also available in IV and rectal forms.
prn; 5 mg every 4–6 hours prn
Opioid Agonists with Moderate Effectiveness
codeine PO; 15–60 mg qid Also for cough; available in IM and
subcutaneous forms; combination drug
with aspirin is called Empirin; available also
as combination drug with acetaminophen
(Tylenol with codeine).
hydrocodone (Hycodan) PO; 5–10 mg every 4–6 hours prn (max: Also for cough; combination drug with
15 mg/dose) acetaminophen is called Vicodin.
oxycodone (OxyContin, Oxecta); oxycodone PO; 5–10 mg qid prn Combination drug with acetaminophen is
terephthalate (Percocet-5, Roxicet, others) Controlled release; 10–20 mg every 12 hours called Percocet or Roxicet; with aspirin is
called Percodan.
Opioid Antagonists
naloxone (Narcan) IV; 0.4–2 mg, may be repeated every 2–3 For opioid overdose and postoperative opioid
min up to 10 mg if necessary depression.
naltrexone (Trexan, ReVia, Vivatrol) PO; 25 mg followed by another 25 mg in For management of opiate or alcohol
1 hour if no withdrawal response (max: dependence; longer lasting effect than
800 mg/day) naloxone.
Opioids With Mixed Agonist–Antagonist Effects
buprenorphine (Buprenex, Butrans, IM/IV; 0.3 mg every 6 hours (max: 0.6 mg For moderate to severe pain; also available in
Suboxone) every 4 hours) subcutaneous, epidural, and rectal forms.
butorphanol (Stadol) IM; 1–4 mg every 3–4 hours prn (max: 4 For obstetrical analgesia during labor, cancer
mg/dose) pain, renal colic, and burns; available in IV
and intranasal forms.
nalbuphine (Nubain) Subcutaneous/IM/IV; 10–20 mg every 3–6 For moderate to severe pain.
hours prn (max: 160 mg/day)
pentazocine (Talwin) PO; 50–100 mg every 3–4 hours (max: 600 For moderate to severe pain (much lower
mg/day); subcutaneous/IM/IV; 30 mg every dose for women in labor).
3–4 hours (max: 360 mg/day)
Buccal fentanyl is indicated for the management of breakthrough cancer pain in adult patients who are al-
ready receiving and who might already be tolerant to traditional opioid therapy. These medications should
not be used to treat pain other than chronic cancer pain or in the management of acute or postoperative
pain, including headaches and migraines. Fentanyl may cause serious harm or death if used accidentally
by a child or by an adult who does not have a higher level of tolerance to opioids. Respiratory depression
and fatal overdose are risks. Alfentanil (Alfenta), remifentanil (Ultiva), and sufentanil (Sufenta) are used to
provide continuous pain relief during and after surgery or for use during the induction and maintenance of
general anesthesia; these are discussed further in Chapter 15.
In the pharmacologic management of pain, it is common practice to combine opioids and nonnarcotic
analgesics into a single tablet or capsule (Core Concept 14.6). The two classes of analgesics work syner- syn 5 together
gistically to relieve pain, and the dose of narcotic can be kept small to avoid dependence and opioid-related erg 5 work
adverse effects. Examples of combination analgesics are as follows: istically 5 ability to
■ Vicodin (hydrocodone, 5 mg; acetaminophen, 500 mg)

■ Percocet (oxycodone HCl, 5 mg; acetaminophen, 325 mg)
■ Percodan (oxycodone HCl, 4.5 mg; oxycodone terephthalate, 0.38 mg; aspirin, 325 mg)
■ Empirin with Codeine No. 2 (codeine phosphate, 15 mg; aspirin, 325 mg)
■ Ascomp with Codeine or Fiorinal (codeine phosphate, 30 mg; aspirin, 325 mg; caffeine, 40 mg;
butalbital, 50 mg)
■ Fioricet with Codeine (codeine phosphate, 30 mg; acetaminophen, 325 mg; caffeine, 40 mg;
butalbital, 50 mg)
■ Tylenol with Codeine (single dose may contain from 15 to 60 mg of codeine phosphate and
from 300 to 1,000 mg of acetaminophen)
Some opioids are used primarily for conditions other than pain relief. Codeine is often prescribed
as a cough suppressant and is covered in Chapter 29. Opiates used in treating diarrhea are presented in
Chapter 30.
Opioid Antagonists
Drugs that block an opioid receptor are called opioid antagonists. Opioid antagonists are substances that
prevent the effects of opioid agonists. These drugs are considered competitive antagonists because they
compete with opioid agonists for access to the opioid receptor site.
Opioid overdose can occur as a result of overly aggressive pain therapy or as a result of substance abuse.
Any opioid may be abused for its psychoactive effects; however, morphine, meperidine, and heroin are sometimes
preferred because of their potency. Although heroin is currently available as a legal analgesic in many countries,
it is considered by the FDA to be too dangerous for therapeutic use and is a major drug of abuse. Once injected
or inhaled, heroin rapidly crosses the blood–brain barrier to enter the brain, where it is metabolized to morphine.
Thus, the effects and symptoms of heroin use are actually caused by the activation of mu and kappa receptors by
morphine. The initial effect is an intense euphoria, called a rush, followed by several hours of deep relaxation.
Opioid antagonists are often used to reverse the symptoms of opioid toxicity or overdose. Symptoms
of overdose include sedation or respiratory distress. Acute opioid intoxication is a medical emergency,
with respiratory depression being the most serious problem. Infusion with the opioid antagonist naloxone
(Narcan) may be used to reverse respiratory depression and other acute symptoms. Naltrexone mixed with
morphine (Embeda) is used for moderate to severe pain control when a continuous, round-the-clock opioid
analgesic is needed for an extended period. In cases in which the patient is unconscious or unclear as to
which drug has been taken, opioid antagonists may be given to diagnose the overdose. If the opioid antago-
nist fails to quickly reverse the acute symptoms, the overdose may be attributed to a nonopioid substance.
Drug Prototype: Naloxone (Narcan)

Therapeutic Class: Drug for treatment of acute opioid overdose and misuse
Pharmacologic Class: Opioid receptor blocker
Actions and Uses: Naloxone is a pure opioid antagonist, atient may experience rapid loss of analgesia, increased blood
p
blocking both mu and kappa receptors. It is used for complete pressure, tremors, hyperventilation, nausea/vomiting, and
or partial reversal of opioid effects in emergency situations drowsiness. It should not be used for respiratory depression
when acute opioid overdose is suspected. Given intravenously, caused by nonopioid medications.
it begins to reverse opioid-initiated CNS and respiratory Drug interactions include a reversal of the analgesic effects
depression within minutes. It will immediately cause opioid of narcotic agonists and agonist–antagonists.
withdrawal symptoms in patients physically dependent on
opioids. It is also used to treat postoperative opioid depression
(after-effect of the opioid therapy applied during surgery). It is Black Box Warning:
occasionally given as adjunctive therapy to reverse hypotension None; however, naltrexone, a similar opioid receptor antag-
caused by septic shock. Naloxone is pregnancy category B. onist, has the capacity to produce hepatic injury when taken
in excessive doses or if taken by patients with hepatic injury
Adverse Effects and Interactions: Naloxone itself has minimal or acute liver disease.
toxicity. However, in reversing the effects of opioids, the
Opioids with Mixed Agonist–Antagonist Effects

Narcotic opioids that have mixed agonist–antagonist activity stimulate the opioid receptor; thus, they cause
analgesia. However, withdrawal symptoms and adverse effects are not as intense due to partial activation
of the receptor subtypes.
Although effective at relieving pain, the opioid agonists have a greater risk for dependence than
almost any other class of medications. Tolerance develops relatively quickly to the euphoric effects of
opioids, causing users to increase their doses and take the drugs more frequently. The higher and more
frequent doses rapidly cause physical dependence in opioid abusers.
When physically dependent patients attempt to discontinue drug use, they experience extremely un-
comfortable symptoms which generally cause them to continue taking the drugs. As long as the drugs
are continued, they feel “normal” and continue to work and engage in social activities. If they abruptly
discontinue the drugs, they experience withdrawal symptoms for about seven days before overcoming the
physical dependence. Beyond this, the intense craving that characterizes psychological dependence may
occur for many months, even years, following discontinuation of opioids. This often results in a return to
drug-seeking behavior unless support groups are established.
One method of treating opioid dependence has been to switch the patient from IV and inhalation forms
of illegal drugs to oral methadone (Dolophine). Although oral methadone is an opioid, it does not cause the
euphoria of the injectable opioids. Methadone also does not cure the dependence, and the patient must con-
tinue taking the drug to avoid withdrawal symptoms. This therapy, called methadone maintenance, may
continue for many months or years, until the patient decides to enter a total withdrawal treatment program.
Methadone maintenance allows patients to return to productive work and social relationships without the
physical, emotional, and criminal risks of illegal drug use.
A newer treatment option is to administer buprenorphine (Buprenex, Butrans, Suboxone), a mixed
opioid agonist–antagonist, by the sublingual or transdermal route. Buprenorphine is used early in opioid
abuse therapy to prevent opioid withdrawal symptoms. Suboxone, contains both buprenorphine and nalox-
one and is used later in the maintenance of opioid addiction.
Healthcare providers should always be aware that when administering mixed agonist–antagonists
with opioid agonists, their pain-blocking properties are reduced. Thus, there may be a tendency to over-
prescribe mixed opioids, promoting drug misuse. This is true even though in most cases the potential for
causing opioid addiction is lower with mixed agonist–antagonists drugs.
Nursing Process Focus Patients Receiving Opioids

neurological, renal and liver conditions, allergies, drug history, ■ Acute or Chronic Pain related to injury, disease process, surgical
likelihood of drug dependency, and possible drug interactions. procedure or inadequate medication
■ Evaluate complaints of pain (quality, intensity, location, duration). ■ Ineffective Breathing Pattern related to adverse effects of drug
■ Acquire the results of a complete phsycial examination including vital therapy
signs and ECG. ■ Constipation related to adverse effect of drug therapy
■ Evaluate laboratory blood findings: CBC, chemistry, renal and liver ■ Risk for Injury related to adverse effect of drug therapy
function studies, and drug screening.
■ Determine neurological status (level of consciousness [LOC], mental
status and identification of recent mood and behavior patterns).
The patient will:

■ Experience therapeutic effects (report of pain relief or a reduction in pain intensity).
Implementation
■ Monitor the use of opioids. (Opioids are Schedule II controlled sub- ■ Inform the patient and caregivers to take necessary steps to safeguard
stances and can produce both physical and psychological dependence.) drug supply and to avoid sharing medications with others.
■ Administer medication correctly and evaluate the patient knowledge Instruct the patient:
of proper administration. (Depending on the drug, they may be ad- ■ That oral capsules may be opened and mixed with cool foods; extended-
ministered PO, subcutaneously, IM, IV, or epidural. Combining opioids release tablets, however, may not be chewed, crushed, or broken.
with some medications or food items may be contraindicated.) ■ That the oral solution for taking sublingually, may be more concen-
trated than the solution for swallowing.
■ To not use opioids concurrently with other medications (including
herbal therapies) without consulting healthcare provider.
■ Monitor laboratory liver function studies. (Opioids are metabolized in Instruct the patient to:
the liver. Hepatic disease can increase blood levels of opioids to toxic ■ Report to healthcare provider the following symptoms: nausea,
levels.) vomiting, diarrhea, rash, jaundice, abdominal pain, tenderness, or
distention, or change in color of stool.
■ Adhere to laboratory testing regimen for liver function as ordered by
the healthcare provider.
■ Monitor vital signs, especially depth and rate of respirations/pulse Instruct the patient to:
oximetry. Withhold the drug if the patient’s respiratory rate is below ■ Monitor vital signs regularly, particularly respirations.

12, and notify the healthcare provider. Keep resuscitative equipment ■ Withhold medication for any difficulty in breathing or respirations
and a narcotic antagonist such as naloxone (Narcan) accessible. below 12 breaths per minute; report symptoms immediately to the
(Opioid antagonists may reverse respiratory depression, decrease level healthcare provider.
of consciousness, and initiate other symptoms of narcotic overdose.)
■ Perform neuro checks regularly. Especially monitor for changes in LOC Instruct the patient to:
or seizure activity. (Decreased LOC and sluggish pupillary response ■ Report headache or any significant change in sensorium, such as an
may occur with high doses, and the drug may increase intracranial aura or other visual effects that may indicate an impending seizure to
pressure.) the healthcare provider.
■ Recognize seizures and methods to ensure personal safety during a
seizure.
■ Report any seizure activity immediately.
■ If ordered prn, administer the medication upon patient’s request or Instruct the patient to:
when nursing observations indicate expressions of pain by the patient. ■ Alert the nurse immediately upon the return or increase of pain.
■ Notify the healthcare provider regarding the drug’s effectiveness.
■ Monitor renal status and urinary output (may cause urinary retention, Instruct the patient to:
which may exacerbate existing symptoms of prostatic hypertrophy). ■ Measure and monitor fluid intake and output.
■ Report symptoms of dysuria (hesitancy, pain, diminished stream),
changes in urine quality, or scanty urine output to the healthcare
provider.
■ Report fever or flank pain that may be indicative of a urinary tract
infection.
■ Monitor for other adverse effects such as restlessness, dizziness, Instruct the patient to:
anxiety, depression, hallucinations, nausea, and vomiting. (Hives ■ Recognize adverse effects and symptoms of an allergic or anaphylactic
or itching may indicate an allergic reaction due to the production reaction.
of histamine. Depression, anxiety and hallucinations may indicate ■ Immediately report to healthcare provider any shortness of breath,
overdose.) tight feeling in the throat, itching, hives or other rash, feelings of
dysphoria, nausea, or vomiting.
■ Avoid the use of sleep-inducing over-the-counter (OTC) antihistamines
without first consulting the healthcare provider.
■ Monitor for constipation. (Drug slows peristalsis.) Instruct the patient to:
■ Maintain adequate fluid and fiber intake to facilitate stool passage.
■ Use a stool softener or laxative as recommended by the healthcare
provider.
■ Ensure patient safety. Monitor ambulation until response to the drug Instruct the patient to:
is known. (Drug can cause sedation and dizziness.) ■ Request assistance when getting out of bed.
■ Avoid driving or performing hazardous activities until effect of the
drug is known.
■ Monitor frequency of requests and stated effectiveness of narcotic Instruct the patient:
administered. (Opioids cause tolerance and dependence.) ■ Regarding cross-tolerance issues.
■ To monitor medication supply to observe for hoarding, which may
signal an impending suicide attempt.
■ Who is suffering from a terminal illness about the issue of drug
dependence as related to reduced life expectancy.
Nonopioid Analgesics for Moderate Pain
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the preferred

Core Concept 14.6 nonopioid analgesics for inflammation and less severe pain.
The nonopioid analgesics involve NSAIDs and a few centrally acting drugs, including acetaminophen. The
role of the NSAIDs in the treatment of inflammation and fever is discussed more thoroughly in Chapter 24.
Therefore, there is only brief mention here. Table 14.4 ◆ highlights the more common nonopioid analgesics.
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

NSAIDs are drugs for mild to moderate pain, especially for pain associated with inflammation. NSAIDs
inhibit cyclooxygenase, an enzyme responsible for the formation of prostaglandins. When cyclooxygen-
ase is inhibited, inflammation and pain are reduced. These drugs have many advantages over the opioids in
that the NSAIDs have antipyretic, anti-inflammatory, and analgesic properties.
mediators 5 middle drugs The NSAIDs act by inhibiting pain mediators at the nociceptor level. When tissue is damaged, local
chemical mediators are released: histamine, potassium ion, hydrogen ion, bradykinin, and prostaglandins.
brady 5 slow Bradykinin is associated with sensory impulses of pain. Prostaglandins prompt pain through the formation
kinin 5 movement of free radicals.
Popular NSAIDs available OTC are aspirin and ibuprofen. Ibuprofen and related medications are
available in many different formulations, including those designed for children. Most are safe and well
tolerated by patients when used at low to moderate doses. Higher and more prolonged doses produce hepa-
toxicity, which is a major concern with these classes of drugs (Chapter 24).
After tissue damage, prostaglandins are formed with the help of two enzymes called cyclooxygen-
ase type 1 (COX-1) and cyclooxygenase typ. 2 (COX-2). Aspirin and ibuprofen-related drugs inhibit both
COX-1 and COX-2. Thus, COX inhibition is the basis of NSAID therapy. Because the COX-2 enzyme is
syn 5 together more specific for the synthesis of inflammatory prostaglandins, the selective COX-2 inhibitors provide a
thesis 5 put more focused peripheral pain relief. Celecoxib (Celebrex) is one of the COX-2 inhibitors still available in
the United States; other COX-2 inhibitors have been discontinued. Figure 14.3 ■ illustrates the mechanism
of pain transmission at the nociceptor level.
Drug Prototype: Aspirin (Acetylsalicylic Acid, ASA)

Therapeutic Class: Nonopioid analgesic, nonsteroidal anti-inflammatory drug (NSAID), antipyretic; drug for
myocardial infarction prophylaxis and transient ischemia
Pharmacologic Class: Salicylate, cyclooxygenase (COX) inhibitor, prostaglandin synthesis inhibitor, platelet
aggregation inhibitor
Actions and Uses: Aspirin inhibits prostaglandin synthesis buffered preparations are available for patients who experience
involved in the processes of pain and inflammation and GI adverse effects.
produces mild to moderate relief of fever. It has limited effects Because aspirin increases bleeding time, it should not
on peripheral blood vessels, causing vasodilation and sweating. be given to patients receiving anticoagulant therapy such as
Aspirin has significant anticoagulant activity, and this property warfarin, heparin, and plicamycin. ASA may increase the action
is responsible for its ability to reduce the risk of mortality of oral hypoglycemic drugs. Effects of NSAIDs, uricosuric drugs
following MI and to reduce the incidence of strokes. Aspirin such as probenecid, beta blockers, spironolactone, and sulfa
has also been found to reduce the risk of colorectal cancer, drugs may be decreased when combined with ASA.
although the mechanism by which it affords this protective Use with phenobarbital, antacids, and glucocorticoids
effect is unknown. may decrease ASA effects. Insulin, methotrexate, phenytoin,
sulfonamides, and penicillin may increase effects. When taken
Adverse Effects and Interactions: At high doses, such as those with alcohol, pyrazolone derivatives, steroids, or other NSAIDs,
used to treat severe inflammatory disorders, aspirin may cause there is an increased risk for gastric ulcers.
gastric discomfort and bleeding because of its antiplatelet Use with caution with herbal supplements, such as
effects. Hepatotoxicity, is also a concern, especially in patients feverfew, which may increase the risk of bleeding.
with pre-existing liver disease. Enteric-coated tablets and
Table 14.4 Nonopioid Analgesics

NSAIDs: Aspirin and Other Salicylates
aspirin (acetylsalicylic acid, ASA) PO; 350–650 mg every four hours Also for fever, inflammation, and
(max: 4 g/day) thromboembolic disorders, prevention of
transient ischemic attacks and heart attacks;
rectal form available
salsalate (Disalcid) PO; 325–3,000 mg daily in divided doses Also for fever, inflammation
(max: 4 g/day)
NSAIDs: Ibuprofen and Ibuprofen-like Drugs
diclofenac (Cambia, Cataflam, Voltaren, PO; 50 mg bid to qid (max: 200 mg/day) Also for inflammation
Zipsor)
diflunisal PO; 1000 mg followed by 500 mg bid to tid Also for inflammation
etodolac PO; 200–400 mg tid to qid Also for inflammation
fenoprofen (Nalfon) PO; 200 mg tid to qid Also for inflammation
flurbiprofen (Ansaid, Ocufen) PO; 50–100 mg tid to qid (max: 300 mg/day) Similar to ibuprofen
ibuprofen (Advil, Motrin, others) PO; 400 mg tid to qid (max: 1,200 mg/day) Also for fever and inflammation
indomethacin (Indocin) PO; 25–50 mg bid or tid (max: 200 mg/day) Also used for moderate to severe rheumatoid
or 75 mg sustained release one to two arthritis and acute gouty arthritis
times/day
ketoprofen (Actron, Orudis) PO; 12.5–50 mg tid to qid Also for inflammation
ketorolac (Toradol) PO; 10 mg qid prn (max: 40 mg/day) Also for allergic conjunctivitis, available in
IM/IV forms
mefenamic acid (Ponstel) PO; loading dose 500 mg, maintenance dose Used for short-term relief of mild to moderate
250 mg every 6 hours prn pain, including menstrual cramps
meloxicam (Mobic) PO; 7.5 mg daily (max: 15 mg/day) Used for osteoarthritis
nabumetone (Relafen) PO; 1,000 mg daily (max: 2,000 mg/day) Inhibits COX-2 more than COX-1
naproxen (Naprosyn, Naprelan) PO; 500 mg followed by 200–250 mg tid to Also for inflammation
qid (max: 1,000 mg/day)
naproxen sodium (Aleve, Anaprox, others) PO; 250–500 mg bid (max: 1,000 mg/day Also for dysmenorrhea
naproxen)
oxaprozin (Daypro) PO; 600–1200 mg daily (max: 1,800 mg/day) Similar to naproxen; once-a-day dosage
piroxicam (Feldene) PO; 10–20 mg daily to bid (max: 20 mg/day) Has prolonged half-life
sulindac (Clinoril) PO; 150–200 mg bid (max: 400 mg/day) Also for inflammation
tolmetin (Tolectin) PO; 400 mg tid (max: 2 g/day) Also for inflammation
NSAIDs: Selective COX-2 Inhibitors
celecoxib (Celebrex) PO; 100–200 mg bid or 200 mg/daily Also for inflammation
Centrally Acting Drugs
acetaminophen (Tylenol) (see page 369 for PO; 325–650 mg every 4–6 hours Also for fever; available in rectal form;
the Drug Prototype Box) centrally acting COX inhibitor
tramadol (Ultram) PO; 50–100 mg every 4–6 hours prn Causes less respiratory depression than
(max: 400 mg/day), may start with 25 mg/ morphine
day and increase by 25 mg every 3 days up to
200 mg/day
ziconotide (Prialt) Intrathecal; 0.1 mcg/hr via infusion, may Also used for muscle spasticity
increase by 0.1 mcg/hr every 2–3 days (max:
0.8 mcg/hr)
Figure 14.3
Mechanisms of pain at COX = Cyclooxygenase

the nociceptor level. PGs = Prostaglandins
PGs PGs
block platelet pain and
aggregation inflammation
Opiates alter the
perception of and Selective
emotional responses COX-2 inhibitors
X
to pain
COX-1 COX-2 • Celecoxib
Nonselective
X
COX inhibitors
Arachidonic acid • Aspirin
• Ibuprofen
Free nerve
endings
(nociceptor) Tissue damage
+
Pain
Pain mediators
transmission K+
Pyrogens*
To spinal
cord
Histamine
m
rea
dst
*To brain to increase Bloo
body temperature
Centrally Acting Drugs

Centrally acting drugs are drugs that exert effects directly within the brain and spinal cord. Any analgesic
drug, which has a central effect bypasses the nociceptor level. Acetaminophen is a centrally acting nono-
pioid analgesic. Acetaminophen reduces fever by direct action at the level of the hypothalamus and causes
dilation of peripheral blood vessels, enabling sweating and dissipation of heat. It is the primary alternative
to NSAIDs when patients cannot take aspirin or ibuprofen. Acetaminophen does not produce GI bleed-
ing or ulcers and it does not exhibit cardiotoxicity. The safety profile of acetaminophen is excellent when
administered in proper therapeutic doses; however, hepatotoxicity can occur with misuse and overdose.
Aspirin and acetaminophen have similar efficacies in relieving pain and reducing fever. Acetaminophen is
featured as a prototype drug for the treatment of fever in Chapter 24.
Tramadol (Ultram) and ziconotide (Prialt) are additional centrally acting analgesics. Of the two drugs,
tramadol is the more widely prescribed. Tramadol has weak opioid activity, although it is not thought to
relieve pain by this mechanism. Its main action is to inhibit reuptake of norepinephrine and serotonin in
spinal neurons. Tramadol is well tolerated, but common adverse effects are vertigo, dizziness, headache,
nausea, vomiting, constipation, and lethargy.
Concept Review 14.4

■ Think about cyclooxygenase inhibitors (NSAIDs) and prostaglandins, and then describe
how pain might be regulated at the nociceptor.
Tension Headaches and Migraine
Headache is one of the most common complaints of patients. Living with headaches can interfere with activi-
ties of daily living and can cause great distress. Pain and difficulty may result in work-related absences and
neglect of home and family life. When headaches are persistent, or as migraines occur, drug therapy is needed.
CAM TherapY
Evening Primrose Oil for Pain and Eczema
Evening primrose (Primula biennis) is a wildflower that grows throughout the United States.
The oil extracted from the seeds of the plant contains high amounts of gamma linolenic acid,
an essential fatty acid that is required by the body for normal growth and development.
Evening primrose oil has been used for a large number of conditions. The strongest
scientific evidence is for treating eczema, a condition characterized by inflamed, itchy
skin. Some data have suggested that the herb may reduce pain in patients with breast
tenderness and rheumatoid arthritis. Other claimed uses include premenstrual syndrome,
diabetic neuropathy, cholesterol reduction, multiple sclerosis, and prevention of stroke;
however, scientific evidence is not adequate to support these indications. Evening primrose
oil is very safe. There is some concern that it may lower the seizure threshold in patients
with epilepsy.
Of the many types of headaches, the most common is the tension headache. It occurs when muscles
of the head and neck tighten in response to stress. The tightness causes a steady and lingering pain.
Although quite painful, tension headaches usually end when the stress is resolved. They are generally
considered an annoyance rather than a medical emergency. Tension headaches are effectively treated with
OTC analgesics such as aspirin, acetaminophen, or ibuprofen. More intense tension headache may be
treated with additional classes of drugs.
The most painful type of headache is the migraine, which is characterized by throbbing or pulsat-
ing pain, sometimes preceded by an aura similar to those that warn of a seizure (see Chapter 13). The
auras of migraines are sensory cues, such as seeing jagged lines or flashing lights, smelling, tasting, or
hearing something strange. They let the patient know that a migraine attack is coming soon. Most pa-
tients with migraines also have nausea and vomiting. Triggers for migraines include nitrates and mono-
sodium glutamate (MSG) found in many Asian foods, red wine, perfumes, food additives, caffeine,
chocolate, and aspartame (a sugar substitute). By avoiding these substances, some patients can prevent
the onset of a migraine attack.
Migraines can be effectively treated with a variety of drug classes. Core Concept 14.7
There are two primary goals for the pharmacologic management of migraines. The first is to prevent mi-
graines from occurring (prophylaxis), and the second is stop migraines in progress. For the most part, the pro = before
drugs used to stop migraines are different than those used for prophylaxis; nevertheless, drug therapy is phylaxis = guarding
most effective if begun before a migraine has reached a severe level. It is not unusual for pharmacotherapy
for mild migraines to begin with acetaminophen or NSAIDs. If OTC analgesics are unable to stop the mi-
graine, then more specific drugs will be necessary.
The two major drug classes used to terminate migraines are the triptans and the ergot alkaloids; both
stimulate receptors to serotonin also called 5-hydroxytryptamine (5-HT). A variety of other drugs classes
are also used to treat migraines. Antimigraine drugs are listed in Table 14.5 ◆.
Triptans
Triptans were introduced in the 1990s for the treatment of migraine. As possible agonists to the 5-HT re-
ceptor, these drugs act to constrict blood vessels in the brain. They are effective in stopping migraines with
or without auras. The first of the triptans marketed in the United States was sumatriptan (Imitrex). Since
1993, more triptans were developed. Although oral forms of the triptans are the most convenient, patients
who experience unpleasant symptoms during a migraine, such as nausea and vomiting, may require an al-
ternate dosage form. Intranasal formulation and prefilled syringes of triptans are available for patients who
are able to self-administer.
Ergot Alkaloids
For patients who are unresponsive to triptans, the ergot alkaloids have been used to terminate migraines.
The actions of the ergot alkaloids have been known for a long time. The first purified alkaloid, ergotamine
(Ergostat), was isolated from the ergot fungus in 1920. Ergotamine is an inexpensive drug that is avail-
able in oral, sublingual, and suppository forms. Modification of the original molecule has produced an-
other useful drug, dihydroergotamine (Migranal). Dihydroergotamine is given parenterally and as a nasal
spray. Because the ergot alkaloids interact with adrenergic and dopaminergic receptors as well as serotonin
receptors, they produce multiple actions and adverse effects such as tachycardia or bradycardia, nausea,
vomiting, muscle pain and stiffness, peripheral constriction (leg weakness, numbness or tingling), lack of
urination, and hypertension. Many ergot alkaloids are pregnancy category X drugs.
Table 14.5 Antimigraine Drugs

Triptans
almotriptan (Axert) PO; 6.25–12.5 mg, may repeat in 2 hours if May cause heart palpitations and rapid
necessary (max: two tablets/day) heartbeat
eletriptan (Relpax) PO; 20–40 mg, may repeat in 2 hours if May cause hypotension in older adult
necessary (max: 80 mg/day) patients
frovatriptan (Frova) PO; 2.5 mg, may repeat in 2 hours if May cause chest pains and heart palpitations
necessary (max: 7.5 mg/day)
naratriptan (Amerge) PO; 1–2.5 mg, may repeat in 4 hours if Serotonin stimulator; for migraine
necessary (max: 5 mg/day) termination
rizatriptan (Maxalt) PO; 5–10 mg, may repeat in 2 hours if May cause myocardial infarction
necessary (max: 30 mg/day); 5 mg with
concurrent propranolol (max: 15 mg/day)
sumatriptan (Imitrex) PO; 25 mg for one dose (max: 100 mg) Serotonin stimulator; subcutaneous and
intranasal forms available; for termination of
migraine
zolmitriptan (Zomig) PO; 2.5–5 mg, may repeat in 2 hours if Serotonin stimulator; for termination of
necessary (max: 10 mg/day) migraine
Ergot Alkaloids
dihydroergotamine mesylate (D.H.E. 45, IM; 1 mg, may be repeated at 1-hour Also available as nasal spray; pregnancy
Migranal) intervals to a total of 3 mg (max: 6 mg/week) category X; for migraine termination; may be
used in combination with low-dose heparin
to prevent postop deep vein thrombosis
ergotamine tartrate (Ergostat), ergotamine PO; 1–2 mg followed by 1–2 mg every 30 Also available in sublingual, inhalant, or
with caffeine (Cafergot, Ercaf, others) minutes until headache stops (max: 6 mg/day rectal forms; may cause physical depen-
or 10 mg/week) dence; pregnancy category X; for migraine
termination
Antiseizure Drugs
topiramate (Topamax) PO; start with 50 mg/day, increase by 50 mg/ Sugar-like chemical molecule; enhances the
week to effectiveness (max: 1,600 mg/day) action of GABA; also for partial seizures
valproic acid (Depakene, Depakote) (see PO; 250 mg bid (max: 100 mg/day) Also for absence seizures and mixed
page 191 for the Drug Prototype box) generalized types of seizures and mania
Beta-Adrenergic Blockers
atenolol (Tenormin) (see page 309 for the PO; 25–50 mg daily (max: 100 mg/day) Also used for hypertension and angina
Drug Prototype box)
metoprolol (Lopressor) PO; 50–100 mg daily bid (max: 450 mg/day) Also for angina and MI; sustained-release
and IV forms available
propranolol (Inderal, InnoPran XL) (see page PO; 80–240 mg/day in divided doses, may Beta-adrenergic blocker for migraine
340 for the Drug Prototype box) need 160–240 mg/day prevention
timolol (Betimol, Timoptic) (see page 604 PO; 10 mg bid, may increase to 60 mg/day in Also for hypertension, angina, and glaucoma
for the Drug Prototype box) two divided doses
Calcium Channel Blockers
nifedipine (Adalat CC, Procardia XL) (see PO; 10–20 mg tid (max: 180 mg/day) Selective for calcium channels in blood
page 279 for the Drug Prototype box) v essels; decreases peripheral vascular
resistance and increases cardiac output;
also for hypertension and angina;
sustained-release form available
nimodipine (Nimotop) PO; 60 mg every 4 hours for 21 days; start Off-label use for migraines; primary use is
therapy within 96 hours of subarachnoid for improvement of neurologic symptoms
hemorrhage following a stroke
verapamil (Calan, Isoptin SR, others) (see PO; 40–80 mg tid Off-label use for migraine prevention
page 342 for the Drug Prototype box)
Table 14.5 Antimigraine Drugs (continued)

Tricyclic Antidepressants
amitriptyline (Elavil) PO; 75–100 mg/day Off-label use for migraine prevention
imipramine (Tofranil) (see page 129 for the PO; 75–100 mg/day (max: 300 mg/day) May cause cardiac dysfunction and abnormal
Drug Prototype box) blood cell count; also for alcohol or cocaine
dependence; may control bedwetting in
children; available IM
protriptyline (Vivactil) PO; 15–40 mg/day in three to four divided For symptoms of depression; few sedative
doses (max: 60 mg/day) qualities; causes increased heart rate
Miscellaneous Drugs
onabotulinumtoxin A (Botox) IM; 155 units administered intramuscularly Direct-acting antispasmodic drug for muscle
(IM) to muscles of the head and neck area spasms and spasticity
methysergide (Sansert) PO; 4–8 mg/day in divided doses Similar to ergotamine; for migraine
prevention
riboflavin (vitamin B2) PO; as a supplement: 5–10 mg/day; for defi- Deficiency caused by chronic diarrhea,
ciency: 5–30 mg/day in divided doses liver disease, alcoholism, or inadequate
consumption of milk or animal products
Other Antimigraine and Tension Headache Drugs

Drugs for migraine prophylaxis include various classes of drugs that are discussed in other chapters of this
textbook. These include antiseizure drugs (Chapter 13), beta-adrenergic blockers (Chapter 22), calcium
channel blockers (Chapter 18), antidepressants (Chapter 10), and neuromuscular blockers (Chapter 12).
Because all these drugs have the potential to produce side effects, prophylaxis is initiated only if the inci-
dence of migraines is high and the patient is unresponsive to the drugs used to abort migraines. Of the vari-
ous drugs, the beta blocker propranolol (Inderal) is one of the most commonly prescribed. Amitriptyline,
an antidepressant, is often prescribed for patients who suffer from insomnia in addition to their migraines.
In 2010, onabotulinumtoxinA (Botox) was approved for the treatment of chronic migraines in cases in
which other medications were not successful. Botox inhibits neuromuscular transmission by blocking the
release of acetylcholine from axon terminals innervating skeletal muscle. With this approach, IM injections
are divided across specific muscles of the head and neck. When muscles are blocked, headaches due to
intense muscle tension subside for a period of up to three months. More indications for Botox therapy are
discussed in Chapter 12.
Drug Prototype: Sumatriptan (Imitrex)

Therapeutic Class: Antimigraine drug
Pharmacologic Class: Triptan, 5-HT (serotonin) receptor drug, vasoconstrictor of intracranial arteries
Actions and Uses: Sumatriptan, a triptan, belongs to a relatively Adverse Effects and Interactions: Some dizziness, drowsiness,
new group of antimigraine drugs known as the triptans. The or a warming sensation may be experienced after taking
triptans act by causing vasoconstriction of cranial arteries; this sumatriptan; however, these effects are not normally
vasoconstriction is moderately selective and does not usually af- severe enough to warrant stopping therapy. Because of its
fect overall blood pressure. This medication is available in oral, vasconstricting action, the drug can cause chest pressure and
intranasal, and subcutaneous forms. Subcutaneous administra- should be used cautiously, if at all, in patients with recent MI, or
tion ends migraine attacks in 10 to 20 minutes; the dose may be with a history of angina pectoris, hypertension, or diabetes.
repeated 60 minutes after the first injection to a maximum of Sumatriptan interacts with several drugs. For example,
two doses per day. If taken orally, sumatriptan should be admin- an increased effect may occur when taken with MAOIs
istered as soon as possible after the migraine is suspected or has and selective serotonin reuptake inhibitors (SSRIs). Further
begun. vasoconstriction can occur when taken with ergot alkaloids and
other triptans.

Patients taking pain medication need to know the following facts and recommendations:
In General
1. Carefully describe pain to your healthcare provider so that the analgesic medication
being taken is suited to the complaint.
2.
Report any OTC medication taken for pain to your healthcare provider to minimize
adverse effects and interactions.
3.
Aspirin has many undesirable adverse effects mainly related to gastric upset and
bleeding.
4. Follow instructions carefully and watch for drug interactions or contraindications.
Regarding Opiates
5. Avoid combining pain medications with alcohol and other CNS depressants (especially
opioids).
6.
Vital signs should be monitored with all opioid medications because of their CNS de-
pressant effects.
7.
Get up slowly from seated positions because certain pain medications cause
lightheadedness.
8.
Avoid operating machinery or driving a car if taking opiates because dizziness, blurred
vision, and drowsiness can occur.
9. Do not abruptly stop taking opioids; this could result in withdrawal. Signs include
chills, abdominal and muscle cramps, severe itching, sweating, restlessness, anxiety,
yawning, and drug-seeking behavior.
Chapter Review
14.1 Pain assessment is the first step to pain allow lower doses to be given with possibly fewer drug-
management. related adverse effects. Other adjunctive approaches
Pain is a subjective experience in which many pa- include FDA approved antiseizure drugs, local anesthet-
tients describe discomfort differently. Pain may ics, and corticosteroids, which reduce inflammation and
be classified as acute (from injury to recovery) or suppress pain in some cases. O ff-label drug categories
chronic (longer than six months). Pain may be clas- include TCAs, and drugs for dysrhythmia.
sified as nociceptor pain and further divided into so-
14.4 Opioid analgesic medications exert their effects by
matic or visceral pain and neuropathic pain.
interacting with specific receptors.
14.2 Pain transmission processes allow several major Different types of receptors mediate analgesia (pain
targets for pharmacologic intervention. relief)—mu receptors and kappa receptors are the most
Pain signals involve nerve impulses along two types of commonly targeted. Both are opioid receptors that re-
sensory neurons, Aδ and C fibers. Once impulses reach spond to natural or synthetic morphine-like substances.
the spinal cord, substance P is thought to transmit pain Natural substances extracted from unripe seeds of the
at the spinal level. The release of substance P is con- poppy plant are called opiates. Narcotic is a general
trolled by ganglia that release neurotransmitters called term referring to morphine-like drugs. In the context of
endogenous opioids. If not blocked, the impulse travels drug enforcement, the term narcotic includes a much
to the brain, where pain information is sensed and a re- broader classification of abused illegal drugs.
sponse to the sensation is initiated. Opioids act at the
14.5 Opioids have multiple therapeutic effects, includ-
level of the central nervous system (CNS); nonsteroi-
ing relief of severe pain.
dal anti-inflammatory drugs (NSAIDs) act at the level
of the peripheral nervous system (PNS). Opioids produce many effects, including analgesia for
intense pain, cough suppression, suppression of GI
14.3 Nonpharmacologic techniques and adjuvant anal- motility in diarrhea treatment, sedation, and euphoria.
gesics assist in providing adequate pain relief. It is common practice to place opioids and nonnar-
Nonpharmacologic techniques may be used in place of cotic analgesics in a single tablet or capsule. Acute
drugs or as adjunctive to drug therapy. When used along opioid intoxication is treated with the opioid antago-
with medication, nonpharmacologic techniques may nist naloxone. All of the narcotic analgesics have the
Chapter Review 215
potential to cause physical and psychological depen- Another antifever drug is acetaminophen, a centrally
dence. The opioids have a greater risk of dependency acting drug that acts as a nonopioid analgesic.
than most of the other classes of medications.
14.7 Migraines can be effectively treated with a variety
14.6 Nonsteroidal anti-inflammatory drugs (NSAIDs) of drug classes.
are the preferred nonopioid analgesics for inflam- Headaches in two categories—tension headaches and
mation and less severe pain. migraines—are the most common complaints of pa-
NSAIDs are nonopioid analgesics used to treat less tients. The two primary goals of migraine therapy are
severe pain associated with inflammation. NSAIDs migraine termination and migraine prevention. The
have antifever and pain-reducing properties. These two major classes of antimigraine drugs are ergot
effects are achieved by inhibition of enzymes called alkaloids and triptans. Drugs for migraine prophy-
cyclooxygenase type one (COX-1) and cyclooxygen- laxis include beta-adrenergic blockers, calcium chan-
ase type two (COX-2). When cyclooxygenase (COX) nel blockers, antidepressants, antiseizure drugs, and
is inhibited, prostaglandin synthesis is prevented. drugs for muscle tension.
One medication is selective for the COX-2 receptor.
Review Questions
The following questions are written in NCLEX-PN® style. An- 6. Prior to administering pain medication, the nurse ob-
swer these questions to assess your knowledge of the chapter tained which of the following information about the patient’s
material, and go back and review any material that is not clear pain? (Select all that apply.)
to you. 1. The patient’s diagnosis
1. The patient has osteoarthritis. Which of the following 2. The location of the pain
drugs would the nurse anticipate being ordered for both pain 3. When the patient last had a meal
and inflammation? 4. The severity of the pain
1. Sumatriptan (Imitrex) 7. The patient has been receiving morphine sulfate for pain
2. Acetaminophen (Tylenol) control. An evaluation of the patient reveals a decreased level
3. Fentanyl (Sublimaze) of consciousness and shallow respirations at a rate of 8 per
4. Meloxicam (Mobic) minute. The nurse anticipates what opioid antagonist being
ordered?
2. The patient is starting on sumatriptan (Imitrex) for mi-
graines. For which of the following should the nurse in- 1. Butorphanol (Stadol)
struct the patient to notify his or her healthcare provider 2. Hydrocodone (Hycodan)
immediately? 3. Naloxone (Narcan)
4. Oxycodone (OxyContin)
1. Chest pressure
2. GI upset 8. Since a patient is allergic to aspirin, the nurse administers
3. Bleeding what drug as an alternative for relief of mild pain?
4. Lethargy 1. Acetaminophen
3. A patient is receiving an NSAID, so the nurse monitors 2. Morphine
the patient for: 3. Etodolac
4. Fentanyl
1. GI upset and bleeding
2. Urinary retention 9. The nurse monitors for which of the following adverse ef-
3. Blurred vision fects of ergotamine (Ergostate): (Select all that apply.)
4. Anorexia 1. Tachycardia
4. The patient is experiencing opioid dependency. The nurse 2. Nausea and vomiting
would expect which drug to be used to treat this condition? 3. Peripheral dilation
4. Peripheral constriction
1. Oxycodone (OxyContin)
2. Tramadol (Ultram) 10. The healthcare provider orders ibuprofen 400 mg, po,
3. Hydromorphone (Dilaudid) three times a day. The pharmacy sends ibuprofen suspension
4. Methadone (Dolophine) 200 mg/5 mL. How many milliliters should the patient receive
in each dose?
5. When planning care for a patient in pain, the nurse un-
derstands that pain signals begin at the ______ and proceed 1. 2 mL
through the CNS. 2. 15 mL
3. 5 mL
1. Spinal cord 4. 10 mL
2. Viscera
3. Nociceptors
4. Substance P
Remember Mr. Coidiuf, who was 2. According to the prescription, which of the following nar-
introduced at the beginning of the cotic analgesics would the nurse expect to give to Mr. Coidiuf?
chapter? Now read the remainder of 1. Percocet
the case study. Based on the informa- 2. Talwin
tion you have learned in this chapter, 3. Dilaudid
answer the questions that follow. 4. Demerol
Mr. Damian Coidiuf, age 32, sustained a back injury three
3. Mr. Coidiuf asks the nurse why the doctor put him on a
years ago, which responded well to treatment with nonsteroi- narcotic that also contains acetaminophen. The nurse replies
dal anti-inflammatory medication. Over the last six months, that: (Select all that apply.)
Mr. Coidiuf has been seeing his healthcare provider again with
complaints of “sharp painful sensations along his right hip.” 1. The two medications work well together to decrease pain.
Despite careful attention, it appears that Mr. Coidiuf ’s pain 2. A lower dose of the narcotic can be used when combined
is no longer responding to anti-inflammatory medication. His with acetaminophen.
healthcare provider prescribes a narcotic analgesic (moder- 3. Because narcotics can have serious adverse effects, using a
ate effectiveness) with acetaminophen, hoping this treatment low dose of a narcotic can help minimize these effects.
might provide relief. Following three physical therapy sessions, 4. Combining the two medication helps to lower the cost.
and the new medication, Mr. Coidiuf reports that he is “feeling 4. While providing Mr. Coidiuf with information about the
better.” use of narcotics, the nurse informs him to report which of the
following adverse effects to his healthcare provider?
1. The nurse understands that when Mr. Coidiuf was given
NSAIDs three years ago, the purpose was to: (Select all that 1. Diarrhea
apply.) 2. Hallucinations
3. Sedation
1. Reduce pain 4. Insomnia
2. Reduce inflammation
3. Acts within the CNS
4. Inhibit pain mediators at the nociceptors

C
“That needle burned, but
then I could only feel a little H
tug with the stitches.” A
Mr. Jeffery Wayland P
T
E
R
Drugs for Anesthesia

15
Core Concepts
15.1 Local anesthesia causes a rapid loss of sensation to a 15.5 General anesthetics are usually administered by the
limited part of the body. inhalation or IV routes.
15.2 Local anesthetics produce their therapeutic effect by 15.6 Intravenous anesthetics are important supplements
blocking the entry of sodium ions into neurons. to inhalant general anesthetics and include benzodi-
15.3 Local anesthetics are classified by their chemical azepines, opioids, and miscellaneous IV drugs.
structures. 15.7 Nonanesthetic drugs are used as adjuncts to anes-
15.4 General anesthesia is a loss of sensation occurring thesia before, during, and after surgery.
throughout the entire body, accompanied by a loss
of consciousness.
Drug Snapshot
Local Anesthetics Gases nitrous oxide 225
Esters Volatile liquids isoflurane (Forane) 225
Amides lidocaine (Xylocaine) 222 Intravenous anesthetics propofol (Diprivan) 227
Miscellaneous drugs Adjuncts to Anesthesia
General Anesthetics Neuromuscular blockers succinylcholine
Inhalation drugs (Anectine) 228
Learning Outcomes
1. Compare and contrast the five 4. Identify the actions of general 7. Categorize drugs used for anesthesia
major routes for administering local anesthetics within the central based on their classifications and
anesthetics. nervous system (CNS). actions in the body.
2. Describe differences between the 5. Compare and contrast the two 8. For each of the classes listed in the
two major chemical classes of local primary ways that general anesthesia Drug Snapshot, identify representative
anesthetics. may be induced. drugs and explain their mechanisms
3. Explain why epinephrine and sodium 6. Identify the four stages of general of drug action, primary actions, and
hydroxide are sometimes included as anesthesia. important adverse effects.
part of the local anesthetic medicine.
218 Chapter 15 Drugs for Anesthesia
Key Terms
amides (AM-ides) 220 esters (ES-turs) 220 local anesthesia 218
anesthesia (ANN-ess-THEE-zee-uh) 218 general anesthesia 218 neuromuscular blockers 227
an 5 without
esthesia 5 sensation
A nesthesia is a medical procedure performed by administering drugs that cause a loss of sensation.
Local anesthesia occurs when sensation is lost to a limited part of the body without loss of con-
sciousness. General anesthesia requires different classes of drugs that cause loss of sensation
to the entire body, usually resulting in a loss of consciousness. This chapter examines drugs used for both
local and general anesthesia, including select drugs used before and after surgical procedures.
Local Anesthesia
Local anesthesia causes a rapid loss of sensation to a limited part

core concept 15.1 of the body.
Local anesthesia is loss of sensation to a relatively small part of the body without loss of consciousness
to the patient. This technique may be necessary when a relatively brief dental or medical procedure is per-
formed. Although local anesthesia often causes a loss of sensation to a small, limited area, it sometimes
affects relatively large portions of the body, such as an entire limb. Because of this action, some local anes-
thetic treatments are more accurately called surface anesthesia or regional anesthesia, depending on how
the drugs are administered and the results they produce.
The five major routes (Figure 15.1 ■) for applying local anesthetics are the following:
■ Topical
■ Infiltration
■ Nerve block
■ Spinal
■ Epidural
The method used depends on the location and amount of anesthesia that is needed, as well as the
s pecific procedure being performed. For example, some local anesthetics are applied topically before a
needlestick or minor skin surgery. Others are used to block sensations to large areas such as limbs or the
lower abdomen. The different methods of local and regional anesthesia are summarized in Table 15.1 ◆.
Fast Facts Anesthesia and Anesthetics

■ The first medical applications of anesthetics involved ether (in 1842) and nitrous oxide (in 1846).
■ Over 20 million people receive anestshetics each year in the United States.
■ Most of the general public associate use of local anesthetic drugs with the practice of dentistry or
topical skin medications.
■ About half of the general anesthetics in medical practice are administered by a nurse anesthetist.
■ Herbal products may interact with anesthetics—for example, St. John’s wort may intensify or
prolong the effects of some opioids and anesthetics.
Concept Review 15.1

■ What is local anesthesia? Name the five general routes for local and regional anesthesia.
F i g u re 1 5 . 1
(a) Topical
(b) Infiltration
(c) Nerve block
(d) Spinal
Pia mater
Arachnoid mater
Dura mater (e) Epidural
Routes for applying local anesthesia include (a) topical, (b) infiltration, (c) nerve block, (d) spinal, and
(e) epidural.
Table 15.1 Methods of Local and Regional Anesthesia

Route Formulation/Method Description
Epidural anesthesia Injection into the epidural space (the Drug causes numbness, without paralysis, of the areas
area between the vertebrae and the below the injection site. A small catheter is often
spinal cord). placed into the epidural space to allow for multiple
injections.
Infiltration (field block) anesthesia Direct injection into tissue immediate Drug diffuses into tissue to block a specific group of nerves in a
to the surgical site. small area very close to the area to be operated on.
Nerve block anesthesia Direct injection into tissue that may be Drug affects the bundle of nerves serving the area to be
distant from the operation site. operated on; used to block sensation in a limb or large area
of the face.
Spinal anesthesia Injection into the cerebrospinal spinal Drug affects large, regional area such as the lower abdomen
fluid (CSF). and legs.
Topical (surface) anesthesia Creams, sprays, suppositories, drops, Applied to mucous membranes, including the eyes, lips,
and lozenges. gums, nasal membranes, and throat; very safe unless
absorbed.
Local anesthetics produce their therapeutic effect by blocking the entry of

Core Concept 15.2 sodium ions into neurons.
Local anesthetics are drugs that produce a rapid loss of sensation to a limited part of the body. The mecha-
nism of action of local anesthetics is well known. Recall that the concentration of sodium is normally
higher outside the neurons compared to the inside. A rapid influx of sodium ions into the cell is necessary
for neurons to fire.
Local anesthetics act by blocking sodium channels, as illustrated in Figure 15.2 ■. The blocking of
sodium channels is nonselective; therefore, both sensory and motor impulses are affected. Sensation and
muscle activity in the treated area will be decreased temporarily. Because of their mechanism of action, lo-
cal anesthetics are called sodium channel blockers.
During a medical or surgical procedure, it is essential for the anesthetic to last long enough to com-
plete the procedure. Small amounts of epinephrine are sometimes added to the anesthetic solution in order
to constrict blood vessels in the immediate area where the local anesthetic is applied. This keeps the drug
active at the injected site and extends its duration of action. The addition of epinephrine to lidocaine (Xylo-
caine), for example, increases the anesthetic effect from about 20 minutes to 60 minutes. This is important
for surgical and dental procedures that take longer than 20 minutes; otherwise, a second injection would be
necessary.
Sometimes an alkaline substance, such as sodium hydroxide or sodium bicarbonate, is added to anes-
thetic solutions to increase the drug’s effectiveness in areas with extensive local infection or abscesses. The
reason for this is that bacteria tend to acidify an infected site, and local anesthetics are less effective in an
acidic environment. Adding alkaline substances neutralizes the infected region and allows the anesthetic to
work better.
Core Concept 15.3 Local anesthetics are classified by their chemical structures.
The two major classes of local anesthetics are esters and amides (Table 15.2 ◆). The terms ester
and amide refer to types of chemical linkages found within the anesthetic molecules, as illustrated in
Figure 15.3 ■. A small number of miscellaneous drugs are neither esters nor amides.
F i g u re 1 5 . 2
(a) In normal nerve

conduction, sodium Na+
ions (Na+) enter the
sodium channels along
a neuron and allow the
neuron to fire (set off
an action potential) and
conduct an impulse.
(b) Local anesthetics
(represented by the Sodium
red x) block the sodium channel
channels. Sodium ions
are not able to enter (a)
the neuronal membrane
through the sodium
channels. Therefore, no
Na1
action potential can be
conducted along the
nerve.
Sodium
channel
blocker
(b)
Table 15.2 Selected Local Anesthetics

Drug Clinical Uses Remarks
Esters
benzocaine (Americaine, Anbesol, Solarcaine, Topical anesthesia For sunburn, sore throat, earache, hemorrhoids,
others) (see page 589 for the Drug Prototype and other minor skins conditions
box)
chloroprocaine (Nesacaine) Infiltration, nerve block, and epidural Short duration
anesthesia
procaine (Novocain) Infiltration, nerve block, epidural, and Short duration
spinal anesthesia
proparacaine (Alcaine, Ophthetic) To numb the eye before surgery, certain Short duration
tests, or procedures
tetracaine (Pontocaine) Topical and spinal anesthesia Longer duration
Amides
articaine (Septocaine, Zorcaine) Infiltration and nerve block anesthesia Longer duration
bupivicaine (Marcaine, Sensorcaine) Infiltration and epidural anesthesia Longer duration
dibucaine (Nupercainal) Topical or spinal anesthesia Longer duration
lidocaine (Anestacon, Dilocaine, Topical anesthesia, infiltration, nerve May be combined as a mixture of lidocaine
Xylocaine, others) block, epidural, and spinal anesthesia and prilocaine (EMLA cream) for topical
application
mepivacaine (Carbocaine, Isocaine, Polocaine) Infiltration, nerve block, and epidural Intermediate duration
anesthesia
prilocaine Infiltration, nerve block, and epidural Intermediate duration
anesthesia
ropivacaine (Naropin) Infiltration, nerve block, and epidural Longer duration
anesthesia
Miscellaneous Drugs
dyclonine (Dyclone) Topical anesthesia For ear, nose, and throat procedures
ethyl chloride or chloroethane Topical anesthesia For minor medical procedures
pramoxine (Tronothane) Topical anesthesia For minor medical procedures
F i g ur e 1 5 . 3
Type General formula Example The esters contain

a type of chemical
O O linkage that includes
C2H5 carbon and oxygen
Ester R C O R H2N C O C2H2 N (-CO-O-). The amides
C2H5 contain a type of
chemical linkage
Procaine
that includes carbon,
nitrogen, and oxygen
(-NH-CO-).
O CH3 O
C2H5
Amide R NH C R NH C CH2 N
C2H5
CH3
Lidocaine
Esters
Cocaine, the first local anesthetic widely used for medical procedures, was used as far back as the
1880s. Cocaine is a natural ester, found in the leaves of the plant Erythroxylon coca, native to the
Andes Mountains of Peru. As late as the 1980s, cocaine was routinely used for eye surgery, nerve
blocks, and spinal anesthesia. Although still available for local anesthesia, cocaine is a Schedule II
drug and rarely used therapeutically in the United States. The abuse potential of cocaine is discussed
in Chapter 7.
Another ester, procaine (Novocain), was the drug of choice for dental procedures from the mid-
1900s to the 1960s. About that time, amide anesthetics were developed, and use of the ester anesthet-
ics declined. One ester, benzocaine (Solarcaine and others), is used as a topical over-the-counter (OTC)
drug for treating a large number of painful conditions, including sunburn, insect bites, hemorrhoids, sore
throat, and minor wounds. Tetracaine is an ester that is often sprayed on the skin and mucous membranes
to cause loss of feeling before and during surgery or for endoscopic procedures. For example, a topical
anesthetic comprising benzocaine, butamben, and teratracaine (Cetacaine) is used in examinations of the
esophagus or colon. Proparacaine (Alcaine, Ophthetic) is a drug used for short-term anesthesia in ocular
procedures.
Amides
Amides have largely replaced the esters because they produce fewer adverse effects and generally have a
longer duration of action. Lidocaine (Xylocaine) is the most widely used amide for short surgical proce-
dures requiring local anesthesia. Ethyl chloride or cloroethane is a mild topical drug supplied as a liquid
in a spray bottle. It is used for basic procedures such as removing splinters or small debris from the skin’s
surface.
Adverse effects to local anesthesia are uncommon. Allergy is rare. When it does occur, it is often due
to sulfites, which are added as preservatives to prolong the shelf life of the anesthetic, or to methylparaben,
which may be added to prevent bacterial growth in anesthetic solutions. Early signs of adverse effects of
local anesthetics include symptoms of CNS stimulation such as restlessness or anxiety. Later, drowsiness
and unresponsiveness may occur due to CNS depression. Cardiovascular effects, including hypotension
and dysrhythmias, are possible. Patients with a history of cardiovascular disease are often given forms of
local anesthetics that contain no epinephrine to reduce the possible effects of this sympathomimetic on the
heart and blood pressure. CNS and cardiovascular adverse effects are rare unless the local anesthetic is
absorbed rapidly or is accidentally injected directly into a blood vessel.
Concept Review 15.2

■ How does a local anesthetic work? How does the anesthetic action of lidocaine with epi-
nephrine differ from that of lidocaine without epinephrine?
Drug Prototype: Lidocaine (Xylocaine)

Therapeutic Class: Anesthetic (local/regional/topical), antidysrhythmic (class IB)
Pharmacologic Class: Sodium channel blocker; amide
Actions and Uses: Lidocaine is the most frequently used in- Adverse Effects and Interactions: When used for anesthesia,
jectable local anesthetic. It is available in solutions ranging adverse effects are uncommon. An early symptom of toxicity is
from 0.5% to 2% for infiltration, nerve block, spinal, or epi- excitement, leading to irritability and confusion. Serious adverse
dural anesthesia. A topical form is also available. When given effects include convulsions, respiratory depression, and cardiac
for anesthesia, its onset of action is 5 to 15 minutes. Several arrest. Until the effect of the anesthetic diminishes, patients
hours may be needed for complete sensation to reappear. may injure themselves by biting or chewing areas of the mouth
Lidocaine is also given IV, IM, or subcutaneously to treat dys- that have no sensation following a dental procedure.
rhythmias, as discussed in Chapter 22. Solutions of lidocaine Barbiturates may decrease activity of lidocaine. Increased
containing preservatives or epinephrine are used for local effects of lidocaine occur if taken with cimetidine, quinidine,
anesthesia only and must never be given parenterally for and beta blockers. If lidocaine is used on a regular basis, its ef-
dysrhythmias. fectiveness may diminish when used with other medications.
Nursing Process Focus Patients Receiving Local Anesthesia

■ Obtain a complete health history including cardiovascular conditions, therapy
allergies (especially for amide-type drugs), drug history, and possible ■ Acute Pain related to administration of drug
drug interactions. ■ Risk for Injury related to lack of sensation to a part of the body
■ Check for the presence of broken skin, infections, burns and wounds caused by the anesthetic
where medication is to be applied.
■ Determine character, duration, location, and intensity of pain where
medication is to be applied.

The patient will:
■ Experience therapeutic effects (no pain during surgical procedure).
Implementation

■ Monitor for cardiovascular adverse effects. (These may occur if ■ Instruct the patient to report any unusual heart palpitations,
anesthetic is absorbed.) lightheadedness, drowsiness, or confusion. If using medication
on a regular basis, instruct the patient to see the healthcare
provider regularly.
■ Check skin or mucous membranes for infection or inflammation. ■ Instruct the patient to report any irritation or increase in discomfort
(Condition could be worsened by the drug.) in areas where medication was used to the healthcare provider.
■ Monitor for length of effectiveness. (Local anesthetics are effective ■ Instruct the patient to report any discomfort during the procedure.
for one to three hours.)
■ Obtain information on and monitor the use of other medications. ■ Instruct the patient to report use of any medications to the
■ Provide for patient safety. (There is a potential for injury related ■ Inform the patient about having no feeling in the anesthetized
to the fact that the area being treated lacks sensation.) area and taking extra caution to avoid injury, including heat-
related injury.
■ Monitor for gag reflex if used in the mouth or throat. (Xylocaine Instruct the patient to:
viscous may interfere with the swallowing reflex.) ■ Not eat within one hour of administration.
■ Not chew gum while any portion of the mouth or throat is
anesthetized to prevent biting injuries.

Cam therapy
Oil of Cloves for Dental Pain
One natural remedy for tooth pain is oil of cloves, a natural substance whose use dates
back thousands of years in Chinese medicine. Extracted from the clove plant Eugenia, eu-
genol is the active chemical that produces a numbing effect. It works especially well for
dental caries (cavities). The herb is applied by soaking a piece of cotton and packing it
around the gums close to the affected tooth. Dentists sometimes recommend it for tempo-
rary relief of a toothache. Clove oil has an antiseptic effect that has been reported to kill
microorganisms.
Other uses of clove oil that lack reliable scientific evidence include treatment
of premature ejaculation, low libido, and fever reduction. Clove oil is very safe, with
rash and gastrointestinal (GI) upset being the most common adverse effects. Clove oil
may increase the risk for bleeding and should be used cautiously in patients taking
anticoagulants.
General Anesthesia
General anesthesia is a loss of sensation occurring throughout the entire

Core Concept 15.4 body, accompanied by a loss of consciousness.
General anesthesia involves loss of sensation to the entire body. General anesthetics are used when it is
necessary for patients to remain still and without pain for a period longer than could be achieved with local
anesthetics. The goal of general anesthesia is to provide a rapid and complete loss of sensation. Signs of
general anesthesia include total analgesia (no feeling of pain) and loss of consciousness, memory, and
body movement. Although these signs are similar to those of sleeping, general anesthesia and sleep are not
exactly the same. General anesthetics depress most nervous activity in the brain, whereas sleeping stops
activity in only very specific areas. In fact, some brain activity actually increases during sleep, as described
in Chapter 9.
General anesthesia is rarely achieved with a single drug. Instead, multiple medications are used to
rapidly induce unconsciousness, cause muscle relaxation, and maintain deep anesthesia. This approach,
called balanced anesthesia, allows the dose of inhalation anesthetic to be lower so that the procedure is
safer for the patient.
General anesthesia is a progressive process that occurs in distinct steps, or stages. The most effective
medications can quickly cause all four stages, whereas others are only able to cause stage 1 (light seda-
tion). Most major surgery occurs in stage 3, where the patient is completely relaxed and sedated. Thus,
stage 3 anesthesia is called surgical anesthesia. When seeking surgical anesthesia, the anesthesiologist
will try to move quickly through stage 2 because this stage produces distressing symptoms. Often an
IV drug will be given to calm the patient during this stage. The stages of general anesthesia are listed in
Table 15.3 ◆.
There are two primary methods of causing general anesthesia. Intravenous drugs are usually admin-
istered first because they act within a few seconds. After the patient loses consciousness, inhaled drugs are
used to maintain the anesthesia. During short surgical procedures or those requiring lower stages of anes-
thesia, the IV drugs may be used alone.
General anesthetics are usually administered by the inhalation

Core Concept 15.5 or IV routes.
General anesthetics are drugs that rapidly produce unconsciousness and total analgesia. To supplement a
general anesthetic, adjunctive drugs are given before, during, and after surgery. Inhaled general anesthet-
ics, listed in Table 15.4 ◆, are gases or volatile liquids. These drugs produce their effects by preventing the
flow of sodium into neurons in the CNS, thus delaying nerve impulses and producing a dramatic reduction
in neural activity. The exact mechanism for how this occurs is not known, although it is likely that gamma-
aminobutyric acid (GABA) receptors in the brain are activated. It is not the same mechanism as is known
for local anesthetics. There is some inconclusive evidence suggesting that the mechanism may be related to
that of some antiseizure drugs. There is no specific receptor that binds to general anesthetics, and they do
not seem to affect neurotransmitter release.
Table 15.3 Stages of General Anesthesia

Stage 1 Loss of pain; the patient loses general sensation but may be awake. This stage proceeds until
the patient loses consciousness.
Stage 2 Excitement and hyperactivity; the patient may be delirious and try to resist treatment.
Heartbeat and breathing may become irregular, and blood pressure can increase. IV drugs
are administered here to calm the patient.
Stage 3 Surgical anesthesia; skeletal muscles become paralyzed. Cardiovascular and breathing
activities stabilize. Eye movements slow down and the patient becomes still.
Stage 4 Paralysis of the medulla region in the brain (responsible for controlling respiratory and
cardiovascular activity). If breathing or the heart stops, death could result. This stage is
usually avoided during general anesthesia.
Table 15.4 Inhaled General Anesthetics

Drug Clinical Uses
GASES
nitrous oxide Used alone in dentistry, obstetrics, and short medical procedures; used in combination with more potent
inhaled anesthetics
Volatile Liquids
desflurane (Suprane) Induction and maintenance of general anesthesia
enflurane (Ethrane) Induction and maintenance of general anesthesia
isoflurane (Forane) Induction and maintenance of general anesthesia; most widely used inhalation anesthetic
sevoflurane (Ultane) Induction and maintenance of general anesthesia
Drug Prototype: Nitrous Oxide

Therapeutic Class: General anesthetic Pharmacologic Class: Inhalation gaseous drug
Actions and Uses: The main action of nitrous oxide is analgesia doses, patients exhibit some adverse signs of stage 2 anesthe-
caused by suppression of pain mechanisms in the CNS. This drug has sia, such as anxiety, excitement, and combativeness. Lowering
a low potency and does not produce complete loss of conscious- the inhaled dose will quickly reverse these adverse effects. As
ness or extreme relaxation of skeletal muscle. Because nitrous oxide nitrous oxide is exhaled the patient may temporarily have some
does not cause surgical anesthesia (stage 3), it is commonly com- difficulty breathing at the end of a procedure. Nausea and vom-
bined with other surgical anesthetic drugs. Nitrous oxide is ideal for iting following the procedure are more common with nitrous
dental procedures because the patient remains conscious and can oxide than with other inhalation anesthetics. Nitrous oxide
follow instruction while experiencing full analgesia. has the potential to be abused by users (sometimes medical
personnel) who enjoy the relaxed, sedated state that the drug
Adverse Effects and Interactions: When used in low to moder- produces.
ate doses, nitrous oxide produces few adverse effects. At higher
Drug Prototype: Isoflurane (Forane)

Therapeutic Class: General anesthetic Pharmacologic Class: Inhalation volatile liquid; GABA and glutamate
receptor agonist
Actions and Uses: Isoflurane produces a potent level of surgi- intracranial pressure. Older adult patients are more susceptible
cal anesthesia that is rapid in onset. It provides the patient to hypotension caused by the drug.
with smooth induction with a low degree of metabolism by the When isoflurane is used concurrently with nitrous oxide,
body. This drug provides excellent muscle relaxation and may coughing, breath holding, and laryngospasms may occur. If
be used off-label as adjuvant therapy in the treatment of status isoflurane is administered with systemic polymyxin and amino-
asthmaticus. Isoflurane with oxygen or with an oxygen/nitrous glycosides, skeletal muscle weakness, respiratory depression, or
oxide mixture may be used. Compared to other inhaled general apnea may occur. Additive effects may occur with isoflurane
anesthetics, cardiac output is well maintained. if administered with other skeletal muscle relaxants. Additive
hypotension may result if used concurrently with antihyper-
Adverse Effects and Interactions: Mild nausea, vomiting, and tensive medications such as beta blockers. Epinephrine, norepi-
tremor are common adverse effects. The drug produces a dose- nephrine, dopamine, and other adrenergic agonists should be
dependent respiratory depression and a reduction in blood administered with caution due to the possibility of dysrhythmias.
pressure. Malignant hyperthermia with elevated temperature Other drugs may cause dysrhythmias including amiodarone,
has been reported. Patients with a known history of genetic ibutilide, droperidol, and phenothiazines. Levodopa should be
predisposition to malignant hyperthermia should not use iso- discontinued six to eight hours before isoflurane administration.
flurane. Caution should be used when treating patients with St. John’s wort should be discontinued two to three weeks prior
head trauma or brain neoplasms due to possible increases in to administration due to the possible risk of hypotension.
Gases
The only gas used routinely for anesthesia is nitrous oxide, commonly called laughing gas. Nitrous
oxide is used for brief obstetrical and surgical procedures and dental procedures. It may also be used
in conjunction with other general anesthetics, making it possible to decrease their doses with greater
effectiveness.
Nitrous oxide should be used cautiously in patients with myasthenia gravis because it may cause re-
spiratory depression and prolonged hypnotic effects. Patients with cardiovascular disease, especially those
with increased intracranial pressure, should be monitored carefully because the hypnotic effects of the drug
may be prolonged or potentiated.
Volatile Liquids
The volatile anesthetics are liquid at room temperature but are converted into a vapor and inhaled to pro-
duce their anesthetic effects. Volatile drugs include desflurane (Suprane), enflurane (Ethrane), isoflurane
(Forane), and sevoflurane (Ultane). Some general anesthetics increase the sensitivity of the heart to drugs
such as epinephrine, norepinephrine, dopamine, and serotonin. Most volatile liquids depress cardiovascular
and respiratory function. Because isoflurane (Forane) has less effect on the heart and does not damage the
liver, it has become the most widely used inhalation anesthetic. The volatile liquids are excreted almost
entirely by the lungs through exhalation.
Intravenous anesthetics are important supplements to inhalant general

anesthetics and include benzodiazepines, opioids, and miscellaneous IV
Core Concept 15.6 drugs.
Intravenous Anesthetics
Intravenous anesthetics may be used alone, for short procedures, or in combination with inhalation
anesthetics. IV general anesthetics, listed in Table 15.5 ◆ are important supplements to general anesthe-
sia. Although occasionally used alone, they are more often administered with inhaled general anesthetics.
Table 15.5 Intravenous Anesthetics

Drug Remarks
Benzodiazepines
diazepam (Valium) (see page 188 for the Drug For induction of anesthesia; prototype drug for the benzodiazepines
Prototype box)
lorazepam (Ativan) (see page 116 for the Drug For induction of anesthesia and to produce conscious sedation; for short medical
Prototype box) procedures or surgery
midazolam (Versed) For induction of anesthesia and to produce conscious sedation; for short diagnostic
procedures
Opioids
alfentanil (Alfenta) Rapid onset and short duration of action; for induction of anesthesia; used as a
supplement to other anesthetic drugs
fentanyl (Sublimaze, others) Short-acting analgesic used during the operative and perioperative period; used to
supplement both general and regional anesthesia
remifentanil (Ultiva) Approximately seven times more potent than fentanyl; onset and duration of action more
rapid than fentanyl; for induction and maintenance of anesthesia
sufentanil (Sufenta) Approximately seven times more potent than fentanyl; onset and duration of action more
rapid than fentanyl; for induction and maintenance of anesthesia
miscellaneous IV drugs
etomidate (Amidate) For induction of anesthesia; for short medical procedures
fospropofol (Lusedra) For induction and maintenance of general anesthesia; for short medical procedures
ketamine (Ketalar) For sedation, amnesia, and analgesia; for short diagnostic, therapeutic, or surgical
procedures; most often used in children
propofol (Diprivan) For induction and maintenance of general anesthesia; for short medical procedures
Drug Prototype: Propofol (Diprivan)

Therapeutic Class: General anesthetic Pharmacologic Class: Intravenous induction drug; N-methy-D-aspartate
(NMDA) receptor agonist
Actions and Uses: Propofol is indicated for the induction and egg products. Diprivan injectable emulsion is not recom-
maintenance of general anesthesia. It has almost an immediate mended for obstetrics, including cesarean section
onset of action and is used effectively for conscious sedation. deliveries, or for use in nursing mothers. The drug should
Emergence is rapid and few adverse effects occur during recov- be used with caution in patients with cardiac or respiratory
ery. Propofol has an antiemetic effect that can prevent nausea impairment.
and vomiting. The dose of propofol should be reduced in patients
receiving preanesthetic medications such as benzodiazepines
Adverse Effects and Interactions: Propofol is contraindicated or opioids. Use with other CNS depressants can cause additive
in patients who have a known hypersensitivity reaction to CNS and respiratory depression.
the medication or its emulsion, which contains soybean and
Concurrent administration of IV and inhaled anesthetics together allows the dose of the inhaled drug to anti 5 against
be reduced, thus lessening the potential for serious adverse effects. Furthermore, when IV and inhaled emetic 5 vomiting
anesthetics are combined, they provide greater analgesia and muscle relaxation than could be provided by
the inhaled anesthetic alone. When IV anesthetics are administered alone, they are generally reserved for
medical procedures that take less than 15 minutes.
Drugs employed as IV anesthetics include benzodiazepines, opioids, and miscellaneous drugs. Opi-
oids offer the advantage of superior analgesia. Combining the opioid fentanyl (Sublimaze) with the anti-
psychotic drug droperidol (Inapsine) produces a state known as neuroleptanalgesia. In this state, patients
are conscious but insensitive to pain and unaware of their surroundings. The premixed combination of
these two drugs is marketed as Innovar. A similar conscious, dissociated (i.e., unaware) state is produced
with the amnestic, ketamine (Ketalar). amnestic 5 loss of memory
Concept Review 15.3

■ What is the role of IV anesthetics in surgical anesthesia? Why are these drugs not used
alone for general anesthesia?
Adjuncts to Anesthesia
Nonanesthetic drugs are used as adjuncts to anesthesia before, during,

and after surgery. Core Concept 15.7
A number of drugs are used either to complement the effects of general anesthetics or to treat anticipated
adverse effects of the anesthesia. These drugs, shown in Table 15.6 ◆, are called adjuncts to anesthesia.
They may be given prior to, during, or after surgery.
Preoperative drugs are given to relieve anxiety and to provide mild sedation. Opioids, such as mor- pre = before
phine, may be given to reduce the amount of general anesthetic required or to reduce any pain that the operative = surgery
patient will experience at the onset of surgery. Anticholinergics such as atropine may be administered to
dry secretions and to suppress the bradycardia caused by some anesthetics. Sedative–hypnotic drugs help sedative 5 drowsy
reduce fear, anxiety, or pain associated with the surgery. hypnotic 5 sleep
During surgery, the primary adjuncts are the neuromuscular blockers (see Chapter 12). Neuromus- neuro 5 nerve
cular blockers cause paralysis without loss of consciousness, which means that without a general anes- muscular 5 muscle
thetic, patients would be awake and without the ability to move. It is important to note that breathing
muscles are skeletal muscle. This is why patients require intubation and mechanical ventilation. Adminis-
tration of these drugs also allows a reduced amount of general anesthetic.
Table 15.6 Selected Adjuncts to Anesthesia

Drug Remarks
Anticholinergic
atropine Used in general anesthesia as a premedication, in emergency situations, or during surgery
to increase heart rate and to reverse the effects of some cholinergic drugs
Benzodiazepine
midazolam (Versed) Generally used before other intravenous agents for induction of anesthesia
Cholinergic Drug
bethanechol (Urecholine) (see page 93 For relief of constipation and urinary retention caused by opioids; stimulates GI motility
Dopamine Blocker
droperidol (Inapsine) For nausea and vomiting caused by opioids; reduces anxiety and relaxes muscles
Neuromuscular Blockers
mivacurium (Mivacron) Short duration; nondepolarizing type
succinylcholine (Anectine) Short duration; depolarizing type
tubocurarine Long duration; nondepolarizing type
Opioids
alfentanil (Alfenta) Short duration; for induction of anesthesia when endotracheal or mechanical ventilation is needed;
provides analgesia
fentanyl (Sublimaze, others) For analgesia during or after anesthesia; the combination of fentanyl and droperidol is called Innovar
morphine (see page 203 for the Drug For analgesia during or after anesthesia
Prototype box)
remifentanil (Ultiva) For analgesia during or after anesthesia; shorter duration of action than fentanyl
sufentanil (Sufenta) For primary anesthesia or to provide analgesia during or after anesthesia
Phenothiazine
promethazine (Phenergan) For nausea and vomiting associated with obstetric sedation and opioids
Drug Prototype: Succinylcholine (Anectine)

Therapeutic Class: Skeletal muscle paralytic, neuromuscular blocker
Pharmacologic Class: Depolarizing blocker, acetylcholine receptor blocking drug
Actions and Uses: Like the natural neurotransmitter acetylcholine, Increased effect of succinylcholine may occur if given with
succinylcholine acts on cholinergic receptor sites at neuromuscu- phenothiazines oxytocin, promazine; tacrine, or thiazide diuretics.
lar junctions. At first, depolarization occurs, and skeletal muscles Decreased effect of succinylcholine occurs if given with diazepam.
contract. After repeated contractions, however, the membrane If this drug is given with nitrous oxide, an increased risk of
is unable to repolarize as long as the drug stays on the receptor. bradycardia, dysrhythmias, sinus arrest, apnea, and malignant
Effects are first noted as muscle weakness and muscle spasms. Even- hyperthermia exists. If succinylcholine is given with cardiac
tually paralysis occurs. Succinylcholine is rapidly broken down by glycosides, there is increased risk of cardiac dysrhythmias. If nar-
the enzyme pseudocholinesterase; when the IV infusion is stopped, cotics are given with succinylcholine, there is increased risk of
the duration of action is only a few minutes. Use of succinylcholine bradycardia and sinus arrest.
reduces the amount of general anesthetic needed for procedures.
Adverse Effects and Interactions: Succinylcholine can cause Black Box Warning:
complete paralysis of the diaphragm and intercostal muscles; Succinylcholine should be administered in a facility with
thus, mechanical ventilation is necessary during surgery. Brady- trained personnel to monitor, assist, and control respiration.
cardia and respiratory depression are expected adverse effects. Cardiac arrest has been reported resulting from hyperkalemia
If doses are high, tachycardia, hypotension, and urinary reten- (elevated potassium blood level) rhabdomyolysis most fre-
tion may occur. Patients with certain genetic defects may experi- quently in infants or children with undiagnosed skeletal mus-
ence rapid onset of extremely high fever with muscle rigidity—a cle myopathy, or Duchenne muscular dystrophy. In children,
serious condition known as malignant hyperthermia. use of this drug is reserved for cases of emergency intubation
Additive skeletal muscle blockade will occur if succinylcho- (process of inserting an endotracheal tube for breathing) or
line is given concurrently with clindamycin, aminoglycosides, when immediate securing of the airway is necessary.
furosemide, lithium, quinidine, or lidocaine.
Chapter Review 229
Neuromuscular blocking agents are classified as depolarizing blockers and nondepolarizing block-
ers. The only depolarizing blocker is succinylcholine (Anectine), which works by binding to acetylcho-
line receptors at neuromuscular junctions to cause total skeletal muscle paralysis. Succinylcholine is junction 5 connection
used in surgery for ease of tracheal intubation. Mivacurium (Mivacron) is the shortest acting of the
nondepolarizing blockers, whereas tubocurarine is a longer-acting neuromuscular blocker. The nonde-
polarizing blockers cause muscle paralysis by competing with acetylcholine for cholinergic receptors
at neuromuscular junctions. Once attached to the receptor, the nonpolarizing blockers prevent muscle
contraction.
Postoperative drugs include analgesics for pain and antiemetics, such as ondansetron (Zofran, Zu- post 5 after
plenz) for the nausea and vomiting that sometimes occur during recovery from the anesthetic. Occasion-
ally, following surgery, a parasympathomimetic, such as bethanechol (Urecholine) is administered to
stimulate the urinary tract and the smooth muscle of the bowel (see Chapter 8).

Patients treated with local anesthetic medications need to know the following:
1. When using topical anesthetics for skin conditions, avoid touching the eyes.
2. Never apply topical medications to large patches of skin or to areas where there is an
open lesion or cut unless instructed to do so by the healthcare provider.
3. Notify the dentist or healthcare providers of any previous adverse reactions to local anes-
thesia before being given additional anesthetic medications.
4. After receiving local anesthetic solutions for the mouth, do not consume food and drink
until it is clear that the anesthetic has worn off.
5. While the area is still numb, do not chew or pick at an area where a dental procedure
has been performed.
6. Be careful not to inhale anesthetic sprays used for topical application.
7. Get immediate assistance if drowsiness, confusion, or blurred vision has occurred after
receiving a local anesthetic. Other signs/symptoms to look for include lightheadedness,
an irregular heartbeat, or feeling faint.
8. Report all medications and conditions to the healthcare provider before receiving
anesthetics.
9. For outpatient dental or medical procedures involving anesthesia, someone should be
available to assist with activities such as transportation.
10. Follow postprocedure instructions carefully after anesthesia.
11. Have sufficient pain medication readily available so that postprocedure pain can be
managed after the effects of the anesthesia are no longer felt.
Chapter Review
15.1 Local anesthesia causes a rapid loss of sensation to nerve. Epinephrine is sometimes added to anes-
a limited part of the body. thetic solutions to increase the duration of action
Local anesthesia is loss of sensation to a relatively small of the anesthetic. A base such as sodium hydrox-
part of the body without causing loss of consciousness. ide is added to make an infected tissue environ-
Sometimes local anesthesia is applied to an entire limb. ment more alkaline.
In these cases, it is more accurately called surface an-
15.3 Local anesthetics are classified by their chemical
esthesia or regional anesthesia, depending on how the
structures.
drugs are administered and the results they produce.
The two major classes of local anesthetics are esters
15.2 Local anesthetics produce their therapeutic effect and amides. Benzocaine (Solarcaine, others) is the
by blocking the entry of sodium ions into neurons. most commonly used ester; lidocaine (Xylocaine) is
Blocking sodium entry into neurons prevents the most widely prescribed amide.
transmission of the electrical impulse along the
15.4 General anesthesia is a loss of sensation occurring benzodiazepines, opioids, and miscellaneous IV
throughout the entire body, accompanied by a drugs.
loss of consciousness. Intravenous drugs may be used along with inhaled
General anesthesia proceeds in stages from light se- anesthetics to lower the potential for serious adverse
dation to total loss of consciousness. The less potent effects. Benzodiazepines, opioids, and other select
anesthetics cause stage 1 anesthesia, whereas more IV drugs are generally reserved for quick medi-
potent drugs cause surgical anesthesia (stage 3). cal procedures and treatments requiring superior
analgesia.
15.5 General anesthetics are usually administered by
the inhalation or IV routes. 15.7 Nonanesthetic drugs are used as adjuncts to anes-
thesia before, during, and after surgery.
Two primary methods for producing rapid uncon-
sciousness and total analgesia are IV drugs and in- A number of drugs are given prior to surgery to re-
haled general anesthetics. Inhalation drugs include lieve anxiety, provide mild sedation, counteract pain,
nitrous oxide, the only gaseous drug, and volatile and dry secretions. Neuromuscular blockers, given
liquids. Many drugs may be used alone or in com- during surgery, relax skeletal muscle and maintain a
bination with other drugs. The mechanism by which proper heart rate. Drugs after surgery include treat-
general anesthetics produce their effect is not com- ment for pain and vomiting and for stimulating the
pletely known. bowel and urinary tract.
15.6 Intravenous anesthetics are important supple-

ments to inhalant general anesthetics and include
Review Questions
The following questions are written in NCLEX-PN® style. Answer 4. “An anesthetic cream will be applied to the skin in the
these questions to assess your knowledge of the chapter material, areas causing your pain. This cream will numb those
and go back and review any material that is not clear to you. areas.”
1. The nurse informs the patient that which of the follow- 4. Before administering propofol, the nurse checks a pa-
ing herbal products may prolong or intensify the effects of tient’s record for allergies. After reviewing the records and
anesthesia? talking to the patient, the nurse notifies the healthcare pro-
1. Kava kava vider and the order is discontinued because the patient is al-
2. Oil of cloves lergic to:
3. Anise 1. Peanuts
4. St. John’s wort 2. Shellfish
3. Egg products
2. While administering lidocaine, the nurse monitors for 4. Milk
toxicity, which is manifested by: (Select all that apply.)
1. Excitement 5. A patient is to receive nitrous oxide during surgery. The
2. Irritability nurse understands that he or she will need to monitor the pa-
3. Tachypnea tient for which adverse effect?
4. Confusion 1. Restlessness
2. Dysrhythmia
3. A patient in labor is advised that she can have epidural 3. Hypertension
anesthesia to help relieve her pain. When she asks the nurse 4. Mania
what will happen, the nurse tells her:
1. “An anesthetic drug will be injected directly into the area 6. The patient being prepared for surgery asks the nurse why
where the pain is occurring, affecting the nerves and block- he or she is receiving morphine and atropine prior to surgery.
ing any sensations.” The nurse’s best response is:
2. “A small tube (catheter) will be placed in the space be- 1. “You will need to speak with your healthcare provider.”
tween the vertebrae and the spinal cord and an anesthetic 2. “The morphine will help to provide some pain relief
drug will be injected through the tube. The medication will before surgery and the atropine will help to decrease
cause numbness in the areas below the injection site, but secretions.”
you will still be able to move your legs.” 3. “The morphine and atropine will help your anesthetic work
3. “You will receive an injection of an anesthetic drug in your more effectively.”
back, directly into the cerebrospinal spinal fluid, which 4. “These medications are routinely used before we send a pa-
will numb the lower half of your body.” tient to surgery.”
Chapter Review 231
7. In reviewing a patient’s preoperative paperwork, the nurse 9. The anesthesiologist orders atropine, 1 mg IM for a pa-
notes that the patient has a history of cardiovascular disease tient in the recovery room. Available is 0.8 mg/mL. How many
and therefore should not receive epinephrine along with the milliliters will be given?
anesthetics because it can cause: 1. 1 mL
1. Tachycardia and hypertension 2. 1.15 mL
2. Bradycardia and hypotension 3. 1.2 mL
3. Tachycardia and hypotension 4. 1.25 mL
4. Bradycardia and hypertension
10. The patient is experiencing nausea in the recovery room.
8. The nurse explains to the patient that he or she will re- The nurse anticipates which medication being ordered?
ceive both isoflurane (Forane) and nitrous oxide: 1. Meperidine
1. To provide the additional anesthesia to put him or her in a 2. Bethanechol
sleeplike state 3. Ondansetron
2. To increase effectiveness of anesthesia with lower dosages 4. Succinylcholine
of each drug
3. Because isoflurane is not effective when used alone
4. Because nitrous oxide should not be used alone
Remember Mr. Wayland, the patient 2. The nurse understands that the addition of epinephrine to
introduced at the beginning of the the lidocaine is to:
chapter? Now read the remainder of 1. Prevent infection
the case study. Based on the informa- 2. Prevent an allergic reaction
tion you have learned in this chapter, 3. Increase the duration of the anesthetic
answer the questions that follow. 4. Decrease pain after the procedure
Mr. Jeffery Wayland, age 38, has a history of cardiovascu-
lar disease. He has collapsed and sustained an injury to his 3. Soon after administering the lidocaine, the nurse monitors
scalp. The wound is substantial, and Mr. Wayland is bleeding Mr. Wayland for:
across his right forehead. The patient is rushed to the emer- 1. Constriction of airways
gency department by his girlfriend. The girlfriend reports that 2. Anxiety
Mr. Wayland is normally very fearful of doctors and nurses. 3. Tachycardia
It is unclear why Mr. Wayland collapsed. The doctor wants to 4. Unresponsiveness
inject the tissue surrounding the wound with 1% lidocaine with
epinephrine for local anesthesia prior to suturing the lacera- 4. As the nurse, would it be advisable to give Mr. Wayland
tion and asks the nurse to prepare the medication. a barbiturate to help him calm down due to his fear of doctors
and nurses in this case?
1. Because he is anxious, Mr. Wayland asks the nurse, “Is 1. No, a barbiturate might increase toxicity symptoms if
the doctor going to numb the area before he begins to put Mr. Wayland is allergic to lidocaine.
stitches in my head?” The nurse replies: 2. Yes, a barbiturate might increase the effectiveness of
1. “Yes, the doctor will apply a topical (surface) anesthetic lidocaine in this situation and help the patient calm
medication to numb the area.” down.
2. “Yes, the doctor will inject an anesthetic medication d irectly 3. No, a barbiturate might decrease the effectiveness of
around the area, or field, of the wound to help prevent pain.” lidocaine in this situation and make the patient more
3. “Yes, the doctor will inject an anesthetic medication that irritable.
will block a bundle of nerve endings.” 4. No, a barbiturate might decrease the effectiveness of
4. “Yes, the doctor will provide an anesthetic drug by inject- lidocaine in this situation, although the medication would
ing it into your epidural space.” normally have a calming effect.

U N I T
3
The Cardiovascular
and Urinary Systems
Unit Contents
Chapter 16 Drugs for Lipid Disorders / 234
Chapter 17 Diuretics and Drugs for Electrolyte and Acid–Base Disorders / 248
Chapter 18 Drugs for Hypertension / 265
Chapter 19 Drugs for Heart Failure / 287
Chapter 20 Drugs for Angina Pectoris, Myocardial Infarction, and Stroke / 301
Chapter 21 Drugs for Shock and Anaphylaxis / 319
Chapter 22 Drugs for Dysrhythmias / 331
Chapter 23 Drugs for Coagulation Disorders / 346

C
“I’ve lived too long to
h change my eating habits
a now. I’ve had bad blood tests
p for years and nothing has
happened to me. Besides,
t I’m too busy to deal with one
e more problem in my life.”
r Mr. Edward Long
16 Drugs for Lipid Disorders
Core Concepts
16.1 Lipids serve essential roles in the body, but too 16.5 Bile acid binding drugs can reduce LDL levels by
much dietary fat can lead to disease. increasing cholesterol excretion.
16.2 Lipoproteins transport lipids through the blood 16.6 Niacin can reduce triglyceride and LDL-cholesterol
for utilization by tissues, storage in adipose levels.
tissue, or excretion by the liver. 16.7 Fibric acid drugs lower triglyceride levels, but have
16.3 Elevated lipid levels can often be prevented or little effect on LDLs.
controlled through therapeutic lifestyle changes. 16.8 Other approaches to treating hyperlipidemia include
16.4 Statins are preferred drugs for reducing blood ezetimibe, omega-3 fatty acids, and fixed-dose
lipid levels. combination therapy.
Drug Snapshot
HMG-CoA reductase atorvastatin (Lipitor) 240
inhibitors (statins)
Bile acid binding drugs cholestyramine (Questran) 240
Fibric acid drugs gemfibrozil (Lopid) 244

(fibrates)
Learning Outcomes
1. Summarize the links among high 4. Compare and contrast the different 7. For each of the classes in the Drug
blood cholesterol, low-density types of lipoproteins. Snapshot, identify representative
lipoprotein (LDL) levels, and 5. Give examples of how blood lipid drugs and explain their mechanisms
cardiovascular disease. levels can be controlled through of drug action, primary actions, and
2. Compare and contrast the different nonpharmacologic means. important adverse effects.
types of lipids. 6. Categorize antihyperlipidemic drugs
3. Describe how lipids are transported based on their classifications and
through the body. mechanisms of action.
Key Terms
atherosclerosis (ath-ur-oh-skler- hypercholesterolemia (HEYE-purr- lipoproteins (LIP-oh-PROH-teen) 236
OH-sis) 235 koh-LESS-tur-ol-EEM-ee-uh) 235 low-density lipoprotein (LDL) 236
bile acids (BEYE-ulz) 241 hyperlipidemia (HEYE-purr-LIP-i- plaque (PLAK) 235
dyslipidemia (dys-lip-i-DEEM-ee-uh) 235 DEEM-ee-uh) 235 therapeutic lifestyle changes 236
high-density lipoprotein (HDL) 236 hypertriglyceridemia (HEYE-purr-tri-gliss- triglycerides (tri-GLISS-ur-ide) 235
ur-i-DEEM-ee-uh) 235
HMG-CoA reductase (ree-DUCK-tase) 238 very low-density lipoprotein (VLDL) 236
R esearch has brought about a nutritional revolution as new knowledge about lipids and their relation-
ship to obesity and cardiovascular disease has allowed people to make more intelligent lifestyle
choices. Advances in the diagnosis of lipid disorders have helped to identify those patients at great-
est risk for cardiovascular disease, and those most likely to benefit from pharmacologic intervention. Safe,
effective drugs for lowering lipid levels are now available that decrease the risk of cardiovascular diseases.
As a result of this knowledge and from advancements in pharmacology, the incidence of death due to car-
diovascular disease has been declining, although it is still the leading cause of death in the United States.
Lipids serve essential roles in the body, but too much dietary
fat can lead to disease. Core Concept 16.1
Lipids, or fats, are organic compounds that are essential for good health. Lipid tissue provides cushioning
and protection of organs and insulates the body to maintain core temperature. Phospholipid is the major
component of all cell membranes in the body.
The most common lipids, the triglycerides, are the major storage form of fat in the body and the only
type of lipid that serves as an important energy source. They account for 90% of the total lipids in the body.
Cholesterol is a lipid that is a major component of cell membranes and which serves as a building
block for other lipid-based biochemicals such as vitamin D, bile salts, cortisol, estrogen, and testoster-
one. Its negative role in promoting atherosclerosis or plaque on the walls of arteries is well known. Fatty athero 5 fatty
plaque deposits narrow arteries, thereby contributing to angina, myocardial infarction (MI), and stroke, as sclera 5 hard
discussed in Chapter 20. Because the body needs only small amounts of cholesterol daily, it is not neces- osis 5 condition of
sary to ingest excess amounts of cholesterol in the diet. Dietary cholesterol is obtained solely from animal
food products; humans do not absorb the sterols produced by plants.
Research is still uncovering the important roles of lipids in the diet. While it is clear that too much of
certain types of dietary fat are associated with disease, some types actually promote wellness. For example,
evidence is strong that intake of saturated fats and trans fats should be limited because they are associated
with obesity, cardiovascular disease, and possibly cancer. However, omega-3 fatty acids, which are found
in abundance in deep, cold-water fish such as salmon, tuna, and herring, may have health benefits. The
richest plant source of omega-3 fatty acids is flaxseed, which has become a popular dietary supplement.
Several terms are used to describe lipid disorders. Dyslipidemia is a general term meaning an ab-
normal amount of lipid in the blood. Hyperlipidemia is a similar term that refers to high levels of lipids hyper 5 above
in the blood. Some patients have only one specific type of lipid that is elevated. Elevated blood choles- lipid 5 fat
terol, or hypercholesterolemia, is the type of dyslipidemia that is most familiar to the general public. emia 5 blood
Hypertriglyceridemia, elevated triglycerides, is a less common disorder.
Fast Facts High Blood Cholesterol

■ Thirty million Americans (15% of U.S. adults) are believed to have both hypertension and high
blood cholesterol levels.
■ The incidence of high blood cholesterol increases until age 65.
■ Moderate alcohol intake does not reduce LDL cholesterol, but it does increase high-density
lipoprotein (HDL, or good) cholesterol.
■ High blood cholesterol occurs more frequently in men than in premenopausal women, but after
age 50, the disease is more common in women.
■ To lower blood cholesterol, dietary intake of both cholesterol and saturated fats must be reduced.
■ Familial hypercholesterolemia affects 1 in 500 people and is a genetic disease that predisposes
people to high cholesterol levels.
236 Chapter 16 Drugs for Lipid Disorders
Lipoproteins transport lipids through the blood for utilization

Core Concept 16.2 by tissues, storage in adipose tissue, or excretion by the liver.
Knowledge of cholesterol metabolism is important to understanding cardiovascular disease and the phar-
macotherapy of lipid disorders. In simplest terms, the greater the amount of cholesterol circulating in the
blood, the greater the risk of cardiovascular disease. This is because the circulating cholesterol binds to
vessel walls, increasing plaque buildup as years pass.
Because they are not soluble in the blood, cholesterol and other lipids are packaged as lipoprotein
complexes by the liver. Lipoproteins contain an inner core of lipid surrounded by an outer shell of carrier
protein, which makes them water soluble and able to be transported freely through the blood. The three most
common lipoproteins are named based on their weight or density, which comes primarily from the amount
of protein present in the complex. Figure 16.1 ■ illustrates the three basic lipoproteins and their composi-
tion. Each type of lipoprotein serves a different function in transporting lipids to their final destination.
Although cholesterol is packaged in all lipoproteins, low-density lipoprotein (LDL) has the great-
est amount: Almost 50% of LDL consists of cholesterol. The liver makes LDL, which is then transported
to tissues and organs, where it is used to build plasma membranes or to synthesize other steroids. Once
in the tissues, cholesterol can also be stored for later use. Storage of cholesterol in the lining of blood
vessels, however, contributes to plaque buildup and atherosclerosis. LDL is often called “bad” choles-
terol because this lipoprotein contributes significantly to plaque deposits and coronary artery disease.
Under normal circumstances, the body makes all the cholesterol it needs to construct cell membranes
and other vital functions. When cholesterol is ingested, the body simply makes less to compensate for the
increased amounts in the diet. If a person includes too much cholesterol in the diet, however, this feedback
loop fails and LDL-cholesterol builds, increasing the risk for health problems.
The body has a remarkable method for keeping blood cholesterol levels in check. A second type of lipo-
protein, high-density lipoprotein (HDL), picks up cholesterol in the blood and other tissues and returns it to
the liver. Once in the liver, the cholesterol is used to make bile, which is essential for digestion of lipids. The
cholesterol component of bile is then excreted in the feces, although some is reabsorbed back into the circulation.
Excretion via bile is the only route the body uses to remove cholesterol. Thus HDL may be thought of as “choles-
terol scavengers” that pick up cholesterol in blood and tissues and transport it for removal from the body. Because
HDL transports cholesterol for destruction and removes it from the body, it is considered “good” cholesterol.
Of course, cholesterol is not the only type of lipid that can lead to cardiovascular disease. Triglycer-
ides must also be monitored and maintained within normal levels. Very low-density lipoprotein (VLDL)
is the primary carrier of triglycerides in the blood. VLDL is made in the liver and converted to LDL as it
travels through the bloodstream as most of the triglycerides in VLDL are transported to adipose tissue for
storage. The health consequences of high blood levels of VLDL are not as clear as for LDL levels. It has
been demonstrated, however, that high levels of VLDL are associated with an increased risk of pancreatitis.
Elevated lipid levels can often be prevented or controlled through

Core Concept 16.3 therapeutic lifestyle changes.
Most patients with dyslipidemias are asymptomatic and do not seek medical intervention until cardiovas-
cular disease has progressed, resulting in hypertension or symptoms such as chest pain. For most patients,
lipid disorders are the result of a combination of genetic and environmental (lifestyle) factors.
When a patient is found to have high LDL-cholesterol levels, a decision must be made regarding the
initiation of drug therapy. Although the drugs used to control lipid levels are generally safe and effective,
other risk factors are considered, such as age, family history of heart disease, hypertension, and cigarette
smoking. The stage at which drug therapy is begun depends on the number and extent of these risk factors.
The more risk factors present, the more aggressive is the therapy. Table 16.1 ◆ gives the desirable, border-
line, and high laboratory values for each of the major lipids and lipoproteins.
Recommendations for the treatment of high blood cholesterol have been set by the National Cho-
lesterol Education Program (NCEP) of the National Institutes of Health. These recommendations, which
are revised periodically, are the gold standard for treating this disorder. In some patients, high blood cho-
lesterol levels can be controlled by initiating therapeutic lifestyle changes without drug therapy. Many
patients with borderline laboratory values can control their hyperlipidemia entirely through nonpharma-
cologic means. Even in patients with high risk for whom drug therapy is indicated, using these changes
is important for reducing cholesterol levels. Following are the features of therapeutic lifestyle changes:
■ Increase physical activity, which raises HDL levels and lowers triglycerides.
■ Maintain weight within a normal range.
■ Implement a medically supervised exercise plan.
■ Reduce dietary saturated fat intake to 7% of total caloric intake.
■ Reduce cholesterol intake to less than 200 mg/day.
■ Increase intake of whole grains, vegetables, and fruits so that total dietary fiber is 10 to 25 g/day.
■ Eliminate tobacco use.
Figure 16.1
Composition of
lipoproteins: (a) HDL;
(b) LDL; (c) VLDL.
45–50%
20%
30%
5%
(a) HDL
25%
45%
20%
10%
(b) LDL
5–10%
10–15%
15–20%
55–65%
(c) VLDL
Triglyceride Protein
Phospholipid Cholesterol
In addition to the recommendations of the NCEP, other lifestyle changes likely contribute to keeping
blood cholesterol levels within normal values and reducing the risk of heart disease. These factors include
maintaining blood pressure within normal limits, reducing stress, and limiting the intake of high-sugar
foods. Increased intake of omega-3 fatty acids has been shown to reduce the risk of cardiovascular disease.
Because trans-fatty acids in the diet can raise blood cholesterol levels, patients should be advised to avoid
foods that are fried or contain vegetable shortening or partially hydrogenated oils.
Table 16.1 Standard Laboratory Lipid Profiles

Type of Lipid Laboratory Value (mg/dl) Standard
Total cholesterol Less than 200 Desirable
200–240 Borderline high risk
Greater than 240 High risk
LDL cholesterol Less than 100 Optimal
100–129 Near or above optimal
130–159 Moderate risk
160–189 High risk
Greater than 189 Very high risk
HDL cholesterol Less than 35 High risk
35–45 Moderate risk
46–59 Low risk
Greater than 60 Desirable
Triglycerides Less than 149 Desirable
150–199 Borderline high risk
200–499 High risk
Greater than 500 Very high risk
CAM Therapy
Red Yeast Rice and Cholesterol
Red yeast rice is a supplement that is produced when rice is fermented with the yeast Monascus
purpureus. The product is sometimes reduced to a powder and used as a coloring or flavoring.
Red yeast rice has been used for centuries in Chinese medicine to treat various digestive and liver
complaints, but more recently it has been used as a supplement to manage high blood cholesterol.
Red yeast rice clearly is effective at lowering blood cholesterol levels. This is likely because
the product contains a chemical identical to the prescription drug lovastatin. In 2007, the
Food and Drug Administration (FDA) decided that red yeast rice should be regulated as a
prescription drug. Some supplement manufacturers remarketed the product after removing
lovastatin from the red yeast rice. To avoid legal action, most red yeast labels do not mention
a cholesterol-lowering effect. It is unclear whether the “lovastatin-removed” product has
any ability to lower blood cholesterol. Patients should discuss this supplement with their
healthcare provider before beginning therapy.
Concept Review 16.1

■ Why is the cholesterol in high-density lipoproteins considered to be “good” cholesterol?
Core Concept 16.4 Statins are preferred drugs for reducing blood lipid levels.
In the late 1970s, compounds were isolated from various species of fungi that were found to inhibit cholesterol
production in human cells in the laboratory. This class of drugs, known as the statins, has since revolutionized
the treatment of lipid disorders. Statins can produce a dramatic 20% to 40% reduction in LDL-cholesterol
levels. In addition to decreasing LDL-cholesterol levels in the blood, statins can also lower triglyceride levels,
lower VLDL levels, and raise “good” HDL-cholesterol levels. These effects have been shown to reduce the
incidence of serious cardiovascular related events by 25% to 30%. Statins are now first-line drugs in the treat-
ment of dyslipidemias and are among the most widely prescribed drugs in the United States.
Cholesterol is made in the liver by a series of more than 25 metabolic steps. Of the many enzymes
involved in this complex pathway, HMG-CoA reductase (hydroxymethylglutaryl-CoenzymeA reductase)
serves as the primary regulator of cholesterol biosynthesis. Under normal conditions, this enzyme is con-
trolled through negative feedback: High levels of LDL cholesterol in the blood will shut down production
of HMG-CoA reductase, thus turning off the cholesterol pathway. Figure 16.2 ■ illustrates some of the
steps in cholesterol biosynthesis and the importance of HMG-CoA reductase.
The statins act by inhibiting HMG-CoA reductase. As the liver makes less cholesterol, the body re-
sponds by making more LDL receptors in order to scavenge more LDL from the blood, thus reducing
blood levels of LDL. The drop in lipid levels is not permanent, however, patients need to remain on these
drugs during the remainder of their lives or until their hyperlipidemia can be controlled through lifestyle
changes. Statins have been shown to slow the progression of coronary artery disease and to reduce deaths
from cardiovascular disease. Doses of the HMG-CoA reductase inhibitors are shown in Table 16.2 ◆.
Figure 16.2
Cholesterol biosynthesis
and excretion.
Acetyl CoA HMG-CoA HMG-CoA

Reductase
HO
Cholesterol
To gallbladder
Bile salts
Excretion
Table 16.2 Drugs for Dyslipidemias

HMG-CoA Reductase Inhibitors
atorvastatin (Lipitor) PO; 10–80 mg/day May be taken with or without food at any time of the day
fluvastatin (Lescol) PO; 20 mg/day (max: 80 mg/day) May be taken with or without food in the evening
lovastatin (Altoprev, Mevacor) PO; 20–40 mg 1–2 times/day Should be taken with food in the evening
pitavastatin (Livalo) PO; 1–4 mg/day (max: 4 mg/day) May be taken with or without food at any time of the day
pravastatin (Pravachol) PO; 10–40 mg/day May be taken with or without food in the evening
rosuvastatin (Crestor) PO; 5–40 mg/day May be taken with or without food at any time of the day
simvastatin (Zocor) PO; 5–40 mg/day May be taken with or without food in the evening
Bile ACID BINDING DRUGS
cholestyramine (Questran) PO; 4–8 g bid–qid Take with large amounts of fluid; take other drugs
one hour before or four hours after
colesevelam (Welchol) PO; 1.9 g bid Take with meals and with at least 8 oz of fluid
colestipol (Colestid) PO; 5–20 g/day in divided doses Taken with large amounts of fluid; take other drugs
one hour before or four hours after
Fibric Acid DRUGS
fenofibrate (Antara, Fibricor, Lofibra, PO; 43–200 mg/day, depending Take with food. Assess periodically for symptoms
Tricor, Trilipix) upon the specific product of myopathy
gemfibrozil (Lopid) PO; 600 mg bid (max: 1500 mg/day) Take 30 min before morning and evening meals
Other DRUGS FOR DYSLIPIDEMIAS
ezetimibe (Zetia) PO; 10 mg/day Newer antihyperlipidemic; inhibits cholesterol absorption
icosapent (Vascepa) PO; 4 g/day Take with food
lomitapide (Juxtapid) PO; 5–60 mg once daily Newer drug for inherited hypercholesterolemia
mipomersan (Kynamro) Subcutaneous; 200 mg once weekly Newer drug for LDL and total cholesterol
niacin (Niacor, Niaspan, others) PO; 1.5–3 g/day (max: 6 g/day) Also used to treat niacin deficiency (10–20 mg/day). Take with food
omega-3-acid ethyl esters (Lovaza) PO; 4 g/day Take with food
Seven statins are currently available and all have very similar actions and adverse effects. All the
statins are given orally. Some statins should be administered in the evening because cholesterol biosyn-
thesis in the body is higher at night. Atorvastatin and rosuvastatin have longer half-lives and are effective
regardless of the time of day they are taken.
The statins are generally safe drugs, having few serious adverse effects. Gastrointestinal (GI) dis-
turbances such as indigestion, flatulence, cramping, and constipation are usually mild and disappear with
continued use. Statins can cause muscle injury, resulting in symptoms such as weakness, soreness, and
pain. Muscle-related side effects are dose related and tend to occur more often in elderly patients. Patients
should be carefully monitored for these symptoms because muscle injury may progress to more serious
conditions. In 2001, cerivastatin was removed from the market because of 31 fatalities due to severe rhab-
domyolysis associated with the use of the drug. Rhabdomyolysis is a medical condition in which muscle
tissue, including cardiac muscle, becomes extremely inflamed, resulting in breakdown of muscle. Patients
reporting muscular soreness or weakness may have their statin dosage reduced, or they may be switched to
a drug of a different class.
Drug Prototype: Atorvastatin (Lipitor)

Therapeutic Class: Antihyperlipidemic drug Pharmacologic Class: HMG-CoA reductase inhibitor (statin)
Actions and Uses: Atorvastatin slows the biosynthesis of diarrhea, and constipation. A small percentage of patients ex-
cholesterol by blocking the rate-limiting enzyme, HMG-CoA perience liver damage; thus, liver function is usually monitored
reductase. The primary indication for atorvastatin is hypercho- periodically during therapy. The most serious adverse effect is
lesterolemia. Although lovastatin (Mevacor) was the first HMG- rhabdomyolysis. Like other statins, atorvastatin is a pregnancy
CoA reductase inhibitor approved for use in the United States, category X drug. Pregnancy testing should be conducted prior
atorvastatin has a long half-life and may be administered to treatment in women of childbearing years, and the patient
without regard to food or time of day. Maximum effects from should be advised to take precautions to prevent pregnancy
atorvastatin are seen in 4–8 weeks. Effectiveness is measured during therapy.
by decreases in LDL, total cholesterol, and triglycerides, and an Atorvastatin interacts with many other drugs. For exam-
increase in HDL. Patients receiving this drug should be placed ple, it may increase digoxin levels by 20%, as well as increase
on a cholesterol-lowering diet, because this will enhance the levels of oral contraceptives. Erythromycin may increase atorv-
drug’s therapeutic effects. The primary goal in atorvastatin astatin levels by 40%.
therapy is to reduce the risk of MI and stroke. Grapefruit juice inhibits the metabolism of statins, allow-
ing them to reach toxic levels. Because HMG-CoA reductase in-
Adverse Effects and Interactions: Adverse effects of atorv- hibitors also decrease the synthesis of coenzyme Q10 (CoQ10),
astatin are rarely severe enough to cause discontinuation of patients may benefit from CoQ10 supplements.
therapy and include GI complaints such as intestinal cramping,
Drug Prototype: Cholestyramine (Questran)

Therapeutic Class: Antihyperlipidemic drug Pharmacologic Class: Bile acid binding drug
Actions and Uses: Cholestyramine is used to treat elevated lev- Adverse Effects and Interactions: Although cholestyramine rarely
els of cholesterol and LDLs. The drug is formulated as a powder produces serious adverse effects, patients may experience constipa-
that is mixed with fluid before being taken once or twice daily. tion, bloating, gas, and nausea that may limit its use. Cholestyr-
It is not absorbed or metabolized once it enters the intestine; amine has the ability to bind to other drugs and interfere with
thus, it does not produce systemic effects. It may take 30 days their absorption. Examples include binding to vitamin K, thiazide
or longer to produce its maximum effect. Cholestyramine is diuretics, and penicillins. To prevent potential interactions, other
sometimes combined with other cholesterol-lowering drugs, medications should be taken one hour before or four hours after
such as the statins or niacin to produce additive effects. administration of cholestyramine. The drug is contraindicated in
patients with biliary obstruction, biliary cirrhosis, or GI obstruction.
NURSING PROCESS FOCUS Patients Receiving Drug Therapy with HMG-CoA Reductase Inhibitors (Statins)
Prior to administration: ■ Deficient Knowledge related to a need for an altered lifestyle and
■ Obtain a complete health history including cardiovascular, musculoskel- lack of information about drug therapy
etal, gastrointestinal, renal and liver conditions, diet, allergies, drug ■ Noncompliance related to difficulty adhering to dietary and drug
history, and possible drug interactions. regimen
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, renal ■ Chronic Pain related to drug-induced myopathy
and liver function studies, glucose and pregnancy testing for women of ■ Ineffective Self-health Maintenance related to insufficient knowledge
childbearing age. of seriousness of disease and drug therapy regimen
■ Acquire the results of a complete physical examination, including vital
signs, height, and weight.
The patient will:

■ Experience therapeutic effects (lowered cholesterol and triglyceride levels).
Implementation
■ Monitor blood cholesterol and triglyceride levels at intervals during ■ Advise the patient of the importance of keeping appointments for
therapy. (Monitoring these levels will help to determine effectiveness laboratory testing.
of therapy.)
■ Monitor patient compliance with dietary regimen. (Maintenance ■ Ensure that patient/family understand that drug therapy is used in
of controlled saturated fat diet is essential to the effectiveness of addition to diet therapy. Provide the patient with information needed
medications.) to maintain a low-saturated fat, low-cholesterol diet.
■ Monitor the patient for alcohol abuse. (Excessive alcohol intake may ■ Instruct the patient to avoid or limit alcohol use.
result in liver damage and interfere with drug effectiveness.)
■ Monitor the patient for adverse effects of drug therapy, e.g. GI effects, ■ Instruct the patient to report symptoms of GI effects such as cramping
muscle soreness or joint pain unrelated to usual activity. (May indicate and diarrhea; unexplained muscle tenderness and pain, tingling of
muscle inflammation related to medication.) extremities, or effects that hinder normal activities of daily living to
■ If complaints of increasing muscle soreness, monitor CPK level. ■ Instruct patient to see healthcare provider immediately if having
(Elevated CPK may be indicative of myopathy.) increased muscle pain and weakness.
■ Obtain the patient’s smoking history. (Smoking increases risk of ■ Encourage smoking cessation. Provide information about medications
cardiovascular disease and may decrease HDL levels.) and smoking cessation programs.
■ Monitor patient’s pregnancy status. (Statins are classified as pregnancy ■ Advise the patient of childbearing age of the dangers of using statins
category X.) while pregnant; to report any prospects of pregnancy or possible side
effects/symptoms.
of proper administration. (Some medications interact with statins and ■ Not to take medication with grapefruit juice.
grapefruit juice inhibits metabolism.) ■ To notify healthcare practitioner when taking oral contraceptives,
erythromycin and some cardiac medication such as digoxin, diltiazem,
and verapamil.
Bile acid binding drugs can reduce LDL levels by increasing

cholesterol excretion. Core Concept 16.5
Prior to the discovery of the statins, the primary means of lowering blood cholesterol was through use of
bile acid binding drugs. Bile acids, contain a high concentration of cholesterol and are secreted by the liver
to aid in the digestion of fats in the small intestine. Once bound in the intestine, the cholesterol in the bile
acids is eliminated in the feces. Although they are no longer considered first-line drugs for dyslipidemias,
they are sometimes combined with statins for patients who are unable to achieve sufficient response from
the statins alone. Doses of these drugs are listed in Table 16.2. Bile acid binding drugs are also called bile
acid resins and bile acid sequestrants. The prototype drug for this drug class is cholestyramine (Questran).
Although effective at producing a 20% decrease in LDL-cholesterol levels, the bile acid binding drugs
tend to cause more frequent adverse effects than do the statins. Taken orally, bile acid binding drugs are not
absorbed into the circulation; therefore, their adverse effects are limited to the GI tract. A high percentage
of patients, however, experience constipation, bloating, nausea, or indigestion. Colesevelam (Welchol) is a
newer drug in this class that is reported to have fewer adverse effects than the older drugs. Also of concern
is that bile acid binding drugs can prevent the absorption of other medications and vitamins that may be
taken at the same time. This can be avoided by teaching the patient to take these drugs one hour before, or
four hours after, other medications.
Core Concept 16.6 Niacin can reduce triglyceride and LDL-cholesterol levels.
Niacin, also called nicotinic acid, is a water-soluble B-complex vitamin whose primary action is
to decrease VLDL levels. When VLDL is diminished, the patient also experiences a reduction in
LDL-cholesterol and triglyceride levels. It also has the desirable effects of reducing triglycerides and
increasing HDL levels. Thus, niacin is unique in that it can improve multiple types of dyslipidemias.
As with other lipid-lowering drugs, maximum therapeutic effects may take a month or longer to
achieve.
Its ability to lower lipid levels is unrelated to its role as a B-vitamin; very high doses are needed to
achieve a lipid-lowering effect. For decreasing cholesterol, the usual dose is 2 to 3 g per day. When taken
as a vitamin, the dose is only 25 mg per day.
Although effective at reducing LDL cholesterol by 20%, niacin produces more adverse effects than
the statins. Flushing and hot flashes occur in almost every patient, although taking one aspirin tablet
30 minutes prior to niacin administration can reduce flushing in many patients. A variety of uncomfortable
intestinal effects such as nausea, excess gas, and diarrhea are commonly reported. Although uncommon,
more serious adverse effects such as liver toxicity and gout are possible. Because of these adverse effects,
niacin is most often used in lower doses in combination with a statin or bile acid binding drug because the
beneficial effects of these drugs are additive. Several fixed-dose combination drugs are available, including
Advicor (niacin with lovastatin) and Simcor (niacin with simvastatin). Extended-release niacin, which is
taken once daily, causes less flushing and GI adverse effects.
As a vitamin, niacin is available without a prescription. However, patients should be instructed not to
attempt self-medication with this drug. One form of niacin, available over the counter as a vitamin supple-
ment called nicotinamide, has no lipid-lowering effects. Patients should be informed that if niacin is used
to lower cholesterol, it should be done under medical supervision.
Concept Review 16.2

■ How does the mechanism of the statins differ from that of niacin?
CAM THERAPY
Coenzyme Q10 for Heart Disease
Coenzyme Q10 (CoQ10) is a vitamin-like substance found in most animal cells. It is an
essential component in the cell’s mitochondria, which produce energy or adenosine tri-
phosphate (ATP). Because the heart requires high levels of ATP, a sufficient level of CoQ10
is essential to that organ. Foods richest in this substance are pork, sardines, beef heart,
salmon, broccoli, spinach, and nuts. Older adults appear to have an increased need for
CoQ10.
Reports of the benefits of CoQ10 for treating heart disease began to emerge in the
mid-1960s. Subsequent reports have claimed that CoQ10 may be beneficial in angina
pectoris, dysrhythmias, periodontal disease, immune disorders, neurologic disease, obesity,
diabetes mellitus, and certain cancers. Considerable research has been conducted on this
antioxidant.
The statins decrease CoQ10 levels. Indeed, many of the adverse effects of statins may
be due to the decrease in CoQ10 levels, including muscle weakness and rhabdomyolysis.
Supplementation with CoQ10 may diminish myopathy symptoms. In addition, there is
scientific evidence to suggest that CoQ10 causes a small decrease in blood pressure in patients
with hypertension. Evidence to support the use of CoQ10 in treating patients with heart
disease, neurologic disorders, or cancer is weak. As for most dietary supplements, controlled
research studies are often lacking and give conflicting results.
Fibric acid drugs lower triglyceride levels, but have little effect on LDLs. Core Concept 16.7
Once commonly prescribed to reduce lipid levels, the fibric acid drugs, or fibrates, have been largely re-
placed by the statins for most indications. They are sometimes used in combination with the statins. In ad-
dition they remain preferred drugs for treating extremely high triglyceride levels. Doses of the fibrates are
listed in Table 16.2.
The first fibric acid drug, clofibrate (Atromid-S), was widely prescribed until studies demonstrated
it did not reduce mortality from cardiovascular disease. Although clofibrate is no longer available in the
United States, two other fibrates, fenofibrate (Antara, Lofibra Tricor, others), and gemfibrozil (Lopid), are
sometimes prescribed for patients who have excessive triglyceride and VLDL levels. Fibrates are the most
effective drugs for reducing VLDLs and blood triglyceride levels. Elevation of “good” HDL cholesterol
is another effect of fibrate therapy. Unfortunately, these drugs have little effect on LDL-cholesterol levels.
Fibrates cause few serious adverse effects. Flushing, dizziness, fatigue, rashes, and GI complaints
are the most common adverse effects. Like the statins, some patients experience muscle pain or weakness;
therefore, patients receiving concurrent therapy with both statins and fibrates should be monitored carefully.
The mechanisms of action of the fibrates and other drugs for dyslipidemias are shown in Figure 16.3 ■.
Dosages of these drugs are listed in Table 16.2.
Figure 16.3
Tissues
Statins
LDL Interfere with HMG-CoA
Lipoprotein
HDL reductase, the critical
lipase
(for excretion) enzyme in the biosynthesis
of cholesterol
VLDL
Niacin Cholesterol
Decreases both VLDL HMG-CoA
and LDL levels
Bile acids
Dietary
lipids
Ezetimibe
Bile acid sequestrants Blocks the absorption
Bind bile acids, thus increasing of cholesterol from the
the excretion of cholesterol in small intestine
the stool Absorbed
lipids
Bile acid and drug

(excretion in feces)
Mechanisms of action of lipid-lowering drugs.

Drug Prototype: Gemfibrozil (Lopid)

Therapeutic Class: Antihyperlipidemic drug Pharmacologic Class: Fibric acid drug
Actions and Uses: Gemfibrozil can cause up to a 50% reduc- nausea, and abdominal cramping. The drug produces few
tion in VLDL with a moderate increase in HDL. Because it is serious adverse effects, but it may increase the likelihood of
less effective than the statins, it is not a drug of first choice gallstones and occasionally affect liver function.
for reducing LDL-cholesterol levels. However, it is useful Using gemfibrozil with oral anticoagulants may increase
for patients with high triglyceride levels who have not re- the risk of bleeding. Concurrent use with statins should be
sponded favorably to diet modification and those at risk for avoided because this increases the risk of myopathy and
pancreatitis. rhabdomyolysis.
Adverse Effects and Interactions: The most common adverse

effects of gemfibrozil are related to the GI system: diarrhea,
Other approaches to treating hyperlipidemia include

ezetimibe, omega-3 fatty acids, and fixed-dose
Core Concept 16.8 combination therapy.
A newer drug for treating high blood cholesterol levels is ezetimibe (Zetia). Ezetimibe blocks the absorp-
tion of cholesterol in the small intestine. LDL-cholesterol and triglyceride levels are reduced, with a slight
increase in HDL cholesterol. When used as monotherapy, it can decrease blood cholesterol levels by about
20%. Adding a statin to the therapeutic regimen reduces LDL by an additional 15% to 20%. Adverse ef-
fects from ezetimibe are uncommon and include abdominal pain, back pain, diarrhea, and arthralgia. The
dose for ezetimibe is listed in Table 16.2. In 2013, the FDA approved Liptruzet, a combination containing
ezetimibe and atorvastatin.
Omega-3-acid ethyl esters (Lovaza) and icosapent (Vascepa) are two prescription forms of omega-3
fatty acids found in fish oil. Fish oil has long been a natural therapy for the treatment of high blood lipid
levels. Both drugs are approved as an adjunct to diet in the treatment of severe hypertriglyceridemia. Most
adverse effects are minor and include burping, fishy taste, and dyspepsia (indigestion). Those patients
allergic to seafood may be allergic to fish oil. High doses of omega-3 fatty acids may prolong clotting time
and should be used with caution in patients taking anticoagulants.
A recent trend in the treatment of hyperlipidemia is to combine drugs from two different classes in a
single tablet. Vytorin combines 10 mg of ezetimibe with 10, 20, 40, or 80 mg of simvastatin. Advicor com-
bines 20 mg of lovastatin with 500, 750, or 1000 mg of niacin. These fixed-dose combinations allow for
lower doses of each individual drug, potentially resulting in fewer adverse effects. Taking a single tablet is
easier for the patient to remember, which increases compliance. Because the combination drugs attack cho-
lesterol levels using two distinct mechanisms of action, it may be possible to get a synergistic, or additive,
effect of the drugs on blood cholesterol levels.
A second trend in treating cardiovascular disease is to combine an antihypertensive drug with an
antihyperlipidemic medication. For example, Caduet combines the antihypertensive amlodipine with ator-
vastatin. Several fixed-dose combinations are available with 5 to 10 mg of amlodipine and 10 to 80 mg of
atorvastatin. These combination agents are targeted for the millions of patients who have both hypertension
and elevated blood cholesterol levels.
Chapter Review 245
patients need to know

Patients treated for lipid disorders need to know the following:
In General
1. Because high cholesterol and triglyceride levels in the blood increase the risk for heart
disease and stroke, follow the healthcare provider’s instructions even when feeling well.
2. Continuation of a low-fat, low-cholesterol diet while taking lipid-lowering drugs
will provide the best results.
Regarding Statin Medications

3. Atorvastatin and rosuvastatin are effective regardless of the time of day they are
taken. Taking other statin drugs in the evening makes them available to work on
the higher amount of cholesterol that the body makes at night.
4. The healthcare provider may prescribe a fibric acid drug to lower triglycerides and
another drug to lower cholesterol. One drug should not be stopped when the sec-
ond drug is ordered, except by practitioner’s advice.
Regarding Bile Acid Binding Drugs

5. Self-medication with niacin can cause gout and liver damage from high doses. It will
not lower cholesterol at low doses. Supervision by a healthcare provider supports
safe and effective use of this drug.
6. If prescribed bile acid resins, such as psyllium (Metamucil), cholestyramine (Questran),
or colestipol (Colestid), take one hour after or four hours before other drugs to avoid
counteracting drug effectiveness. Dissolving the bile acid resin in water and keeping
fluid intake high helps to avoid irritation of the mouth and constipation.
CHAPTER REVIEW
16.1 Lipids serve essential roles in the body, but too 16.4 Statins are preferred drugs for reducing blood
much dietary fat can lead to disease lipid levels.
Lipids, or fats, have important roles in human physi- Drugs in the statin class inhibit HMG-CoA reductase,
ology. Excessive dietary triglyceride or cholesterol a critical enzyme in the biosynthesis of cholesterol.
can cause dyslipidemias, an abnormal amount of lipid They are safe and effective at lowering LDL cho-
in the blood. Dyslipidemias are major risk factors for lesterol and are the most widely prescribed class of
cardiovascular disease. drugs for hyperlipidemias.
16.2 Lipoproteins transport lipids through the blood for 16.5 Bile acid binding drugs can reduce LDL levels by
utilization by tissues, storage in adipose tissue, or increasing cholesterol excretion.
excretion by the liver. The bile acid binding drugs are effective at lowering
Lipids are packaged for travel through the blood in li- LDL cholesterol, although they produce more ad-
poprotein complexes. High VLDL and LDL are asso- verse effects than the statins. They should be taken
ciated with an increased incidence of cardiovascular separately from other medications because they can
disease, whereas HDL provides a protective effect. interfere with drug absorption.
16.3 Elevated lipid levels can often be prevented or 16.6 Niacin can reduce triglyceride and LDL-cholesterol
controlled through therapeutic lifestyle changes. levels.
Before starting pharmacotherapy for hyperlipidemia, Niacin, or nicotinic acid, can be effective at lower-
patients are usually advised to manage the condi- ing LDL cholesterol and triglycerides when given in
tion through lifestyle changes, such as restriction of large amounts. It is not usually a first-choice drug but
dietary saturated fats and cholesterol, increased exer- is sometimes combined in smaller doses with other
cise, and smoking cessation. lipid-lowering drugs.
16.7 Fibric acid drugs lower triglyceride levels, but have 16.8 Other approaches to treating hyperlipidemia
little effect on LDLs. include ezetimibe, omega-3 fatty acids, and fixed-
Fibric acids such as gemfibrozil are effective at low- dose combination therapy.
ering triglycerides but less effective than the statins Ezetimibe lowers LDL levels by blocking the absorp-
at lowering blood lipids. Their use is limited because tion of cholesterol from the intestine. Omega-3 fatty
of frequent adverse effects. However, they are some- acids are available by prescription to lower LDL
times combined with other drugs to produce an addi- cholesterol. Combination drugs such as Advicor and
tive effect. Vytorin attack high blood cholesterol levels using two
different mechanisms.
Review Questions
The following questions are written in NCLEX-PN® style. Answer 3. Administers the drug at least one hour before or four hours
these questions to assess your knowledge of the chapter material, after meals
and go back and review any material that is not clear to you. 4. Administers the drug at bedtime
1. This lipoprotein is responsible for transporting choles-
7. A patient is interested in taking niacin to help reduce his
terol from the blood to the liver.
or her cholesterol. When he or she asks the nurse about pos-
1. LDL sible adverse effects, the nurse informs him or her that niacin
2. VLDL can cause: (Select all that apply.)
3. HDL
1. Flushing
4. Triglycerides
2. Excess gas
2. The nurse understands that which of the following HMG- 3. Constipation
CoA reductase inhibitors should be taken with meals? 4. Diarrhea
1. Atorvastatin (Lipitor)
2. Simvastatin (Zocor) 8. On assessment, the patient is found to have a total cho-
3. Lovastatin (Mevacor) lesterol level of 326 mg/dL and prehypertension. When assist-
4. Rosuvastatin (Crestor) ing the RN in the development of a care plan, the LPN or LVN
recognizes that the best treatment for this patient would be a
3. The nurse is instructing a patient on how to take statin low-fat diet and:
drugs. The patient is informed that statin drugs are most effec- 1. An exercise program only
tive when taken: 2. Cholesterol-lowering medication
1. In the morning 3. Over-the-counter supplements
2. In the evening 4. An antihypertensive
3. With other medications
4. On an empty stomach 9. After a review of a patient’s chart, the nurse notices that
the patient has developed gallstones and elevated liver en-
4. The healthcare practitioner orders lovastatin (Mevacor)
zymes. Which of the following cholesterol-lowering medica-
20 mg at bedtime. The supply is 10 mg tablets. How many tab-
tions could cause this?
lets will the nurse give?
1. Cholestyramine (Questran)
1. 1 tablet
2. Niacin (Nicotinic acid)
2. 1½ tablets
3. Gemfibrozil (Lopid)
3. 2 tablets
4. Lovastatin (Mevacor)
4. 2½ tablets
5. Which of the following patient complaint would the nurse 10. A patient hears that taking fish oil is good for helping to
consider to be an adverse reaction to a bile acid resin? bring down triglyceride levels. He asks the nurse about infor-
1. Constipation mation concerning this form of treatment. The nurse would ex-
2. Headache plain that: (Select all that apply.)
3. Anxiety 1. A minor adverse effect of this drug is dyspepsia.
4. Double vision 2. Some people who are allergic to seafood may be allergic to
fish oil.
6. When administering colestipol (Colestid), the nurse: 3. Omega-3 fatty acids are the beneficial component found in
1. Administers the drug with large amounts of fluid to prevent fish oil.
GI upset 4. No matter what the dose, omega-3-fatty acids may decrease
2. Administers the drug 30 minutes prior to meals the ability of the blood to clot.
Chapter Review 247
Remember Mr. Long, the patient 2. After two months of therapy, the physician switched
introduced at the beginning of the the prescription to lovastatin (Mevacor). Mr. Long asks what
chapter? Now read the remainder makes this drug different from the other one he was on. You
of the case study. Based on the in- reply that this drug acts by:
formation you have learned in this 1. Inhibiting enzymes that make cholesterol.
chapter, answer the questions that 2. Binding bile acids in the intestine, which increase choles-
follow. terol excretion.
Mr. Edward Long is a 50-year-old office worker who has 3. Increasing the breakdown of cholesterol in the liver.
gained 50 pounds over the past five years. His blood pressure 4. Making more bile acids, which bind cholesterol.
has consistently been high, but he has declined to take medi- 3. After several weeks of lovastatin therapy, Mr. Long re-
cation for the condition. His LDL-cholesterol level has been turns to the office for follow-up. What question should you ask
above 210 mg/dL on his last three office visits. He claims to to determine if he may be suffering from a very serious adverse
have no chronic diseases and is at the office seeking assistance effect of the statins?
concerning his weight gain.
1. “Do you have bloody diarrhea more than once a week?”
1. The physician ordered cholestyramine for Mr. Long. As 2. “Have you felt confused, lethargic, or drowsy since starting
the nurse, you inform Mr. Long that this drug acts by: the drug?”
3. “Have you experienced excessive muscle weakness or pain?”
1. Inhibiting enzymes that make cholesterol.
4. “Have you experienced acid indigestion or nausea?”
2. Binding bile acids in the intestine, which increases choles-
terol excretion. 4. You are checking the results of Mr. Long’s lab work.
3. Increasing the breakdown of cholesterol in the liver. Which of the following therapeutic results would you expect to
4. Making more bile acids, which bind cholesterol. see now that he has been taking lovastatin?
1. Higher LDL level
2. Higher VLDL level
3. Lower HDL level
4. Higher HDL level

C
“I did everything the nurse
h told me to do. Why is my
a blood pressure so high when
p I’ve been taking all my
medications?”
t
Mr. Joseph Grant
e
r
17 Diuretics and Drugs for Electrolyte

and Acid–Base Disorders
Core Concepts
17.1 The kidneys regulate fluid volume, electrolytes, 17.6 The thiazides are the most widely prescribed class
acids, and bases. of diuretics.
17.2 The composition of filtrate changes dramatically 17.7 Although less effective than the loop diuret-
as a result of the processes of reabsorption and ics, potassium-sparing diuretics may help prevent
secretion. hypokalemia.
17.3 Renal failure significantly impacts 17.8 Several less commonly prescribed diuretics have
pharmacotherapy. specific indications.
17.4 Diuretics are used to treat hypertension, heart 17.9 Electrolytes are charged substances that play
failure, and fluid retention disorders. important roles in maintaining homeostasis.
17.5 The most effective diuretics are those that 17.10 Acidic and basic drugs can be administered to
affect the loop of Henle. correct pH imbalances.
Drug Snapshot
Loop (high-ceiling) furosemide (Lasix) 254 Miscellaneous diuretics

diuretics Electrolytes potassium chloride (KCl) 260
Thiazide diuretics hydrochlorothiazide Acid–base agents sodium bicarbonate
(Microzide) 255 (NaHCO3) 261
Potassium-sparing spironolactone
diuretics (Aldactone) 256
Learning Outcomes
1. Explain the role of the kidneys in 4. Identify common causes of alkalosis 6. For each of the classes in the Drug
maintaining fluid, electrolyte, and and acidosis and the drugs used to Snapshot, identify representative
acid–base balance. treat these conditions. drugs and explain their mechanisms
2. Compare and contrast the loop, 5. Categorize drugs used in the of drug action, primary actions, and
thiazide, and potassium-sparing treatment of urinary system important adverse effects.
diuretics. electrolyte and acid–base disorders
3. Explain the pharmacotherapy of based on their classifications and
sodium and potassium imbalances. mechanisms of action.
Key Terms
acidosis (ah-sid-OH-sis) 260 erythropoietin (ee-rith-ro-po-EE-tin) 252 hyponatremia (hy-po-nay-TREE-
aldosterone (al-DOH-stair-own) 256 filtrate (FIL-trate) 250 mee-uh) 259
alkalosis (al-kah-LOH-sis) 260 hyperkalemia (heye-purr-kah-LEE- nephrons (NEF-ron) 249
carbonic anhydrase (kar-BON-ik mee-ah) 256 pH 260
an-HY-drase) 256 hypernatremia (heye-purr-nuh-TREE- reabsorption 250
diuretic (dye-your-ET-ik) 252 mee-ah) 259 renal failure 251
electrolytes (ee-LEK-troh-lites) 258 hypokalemia (heye-poh-kah-LEE- secretion 251
mee-uh) 252
end-stage renal disease (ESRD) 251
T he volume and composition of fluids in the body must be maintained within narrow limits. Excess
fluid volume can lead to hypertension or heart failure, whereas depletion may result in dehydration or
shock. Body fluids must also contain specific amounts of essential ions or electrolytes and be main-
tained at specific pH values. The kidneys serve a remarkable role in keeping the volume and composition of
body fluids within normal limits. This chapter examines diuretics and drugs used to reverse electrolyte and
acid–base imbalances.
The kidneys regulate fluid volume, electrolytes, acids, and bases. core concept 17.1
When most people think of the kidneys, they think of excretion. Although this is certainly one of their
roles, the kidneys have many other essential functions. The kidneys are the primary organs for regulating
fluid volume, electrolyte composition, and the acid–base balance of body fluids. They also secrete the
enzyme renin, which helps to regulate blood pressure (see Chapter 18), and the hormone erythropoietin,
which stimulates red blood cell production. In addition, the kidneys are responsible for the production of
calcitriol, the active form of vitamin D, which helps maintain bone homeostasis (see Chapter 35). It is not
surprising that overall wellness is strongly dependent on proper functioning of the kidneys.
The urinary system consists of two kidneys, two ureters, a urinary bladder, and a urethra. These struc-
tures are shown in Figure 17.1 ■. Each kidney contains more than 2 million nephrons, the functional units
Figure 17.1
The urinary system.
Suprarenal gland
Suprarenal gland Left kidney
Right kidney
Right renal
Left renal
artery and vein
artery and vein
Abdominal aorta
Ureter
Ureter
Rectum
Urinary bladder
Prostate gland
Urethra
250 Chapter 17 Diuretics and Drugs for Electrolyte and Acid–Base Disorders
Figure 17.2
The nephron. Efferent

Peritubular
arteriole
capillaries
Proximal tubule
F R
Distal tubule
Collecting
duct
R
Afferent Glomerulus Bowman’s
arteriole capsule S
R R R
Loop of
Henle
Urine
F = Filtration: blood to tubule
R= Reabsorption: tubule to blood E
S= Secretion: blood to tubule
To renal
E= Excretion: tubule to
To bladder and vein
external environment
external environment
Fast Facts Renal Disorders

■ Although more than 16,000 kidney transplants are performed annually, more than 80,000 people
are on a waiting list for kidney transplants.
■ One out of every 750 people is born with a single kidney. A single kidney is larger and more
vulnerable to injury from heavy contact sports.
■ About 526,000 Americans suffer from chronic kidney failure, and 87,000 die annually from causes
related to the disease.
■ Type 2 diabetes is the leading cause of chronic kidney failure, accounting for 30–40% of all new
cases each year.
of the kidney. As blood enters a nephron, it is filtered through a porous capillary known as the glomerulus.
Once in the nephron, the fluid is called filtrate. Water and other small molecules readily pass through and
enter the Bowman’s capsule, the first section of the renal tubule. After leaving Bowman’s capsule the fil-
trate travels through the proximal tubule, the loop of Henle, and, subsequently, the distal tubule. Nephrons
empty their filtrate into tubes called common collecting ducts, and then into larger and larger collecting
structures inside the kidney. Fluid leaving the collecting ducts and entering subsequent portions of the kid-
ney is called urine. The parts of the nephron are illustrated in Figure 17.2 ■.
The composition of filtrate changes dramatically as a result of the

core concept 17.2 processes of reabsorption and secretion.
When filtrate enters the Bowman’s capsule, its composition is very similar to that of plasma. Plasma pro-
teins such as albumin, however, are too large to have passed through the glomerulus and will not be present
in the filtrate or in the urine of healthy patients. As filtrate travels through the nephron, its composition
changes dramatically. Some substances in the filtrate cross the walls of the nephron to reenter the blood, a
process known as reabsorption. Water is the most important molecule reabsorbed in the tubule. For every
180 liters (47 gallons) of water entering the filtrate each day, 178.5 liters (45.5 gallons) are reabsorbed,
leaving only 1.5 liters to be excreted in the urine. Glucose, amino acids, and essential ions such as sodium,
chloride, calcium, and bicarbonate are also reabsorbed.
Certain ions and molecules too large to pass through the glomerulus can still enter the urine by cross-
ing from the blood to the filtrate through a process known as tubular secretion. Potassium, phosphate,
hydrogen, and ammonium ions enter the filtrate through secretion. Examples of drugs secreted in the proxi-
mal tubule include penicillin G, ampicillin, nonsteroidal anti-inflammatory drugs (NSAIDs), furosemide,
epinephrine, and trimethoprim.
Reabsorption and secretion are critical to the pharmacokinetics of many drugs. Some drugs are
reabsorbed, whereas others are secreted into the filtrate. For example, approximately 90% of a dose of
penicillin G enters the urine through secretion. When the kidney is damaged, reabsorption and secretion
mechanisms are impaired and serum drug levels may be dramatically affected. The processes of reabsorp-
tion and secretion are depicted in Figure 17.2.
Concept Review 17.1

■ How does the composition of filtrate differ from that of blood?
Renal failure significantly impacts pharmacotherapy. core concept 17.3
Renal failure is a decrease in the kidneys’ ability to maintain electrolyte and fluid balance and to excrete
waste products. If renal excretion is impaired, drugs will accumulate to high concentrations in the blood
and tissues, resulting in toxicity. Because the kidneys excrete most drugs, the majority of medications will
require a significant dosage reduction in patients with moderate to severe renal failure. The importance of
this cannot be overemphasized: Administering the “average” dose to a patient in severe renal failure can
kill a patient.
The healthcare provider has a critical role in preventing serious adverse drug effects in patients with
renal impairment. Monitoring kidney function tests, such as urinalysis and serum creatinine helps to iden-
tify impending renal failure. Notifying the prescriber at the first indication of renal failure allows drug dos-
ages to be lowered, thereby preventing toxicity. Because healthcare providers frequently encounter patients
with renal failure, special note should be taken of nephrotoxic drugs when learning pharmacology. Once a
diagnosis of renal impairment is established, all nephrotoxic medications should be either discontinued or
used with extreme caution.
Renal failure is classified as acute or chronic, depending on its onset. Acute renal failure requires im-
mediate treatment because accumulation of waste products, such as urea and creatinine can result in death
if untreated. The cause of acute renal failure must be quickly identified and corrected. The most common
cause of acute renal failure is lack of sufficient blood flow through the kidneys due to underlying condi-
tions such as heart failure, dysrhythmias, hemorrhage, or dehydration.
Chronic renal failure occurs over a period of months or years. Over half of patients with chronic renal
failure have a medical history of longstanding hypertension (HTN) or diabetes mellitus. Because of its
long, gradual development and nonspecific symptoms, chronic renal failure may go undiagnosed for many
years until the impairment becomes irreversible. When the kidneys are no longer able to function at a level
necessary for day-to-day living, the patient has end-stage renal disease (ESRD) and dialysis and kidney
transplantation become treatment alternatives.
CAM Therapy
Cranberry for Urinary System Health
Nearly everyone is familiar with the bright red cranberries that are eaten during holiday
times. Native Americans used the colorful, ripe berries to treat wounds and to cure anorexia
and for other digestive complaints. In the 1900s, it was noted that the acidity of the urine
increases after eating cranberries; thus began the belief that cranberry juice is a natural cure
for urinary tract infections.
Cranberry juice or berries contain a significant amount of vitamin C and other antioxidants
that can promote health. They contain a substance that can prevent bacteria from sticking on the
walls of the bladder. Research suggests that cranberries can prevent symptomatic urinary tract
infections in some patients, especially in women who have recurrent infections.
Cranberry is a safe supplement, although large amounts may cause GI upset and diarrhea.
The juice should be 100% cranberry and not “cocktail” juice because that contains sugar,
which enhances bacteria growth and may be contraindicated in patients with diabetes. Some
individuals may prefer to take cranberry capsules, which are available at most pharmacies.
Pharmacotherapy of renal impairment includes administering diuretics, which can increase urine out-
put. In addition, cardiovascular drugs are commonly administered to treat underlying HTN or heart fail-
ure. Dietary management, such as protein restriction and reduction of sodium, potassium, phosphorus, and
magnesium intake, is often necessary to prevent worsening of renal impairment.
Many patients with chronic renal failure will also have a deficiency of erythropoietin, a hormone
secreted by the kidney. Erythropoietin serves as a primary signal to increase red blood cell production in
the bone marrow. A synthetic form of erythropoietin, epoetin alfa (Epogen, Procrit) is effective in treating
several disorders caused by a deficiency in red blood cells. Epoetin is sometimes given to patients under-
going cancer chemotherapy to counteract the anemia caused by antineoplastic drugs (see Chapter 28). It
is occasionally prescribed for patients prior to blood transfusions or surgery and to treat anemia in HIV-
infected patients. Epoetin alfa is usually administered three times per week until an increase in the number
of red blood cells is achieved.
Diuretics are used to treat hypertension, heart failure,

core concept 17.4 and fluid retention disorders
dia 5 thoroughly A diuretic is a drug that increases urine output. The goal of most diuretic therapy is to reverse abnormal
uretic 5 to urinate fluid retention by the body. Excretion of excess fluid in the body is particularly desirable in the following
conditions:
■ Hypertension
■ Heart failure
■ Kidney failure
■ Pulmonary edema
■ Liver failure or cirrhosis
The most common mechanism by which diuretics act is by blocking sodium ion (Na+) reabsorption in
the nephron, thus sending more Na+ to the urine. Chloride ion (Cl–) follows Na+. Because water molecules
travel with sodium, blocking the reabsorption of Na+ will increase the volume of urination, or diuresis.
Some drugs, such as furosemide (Lasix), act by preventing the reabsorption of Na+ in the loop of Henle,
and thus they are called loop diuretics. Because of the abundance of Na+ in the loop of Henle, furosemide
is capable of producing large increases in urine output. Other drugs, such as the thiazides, act on the distal
tubule. Because most Na+ has already been reabsorbed from the filtrate by the time it reaches this point in
the nephron, the thiazides produce less diuresis than does furosemide. The sites at which the various diuret-
ics act are shown in Figure 17.3 ■.
core concept 17.5 The most effective diuretics are those that affect the loop of Henle.
The most effective diuretics are the loop or high-ceiling diuretics. Drugs in this class act by blocking the
reabsorption of Na+ and Cl– in the loop of Henle. When given by IV, they have the ability to cause large
amounts of fluid to be excreted by the kidney in a very short time. Loop diuretics are used to reduce the fluid
accumulation associated with heart failure, hepatic cirrhosis, or chronic renal failure. Furosemide (Lasix)
and torsemide (Demadex) are also approved for HTN.
Furosemide is the most frequently prescribed loop diuretic. Unlike the thiazide diuretics, furosemide
is able to increase urine output even when blood flow to the kidneys is diminished. Torsemide (Demadex)
has a longer half-life than furosemide, which offers the advantage of once-a-day dosing. Bumetanide
(Bumex) is 40 times more potent than furosemide but has a shorter duration of action.
The rapid excretion of large amounts of water caused by loop diuretics may produce adverse
de 5 not/without
effects such as dehydration and electrolyte imbalances. Signs of dehydration include thirst, dry mouth,
hydration 5 water
weight loss, and headache. Hypotension, dizziness, and even fainting can result from the rapid fluid loss.
hypo 5 low or below normal When urine flow increases, potassium ion is lost from the body. Potassium depletion, or hypokalemia,
kal 5 potassium may cause dysrhythmias, and thus potassium supplements may be indicated during loop diuretic therapy.
emia 5 blood condition Potassium loss is of particular concern to patients who are also taking digoxin (Lanoxin). Although rare,
impairment of hearing or balance (ototoxicity) is possible. Because of the potential for serious adverse
effects, the loop diuretics are normally reserved for patients with moderate to severe fluid retention, or
Figure 17.3
Miscellaneous diuretics
• Carbonic anhydrase inhibitors

• Mannitol
Proximal tubule
Thiazide diuretics
• Hydrochlorothiazide
Na+ Cl– Early distal Potassium-

tubule sparing
diuretics
65%
Na+ Cl– • Spironolactone
• Triamterene
10% Late distal

Na+ tubule and
Ascending limb 20%
Cl– collecting
of loop of Henle
Na+ duct
1% to
Loop diuretics 5%
K+
• Furosemide
Sites of action of diuretics.
when other diuretics have failed to achieve therapeutic goals. Information on the loop diuretics is given
in Table 17.1 ◆.
Concept Review 17.2

■ Why are drugs that block Na+ reabsorption at the loop of Henle more effective than
those that act on the distal tubule?
Table 17.1 Loop Diuretics

bumetanide (Bumex) PO; 0.5–2 mg daily (max: 10 mg/day) IV form available; this drug is 40 times more potent than
furosemide
ethacrynic acid (Edecrin) PO; 50–100 mg once or twice per day IV form available; exhibits the most ototoxicity of the drugs
(max: 400 mg/day) in this class
furosemide (Lasix) PO; 20–80 mg daily (max: 600 mg/day) IV and IM forms available
IV/IM; 20–40 mg in one or more divided doses
(max: 600 mg/day)
torsemide (Demadex) PO; 4–20 mg daily (max: 200 mg/day) IV form available; exhibits the lowest risk of ototoxicity of
the drugs in this class
Drug Prototype Furosemide (Lasix)

Therapeutic Class: Drug for heart failure (HF), edema, and HTN Pharmacologic Class: Diuretic (loop type)
Actions and Uses: Furosemide is used for conditions in the most important of which is hypokalemia. Because
which the patient is retaining fluid. In the treatment hypokalemia may cause dysrhythmias in patients taking
of acute HF furosemide has the ability to remove large digoxin, combination therapy with furosemide and digoxin
amounts of edema fluid from the patient in a short time. must be carefully monitored. When furosemide is given with
Patients often receive quick relief from their distressing corticosteroids and amphotericin B, it can increase the risk for
symptoms. Compared to other diuretics, furosemide is par- hypokalemia. When given with lithium, elimination of lithium
ticularly beneficial when cardiac output and renal flow are is decreased, causing higher risk of toxicity. When given with
severely diminished. sulfonylureas and insulin, furosemide may diminish their
Furosemide acts by preventing the reabsorption of sodium hypoglycemic effects. Because furosemide is such a potent
and chloride in the loop of Henle. By blocking sodium chloride drug, fluid loss must be carefully monitored to prevent possible
(NaCl) reabsorption, furosemide interferes with water reab- dehydration and hypotension.
sorption. When water reabsorption is blocked, increased Furosemide should be monitored carefully in patients
urination results. receiving aminoglycoside antibiotics because additive oto-
toxicity may result. Patients allergic to sulfur or sulfonamide
Adverse Effects and Interactions: Adverse effects of furosemide, antibiotics should not receive furosemide because of potential
like those of most diuretics, include electrolyte imbalances, allergic response.
core concept 17.6 The thiazides are the most widely prescribed class of diuretics.
The thiazides comprise the largest, most frequently prescribed class of diuretics. These drugs act on the
distal tubule to block sodium reabsorption and increase water excretion. Their primary use is for the treat-
ment of mild to moderate HTN. They are less effective at producing diuresis than the loop diuretics, and
they are ineffective in patients with severe renal disease. All the thiazide diuretics are available by the oral
route and have equivalent efficacy and safety profiles. Three drugs—chlorthalidone (Hygroton), indap-
amide (Lozol), and metolazone (Zaroxolyn)—are not true thiazides, although they are included with this
drug class because they have similar mechanisms of action and adverse effects. The thiazide and thiazide-
like diuretics are listed in Table 17.2 ◆.
The frequency of adverse effects with the thiazides is lower than that of the loop diuretics. As is true
with other diuretics, dehydration is possible because of excessive or rapid fluid loss, and patients may
experience dizziness due to hypotension when moving from a supine to an upright position. Electrolyte
levels are monitored periodically to prevent hypokalemia. To avoid adverse effects from the drug, patients
Table 17.2 Thiazide and Thiazide-Like Diuretics

bendroflumethiazide and PO; 1 tablet/day (40–80 mg nadolol/5 mg Intermediate acting
nadolol (Corzide) bendroflumethiazide)
chlorothiazide (Diuril) PO; 250–500 mg one or two times/day IV form available; short acting
chlorthalidone (Hygroton) PO; 50–100 mg/day Thiazide-like; long acting
hydrochlorothiazide (Microzide) PO; 25–100 mg/day Short acting
indapamide (Lozol) PO; 1.25–2.5 mg once daily Thiazide-like; long acting
methyclothiazide (Aquatensen, Enduron) PO; 2.5–10 mg/day Long acting
metolazone (Zaroxolyn) PO; 2.5–10 mg once daily Thiazide-like; intermediate acting
Drug Prototype: Hydrochlorothiazide (Microzide)

Therapeutic Class: Drug for hypertension and edema Pharmacologic Class: Thiazide diuretic
Actions and Uses: Hydrochlorothiazide is the most widely pre- deficiency may cause cardiac conduction abnormalities, patients
scribed diuretic, belonging to a class of drugs known as the are usually asked to increase their intake of dietary potassium
thiazides. Hydrochlorothiazide is approved to treat ascites, as a precaution.
edema, HF, and HTN. Like many diuretics, it produces few seri- Hydrochlorothiazide increases the action of antihyperten-
ous adverse effects and is effective at producing a 10–20 mmHg sives and skeletal muscle relaxants. It may reduce the effective-
reduction in blood pressure. Patients with severe HTN require ness of anticoagulants, antigout drugs, and antidiabetic drugs,
the addition of a second drug from a different class to control including insulin.
the disease. Central nervous system (CNS) depressants such as alcohol,
Hydrochlorothiazide acts on the kidney tubule to decrease barbiturates, and opioids may increase the orthostatic hypoten-
the reabsorption of Na+. When hydrochlorothiazide blocks this sion caused by hydrochlorothiazide. Steroids or amphotericin B
reabsorption, more Na+ and water are sent into the urine, thus increase K+ loss when given in conjunction with hydrochloro-
reducing blood volume and decreasing blood pressure. The vol- thiazide, leading to hypokalemia.
ume of urine produced is directly proportional to the amount Hydrochlorothiazide increases the risk of serum toxicity of
of Na+ reabsorption blocked by the diuretic. the following drugs: digoxin, lithium, allopurinol, anesthetics,
and antineoplastics. It also alters vitamin D metabolism and cal-
Adverse Effects and Interactions: The most common adverse cium conservation; use of calcium supplements may cause hy-
effects of hydrochlorothiazide include possible electrolyte imbal- percalcemia. It should be used with caution with ginkgo biloba,
ances, especially loss of excessive K+ and Na+. Because potassium which may cause an increase in blood pressure.
taking thiazides should be advised to drink plenty of water and beverages containing electrolytes and to
eat a balanced diet. Diabetic patients should be aware that thiazide diuretics sometimes raise blood glu-
cose levels.
Hydrochlorothiazide is often combined with drugs from other classes for the pharmacotherapy of hy-
pertension. The combination of hydrochlorothiazide with another antihypertensive allows for lower doses
of each individual drug, thus decreasing the incidence of side effects. In addition, a combination drug can
sometimes cause a greater reduction in blood pressure than using a single drug. Examples of combination
drugs include the following:
Apresazide: hydrochlorothiazide with hydralazine (a direct vasodilator)
Benicar HCT: hydrochlorothiazide with olmesartan (an angiotensin II receptor blocker)
Lopressor HCT: with metoprolol (a beta adrenergic blocker)
Zestoretic: hydrochlorothiazide with lisinopril (an angiotensin-converting enzyme inhibitor)
Although less effective than the loop diuretics, potassium-sparing

diuretics may help prevent hypokalemia. core concept 17.7
Potassium depletion is a potentially serious adverse effect of the thiazide and loop diuretics. The therapeu-
tic advantage of the potassium-sparing diuretics is that they are able to increase diuresis without adversely
affecting blood potassium levels. These diuretics are shown in Table 17.3 ◆.
Normally, Na+ and K+ are exchanged in the distal tubule; Na+ is reabsorbed into the bloodstream and
K+ is secreted into the tubule. Potassium-sparing diuretics block this exchange, causing sodium to stay in
the tubule and ultimately leave through the urine. When Na+ is blocked, the body retains more K+. Because
most of the Na+ has already been removed by the time the filtrate reaches the distal tubule, potassium-
sparing diuretics produce only a mild diuresis. Their primary use is in combination with thiazide or loop
diuretics to minimize potassium loss.
Table 17.3 Potassium-Sparing Diuretics

amiloride (Midamor) PO; 5 mg/day (max: 20 mg/day) Moduretic is a fixed-dose combination of amiloride and
hydrochlorothiazide.
spironolactone (Aldactone) PO; 25–100 mg one or two times/day Used in combination with other antihypertensives
to increase diuresis; monitor serum potassium level
carefully
eplerenone (Inspra) PO; 25–50 mg once daily Newer drug in class; actions very similar to
spironolactone
triamterene (Dyrenium) PO; 50–100 mg bid Dyazide is a fixed-dose combination of triamterene
and hydrochlorothiazide.
Spironolactone and eplerenone (Inspra) are potassium-sparing diuretics that act by blocking the ac-
tions of the hormone aldosterone; thus they are commonly called aldosterone antagonists. Secreted by the
adrenal cortex, the normal function of aldosterone is to promote the retention of sodium ion. Although it
produces only a mild diuresis, spironolactone has been found to significantly reduce mortality in patients
with heart failure.
Unlike the loop and thiazide diuretics, patients taking potassium-sparing diuretics should not take
potassium supplements and should not add potassium-rich foods to their diet. Intake of excess potassium
when taking these medications may lead to hyperkalemia.
Drug Prototype: Spironolactone (Aldactone)

Therapeutic Class: Antihypertensive, drug for reducing edema
Pharmacologic Class: Potassium-sparing diuretic, aldosterone antagonist
Actions and Uses: Spironolactone, the most frequently pre- Adverse Effects and Interactions: Spironolactone does such an
scribed potassium-sparing diuretic, is primarily used to treat mild efficient job of retaining potassium that hyperkalemia may de-
HTN, often in combination with other antihypertensives. It may velop. The risk of hyperkalemia is increased if the patient takes
also be used to reduce edema associated with kidney or liver potassium supplements or is also taking angiotensin-converting
disease, and it is effective in slowing the progression of heart enzyme (ACE) inhibitors. Signs and symptoms of hyperkalemia
failure. include muscle weakness, fatigue, and bradycardia. When po-
Spironolactone blocks sodium reabsorption in the distal tassium levels are monitored carefully and maintained within
tubule by inhibiting aldosterone. Aldosterone is a hormone normal values, adverse effects from spironolactone are uncom-
secreted by the adrenal cortex that is responsible for increas- mon. Spironolactone is contraindicated during pregnancy and
ing the renal reabsorption of Na+ in exchange for K+, thus lactation.
causing water retention. When blocked by spironolactone, When spironolactone is combined with ammonium chlo-
sodium and water excretion is increased, and the body retains ride, acidosis may occur. Aspirin and other salicylates may
more potassium. decrease the diuretic effect of the medication. Use of spirono-
lactone with digoxin may decrease the effects of digoxin.
core concept 17.8 Several less commonly prescribed diuretics have specific indications.
A few miscellaneous diuretics have very limited and specific indications. Two of these drugs inhibit
carbonic anhydrase, an enzyme involved with acid–base balance. Acetazolamide (Diamox) is a carbonic
intra 5 within anhydrase inhibitor used to decrease intraocular pressure in patients with glaucoma (see Chapter 37). Unre-
ocular = eye lated to its diuretic effect, acetazolamide is also used to treat acute mountain sickness in patients at very high
altitudes. The carbonic anhydrase inhibitors are not commonly used as diuretics, because they produce a
very weak diuresis and have a higher incidence of adverse effects than other diuretics.
Table 17.4 Miscellaneous Diuretics

acetazolamide (Diamox) PO; 250–375 mg/day in a.m. Carbonic anhydrase inhibitor; IV form available
glycerin (Colace, Osmoglyn) PO; 1–1.8 g/kg, 1–2 hours before ocular Osmotic type; also used to treat constipation
surgery and acute glaucoma
mannitol (Osmitrol) IV; 100 g infused over 2–6 hours Osmotic type
methazolamide (Neptazane) PO; 50–100 mg bid or tid Carbonic anhydrase inhibitor
urea (Ureaphil) IV; 1–1.5 g/kg over 1–2.5 hours Osmotic type
The osmotic diuretics also have very specific applications. Mannitol (Osmitrol) is used to main-
tain urine flow in patients with acute renal failure during prolonged surgery. Mannitol is also used to
reduce swelling in the brain (increased intracranial pressure) and lower intraocular pressure in certain
types of glaucoma. It is a very potent diuretic that is only given by the IV route. Osmotic diuretics are
rarely drugs of first choice due to their potential toxicity. Table 17.4 ◆ lists some of the miscellaneous
diuretics.
NURSING PROCESS FOCUS Patients Receiving Diuretic Therapy

Prior to administration: ■ Fluid Volume related to effects of medical condition
■ Obtain a complete health history including cardiovascular disease, ■ Deficient Fluid Volume related to effects of drug therapy
renal and liver conditions, diabetes, pregnancy, allergies, diet, and ■ Urinary Elimination related to diuretic use
data on recent surgeries or trauma. ■ Risk for Electrolyte Imbalance related to diuretic use
■ Acquire the results of a complete physical examination, including ■ Deficient Knowledge related to a lack of information about drug
vital signs, height, and weight. therapy
■ Obtain the patient’s medication history, including cardiac ■ Noncompliance related to adverse effects of medications
medications, nicotine and alcohol consumption, and use of over-the
counter/herbal supplements or alternative therapies. Determine
possible drug allergies and/or interactions.
■ Evaluate laboratory blood findings: CBC, electrolytes, renal and liver
function studies.
The patient will:

■ Experience therapeutic effects (normal fluid balance and maintenance of normal electrolyte levels).
Implementation
■ Monitor for fluid overload by measuring intake, output, and daily Instruct the patient to:
weights. (Intake, output, and daily body weight can be indications of ■ Immediately report any severe shortness of breath, frothy sputum,
the effectiveness of diuretic therapy.) profound fatigue, edema in extremities, potential signs of heart
failure, or pulmonary edema.
■ Accurately measure fluid intake, fluid output, and body weight, and
report decrease in output or weight gain of 2 lb or more within two
days.
■ Avoid excessive heat, which contributes to fluid loss through
perspiration.
■ Consume adequate amounts of plain water.
■ Monitor laboratory findings, especially potassium and sodium. (Diuret- ■ Advise the patient of the importance of keeping appointments for
ics can cause electrolyte imbalances.) laboratory testing.
■ Instruct the patient to inform laboratory personnel of diuretic therapy
when providing blood or urine samples.
continued . . .

■ Monitor vital signs, especially blood pressure. (Diuretics reduce blood Instruct the patient to:
volume, resulting in lowered blood pressure.) ■ Monitor blood pressure as specified by the healthcare provider and
ensure proper use of home equipment.
■ Stop medication if severe hypotension exists, as specified by the
healthcare provider (e.g., “hold for levels below 88/50 mmHg”).
■ Observe for changes in level of consciousness, dizziness, fatigue, and Instruct the patient to:
postural hypotension. (Reduction in blood volume due to diuretic ■ Immediately report any change in consciousness, especially feeling
therapy may produce changes in level of consciousness or syncope.) faint.
■ Change positions slowly.
■ Obtain blood pressure readings in sitting, standing, and lying
positions.
■ Monitor nutritional status, especially intake of foods with sodium and Instruct patients:
potassium. (These electrolytes can become depleted with thiazide or ■ Receiving loop or thiazide diuretics to eat foods high in potassium.
loop diuretics. Potassium sparing diuretics may cause sodium loss but ■ Receiving potassium-sparing diuretics to avoid foods high in
potassium increase.) potassium.
■ To consult with healthcare provider before using vitamin/mineral sup-
plements or electrolyte-fortified sports drinks. Combining potassium
supplements with a high potassium diet may lead to hyperkalemia.
■ Observe for signs of hypersensitivity reaction. (Allergic responses may Instruct the patient or caregiver to report:
be life threatening.) ■ Difficulty breathing, throat tightness, hives or rash, or bleeding.
■ Flu-like symptoms such as shortness of breath, fever, sore throat,
malaise, joint pain, profound fatigue.
■ Monitor hearing and vision. (Loop diuretics are ototoxic. Thiazide ■ Instruct the patient to report any changes in hearing or vision such
diuretics increase serum digoxin levels, which produce visual changes.) as ringing or buzzing in the ears, becoming “hard of hearing,” or
experiencing dimness of sight, seeing halos, or having “yellow vision.”
■ Monitor reactivity to light exposure. (Some diuretics cause Instruct the patient to:
photosensitivity.) ■ Limit exposure to the sun.
■ Wear dark glasses and light-colored loose-fitting clothes when
outdoors.
■ Administer medication correctly and evaluate the patient’s knowl- Instruct the patient:
edge of proper administration. (Some medications interact with other ■ About the appropriate dosing and administration of the specific
medications.) diuretic being taken.
■ To take diuretic in the morning instead of at night to avoid
interruption of sleep.

through 17.4 for lists of drugs to which these nursing actions apply.
Electrolytes are charged substances that play important

core concept 17.9 roles in maintaining homeostasis.
Minerals are inorganic substances needed in very small amounts by the body (see Chapter 31). When
placed in water, some of these minerals become ions and possess a positive or negative charge. Small, inor-
electro 5 conducts electricity ganic molecules possessing a positive or negative charge are called electrolytes. Electrolytes are essential
lyte 5 solution to many body functions, including nerve conduction, muscle contraction, and bone growth and remodeling.
Too little or too much of an electrolyte may result in serious disease and must be quickly corrected.
Levels of electrolytes in body fluids are maintained within very narrow ranges, primarily by the kid-
ney and gastrointestinal (GI) tract. As electrolytes are lost due to normal excretory functions, they must
be replaced by adequate fluid intake; otherwise, electrolyte imbalances can result. Although imbalances
can occur in any ion, sodium, potassium, and calcium are of greatest importance. Calcium homeostasis is
presented in vitamins, minerals, and nutritional supplements because it is associated with the pharmaco-
therapy of bone disorders. Sodium and potassium are discussed in the following paragraphs. The major
electrolyte imbalances and their treatments are described in Table 17.5 ◆.
An electrolyte imbalance is a sign of an underlying medical condition that needs attention. The most
common cause is renal impairment. In some cases, drug therapy itself can cause the electrolyte imbalance.
For example, aggressive therapy with loop diuretics such as furosemide (Lasix) can rapidly deplete the
Table 17.5 Electrolyte Imbalances

Abnormal Serum
Ion Condition Value (mEq/L) Supportive Treatment*
Calcium Hypercalcemia Greater than 11 Hypotonic fluid or calcitonin
Hypocalcemia Less than 4 Calcium supplements or vitamin D
Chloride Hyperchloremia Greater than 112 Hypotonic fluid
Hypochloremia Less than 95 Hypertonic salt solution
Magnesium Hypermagnesemia Greater than 4 Hypotonic fluid
Hypomagnesemia Less than 0.8 Magnesium supplements
Phosphate Hyperphosphatemia Greater than 6 Dietary phosphate restriction
Hypophosphatemia Less than 1 Phosphate supplements
Potassium Hyperkalemia Greater than 5 Hypotonic fluid, buffers, or dietary potassium
restriction
Hypokalemia Less than 3.5 Potassium supplements
Sodium Hypernatremia Greater than 145 Hypotonic fluid or dietary sodium restriction
Hyponatremia Less than 135 Hypertonic salt solution or sodium supplement
*For all electrolyte imbalances, the primary therapeutic goal is to identify and correct the cause of the imbalance.
body of Na+ and K+. Treatment includes correcting the electrolyte imbalance as well as treating the under-
lying medical condition. Treatments for electrolyte imbalances range from simple changes in dietary intake
for mild imbalances to rapid electrolyte infusions in severe cases.
Sodium Imbalances
Because Na+ is the major electrolyte in extracellular fluid, imbalances of this ion can have serious con-
sequences. Sodium excess, or hypernatremia, is most commonly caused by kidney disease; Na+ accu- hyper 5 high or above normal
mulates in the blood due to decreased excretion. Another cause of hypernatremia is high net water losses, natri 5 sodium
such as occur from inadequate water intake, watery diarrhea, fever, or burns. A high serum Na+ level can emia 5 blood condition
cause cellular dehydration with symptoms such as thirst, fatigue, weakness, muscle twitching, convulsions,
and a decreased level of consciousness. For minor hypernatremia, a salt-restricted diet may be effective in
returning serum Na+ to normal levels. In patients with acute hypernatremia, however, IV fluids such as 5%
dextrose in water or diuretics may be administered to quickly remove sodium from the body.
Sodium deficiency, or hyponatremia, may occur when Na+ is lost because of serious skin burns,
vomiting, diarrhea, kidney disease, and with conditions associated with excessive sweating or prolonged
fever. Symptoms of hyponatremia include nausea, vomiting, anorexia, abdominal cramping, confusion,
lethargy, convulsions, coma, and muscle twitching or tremors. Hyponatremia is usually treated with solu-
tions of sodium chloride or with IV fluids containing salt, such as normal saline or lactated Ringer’s solu-
tion. Tolvaptan (Samsca) is a newer drug administered to raise sodium levels in hospitalized patients with
serious hyponatremia.
Potassium Imbalances
Potassium levels must be carefully balanced between adequate dietary intake and renal excretion. Levels of
K+ in the blood must be maintained within narrow limits because too little or too much of this electrolyte is
associated with fatal cardiac dysrhythmias and serious neuromuscular disorders.
Hyperkalemia may be caused by high consumption of potassium-rich foods or dietary supplements,
particularly when patients are taking potassium-sparing diuretics such as spironolactone. Excess potassium
may also accumulate when renal excretion is diminished due to kidney pathology. The most serious conse-
quences of hyperkalemia are cardiac dysrhythmias.
In mild cases of hyperkalemia, K+ levels may be returned to normal by restricting major dietary
sources of potassium such as bananas, dried fruits, peanut butter, broccoli, and green leafy vegetables. If
the patient is taking a potassium-sparing diuretic, the dose is lowered or an alternate drug is considered. In
acute cases, administration of furosemide (Lasix) can increase potassium excretion within minutes. Serum
potassium levels may also be lowered by administering sodium polystyrene sulfate (Kayexalate), a resin
that removes K+ by exchanging it for Na+ in the large intestine. This drug is given concurrently with a
laxative to promote rapid evacuation of the potassium. Sodium polystyrene sulfate is available in oral and
enema formulations. An additional method of treating hyperkalemia is to administer glucose and insulin,
which causes potassium to leave the extracellular fluid and enter cells.
Drug Prototype: Potassium Chloride (KCl)

Therapeutic Class: Potassium supplement Pharmacologic Class: Electrolyte
Actions and Uses: Potassium is one of the most important elec- of the unpleasant taste of the drug. Intravenous forms may be
trolytes in body fluids, and levels must be maintained within a given in critical care situations.
narrow range of values between 3.5 and 5.5 mEq/L. Too much
or too little K+ may lead to serious consequences and must be Adverse Effects and Interactions: KCl irritates the GI mu-
immediately corrected. Neurons and muscle fibers are most cosa; therefore, nausea and vomiting are common. The drug
sensitive to potassium loss. Muscle weakness, dysrhythmias, may be taken with meals or antacids to lessen the gastric
and cardiac arrest are possible consequences. KCl is also distress. Taking too much KCl can cause hyperkalemia, espe-
used to treat mild forms of alkalosis. cially when it is combined with a diet that contains potas-
KCl is the drug of choice for treating or preventing hy- sium-rich foods.
pokalemia. Therapy with loop or thiazide diuretics is the most Potassium supplements interact with potassium-sparing
common cause of excessive potassium loss. Patients taking thia- diuretics and ACE inhibitors to increase the risk of hyper-
zide or loop diuretics are usually instructed to take oral potas- kalemia. If patients are taking these drugs, the healthcare
sium supplements to prevent hypokalemia. Oral forms include provider should warn them not to take OTC potassium
tablets, powders, and liquids, usually heavily flavored because supplements.
Hypokalemia is a relatively common adverse effect resulting from high doses of loop diuretics
such as furosemide. Strenuous muscular activity and severe vomiting or diarrhea can also result in
significant potassium loss. Mild hypokalemia is treated by increasing the dietary intake of potassium-
rich foods. More severe deficiencies require oral or parenteral potassium supplements. Potassium
chloride (KCl) is available in IV and a wide variety of oral formulations to increase blood potassium
levels.
core concept 17.10 Acidic and basic drugs can be administered to correct pH imbalances.
One of the most important homeostatic functions of the blood is to neutralize strong acids and bases. Much
of the food we eat is either more acidic or more alkaline than body fluids. Furthermore, during the break-
down of food, the body generates significant amounts of acid. If body fluids become too acidic or too alka-
line, enzymes will not function efficiently and cells may be injured.
The degree of acidity or alkalinity of a solution is measured by its pH. A pH of 7 is defined as neutral,
above 7 as basic or alkaline, and below 7 as acidic. To maintain homeostasis, the pH of plasma and most
alkal 5 basic body fluids must be kept within the very narrow range of 7.35 to 7.45. At pH values above 7.45, alkalosis
osis 5 condition develops, and symptoms of CNS stimulation occur that include nervousness and convulsions. Acidosis
occurs below a pH of 7.35, and symptoms of CNS depression may result in coma. In either alkalosis or
acidosis, death may result if large changes in pH are not corrected immediately.
Acidosis and alkalosis are not diseases; they are symptoms of underlying disorders. Primary treat-
ment of acid–base disorders is always targeted to correct the underlying cause. Drugs are administered to
support the patient’s vital functions while the disease is being treated. Common causes of alkalosis and
acidosis are listed in Table 17.6 ◆.
Treatment of alkalosis is directed toward addressing the underlying condition that is causing the
excess bases to be retained. In mild cases, alkalosis may be corrected by administering sodium chloride
concurrently with KCl. This combination increases the renal excretion of bicarbonate ion (a base), which
indirectly increases the acidity of the blood. For acute patients, acidifying agents may be used. Hydro-
chloric acid and ammonium chloride are two drugs that can quickly lower the pH in patients with severe
alkalosis.
In patients with acidosis, the goal is to quickly reverse the level of acids in the blood. A preferred
treatment for acute acidosis is to administer infusions of sodium bicarbonate. Bicarbonate ion acts as a
base to quickly neutralize acids in the blood and other body fluids. The patient must be carefully monitored
during infusions because this drug can “over-correct” the acidosis, causing blood pH to turn alkaline. The
correction of acid–base imbalances is illustrated in Figure 17.4 ■.
Table 17.6 Causes of Acidosis and Alkalosis
Acidosis Alkalosis
Respiratory Origins of Acidosis Respiratory Origin of Alkalosis
■ Hypoventilation or shallow breathing ■ Hyperventilation due to asthma, anxiety, or high altitude
■ Airway constriction
■ Damage to respiratory center in medulla
Metabolic Origins of Acidosis Metabolic Origins of Alkalosis

■ Severe diarrhea ■ Constipation for prolonged periods
■ Kidney failure ■ Ingestion of excess sodium bicarbonate
■ Diabetes mellitus ■ Diuretics that cause potassium depletion
■ Excess alcohol ingestion ■ Severe vomiting
■ Starvation
Figure 17.4
Acids pH = 7.35–7.45 Bases
Normal plasma
Sodium Ammonium chloride

bicarbonate or
Sodium chloride
with potassium
chloride
es Acid
Bas s
35 pH
< 7. > 7.
45
pH
s Bas
Acid es
Acidosis Alkalosis
CNS depression CNS stimulation
Coma Convulsions
Correction of acid–base imbalances.
Drug Prototype: Sodium Bicarbonate (NaHCO3 )

Therapeutic Class: Agent to treat acidosis or bicarbonate deficiency Pharmacologic Class: Electrolyte
Actions and Uses: Acidosis is a more common event than alka- by too much bicarbonate ion. Symptoms may include confu-
losis, occurring during shock or cardiac arrest, or with diabetes sion, irritability, slow respiration rate, and vomiting. Sim-
mellitus. Sodium bicarbonate is the drug of choice for correct- ply discontinuing the sodium bicarbonate infusion often
ing acidosis: The bicarbonate ion (HCO3–) directly raises the pH reverses these symptoms; however, potassium chloride or
of body fluids. Sodium bicarbonate may be given orally if aci- ammonium chloride may be administered to reverse the
dosis is mild, or IV in cases of acute disease. Although sodium alkalosis.
bicarbonate neutralizes gastric acid, it is rarely used to treat Sodium bicarbonate may decrease the absorption of
peptic ulcers because of its tendency to cause gas and gastric ketoconazole and may decrease elimination of dextroamphet-
distention. amine, ephedrine, pseudoephedrine, and quinidine. Sodium
Sodium bicarbonate may also be used to make the urine bicarbonate may increase the elimination of lithium, salicylates,
more basic. An alkaline urine will speed the excretion of acidic and tetracyclines. Chronic use of sodium bicarbonate with milk
drugs, such as barbiturates and aspirin. or calcium supplements may cause milk–alkali syndrome, a
condition characterized by very high serum calcium levels and
Adverse Effects and Interactions: Most of the adverse effects of possible kidney failure.
sodium bicarbonate therapy are the result of alkalosis caused

Patients treated for urinary, acid–base, and fluid disorders need to know the following:
Regarding Diuretics
1. See the healthcare provider regularly and have serum electrolytes, complete blood
count (CBC), and glucose levels monitored as instructed.
2. When taking diuretics, drink plenty of water if dry mouth or thirst develops, unless
otherwise directed by a healthcare provider.
3. Take diuretics in the morning or at least two hours before bedtime to avoid night-
time diuresis.
4. If diabetes is present, monitor blood sugar levels very closely when taking thiazide
diuretics because these drugs may elevate blood glucose levels.
5. Do not take thiazide diuretics during pregnancy or when breast-feeding.
6. When taking loop or thiazide diuretics, increase dietary sources of potassium-rich
foods such as dark leafy vegetables, nuts, citrus fruits, bananas, and potatoes. If
taking a potassium-sparing diuretic, avoid these foods unless otherwise instructed
by a healthcare provider.
7. Avoid caffeinated beverages when taking diuretics. The diuretic effect of the
caffeine combined with the effects of these medications may cause dehydration.
Regarding Potassium Supplements

8. Because KCl tablets are irritating to the GI mucosa, they should be taken with food.
Do not crush or suck the tablets. If nausea or heartburn occurs, take antacids along
with the KCl.
Chapter Review
core concepts summary
17.1 The kidneys regulate fluid volume, electrolytes, erythropoietin used to treat anemia in which there is a
acids, and bases. deficiency in red blood cell production.
The kidneys are essential to the overall health of the
17.4 Diuretics are used to treat hypertension, heart fail-
patient, and to control fluid volume, electrolyte com-
ure, and fluid retention disorders.
position, and acid–base balance. The functional unit
of the kidney is the nephron. Diuretics are drugs that increase urine output, usu-
ally by blocking sodium reabsorption. Indications for
17.2 The composition of filtrate changes dramatically diuretics include hypertension, heart failure, kidney
as a result of the processes of reabsorption and failure, and liver disease.
secretion.
17.5 The most effective diuretics are those that affect
Filtrate entering the proximal tubule resembles
the loop of Henle.
plasma without proteins. Through the processes of
reabsorption and secretion, the filtrate composition The high-ceiling or loop diuretics such as furosemide
changes, producing urine. act by blocking sodium reabsorption in the loop of
Henle. They are the most effective diuretics but are
17.3 Renal failure significantly impacts pharma more likely to cause dehydration and electrolyte loss.
cotherapy.
17.6 The thiazides are the most widely prescribed class
Because the kidneys excrete most drugs, a large
of diuretics.
number of medications require a significant dosage
reduction in patients with moderate to severe renal The thiazide diuretics block sodium reabsorption in
failure. Renal failure is classified as acute or chronic. the distal tubule. Although less effective than the loop
Pharmacotherapy of renal failure attempts to cure diuretics, the thiazides are more frequently prescribed
the cause of the dysfunction. Diuretics may be used because of their lower incidence of serious adverse
to maintain urine output. Epoetin alfa is a form of effects.
Chapter Review 263
17.7 Although less effective than the loop diuretics, adverse effect of drug therapy with certain diuretics.
potassium-sparing diuretics may help prevent Oral or IV potassium chloride can reverse symptoms
hypokalemia. of hypokalemia. Although less common, hyperkale-
Potassium-sparing diuretics act on the distal tubule, mia may be just as serious and may be reversed by
although they are less effective than the loop diuret- administration of glucose or insulin.
ics. Their primary advantage is that they do not cause
17.10 Acidic and basic drugs can be administered to
potassium loss.
correct pH imbalances.
17.8 Several less commonly prescribed diuretics have Sodium chloride with potassium chloride may be
specific indications. administered to reverse mild to moderate alkalosis.
Carbonic anhydrase inhibitors and osmotic diuret- Hydrochloric acid or ammonium chloride may be ad-
ics are not commonly prescribed. They have specific ministered for acute alkalosis. Sodium bicarbonate is
applications, such as decreasing intraocular pressure used to reverse acidosis.
and maintaining urine flow during renal failure.
17.9 Electrolytes are charged substances that play

important roles in maintaining homeostasis.
Electrolyte imbalances can cause significant signs
and symptoms. Hypokalemia is a serious potential
Review Questions
The following questions are written in NCLEX-PN ® style. 3. Serum pH

Answer these questions to assess your knowledge of the chapter ma- 4. Glucose levels
terial, and go back and review any material that is not clear to you.
6. The nurse is monitoring a patient for which of the follow-
1. Which of the following is not a function of the kidneys? ing common adverse effects of oral potassium chloride?
1. Acid–base balance 1. Drowsiness
2. Secretion of renin 2. Nausea and vomiting
3. Production of white blood cells 3. Hypoglycemia
4. Production of calcitriol 4. Muscle weakness
2. While collecting data on a patient suspected of being 7. When instructing a patient about taking potassium-
dehydrated, the nurse is looking for: sparing diuretics, the nurse teaches the patient to:
1. Headache and increased urinary output 1. Take potassium supplements.
2. Weight gain and edema 2. Not take potassium supplements
3. Hypertension and decreased urinary output 3. Add potassium rich foods to his or her diet.
4. Hypotension, headache, and dry mouth 4. Have his or her magnesium levels monitored regularly
3. A patient, newly diagnosed with hypertension, was just 8. The patient is receiving IV normal saline because of
seen by his or her healthcare provider. The office nurse was hyponatremia. On assessment, the nurse determines that the
asked to give him or her samples of the most commonly pre- hyponatremia may have been caused by: (Select all that apply.)
scribed diuretic used for this condition. The nurse gives the 1. Constipation
patient which of the following diuretics? 2. Severe diarrhea and vomiting
1. Ethacrynic acid (Edecrin) 3. Prolonged fever and sweating
2. Chlorothiazide (Diuril) 4. Hemorrhage
3. Spironolactone (Aldactone)
4. Mannitol (Osmitrol) 9. When taking diuretics, the patient is instructed to de-
crease or avoid the intake of:
4. A female patient, recently started on diuretic therapy, is 1. Dark green, leafy vegetables
taught by the nurse that she should: 2. Nuts
1. Take medication at night. 3. Fruits
2. Rise slowly from a sitting position. 4. Caffeine
3. Increase sodium intake.
4. Decrease fluid intake. 10. The healthcare provider orders 1,000 mL of 0.9% NaCl to
infuse IV over eight hours. In monitoring the IV, how many mL
5. A patient is receiving intravenous sodium bicarbonate for should the nurse expect to infuse in one hour?
treatment of metabolic acidosis. During this infusion, how will 1. 100 mL
the nurse monitor for therapeutic effect? 2. 125 mL
1. Liver function tests 3. 135 mL
2. White blood cell count 4. 150 mL
Remember Mr. Grant, the patient 2. Given the previous information, the nurse believes it is
introduced at the beginning of the quite possible that Mr. Grant’s cardiac symptoms and weakness
chapter? Now read the remainder of were caused by:
the case study. Based on the informa- 1. Hyperkalemia
tion you have learned in this chapter, 2. Hypokalemia
answer the questions that follow. 3. Hypernatremia
4. Hyponatremia
3. The physician examines Mr. Grant and decides to admin-
ister a dose of sodium polystyrene sulfonate (Kayexalate). The
nurse explains to Mr. Grant that the reason for administering
this drug is to:
Mr. Joseph Grant has been placed on hydrochlorothiazide (Micro-
zide) for high blood pressure, and potassium chloride as a dietary 1. Increase fluid volume.
supplement. His wife tells him to eat lots of bananas because she 2. Decrease fluid volume.
read that this was necessary when taking diuretics. After a few 3. Increase serum potassium levels.
weeks, Mr. Grant becomes weak and feels as if his heart is skipping 4. Decrease serum potassium levels.
beats. His blood pressure remains high, despite the diuretic. 4. After Mr. Grant’s condition stabilized, the physician de-
cided to select furosemide (Lasix), a more effective diuretic to
1. When providing education on his medications, which of treat hypertension. Which of the following information should
the following should have been explained to Mr. Grant? the nurse provide to Mr. Grant?
1. Never eat bananas when taking Microzide. 1. Never eat bananas when taking Lasix.
2. Eat lots of bananas when taking Microzide. 2. Eat lots of bananas when taking Lasix.
3. Limit potassium-rich foods when taking potassium 3. Limit potassium-rich foods when taking potassium
supplements. supplements.
4. Never eat bananas and take Microzide at the same meal. 4. Never eat bananas and take Lasix at the same meal.
website.

C
“I have all these reports to
finish by Friday. I just don’t h
have time to deal with high a
blood pressure.” p
Mr. Paul Rodriguez t
e
r
Drugs for Hypertension

18
Core Concepts
18.1 Hypertension is characterized by the consistent 18.7 Selection of specific antihypertensive drugs depends
elevation of arterial blood pressure. on the severity of the disease.
18.2 Failure to treat hypertension can lead to stroke, 18.8 Diuretics are often preferred drugs for treating mild
heart failure, or myocardial infarction. to moderate hypertension.
18.3 Blood pressure is caused by the pumping action of 18.9 Calcium channel blockers have emerged as impor-
the heart. tant drugs in the treatment of hypertension.
18.4 The primary factors responsible for blood pressure 18.10 Blocking the renin-angiotensin-aldosterone system
are cardiac output, the resistance of the small leads to a decrease in blood pressure.
arteries, and blood volume. 18.11 Adrenergic blockers are commonly used to treat
18.5 Many nervous and hormonal factors help to keep hypertension.
blood pressure within normal limits. 18.12 Vasodilators lower blood pressure by relaxing
18.6 Positive lifestyle changes can reduce blood pressure arteriolar smooth muscle.
and lessen the need for medications.
Drug Snapshot
Diuretics Adrenergic blockers doxazosin

(Cardura) 282
Renin-angiotensin- enalapril (Vasotec) 277
aldosterone modifiers Direct-acting vasodilators hydralazine
(Apresoline) 283
Calcium channel blockers nifedipine (Adalat CC,
Procardia XL) 279
Learning Outcomes
1. Explain how hypertension is defined and blood volume on blood 7. Describe general principles that
and classified. pressure. guide the selection of specific
2. Identify the long-term consequences 5. Discuss nervous and hormonal medications for hypertension.
of untreated hypertension. factors that influence blood 8. For each of the classes listed in the
3. Describe how the pumping action pressure. Drug Snapshot, identify representative
of the heart creates blood pressure. 6. Discuss the role of positive lifestyle drugs and explain their mechanisms
changes in the management of of drug action, primary actions, and
4. Explain the effects of cardiac important adverse effects.
output, peripheral resistance, hypertension.
266 Chapter 18 Drugs for Hypertension
Key Terms
aldosterone (al-DOH-stair-own) 274 diastolic pressure (DEYE-ah-stall-ik) 267 lumen (LOO-men) 269
angiotensin II (AN-geo-TEN-sin) 274 diuretics (deye-your-ET-ik) 269 orthostatic hypotension (or-tho-STAT-ik)
angiotensin-converting enzyme (ACE) electrolytes (ee-LEK-troh-lites) 273 282
(angeo-TEN-sin) 274 false neurotransmitter (NYUR-oh-TRANS- peripheral resistance (per-IF-ur-ul) 269
antidiuretic hormone (ADH) (ANT-eye- mitt-ur) 282 reflex tachycardia (ta-kee-CAR-dee-ah)
deye-your-ET-ik) 270 hyperkalemia (heye-purr-kah-LEE-mee- 270
baroreceptors (BARE-oh-ree-sep- ah) 274 renin-angiotensin-aldosterone system
tours) 270 hypertension (HTN) (heye-purr-TEN-shun) (RAAS) (REN-in–an-geo-TEN-sin-al-
bradycardia (bray-dee-KAR-DEE-ah) 282 266 DOS-ter-own) 274
calcium channel blockers (CCBs) 278 hypokalemia (heye-poh-kah-LEE-mee-ah) systolic pressure (SIS-tol-ik) 267
cardiac output 269 274 vasomotor center (VAZO-mo-tor) 270
C ardiovascular disease, which includes all conditions affecting the heart and blood vessels, is the
most common cause of death in the United States. Hypertension (HTN), or high blood pressure,
is the most common of the cardiovascular diseases. Because healthcare providers encounter nu-
merous patients with this disease, a firm grasp of the underlying principles of antihypertensive therapy
is critical. By improving public awareness of HTN and teaching the importance of early intervention, the
healthcare provider can contribute significantly to reducing cardiovascular mortality.
Hypertension is characterized by the consistent elevation of arterial

core concept 18.1 blood pressure.
hyper =high Hypertension (HTN) is defined as the consistent elevation of arterial blood pressure. A patient is said to
tension = pressure have chronic HTN if he or she presents with a sustained systolic blood pressure of greater than 140 mmHg
or diastolic pressure of greater than 90 to 99 mmHg after multiple measurements are made over several
clinic visits.
Many attempts have been made to further define HTN, with the goal of developing guidelines for
treatment. The National High Blood Pressure Education Program Coordinating Committee of the National
Heart, Lung, and Blood Institute of the National Institutes of Health has issued guidelines for treating
HTN that have become well accepted in the medical community. The committee classified HTN into three
categories—prehypertension, Stage 1, and Stage 2. The recommendations from Committee Report JNC-7
are summarized in Table 18.1 ◆. In addition to measurements of blood pressure, the classification of HTN
also considers compelling conditions that have been shown to worsen the health outcomes for people
with untreated HTN. These include heart failure, post-myocardial infarction, high risk for coronary artery
disease, diabetes, chronic kidney disease, and previous stroke.
Blood pressure changes throughout the life span, gradually and continuously rising from child-
hood through adulthood. What is considered normal blood pressure at one age may be considered
abnormal in someone older or younger. HTN has the greatest impact on older adults, affecting
approximately 30% of those older than 50 years, 64% of men older than age 65, and 75% of women
older than age 75.
Table 18.1 Classification and Management of Hypertension in Adults

Systolic/Diastolic Initial Antihypertensive Therapy
Blood Pressure Blood Pressure
Classification (mmHg) Without Compelling Indication* With Compelling Indication*
Normal 119/79 or lower No antihypertensive indicated No antihypertensive indicated
Prehypertension 120–139/80–89 — —
Stage 1 Hypertension 140–159/90–99 Thiazide diuretic (for most patients) Other antihypertensives, as needed
Stage 2 Hypertension 160 or higher/100 or higher Two-drug combination antihypertensive —
(for most patients)
*Compelling conditions include: heart failure, postmyocardial infarction, high risk for coronary artery disease, diabetes, chronic kidney disease, and
recurrent stroke prevention.
Source: National High Blood Pressure Education Program National Heart, Lung, and Blood Institute. (2003). JNC-7 Express: The Seventh Report of the
Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.
Failure to treat hypertension can lead to stroke, heart failure, or

myocardial infarction. core concept 18.2
HTN is a complex disease that is caused by a combination of genetic and environmental factors. In 90% of
the patients with HTN, no specific cause for the elevated blood pressure can be identified. This type of HTN
is called primary or essential. Although the actual cause of primary HTN may not be known, many conditions
or risk factors are associated with the disease. Advanced age and weight gain, particularly around the hips and
thighs, tends to be associated with HTN. The disease is most prevalent in blacks and least prevalent in Mexican
Americans. Men in all ethnic groups experience more HTN compared to women. The disease also has a heredi-
tary component, with family members of patients with HTN having greater risk of acquiring the disease than
nonfamily members. Other factors, such as tobacco use and high-fat diets, clearly contribute to the disease.
In 10% of patients, a specific cause of the HTN can be identified. This is called secondary hyperten-
sion. Certain diseases, such as Cushing’s syndrome, hyperthyroidism, and chronic renal disease, cause
elevated blood pressure. Certain drugs are also associated with HTN, including corticosteroids, oral con-
traceptives, and epoetin alfa (Epogen). The therapeutic goal for secondary HTN is to treat or remove the
underlying condition that is causing the blood pressure elevation. In many cases, correcting this underlying
condition will cure the associated HTN.
Because chronic HTN may produce no identifiable symptoms for as long as 10 to 20 years, many
people are not aware of their condition. Convincing patients to control their diets, spend money on medica-
tion, and take drugs on a regular basis when they are feeling healthy is a difficult task for the healthcare
provider. Failure to control HTN, however, can result in serious consequences. Prolonged high blood pres-
sure can lead to accelerated narrowing of the arteries, resulting in strokes, kidney failure, and even cardiac
arrest. One of the most serious consequences of chronic HTN is that the heart must work harder to pump
blood to organs and tissues. This excessive workload can cause the heart to fail and the lungs to fill with
fluid, a condition known as heart failure (HF). Drug therapy of HF is covered in Chapter 19.
The death rate from cardiovascular-related diseases has dropped significantly over the past 30 years
because of the improved diagnosis and treatment of HTN, as well as the acceptance of healthier lifestyle
habits. Early treatment is essential; the long-term cardiovascular damage caused by HTN is irreversible if
the disease is allowed to progress unchecked.
Blood pressure is caused by the pumping action of the heart. core concept 18.3
Although pressure can be measured in nearly any vessel in the body, the term blood pressure commonly
refers to the pressure in the large arteries. Because the pumping action of the heart is the source of blood
pressure, those arteries closest to the heart, such as the aorta, have the highest pressure. Pressure decreases
gradually as the blood travels farther from the heart, until it falls close to zero in the largest veins. This is
When the ventricles of the heart contract and eject blood, the pressure created in the arteries is called
systolic pressure. When the ventricles relax and the heart temporarily stops ejecting blood, pressure in the
arteries will fall, and this results in diastolic pressure. Blood pressure is measured in units of millimeters
of mercury, abbreviated as mmHg. (Hg is the chemical symbol for the element mercury.) The average
normal systolic pressure in a healthy adult is considered to be less than 120 mmHg, whereas the average
normal diastolic pressure is less than 80 mmHg. The systolic and diastolic pressures are usually measured
and reported together, with the systolic given first. For example, average normal blood pressure is said to
be less than 120/80 mmHg. Figure 18.2 ■ illustrates how the pumping action of the heart determines sys-
tolic and diastolic blood pressure.
Fast Facts Hypertension

■ High blood pressure affects more than 70 million U.S. adults, or approximately one in three Americans.
■ Among people with HTN, more than 28% do not realize they have the condition.
■ African American men have the highest rate of HTN.
■ Approximately 65% of Americans diagnosed with HTN do not have their condition under adequate
control.
■ HTN is the most common complication of pregnancy.
■ Prehypertension (120–139/80–89 mmHg) affects over 20% of the adult population, almost 45 million
people.
■ Approximately 54,000 Americans die of HTN per year; it is a contributing factor in 300,000 addi-
tional deaths each year.
Figure 18.1
Blood pressure changes Vena cavae Aorta

throughout the
circulation. 7 mm 120 mm
Large veins Large arteries
16 mm 100 mm
16 90
mm Heart mm
Small veins Small arteries
20
m
m
m
m
50
Venules Arterioles
Capillaries
Figure 18.2
Aorta
Aorta
Peripheral Peripheral
resistance resistance
120 mm 80 mm
Cardiac
output
Arterioles Arterioles
Valve open Valve closed
(a) Systolic (b) Diastolic
(a) Systolic pressure occurs when the heart ejects blood, creating high pressure in the arteries.
(b) Diastolic pressure occurs when the heart relaxes, resulting in less pressure in the arteries.
The primary factors responsible for blood pressure are cardiac output,
the resistance of the small arteries, and blood volume. core concept 18.4
In order to understand how drugs affect blood pressure, the student must have an excellent knowledge of
cardiovascular physiology. Investing time to understand the details of how this system functions will reap
great rewards later when studying the cardiovascular and respiratory drugs.
Although many factors can influence blood pressure, three factors are truly responsible for determin-
ing the pressure. The three primary factors—cardiac output, peripheral resistance, and blood volume—are
The volume of blood pumped per minute is called the cardiac output. Although resting cardiac out-
put is approximately 5 liters per minute (L/min), strenuous exercise can increase this output to as much as
35 L/min. This is important to pharmacology because drugs that change the cardiac output have the poten-
tial to influence a patient’s blood pressure. It is important to remember that the higher the cardiac output,
the higher the blood pressure.
As blood flows at high speeds through the vascular system, it bumps and drags across the walls
of the vessels. Although the vessel walls are extremely smooth, this friction reduces the velocity of the
blood. This dragging or friction in the arteries is called peripheral resistance. Arteries have smooth
muscle in their walls that, when constricted, will cause the inside diameter or lumen to become smaller,
thus creating more resistance and higher pressure. This is how the body controls normal minute-by-min-
ute changes in blood pressure. This is also important to pharmacology because a number of drugs affect
vascular smooth muscle, causing vessels to constrict, thus raising blood pressure. Other drugs cause the
smooth muscle to relax, thereby opening the lumen and lowering blood pressure. These drugs are among
those used to treat HTN. The role of the autonomic nervous system in controlling peripheral resistance is
presented in Chapter 8.
The third factor responsible for blood pressure is the total amount of blood in the vascular system, or
blood volume. Although the average person maintains a relatively constant blood volume of approximately
5 L, this can change as a result of certain regulatory factors and with certain disease states. More blood in
the vascular system will exert additional pressure on the walls of the arteries and raise blood pressure. For
example, high sodium diets cause water to be retained by the body, thus increasing blood volume and rais-
ing blood pressure. On the other hand, drugs called diuretics can cause fluid loss through urination, thus
decreasing blood volume and lowering blood pressure. Diuretics are discussed later in this chapter and
were presented in Chapter 17.
Many nervous and hormonal factors help to keep blood pressure within
normal limits. core concept 18.5
It is critical that the body maintains a normal range of blood pressure and that it has the ability to safely and
rapidly change pressure as it proceeds through daily activities, such as sleep and exercise. Too little blood
pressure can cause dizziness and lack of urine formation, whereas too much pressure can cause vessels
to rupture. A diagram explaining how the body maintains homeostasis during periods of blood pressure
change is shown in Figure 18.4 ■
Figure 18.3
Blood pressure
Peripheral resistance/
Blood volume Cardiac output
diameter of arterioles
Primary factors affecting blood pressure.

Figure 18.4
Blood pressure is
controlled by the Blood pressure
actions of the cardio-
vascular system and
kidneys.
Compensatory action by Compensatory action

cardiovascular system by kidneys
Vasodilation Stroke volume Heart rate Urine output
Cardiac output Blood volume
Blood pressure
returns to normal
Blood pressure is regulated on a minute-to-minute basis by a cluster of neurons in the medulla ob-
longata called the vasomotor center. Nerves travel from the vasomotor center to the arteries, where the
smooth muscle is directed to either constrict (raise blood pressure) or relax (lower blood pressure).
Receptors in the aorta and the carotid artery act as sensors to provide the vasomotor center with
baro 5 pressure vital information on current conditions in the vascular system. Some of these neurons, called barorecep-
receptor 5 sensor tors, have the ability to sense blood pressure within these large vessels. The baroreceptors are impor-
tant to the pharmacotherapy of HTN. When a drug is given to lower blood pressure, the baroreceptors
respond by trying to return pressure to its original (high) level. The baroreceptor response includes an
tachy = rapid immediate increase in heart rate, known as reflex tachycardia. In time, the body will recognize the
cardia = heart lower blood pressure as normal, “reset” the baroreceptors, and reflex tachycardia will diminish. If reflex
tachycardia does not decrease, a patient may be administered a beta-adrenergic blocker to prevent heart
rate increase.
Emotions can also have a profound effect on blood pressure. Anger and stress can cause blood pres-
sure to rise, whereas mental depression and lethargy may cause it to fall. Strong emotions, if present for a
long time, may be important contributors to chronic HTN.
A number of hormones and other agents affect blood pressure on a daily basis. When given as medi-
cations, some of these agents may have a profound effect on blood pressure. For example, an injection of
anti 5 against epinephrine or norepinephrine will immediately raise blood pressure. Antidiuretic hormone (ADH) is a
diuretic 5 urination strong vasoconstrictor that can increase blood pressure by raising blood volume. The renin-angiotensin-
aldosterone system is particularly important in the pharmacotherapy of HTN and is discussed in core con-
cept 18.9. A summary of the various nervous and hormonal factors influencing blood pressure is shown in
Figure 18.5 ■.
Concept Review 18.1

■ Because hypertension may cause no symptoms, how would you convince a patient to take
his or her medication regularly?
Figure 18.5
Hormonal and nervous

factors influencing
blood pressure.
ine ne
hr
ep hri
nep
No in
pi
Ep
re
Adrenal
Vasomotor center
Nore
gland
in medulla
pine
phrin
e
Aldosterone
+
+ es
iol
ter
Angiotensin II
Ar
(lungs)
+
Angiotensin I
ADH
(liver)
ADH Renin
Baroreceptors Hypothalamus Kidney
+ = Vasoconstriction Changes in
blood volume
Positive lifestyle changes can reduce blood pressure and lessen the need
for medications. core concept 18.6
When a patient is first diagnosed with HTN, the healthcare provider obtains a comprehensive medical his-
tory to determine if the disease can be controlled without medications. Positive lifestyle changes should be
recommended for all patients with prehypertension or HTN. Of great importance is maintaining optimum
weight, because obesity is closely associated with blood lipid elevation and HTN. Combining a safe weight Life Span Fact
loss program with proper nutrition can delay the progression from prehypertension to HTN.
Control of blood pressure
In many cases, implementing positive lifestyle changes may eliminate the need for pharmacotherapy is particularly important in
altogether. Even if pharmacotherapy is required, it is important that the patients continue these lifestyle older adults. Age often causes
modifications so that dosages can be minimized. Because all blood pressure medications have potential ad- blood vessels to be less elastic,
verse effects, it is important that patients attempt to control their disease through nonpharmacologic means thus impairing their ability to
to the greatest extent possible. Important nonpharmacologic methods for controlling HTN are as follows: dilate or constrict with activi-
ties of daily living. Healthcare
■ Implement a medically supervised, safe weight-reduction plan, if 20% or more over normal providers should emphasize to
body weight. their older adult patients the
importance of blood pressure
■ Stop using tobacco. monitoring and control.
■ Restrict salt (sodium) intake and eat foods rich in potassium and magnesium.
■ Limit alcohol consumption.
■ Implement a medically supervised aerobic exercise plan.
■ Reduce sources of stress and learn to implement coping strategies.
Selection of specific antihypertensive drugs depends on the severity of

core concept 18.7 the disease.
The goal of antihypertensive therapy is to reduce blood pressure to normal levels so that the long-term
consequences of HTN may be prevented. Keeping blood pressure within normal limits has been shown to
reduce the risk of HTN-related diseases, such as stroke and heart failure. Several therapeutic strategies are
used to achieve this goal, as summarized in Figure 18.6 ■.
Figure 18.6
Mechanism of action of
antihypertensive drugs.
Alpha2 agonists
Decrease sympathetic
Brain impulses from the CNS to
the heart and arterioles,
causing vasodilation
Arterioles
a2
Alpha1 blockers
Inhibit sympathetic
activation in
2 arterioles, causing
vasodilation
Sympathetic a1
nervous system
2
Direct vasodilators
2
Act on the smooth
muscle of arterioles,
Beta blockers b1
Decrease the heart Ca21
rate and myocardial
contractility, 2 Calcium channel
reducing cardiac
blockers
output
2 Block calcium ion
channels in arterial
smooth muscle,
Heart
causing
vasodilation
Angiotensin
receptor blockers
Prevent angiotensin
II from reaching its
receptors, causing
Angiotensin II
vasodilation
Renin
Kidney
ACE inhibitors
Diuretics Block formation of angiotensin II, causing
Increase urine output and vasodilation, and block aldosterone
decrease fluid volume secretion, decreasing fluid volume
– = Inhibitory Effect
The pharmacologic management of HTN is individualized to the patient’s risk factors, comorbid med-
ical conditions, and degree of blood pressure elevation. Patient responses to antihypertensive medications
vary widely because of the many complex genetic and environmental factors affecting blood pressure. A
large number of antihypertensive drugs are available, and choice of therapy is often based on the experi-
ence of the healthcare provider. Although antihypertensive treatment varies, there are several principles
that guide pharmacotherapy.
Pharmacotherapy usually begins with low doses of a single antihypertensive medication. The patient
is reevaluated after an appropriate time interval, when, if necessary, the prescriber may increase the dose
of the initial drug or substitute another antihypertensive drug from a different drug class. The following are
considered primary antihypertensive drug classes:
■ Diuretics
■ Renin-angiotensin-aldosterone inhibitors
■ Calcium channel blockers (CCBs)
■ Beta-adrenergic blockers
The JNC-7 report recommends thiazide diuretics as the initial drugs for mild to moderate HTN.
atients with a compelling condition, however, may benefit from a second drug, either in combination
P
with the diuretic or in place of the diuretic. The use of two drugs from different classes often produces an
additive reduction in blood pressure. Another advantage of this approach is that it allows lower doses of
each drug than would be needed if a single one were used. Lower doses usually produce fewer side effects,
which improves patient adherence to therapy. However, adherence decreases when patients need to take
more than one drug or when they need to take them more often. For convenience, drug manufacturers often
combine two drugs into a single pill or capsule. The diuretic hydrochlorothiazide (Microzide) is the most
common drug used in combination antihypertensive products. Examples of antihypertensive combination
drugs include Diovan HCT (hydrochlorothiazide and valsartan), Zestoretic (hydrochlorothiazide and lisin-
opril), and Lotrel (benazepril and amlodipine).
Certain antihypertensive classes cause more frequent or serious adverse effects and are generally pre-
scribed only when first-line medications do not produce a satisfactory response. The alternative antihyper-
tensive drug classes include the following:
■ Alpha1-adrenergic blockers
■ Alpha2-adrenergic agonists (centrally-acting agents)
■ Direct-acting vasodilators
In designing outcomes for patients with HTN, special attention should be placed on African Americans
with this disorder. The incidence of HTN is significantly higher in African Americans than in other ethnic
groups, and aggressive antihypertensive therapy may be necessary to manage the disorder. Some physi-
cians recommend initiating therapy with two drugs to ensure adequate response. Based on clinical trials in
African Americans, the Food and Drug Administration (FDA) recently approved BiDil, a fixed-dose com-
bination of isosorbide dinitrate and hydralazine that appears to be particularly effective at lowering blood
pressure in this population.
Diuretics are often preferred drugs for treating mild to moderate

hypertension. core concept 18.8
Diuretics act by increasing the amount of urine produced by the kidneys. They are widely used in the
treatment of HTN, HF, and fluid balance disorders. Diuretics were presented in detail in Chapter 17, and
prototype drug features for hydrochlorothiazide (Microzide), furosemide (Lasix), and spironolactone
(Aldactone) are included in that chapter. This section focuses on the role of diuretics in treating hyperten-
sion. Table 18.2 ◆ lists diuretics commonly used to treat HTN.
Diuretics were the first widely prescribed class of drugs used to treat HTN in the 1950s. Despite many
advances in drug therapy since then, diuretics are still considered drugs of first choice because they pro-
duce few adverse effects and are very effective at controlling mild to moderate HTN. For more advanced
disease, they are prescribed in combination with antihypertensive medications from other classes.
Although many different diuretics are available for HTN, all produce a similar outcome: the reduction
of blood volume through the urinary excretion of water and electrolytes. Electrolytes are ions such as so-
dium (Na+), calcium (Ca2+), chloride (Cl–), and potassium (K+). The mechanisms by which diuretics reduce
blood volume differ among the various diuretics. Differences among the diuretic classes are presented in
Chapter 17.
A common adverse effect of diuretic therapy is dehydration, the excessive loss of water from de 5 without or absence of
the body. Early signs of dehydration include thirst, dry mouth, dizziness, lethargy, and a fall in blood hydra 5 water
pressure. tion 5 condition
Table 18.2 Diuretics for Hypertension

amiloride (Midamor) PO; 5–10 mg/day (max: 20 mg/day) Potassium sparing type
bumetanide (Bumex) PO; 0.25–2 mg once daily (max: 10 mg/day) Loop diuretic type; decreases blood potassium
levels; IV and IM forms available
chlorothiazide (Diuril) PO/IV; 250 mg–1 g/day in one or two divided Thiazide type; decreases blood potassium levels
doses (max: 2 g/day)
chlorthalidone (Thalitone) PO; 12.5–25 mg daily (max: 50 mg/day) Thiazide type; decreases blood potassium levels
eplerenone (Inspra) PO; 25–50 mg once daily (max: 100 mg/day) A newer potassium-sparing diuretic
furosemide (Lasix) (see page 254 for the PO; 20–80 mg/day (max: 600 mg/day) Loop diuretic type; decreases blood potassium
Drug Prototype box) levels; IV and IM forms available
hydrochlorothiazide (Microzide) (see page PO; 25–100 mg in one to two divided doses Thiazide type; decreases blood potassium levels
255 for the Drug Prototype box) (max: 200 mg/day)
indapamide (Lozol) PO; 2.5–5 mg daily (max: 5 mg/day) Similar to thiazide type; decreases blood
potassium levels
spironolactone (Aldactone) (see page 256 PO; 25–100 mg 1–2 times/day (max: 400 mg/day) Potassium-sparing type
torsemide (Demadex) PO/IV; 10–20 mg/day (max: 200 mg/day) Loop diuretic type; decreases blood potassium
levels
triamterene (Dyrenium) PO; 50–100 mg bid (max: 300 mg/day) Potassium sparing type
Electrolyte imbalances of potassium, sodium, and magnesium ions are additional adverse effects of
Life Span Fact diuretic therapy. Loss of K+, or hypokalemia, is of particular concern because it can lead to serious ab-
Older adults are especially at normalities in cardiac rhythm. When taking thiazide or loop diuretics, patients should be encouraged to
risk for dehydration and must include a potassium supplement or to eat foods rich in potassium content, such as bananas, oranges, toma-
be carefully monitored during toes, milk, salmon, and beef.
the initial stages of diuretic Certain diuretics such as spironolactone (Aldactone) have fewer tendencies to cause K+ depletion,
therapy. and, for this reason, are called potassium-sparing diuretics. Taking potassium supplements with potas-
hyper 5 high sium-sparing diuretics may lead to dangerously high K+ levels in the blood, or hyperkalemia, which can
hypo 5 low cause cardiac conduction abnormalities.
ka 5 potassium
emia 5 blood
Concept Review 18.2
■ State the major reasons why patients should continue lifestyle changes even though their
antihypertensive drugs appear to be effective.
Blocking the renin-angiotensin-aldosterone system leads to a decrease

core concept 18.9 in blood pressure.
The renin-angiotensin-aldosterone system (RAAS) is one of the primary homeostatic mechanisms con-
trolling blood pressure and fluid balance in the body. Drugs that modify the RAAS decrease blood pressure
and increase urine output. They are widely used in the treatment of HTN, HF, and MI. Table 18.3 ◆ lists
the RAAS modifiers commonly used to treat HTN.
Renin is an enzyme secreted by specialized cells in the kidneys when blood pressure falls or when
angio = vessels there is a decrease in Na+ flowing through the kidney tubules. In a series of enzymatic steps, angiotensin II,
tensin =pressure one of the most potent natural vasoconstrictors known, is formed. The enzyme responsible for the final step
of this pathway is called angiotensin-converting enzyme (ACE). The intense vasoconstriction of arteri-
oles caused by angiotensin II raises blood pressure by increasing peripheral resistance.
A second, equally important effect of angiotensin II is stimulation of the secretion of aldosterone, a
hormone from the adrenal gland that increases Na+ reabsorption in the kidney. The enhanced Na+ reabsorp-
tion causes the body to retain water, which raises blood volume and increases blood pressure. Drugs that
inhibit the RAAS block the effects of angiotensin II, thus decreasing blood pressure through two mecha-
nisms: dilating arteries and decreasing blood volume.
First detected in the venom of pit vipers in the 1960s, drugs that inhibit ACE have been approved for
hypertension since the 1980s. Since then, the ACE inhibitors have become important drugs in the treatment
of HTN. ACE inhibitors are preferred drugs for patients with both diabetes and HTN because they have
Table 18.3 ACE Inhibitors and Angiotensin-Receptor Blockers for Hypertension

Drug Route and Adult dose Remarks
Ace Inhibitors
benazepril (Lotensin) PO; 10–40 mg in one to two divided doses May be used in combination with thiazide
(max: 40 mg/day) diuretics
captopril (Capoten) PO; 6.25–25 mg tid (max: 450 mg/day) Also for HF
enalapril (Vasotec) PO; 5–40 mg in 1–2 divided doses Also for HF; IV form available
(max: 40 mg/day)
fosinopril (Monopril) PO; 5–40 mg daily (max: 80 mg/day) Also for HF
lisinopril (Prinivil, Zestril) (see page 292 for PO; 10 mg daily (max: 80 mg/day) Also for HF
moexipril (Univasc) PO; 7.5–30 mg daily (max: 30 mg/day) Approved for HTN only
perindopril (Aceon) PO; 4 mg once daily (max: 16 mg/day) Also for HF, stable angina, and post MI
therapy
quinapril (Accupril) PO; 10–20 mg daily (max: 80 mg/day) Also for HF
ramipril (Altace) PO; 2.5–5 mg daily (max: 20 mg/day) Also for HF, stroke prophylaxis and post-MI
therapy
trandolapril (Mavik) PO; 1–4 mg daily (max: 8 mg/day) Also for post-MI therapy
Angiotensin-Receptor Blockers
azilsartan (Edarbi) PO; 40–80 mg once daily Approved for HTN only. Newer drug in this
class
candesartan (Atacand) PO; start at 16 mg/day (max: 32 mg/day) Also for HF
eprosartan (Teveten) PO; 600 mg/day or 400 mg qid–bid (max: Approved for HTN only
800 mg/day)
irbesartan (Avapro) PO; 150–300 mg/day (max: 300 mg/day) Approved for HTN only; Maximum effect may
take 6–12 weeks
losartan (Cozaar) PO; 25–50 mg in one to two divided doses Approved for HTN only
(max: 100 mg/day)
olmesartan (Benicar) PO; 20–40 mg/day (max: 40 mg/day) Approved for HTN only
telmisartan (Micardis) PO; 40–80 mg/day (max: 80 mg/day Approved for HTN only
valsartan (Diovan) PO; 80 mg/day (max: 320 mg/day) Also for HF
been shown to reduce the progression of kidney failure that often occurs in patients with diabetes. Because
of cardiovascular changes associated with diabetes, these patients often require therapy with at least two
antihypertensive drugs. Adverse effects of ACE inhibitors are relatively minor and include persistent dry
cough and hypotension following the first dose of the drug. Though rare, the most serious adverse effect
of ACE inhibitors is the development of angioedema, an intense swelling around the lips, eyes, throat, and
other body regions. In advanced cases, angioedema may lead to airway closure due to serious swelling in
the neck. When angioedema does occur, it most often develops within hours or days after beginning ACE
inhibitor therapy.
A second method of modifying the RAAS is blocking the action of angiotensin II after it is formed.
This class of drugs is called the angiotensin-receptor blockers (ARBs). These drugs, which include irbesar-
tan (Avapro), losartan (Cozaar), and valsartan (Diovan), block the receptors for angiotensin II in arteriolar
smooth muscle and in the adrenal gland, thus causing blood pressure to fall. Their actions of arteriolar
dilation and increased renal Na+ excretion are quite similar to those of the ACE inhibitors. ARBs have
relatively few adverse effects, such as headache, dizziness, and facial flushing, most of which are related
to hypotension. Unlike the ACE inhibitors, they do not cause cough, and angioedema is rare. Drugs in this
class are usually combined with drugs from other classes; for example, the drug Hyzaar combines losartan
with the diuretic hydrochlorothiazide.
The newest method of modifying the RAAS is to inhibit the effects of renin itself. The direct renin
inhibitors prevent the formation of angiotensin I and II. Aliskiren (Tekturna) was the first drug marketed in
this class of antihypertensives. Pharmaceutical companies were quick to add aliskiren to other drugs to cre-
ate fixed-dose combination drugs containing hydrochlorothiazide (Tekturna HCT), amlodipine (Tekamlo),
and valsartan (Valturna). The most common adverse effects of aliskiren are diarrhea, cough, flu-like symp-
toms, and rash.
Nursing Process Focus Patients Receiving ACE Inhibitor Therapy

Prior to administration: ■ Risk for Injury related to orthostatic hypotension
■ Obtain a complete health history including cardiovascular conditions, ■ Deficient Knowledge related to a lack of information about drug
neurological status, any incidence of angioedema, allergies, drug his- therapy
tory, and possible drug interactions. ■ Ineffective Tissue Perfusion related to decreased blood volume
■ Acquire the results of a complete physical examination, including vital ■ Risk for Imbalanced Nutrition: More than body requirements related
signs, height weight and ECG (compare to previous baseline values.) to hyperkalemia
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, and ■ Noncompliance related to adverse effects of medications
renal and liver function studies.

The patient will:
■ Experience therapeutic effects (a reduction in systolic/diastolic blood pressure and normal electrolyte levels).
Implementation

■ Monitor for first-dose phenomenon of profound hypotension. ■ Warn the patient about the first-dose phenomenon; reassure that this
(First-dose phenomenon includes the relatively minor adverse effects effect diminishes with continued therapy.
of dry cough and hypotension.)
■ Monitor vital signs, especially blood pressure. (ACE inhibitors can cause Instruct the patient:
hypotension.) ■ To monitor blood pressure as specified by the healthcare provider and
ensure proper use of home equipment.
■ That changes in consciousness may occur due to rapid reduction in
blood pressure and to immediately report feelings of faintness.
■ That the drug takes effect in approximately one hour and peaks in
three to four hours.
■ To rest in the supine position beginning one hour after administration
and for three hours after the first dose.
■ To always rise slowly, avoiding sudden posture changes.
■ Monitor for changes in level of consciousness, dizziness, drowsiness, Instruct the patient to:
or lightheadedness. (Signs of decreased blood flow to the brain are ■ Report dizziness or fainting that persists beyond the first dose as well
due to the drug’s hypotensive action. Sudden fainting episodes are as unusual sensations (e.g., numbness and tingling) or other changes in
possible.) the face or limbs to the healthcare provider.
■ Contact the healthcare provider before the next scheduled dose of the
drug if fainting occurs.
■ Ensure patient safety. (Postural hypotension may cause dizziness, Instruct the patient to:
affecting the ability to perform normal activities.) ■ Obtain help prior to getting out of bed or attempting to walk alone.
■ Avoid driving or other activities that require mental alertness or
physical coordination until effects of the drug are known.
■ Observe for hypersensitivity reaction, particularly angioedema. Instruct the patient:
(Angioedema may arise at any time during ACE inhibitor therapy, but ■ To immediately report any difficulty breathing, throat tightness,
it is generally expected shortly after initiation of therapy.) muscle cramps, hives or rash, or tremors to the healthcare provider.
(These symptoms can occur as early as the first dose or much later
as a delayed reaction.)
■ That angioedema can be life threatening and to call emergency
medical services if severe dyspnea or hoarseness is accompanied by
swelling of the face or mouth.
■ Monitor for persistent dry cough, a possible adverse effect of the drug. Instruct the patient to:
Monitor changes in cough pattern. (This may indicate another disease ■ Expect persistent dry cough.
process.) ■ Report any change in the character or frequency of cough. (Any cough
accompanied by shortness of breath, fever, or chest pain should be
reported immediately to the healthcare provider because it may
indicate MI.)
■ Sleep with the head elevated if cough becomes troublesome when in
the supine position.
■ Use nonmedicated sugar-free lozenges or hard candies to relieve
cough.
continued . . .

■ Monitor for dehydration or fluid overload. (Dehydration causes low Instruct the patient to:
circulating blood volume and will exacerbate hypotension. Severe de- ■ Observe for signs of dehydration, such as oliguria, dry lips and mucous
hydration may trigger syncope and collapse.) membranes, or poor skin turgor.
■ Report any bodily swelling that leaves sunken marks on the skin when
pressed to the healthcare provider.
■ Measure and monitor fluid intake and output, and weigh daily.
■ Monitor increased need for fluids caused by vomiting, diarrhea, or ex-
cessive sweating.
■ Avoid excessive heat that contributes to sweating and fluid loss.
■ Consume adequate amounts of plain water.
■ Monitor for high potassium levels. (Hyperkalemia is a potentially life- Instruct the patient to:
threatening complication. Patients on ACE inhibitors should regularly ■ Immediately report any signs of hyperkalemia to the healthcare pro-
have blood tests to measure potassium levels.) vider: nausea, irregular heartbeat, profound fatigue/muscle weakness,
and slow or faint pulse.
■ Avoid consuming electrolyte-fortified snacks, or sports drinks that may
contain potassium.
■ Avoid using salt substitute (KCl) to flavor foods.
■ Consult the healthcare provider before taking any nutritional supple-
ments containing potassium.
■ Monitor for liver and kidney function. (ACE inhibitors are metabolized Instruct the patient to:
by the liver and excreted by the kidneys.) ■ Report signs of liver toxicity such as nausea; vomiting; anorexia; diar-
rhea; rash; jaundice; abdominal pain, tenderness, or distension; or
change in the color or character of stools to the healthcare provider.
■ Discontinue the drug immediately and contact the healthcare provider
if jaundice occurs.
■ Adhere to laboratory testing regimen as ordered by the healthcare
provider.
level of proper administration. (Some medications interact with other ■ That taking other antihypertensive drugs may increase risk for
medications.) hypotension.
■ Not to take medication with grapefruit juice.
■ To consult a healthcare provider before taking potassium supplements
or potassium-sparing diuretics.
■ That nonsteroidal anti-inflammatory drugs may reduce the actions of
ACE inhibitors.

Drug Prototype: Enalapril (Vasotec)

Therapeutic Class: Drug for hypertension and heart failure Pharmacologic Class: ACE inhibitor
Actions and Uses: Enalapril is one of the most common ACE fainting. Care must be taken because a rapid fall in blood
inhibitors prescribed for HTN. Unlike captopril, the first ACE pressure may occur following the first dose. Most drugs in
inhibitor to be marketed, enalapril has a prolonged half-life, this class cause a persistent, dry cough. Other adverse effects
which permits administration once or twice daily. Enalapril acts include headache and dizziness.
by reducing angiotensin II and aldosterone levels to produce a Thiazide diuretics increase the risk of excessive potassium
significant reduction in blood pressure, with few adverse effects. loss when used with enalapril. On the other hand, potassium-
Enalapril has effectiveness comparable to the thiazide diuretics sparing diuretics increase the risk of hyperkalemia when used
and the beta-adrenergic blockers. It may be used by itself or in with ACE inhibitors.
combination with other antihypertensives. Vaseretic is a fixed- Enalapril may induce lithium toxicity by reducing renal
dose combination of enalapril and hydrochlorothiazide. clearance of lithium. Nonsteroidal anti-inflammatory drugs
(NSAIDs) may reduce the effectiveness of ACE inhibitors.
Adverse Effects and Interactions: Unlike diuretics, ACE inhibitors
such as enalapril have little effect on electrolyte balance, and
unlike beta-adrenergic blockers, they cause few cardiac adverse
effects. Like other antihypertensive drugs, enalapril may cause Black Box Warning:
hypotension, especially when moving quickly from a supine Fetal injury and death may occur when ACE inhibitors or
to an upright position. This condition, known as postural or ARBs are taken during pregnancy. When pregnancy is de-
orthostatic hypotension, can cause lightheadedness and even tected, they should be discontinued as soon as possible.
Calcium channel blockers have emerged as important drugs in the

core concept 18.10 treatment of hypertension.
Calcium channel blockers (CCBs) comprise a group of drugs that are used to treat a number of cardiovas-
cular diseases, including angina pectoris, cardiac dysrhythmias, and HTN. When CCBs were first approved
for the treatment of angina in the early 1980s, it was quickly noted that a “side effect” of the drugs was
the lowering of blood pressure in patients with HTN. Although not usually prescribed as monotherapy for
chronic HTN, CCBs are useful in treating patients who are unresponsive to other antihypertensive classes,
such as elderly patients and blacks. Table 18.4 ◆ lists CCBs that are commonly used to treat HTN.
Contraction of a muscle is regulated by the amount of calcium ions inside the muscle cell. Muscular
contraction occurs when Ca2+ enters the cell through channels in the plasma membrane. CCBs block these
channels and prevent Ca2+ from entering the cell, thus inhibiting muscular contraction. At low doses, CCBs
cause vasodilation in arterioles, thus decreasing blood pressure. Some CCBs, such as nifedipine (Adalat
CC, Procardia XL), are selective for calcium channels in arterioles, whereas others, such as verapamil (Ca-
lan, Isoptin, others), affect channels in both arterioles and cardiac muscle. CCBs vary in their potency and
in the frequency and types of adverse effects produced. The use of CCBs in the treatment of dysrhythmias
and angina is discussed in Chapters 22 and 20, respectively.
Two CCBs, clevidipine (Cleviprex) and nicardipine (Cardene) are important drugs for treating pa-
tients with serious, life-threatening HTN. Clevidipine has an ultrashort half-life of one minute and is only
available by the IV route for hypertensive emergencies.
The high safety profile of CCBs has contributed to their popularity in treating HTN. Common adverse
effects related to their vasodilation action include headache, facial flushing, and dizziness. The CCBs that
affect the heart should be used cautiously in patients with preexisting cardiac disease.
Table 18.4 Calcium Channel Blockers for Hypertension

Drug Route And Adult Dose Remarks
amlodipine (Norvasc) PO; 5–10 mg once daily (max: Works primarily on peripheral circulation; reduces
10 mg/day) systolic, diastolic, and mean blood pressure; also for
angina
diltiazem (Cardizem, Cartia XT, PO; 120–240 mg daily or 20–120 mg Dilates coronary arteries; affects calcium channels in
Dilacor XR, others) (see page 309 bid both heart and blood vessels; extended-release and IV
for the Drug Prototype box) forms are available; also for angina and dysrhythmias
felodipine (Plendil) PO; 5–10 mg/day (max: 20 mg/day) Selective for calcium channels in blood vessels; also for
angina and HF
isradipine (DynaCirc) PO; 1.25–10 mg bid (max: 20 mg/day) Affects calcium channels in both heart and blood vessels;
also for angina
nicardipine (Cardene) PO; 20–40 mg tid (max: 120 mg/day) Selective for calcium channels in blood vessels; also for
PO (Sustained release): angina; IV form is available
30–60 mg bid
nifedipine (Adalat CC, PO; 10–20 mg tid (max: 180 mg/day) Selective for calcium channels in blood vessels; decreases
Procardia XL) PO (extended release); 30–60 mg peripheral vascular resistance, and increases cardiac output;
once daily also for angina
nisoldipine (Nisocor) PO; 10–20 mg bid (max: 60 mg/day) Structurally similar to nifedipine; affects calcium
channels in both the heart and blood vessels; also for
angina and HF
verapamil (Calan, Isoptin SR, others) PO; 40–80 mg tid (max: 480 mg/day) Affects calcium channels in both heart and blood
(see page 342 for the Drug Prototype PO (sustained release): 90–240 mg vessels; IV form available for specific dysrhythmias
box) 1–2 times/day
Drug Prototype: Nifedipine (Adalat CC, Procardia XL)

Therapeutic Class: Drug for hypertension and angina Pharmacologic Class: Calcium channel blocker
Actions and Uses: Nifedipine is a CCB prescribed for angina as Nifedipine may increase serum levels of digoxin, cimetidine,
well as for HTN. Nifedipine selectively blocks calcium channels and ranitidine, and increase the effects of warfarin, result-
in myocardial and vascular smooth muscle, including that in ing in increased partial thromboplastin time (PTT). It may also
the coronary arteries. This results in reduced oxygen demands increase the effects of fentanyl anesthesia, resulting in severe
by the heart, an increase in cardiac output, and a fall in blood hypotension and an increased need for fluids. Grapefruit juice
pressure. It is available as immediate-release capsules and as may enhance the absorption of nifedipine.
extended-release tablets (XL). Alcohol increases the vasodilating action of nifedipine and
can lead to a severe drop in blood pressure. Nicotine causes
Adverse Effects and Interactions: Adverse effects of nifedipine vasoconstriction, countering the desired effect of nifedipine.
are generally minor and related to vasodilation, such as Use with melatonin may increase blood pressure and
headache, dizziness, and flushing. Fast-acting forms of heart rate.
nifedipine can cause significant reflex tachycardia. To avoid
rebound hypotension, discontinuation of drug therapy should
occur gradually.
Nursing Process Focus Patients Receiving Calcium Channel Blocker Therapy

Prior to administration: ■ Ineffective Self-health Maintenance related to insufficient knowledge
■ Obtain a complete health history including cardiovascular, respiratory, of seriousness of disease and drug therapy regimen
neurological, renal and liver conditions, allergies, drug history, and ■ Deficient Knowledge related to a lack of information about drug
possible drug interactions. therapy unfamiliarity with medication information
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, and ■ Decreased Cardiac Output related to effects of drug therapy
renal and liver function studies. ■ Risk for Injury related to possible orthostatic hypotension
■ Acquire the results of a complete physical examination, including vital ■ Noncompliance related to adverse effects of medications
signs, height, weight, ECG, neurological status and signs of edema.

The patient will:
■ Experience therapeutic effects (reduction in systolic/diastolic blood pressure).
Implementation
■ Monitor vital signs and ECG. Obtain blood pressure readings in sitting, Instruct the patient to:
standing, and supine positions to monitor fluctuations in blood ■ Monitor vital signs as specified by the nurse, particularly the blood
pressure. (CCBs dilate the arteries, reducing blood pressure and pressure, ensuring proper use of home equipment.
possibly causing hypotension.) ■ Withhold medication for severe hypotensive readings as specified by
the nurse (e.g., “hold for levels below 88/50 mmHg”).
■ Immediately report palpitations or rapid heartbeat.
■ Observe for changes in level of consciousness, dizziness, fatigue, Instruct the patient to:
postural hypotension. (These adverse effects can be caused by ■ Report dizziness or lightheadedness to the healthcare provider.
vasodilation.) ■ Rise slowly from prolonged periods of sitting or lying down.
■ Observe for paradoxical increase in chest pain, angina symptoms, or ■ Inform patient to report chest pain or other angina-like symptoms
increase in heart rate. (These complaints may be related to severe immediately to the healthcare provider.
hypotension.)
■ Monitor for signs of HF. (CCBs can decrease myocardial contractility, ■ Instruct the patient to immediately report any severe shortness
increasing the risk of HF.) of breath, frothy sputum, profound fatigue, and swelling to the
healthcare provider. These may be signs of HF or fluid accumulation
in the lungs.
continued . . .

■ Monitor for fluid accumulation. Measure intake and output, and daily Instruct the patient to:
weights. (Edema is an adverse effect of some CCBs.) ■ Avoid excessive heat, which contributes to excessive sweating and
fluid loss.
■ Measure and monitor fluid intake and output, and weigh daily.
■ Consume enough plain water to remain adequately, but not overly,
hydrated.
■ Observe for hypersensitivity reaction. (Allergic responses may be life ■ Instruct the patient to immediately report difficulty breathing, throat
threatening.) tightness, hives or rash, muscle cramps, or tremors to the healthcare
provider.
■ Monitor liver and kidney function. (CCBs are metabolized in the liver Instruct the patient to:
and excreted by the kidneys.) ■ Report signs of liver toxicity to the healthcare provider: nausea, vom-
iting, anorexia, bleeding, severe upper abdominal pain, heartburn,
jaundice, or a change in the color or character of stools.
■ Report signs of renal toxicity to the healthcare provider: fever, flank pain,
changes in urine output, color, or character (cloudy, with sediment).
■ Adhere to laboratory testing regimens as ordered by the healthcare
provider.
■ Observe for constipation. May need to increase dietary fiber or admin- Advise the patient to:
ister laxatives. (CCBs may cause constipation.) ■ Maintain adequate fluid and fiber intake to facilitate stool passage.
■ Use a bulk laxative or stool softener, as recommended by the health-
care provider.
■ Ensure patient safety. Monitor ambulation until response to the drug ■ Instruct the patient to avoid driving or other activities that require
is known. (Some CCBs may cause drowsiness.) mental alertness or physical coordination until the effects of the drug
are known.
level of proper administration. (Some medications interact with other ■ That taking other antihypertensive drugs may increase risk for
medications.) hypotension.
■ To avoid rebound hypotension, this drug should be discontinued
gradually
■ Not to take nifedipine with grapefruit juice because it may enhance
absorption.
■ That alcohol potentiates vasodilating action of nifedipine
CAM Therapy
Grape Seed Extract for Hypertension
Grapes and grape seeds have been used to enhance wellness for thousands of years. Their
primary use has been for cardiovascular conditions such as HTN, high blood cholesterol, ath-
erosclerosis, and to generally improve circulation. Some claim that grape seed extract im-
proves wound healing, prevents cancer, and lowers the risk for the long-term consequences
of diabetes.
The grape seeds, usually obtained from winemaking, are crushed and placed into tablet,
capsule, or liquid forms. Grape seed extract has antioxidant properties. In general, antioxidants
improve wound healing and repair cellular injury. Preliminary evidence suggests that it may
have some benefit in repairing blood vessel damage that could lead to atherosclerosis and
HTN. Controlled, long-term studies on the effects of grape seed extract on HTN have not been
conducted. It has few adverse effects, but caution should be used if taking anticoagulant
drugs because increased bleeding may result. Overall, the benefits of grape seed extract are
no different than those of a diet balanced with natural antioxidants and an occasional glass
of red wine.
Adrenergic blockers are commonly used to treat hypertension. core concept 18.11
Stimulation of the sympathetic division of the autonomic nervous system causes “fight-or-flight” responses
such as faster heart rate, an increase in blood pressure, and bronchodilation. By blocking the sympathetic
fight-or-flight responses, adrenergic drugs can cause the heart rate to slow, blood pressure to decline, and
the bronchi to dilate. Adrenergic antagonists (or blockers) that are important in managing HTN are listed
in Table 18.5 ◆.
Because of their beneficial effects on the heart and vessels, adrenergic blockers are used for a wide
variety of cardiovascular disorders. These drugs can block the effects of the sympathetic division through a
number of different mechanisms, although they all have in common the effect of lowering blood pressure.
These mechanisms include the following:
■ Blockade of alpha1-receptors in the arterioles
■ Blockade of beta1-receptors in the heart
■ Nonselective blockade of both beta1- and beta2-receptors
■ Stimulation of alpha2-adrenergic receptors in the brainstem (centrally acting)
Table 18.5 Adrenergic Blockers and Central-Acting Drugs for Hypertension

acebutolol (Sectral) PO; 400–800 mg/day (max: 1200 mg/day) Selective beta1-blocker; also for premature ventricular
beats
atenolol (Tenormin) (see page 309 PO; 25–50 mg/day (max: 100 mg/day) Selective beta1-blocker; IV form available for MI; monitor
for the Drug Prototype box) apical pulse prior to administration
betaxolol (Kerlone) PO; 10–40 mg/day (max: 40 mg/day) Selective beta1-blocker; approved for HTN only; discontinue
drug gradually to avoid
rebound HTN
bisoprolol (Zebeta) PO; 2.5–5 mg daily (max: 20 mg/day) Selective beta1-blocker; also for angina;
discontinue the drug gradually to avoid
rebound HTN
carvedilol (Coreg) (see page 296 PO; 6.25 mg bid (max: 50 mg/day) Blocks both alpha and beta receptors; also for HF
clonidine (Catapres) PO; 0.1 mg bid–tid (max: 0.8 mg/day) Central-acting alpha2-adrenergic drug; transdermal
patch available; epidural infusion form available for
management of cancer pain
doxazosin (Cardura) PO; 1 mg at bedtime; may increase to Selective alpha1-blocker; also for benign prostatic
16 mg/day in one to two divided doses hyperplasia (BPH)
(max: 16 mg/day)
methyldopa (Aldomet) PO; 250 mg bid or tid (max: 3 g/day) Central-acting alpha2-adrenergic drug; IV form available;
lowers standing and supine blood pressure
metoprolol (Lopressor, Toprol) PO; 50–100 mg daily or bid (max: Selective beta1-blocker; sustained-release and IV forms
450 mg/day) available; also for angina and MI
nadolol (Corgard) PO; 40 mg/day (max: 320 mg/day) Nonselective beta blocker; also for angina
pindolol (Visken) PO; 5 mg bid (max: 60 mg/day) Nonselective beta1- and beta2-blocker; for HTN only
prazosin (Minipress) (see page 100 PO; 1 mg at bedtime; increase to Selective alpha1-blocker used in combination with other
for the Drug Prototype box) 1 mg bid–tid (max: 20 mg/day) antihypertensives; also for BPH, Raynaud’s disease, and
pheochromocytoma
propranolol (Inderal, InnoPran XL) PO; 40 mg bid but may be increased to Nonselective beta1- and beta2-blocker; also for angina, MI,
(see page 340 for the Drug 160–480 mg/day in divided doses dysrhythmias, and migraine prophylaxis; IV form available
Prototype box) (max: 480 mg/day)
Terazosin (Hytrin) PO; 1 mg at bedtime; increase 1–5 mg/day Selective alpha1-blocker; also for BPH
(max: 20 mg/day)
timolol (Betimol, Timoptic, PO; 10 mg bid (max: 60 mg/day) Nonselective beta1- and beta2-blocker; also for MI and mi-
others) (see page 604 for graine prophylaxis and for glaucoma
Drug Prototype: Doxazosin (Cardura)

Therapeutic Class: Drug for hypertension and BPH Pharmacologic Class: Alpha1-adrenergic blocker
Actions and Uses: Doxazosin is an adrenergic blocker available Adverse Effects and Interactions: When starting doxazosin
only in oral form. Because it is selective for blocking alpha1- therapy, some patients experience orthostatic hypotension,
receptors in vascular smooth muscle, it has few adverse effects although tolerance normally develops to this adverse effect
on other autonomic organs and is sometimes preferred over after a few doses. Dizziness and headache are also common
nonselective beta blockers such as propranolol. Doxazosin di- adverse effects, although they are rarely severe enough to
lates both arteries and veins and is capable of causing a rapid, cause discontinuation of therapy. Oral cimetidine may cause a
profound fall in blood pressure. Although prazosin was the first mild increase (10%) in the half-life of doxazosin. Concurrent
alpha blocker available for hypertension, other alpha blockers administration of doxazosin with phosphodiesterase–5
such as doxazosin and terazosin (Hytrin) are more widely used inhibitors, such as sildenafil (Viagra) can result in additive BP
because they can be taken once daily. lowering effects and hypotension.
Doxazosin and several other alpha blockers also relax
smooth muscle around the prostate gland. Patients who have
difficulty urinating due to an enlarged prostate, a condition
known as benign prostatic hyperplasia (BPH), sometimes receive
these drugs to relieve symptoms of this disease, as discussed in
Chapter 34‌.
Some drugs, such as epinephrine, affect both beta- and alpha-adrenergic receptors and can cause seri-
ous adverse effects. Drugs that affect only one receptor subtype produce fewer adverse effects. Prazosin
(Minipress), for example, is specific to alpha1-receptors and thus has less effect on the heart, which con-
tains beta1-receptors. On the other hand, atenolol (Tenormin) and metoprolol (Lopressor, Toprol) are se-
lective for beta1-receptors and thus have little effect on the bronchi, which have beta2-receptors. Of the
adrenergic antagonists, only the beta-blockers are considered first-line drugs for the pharmacotherapy of
HTN.
The adverse effects of adrenergic antagonists are predictable because they are extensions that would
ortho = straight be expected from blocking the fight-or-flight response. The alpha 1-blockers tend to cause orthostatic
static = causing to stand hypotension in patients when they move quickly from a supine to an upright position. Dizziness, nausea,
bradycardia, and dry mouth are also common. Less common, though sometimes a major cause for non-
brady = slow
adherence, is their adverse effect on male sexual function (impotence). Because nonselective beta blockers
cardia = heart
slow the heart rate and cause bronchoconstriction, they should be used with caution in patients with asthma
or HF.
Some adrenergic blockers affect the production of neurotransmitters in the central nervous system
rather than affecting the peripheral nervous system. For example, methyldopa (Aldomet) is converted to a
false neurotransmitter in the brainstem, thus causing a shortage of the “real” neurotransmitter and inhibi-
tion of the sympathetic nervous system. Clonidine (Catapres), an alpha2 blocker, affects alpha-adrenergic
receptors in the cardiovascular control centers in the brainstem. The central acting drugs have a tendency to
produce sedation and are infrequently prescribed.
Concept Review 18.3

■ Why is it important for the patient to weigh himself or herself on a regular basis when
taking antihypertensive drugs?
core concept 18.12 Vasodilators lower blood pressure by relaxing arteriolar smooth muscle.
Many of the antihypertensive drugs discussed thus far lower blood pressure through indirect means by af-
fecting enzymes (ACE inhibitors), autonomic nerves (alpha and beta blockers), or fluid volume (diuretics).
It would seem that a more efficient way to reduce blood pressure would be to cause a direct relaxation of
arteriolar smooth muscle. Indeed, drugs that directly affect vascular smooth muscle are highly effective at
lowering blood pressure, but they produce too many adverse effects to be drugs of first choice. The direct-
acting vasodilators used for hypertension are listed in Table 18.6 ◆.
Table 18.6 Direct-Acting Vasodilators for Hypertension

hydralazine (Apresoline) PO; 10–50 mg qid (max: 300 mg/day) Diastolic response usually greater than systolic; IV and IM forms
available.
minoxidil (Loniten) PO; 5–40 mg/day (max: 100 mg/day) Reserved for severe hypertension; topical form used to promote hair
growth.
nitroprusside (Nitropress) IV; 0.5–10 mcg/kg/min For hypertensive crisis; produces both arteriolar and venous dilation;
infusion not to exceed 10 min.
Direct vasodilators produce reflex tachycardia, a normal physiologic response to the sudden decrease
in blood pressure caused by the drug. Reflex tachycardia forces the heart to work harder, and blood pres-
sure increases, counteracting the effect of the antihypertensive drug. Patients with coronary artery disease
could experience an acute angina attack. Fortunately, reflex tachycardia can be prevented by the concurrent
administration of a beta blocker, such as propranolol.
A second potentially serious adverse effect of direct vasodilator therapy is sodium and water reten-
tion. As the kidney retains more sodium and water, blood volume increases, thus raising blood pressure
and canceling the antihypertensive action of the vasodilator. A diuretic may be administered concurrently
with a direct vasodilator to prevent fluid retention.
One direct-acting vasodilator, nitroprusside (Nitropress), is the traditional drug of choice for hyper-
tensive emergency, a condition in which diastolic pressure is greater than 120 mmHg and there is evidence
of organ damage, usually to the heart, kidney, or brain. This potentially life-threatening condition must
be controlled quickly. Nitroprusside has the ability to lower blood pressure almost instantaneously on IV
administration. Care must be taken not to decrease blood pressure too quickly because this can result in
hypotension and severe restriction of blood flow to the cerebral, coronary, or renal capillaries.
Drug Prototype: Hydralazine (Apresoline)

Therapeutic Class: Drug for hypertension and heart failure Pharmacologic Class: Direct-acting vasodilator
Actions and Uses: Hydralazine was one of the first oral anti- Adverse Effects and Interactions: Headache, reflex tachycardia,
hypertensive drugs marketed in the United States. Therapy is palpitations, flushing, nausea, and diarrhea are common but
generally begun with low doses, which are gradually increased may resolve as therapy progresses. Patients taking hydralazine
until the desired therapeutic response is obtained. After sev- often receive a beta blocker to counteract reflex tachycardia.
eral months of therapy, tolerance to the drug develops and The drug may produce a lupus-like syndrome with extended
a dosage increase may be necessary. Although it produces an use. Sodium and fluid retention is another potentially serious
effective reduction in blood pressure, drugs in other antihy- adverse effect. The use of hydralazine is mostly limited to pa-
pertensive classes have largely replaced hydralazine because of tients whose HTN cannot be controlled with safer medications.
its many adverse effects. However, this may change due to the Administering hydralazine with other antihypertensives
approval of BiDil, a fixed-dose combination of isosorbide dini- or monoamine oxidase (MAO) inhibitors may cause severe
trate and hydralazine that appears to be effective at lowering hypotension. This includes all drug classes used as antihyper-
blood pressure in African Americans. tensives. NSAIDs may decrease the antihypertensive response
of hydralazine.
Patients treated for HTN need to know the following:
1. Take medications as prescribed.
2. Never discontinue the medication without approval from a healthcare provider.
3. To control HTN, incorporate lifestyle changes such as diet and exercise, even if blood
pressure is brought into normal limits by the medication.
4. Check blood pressure on a regular basis and report significant variations to the health-
care provider.
5. Get out of bed slowly to avoid dizziness.
6. If taking loop or thiazide diuretics, potassium supplements or an increased intake
of potassium-rich foods such as bananas, dried fruits, and orange juice may be
necessary.
7. Take weight measurements regularly and report abnormal weight gains or losses.
8. Do not take any over-the-counter (OTC) medications for colds, flu, or allergies without
first checking with a healthcare provider.
Safety Alert
Drug-to-Food Interactions
Certain drug–food interactions can be very dangerous. For example, the combination of grape-
fruit juice and certain blood pressure-lowering drugs or some cholesterol-lowering drugs can
cause toxic levels of the drug in the blood. It is advisable for patients to keep medications in
their original, labeled containers so that instructions are readily available. The nurse should en-
sure that patients are fully informed about how to take their drugs by providing both oral and
written instructions.
Chapter Review
18.1 Hypertension is characterized by the consistent pressure, and that present during the heart’s relax-
elevation of arterial blood pressure. ation is called diastolic pressure.
A patient having a sustained blood pressure of 18.4 The primary factors responsible for blood pressure
140/90 mmHg after multiple measurements made are cardiac output, the resistance of the small ar-
over several clinic visits is said to have hypertension teries, and blood volume.
(HTN). HTN is classified into three categories—
prehypertension, Stage 1, and Stage 2. As blood leaves the heart, its pressure depends on
how much blood is present in the vessels (blood vol-
ume), how much is ejected per minute, and how much
18.2 Failure to treat hypertension can lead to stroke,
resistance it encounters from the small arteries (pe-
heart failure, or myocardial infarction.
ripheral resistance). These are considered the primary
HTN is one of the most common diseases. Uncon- factors controlling blood pressure.
trolled HTN can cause chronic and debilitating dis-
orders such as stroke, heart attack, and heart failure. 18.5 Many nervous and hormonal factors help to keep
blood pressure within normal limits.
18.3 Blood pressure is caused by the pumping action of Clusters of neurons in the medulla known as the vaso-
the heart. motor center regulate blood pressure. Feedback is pro-
As the heart pumps, it creates pressure that is great- vided to the vasomotor center by baroreceptors in the
est in the arteries closest to the heart. The pressure aorta and carotid arteries. Hormones such as epinephrine
created by the heart’s contraction is called systolic or ADH may have profound effects on blood pressure.
Chapter Review 285
18.6 Positive lifestyle changes can reduce blood pres- also decrease blood volume, which aids in producing
sure and lessen the need for medications. their antihypertensive effect.
Because antihypertensive drugs may have uncomfort- 18.10 Calcium channel blockers have emerged as impor-
able adverse effects, lifestyle changes such as proper tant drugs in the treatment of hypertension.
diet and exercise are often implemented prior to and
during drug therapy to enable lower drug doses. Calcium channel blockers (CCBs) block calcium
ions from entering smooth muscle cells, causing ar-
18.7 Selection of specific antihypertensive drugs de- terioles to relax, thus reducing blood pressure. Some
pends on the severity of the disease. CCBs are also used to treat angina, heart failure, and
dysrhythmias.
Drug therapy of HTN often begins with low doses of
a single drug. If ineffective, a second drug from a dif- 18.11 Adrenergic blockers are commonly used to treat
ferent class may be added to the regimen. Multidrug hypertension.
therapy is common.
Autonomic drugs that block alpha1-receptors, block
beta 1- and/or beta 2-receptors, or stimulate alpha 2-
18.8 Diuretics are often preferred drugs for treating
receptors in the brainstem (centrally acting) to lower
mild to moderate hypertension.
blood pressure are available. Although acting by
Diuretics are often drugs of first choice for HTN be- different mechanisms, these drugs all lower blood
cause they have few adverse effects and can control pressure.
minor to moderate HTN. Electrolytes should be care-
fully monitored in patients taking diuretics. 18.12 Vasodilators lower blood pressure by relaxing ar-
teriolar smooth muscle.
18.9 Blocking the renin-angiotensin-aldosterone sys- A few drugs lower blood pressure by directly relax-
tem leads to a decrease in blood pressure. ing arteriolar smooth muscle. Other than their use
Blocking angiotensin-converting enzyme (ACE) or in treating hypertensive crisis, drugs in this class are
the angiotensin II receptor can prevent the intense not widely used because of their numerous adverse
vasoconstriction caused by angiotensin. These drugs effects.
Review Questions
The following questions are written in NCLEX-PN® style. 3. There is less daily medication dosing.
Answer these questions to assess your knowledge of the chap- 4. Multidrug therapy treats the patient’s other medical
ter material, and go back and review any material that is not conditions.
clear to you.
4. The patient is taking furosemide (Lasix) 40 mg bid. The
1. The nurse takes a patient’s blood pressure at 142/92 mm Hg. nurse monitors the patient’s lab report for:
In an adult patient, this level is considered: 1. Hyperkalemia
1. Normal 2. Hypokalemia
2. Prehypertension 3. Hypernatremia
3. Hypertension, stage 1 4. Hypercalcemia
4. Hypertension, stage 2
5. The patient has been taking losartan (Cozaar) for his
2. Just prior to starting antihypertensive therapy, the nurse hypertension. The physician has determined that the current
obtains an ECG and the baseline heart rate of a patient. This medication regimen is not effective. Which of the following
was done because the effects of the medication he or she will drugs may be added to the treatment plan?
be taking affects heart function and rate. What medication will 1. Felodipine (Plendil)
the patient most likely be taking? 2. Methyldopa (Aldomet)
1. Cardizem 3. Atenolol (Tenormin)
2. Micardis 4. Hydrochlorothiazide (Microzide)
3. Diuril
4. Nitropress 6. The patient has been started on antihypertensives. The
nurse monitors the patient for:
3. The patient is on two antihypertensive drugs. The nurse 1. Nausea and vomiting
recognizes that the advantage of multidrug treatment is: 2. Diarrhea
1. Blood pressure decreases faster. 3. Dizziness
2. Adverse effects are fewer. 4. Tetany
7. A patient with hypertension has a medication order for 9. The patient has started on a direct-acting vasodilator. To
diltiazem HCL 60 mg po twice a day. How many tablet(s) will make sure the patient understands how this medication works,
the nurse administer in a day if the medication comes only as the nurse includes what information in the teaching plan?
120 mg per tablet: 1. They block calcium from entering smooth muscle, causing
1. Half tablet in the morning arterioles to relax.
2. Half tablet, once in the morning and one in the evening 2. They block receptors in the brainstem to lower blood
3. One tablet in the morning pressure.
4. One tablet in the morning and one in the evening 3. They block the angiotensin-converting enzyme to prevent
vessel constriction.
8. The nurse is helping to develop a presentation on the dif- 4. They relax smooth muscles in the blood vessels to decrease
ferent types of medications used for hypertension. The presen- peripheral resistance.
tation will be conducted at a local church as part of their health
ministry. One of the types of antihypertensive medications that 10. The patient is on an ACE inhibitor. As a result of this ther-
will be included is the one that affects the renin-angiotensin- apy, the nurse checks for which of the following:
aldosterone system to increase urine. This medication is a(n): 1. Hypokalemia
1. Calcium channel blocker 2. Hyperkalemia
2. Adrenergic blocker 3. Hypernatremia
3. ACE inhibitor 4. Hyperglycemia
4. Direct-acting vasodilator
Remember Mr. Rodriguez, the pa- 2. What two drug classes are contained in Hyzaar?
tient introduced at the beginning of 1. Thiazide diuretic and angiotensin-receptor blocker
the chapter? Now read the remainder 2. Thiazide diuretic and potassium-sparing diuretic
of the case study. Based on the infor- 3. ACE inhibitor and potassium-sparing diuretic
mation you have learned in this chap- 4. Alpha-adrenergic blocker and ACE inhibitor
ter, answer the questions that follow.
Mr. Paul Rodriguez was admitted to the emergency depart- 3. What instructions did the nurse provide to Mr. Rodriguez
ment unconscious with a nose bleed that wouldn’t stop. His about Hyzaar?
blood pressure was measured as 210/120 mmHg, and the doc- 1. Always rise slowly and avoid sudden changes in posture.
tor ordered that he be immediately placed on nitroprusside 2. Take a daily potassium supplement.
(Nitropress). He stayed in the hospital for two days and was 3. Eat plenty of calcium-rich foods such as yogurt.
discharged with a blood pressure of 135/88 mmHg. On dis- 4. Do not exercise regularly because exercise may interfere
charge, Mr. Rodriguez was given a prescription for Hyzaar with blood pressure regulation.
with instructions on how it works, monitoring, possible adverse
effects, and precautions. 4. After eight months on Hyzaar, the physician switched
Mr. Rodriguez to nifedipine (Procardia). He then reported to
1. Why was nitroprusside, rather than Hyzaar, used in the the nurse that he stopped taking the Procardia because it made
emergency department? him dizzy, and he felt his heart was racing. The nurse explained
1. Nitroprusside is safer. that this common adverse effect was probably due to:
2. Nitroprusside has a longer duration of action. 1. Electrolyte imbalance
3. Nitroprusside has a faster onset of action. 2. Underdosing of nifedipine
4. Mr. Rodriguez is allergic to Hyzaar. 3. Excessive vasodilation of arteries
4. Reflex tachycardia
NOTE: Answers to the Review and Case Study Questions appear in Appendix B. The complete rationales and answers are located
on the textbook’s website.

c
“My parents and
grandparents smoked h
their whole lives and a
lived to their 90s. I just p
can’t believe smoking has
damaged my heart.” t
Mr. Albert Novi
e
r
Drugs for Heart Failure

19
Core Concepts
19.1 Heart failure is closely associated with disorders such 19.6 Diuretics relieve symptoms of heart failure by reduc-
as chronic hypertension, coronary artery disease, and ing fluid overload and decreasing blood pressure.
diabetes. 19.7 Cardiac glycosides increase the force of myocardial
19.2 The central cause of heart failure is weakened heart contraction and were once the traditional drugs of
muscle. choice for heart failure.
19.3 The three primary characteristics of heart function 19.8 Beta-adrenergic blockers are used in combination with
are force of contraction, heart rate, and speed of other drugs to slow the progression of heart failure.
impulse conduction. 19.9 Vasodilators reduce symptoms of heart failure by
19.4 The specific therapy for heart failure depends on the decreasing cardiac workload.
severity of the disease. 19.10 Phosphodiesterase inhibitors and other miscella-
19.5 Angiotensin-converting enzyme (ACE) inhibitors are neous drugs are used for short-term therapy of
the preferred drugs for heart failure. advanced heart failure.
Drug Snapshot
Angiotensin-converting lisinopril (Prinivil, Zestril) Vasodilators

enzyme (ACE) inhibitors 292
Phosphodiesterase inhibitors milrinone (Primacor)
Diuretics and miscellaneous agents 297
Cardiac glycosides digoxin (Lanoxin,
Lanoxicaps) 295
Beta-adrenergic blockers carvedilol (Coreg) 296
Learning Outcomes
1. Identify the major risk factors for the pharmacotherapy of heart 6. For each of the classes listed
associated with the progression to failure. in the Drug Snapshot, identify
heart failure. 4. Explain several means by which representative drugs and explain
2. Relate how the symptoms patients may manage their heart their mechanisms of drug action,
associated with heart failure may be failure without drugs. primary actions, and important
caused by weakened heart muscle. adverse effects.
5. Categorize heart failure drugs
3. Identify drug classes that are used based on their classifications and
as first-line and second-line choices mechanisms of action.
288 Chapter 19 Drugs for Heart Failure
Key Terms
afterload 289 natriuretic peptide (hBNP) phosphodiesterase
contractility (kon-trak-TILL-eh-tee) 289 (na-tree-ur-ET-ik) 297 (fos-fo-die-ES-tur-ase) 297
heart failure (HF) 288 peripheral edema (purr-IF-ur-ul preload 289
eh-DEE-mah) 289
inotropic effect (in-oh-TRO-pik) 289
H eart failure (HF) is one of the most common and fatal of the cardiovascular diseases, and its inci-
dence is expected to increase as the population ages. Despite the dramatic decline in death rates for
most cardiovascular disease that has occurred over the past two decades, the death rate for HF has
only recently begun to decrease. Although improved treatment of myocardial infarction (MI) and hyperten-
sion (HTN) has led to declines in mortality due to HF, approximately one in five patients dies within one
year of diagnosis of HF, and 50% die within five years.
Heart failure is closely associated with disorders such as chronic

Core Concept 19.1 hypertension, coronary artery disease, and diabetes.
Heart failure (HF) is the inability of the ventricles to pump enough blood to meet the body’s metabolic
demands. HF can be caused by any disorder that affects the heart’s ability to receive or eject blood.
Although weakening of cardiac muscle is a natural consequence of aging, the process can be accelerated
by a number of diseases associated with HF that are shown in Table 19.1 ◆. There is no cure for HF;
however, effective drug therapy can relieve many of the distressing symptoms of HF and may prolong
patients’ lives.
For many patients, HF is considered a preventable condition; controlling associated diseases will
greatly reduce the risk of eventual HF. For example, controlling lipid levels and keeping blood pressure
within normal limits will reduce the incidence of MI. Maintaining blood glucose within normal values can
reduce the cardiovascular consequences of uncontrolled diabetes. Therefore, the therapy of HF is no longer
just focused on end stages of the disorder. Pharmacotherapy is now targeted at prevention and slowing the
progression of HF. This change in emphasis has led to significant improvements in survival and quality of
life for patients with HF.
Table 19.1 Disorders Commonly Associated with Heart Failure

Disease Description
Chronic hypertension Sustained high systemic blood pressure
Coronary artery disease Atherosclerosis of the coronary arteries
Diabetes Lack of insulin or inability to tolerate carbohydrates
Mitral stenosis Inability of the mitral valve to open fully
Myocardial infarction Heart muscle death due to coronary artery obstruction
Fast Facts Heart Failure

■ HF affects 10% of those over age 70.
■ More than 58,000 people die of HF each year.
■ African Americans have one-half to two times the incidence of HF as Whites.
■ HF occurs slightly more frequently in men than in women.
■ HF is twice as frequent in patients with hypertension and five times as frequent in persons who have
experienced an MI.
The central cause of heart failure is weakened heart muscle. Core Concept 19.2
Although a number of diseases can lead to HF, the end result is the same: The heart is unable to pump out
the volume of blood required to meet the needs of the other organs. To understand how drugs act on the
weakened heart muscle, it is essential to understand the underlying cardiac physiology.
The right side of the heart receives blood from the venous system and sends it to the lungs, where the
blood receives oxygen and gives up its carbon dioxide. The blood returns to the left side of the heart, which
sends it out to the rest of the body through the aorta. The amount of blood received by the right side should
exactly equal that sent out by the left side. If this does not happen, HF may occur. The amount of blood
pumped by each ventricle per minute is the cardiac output. The relationship between cardiac output and
blood pressure is explained in Chapter 18.
Although many variables affect cardiac output, the two most important factors are preload and after-
load. Just before the chambers of the heart contract (systole), they are filled to their maximum capacity
with blood. The degree to which the cardiac muscle fibers are stretched just prior to contraction is preload.
The more these fibers are stretched, the more forcefully they will contract. This is somewhat analogous to a
rubber band: The more it is stretched, the more forcefully it will snap back. This strength of contraction of
the heart is called contractility.
The second important factor affecting cardiac output is afterload. For the left ventricle to pump blood
out of the heart, it must overcome a fairly substantial pressure in the aorta. The afterload is the amount
of pressure in the aorta that must be overcome for blood to be ejected from the left ventricle. The greater
afterload that occurs with chronic HTN creates a constant increased workload for the heart. This explains
why patients with chronic HTN are more likely to experience HF. Lowering blood pressure results in less
workload for the heart.
In HF, the myocardium becomes weakened, and the heart cannot eject all the blood it receives. This
weakening may occur on the left side, the right side, or both sides of the heart. If it occurs on the left
side, excess blood accumulates in the left ventricle. The wall of the left ventricle thickens and enlarges
(hypertrophy) in an attempt to compensate for the increased workload. Because the left ventricle has
limits to its ability to compensate, blood “backs up” into the lungs, resulting in the classic symptoms of
cough and shortness of breath, particularly when the patient is lying down. Left HF is sometimes called
congestive HF.
Although left-sided HF is more common, the right side of the heart can also become weak,
either simultaneously with the left side or independently from the left side. In right HF, the blood
“backs up” into the peripheral veins. This results in swelling of the feet and ankles, a condition
known as peripheral edema, and engorgement of organs such as the liver. Figure 19.1 ■ illustrates
the underlying pathophysiology of HF. Figure 19.2 ■ illustrates the signs and symptoms of the
patient in HF.
The three primary characteristics of heart function are force of

contraction, heart rate, and speed of impulse conduction. Core Concept 19.3
Cardiac physiology is quite complex, particularly when the heart is challenged with a chronic disease such
as HF. A simplified method for understanding cardiac function, and one that is quite useful for understand-
ing drug therapy, is to visualize the heart as having three fundamental characteristics:
1.
It contracts with a specific force or strength (contractility).
2.
It beats at a certain rate (beats per minute).
3.
It conducts electrical impulses at a particular speed.
The ability to change the force of contraction, or contractility, is of particular interest to the pharma-
cotherapy of HF. Because the fundamental cause of HF is a weak myocardium, causing the muscle to beat
more forcefully seems to be an ideal solution. The ability to increase the strength of contraction is called
a positive inotropic effect and is a fundamental characteristic of the class of drugs known as the cardiac ino 5 fiber
glycosides. tropic 5 to influence
The ability of the heart to speed up or slow down is a second characteristic important to pharmacol-
ogy. A faster heart works harder but not necessarily more efficiently. A slower heart has a longer time to
rest between beats, thus decreasing the workload on the heart.
Figure 19.1
Pathophysiology of
heart failure. Decreased myocardial contractility/stroke volume
Decreased cardiac output
Increased preload Decreased blood pressure
Decreased blood Increased

Pulmonary edema
flow to kidneys heart rate
Decreased oxygen ADH Renin-angiotensin

supply system activated
Aldosterone secreted
Sodium and Increased

water peripheral
retention resistance
Edema of limbs/
Increased
Increased
afterload
blood volume
Increased
myocardial
workload
Figure 19.2
Signs and symptoms of

the patient with heart
failure.
Upright posture/
leaning forward
Persistent cough
Anxiety/restlessness
Rapid breathing
Skin cyanotic and clammy

Fast heart rate
Edema of lower limbs
290
Figure 19.3
1 = Stimulation
2 = Inhibition
Arterioles
Adrenergic blockers
Decrease cardiac workload by 2 2 2

slowing the heart rate (b1) and
decreasing blood pressure (a1)
(Example: carvedilol)
Vasodilators
Decrease cardiac workload by

dilating vessels and reducing
Sympathetic a1 preload (Example: isosorbide
b1 neurons dinitrate with hydralazine)
ACE inhibitors and

2 Phosphodiesterase angiotensin
inhibitors receptor blockers
1
Increase cardiac output by Increase cardiac output by
1 increasing the force of lowering blood pressure and
myocardial contraction decreasing blood volume
(Example: milrinone) (Example: lisinopril)
Heart
Diuretics
Cardiac glycosides Increase cardiac output by

reducing fluid volume and
Increase cardiac output by Kidney
1 decreasing blood pressure
increasing the force of (Example: furosemide)
myocardial contraction
1
(Example: digoxin)
Increased urine output
Mechanisms of action of drugs used to treat heart failure.
A third fundamental characteristic of cardiac physiology is the electrical conduction through the heart.
Some cardiovascular drugs influence the speed of this conduction. Slowing the conduction speed through
the heart will cause the heart to beat slower, thus lessening cardiac workload.
These primary characteristics of cardiac function can be modified through pharmacotherapy to assist
the heart in meeting the body’s metabolic demands. The mechanisms by which HF medications accom-
plish this are shown in Figure 19.3 ■.
The specific therapy for heart failure depends on the severity

of the disease. Core Concept 19.4
Although HF can be acute and require immediate treatment, it is often considered a progressive, chronic dis-
order. In its early stages, many of its symptoms can be improved through nonpharmacologic interventions.
Through certain lifestyle changes, the patient can experience a higher quality of life either without drug
therapy or with lower drug doses that have less risk for adverse effects. It should be noted that the following
nonpharmacologic methods for controlling HF are the same strategies also used to manage hypertension.
■ Stop using tobacco.

■ Restrict salt (sodium) intake, and be sure to eat foods rich in potassium and magnesium.
■ Limit alcohol consumption.
■ Implement a medically supervised aerobic exercise plan.
■ Reduce sources of stress and learn to implement coping strategies.
■ Reduce weight to (or maintain it at) an optimum level.
■ Limit caffeine consumption.
Once heart disease progresses such that it significantly affects activities of daily living, drug therapy
is indicated. Drugs for HF may be classified as first-line or second-line drugs. If first-line drugs are not
effective, then second-line drugs will be tried or added to the regimen. The first-line drugs are the ACE
inhibitors and diuretics. These medications relieve most symptoms of mild to moderate HF and produce
the fewest number of adverse effects. Sometimes considered first-line drugs, the cardiac glycosides are
effective but have the potential for more serious adverse effects. Drugs of second choice are those used in
acute HF, or when the ACE inhibitors and diuretics prove ineffective. Second-line drugs include the phos-
phodiesterase inhibitors, vasodilators, and beta-adrenergic blockers. The use of multiple drugs is common
in the pharmacotherapy of HF.
Angiotensin-converting enzyme (ACE) inhibitors are the preferred

Core Concept 19.5 drugs for heart failure.
Drugs affecting the renin-angiotensin-aldosterone system reduce the workload on the heart by lowering
blood pressure. They are drugs of choice for the treatment of HF. Table 19.2 ◆ lists the ACE inhibitors
approved to treat HF.
The basic pharmacology of the ACE inhibitors and their effects on the renin-angiotensin-aldosterone
pathway are discussed in Chapter 18. Approved for the treatment of HTN since the 1980s, ACE inhibitors
have since been shown to slow the progression of HF and to reduce deaths from this disease. They have
replaced digoxin as the preferred drugs for the treatment of chronic HF.
Drug Prototype Lisinopril (Prinivil, Zestril)

Therapeutic Class: Drug for HF, HTN, and MI prevention Pharmacologic Class: ACE inhibitor
Actions and Uses: Lisinopril is one of the most frequently pre- headache, dizziness, orthostatic hypotension, and rash. Because
scribed drugs for HTN and HF. An additional indication for this high potassium levels may occur during therapy, use of potassium
medication is to improve survival in patients when given within supplements or potassium-sparing diuretics should be avoided.
24 hours of an acute MI. Thus, electrolyte levels are usually monitored periodically. Angio-
Lisinopril lowers blood pressure by blocking ACE. Like edema is a rare, though potentially serious, adverse effect.
other ACE inhibitors, doses of lisinopril may require two to Lisinopril interacts with nonsteroidal anti-inflammatory
three weeks of therapy for optimum effectiveness, and several drugs (NSAIDs) to cause decreased antihypertensive activity.
months of therapy may be needed for a patient’s cardiac func- Lisinopril may increase lithium levels and toxicity.
tion to return to normal. Because of their combined hypoten-
sive action, concurrent therapy with lisinopril and diuretics Black Box Warning:
should be carefully monitored.
Fetal injury and death may occur when ACE inhibitors are
taken during pregnancy. When pregnancy is detected, they
Adverse Effects and Interactions: Lisinopril exhibits few serious should be discontinued as soon as possible.
adverse effects. The most common adverse effects are cough,
Table 19.2 First-Line Drugs for Heart Failure

ACE Inhibitors and Angiotensin receptor blockers
candesartan (Atacand) PO; start at 4 mcg once daily, and slowly increase Also for HTN
to a dose of 32 mg
captopril (Capoten) PO; 25–50 mg bid or tid (max: 450 mg/day) Decreases central venous and pulmonary wedge
pressure; also for HTN and post MI therapy
enalapril (Vasotec) (see page 277 for PO; 2.5 mg qid–bid (max: 40 mg/day) Increases cardiac output; IV form available; also
the Drug Prototype box) for HTN
fosinopril (Monopril) PO; 5–40 mg daily (max: 40 mg/day) Also for HTN
lisinopril (Prinivil, Zestril) PO; 10 mg daily (max: 80 mg/day) Therapy should not begin until two to three days
after diuretics are stopped; also for HTN and post
MI therapy.
quinapril (Accupril) PO; 10–20 mg daily (max: 40 mg/day) Observe for signs of hyperkalemia; also for HTN.
ramipril (Altace) PO; 2.5–5 mg bid (max: 10 mg/day) Also for HTN, stroke prophylaxis and post-MI therapy
valsartan ( Diovan) PO; Start with 40 mg bid and slowly increase 160 mg bid Also for HTN
Selected Diuretics
bumetanide (Burinex, Bumex) PO; 0.5–2 mg daily (max: 10 mg/day) Affects loop of Henle; diuretic activity is 40 times
greater and duration of action is shorter than fu-
rosemide; IM and IV forms available.
eplerenone (Inspra) PO; 25–50 mg once daily (max: 100 mg/day) Potassium-sparing diuretic; originally approved
for HTN
furosemide (Lasix) (see page 254 for PO; 20–80 mg in one or more divided doses Monitor for signs and symptoms of hypokalemia; also
the Drug Prototype box) (max: 600 mg/day) for HTN; IV and IM forms available; loop diuretic.
hydrochlorothiazide (Microzide) (see PO; 25–200 mg in one to three divided doses May bring on diabetes in patients with prediabe-
page 255 for the Drug Prototype box) (max: 200 mg/day) tes; also for HTN; thiazide diuretic
spironolactone (Aldactone) (see PO; 5–200 mg in divided doses (max: 200 mg/day) Used for refractory edema with HF; also for HTN;
page 256 for the Drug Prototype box) potassium-sparing diuretic
torsemide (Demadex) PO; 10–20 mg/day (max: 200 mg/day) Affects loop of Henle; also for HTN; IV form available
CAM TherapY
Carnitine and Heart Disease
Carnitine is a natural substance structurally similar to amino acids. Its primary function in
metabolism is to move fatty acids from the bloodstream into cells, where carnitine assists in
the breakdown of lipids and the production of energy. The best food sources of carnitine are
organ meat, fish, muscle meats, and milk products. Carnitine is available as a supplement in
several forms, including L-carnitine, D-carnitine, and actetyl-carnitine. D-carnitine is associ-
ated with potential adverse effects and thus should be avoided.
Carnitine has been claimed to enhance energy and sports performance, heart health,
memory, immune function, and male fertility. It is also being marketed as a “fat burner” for
weight reduction.
Carnitine has been extensively studied. There is solid evidence to support supplementation
in patients who are deficient in carnitine. Certain patients, such as vegetarians or those with
heart disease, may need additional amounts. Carnitine supplementation has been shown
to improve exercise tolerance in patients with angina. The use of carnitine may prevent the
occurrence of dysrhythmias in the early stages of heart disease. Carnitine has also been shown dys 5 difficult or bad
to decrease triglyceride levels while increasing high-density lipoprotein (HDL) serum levels, rhythmia 5 rhythm
thus helping to minimize one of the major risk factors associated with heart disease. Research
has not shown carnitine supplementation to be of significant benefit in enhancing sports
performance or weight loss.
The ACE inhibitors produce their effects by blocking ACE, thus preventing the formation of an-
giotensin, an extremely potent vasoconstrictor. The primary actions of the ACE inhibitors are to lower
blood pressure and reduce blood volume by enhancing the excretion of sodium and water. The resultant
reduction of arterial blood pressure increases cardiac output. An additional effect of the ACE inhibitors
is dilation of the veins returning blood to the heart. This action decreases preload and reduces pulmo-
nary congestion and peripheral edema. The combined actions of ACE inhibitors substantially decrease
the workload on the heart and allow it to work more efficiently. ACE inhibitors have been shown to
reduce mortality following acute MI when therapy is started soon after the onset of symptoms (see
Chapter 20).
A related group of drugs act by blocking the effects of angiotensin after it is formed. Angiotensin-
receptor blockers (ARBs) are newer drugs that have similar effectiveness to the ACE inhibitors. Although
the ARBs are usually prescribed for HTN, valsartan (Diovan) and candesartan (Atacand) are also approved
for HF. Because research has not yet demonstrated a clear advantage of ARBs over other medications, their
use in the treatment of HF is usually reserved for patients unable to tolerate the adverse effects of ACE
inhibitors.
Diuretics relieve symptoms of heart failure by reducing

Core Concept 19.6 fluid overload and decreasing blood pressure.
Diuretics are commonly used for the symptomatic treatment of HF. They produce few adverse effects
and are effective at increasing urine flow, lowering blood volume, and reducing edema and congestion.
When diuretics reduce fluid overload and lower blood pressure, the workload on the heart is reduced and
cardiac output increases. They are widely used in the treatment of cardiovascular disease in patients with
fluid overload. When used to treat HF, diuretics are usually prescribed in combination with ACE inhibitors
and other HF medications in patients who have edema.
The most common adverse effects from diuretic therapy are electrolyte imbalances. Of greatest con-
cern are the effects of diuretics on potassium levels, because too little or too much potassium can greatly
affect a failing heart. This can be especially important in patients taking cardiac glycosides; patients with
potassium or magnesium deficiencies are at greater risk for toxicity from digoxin. Potassium or magne-
sium supplements may be prescribed to prevent this adverse effect. Frequent laboratory testing may be
necessary to monitor electrolyte levels in patients with HF.
The mechanism by which diuretics reduce blood volume, specifically where and how the nephron of
the kidney is affected among the various drugs are discussed in Chapter 17. A Nursing Process Focus chart
for diuretics, and prototype features for furosemide (Lasix), hydrochlorothiazide (Microzide) and spirono-
lactone (Aldactone) are also included in Chapter 17.
Cardiac glycosides increase the force of myocardial contraction and were

core concept 19.7 once the traditional drugs of choice for heart failure.
The value of the cardiac glycosides in treating heart disorders has been known for over 2,000 years.
They have been used as arrow poisons by African tribes and as medicines by the ancient Egyptians and
Romans.
Extracted from the common plants Digitalis purpura (purple foxglove) and Digitalis lanata
(white foxglove), drugs from this class are sometimes called digitalis glycosides. Until the discovery
of the ACE inhibitors, the cardiac glycosides were the mainstay of HF treatment. Digoxin (Lanoxin)
is the only drug in this class available in the United States. The routes and dose for digoxin are listed
in Table 19.3 ◆.
The primary action of digoxin is an increase in the force of myocardial contraction. This action, a
positive inotropic effect, allows the weakened heart to eject more blood per beat, thus increasing cardiac
output. The increased cardiac output helps the heart to meet the metabolic demands of the tissues.
A second important action of digoxin is its ability to slow electrical conduction through the heart. This
results in fewer beats per minute. The reduced heart rate, combined with more forceful contractions, allows
for much greater efficiency of the heart.
Unfortunately, digoxin has the potential to cause serious adverse effects at high doses and in certain
patients. The margin of safety between a beneficial dose and a toxic dose is very small; thus, therapy
should be closely monitored to prevent severe adverse effects. Serum digoxin levels above 1.8 mg/mL are
considered toxic. Initial adverse effects are gastrointestinal (GI) related and include loss of appetite, vomit-
ing, and diarrhea. Headache, drowsiness, confusion, and blurred vision may occur. Excessive slowing of
the heart rate and other cardiac abnormalities can be fatal if not corrected.
The antidote for digoxin toxicity is administration of digoxin immune fab (Ovine). This drug binds
digoxin, preventing it from reaching the tissues. Onset of action is rapid—less than one minute after the IV
infusion is begun.
Table 19.3 Second-Line Drugs for Heart Failure

Cardiac glycoside
digoxin (Lanoxin, Lanoxicaps) PO; 0.125–0.5 mg/day (max: 0.5 mg/day) Increases cardiac output; larger dose may be
given to initiate therapy; IV form available;
also used for dysrhythmias
Beta-adrenergic blockers
carvedilol (Coreg) PO; 3.125 mg bid for 2 weeks, then gradually Reduces cardiac workload; dose must be
increase dose (max: 25 mg bid) increased very slowly to prevent adverse
effects; primary use is for HTN
metoprolol (Lopressor, Toprol XL) PO; 25 mg/day for 2 weeks, then gradually Also for HTN, angina, and post-MI therapy
increase dose; (max: 200 mg/day)
Direct-Acting Vasodilators
hydralazine with isosorbide dinitrate (BiDil) PO; 1–2 tablets tid (each tablet contains 20 mg Increases heart rate and cardiac output;
isosorbide dinitrate and 37.5 mg hydralazine) decreases myocardial oxygen consumption;
(max: 2 tablets/day) hydralazine also for HTN and isosorbide
dinitrate for angina
nesiritide (Natrecor) IV; 2 mcg/kg bolus followed by continuous Also called atrial natriuretic peptide; only
infusion at 0.01 mcg/kg/min for acute HF
Phosphodiesterase Inhibitors
inamrinone (Inocor) IV; 0.75 mg/kg bolus given slowly over 2–3 min; Larger dose is given to initiate therapy; peak
then 5–10 mcg/kg/min (max: 10 mg/kg/day) effect reached in 10 min.
milrinone (Primacor) IV; 50 mcg/kg over 10 min; then 0.375–0.75 Larger dose is given to initiate therapy; peak
mcg/kg/min effect reached in 2 min.
Concept Review 19.1

■ If cardiac glycosides are so effective at increasing myocardial contraction, why are they no
longer first-line drugs for HF?
Drug Prototype: Digoxin (Lanoxin, Lanoxicaps)

Therapeutic Class: Drug for heart failure Pharmacologic Class: Cardiac glycoside
Actions and Uses: The primary benefit of digoxin is its ability to Adverse Effects and Interactions: The most dangerous adverse
increase the strength of cardiac contraction (positive inotropic effect of digoxin is its ability to create dysrhythmias, par-
effect). Digoxin accomplishes this by inhibiting Na+–K+ ATPase, ticularly in patients who have hypokalemia. Because diuret-
an enzyme in myocardial cells. ics can cause hypokalemia and are also often used to treat
By increasing myocardial contractility, digoxin directly in- HF, use of digoxin and diuretics together must be carefully
creases cardiac output, thus alleviating symptoms of HF and monitored. Levels of potassium, magnesium, calcium, blood
improving exercise tolerance. The increased cardiac output also urea nitrogen (BUN), and creatinine should be monitored
results in increased urine production and a desirable reduction frequently (hypokalemia predisposes the patient to digoxin
in blood volume, thus relieving the distressing symptoms of toxicity). Other adverse effects of digoxin therapy include
lung congestion and peripheral edema. nausea, vomiting, and anorexia and abnormalities of the
In addition to its positive inotropic effect, digoxin also has the nervous system such as blurred vision. Periodic serum levels
ability to suppress the sinoatrial (SA) node (the pacemaker of the are checked to determine if the digoxin level is within the
heart) and slow electrical conduction through the atrioventricular therapeutic range, and the dosage may be adjusted based on
(AV) node. Because of these actions, digoxin is sometimes used to the laboratory results. Digoxin also interacts with many other
treat cardiac rhythm abnormalities known as dysrhythmias, which medications. Concurrent use with beta blockers may result in
is discussed in Chapter 22. Pulse rate should be monitored daily, additive bradycardia. Because small changes in digoxin levels
and values less than 60 beats per minute or greater than 100 can produce serious adverse effects, the healthcare provider
beats per minute should be reported to the healthcare provider. must constantly be alert for drug–drug interactions.
Beta-adrenergic blockers are used in combination with other

core concept 19.8 drugs to slow the progression of heart failure.
Drugs that produce a positive inotropic effect, such as the cardiac glycosides and phosphodiesterase in-
hibitors, play important roles in treating the diminished contractility that is the hallmark of HF. It may
seem somewhat unusual then to find medications that exhibit a negative inotropic effect prescribed for this
disease. Yet such is the case with the beta-adrenergic blockers. Beta blockers have been shown to dramati-
cally reduce the number of hospitalizations and deaths associated with HF.
Beta-adrenergic antagonists block the cardiac actions of the sympathetic nervous system, thus slow-
ing the heart rate and reducing blood pressure. Workload on the heart is decreased. Carvedilol (Coreg) and
metoprolol (Lopressor, Toprol XL) are the two beta blockers approved to treat HF. Patients with HF must
be carefully monitored when taking beta blockers because these drugs have the potential to worsen HF.
They are always used in combination with other agents, usually ACE inhibitors. The basic pharmacology
of the beta blockers is presented in Chapter 8. Other indications, routes, and dosages of the beta-adrenergic
blockers are discussed elsewhere in this text: hypertension in Chapter 18, dysrhythmias in Chapter 22, and
angina/myocardial infarction in Chapter 20.
Vasodilators reduce symptoms of heart failure by decreasing

core concept 19.9 cardiac workload.
The two direct-acting vasodilators, hydralazine (Apresoline) and isosorbide dinitrate (Isordil), act directly
on vascular smooth muscle to relax blood vessels and lower blood pressure. Hydralazine acts on arterioles,
whereas isosorbide dinitrate acts on veins. Because the two drugs act synergistically, isosorbide dinitrate is
combined with hydralazine in the treatment of HF. BiDil is a fixed-dose combination of 20 mg of isosor-
bide dinitrate with 37.5 mg of hydralazine. Dosing for the drug is shown in Table 19.2.
Because of a high incidence of reflex tachycardia and orthostatic hypotension, vasodilators play a
minor role in the drug therapy of HF. They are generally reserved for patients with more severe disease,
or those who cannot tolerate ACE inhibitors. BiDil appears to be especially effective in treating HF in
African American patients, who often exhibit resistance to standard therapies. Hydralazine is featured as a
prototype drug for direct vasodilators in the treatment of HTN in Chapter 18. Isosorbide dinitrate belongs
to a class of drugs called organic nitrates that are widely used in the treatment of angina pectoris (see
Chapter 20).
Concept Review 19.2

■ Why are the ACE inhibitors preferred over both the nitrates and the diuretics in the treat-
ment of HF?
Drug Prototype: Carvedilol (Coreg)

Therapeutic Class: Drug for heart failure and HTN Pharmacologic Class: Beta-adrenergic blocker
Actions and Uses: Carvedilol was the first beta-adrenergic and weight gain. It should be used with caution in patients
blocker approved for the treatment of HF. It has been found with asthma or cardiac dysrhythmias.
to reduce symptoms, slow the progression of the disease, and Carvedilol’s effect in decreasing heart rate and contractil-
increase exercise tolerance when combined with other HF ity has the potential to worsen HF; therefore, dosage must
drugs, such as ACE inhibitors. Unlike many drugs in this class, be carefully monitored. Because of the potential for adverse
carvedilol blocks beta1- and beta2- as well as alpha1-adrenergic cardiac effects, beta-adrenergic blockers such as carvedilol are
receptors. The primary therapeutic effects relevant to HF are usually given concurrently with other drugs in the treatment
a reduction in heart rate and a drop in blood pressure. The of HF.
lower blood pressure reduces the workload on the heart. The Carvedilol interacts with many drugs. For example, levels
drug is also approved to treat HTN and for reducing cardiac of carvedilol are significantly increased when the drug is taken
complications following an MI. with rifampin. MAO inhibitors, clonidine, and reserpine can
cause hypotension or bradycardia when given with carvedilol.
Adverse Effects and Interactions: The most frequent adverse When given with digoxin, carvedilol may increase digoxin lev-
effects of carvedilol include back pain, bradycardia, dizzi- els. It may also enhance the hypoglycemic effects of insulin and
ness, shortness of breath, fatigue, orthostatic hypotension, oral hypoglycemic agents.
Drug Prototype: Milrinone (Primacor)

Therapeutic Class: Drug for severe heart failure Pharmacologic Class: Phosphodiesterase inhibitor
Actions and Uses: Of the two phosphodiesterase inhibitors avail- more than 1 of every 10 patients taking the drug. The patient’s
able, milrinone is generally preferred because it has a shorter electrocardiogram (ECG) should be monitored continuously
half-life and fewer adverse effects. It is given IV only and is primar- during the infusion of the drug. Less serious adverse effects in-
ily used for the short-term support of advanced HF. Peak effects clude headache, nausea, and vomiting.
occur in two minutes. Immediate effects of milrinone include an Use with disopyramide may cause excessive hypoten-
increased force of contraction and an increase in cardiac output. sion. Caution should be used when administering milrinone
with digoxin, dobutamine, or other inotropic drugs because
Adverse Effects and Interactions: The most serious adverse their positive inotropic effects on the heart may be additive.
effect of milrinone is ventricular dysrhythmia, which can occur in
Phosphodiesterase inhibitors and other miscellaneous drugs

are used for short-term therapy of advanced heart failure. core concept 19.10
Phosphodiesterase inhibitors are drugs with a very brief half-life that are occasionally used for the short-
term control of acute HF. The doses of phosphodiesterase inhibitors are given in Table 19.3.
The two drugs in this class block the enzyme phosphodiesterase in cardiac and smooth muscle.
Blocking phosphodiesterase has the effect of increasing the amount of calcium available for myocardial
contraction. The inhibition results in two main actions that benefit patients with HF: an increased force of
contraction (positive inotropic response) and vasodilation. Because of their toxicity, however, phosphodi-
esterase inhibitors are reserved for patients who have not responded to ACE inhibitors or cardiac glyco-
sides, and they are generally used for two to three days only.
A third vasodilator used for HF is very different from hydralazine or isosorbide dinitrate. Nesirit-
ide (Natrecor) is a small peptide hormone that is structurally identical to a hormone known as human
beta-type natriuretic peptide (hBNP), which is secreted by the heart when the heart begins to fail. natri 5 sodium
Nesiritide reduces both preload and afterload, improving cardiac efficiency in patients with HF. Nesirit- uretic 5 urinary excretion
ide has limited uses because of its ability to cause severe hypotension. The medication is given only by
IV infusion, and patients require continuous monitoring. It is approved for patients with severe HF.
Patients treated for HF need to know the following:
In General
1. Take blood pressure regularly because many drugs for HF affect blood pressure.
Report any persistent changes.
2. Take weight measurements regularly and report abnormal weight gains or losses.
3. Salt intake should be limited.
Regarding ACE Inhibitors
4. Avoid sudden position changes because these can cause lightheadedness.
Regarding Cardiac Glycosides
5. Check pulse rate before taking digoxin. If the rate is less than 60 beats per minute or
the rate designated by a healthcare provider, the drug should not be taken.
6. Many drugs interact with digoxin to increase or decrease its effects on the heart. For
this reason, it is important to consult with a healthcare provider before taking any
other medication.
7. Report visual disturbances (seeing halos or a yellow-green tinge, blurring), nausea,
headaches, or irregular heartbeat without delay because they are signs and symp-
toms of digoxin toxicity.
Regarding Diuretics
8. Limit salt intake as directed by the healthcare provider.
9. Drink at least six to eight glasses of water daily.
10. Report any of the following adverse effects: abdominal pain, jaundice, dark urine,
flu-like symptoms.
11. To prevent dizziness, avoid sudden position changes.
12. An increased intake of potassium-rich foods such as bananas, dried fruits, and orange
juice, or a potassium supplement may be necessary if certain diuretics are taken. Tak-
ing potassium supplements with food reduces stomach irritation.
Chapter Review
19.1 Heart failure is closely associated with disorders 19.6 Diuretics relieve symptoms of heart failure by
such as chronic hypertension, coronary artery dis- reducing fluid overload and decreasing blood
ease, and diabetes. pressure.
Heart failure (HF) is not considered a distinct disease Diuretics produce few serious adverse effects and
in itself. Instead, a number of diseases that affect the are often used in combination with other HF drugs
heart, such as chronic hypertension (HTN), coronary to reduce patients’ symptoms. Potent diuretics such
artery disease, and diabetes, lead to the collection of as furosemide are particularly valuable in treating
symptoms known as HF. acute HF.
19.2 The central cause of heart failure is weakened 19.7 Cardiac glycosides increase the force of myocardial
heart muscle. contraction and were once the traditional drugs of
HF occurs when the heart cannot pump enough blood choice for heart failure.
to meet the demands of the tissues. This usually oc- Cardiac glycosides, long the mainstay for pharmaco-
curs when the heart muscle cannot contract with suf- therapy of HF, increase myocardial contractility and
ficient force. HF may occur on the right side, left are effective. The large number of drug–drug interac-
side, or both sides of the heart, producing symptoms tions and the potential for serious adverse effects such
such as shortness of breath, coughing, and peripheral as dysrhythmias limit their use.
edema.
19.8 Beta-adrenergic blockers are used in combination
19.3 The three primary characteristics of heart function with other drugs to slow the progression of heart
are force of contraction, heart rate, and speed of failure.
impulse conduction. Although beta blockers decrease myocardial con-
The ability of the heart to effectively pump blood de- tractility, they also lower heart rate and blood pres-
pends on the strength of contraction of the myocardial sure, which is beneficial in reducing the symptoms
fibers. Heart rate and the speed of the impulse con- of HF. When administered to treat patients with HF,
duction across the myocardium also directly affect they are nearly always used in combination with
the ability of the heart to pump blood. other drugs.
19.4 The specific therapy for heart failure depends on 19.9 Vasodilators reduce symptoms of heart failure by
the severity of the disease. decreasing cardiac workload.
Mild HF can be improved through lifestyle Direct vasodilators are effective at relaxing blood ves-
changes such as tobacco cessation and maintain- sels, thus reducing myocardial oxygen demand on the
ing optimum weight. As HF progresses, pharma- heart. BiDil is a combination of two vasodilators: iso-
cotherapy with drugs of first choice, such as ACE sorbide dinitrate and hydralazine. Their use is limited
inhibitors or diuretics, is indicated. More advanced by their high incidence of adverse effects.
disease may require therapy with cardiac glyco-
sides, phosphodiesterase inhibitors, beta blockers, 19.10 Phosphodiesterase inhibitors and other miscel-
or vasodilators. laneous drugs are used for short-term therapy of
advanced heart failure.
19.5 Angiotensin-converting enzyme (ACE) inhibitors Phosphodiesterase inhibitors are a relatively new
are the preferred drugs for heart failure. class of drugs used for the short-term treatment of
ACE inhibitors improve HF by reducing peripheral HF. Although effective, they are given IV only and
edema and increasing cardiac output. Because of their can produce potentially serious adverse effects. Ne-
effectiveness and their relatively low potential for siritide (Natrecor) is a small peptide hormone that is
serious adverse effects, they have become preferred approved only for severe HF because of its potentially
drugs in the treatment of HF. serious adverse effects.
Chapter Review 299
Review Questions
The following questions are written in NCLEX-PN® style. An- 6. The nurse is assisting in the development of a medication in-
swer these questions to assess your knowledge of the chapter ma- formation pamphlet to be given to those patients taking ACE inhib-
terial, and go back and review any material that is not clear to you. itors. Which of the following should be included in the education
provided to a patient on lisinopril (Prinivil)? (Select all that apply.)
1. The patient has developed a cough and shortness of breath
when he or she lies down. After thoroughly collecting data on 1. “It may take several weeks for your blood pressure to re-
the patient, the nurse suspects: turn to normal.”
2. “You must have your potassium monitored from time to
1. Right HF
time.”
2. Left HF
3. “This medication may change your vision from time to
3. Liver engorgement
time.”
4. Peripheral edema
4. “It interacts with NSAIDs to cause decreased antihyperten-
2. The patient has been started on digoxin (Lanoxin) therapy. sive activity.”
Which of the following should the nurse monitor carefully?
7. In addition to decreasing cardiac contractility, the nurse
1. SGOT levels informs the patient that beta blockers:
2. Amylase levels 1. Lower heart rate and blood pressure.
3. Sodium levels 2. Increase heart rate and afterload.
4. Potassium levels 3. Produce systemic vasoconstriction.
3. The nurse is teaching a patient about beta blockers. The pa- 4. Increase the force of myocardial contraction.
tient states that he or she is already taking another kind of medica- 8. A patient is taking digoxin. Just in case the patient devel-
tion for his or her HF. The nurse tells him or her that this is not ops digoxin toxicity, which drug would the nurse expect to be
uncommon. What other drug is usually given with beta-blockers? ordered for this patient?
1. Cardiac glycosides 1. Digoxin immune fab
2. Diuretics 2. Milrinone (Primacor)
3. Phosphodiesterase inhibitors 3. Inamrinone (Inocor)
4. ACE inhibitors 4. Flecainide (Tambocor)
4. A patient who is taking hydralazine for HF is also experienc- 9. A patient is receiving digoxin and furosemide (Lasix).
ing angina. Which of the following drugs would be used in com- Which of the following electrolyte levels should the nurse
bination with hydralazine to help relieve this patient’s symptoms? most carefully monitor?
1. Isosorbide dinitrate (Isordil) 1. Potassium
2. Carvedilol (Coreg) 2. Creatinine
3. Chlorothiazide (Diuril) 3. Sodium
4. Milrinone (Primacor) 4. Calcium
5. The patient is admitted with HF. The physician orders IV 10. The healthcare provider orders a patient to have 0.5 mg of
milrinone (Primacor). The nurse observes for the most serious digoxin. On hand, you have a bottle labeled digoxin 0.25 mg
adverse effect of this drug, which is: per tablet. How many tablet(s) will you give?
1. Headache 1. One tablet
2. Dysrhythmias 2. One and one-half tablets
3. Confusion 3. Two tablets
4. Drowsiness 4. Half tablet
Remember Mr. Novi, the patient intro- starting him on some medication to help his heart function
duced at the beginning of the chapter? more effectively, in addition to providing information on a
Now read the remainder of the case study. smoking cessation program.
Based on the information you have learned
in this chapter, answer the questions that 1. Which of the following drugs would most likely be
follow. p rescribed for Mr. Novi?
1. Isosorbide dinitrate (Isordil)
Mr. Albert Novi, age 45, has smoked since age 12. He recently 2. Enalapril (Vasotec)
has had trouble breathing when mowing the lawn, and he 3. Milrinone (Primacor)
coughs when he lies down to sleep at night. The physician 4. Digoxin (Lanoxin)
has diagnosed Mr. Novi with early HF and is planning on
2. Which of the following actions would be most desirable 4. Mr. Novi has eventually been placed on digoxin and
for a drug used to treat HF in Mr. Novi? furosemide. Which of the following adverse effects of furo-
1. Increase the heart rate. semide should nurse tell the patient about because it could
2. Increase cardiac output. lead to dysrhythmias and other cardiac disease while taking
3. Increase arterial blood pressure. digoxin?
4. Increase blood volume by retaining water. 1. Hypotension
2. Bradycardia
3. After a year, Mr. Novi enters the emergency department 3. Hypokalemia
with acute shortness of breath and severe congestion in both 4. Hyperkalemia
lungs. The nurse understands that the plan of care for a patient
presenting in the emergency room with these symptoms will
most likely include which medication?
1. Inamrinone (Inocor)
2. Captopril (Capoten)
3. Carvedilol (Coreg)
4. Spironolactone (Aldactone)

C
“Every time I mow the lawn
it happens. The pain is so h
crushing, all I can do is cry a
in my yard.” p
Ms. Shirley Bush t
e
r
Drugs for Angina Pectoris,

Myocardial Infarction, and Stroke 20
Core Concepts
20.1 Coronary heart disease is caused by a restriction in 20.7 Calcium channel blockers relieve angina pain by
blood flow to the myocardium. reducing the cardiac workload.
20.2 Angina pectoris is characterized by severe chest pain 20.8 The early diagnosis and treatment of myocardial
caused by lack of sufficient oxygen flow to heart infarction (MI) increases chances of survival.
muscle. 20.9 Thrombolytics dissolve clots blocking the coronary
20.3 Angina pain can often be controlled through posi- arteries.
tive lifestyle changes and surgical procedures. 20.10 Drugs are used to treat the symptoms and complica-
20.4 The pharmacologic management of angina is tions of acute MI.
achieved by reducing cardiac workload. 20.11 Aggressive treatment of stroke can increase
20.5 The organic nitrates relieve angina pain by dilating survival.
veins and the coronary arteries.
20.6 Beta-adrenergic blockers are sometimes preferred
drugs for reducing the frequency of angina attacks.
Drug Snapshot
Drug Classes Drug PROTOTYPES

Organic nitrates nitroglycerin (Nitrostat, Nitro-Bid,
Nitro-Dur, others) 307
Beta-adrenergic blockers atenolol (Tenormin) 309
Calcium channel blockers diltiazem (Cardizem, Cartia XT,
Dilacor XR, others) 309
Thrombolytics reteplase (Retavase) 312
Learning Outcomes
1. Describe how the myocardium 4. Explain the pharmacologic 7. For each of the classes listed
receives its oxygen and nutrient treatment of MI. in the Drug Snapshot, identify
supply. 5. Describe the pharmacologic representative drugs and explain
2. Explain the pathophysiology of treatment of stroke. their mechanisms of drug action,
angina pectoris. primary actions, and important
6. Categorize drugs used to treat adverse effects as they relate to
3. Identify positive lifestyle changes angina, MI, and stroke based on the treatment of angina, MI, or
that may be implemented to their classification and mechanisms stroke.
manage symptoms of angina. of action.
302 Chapter 20 Drugs for Angina Pectoris, Myocardial Infarction, and Stroke
Key Terms
angina pectoris (an-JEYE-nuh myocardial infarction (MI) (meye-oh-KAR- plaque (plak) 302
PEK-tore-us) 302 dee-ul in-FARK-shun) 310 stable angina 303
atherosclerosis (ath-ur-oh-skler-OH-sis) 302 myocardial ischemia (meye-oh-KAR-dee- stroke 314
coronary arteries (KOR-un-air-ee ul ik-SKEE-mee-uh) 302 thrombotic stroke (throm-BOT-ik) 314
AR-tur-ees) 302 percutaneous transluminal coronary unstable angina 303
coronary artery bypass graft (CABG) angioplasty (PTCA) (per-cue-TAIN-ee-
vasospastic (Prinzmetal’s) angina 303
surgery 304 us trans-LOO-min-ul KOR-un-air-ee
ANN-gee-oh-plas-tee) 304
hemorrhagic stroke (hee-moh-RAJ-ik) 314
A ll tissues in the body are dependent on a continuous supply of oxygen and vital nutrients to sup-
port life and health. The heart and brain are especially demanding. Should the blood supply to
cardiac muscle become compromised, cardiovascular function may become impaired, resulting
in angina pectoris, myocardial infarction (MI), and, possibly, death. Interruption of blood supply to the
brain can cause fainting or stroke. This chapter focuses on the pharmacologic interventions related to an-
cerebro = head or brain
vascular = vessels gina pectoris, MI, and stroke (also called cerebrovascular accident or CVA).
Coronary heart disease is caused by a restriction in blood flow

Core Concept 20.1 to the myocardium.
The heart is the hardest working organ in the body. Whereas the activity of most organs slows considerably
during rest and sleep, the heart must continue pumping so that the tissues can receive the nutrients they need
myo 5 muscle and dispose of the wastes they have accumulated. Because it is such a vital organ, the heart muscle (myocar-
cardium 5 heart dium) must receive a continuous supply of oxygen and nutrients. Any disturbance in blood flow to the vital
organs or to the myocardium itself—even for brief episodes—can result in life-threatening consequences.
Because the heart chambers fill with blood more than 60 times per minute, one would think that the
myocardium would have an ample supply of oxygen and nutrients. The myocardium, however, receives es-
sentially no nutrients from the blood traveling through the heart’s chambers. Instead, heart muscle receives
its nutrients from the first two arteries branching off the aorta, the right and left coronary arteries. As these
arteries branch, they circle the heart, bringing cardiac muscle a continuous supply of oxygen and nutrients.
Coronary heart disease, also called coronary artery disease (CAD), is the term used to describe im-
paired blood flow in the coronary arteries. Moderate restriction of flow leads to angina pectoris. Severe
impairment or complete loss of blood flow causes MI and a high risk of sudden death. CAD can also cause
dysrhythmias and lead to heart failure.
Angina Pectoris
Angina pectoris is acute chest pain caused by insufficient oxygen to a portion of the myocardium. Angina
is characterized by chest pain on physical exertion or emotional stress. Although it produces many of the
same symptoms as a heart attack, its pharmacologic treatment is quite different.
Angina pectoris is characterized by severe chest pain caused by lack

Core Concept 20.2 of sufficient oxygen flow to heart muscle.
athero 5 fatty The most common cause of angina is atherosclerosis: a buildup of fatty, fibrous material called plaque
sclera 5 hard in the walls of arteries. Although plaque may take as long as 40 to 50 years to accumulate to a level that
osis 5 abnormal condition would cause symptoms, plaque deposition actually begins very early in life. If plaque accumulates in a
coronary artery, the myocardium downstream from the affected artery begins to receive less oxygen than
it needs to perform its metabolic functions. This condition of having a reduced blood supply to cardiac
muscle cells is called myocardial ischemia. Figure 20.1 ■ illustrates the progressive accumulation of
plaque that is characteristic of atherosclerosis.
The classic presentation of angina pectoris is intense pain in the chest, often moving to the left side
of the neck and lower jaw and down the left arm. Angina pain is usually preceded by physical exertion or
emotional excitement—events associated with increased myocardial oxygen demand. The plaque-filled
coronary artery is unable to supply the amount of nutrients needed by the stressed myocardium. With rest,
angina pain usually diminishes in less than 15 minutes.
Figure 20.1
Plaque and thrombus

formation in the
coronary artery.
Platelets and fibrin deposit

on plaque and initiate clot
formation
(a) Smooth muscle
Plaque
Moderate Thrombus Thrombus

narrowing partially completely
of lumen occluding lumen occluding lumen
(b)
There are several types of angina. Angina pectoris that is predictable in its frequency, intensity, and
duration is called stable angina. If angina episodes become more frequent or severe and occur during pe-
riods of rest, the condition is called unstable angina. Unstable angina requires more aggressive medical
intervention. It is sometimes considered a medical emergency because it is associated with an increased
risk of MI. A third type of angina is known as vasospastic or Prinzmetal’s angina. This type is caused
by spasms of the coronary arteries, which may or may not contain plaque. Vasospastic angina pain occurs
most often during periods of rest.
Angina pain may closely mimic that of an MI. It is necessary for the healthcare provider to distinguish
quickly between the two diseases because the pharmacologic treatment of angina is much different than
that of MI. Angina is rarely fatal. In contrast, MI has a high mortality rate if treatment is delayed, so drug
therapy must begin immediately.
Chest pain is a common complaint of patients seeking care in physicians’ offices and emergency de-
partments. It is also one of the most frightening symptoms for patients, who often equate their pain to hav-
ing MI with a real risk of sudden death. The pain experienced by the patient, however, is only a symptom of
an underlying disorder. A number of diverse diseases can produce pain in the chest, and some of these are
unrelated to the heart. A major goal of the healthcare provider is to quickly determine the cause of the pain
so that the proper treatment can be administered. Table 20.1 ◆ lists some of the common diseases that can
produce chest pain as a symptom.
Table 20.1 Examples of Disorders That May Produce Chest Pain

Name of Disease Description
Coronary artery disease Atherosclerosis of the coronary arteries
Diabetes Lack of insulin or inability to tolerate carbohydrates
Gastric reflux Backflow of stomach contents into the esophagus
Hypertension High systemic blood pressure
Mitral stenosis Inability of the mitral valve to fully open
Myocardial infarction Cardiac muscle tissue death due to clots in coronary arteries
Peptic ulcer disease Erosion of the mucosa of the stomach or small intestine
Fast Facts Angina Pectoris and Coronary Heart Disease

■ Coronary heart disease causes one out of every five deaths in the United States.
■ Almost 10 million Americans have angina pectoris; 500,000 new cases occur each year.
■ Among ethnic groups, the incidence of angina is highest among African Americans, intermediate in
Mexican Americans, and lowest in non-Hispanic Whites.
■ Angina occurs more frequently in women than men; African American women have approximately
twice the risk of African American men.
Angina pain can often be controlled through positive lifestyle changes

Core Concept 20.3 and surgical procedures.
A combination of variables influences the development and progression of CAD, including dietary patterns
and lifestyle choices. A number of dietary and lifestyle factors are associated with an increased incidence
of angina. The healthcare provider should help the patient control the frequency of angina episodes by ad-
vising him or her to implement some or all of the following lifestyle changes:
■ Limit alcohol consumption to small amounts.
■ Eliminate foods high in cholesterol or saturated fats.
■ Keep blood cholesterol and other lipid indicators within the normal ranges.
■ Do not use tobacco.
■ Keep blood pressure within the normal range.
■ Exercise regularly and maintain optimum weight.
■ Keep blood glucose levels within normal range.
■ Limit salt (sodium) intake.
■ Reduce stress levels as much as possible.
When the coronary arteries are significantly obstructed, the two most common interventions are
per = through procedure ercutaneous transluminal coronary angioplasty (PTCA) with stent insertion, and coronary artery
p
cutaneous = skin bypass graft (CABG) surgery. PTCA is a procedure whereby the area of narrowing is dilated using either
a balloon catheter or a laser. Because the artery may return to its narrowed state after the procedure, a stent
angio = vessel
is sometimes used in conjunction with balloon angioplasty. Angioplasty with stenting typically relieves
plasty = shaped or molded by
a surgical procedure 90% of the original blockage in the artery.
Concept Review 20.1

■ How can a healthcare provider distinguish between stable angina and unstable angina?
The pharmacologic management of angina is achieved by reducing

Core Concept 20.4 cardiac workload.
The treatment goals for a patient with angina are twofold: to reduce the frequency of angina episodes and
to terminate acute angina pain in progress. Long-term goals include extending the patient’s life span by
preventing serious consequences of ischemic heart disease, such as dysrhythmias, heart failure, and MI.
The primary means by which antiangina drugs act is by reducing the myocardial demand for oxygen. This
reduced demand can be accomplished by at least four mechanisms:
■ Slowing the heart rate
■ Dilating veins so that heart receives less blood (reduced preload)
■ Causing the heart to contract with less force (reduced contractility)
■ Lowering blood pressure, thus offering the heart less resistance when ejecting blood from the
ventricles (reduced afterload)
Three classes of drugs—organic nitrates, beta-adrenergic blockers, and calcium channel blockers—
are used to treat angina. Rapid-acting organic nitrates are preferred drugs for terminating acute angina
Figure 20.2
Arterioles Mechanisms of action

of drugs used to treat
angina pectoris.
Beta-adrenergic antagonists
• Decrease the heart rate and 2
myocardial contractility
• Reduce cardiac output and
workload Ca11
b1
Sympathetic Calcium channel blockers
nervous system
• Dilate arterial smooth muscle,
reducing blood pressure and
decreasing cardiac workload
• Some also decrease the heart
2 rate, reducing the workload on
Heart rate the heart, and dilate the
and 2 coronary arteries
contractility 2
2
Vasodilation
Venous
return/ Organic nitrates
preload • Dilate veins, reducing the amount of
2 blood returning to the heart
• Dilate the coronary arteries, bringing
more blood to the myocardium
pain. Beta-adrenergic blockers are considered first-line drugs for preventing angina pain. Calcium channel
blockers are used when beta blockers or long-acting organic nitrates are not tolerated well by a patient. It
is important to understand that the antiangina medications relieve symptoms but do not cure the underlying
disorder. A summary of the drugs used to prevent and treat CAD is shown in Figure 20.2 ■.
Patients with angina will also likely be taking several secondary medications. Daily low-dose aspirin
reduces the risk of serious cardiovascular events. Statins may be prescribed to lower blood cholesterol
levels and reduce the advancement of coronary atherosclerosis. Inclusion of omega-3 fatty acids is some-
times recommended in patients with stable CAD. Ranolazine (Ranexa) is a newer drug for angina that is
approved for chronic angina that has not responded to other agents.
The organic nitrates relieve angina pain by dilating veins and the
coronary arteries. Core Concept 20.5
All drugs in this chemical class possess at least one nitrate (NO2) group. The vasodilation effect of these
agents is a result of the conversion of nitrate to its active form, nitric oxide (NO). Another nitrogen-
containing drug, nitrous oxide (N 2O), is used in anesthesia (see the chapter on Chapter 13). Organic
nitrates used to treat angina are listed in Table 20.2 ◆.
Since the discovery of their medicinal properties in 1857, the organic nitrates have been the mainstay
for the treatment of angina. The primary therapeutic action of these agents is their ability to relax both arte-
rial and venous smooth muscle. Dilation of veins reduces the amount of blood returning to the heart (pre-
load), so the chambers contain a smaller volume. With less blood for the ventricles to pump, the workload
on the heart is decreased, thereby lowering myocardial oxygen demand. The therapeutic outcome is that
chest pain is terminated and episodes of angina become less frequent.
Organic nitrates also have the ability to dilate coronary arteries, and this was once thought to be their
primary mechanism of action. It seems logical that dilating a partially occluded coronary vessel would
allow more oxygen to reach ischemic myocardial tissue. Although this effect does indeed occur, it is not
believed to be the primary mechanism of nitrate action in stable angina. This action, however, is important
in treating the less common form of angina known as vasospastic angina. The organic nitrates can relax
these spasms and stop the pain.
Table 20.2 Selected Drugs for Angina and Myocardial Infarction

Organic Nitrates
isosorbide dinitrate (Dilatrate PO; 2.5–30 mg qid (max: 480 mg/day) For both acute attacks and long-term management; sublin-
SR, Isordil) gual and chewable forms smaller dose is given to initiate
therapy; extended-release form available
isosorbide mononitrate (Imdur, PO (regular release); 20 mg bid; For the prevention of angina; a smaller dose is given to
Ismo, Monoket) PO (sustained release); 30–60 mg once daily initiate therapy; give in morning, if taking once daily
nitroglycerin (Nitrostat, Sublingual: 1 tablet (0.3–0.6 mg) or 1 spray Dilates both arteries and veins; sublingual, oral, translingual,
Nitro-Bid, Nitro-Dur, others) (0.4–0.8 mg) every 3–5 minutes (max: three IV, transmucosal, transdermal, and topical forms available;
doses in 15 minutes) extended-release form available
acebutolol (Sectral) PO; 400–800 mg/day in 1–2 divided doses Cardioselective beta1 blocker; decreases cardiac output; for
(max: 1,200 mg/day) hypertension, dysrhythmias, and stable angina
atenolol (Tenormin) PO; 25–50 mg daily (max: 100 mg/day) Cardioselective beta1 blocker; for angina, dysrhythmias, MI,
and hypertension
metoprolol (Lopressor, For angina: PO; 100 mg bid (max: 400 mg/day) Cardioselective beta1 blocker; for angina, MI, and
Toprol XL) For MI: IV; 5 mg every two minutes for three hypertension
doses followed by PO doses
nadolol (Corgard) PO; 40 mg once daily (max: 320 mg/day) Nonselective beta1 and beta2 blocker; for long-term
prevention of angina and hypertension
propranolol (Inderal, InnoPran XL) PO; 10–80 mg bid–tid (max: 320 mg/day) Nonselective beta1 and beta2 blocker; IV form available;
(see page 340 for the Drug for angina, hypertension, dysrhythmias, MI, and migraine
Profile box) prophylaxis
timolol maleate (Betimol) PO; 15–45 mg tid (max: 60 mg/day) Nonselective beta1 and beta2 blocker; for hypertension, post
MI and angina; topical form available for glaucoma
Calcium Channel Blockers
amlodipine (Norvasc) PO; 5–10 mg daily (max: 10 mg/day) Also for hypertension; Lotrel contains amlodipine and the
ACE inhibitor benazepril
bepridil (Vascor) PO; 200 mg daily (max: 400 mg/day) Also blocks sodium channels; usually reserved for patients
unresponsive to safer antianginals
diltiazem (Cardizem, Cartia PO (regular release); 30 mg tid-qid (max: Dilates coronary arteries and decreases coronary
XT, Dilacor XR, others) 480 mg/day) artery spasm; also for hypertension; IV form available
PO (extended release); 20–240 mg bid (max: for dysrhythmias
540 mg/day)
nicardipine (Cardene) PO; 20–40 mg tid or 30–60 mg Also for hypertension; IV form available
PO (sustained release); bid (max: 120 mg/day)
nifedipine (Adalat CC, Procardia PO; 10–20 mg tid (max: 180 mg/day) Used in the treatment of vasospastic angina; also for
XL, others) (see page 279 for the PO (extended release); 30–90 mg once daily hypertension
Drug Profile box)
verapamil (Calan, Isoptin SR, PO (regular release); 80 mg tid–qid (max: Dilates coronary arteries and inhibits coronary artery spasm;
others) (see page 342 for the 480 mg/day) also for hypertension; IV form available for dysrhythmias
Drug Profile box) PO (sustained release); 180 mg once daily
MISCELLANEOUS DRUG
ranolazine (Ranexa) PO; 500–1,000 mg bid (max: 1,000 mg bid) Acts by shifting myocardial metabolism from fatty acids to
glucose, which decreases the oxygen demands of the heart
trans = across or through Organic nitrates are of two types: short acting and long acting. The short-acting agents, such as ni-
dermis = skin troglycerin, are taken sublingually to quickly stop an acute angina attack in progress. Long-acting nitrates,
such as isosorbide dinitrate (Dilatrate SR, Isordil), are taken orally or delivered through a transdermal
patch to decrease the frequency and severity of angina episodes. Long-acting nitrates are also useful in
reducing the symptoms of heart failure (see Chapter 18).
Drug Prototype: Nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, Others)

Therapeutic Class: Antiangina drug Pharmacologic Class: Organic nitrate, vasodilator
Actions and Uses: Nitroglycerin, the oldest and most widely Adverse Effects and Interactions: Adverse effects of nitro-
used of the organic nitrates, can be delivered by a number of glycerin are usually cardiovascular and rarely life threatening.
different routes, including sublingual, lingual spray, oral, IV, Because nitroglycerin can dilate vessels in the head, headache
transmucosal, transdermal, topical, and extended-release forms. is common and may be persistent and severe. Occasionally, the
It is normally taken while an acute angina episode is in prog- venodilation created by nitroglycerin causes reflex tachycardia.
ress or just prior to physical activity. When given sublingually, A beta-adrenergic blocker may be prescribed to diminish this
it reaches peak plasma levels in only four minutes and thus undesirable increase in heart rate. Many adverse effects of ni-
can stop angina pain rapidly. Chest pain that does not respond troglycerin diminish after a few doses.
quickly to sublingual nitroglycerin may indicate MI. The trans- Using with sildenafil (Viagra) may cause life-threatening
dermal and oral sustained-release forms are for prophylaxis hypotension and CV collapse. Nitrates should not be taken 24
only, because they have a relatively slow onset of action. hours before or after taking Viagra.
Although nitrates are safe drugs that have few serious adverse effects, some adverse effects may be
troublesome to patients. Dilation of veins can reduce blood pressure and cause patients to become dizzy
when moving to a standing position. This fall in blood pressure can result in reflex tachycardia, causing tachy = rapid
patients to feel as if their heart is having palpitations or skipping a beat. Dilation of cerebral vessels may cardia = heart
cause headache, which can sometimes be severe. Flushing of the skin is common. Most of these effects are
temporary and rarely cause discontinuation of drug therapy.
Tolerance commonly occurs with the long-acting organic nitrates when they are taken for extended
periods. The magnitude of the tolerance depends on the dosage and the frequency of drug administration.
Patients are often instructed to remove the transdermal patch for 6–12 hours each day or withhold the
nighttime dose of the oral organic nitrate to delay the development of tolerance.
Beta-adrenergic blockers are sometimes the preferred drugs for reducing

the frequency of angina attacks. Core Concept 20.6
Beta-adrenergic blockers reduce the workload on the heart and are used for angina prophylaxis. Drugs for
angina include cardioselective beta1-blockers and mixed beta1-beta2-blockers. The beta-adrenergic block-
ers of importance in treating angina are listed in Table 20.2.
The pharmacology of the beta-adrenergic blockers, including a Nursing Process Focus, was presented
in Chapter 8. Beta blockers are widely used in medicine, including for the treatment of hypertension (see
Chapter 18), heart failure (see Chapter 19), and dysrhythmias (see Chapter 22). Because of their ability to
reduce the workload on the heart by slowing heart rate and reducing contractility, several beta blockers are
used to decrease the frequency and severity of angina attacks caused by exertion.
Beta-adrenergic blockers are well tolerated by most patients. In some patients, fatigue, lethargy, and
depression occur. Because beta blockers slow the heart rate, they are contraindicated in patients with bra-
dycardia and heart block. Heart rate should be closely monitored so that it does not fall below 60 beats per
minute (bpm) at rest or 100 bpm during exercise. Patients with diabetes should be aware that blood glucose
levels should be monitored more frequently and that insulin doses may need to be adjusted accordingly.
Patients should be advised against abruptly stopping beta-blocker therapy because this may result in a sud-
den increase in workload on the heart and acute angina symptoms. Patients should also be advised to make
position changes slowly when going from a recumbent to an upright position to prevent dizziness and pos-
sible fainting.
Calcium channel blockers relieve angina pain by reducing

the cardiac workload. Core Concept 20.7
Several calcium channel blockers (CCBs) reduce myocardial oxygen demand by lowering blood pressure
and slowing the heart rate. They are widely used in the treatment of cardiovascular diseases. The first ap-
proved use of CCBs was for the treatment of angina. CCBs’ importance to the pharmacotherapy of angina
is listed in Table 20.2.
Nursing Process Focus Patients Receiving Organic Nitrate Therapy

Prior to administration: ■ Risk for Ineffective Tissue Perfusion related to hypotension from drug
■ Obtain a complete health history including cardiovascular conditions, therapy
allergies, drug history, and possible drug interactions. ■ Risk for Injury (dizziness or fainting) related to hypotension from drug
■ Acquire the results of a complete physical examination, including vital therapy
signs, height, weight, and ECG. ■ Acute Pain (headache) related to adverse effects of drug
■ Evaluate laboratory blood findings: CBC, electrolytes, cardiac enzymes, ■ Deficient Knowledge related to a lack of information about drug
lipid panel, and renal and liver function studies. therapy
■ Attain information regarding cardiac-related medications such as ■ Ineffective Self-health Maintenance related to lack of knowledge
sildenafil (Viagra), vardenafil (Levitra), or tadalafil (Cialis) used within about seriousnesss of disease and drug therapy regimen
the past 24 hours.
The patient will:

■ Experience therapeutic effects (relief or prevention of chest pain).
Implementation

■ In cases of chest pain, administer medication correctly and evaluate In case of chest pain, instruct the patient to:
the patient’s knowledge of proper administration. Ask the patient to ■ Place one tablet under the tongue every five minutes during an attack,
describe and rate pain prior to and throughout drug administration up to three times/tablets, until pain is relieved.
for description/documentation of angina episode. (Location and qual- ■ Place SL tablet under the tongue or spray under the tongue; do not
ity of pain will determine need for medication; patients at risk for inhale spray.
angina or MI will need to carry drug in case of emergencies for.) ■ Call emergency medical services (EMS) if chest pain is not relieved after
two or three doses.
■ Obtain a 12-lead ECG to differentiate between angina and infarction. ■ Explain to the patient the reason for and importance of conducting
(Pharmacotherapy depends on which disorder is presenting.) an ECG.
■ Monitor vital signs, especially blood pressure and pulse. Do not admin- Instruct the patient to:
ister drug if the patient is hypotensive. (Drug will further reduce blood ■ Monitor blood pressure as specified by the healthcare provider and
pressure.) ensure proper use of home equipment.
■ Sit or lie down before taking medication and to avoid abrupt changes
in position.
■ Explain to the patient the reason for and importance of monitoring
blood levels that indicate cardiac function.
■ Monitor laboratory findings, especially cardiac enzymes, CBC, blood ■ Advise the patient of the importance of keeping appointments for
urea nitrogen (BUN), creatinine, and liver function test. (Monitoring laboratory testing.
blood levels supplies valuable information on patient’s status.)
■ Monitor alcohol use. (Use of alcohol with nitrates may cause extremely ■ Emphasize the importance of avoiding alcohol while taking
low blood pressure.) nitroglycerin.
■ Monitor for headache in response to use of nitrates. (Nitrates cause Instruct the patient that:
vasodilation including vessels in the head, which may cause pain.) ■ Headache is a common adverse effect that usually decreases over time.
■ Over-the-counter (OTC) medicines usually relieve the headache.
■ He or she must notify the healthcare provider if headaches continue.
■ Monitor for use of erectile dysfunction drugs (e.g., sildenafil) concur- Instruct the patient to:
rently with nitrates. (Life-threatening hypotension may result with ■ Not take erectile dysfunction drugs within 24 hours after taking
concurrent use of these drugs.) nitrates.
■ Wait at least 24 hours after taking erectile dysfunction drugs to
resume nitrate therapy.
■ For use of prophylactic nitrates, administer medication correctly and ■ Instruct patient in the appropriate dosing and administration of the
evaluate the patient’s knowledge of proper administration. (Some specific nitrate being taken.
patients may need the vasodilation effect of nitrates on a continuous ■ Advise the patient to take medication prior to a stressful event or
basis.) physical activity to prevent angina.
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see Planning). See Table 20.2 for a
Drug Prototype: Atenolol (Tenormin)

Therapeutic Class: Drug for angina, hypertension, or MI Pharmacologic Class: Beta-adrenergic blocker
Actions and Uses: Atenolol is one of the most frequently pre- Using atenolol together with calcium channel block-
scribed drugs in the United States due to its relative safety and ers may cause excessive cardiac suppression. Using atenolol
effectiveness in treating a number of chronic disorders, includ- together with digoxin may cause slowed atrioventricular
ing heart failure, hypertension, stable angina, and MI. Atenolol conduction leading to heart block. Patients should avoid
selectively blocks beta1 receptors in the heart. Its effectiveness in using this drug with nicotine or caffeine because their va-
angina is attributed to its ability to slow heart rate and reduce soconstriction action will diminish the beneficial effects of
contractility (negative inotropic effect), both of which lower atenolol.
myocardial oxygen demand. Because of its seven- to nine-hour
half-life, it may be taken once a day.
Adverse Effects and Interactions: As a cardioselective beta1

blocker, atenolol has few adverse effects on the lungs and is Black Box Warning:
useful for patients experiencing bronchospasm. Like other beta Abrupt discontinuation of atenolol should be avoided in
blockers, therapy generally begins with low doses, which are patients with ischemic heart disease because this can cause
gradually increased until the therapeutic effect is achieved. The acute angina pain; doses should be reduced over a one- to
most frequent adverse effects of atenolol include fatigue, weak- two-week period.
ness, dizziness, and hypotension.
Blockade of calcium ion channels has a number of effects on the heart, most of which are similar to
those of beta-adrenergic blockers. Like beta blockers, actions of the CCBs are presented in several chapters
in this text for the treatment of hypertension (see Chapter 18) and dysrhythmias (see Chapter 22). A Nurs-
ing Process Focus for this drug class is included in Chapter 18.
CCBs cause arteriolar smooth muscle to relax, thus lowering peripheral resistance and reducing blood
pressure. This decreases the myocardial oxygen demand, thus reducing the frequency of angina pain. Some
CCBs are selective for arterioles. Others, such as verapamil and diltiazem, have an additional beneficial ef-
fect of slowing the heart rate (negative chronotropic effect). An additional effect of the CCBs is their abil-
ity to dilate the coronary arteries, bringing more oxygen to the myocardium. This is especially important in
patients with vasospastic angina. Because they are able to relieve the acute spasms of vasospastic angina,
CCBs are considered drugs of choice for this condition.
Most adverse effects of CCBs are related to vasodilation, such as headache, dizziness, and edema of
the ankles and feet. CCBs should be used with caution in patients taking other cardiovascular medications
that slow conduction through the atrioventricular (AV) node, particularly digoxin or beta-adrenergic block-
ers. The combined effects of these drugs may cause partial or complete AV heart block, heart failure, or
dysrhythmias.
Concept Review 20.2

■ How does decreasing the workload on the heart result in reduction in angina pain?
Drug Prototype: Diltiazem (Cardizem, Cartia XT, Dilacor XR, Others)

Therapeutic Class: Drug for angina and hypertension Pharmacologic Class: Calcium channel blocker
Actions and Uses: Diltiazem inhibits the transport of calcium as headache, dizziness, and edema of the ankles and feet. Al-
ions into myocardial cells and has the ability to relax both though diltiazem produces few adverse effects on the heart or
coronary and peripheral blood vessels. It is useful in the vessels, it should be used with caution in patients taking other
treatment of atrial dysrhythmias and hypertension as well as cardiovascular medications, particularly digoxin or beta-adren-
angina. When given as sustained-release capsules, it may be ergic blockers; the combined effects of these drugs may cause
administered once daily. heart failure or dysrhythmias.
Diltiazem increases the levels of digoxin or quinidine if
Adverse Effects and Interactions: Adverse effects of diltiazem are taken together. It should be used cautiously with ginger because
generally not serious and are related to vasodilation such this combination may interfere with blood clotting.
Myocardial Infarction
A myocardial infarction (MI) is the result of a sudden occlusion of a coronary artery. Immediate pharma-
cologic treatment may reduce patient mortality.
The early diagnosis and treatment of myocardial infarction (MI) increases

Core Concept 20.8 chances of survival.
MIs are responsible for a substantial number of deaths each year. Some patients die before reaching a med-
ical facility for treatment, and many others die within 48 hours after the initial MI. Clearly, MI is a serious
and frightening disease and is responsible for a large percentage of sudden deaths.
The primary cause of MI is advanced CAD. Plaque buildup can severely narrow one or more branches
of the coronary arteries. Pieces of plaque may break off and lodge in a small vessel that serves a portion of
the myocardium. Deprived of its oxygen supply, the affected area of the myocardium becomes ischemic
and cardiac muscle cells begin to die unless the blood supply is quickly restored. Figure 20.3 ■ illustrates
this blockage and the resulting reperfusion process.
Goals for the pharmacologic treatment of acute MI include the following:
■ Restore blood supply (perfusion) to the damaged myocardium as quickly as possible through the
use of thrombolytics
■ Reduce myocardial oxygen demand with organic nitrates, beta blockers, or CCBs to prevent
another MI
■ Control or prevent MI-associated dysrhythmias with beta blockers or other antidysrhythmics
■ Reduce post-MI mortality with aspirin, beta blockers, and angiotensin-converting enzyme
(ACE) inhibitors
■ Manage severe chest pain and associated anxiety with analgesics
■ Prevent enlargement of the clot with anticoagulants and antiplatelet drugs
Fast Facts Myocardial Infarction

■ About 1.5 million Americans experience a new or recurrent MI each year.
■ About one third of patients experiencing an MI will die; half the deaths occur prior to arrival at the
hospital.
■ About 60% of patients who died suddenly of MI had no previous symptoms of the disease.
■ Mortality from MI is slightly higher in men than in women.
■ More than 20% of men and 40% of women will die from an MI within 1 year of being diagnosed.
Core Concept 20.9 Thrombolytics dissolve clots blocking the coronary arteries.
Thrombolytics are medications that are administered to dissolve an existing blood clot. In the treatment
of MI, the goal of thrombolytic therapy is to dissolve clots that are obstructing the coronary arteries and
restore circulation to the myocardium as quickly as possible. Thrombolytics are most effective when ad-
ministered from 20 minutes to 12 hours after the onset of MI symptoms. Quick restoration of cardiac
circulation has been found to prevent permanent damage to the myocardium and reduce mortality from the
disease. After the clot is successfully dissolved, anticoagulant or antiplatelet therapy is initiated to prevent
the formation of additional thrombi.
Thrombolytics have a narrow margin of safety and the primary risk is excessive bleeding from
interference in the clotting process. Older adults have an increased risk of serious bleeding and intracranial
hemorrhage. Patients with recent trauma or surgery should not receive these drugs. Vital signs must be
monitored continuously, and any signs of bleeding generally call for discontinuation of therapy. Because
these medications are rapidly destroyed in the blood, stopping the infusion normally results in the rapid
termination of any adverse effects.
Figure 20.3
1
Patient experiencing a
myocardial infarction:
must arrive at the hospital
within 20 minutes to 12
hours for thrombolytic
Left coronary
therapy to be effective.
artery
Coronary
thrombosis
Left
ventricle
Area of
ischemia
2
Large clot lodged Catheter
in the left coronary
artery. Tissue distal
to the clot becomes Clot
inflamed and ischemic.
3
Thrombolytic therapy is
initiated in close proximity
to the clot.
Clot
4
Thrombolytic drug dissolves Ischemia
clot. Circulation is restored to clearing
the myocardium and ischemia
begins to resolve.
Blockade and reperfusion following myocardial infarction (mi): (1) blockage of left coronary artery with myocardial
ischemia, (2) infusion of thrombolytics, (3) blood supply returning to myocardium, and (4) thrombus dissolving and
ischemia clearing.
Table 20.3 Thrombolytics

alteplase (Activase) (see page IV; 60 mg initially, then 20 mg/hr infused Naturally occurring tissue plasminogen activator; must be given
357 for the Drug Profile box) over next two hours within six hours of start of MI or three hours of thrombotic stroke
reteplase (Retavase) IV; 10 units over two minutes; repeat Given during an acute MI to decrease the risk of HF and death
dose in 30 minutes
streptokinase (Kabikinase) IV; 250,000–1.5 million units over For acute DVT, pulmonary embolism, and MI
60 minutes
tenecteplase (TNKase) IV; 30–50 mg infused over five seconds Newer thrombolytic with longer half-life
Drug Prototype: Reteplase (Retavase)

Therapeutic Class: Drug for dissolving clots Pharmacologic Class: Thrombolytic
Actions and Uses: Like other drugs in this class, reteplase is most in recognizing and reporting any abnormal bleeding that may
effective if given within 30 minutes but not later than 12 hours occur during thrombolytic therapy. The drug is contraindicated
of the onset of MI symptoms. It usually acts within 20 minutes. A in patients with active bleeding.
second bolus may be delivered after the first, if necessary. After Drug interactions with anticoagulants and platelet aggre-
the clot has been dissolved, therapy with heparin or another anti- gation inhibitors will produce an additive effect and increase
coagulant is started to prevent additional clots from forming. the risk of bleeding.
Adverse Effects and Interactions: The major adverse effect of
reteplase is hemorrhage. Healthcare providers must be vigilant
Since the discovery of streptokinase, the first thrombolytic, there have been a number of generations
of thrombolytics. The more recent drugs such as tenecteplase (TNKase) have a more rapid onset and a
longer duration and may produce fewer adverse effects than older drugs in this class. Table 20.3 ◆ lists the
major thrombolytics.
Core Concept 20.10 Drugs are used to treat the symptoms and complications of acute MI.
The most immediate needs of the patient with MI are to ensure that the heart continues functioning and
that permanent damage from the infarction is minimized. Drugs from several classes are administered
soon after the onset of symptoms to prevent reinfarction and, ultimately, to reduce mortality from the
episode.
Beta blockers are used for MI, as they are for angina, to reduce the cardiac workload. Beta blockers have
the ability to slow the heart rate, decrease contractility, and reduce blood pressure. These three actions
reduce the cardiac oxygen demand, which is beneficial for those who have experienced a recent MI. In
addition, the ability of beta blockers to slow impulse conduction through the heart tends to suppress dys-
rhythmias, which can be serious and sometimes fatal complications can occur following MI. Their use has
been found to reduce mortality following an MI if given within eight hours.
Antiplatelet and Anticoagulant Drugs

Aspirin has been found to dramatically reduce mortality, as much as 50%, in the weeks following an acute
MI. Unless contraindicated, 160–324 mg of aspirin is given as soon as possible following a suspected MI.
Clopidogrel (Plavix) is another effective antiplatelet agent that has been shown to reduce mortality as-
sociated with thrombi formation following an MI. Patients at high risk for thrombi formation may receive
Nursing Process Focus Patients Receiving Thrombolytic Therapy

Prior to administration: ■ Risk for Injury (bleeding) related to adverse effects of thrombolytic
■ Obtain complete health history including cardiovascular, renal, and therapy
liver conditions; recent surgeries or trauma; allergies; drug history ■ Ineffective Tissue Perfusion related to increase in size of thrombus, al-
(especially cardiovascular and OTC); and possible drug interactions. tered blood flow
■ Acquire the results of a complete physical examination, including vital ■ Deficient Knowledge related to a lack of information about drug
signs, height, and weight. therapy
■ Evaluate laboratory blood findings: CBC, electrolytes, clotting factors
(aPTT, PT, platelet count), and renal and liver function studies.
The patient will:

■ Experience therapeutic effects (dissolving of preexisting blood clot(s).
Implementation
Interventions and Rationales Patient Education/Discharge Planning

■ Administer medication correctly; have IV lines initiated or Foley cath- ■ Instruct the patient about procedures and why they are necessary prior
eter inserted prior to beginning therapy. (This allows for monitoring to beginning thrombolytic therapy.
the patient’s condition.)
■ Monitor vital signs every 15 minutes during the first hour of infusion, ■ Advise the patient on the need for frequent monitoring of vital signs.
then every 30 minutes during the remainder of infusion. (A change in
vital signs may indicate indication excessive bleeding, a major adverse
effect of thrombolytic therapy.)
■ Patient should be moved as little as possible during the infusion. (This ■ Advise the patient that activity will be limited during infusion and that
is done to prevent internal injury.) a pressure dressing may be needed to prevent any active bleeding.
■ If given for thrombotic stroke, monitor neurologic status frequently. ■ Advise the patient about assessments and why they are necessary.
(Changes in LOC can indicate excessive bleeding.)
■ Have cardiac rhythm monitored while medication is infusing. ■ Advise the patient that cardiac rhythm will be monitored during
(Dysrhythmias may occur with reperfusion of myocardium.) therapy.
■ Monitor laboratory findings (CBC, clotting factors and ABG) during ■ Instruct the patient on increased risk for bleeding and on the need for
and after therapy for indications of blood loss due to internal activity restriction and frequent monitoring during this time.
bleeding. (Patient has increased risk of bleeding for two to four
days post infusion.)

anticoagulants such as heparin, low-molecular weight heparin, or warfarin (Coumadin) following an MI.
Some patients may remain on anticoagulant therapy on a chronic basis after hospital discharge. The vari-
ous coagulation modifiers are presented in Chapter 23.
Angiotensin-Converting Enzyme (ACE) Inhibitors

The ACE inhibitors captopril (Capoten) and lisinopril (Prinivil, Zestril) have also been found to reduce
mortality following MI. These drugs are most effective when therapy is started within one or two days of
the onset of symptoms. Oral therapy with the ACE inhibitors normally begins after thrombolytic therapy
has been completed and the patient’s condition has stabilized. The pharmacology of the ACE inhibitors is
presented in Chapter 18.
Pain Management
Pain control is essential following acute MI to ensure the patient’s comfort and reduce stress. Opioids such
as morphine sulfate are sometimes given to ease the severe pain associated with acute MI and to sedate the
anxious patient. Details on the pharmacology of the opioids were presented in Chapter 14.
Concept Review 20.3

■ Why is it important to treat an MI within the first 24 hours after symptoms have begun?
What classes of drugs are used for this purpose?
Stroke
A stroke is caused by a thrombus within or bleeding from a vessel serving the brain. Although drug therapy
is limited, immediate treatment may reduce the degree of permanent disability resulting from a stroke.
Core Concept 20.11 Aggressive treatment of stroke can increase survival.
Stroke is a major cause of permanent disability caused by blockage of blood to the brain or rupture of a
blood vessel in the brain. The majority of strokes are caused by a thrombus in a vessel serving the brain
(thrombotic stroke). Areas downstream from the clot lose their oxygen supply, and neural tissue will be-
gin to die unless circulation is quickly restored. A smaller percentage of strokes, about 20%, are caused by
rupture of a cerebral vessel and its associated bleeding into neural tissue (hemorrhagic stroke). Symptoms
are the same for the two types of strokes. Specific symptoms will vary widely depending on the affected
area of the brain and may include blindness, paralysis, speech problems, coma, and even dementia. Mortal-
ity from stroke is very high: As many as 40% of patients will die within the first year of a stroke.
Drug therapy of thrombotic stroke focuses on two main goals: prevention of strokes through the use
of anticoagulants and antihypertensive agents, and restoration of blood supply to the affected portion of the
brain as quickly as possible after an acute stroke through the use of thrombolytics.
Treatment for hemorrhage strokes depends on the cause and severity of the bleeding. Drugs used in
the treatment of acute hemorrhagic stroke may include anticonvulsants to prevent seizure activity, anti-
hypertensive agents to reduce BP, and osmotic diuretics to decrease intracranial pressure. Thrombolytic
therapy is contraindicated in hemorrhagic strokes because its use would prolong bleeding into the intracra-
nial space and cause further damage.
As discussed in Chapter 18, sustained, chronic hypertension is closely associated with stroke. Anti-
hypertensive therapy with beta-adrenergic blockers, CCBs, diuretics, and ACE inhibitors can help manage
blood pressure and reduce the probability of stroke.
In very low doses, aspirin reduces the incidence of stroke by discouraging the formation of thrombi by
inhibiting platelet aggregation. Patients are often placed on low-dose aspirin therapy on a continual basis
following their first stroke. Clopidogrel (Plavix) is an antiplatelet drug that may be used to provide anti-
platelet activity in patients who cannot tolerate aspirin. Other anticoagulants such as warfarin may be given
to prevent stroke in high-risk patients such as those with prosthetic heart valves.
The single most important breakthrough in the treatment of stroke was development of the thrombo-
lytic agents. Prior to the discovery of these drugs, the treatment of thrombotic stroke was largely a passive,
wait-and-see strategy. Now stroke is aggressively treated with thrombolytics as soon as the patient arrives
at the hospital: These agents are most effective if administered within three hours of the attack. Use of
aggressive thrombolytic therapy can completely restore brain function in a significant number of patients
with stroke.
CAM THERAPY
Ginseng and Cardiovascular Disease
Ginseng is one of the oldest known herbal remedies. Panax ginseng is distributed throughout
China, Korea, and Siberia, whereas Panax quinquefolius is native to Canada and the United
States. American ginseng is not considered equivalent to Siberian ginseng.
Ginseng has been used for centuries to promote general wellness, boost immune function,
and reduce fatigue. There are some claims that the herb lowers blood glucose and can help in
the management of hypertension.
Ginseng is thought to have calcium channel blocking actions. The herb appears to improve
blood flow to the heart in times of low oxygen supply, such as with myocardial ischemia. Some
research has shown that ginseng lowers blood sugar levels in patients with type 2 diabetes.
In addition, some studies have found ginseng to boost the immune system. The healthcare
provider should caution patients who take ginseng, because herb–drug interactions are
possible with CCBs, oral hypoglycemics, warfarin, and loop diuretics.
Chapter Review 315
Fast Facts Stroke

■ Stroke is the third leading cause of death, behind heart disease and cancer.
■ The incidence of stroke increases with age, although 25% of all strokes occur in people younger
than age 65:
■ 14% of those 65–74 years old have had a stroke
■ 25% of those 75–84 years old have had a stroke
■ 28% of those older than age 85 have had a stroke
■ The highest incidence of stroke is in African American men—more than double that of white
women.
■ Stroke occurs more frequently in men than in women, although females account for about 60% of
all deaths due to strokes.
■ Over 160,000 Americans die of strokes each year.
patients need to know

Patients treated for chest pain need to know the following:
Regarding Drugs for Angina

1. Dissolve one nitroglycerin tablet under the tongue as soon as angina pain is felt. If pain
is not relieved in five minutes, use another. Many practitioners recommend a third nitro-
glycerin tablet for pain not relieved five minutes after the second dose. If chest pain/
pressure is not relieved by three doses of nitroglycerin, call EMS.
2. Rotate the application site of transdermal patches and do not apply a new patch until
after the old patch has been removed.
3. Change positions slowly. Postural hypotension may cause dizziness and even fainting.
4. Monitor blood pressure regularly, and report any consistent changes to a healthcare
provider.
Regarding Drugs for MI or Stroke

5. A variety of drugs are used in the treatment of MI and stroke. It is important to under-
stand and comply with the drug therapy regimen prescribed by the healthcare provider.
Chapter Review
20.1 Coronary heart disease is caused by a restriction in 20.2 Angina pectoris is characterized by severe chest
blood flow to the myocardium. pain caused by lack of sufficient oxygen flow to
The high metabolic rate of the heart requires that a heart muscle.
continuous supply of oxygen be maintained in the The coronary arteries can become partially occluded
coronary arteries. Restriction of flow can lead to with plaque, resulting in ischemia. Lack of sufficient
angina pectoris or MI. Because both of these disor- oxygen to the myocardium upon emotional or physi-
ders can cause severe chest pain, the healthcare pro- cal exertion causes sharp chest pain, the characteristic
vider must quickly determine the cause of the pain, symptom of angina.
so that appropriate treatment may be administered.
20.3 Angina pain can often be controlled through posi- prescribed to reduce the frequency of acute angina
tive lifestyle changes and surgical procedures. attacks.
A number of lifestyle changes can reduce the deposi-
tion of plaque in the coronary arteries and help pre- 20.8 The early diagnosis and treatment of myocardial
vent coronary heart disease. These include stopping infarction (MI) increases chances of survival.
tobacco use, limiting alcohol consumption, and get- MI is caused by a thrombus in a coronary artery and
ting adequate exercise. Surgical procedures may be is responsible for a substantial number of sudden
necessary to control severe angina. deaths. Fast, effective diagnosis and treatment can re-
duce mortality.
20.4 The pharmacologic management of angina is
achieved by reducing cardiac workload. 20.9 Thrombolytics dissolve clots blocking the coronary
Reducing the workload on the heart can relieve an- arteries.
gina pain. This can be accomplished by slowing the When used within hours of the onset of an MI, throm-
heart rate, dilating the vessels, reducing the force of bolytics can dissolve clots and restore circulation to
myocardial contraction, or reducing blood pressure. the myocardium.
20.5 The organic nitrates relieve angina pain by dilating 20.10 Drugs are used to treat the symptoms and compli-
veins and the coronary arteries. cations of acute MI.
Fast-acting organic nitrates can quickly terminate Beta blockers can slow the heart rate and reduce
angina pain by causing venodilation, which reduces blood pressure and have been shown to reduce
the workload on the heart. They also dilate the coro- mortality when given soon after MI symptoms ap-
nary arteries, bringing more oxygen to the myocar- pear. Aspirin and ACE inhibitors have been shown
dium. Long-acting nitrates can prevent acute angina to reduce mortality when given soon after the on-
episodes, but the patient may become tolerant to their set of MI. Narcotic analgesics are sometimes given
protective effect. to reduce the pain and anxiety associated with
an MI.
20.6 Beta-adrenergic blockers are sometimes pre-
ferred drugs for reducing the frequency of angina
attacks. 20.11 Aggressive treatment of stroke can increase
survival.
Beta blockers lower blood pressure, slow the heart
rate, and reduce the force of contraction, thus reducing Stroke is now viewed as an emergency condition
the workload on the myocardium. They are prescribed requiring immediate treatment to improve survival.
to reduce the frequency of acute angina episodes. Thrombolytics, when given quickly after the onset
of thrombotic strokes, can restore some or all brain
20.7 Calcium channel blockers (CCBs) relieve angina function. Some degree of stroke prevention can be
pain by reducing the cardiac workload. achieved by using anticoagulants and by controlling
blood pressure.
CCBs are effective at lowering blood pressure,
thus reducing the workload on the heart. They are
Review Questions
The following questions are written in NCLEX-PN® style. An- 3. “Call your physician when you have chest pain. The physi-
swer these questions to assess your knowledge of the chapter cian will tell you how many tablets to take.”
material, and go back and review any material that is not clear 4. “Place three tablets under your tongue and call 911.”
to you.
2. The most common adverse effect of nitroglycerin that the
nurse monitors the patient for is:
1. The patient is being discharged with nitroglycerin (Nitro- 1. Headache
stat) tablets. The nurse would teach the patient to: 2. Hypertension
1. “Swallow 3 tablets immediately for pain and call 911.” 3. Diuresis
2. “Put one tablet under your tongue for chest pain.” 4. Bradycardia
Chapter Review 317
3. The licensed practical/vocational nurse (LPN/LVN) is 7. The healthcare provider ordered an IV drip of D5W at 150
assisting the registered nurse in the development of a patient mL/hr. The tubing has a drip factor of 15 drops/mL. The nurse
care plan. She recognizes that the patient is going to be receiv- maintains the IV drip rate at how many drops per minute?
ing what class of medication that decreases heart rate, contrac- 1. 25 drops/minute
tility, and blood pressure, and is used to increase survival rates 2. 28 drops/minute
in post-MI patients? 3. 35 drops/minute
1. ACE inhibitors 4. 38 drops/minute
2. Beta blockers
3. Vasodilators 8. When treating angina, the nurse knows that the mecha-
4. Diuretics nism of action of a beta-adrenergic blocker is:
1. Slowed heart rate and decreased contractility of the heart
4. The nurse assesses for the most common adverse effect of 2. Relaxation of arterial and venous smooth muscle
reteplase (Retavase), which is: 3. Increased contractility and heart rate
1. Dehydration 4. Decreased peripheral resistance
2. Bleeding
9. The patient is instructed when taking calcium chan-
3. Confusion
nel blockers that he should use extreme caution when taking
4. Increased clotting times
which of the following medications?
5. The healthcare provider should be vigilant in observing 1. Acetaminophen (Tylenol)
for which of the following adverse effects during a reteplase 2. Ibuprofen (Motrin)
infusion? 3. Digoxin (Lanoxin)
1. An increase in blood pressure 4. Ranitidine (Zantac)
2. An increase in heart rate 10. The patient is complaining of a viselike pain in his chest
3. Abnormal bleeding and has been diagnosed with an MI. The nurse anticipates that
4. Vomiting or diarrhea he may be giving the patient which of the following medica-
6. The patient has a history of thrombotic stroke. Which of tions? (Select all that apply.)
the following drug(s) might be used in her treatment? (Select 1. Aspirin
all that apply.) 2. A beta blocker
1. Aspirin 3. Thrombolytics
2. Warfarin (Coumadin) 4. An ACE inhibitor
3. Protamine sulfate
4. Ticlopidine (Ticlid)
Remember Ms. Bush, the patient 3. Prevent MI or stroke.

introduced at the beginning of the 4. Relieve epigastric pain.
chapter? Now read the remainder of
the case study. Based on the informa- 2. What instructions should the nurse provide to Ms. Bush
tion you have learned in this chapter, about taking sublingual nitroglycerin?
answer the questions that follow. 1. Take before exercising.
2. Take on first indication of chest pain.
Ms. Shirley Bush, a 65-year-old woman arrives in your office 3. Take three or four times per day to prevent chest pain.
with a complaint of chest pain when she exercises. Subsequent 4. Take before bedtime and when rising.
tests show a 10% occlusion of two coronary arteries. Her blood
pressure is 126/78 mmHg. The physician prescribes one aspirin 3. Ms. Bush says, “What about the metoprolol?” The nurse
per day, sublingual nitroglycerin, and metoprolol. tells her that she has been prescribed metoprolol to:
1. Prevent acute angina attacks.
1. The nurse teaches Ms. Bush that the purpose of the nitro- 2. End an angina attack in progress.
glycerin is to: 3. Prevent MI or stroke.
1. Prevent acute angina attacks. 4. Lower blood pressure.
2. End an angina attack in progress.
Ms. Bush discontinues her drugs without notifying her physi- 4. As the nurse starts the infusion, Ms. Bush asks, “What is this
cian. Three months later, she arrives in the ED with a throm- drug for?” The nurse tells her that the function of reteplase is to:
botic stroke. Her blood pressure is 186/100 mmHg. The 1. Dissolve existing blood clots.
physician orders a reteplase infusion. 2. Prevent possible formation of blood clots.
3. Stabilize blood pressure.
4. Reduce workload on the heart.
Note: Answers to the Review and Case Study Questions appear in Appendix B. The complete rationales and answers are located
on the textbook’s website.
Pearson Nursing Student Resources Find additional review materials at nursing.nursing.pearsonhighered.com.

C
“Where am I? What
happened? I really hurt.” h
a
Mr. Joshua Hanks
p
t
e
r
Drugs for Shock and Anaphylaxis

21
Core Concepts
21.1 Shock is a syndrome characterized by the collapse of 21.4 Vasoconstrictors are administered during shock to
the circulatory system. raise and maintain blood pressure.
21.2 The initial treatment of shock includes basic life 21.5 Inotropic drugs are useful in reversing the decreased
support and identification of the underlying cause. cardiac output that occurs during shock.
21.3 Intravenous (IV) infusions are given to replace fluids 21.6 Anaphylaxis is a type of shock caused by a hyper-
lost during shock. response of body defense mechanisms.
Drug Snapshot
Fluid replacement ormal serum albumin (Albuminar,
n
drugs Plasbumin, others) 323
Vasoconstrictors norepinephrine (Levophed) 326
Inotropic drugs dopamine (Dopastat, Intropin) 326

Drug for anaphylaxis epinephrine (Adrenalin) 327
Learning Outcomes
1. Compare and contrast the different 4. Compare and contrast the use 6. For each of the classes in the Drug
types of shock. of blood products, colloids, and Snapshot, identify representative
2. Relate the symptoms of shock to crystalloids in the pharmacotherapy drugs and explain their mechanisms
their physiologic causes. of shock. of drug action, primary actions, and
5. Identify the indications for the use of important adverse effects.
3. Explain the initial treatment of a
patient with shock. vasoconstrictors and inotropic drugs.
Key Terms
anaphylactic (ann-ah-fuh-LAK-tick) colloids (KO-loyds) 323 inotropic drug (eye-noh-TROW-pik) 325
shock 320 crystalloids (KRIS-tuh-loyds) 323 neurogenic shock (nyoor-oh-JEN-ik) 320
antigen (ANN-tuh-jen) 326 hypovolemic shock (high-poh- septic shock (SEP-tik) 320
cardiogenic shock (kar-dee-oh-JEN-ik) 320 voh-LEEM-ik) 320 shock 320
320 Chapter 21 Drugs for Shock and Anaphylaxis
S hock is a condition in which vital organs are not receiving enough blood to function properly. With-
out an adequate supply of oxygen and other nutrients, cells cannot carry on normal metabolism.
Shock is a medical emergency; failure to reverse the causes and symptoms of shock may lead to
irreversible organ damage and death. This chapter examines how drugs are used to aid in the treatment of
different types of shock.
SHOCK
Shock is a syndrome characterized by the collapse
Core Concept 21.1 of the circulatory system.
There are several types of shock, each having different causes. A simple method for classifying shock is
by naming the underlying pathologic process or organ system causing the disease. Table 21.1 ◆ describes
the different types of shock and their primary causes. This chapter focuses on the pharmacologic therapy of
three common types of shock: hypovolemic, cardiogenic, and anaphylactic.
Shock is a collection of signs and symptoms, many of which are nonspecific. Although symptoms
vary among the different kinds of shock, there are some similarities. The patient may appear pale and claim
to feel sick or weak without reporting any specific symptoms. Behavioral changes are often some of the
earliest symptoms and may include restlessness, anxiety, confusion, depression, and lack of interest. Thirst
is a common complaint. The skin may feel cold or clammy.
Assessing the patient’s cardiovascular status may provide important clues for a diagnosis of shock.
Blood pressure is usually low, with a diminished cardiac output. Heart rate may be rapid, with a weak pulse.
Breathing is rapid and shallow. Figure 21.1 ■ illustrates some of the common symptoms of a patient in shock.
Diagnosis of shock is rarely based on such nonspecific symptoms. A careful medical history, however,
will provide the healthcare provider with valuable clues as to what type of shock may be present. For example,
hypo 5 below obvious trauma or bleeding combined with the symptoms mentioned previously would suggest hypovolemic
vol 5 volume shock. If trauma to the brain or spinal cord is evident, neurogenic shock may be suspected. A history of heart
emic 5 pertaining to the disease would suggest cardiogenic shock, whereas a recent infection may indicate septic shock. A history of
blood
allergy with a sudden onset of symptoms following food or drug intake suggests anaphylactic shock.
neuro 5 nervous system The brain and heart are affected early in the progression of shock. Lack of blood to the brain may
genic 5 origin result in fainting, whereas disruption of blood supply to the myocardium can result in permanent damage to
the heart. Immediate treatment is necessary to prevent failure of other organ systems, including respiratory
cardio 5 heart collapse or renal failure.
genic 5 origin
The initial treatment of shock includes basic life support and

Core Concept 21.2 identification of the underlying cause.
Acute shock is treated as a medical emergency, and the first goal is to provide basic life support. Rapid
identification of the underlying cause is essential because the patient’s condition may deteriorate rapidly
without specific, emergency measures. Keeping the patient quiet and warm until specific therapy can be
Table 21.1 Classification of Shock

Type of Shock Definition Underlying Pathology
Anaphylactic Acute allergic reaction Severe reaction to allergens such as
penicillin, nuts, shellfish, or animal proteins
Cardiogenic Failure of the heart to pump Left heart failure, myocardial ischemia, MI,
sufficient blood to tissues dysrhythmias, pulmonary embolism, and
myocardial or pericardial infection
Hypovolemic Loss of blood volume Hemorrhage, burns, profuse sweating,
excessive urination, vomiting, or diarrhea
Neurogenic Vasodilation due to overstimulation Trauma to the spinal cord or medulla, severe
of the parasympathetic nervous emotional stress or pain, drugs that depress
system or understimulation of the the central nervous system
sympathetic nervous system
Septic Multiple organ dysfunction as a Widespread inflammatory response to
result of pathogenic organisms in bacterial, fungal, or parasitic infection
the blood
Figure 21.1
Symptoms of a patient
Neurologic
in shock.
• Restlessness
• Anxiety
• Lethargy
• Confusion
Skin
• Pale Cardiovascular
• Clammy
• Cool • Tachycardia
• Thready pulse
• Low cardiac output
• Low blood pressure
Respiratory
• Rapid breathing
• Shallow
respiration
Metabolism
• Low temperature
• Thirst
• Acidosis
• Low urine output
initiated is important. Maintaining the ABCs of life support—airway, breathing, and circulation—is criti-
cal. Once basic life support is established, the healthcare provider can begin more specific treatment of the
underlying causes of the shock.
The remaining therapies for shock depend on the specific cause of the condition. The two primary
pharmacotherapeutic goals are to restore normal fluid volume and composition and to maintain adequate
blood pressure. Unless contraindicated, oxygen is administered. For anaphylaxis, an additional therapeutic
goal is to prevent or stop the hypersensitive inflammatory response. Specific pharmacotherapies are illus-
trated in Figure 21.2 ■.
Concept Review 21.1

■ What signs or symptoms might help a paramedic arriving on the scene of a motorcycle
accident determine the cause of the patient’s shock?
Fast Facts Shock

■ Cardiogenic shock occurs in about 5–10% of the patients suffering from an acute myocardial
infarction (MI).
■ Cardiogenic shock is the leading cause of death in patients hospitalized with acute MI, with a
mortality rate of up to 70–80%.
■ The mortality rate for patients with sepsis who develop septic shock is 40–75%.
■ The estimated death rate for anaphylaxis is 0.65–2% of all patients who experience the condition.
■ Fewer than 100 fatal cases of anaphylaxis caused from insect stings occur annually in the United
States.
Figure 21.2
Physiologic changes
occurring during
shock and their
pharmacologic
interventions.
Falling Blood Pressure Loss of Blood Volume
Treatment Treatment
Vasoconstrictors Fluid replacement

• Norepinephrine agents
• Blood products
Inotropic drugs • Colloids
• Dopamine • Crystalloids
Intravenous (IV) infusions are given to replace fluids lost

Core Concept 21.3 during shock.
When a patient loses significant amounts of blood or other body fluids, immediate treatment with fluid
replacement drugs is essential. Fluid loss can occur due to hemorrhage, extensive burns, severe dehydra-
tion, persistent vomiting or diarrhea, or aggressive diuretic therapy. Fluid loss can lead to dehydration and
death if the fluid imbalance is not corrected. Fluid replacement drugs are sometimes referred to as fluid
expanders.
The immediate goal in treating hypovolemic shock is to replace the lost fluid. In mild cases, this may
be accomplished by drinking extra water or beverages containing electrolytes. In acute situations, therapy
with IV infusions can immediately replace lost fluids. Regardless of how fluids are administered, careful
attention must be paid to restoring normal levels of electrolytes as well as fluid volume.
Fluid replacement agents may be categorized as blood products, colloids, or crystalloids. Colloid and
crystalloid infusions are often used when up to one-third of an adult’s blood volume is lost. Examples of
fluid replacement drugs are listed in Table 21.2 ◆.
Blood Products
Whole blood may be used for the treatment of acute, massive blood loss when there is the need to replace
plasma volume and supply red blood cells. The supply of blood products, however, depends on human
donors and requires careful cross-matching to ensure compatibility between the donor and the patient.
Furthermore, the use of whole blood has the potential to transmit serious infections such as hepatitis or
HIV. The administration of whole blood to expand fluid volume has been largely replaced with the use of
specific blood components, along with colloids and crystalloids.
A single unit of whole blood can be separated into its specific constituents (red and white blood cells,
platelets, plasma proteins, fresh frozen plasma, and globulins). This allows a single blood donation to be
used to treat more than one patient.
Table 21.2 Fluid Replacement Drugs

Drug Examples
Blood products ■ Whole blood
■ Plasma protein fraction
■ Fresh frozen plasma
■ Packed red blood cells
Colloids ■ Plasma protein fraction (Plasmanate, Plasma-Plex, Plasmatein, PPF, Protenate)
■
Normal serum albumin (Albuminar, Plasbumin, others)
■ Dextran 40 (Gentran 40, Hyskon, Rheomacrodex) or dextran 70 (Macrodex)
■ Hetastarch (Hespan)
Crystalloids ■ Normal saline (0.9% sodium chloride), an isotonic solution
■ Lactated Ringer’s, an isotonic solution
■ 0.45% normal saline (0.45% sodium chloride), a hypotonic solution
■ 5% dextrose in normal saline (D5W), a hypertonic solution
■ 5 % dextrose in water (D5W), although the solution is isotonic, it becomes hypotonic once infused and
metabolized
Colloids
Colloids are proteins or other large molecules that stay suspended in the blood for a long period and draw
water molecules from the body’s cells and tissues into the blood vessels. Colloids include normal human
serum albumin, dextran, and hetastarch (Hespan). These drugs are administered to provide life-sustaining
support following massive hemorrhage and to treat shock, burns, acute liver failure, and neonatal hemo-
lytic disease.
Crystalloids
Crystalloids are IV solutions that contain electrolytes in amounts resembling those of natural plasma.
Unlike colloids, crystalloid solutions can readily leave the blood and enter the cells or tissues. They
are used to replace fluids that have been lost and to increase urine output. Crystalloid solutions are
classified by their tonicity in relation to plasma. Tonicity refers to the concentration of dissolved
molecules (solutes) within the solution. These solutions are classified as either isotonic (having the
same concentration of solutes as plasma), hypertonic (having a greater concentration of solutes than
plasma), or hypotonic (having a lesser concentration of solutes than plasma). The most common crys-
talloids used for the treatment of shock are isotonic solutions; they are primarily used to replace the
loss of fluid volume.
Drug Prototype: Normal Serum Albumin (Albuminar, Plasbumin, Others)

Therapeutic Class: Fluid replacement drug Pharmacologic Class: Blood product, colloid
Actions and Uses: Normal serum albumin is a protein extracted Adverse Effects and Interactions: Because albumin is a
from whole blood or plasma. Because of this, it may be natural blood product, the patient may have antibodies
classified as both a blood product and a colloid. Its functions to the donor’s albumin, and allergic reactions are possible.
are to maintain plasma osmotic pressure and to shuttle certain Signs of allergy include fever, chills, rash, dyspnea, and
substances through the blood, including a substantial number possibly hypotension. Protein overload may occur if
of drug molecules. After extraction from blood or plasma, excessive albumin is infused.
albumin is sterilized to remove possible contamination by the No clinically significant drug interactions have been
hepatitis viruses or HIV. identified.
Administered IV, albumin is used to restore plasma
volume during hypovolemic shock or to restore blood
proteins in patients with hypoproteinemia. It has an
immediate onset of action and is available in concentrations
of 5% and 25%.
Nursing Process Focus Patients Receiving Intravenous Fluid Therapy

Prior to administration: ■ Deficient Fluid Volume related to injury

■ Obtain a complete health history including cardiovascular, respiratory, ■ Ineffective Tissue Perfusion related to decreased blood volume.
neurological, renal and skin conditions, allergies, drug history, and ■ Risk for Injury related to loss of blood or adverse effect of drug
possible drug interactions. therapy
■ Acquire the results of a complete physical examination, including vital ■ Risk for Electrolyte Imbalance related to fluid loss
signs, height, weight, presence of burns, lung sounds, LOC and urinary ■ Risk for Imbalanced Fluid Volume related to drug therapy
and cardiac output. ■ Deficient Knowledge related to a lack of information about drug
■ Evaluate laboratory blood findings: CBC, electrolytes, ABG, clotting therapy
factors, total protein/albumin, lipid panel, and renal and liver function
studies.
The patient will:

■ Experience therapeutic effects (urinary output of at least 50 mL/hr and systolic blood pressure greater than 90 mm Hg).
Implementation
■ Administer intravenous fluids correctly, checking type of fluid and ■ Inform patient about the need for IV fluids and the reason for
frequently monitoring flow rate and IV site. (Frequently monitoring frequent monitoring.
the infusion of IV fluids will help prevent adverse effects.)
■ Monitor respiratory status: respirations, effort, O2 saturation, and Instruct the patient to:
lung sounds. Report any signs of distress immediately to healthcare ■ Report any signs of respiratory distress such as shortness of breath to
provider. (Effects of drugs and rapid infusion may result in fluid healthcare provider.
overload.) ■ Report changes in sensorium such as lightheadedness, drowsiness,
or dizziness to the healthcare provider.
■ Monitor cardiac function: BP, pulse, heart rate/rhythm, cardiac ■ Inform the patient about the rationale for monitoring cardiac function
output, ECG, and laboratory blood tests. (Effects of drugs and rapid and to immediately report any palpitations, chest pain, or headache.
infusion may result in fluid overload and put stress on the circulatory ■ Instruct the patient about the rationale for monitoring fluid intake
system.) and output, laboratory tests, and possible need for a Foley catheter.
■ Monitor renal function: Intake/output, urine color, BUN, creatinine,
presence of edema, or dehydration. (Renal function changes with an
increase or decrease in fluid volume. A decrease is usually seen with
shock.)
■ Weigh patient daily. (Daily weight is an accurate measure of fluid ■ Teach the patient the rationale for monitoring weight to report any
status.) evidence of weight gain.
■ Monitor electrolytes. (Crystalloid drugs may cause hypernatremia and ■ Instruct the patient to report any evidence of edema.
the resulting fluid retention.)
■ Observe the patient for signs of allergic reactions. (Administration of Instruct the patient:
blood and blood products could cause allergic reactions.) ■ To report itching, rash, chills, and difficulty breathing to the healthcare
provider.
■ That frequent blood draws are necessary to monitor possible
complications of drug administration.
Evaluation of Outcome CriteriaM
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see Planning).
Vasoconstrictors are administered during shock to maintain

Core Concept 21.4 blood pressure.
In the early stages of shock, the body compensates for the rapid fall in blood pressure by activating the
sympathetic nervous system. This sympathetic activity causes vasoconstriction, which raises blood pres-
sure and increases the heart rate and force of myocardial contractions. These compensatory measures help
to maintain blood flow to vital organs such as the heart and brain and to decrease the flow to “less essen-
tial” organs such as the kidneys and liver.
The body’s ability to compensate is limited, however, and profound hypotension may develop as
shock progresses. In severe cases, vasoconstrictors, also called vasopressors, may be needed to help sta-
bilize blood pressure. Because of the potential for serious adverse effects and potential organ damage due
to the rapid and intense vasoconstriction, vasopressors are used only after fluid infusions have failed to
raise blood pressure. Patients receiving these drugs must be monitored continuously during the infusion to
avoid hypertension. Vasoconstrictor therapy is discontinued as soon as the patient’s condition stabilizes.
Discontinuation is always gradual, due to the possibility of rebound hypotension and undesirable cardiac
effects.
Vasoconstrictors used to treat shock include dopamine (Dopastat, Intropin), norepinephrine
(Levophed), phenylephrine (Neo-Synephrine), and epinephrine. Because dopamine also affects the
strength of myocardial contraction, it is considered both a vasopressor and an inotropic drug (see Con-
cept Section 21.5). Epinephrine is usually associated with the treatment of anaphylaxis (Section 21.6).
The basic pharmacology of the sympathomimetic drugs is presented in Chapter 8. Table 21.3 ◆ gives
the dosages for these drugs.
Inotropic drugs are useful in reversing the decreased cardiac output

that occurs during shock. Core Concept 21.5
As shock progresses, the heart begins to fail and cardiac output declines. This lowers the amount of blood
reaching vital tissues and deepens the degree of shock. Inotropic drugs, also called cardiotonic drugs,
have the potential to reverse the cardiac symptoms of shock by increasing the force of myocardial contrac-
tion. The role of the inotropic drug digoxin (Lanoxin) in treating patients with heart failure was presented
in Chapter 19. Digoxin increases myocardial contractility and cardiac output, thus rapidly bringing tissues
their needed oxygen. Chapter 19 should be reviewed because drugs prescribed for heart failure are some-
times used for the treatment of shock.
Dopamine is often a preferred drug for increasing the cardiac output in acute situations because it has
both inotropic and vasoconstriction actions. Dobutamine (Dobutrex) is a beta 1-adrenergic agent that has
value in the short-term treatment of certain types of shock because of its ability to cause the heart to beat
more forcefully without significantly increasing heart rate. The resulting increase in cardiac output assists
in maintaining blood flow to vital organs. Although very effective, dobutamine has a half-life of only
2 minutes, and therapy is limited to 72 hours.
Table 21.3 Vasoconstrictors and Inotropic Drugs for Shock

Drug Rate and Adult Dose Remarks
digoxin (Lanoxin, Lanoxicaps) IV; digitalizing dose 2.5–5 mcg every Doses are highly individualized for each patient; oral
(see page 295 for the Drug 6 hours for 24 hours; maintenance dose forms available; also for dysrhythmias and heart
Prototype box) 0.125–0.5 mg/day failure.
dobutamine (Dobutrex) IV; infused at a rate of 2.5–40 mcg/kg/min Selective to beta1-adrenergic receptors; for cardiac
for a max of 72 hours decompensation
dopamine (Dopastat, IV; 2–5 mcg/kg/min initial dose; may be May activate dopaminergic, beta1- or alpha1-adrenergic
Intropin) increased to 20–50 mcg/kg/min receptors, depending on dose
epinephrine (Adrenalin) Subcutaneous; 0.1–0.5 mL of 1:100 every Nonselective adrenergic drug; available by other routes
10–15 min; IV 0.1–0.25 mL of 1:1,000 for cardiac arrest and asthma and as an adjunct to local
every 10–15 min anesthesia
norepinephrine IV; Initial 0.5–1 mcg/min, titrate to response; Activates alpha- and beta1-adrenergic receptors; also for
(Levophed) usual range 8–30 mcg/min cardiac arrest
phenylephrine (Neo-Synephrine) IV; 0.1–0.18 mg/min until pressure Selective to alpha1-receptors; used to maintain blood
(see page 98 for the Drug stabilizes, then 0.04–0.06 mg/min for pressure during general anesthesia; also for certain
Prototype box) maintenance dysrhythmias, nasal congestion, and glaucoma, and to
dilate the pupil during eye exams; subcutaneous, IM,
ophthalmic, and intranasal forms available
Drug Prototype Norepinephrine (Levophed)

Therapeutic Class: Drug for shock Pharmacologic Class: Sympathomimetic, vasoconstrictor
Actions and Uses: Norepinephrine acts directly on alpha- Norepinephrine interacts with many drugs, including
adrenergic receptors in the smooth muscle of blood vessels to alpha and beta blockers, which may decrease the drug’s effects
immediately raise blood pressure. Its stimulation of beta1-receptors on blood pressure. Conversely, ergot alkaloids and tricyclic
in the heart increases the force of contraction and increases cardiac antidepressants may increase vasopressor effects.
output. It is given by the IV route and has a duration of only one
to two minutes after the infusion is terminated.
Black Box Warning:
Adverse Effects and Interactions: Norepinephrine is a powerful Following extravasation, the affected area should be
vasoconstrictor; thus, continuous monitoring of blood pressure infiltrated immediately with 5–10 mg of phentolamine,
is required to prevent the development of hypertension. When an adrenergic blocker.
first administered, reflex bradycardia is sometimes experienced.
It also has the ability to produce various types of dysrhythmias.
Because of its potent effects on the cardiovascular system, it
should be used with great caution in patients with heart disease.
Drug Prototype Dopamine (Dopastat, Intropin)

Therapeutic Class: Drug for shock Pharmacologic Class: Nonselective adrenergic agonist, inotropic drug
Actions and Uses: Dopamine is the immediate metabolic hypotension. Adverse effects are normally self-limiting because
precursor to norepinephrine. Although classified as a of the short half-life of the drug.
sympathomimetic, the mechanism of dopamine’s action is Dopamine interacts with many other drugs. For example,
dependent on the dose. At low doses, dopamine selectively administering it with monoamine oxidase (MAO) inhibitors and
increases blood flow through the kidneys. This makes dopamine ergot alkaloids increases alpha-adrenergic effects. Phenytoin
of particular value in treating hypovolemic and cardiogenic may decrease dopamine action. Beta blockers may block the
shock. At higher doses, dopamine stimulates beta1-adrenergic cardiac effects of dopamine. Alpha blockers decrease peripheral
receptors, causing the heart to beat with more force and vasoconstriction. Halothane increases the risk of hypertension
increasing cardiac output. Another beneficial effect of and ventricular dysrhythmias.
dopamine when given in higher doses is its ability to stimulate
alpha-adrenergic receptors, thus causing vasoconstriction and
raising blood pressure. Black Box Warning:
Following extravasation, the affected area should be infil-
Adverse Effects and Interactions: Because of its intense effects trated immediately with 5 mg to 10 mg of phentolamine, an
on the cardiovascular system, patients receiving dopamine are adrenergic blocker.
continuously monitored for signs of dysrhythmias and
ANAPHYLAXIS
Anaphylaxis is a type of shock caused by a hyper-response of body
Core Concept 21.6 defense mechanisms.
an 5 without or against Anaphylaxis is a condition in which the natural body defenses produce a hyper-response to an antigen. An
phylaxis 5 protection antigen is anything that is recognized as foreign by the body. Certain foods, industrial chemicals, drugs,
pollen, animal proteins, and even latex gloves can be antigens. A more detailed discussion of the immune
system and the pharmacotherapy of immune disorders are included in Chapter 24.
Following the exposure to an antigen, the body normally responds with actions such as inflamma-
tion, antibody production, and activation of lymphocytes that rid the body of the foreign substance. During
anaphylaxis, however, the body responds quickly—usually within minutes after exposure to the antigen—
by releasing massive amounts of histamine and other inflammatory mediators. The patient may experi-
ence itching, hives, and a tightness in the throat or chest. Swelling occurs around the larynx, causing a
hoarse voice and a nonproductive cough. As anaphylaxis progresses, the patient experiences a rapid fall
in blood pressure and difficulty breathing due to bronchoconstriction. The fall in blood pressure causes
reflex tachycardia, a rebound speeding up of the heart. Untreated anaphylactic shock may result in death.
Figure 21.3 ■ illustrates the signs and symptoms of anaphylaxis.
Figure 21.3
Symptoms of
anaphylaxis.
Arterioles
• Vasodilation
Heart • Edema
• Fast heart rate
• Decreased cardiac Histamine
output release
Plasma Granules
membrane containing
histamine
Mast
cell
Nucleus
Lungs Skin
• Bronchoconstriction • Itching
• Dyspnea • Hives
It is always easier to prevent anaphylaxis than it is to treat it. Patients should be strongly advised to
avoid substances that might trigger acute allergic reactions. This includes carefully reading all food and
cosmetic labels to avoid exposure to known allergens. Individuals with known allergies to insect stings or
food should carry a portable form of epinephrine, such as an EpiPen or Auvi-Q, a newer self-administra-
tion device that has built-in verbal instructions. The healthcare provider should always obtain a compre-
hensive drug allergy history before administering medications. Common allergens include the penicillin
antibiotics and iodine-based contrast media used for radiologic exams. The patient should be observed in
Drug Prototype Epinephrine (Adrenalin)

Therapeutic Class: Drug for anaphylaxis and shock Pharmacologic Class: Sympathomimetic, vasoconstrictor
Actions and Uses: Subcutaneous or IV epinephrine is a drug Adverse Effects and Interactions: The most common adverse
of choice for acute anaphylactic shock because it can reverse effects of epinephrine are nervousness, tremors, palpitations,
many of the distressing symptoms within minutes. Epinephrine dizziness, headache, and stinging/burning at the site of
is nonselective and activates both alpha- and beta-adrenergic application. When administered parenterally, hypertension
receptors. Almost immediately after injection, blood pressure and dysrhythmias may occur rapidly; therefore, the patient
rises due to the stimulation of alpha1-receptors. Activation of is monitored continuously following IV or subcutaneous
beta2-receptors in the bronchi opens the airways to relieve injections.
shortness of breath. Cardiac output increases due to stimulation Epinephrine interacts with many drugs. For example, it
of beta1-receptors in the heart. Epinephrine can also be may increase hypotension with phenothiazines and oxytocin.
administered topically, by inhalation, or by the intracardiac There may be additive toxicities with other sympathomimetics.
route. MAO inhibitors, tricyclic antidepressants, and alpha- and beta-
adrenergic drugs inhibit the actions of epinephrine.
the outpatient setting for 20 to 60 minutes after a drug injection because delayed anaphylactic reactions are
possible.
The pharmacotherapy of anaphylaxis involves supporting the cardiovascular system and preventing
further hyper-response by body defenses. Various medications are used to treat the symptoms of anaphy-
laxis, depending on the severity of the symptoms.
At the first suspicion of anaphylaxis, epinephrine is administered and IV fluid infusions are begun.
Epinephrine is an initial drug for acute shock because it causes vasoconstriction and can rapidly relieve
symptoms of bronchoconstriction. It may be necessary to use other vasoconstrictors (see Table 21.3) to
overcome severe hypotension. Infusion of large amounts of fluids may be needed to overcome circulatory
shock. These may include blood products, colloids, or crystalloids. Fluid infusions continue until systolic
blood pressure reaches at least 90 mmHg and is stable.
A number of other drugs are useful in treating symptoms of anaphylaxis. Oxygen is usually admin-
istered immediately. Antihistamines such as diphenhydramine (Benadryl) may be administered intramus-
cularly or intravenously to prevent additional release of histamine. A bronchodilator such as albuterol
(Ventolin, Proventil) is sometimes administered by inhalation to relieve the acute shortness of breath
caused by histamine release. Corticosteroids such as hydrocortisone may be administered to dampen the
acute inflammatory response that occurs during anaphylaxis. Corticosteroids may be administered for
24 hours or longer to prevent the possibility of delayed anaphylactic reactions. Additional effects of anti-
histamines are discussed in Chapter 24, bronchodilators in Chapter 29, and corticosteroids in Chapter 32,
respectively.
Concept Review 21.2

■ How can inotropic drugs reduce the symptoms of shock without causing
vasoconstriction?

Patients treated for shock need to know the following:
1. Seek emergency medical assistance immediately if signs or symptoms of shock are
being experienced.
2. While waiting for medical assistance, keep warm by using blankets.
3. Have a caregiver, if present, monitor temperature, pulse, and blood pressure until
emergency medical assistance arrives.
4. Do not move around. Lie down and elevate the feet.
5. Report any changes in mental status, such as depression, confusion, or anxiety, to the
healthcare provider immediately.
6. If allergies to bee or wasp stings are known, carry medications such as an EpiPen for all
outside activities. Inform others of any allergies, where medications are kept, and how
to administer them.
7. Take medications for shock (such as epinephrine) exactly as prescribed.
Chapter Review
21.1 Shock is a syndrome characterized by the collapse 21.2 The initial treatment of shock includes basic life
of the circulatory system. support and identification of the underlying
Basic types of shock include cardiogenic, hypovo- cause.
lemic, neurogenic, septic, and anaphylactic shock. Shock may be life threatening if allowed to pro-
Nonspecific symptoms of shock include hypoten- ceed without medical intervention. Immediate
sion, cold or clammy skin, reduced cardiac output, therapy is targeted at restoring or maintaining vital
and behavioral changes such as confusion, apathy, or processes such as respiratory function, blood pres-
disorientation. sure, and cardiac output. Immediate drug therapy
Chapter Review 329
includes vasoconstrictors, inotropic drugs, and IV 21.5 Inotropic drugs are useful in reversing the de
fluid agents. creased cardiac output that occurs during shock.
Circulatory failure can occur during shock if the car-
21.3 Intravenous (IV) infusions are given to replace diac output falls below a critical level. A number of
fluids lost during shock. inotropic drugs are used to strengthen myocardial
Intravenous fluid agents include blood products, col- function and to improve cardiac output.
loids, and crystalloids. These drugs help to maintain
circulation and raise blood pressure. 21.6 Anaphylaxis is a type of shock caused by a hyper-
response of body defense mechanisms.
21.4 Vasoconstrictors are administered during shock to When the body mounts a hyper-response to an anti-
maintain blood pressure. gen, anaphylactic shock may result. Epinephrine is
An immediate concern for the patient in shock is a a drug of choice for immediately reversing the car-
fall in blood pressure. A variety of adrenergic drugs, diovascular symptoms. Intravenous fluid infusion
both selective and nonselective, are used to maintain agents, antihistamines, and corticosteroids also serve
blood pressure and cardiac function. roles in treating this form of shock.
Review Questions
The following questions are written in NCLEX-PN ® style. 3. Digoxin (Lanoxin)

Answer these questions to assess your knowledge of the chapter 4. Dopamine
to you. 6. In reviewing a plan of care for a patient exhibiting the
symptoms of anaphylaxis, which of the following medications
1. The patient with severe burns has just been admitted to would be avoided?
hospital. The nurse will monitor for signs/symptoms of: 1. Antihistamines
1. Cardiogenic shock 2. Corticosteroids
2. Hypovolemic shock 3. Bronchodilators
3. Septic shock 4. Vasodilators
4. Anaphylactic shock
7. After administering an inotropic medication to a patient
2. In the plan of care, the most important intervention for a in shock, the nurse monitors the patient for signs of:
patient experiencing shock is assessing: 1. Decreased cardiac output
1. Temperature 2. Increased cardiac output
2. Heart rate 3. Slowing of the heart rate
3. Respirations rate 4. Increased afterload
4. Blood pressure
8. When administering norepinephrine (Levophed), the
3. The nurse is preparing an IV solution for a patient in hy- nurse monitors the patient for:
povolemic shock. Which IV solution would be most appropri- 1. Tachycardia
ate for this patient? 2. Hypotension
1. 0.45% NS 3. Hypertension
2. Normal serum albumin 4. Liver failure
3. 0.33% NS
4. D5W 9. Dobutamine (Dobutrex) is used to treat shock because:
1. It increases myocardial contractility and heart rate.
4. The patient’s family is asking questions about the medi- 2. It increases myocardial contractility without significantly
cations used in the treatment for shock. The nurse explains increasing heart rate.
that dopamine is one of the drugs being used and that it works: 3. It decreases cardiac output.
(Select all that apply.) 4. It is a powerful vasoconstrictor.
1. At low doses, to cause increased blood flow to the kidneys
2. At high doses, to increase cardiac output 10. The healthcare provider has ordered 1,000 mL of 0.9%
3. To cause vasoconstriction and increases blood pressure sodium chloride to be administered intravenously over five
4. At high doses, to treat anaphylaxis hours. The drop factor on the tubing is 15 drops/mL. How
many milliliters per hour will you administer and how many
5. The patient is experiencing anaphylaxis. The nurse would drops per minute?
administer which drug to increase blood pressure and treat 1. 250 mL/hr and 50 drops/min
bronchospasm related to anaphylaxis? 2. 200 mL/hr and 50 drops/min
1. Epinephrine 3. 200 mL/hr and 45 drops/min
2. Dobutamine (Dobutrex) 4. 250 mL/hr and 45 drops/min
Remember Mr. Hanks from the be- 2. Which drug was given to replace the fluids lost during
ginning of the chapter? Now read Mr. Hanks’ accident?
the remainder of the case study. 1. 0.9% sodium chloride
Based on the information you have 2. Dobutamine
learned in this chapter, answer the 3. Hydrocortisone
questions that follow. 4. Epinephrine
Mr. Joshua Hanks arrives in the emergency department having
3. Within two minutes, Mr. Hanks’ blood pressure increases
lost a considerable amount of blood in an automobile acci- to 100/60 mmHg. The nurse understands that which drug most
dent. His blood pressure is 60/30 mmHg. His skin is clammy, likely caused this effect?
and he is going in and out of consciousness. He is gasping
for breath. The physician orders an infusion of 0.9% sodium 1. 0.9% sodium chloride
chloride, IV dobutamine, IM hydrocortisone, and subcutane- 2. Dobutamine
ous epinephrine. 3. Hydrocortisone
4. Epinephrine
1. The nurse notices that Mr. Hanks’ breathing is labored and 4. After four hours, Mr. Hanks has stabilized, but he still has
he appears anxious. The nurse administers which of the pre- some difficulty breathing. As ordered by the physician, which
scribed medications to help reduce Mr. Hanks’ bronchospasm? of the following drugs would the nurse most likely be adminis-
1. 0.9% sodium chloride tering to help Mr. Hanks with his breathing difficulties?
2. Dobutamine 1. Diphenhydramine (Benadryl)
3. Hydrocortisone 2. Hydrocortisone
4. Epinephrine 3. Phenylephrine (Neo-Synephrine)
4. Albuterol (Ventolin)

C
“I’ve never had anything
happen like this. I was H
watching TV, and all of a A
sudden, my heart started P
racing.”
T
Mrs. Margaret Duncan
E
R
Drugs for Dysrhythmias 22

Core Concepts
22.1 Some types of dysrhythmias produce no 22.6 Sodium channel blockers slow the rate of impulse
patient symptoms, whereas others may conduction through the heart.
be life threatening. 22.7 Beta-adrenergic blockers reduce automaticity and
22.2 Dysrhythmias are classified by the type of rhythm slow conduction velocity in the heart.
abnormality produced and its location. 22.8 Potassium channel blockers prolong the refractory
22.3 The electrical conduction pathway in the period of the heart.
myocardium keeps the heart beating in a 22.9 Calcium channel blockers are available to treat
synchronized manner. supraventricular dysrhythmias.
22.4 Most antidysrhythmic drugs act by blocking ion 22.10 Digoxin and adenosine are used for specific
channels in myocardial cells. dysrhythmias but do not act by blocking ion
22.5 Antidysrhythmic drugs are classified by their channels.
mechanisms of action.
Drug Snapshot
Sodium channel procainamide 339 Calcium channel verapamil (Calan, Isoptin
blockers blockers SR, others) 342
Beta-adrenergic propranolol (Inderal, Miscellaneous drugs
blockers InnoPran XL) 340
Potassium channel amiodarone (Cordarone) 341
blockers
Learning Outcomes
1. Explain how rhythm abnormalities 4. Explain the importance of ion 7. Categorize antidysrhythmic drugs
can affect cardiac function. channels to cardiac function and the based on their classifications and
2. Illustrate the flow of electrical pharmacotherapy of dysrhythmias. mechanisms of action.
impulses through the normal heart. 5. Identify the importance of 8. For each of the classes in the Drug
3. Classify dysrhythmias based on their nonpharmacologic therapies in the Snapshot, identify representative
location and type of conduction treatment of dysrhythmias. drugs and explain their mechanisms
abnormality. 6. Identify basic mechanisms by which of drug action, primary actions, and
antidysrhythmic drugs act. important adverse effects.
332 Chapter 22 Drugs for Dysrhythmias
Key Terms
atrioventricular (AV) node (ay-tree-oh- depolarization (dee-po-lur-eye-ZAY-shun) potassium ion channels (po-TASS-ee-um)
ven-TRIK-you-lur noad 333 335 335
atrioventricular bundle (ay-tree-oh-ven- dysrhythmias (diss-RITH-mee-uh) 332 Purkinje fibers (purr-KEN-gee FI-burrs)
TRIK-you-lur BUN-dul) 333 ectopic foci/pacemakers (ek-TOP-ik FO-si) 333
automaticity (aw-toh-muh-TISS-uh-tee) 335 refractory period (ree-FRAK-tor-ee) 335
333 electrocardiogram (ECG) (e-lek-tro-KAR- sinoatrial (SA) node (si-no-AYE-tree-ul
bundle branches (BUN-dul BRAN-chez) dee-oh-gram) 333 noad) 333
333 fibrillation (fi-bruh-LAY-shun) 332 sinus rhythm (SI-nuss) 333
calcium ion channels (KAL-see-um) 335 polarized (POLE-uh-rized) 335 sodium ion channels (SO-dee-um) 335
dys 5 difficult or bad

rhythm 5 rhythm
ia 5condition D ysrhythmias are abnormalities of electrical conduction or rhythm in the heart. Sometimes called
arrhythmias, they encompass a number of different disorders that range from harmless to life
threatening. Diagnosis is often difficult because patients usually must be connected to an elec-
trocardiogram (ECG) and be experiencing symptoms to determine the exact type of rhythm disorder.
Proper diagnosis and optimum pharmacologic treatment can significantly reduce the frequency of serious
dysrhythmias and their consequences.
Some types of dysrhythmias produce no patient symptoms, whereas

core concept 22.1 others may be life threatening.
Whereas some dysrhythmias produce no symptoms and have negligible effects on heart function, others are
life threatening and require immediate treatment. Typical symptoms of a dysrhythmia include dizziness,
weakness, decreased exercise tolerance, shortness of breath, and fainting. Many patients report palpitations
or a sensation that their heart has skipped a beat. Persistent dysrhythmias are associated with increased risk
a 5 no or not of stroke and heart failure. Severe dysrhythmias may cause sudden death. Because asymptomatic patients
symptomat 5 symptoms may not seek medical attention, it is difficult to estimate the frequency of the disease, although it is likely
ic 5 pertaining to that dysrhythmias are quite common in the population.
Dysrhythmias are classified by the type of rhythm abnormality produced

core concept 22.2 and its location.
There are many types of dysrhythmias, and they may be classified by a number of different methods.
The simplest method is to name dysrhythmias according to the type of rhythm abnormality produced
and their locations. A summary of the different types of dysrhythmias along with a brief description
of each abnormality is given in Table 22.1 ◆. Dysrhythmias that originate in the atria are sometimes
supra 5 above referred to as supraventricular. Those that originate in the ventricles are generally more serious because
ventricular 5cardiac ventricle they are more likely to interfere with the normal function of the heart. Although obtaining a correct
diagnosis of the type of dysrhythmia is sometimes difficult, it is essential for effective treatment.
Atrial fibrillation, a complete disorganization of rhythm, is thought to be the most common type of
dysrhythmia.
Fast Facts Dysrhythmias

■ Dysrhythmias are responsible for more than 44,000 deaths each year.
■ Atrial dysrhythmias occur more commonly in men than in women.
■ The incidence of atrial dysrhythmias increases with age. They affect:
■ Less than 0.5% of those aged 25–35
■ About 1.5% of those up to age 60
■ About 9% of those over age 75
■ About 15% of strokes occur in patients with atrial dysrhythmias.

■ A large majority of sudden cardiac deaths are believed to be caused by ventricular dysrhythmias.
Table 22.1 Types of Dysrhythmias

Name of Dysrhythmia Description
Atrial or ventricular flutter and/or Very rapid, uncoordinated beats; atrial may require treatment but is
fibrillation not usually fatal; ventricular flutter or fibrillation requires immediate
treatment
Atrial or ventricular tachycardia Rapid heartbeat greater than 100 beats per minute in adults;
ventricular tachycardia is more serious than atrial tachycardia
Heart block Area of nonconduction in the myocardium; may be partial or c omplete;
classified as first, second, or third degree
Premature atrial or premature An extra beat often originating from a source other than the sinoatrial
ventricular contractions (PVCs) (SA) node; not normally serious unless it occurs in high frequency
Sinus bradycardia Slow heartbeat, less than 60 beats per minute; may require a pacemaker
Dysrhythmias can occur in both healthy and diseased hearts. Although the actual cause of most
d ysrhythmias is elusive, dysrhythmias are often associated with certain conditions, primarily heart disease
and myocardial infarction (MI). Following are some conditions associated with dysrhythmias:
■ Hypertension (HTN)
■ Cardiac valve disease, such as mitral stenosis
■ Coronary artery disease
■ Medications such as digoxin
■ Low potassium levels in the blood
■ Myocardial infarction
■ Adverse effect from antidysrhythmic medication
■ Stroke
■ Diabetes mellitus
■ Congestive heart failure
The electrical conduction pathway in the myocardium keeps the heart

beating in a synchronized manner. Core Concept 22.3
Although there are many different types of dysrhythmias, all have in common a defect in the formation
or conduction of electrical impulses across the myocardium. These electrical impulses carry the s ignal for
cardiac muscle cells to contract and must be coordinated precisely for the chambers to beat in a s ynchronized
manner. For the heart to function properly, the atria must contract simultaneously, sending their blood into
the ventricles. Following atrial contraction, the right and left ventricles then must contract simultaneously.
Lack of synchronization of the atria and ventricles or of the right and left sides of the heart may have serious
consequences. The normal conduction pathway in the heart is illustrated in Figure 22.1 ■.
Control of this synchronization begins in a small area of tissue in the wall of the right atrium called
the sinoatrial (SA) node. The SA node or pacemaker of the heart has a property called automaticity, the
ability of certain cells to spontaneously generate an electrical impulse known as an action potential, with-
out instructions from the nervous system. The SA node generates a new action potential approximately 75
times every minute under resting conditions. This is referred to as the normal sinus rhythm.
On leaving the SA node, the action potential travels quickly across both atria to the atrioventricular
(AV) node, a small area of specialized fibers that lies in the wall of the right atrium. The AV node also has
the property of automaticity, although less than the SA node. If the SA node malfunctions, the AV node
has the ability to spontaneously generate action potentials and continue the heart’s contraction.
As the action potential leaves the AV node, it travels rapidly to the atrioventricular bundle or bundle
of His, which is responsible for carrying the electrical signal from the atria to the ventricles. The impulse is
then conducted down the right and left bundle branches (tissue that carries electrical signal impulse from
the AV bundle to the Purkinje fibers). The Purkinje fibers carry the electrical impulse to all regions of the
ventricles almost simultaneously.
The wave of electrical activity across the myocardium can be measured by an electrocardiogram
(ECG). The total time for the electrical impulse to travel across the heart is about 0.22 second. A normal
ECG and its relationship to impulse conduction in the heart are shown in Figure 22.2 ■.
Figure 22.1
Normal conduction
pathway in the heart.
SA node Internodal
atrial pathways
AV junction
AV node
Bundle of His
Interventricular
septum Left bundle branch
Right bundle branch
Purkinje fibers
Purkinje system
Figure 22.2
Normal ECG tracing.
T Wave
• Ventricles repolarize
and relax
P T
P Wave
• Atria depolarize
and contract Q
PR Interval S
QT Interval
QRS Complex –
• Ventricles depolarize
and contract
Although action potentials normally begin at the SA node and spread across the myocardium in a
c oordinated manner, other regions of the heart may begin to initiate beats. These areas, known as ectopic ec 5 outside
foci or ectopic pacemakers, may send impulses across the myocardium that compete with those from top 5 place
the normal conduction system. Although healthy hearts often experience an extra beat without incident, ic 5pertaining to
ectopic foci in diseased hearts have the potential to cause many of the types of dysrhythmias noted in
Table 22.1.
It is important to understand that the underlying purpose of this conduction system is to keep the heart
beating in a regular, synchronized manner so that cardiac output can be maintained. Some dysrhythmias
occur sporadically, produce no symptoms, and cause little or no effect on cardiac output. These types of
abnormalities may go unnoticed by the patient and rarely require treatment. Some dysrhythmias, however,
seriously affect cardiac output, producing patient symptoms and resulting in potentially serious, if not
mortal, consequences. It is these types of dysrhythmias that require pharmacotherapy.
Concept Review 22.1

■ Trace the flow of electrical conduction across the heart. What would happen if the
impulse never reached the AV node?
Most antidysrhythmic drugs act by blocking ion channels in

myocardial cells. Core Concept 22.4
Because most antidysrhythmic drugs act by interfering with the cardiac action potential, a firm grasp of
this phenomenon is necessary for understanding drug mechanisms. Action potentials occur in both neurons
and cardiac muscle cells due to differences in the concentration of certain ions found inside and outside the
cell. Under resting conditions, sodium ions (Na+) and calcium ions (Ca2+) are found in higher concentra-
tions outside the myocardial cells, whereas potassium ions (K+) are found in higher concentrations inside
these cells. These imbalances are, in part, responsible for the inside of a myocardial cell membrane being
slightly negatively charged relative to the outside of the membrane. A cell having this negative membrane
potential is said to be polarized.
An action potential begins when sodium ion channels located in the plasma membrane open and Na+
rushes into the cell, producing a rapid depolarization, or loss of membrane potential. During this period,
Ca2+ also enters the cell through calcium ion channels. It is this influx of Ca2+ that is responsible for the
contraction of cardiac muscle. The cell returns to its polarized state by the removal of Na+ from the cell via
the sodium pump and movement of K+ back into the cell through potassium ion channels. In cells located
in the SA and AV nodes, it is the influx of Ca2+, rather than Na+, that generates the rapid depolarization of
the membrane.
Although it may seem complicated to learn the different ions involved in an action potential, this
knowledge is vital to understanding cardiac pharmacology. Blocking potassium, sodium, or calcium ion
channels is the primary pharmacologic strategy used to prevent or terminate dysrhythmias. Figure 22.3 ■
illustrates the flow of ions during the action potential.
The pumping action of the heart requires alternating periods of contraction and relaxation. There is
a brief period following depolarization when the cell cannot initiate another action potential. This time,
known as the refractory period, ensures that the myocardial cell finishes contracting before a second
action potential begins. Some antidysrhythmic drugs produce their effects by prolonging the refractory
period.
Antidysrhythmic drugs are classified by their

mechanisms of action. Core Concept 22.5
The therapeutic goal of antidysrhythmic pharmacotherapy is to prevent or terminate dysrhythmias to reduce

the risk for sudden death, stroke, or other complications resulting from the disease. All antidysrhythmic
drugs have the potential to profoundly affect the heart’s conduction system. Because they can cause seri-
ous adverse effects, antidysrhythmic drugs are normally reserved for patients experiencing symptoms of
dysrhythmia or for those whose condition cannot be controlled by other means. Treating asymptomatic
dysrhythmias with medications provides little or no benefit to the patient.
Figure 22.3
Na+ K+ Ca2+
channel channel channel
Ca2+ Ca2+
Na+ Na+
+ +
+ K +
2+
Ca + + + K
Na 2+ Na+ Na Na K Ca 2+ Na 2+
K
+ Ca +
K Ca
– – – –
+ + + +
+
K + K+ + K +
2+ Na + K K+ K+
Na K
+ Ca K+
K
+
Na+ Ca2+ 2+
Ca K
+
Na+ Ca2+
(a) Resting state before (b) Depolarization (c) Repolarization (d) Return to resting state
action potential • Sodium and calcium • Potassium channel • All channel gates closed
• All channel gates closed channel gates open gates open
The flow of ions through ion channels in myocardial cells.
Antidysrhythmic drugs are grouped by the stage at which they affect the action potential. These drugs
fall into four primary classes and a miscellaneous group that does not act by one of the first four mecha-
nisms. Classes of antidysrhythmics include the following:
■ Sodium channel blockers (Class I)
■ Beta-adrenergic blockers (Class II)
■ Potassium channel blockers (Class III)
■ Calcium channel blockers (Class IV)
■ Miscellaneous antidysrhythmic drugs
The use of antidysrhythmic drugs has significantly declined in the past 20 years. Research has
d etermined that the use of antidysrhythmic medications for prophylaxis can actually increase mortality in
some patients. This is because there is a narrow margin between a therapeutic effect and a toxic effect with
drugs that affect cardiac rhythm. They have the ability not only to correct dysrhythmias but also to worsen
or even create new dysrhythmias. The healthcare provider must carefully monitor patients taking antidys-
rhythmic drugs. Often, the patient is hospitalized during the initial stages of therapy so that the optimum
dose can be accurately determined.
Another reason for the decline in antidysrhythmic drug use is the success of nonpharmacologic
techniques. Research has demonstrated that catheter ablation and implantable cardioverter defibrillators
(ICDs) are more successful in managing certain types of dysrhythmias than is the prophylactic use of medi-
cations. Catheter ablation is a treatment used to identify and destroy the myocardial cells responsible for
the abnormal conduction. ICDs are devices that restore normal rhythm by either pacing the heart or giving
it an electric shock when dysrhythmias occur.
Nursing Process Focus Patients Receiving Antidysrhythmic Drugs
Prior to administration: ■ Risk for Ineffective Tissue Perfusion related to cardiac conduction
■ Obtain a complete health history including cardiovascular, neurologi- abnormality
cal, renal and liver conditions, allergies, drug history, and possible drug ■ Risk for Injury related to adverse effects of drug therapy
interactions. ■ Deficient Knowledge related to a lack of information about drug
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, and therapy
renal and liver function studies. ■ Ineffective Self Health Maintenance related to insufficient knowledge
■ Acquire the results of a complete physical examination, including vital of seriousness of disease and drug therapy regimen
signs, height, weight, ECG, LOC, and urinary output.
Nursing Process Focus (continued)
The patient will:

■ Experience therapeutic effects (stabilization of heart rate, heart rhythm, sensorium, urinary output, and vital signs).
Implementation
of proper administration. (Proper use of medication ensures that the ■ Never discontinue the drug abruptly.
patient will receive intended results and minimize adverse effects.) ■ Take the drug exactly as prescribed, even if feeling well.
■ Take the pulse prior to taking the drug (may need to demonstrate
technique).
■ Immediately notify the healthcare provider for further instructions
if pulse is below the “reportable” pulse rate, usually 60 beats per
minute.
■ Take blood pressure frequently if taking an antidysrhythmic medica-
tion that also lowers blood pressure.
■ Ensure cardiac rate and rhythm are monitored continuously if admin- ■ Explain the need for continuous ECG monitoring when administering
istering drug IV and regularly if administered orally. (IV route is used the medication intravenously.
when rapid therapeutic effects are needed. Monitoring is needed to
detect any potential serious dysrhythmias. Immediately report any
changes in heart sounds or rhythm.)
■ Monitor the IV site and administer all intravenous medications via an ■ Instruct the patient to report any burning or stinging pain, swelling,
infusion pump. (Administering IV cardiac medications via an infusion warmth, redness, or tenderness at the IV insertion site.
pump helps to ensure safety and accuracy.)
■ Obtain information regarding possible causes of the dysrhythmia. Instruct the patient to:
(Electrolyte imbalances, hypoxia, pain, anxiety, caffeine ingestion, and ■ Maintain a diet low in sodium and fat with sufficient potassium.
tobacco use can contribute to dysrhythmias.) ■ Report illness such as flu, vomiting, diarrhea, and dehydration to the
healthcare provider to avoid adverse effects.
■ Avoid the use of caffeine and tobacco products.
■ Observe for adverse effects specific to the antidysrhythmic used. (These Instruct the patient to:
drugs affect heart function and can cause serious adverse effects. Con- ■ Report to healthcare provider any adverse effects specific to the
tinuing or worsening cardiac symptoms may indicate inadequate drug prescribed antidysrhythmic, such as visual disturbances or skin rashes
therapy.) caused by potassium channel blockers.
■ Report any cardiac-related symptoms such as dizziness, hypotension,
palpitations, chest pain, dyspnea, unusual fatigue and weakness.
■ Check for edema, noting location and character. Weigh patient daily Have the patient:
and report a weight gain or loss of 1 kg or more in a 24-hour period. ■ Weigh and record their weight daily, ideally at the same time of day.
(Daily weight is an accurate measure of fluid status; weight gain or ■ Report to healthcare provider a weight loss or gain of more than 1 kg
edema may indicate adverse drug effect or worsening cardiac disease.) (2 lb) in a 24-hour period.
■ Monitor ongoing laboratory results of electrolytes, especially potas- Instruct the patient on the need to:
sium and magnesium; renal function and drug levels. (Hypokalemia ■ Return periodically for lab work.
or hypomagnesemia increases the risk of dysrhythmias. Inadequate or ■ Carry a wallet ID card or wear medical alert jewelry indicating
high drug levels may lead to increased dysrhythmias.) antidysrhythmia medication.
■ Monitor lung sounds. Immediately report if patient is experiencing ■ Instruct the patient to immediately report to healthcare provider any
worsening dyspnea, crackles or pink, frothy pink-tinged sputum. (New severe shortness of breath, frothy sputum, profound fatigue, or swell-
or worsening dysrhythmias may cause lung congestion and possible ing of extremities.
heart failure.)
Sodium channel blockers slow the rate of impulse conduction

Core Concept 22.6 through the heart.
The first medical uses of the sodium channel blockers were recorded in the 18th century. Quinidine,
the oldest antidysrhythmic drug, was originally obtained as a natural substance from the bark of the
South American Cinchona tree. Although a prototype for many decades, quinidine (Quinidex, others) is
rarely used today owing to the availability of safer antidysrhythmics. Sodium channel blockers used as
antidysrhythmics are listed in Table 22.2 ◆.
Sodium channel blockers, the Class I drugs, are the largest group of antidysrhythmics. They are
divided into three subgroups—IA, IB, and IC—based on subtle differences in their mechanisms of action.
Because the action potential is dependent on the opening of sodium ion channels, a blockade of these chan-
nels will slow the spread of impulse conduction across the myocardium. This slowing of conduction will
suppress ectopic pacemaker activity.
The chemical structures and actions of the sodium channel blockers are similar to those of the local
anesthetics. In fact, the antidysrhythmic drug lidocaine is a prototype local anesthetic in Chapter 15. This
anesthetic-like action slows impulse conduction across the heart. A few, such as quinidine and procain-
amide, are effective against many different types of dysrhythmias. The remaining Class I drugs are more
specific and indicated only for life-threatening ventricular dysrhythmias.
All the sodium channel blockers have the potential to cause new dysrhythmias or worsen existing
ones; thus, frequent ECGs should be obtained. The reduced heart rate caused by the drugs can result in hy-
potension, dizziness, and fainting. Some Class I drugs have significant anticholinergic adverse effects such
as dry mouth, constipation, and urinary retention.
Concept Review 22.2

■ Why does slowing the speed of the electrical impulse across the myocardium sometimes
correct a dysrhythmia?
Table 22.2 Sodium Channel Blockers (Class I)

disopyramide (Norpace) PO (immediate release); 400–800 mg in Class 1A; sustained-release form available;
divided doses usually reserved for serious ventricular
PO (extended release); 300 mg bid dysrhythmias
flecainide (Tambocor) PO; 100 mg bid (max: 400 mg/day) Class 1C; usually reserved for serious ventricular
dysrhythmias
lidocaine (Xylocaine) (see page 222 for the IV; 1–4 mg/min infusion rate (max: 3 mg/kg Class 1B; usually reserved for rapid control of
Drug Prototype box) per 5–10 min) ventricular dysrhythmias; IM, subcutaneous,
and topical forms available; also widely used as
a local anesthetic
mexiletine (Mexitil) PO; 200–300 mg tid (max: 1,200 mg/day) Class 1B; usually reserved for serious ventricular
dysrhythmias
phenytoin (Dilantin) (see page 190 for the PO; 100–200 mg tid (max: 625 mg/day) Class 1B; off-label use for dysrhythmias induced
Drug Prototype box) IV; 50–100 mg every 10–15 min until by cardiac glycosides; oral form is used to treat
dysrhythmia is terminated (max: 1 g/day) convulsions
procainamide PO; 50 mg/kg/day in divided doses Class 1A; IM, IV, and sustained-release forms
available; for both atrial and ventricular
dysrhythmias
propafenone (Rythmol) PO (sustained release); 225 mg bid Class 1C; usually reserved for serious ventricular
dysrhythmias
quinidine sulfate PO; 200–400 mg tid or qid (max: 3–4 g/day) Class 1A; gluconate salt is also available in IM
and IV forms; sustained-release forms available
for the sulfate and gluconate salts
Drug Prototype: Procainamide

Therapeutic Class: Antidysrhythmic (Class 1A) Pharmacologic Class: Sodium channel blocker
Actions and Uses: Procainamide is an older drug, approved in Additive cardiac depressant effects may occur if procain-
1950, that is chemically related to the local anesthetic procaine. amide is administered with other antidysrhythmics. Additive
Procainamide blocks sodium ion channels in myocardial cells, anticholinergic adverse effects will occur if procainamide is used
thus slowing conduction of the action potential across the myo- concurrently with other medications that have anticholinergic
cardium. This slight delay in conduction velocity prolongs the effects.
refractory period and can suppress dysrhythmias. Procainamide
has the ability to correct many different types of dysrhythmias.
The most common dosage form is the extended-release tablet;
however, procainamide is also available in IV and IM formula- Black Box Warning:
tions for emergency conditions. Chronic administration may result in a lupus-like syndrome
in 30% to 50% of patients who are taking the drug for
Adverse Effects and Interactions: Procainamide has a narrow more than a year. Procainamide should be reserved for
margin of safety, and dosage must be monitored carefully to life-threatening dysrhythmias because it has the ability to
avoid serious adverse effects. Nausea, vomiting, abdominal produce new dysrhythmias or worsen existing ones.
pain, and headache are common during therapy. The drug can Complete blood counts should be monitored carefully
cause fever accompanied by anorexia, weakness, and nausea/ and the drug discontinued at the first sign of potential blood
vomiting. High doses may produce central nervous system (CNS) abnormalities.
effects such as confusion or psychosis.
Beta-adrenergic blockers reduce automaticity and slow

conduction velocity in the heart. Core Concept 22.7
Beta-adrenergic blockers are used to treat a large number of cardiovascular diseases, including HTN,
MI, heart failure, and dysrhythmias. Their ability to slow the heart rate and conduction velocity can
suppress several types of dysrhythmias. Beta blockers of importance to dysrhythmias are listed in
Table 22.3 ◆.
The basic pharmacology of beta-adrenergic blockers is explained in Chapter 8. Although the effects
of beta blockers on the heart are complex, their basic actions are to slow the heart rate and decrease con-
duction velocity through the AV node. Myocardial automaticity is reduced, and many types of dysrhyth-
mias are stabilized. The main value of beta blockers as antidysrhythmic drugs is to treat atrial dysrhythmias Life Span Fact
that are associated with heart failure.
Only a few beta blockers are approved for dysrhythmias because of the potential for adverse effects. Special attention should be
given to older adults because
Blockade of beta receptors in the heart may result in bradycardia, and hypotension may cause dizziness and
anticholinergic adverse effects
possible fainting. Beta blockers that affect beta2-receptors will also affect the lungs, increasing the risk for may worsen urinary hesitancy
bronchospasm. This is of particular concern in patients with asthma and in elderly patients with chronic in patients with prostate
obstructive pulmonary disease (COPD). enlargement.
Table 22.3 Beta-Adrenergic Blockers Used for Dysrhythmias (Class II)

acebutolol (Sectral) PO; 200–600 mg bid (max: 1,200 mg/day) Cardioselective beta1 blocker; usually reserved for ventricular
dysrhythmias; also for HTN and angina
esmolol (Brevibloc) IV; 50 mcg/kg/min maintenance dose Cardioselective beta1 blocker; usually reserved for immediate
(max: 200 mcg/kg/min) control of severe atrial dysrhythmias; very short half-life of
9 minutes
propranolol (Inderal, PO; 10–30 mg tid or qid (max: 480 mg/ Sustained-release forms available; also for HTN, prevention of MI,
InnoPran XL) day) angina, and migraines
IV; 0.5–3.1 mg every 4 hours
Drug Prototype: Propranolol (Inderal, InnoPran XL)

Therapeutic Class: Antidysrhythmic (Class II) Pharmacologic Class: Beta-adrenergic blocker
Actions and Uses: Propranolol is a nonselective beta-adrenergic Propranolol interacts with many other drugs, including
blocker, affecting both beta1-receptors in the heart and beta2- phenothiazines, which have additive hypotensive effects.
receptors in the lungs. Propranolol reduces heart rate, slows Propranolol should not be given within two weeks of a
conduction velocity, and lowers blood pressure. Propranolol is monoamine oxidase (MAO) inhibitor. Beta-adrenergic drugs
most effective in treating tachycardia. It is approved to treat a such as albuterol block the actions of propranolol.
wide variety of disorders, including HTN, angina, and migraine
headaches, and to prevent MI.
Adverse Effects and Interactions: Frequent adverse effects of Black Box Warning:
propranolol include hypotension and bradycardia. Because of its Abrupt withdrawal is not advised in patients with angina or
ability to slow the heart rate, patients with serious cardiac disor- heart disease. Dosage should gradually be reduced over one
ders such as heart failure must be carefully monitored. Adverse to two weeks and the drug should be restarted if angina
effects such as diminished sex drive and impotence may result in symptoms develop during this period.
nonadherence.
Concept Review 22.3

■ Why are selective alpha-adrenergic blockers such as doxazosin (Cardura) of no value in
treating dysrhythmias?
core concept 22.8 Potassium channel blockers prolong the refractory period of the heart.
Although a small class of drugs, the potassium channel blockers (Class III) have important
applications to the treatment of dysrhythmias. Potassium channel blockers used as antidysrhythmics are
listed in Table 22.4 ◆.
The drugs in Class III exert their actions by blocking potassium ion channels in myocardial cells. Af-
ter the action potential has passed and the myocardial cell is in a depolarized state, repolarization depends
on removal of potassium from the cell. The Class III drugs prolong the duration of the action potential by
lengthening the refractory period (resting stage), which tends to stabilize dysrhythmias.
Potassium channel blockers are reserved for serious dysrhythmias because of potentially serious ad-
verse effects. Like other antidysrhythmics, potassium channel blockers slow the heart rate, resulting in
bradycardia and possible hypotension. These adverse effects occur in a significant number of patients.
These medications can worsen dysrhythmias, especially following the first few doses. Older adults with
preexisting heart failure must be carefully monitored because they are particularly at risk for adverse car-
diac effects of potassium channel blockers.
Table 22.4 Potassium Channel Blockers (Class III)

amiodarone (Cordarone, PO; 400–600 mg/day (max: 1,600 mg/day IV form available; usually reserved for serious ventricular
Pacerone) as loading dose) dysrhythmias
dofetilide (Tikosyn) PO; 125–500 mcg bid based on creatinine Usually for atrial dysrhythmias
clearance
dronedarone (Multaq) PO; 400 mg bid Newer drug; given to reduce the risk of cardiovascular
hospitalization in patients with atrial dysrhythmias
ibutilide (Corvert) IV; 1 mg (10 mL) infused over 10 minutes Usually reserved for atrial flutter or fibrillation
sotalol (Betapace, Betapace AF, PO; 80 mg bid (max: 320 mg/day) Usually reserved for serious ventricular dysrhythmias; also a
Sorine) nonselective beta-adrenergic blocker
Drug Prototype: Amiodarone (Cordarone)

Therapeutic Class: Antidysrhythmic (Class III) Pharmacologic Class: Potassium channel blocker
Actions and Uses: Amiodarone is approved for the treatment of Amiodarone interacts with many other drugs. For example,
resistant ventricular tachycardia that may prove life threaten- it increases digoxin levels in the blood and enhances the actions
ing, and it is a preferred drug for treating atrial dysrhythmias in of anticoagulants. If used together with beta blockers, sinus
patients with heart failure. In addition to blocking potassium ion bradycardia may increase, and sinus arrest and atrioventricular
channels, some of amiodarone’s actions on the heart relate to its block may occur. Amiodarone increases phenytoin levels two- to
blockade of sodium ion channels. Amiodarone is available as oral threefold.
tablets and as an IV infusion. IV infusions are limited to short-term Use cautiously with herbal supplements such as echinacea,
therapy, normally only two to four days. Its onset of action may which may cause increased liver toxicity. Aloe may increase the
take several weeks when the drug is given orally. Its effects, how- effect of amiodarone.
ever, can last four to eight weeks after the drug is discontinued
because it has an extended half-life that may exceed 100 days.
Black Box Warning:
Adverse Effects and Interactions: Amiodarone may cause (oral form only): Amiodarone causes a pneumonia-like syn-
blurred vision, rashes, photosensitivity, nausea, vomiting, an- drome in the lungs. Because the pulmonary toxicity may be
orexia, fatigue, dizziness, and hypotension. Because this medi- fatal, baseline and periodic assessment of lung function is
cation is concentrated by certain tissues and has a prolonged essential. Amiodarone has prodysrhythmic action and may
half-life, adverse effects may be slow to resolve. As with other cause bradycardia, cardiogenic shock, or AV block. Mild liver
antidysrhythmics, patients must be closely monitored to avoid injury is frequent with amiodarone.
serious toxicity.
Calcium channel blockers are available to treat supraventricular

dysrhythmias. core concept 22.9
Like the beta blockers, the calcium channel blockers (Class IV) are widely prescribed for various car-
diovascular disorders. By slowing conduction velocity, they are able to stabilize certain dysrhythmias.
Although about 10 calcium channel blockers (CCBs) are available to treat cardiovascular diseases, only a
limited number have been approved for dysrhythmias. Doses for the CCBs used for treating dysrhythmias
are listed in Table 22.5 ◆. The basic pharmacology of this drug class is presented in Chapter 18. Diltiazem
is featured as a prototype drug in Chapter 20.
Blockade of calcium ion channels produces effects on the heart that are similar to those of beta-
adrenergic blockers. Effects include reduced automaticity in the SA node and slowed impulse conduction
Table 22.5 Calcium Channel Blockers (Class IV) and Miscellaneous Drugs for Dysrhythmias
diltiazem (Cardizem, Cartia XT, Dilacor IV; 5–15 mg/hr continuous infusion for a Oral and sustained-release forms available
XR, others) (see page 309 for the Drug maximum of 24 hours (max: 15 mg/hr) for HTN and angina
Prototype box)
verapamil (Calan, Isoptin SR, others) PO; 240–480 mg/day Sustained-release and IV forms available;
IV; 5–10 mg direct: may repeat in also for HTN, angina, and migraines
15–30 minutes if needed
Miscellaneous Drugs
adenosine (Adenocard, Adenoscan) IV; 6–12 mg given as a bolus injection every Usually reserved for atrial dysrhythmias;
1–2 minutes as needed (max: 12 mg/dose) half-life is only 10 seconds
digoxin (Lanoxin) (see page 295 for the Drug PO; 0.125–0.5 mg qid; dose is individualized Usually reserved for atrial dysrhythmias;
Prototype box) for each patient IV and IM forms available; also for heart
failure
Drug Prototype: Verapamil (Calan, Isoptin SR, Others)

Therapeutic Class: Antidysrhythmic (Class IV) Pharmacologic Class: Calcium channel blocker
Actions and Uses: Verapamil was the first CCB approved and hypotension. Because verapamil can cause bradycardia,
by the Food and Drug Administration (FDA). The drug acts patients with heart failure should be carefully monitored.
by inhibiting the flow of Ca2+ into myocardial cells and in Like many other antidysrhythmics, it has the ability to
vascular smooth muscle. In the heart, this action slows con- elevate blood levels of digoxin. Because both digoxin and
duction velocity and stabilizes dysrhythmias. In the vessels, verapamil have the effect of slowing conduction through
calcium ion channel inhibition lowers blood pressure. the AV node, their concurrent use must be carefully
Verapamil also dilates the coronary arteries, an action monitored.
that is important when the drug is used to treat angina Grapefruit juice may increase verapamil levels. The drug
(see Chapter 20)‌. should be used cautiously with hawthorn, which may have
additive hypotensive effects.
Adverse Effects and Interactions: Adverse effects are
generally minor and may include headache, constipation,
through the AV node. This prolongs the refractory period and stabilizes many types of dysrhythmias. CCBs
Life Span Fact are only effective against atrial dysrhythmias.
The healthcare provider should CCBs are well tolerated by most patients. As with other antidysrhythmics, patients should be carefully
carefully monitor older adults monitored for bradycardia and hypotension. Because their cardiac effects are almost identical to those of
with preexisting heart failure beta-adrenergic blockers, patients concurrently taking drugs from both classes are especially at risk for
because these patients are bradycardia and possible heart failure. Because older patients often have multiple cardiovascular disorders,
particularly at risk from the such as HTN, heart failure, and dysrhythmias, it is not unusual to find elderly patients taking drugs from
cardiac effects of potassium
multiple classes.
channel blockers.
Concept Review 22.4

■ Remembering the effects of digoxin on the heart from Chapter 19, explain why most an-
tidysrhythmic drugs have the potential to cause serious adverse effects in patients taking
cardiac glycosides.
Digoxin and adenosine are used for specific dysrhythmias but do not act
core concept 22.10 by blocking ion channels.
Two other drugs, adenosine and digoxin, are used to treat specific dysrhythmias, but they do not act by the
mechanisms described previously. These drugs are summarized in Table 22.5.
Adenosine (Adenocard, Adenoscan) is given as a one- to two-second bolus IV injection to terminate
serious atrial tachycardia by slowing conduction through the AV node and decreasing automaticity of the
SA node. Its primary indication is a specific dysrhythmia known as paroxysmal supraventricular tachycar-
dia (PSVT), for which it is a preferred drug. Although dyspnea is common, adverse effects are generally
brief, because of its 10-second half-life.
Although digoxin (Lanoxin) is primarily used to treat heart failure, it is also prescribed for certain
types of atrial dysrhythmias because it decreases automaticity of the SA node and slows conduction
through the AV node. Excessive levels of digoxin can produce serious dysrhythmias, and interactions
with other medications are common; therefore, patients must be carefully monitored during therapy. The
adverse effects of digoxin are described in Chapter 19.
Chapter Review 343

Patients treated for dysrhythmias need to know the following recommendations:
In General
1. Monitor blood pressure regularly during treatment.
2. Monitor for a decreased heart rate and changes in rhythm while taking antidysrhythmic
drugs. Report changes to a healthcare provider.
Regarding CCBs
3. Notify healthcare provider if a very slow heart rate (less than 60 beats per minute),
dizziness when standing up quickly, headache, or constipation is experienced.
4. Inform a healthcare provider if systolic blood pressure is less than 90 mmHg, and
do not take the next dose of CCB until instructed to do so.
5. Do not discontinue medication suddenly. It should be stopped gradually under the
supervision of a healthcare provider.
Regarding Beta Blockers

6. Notify the healthcare provider if experiencing a very slow heart rate (less than
60 beats per minute), systolic pressure less than 90 mmHg, dizziness when standing
up quickly, or headache.
7. Notify dentists, surgeons, and eye doctors if taking propranolol (Inderal, InnoPran XL).
This drug lowers intraocular pressure.
8. For those with diabetes, check blood glucose regularly while taking beta blockers. These
medications can change how the body uses sugars and starches.
Chapter Review
22.1 Some types of dysrhythmias produce no pa- cause certain consequences such as stroke or heart
tient symptoms, whereas others may be life failure.
threatening.
22.4 Most antidysrhythmic drugs act by blocking ion
Some dysrhythmias produce no symptoms and are
channels in myocardial cells.
harmless, whereas others are life threatening. The
frequency of dysrhythmias is difficult to ascertain, Antidysrhythmic drugs affect the action potential in
although they are thought to be quite common, par- myocardial cells. They act by blocking sodium, po-
ticularly in the geriatric population. tassium, or calcium channels in the cell membrane.
22.5 Antidysrhythmic drugs are classified by their

22.2 Dysrhythmias are classified by the type of rhythm mechanisms of action.
abnormality produced and its location.
All antidysrhythmic drugs have the ability to cause
Dysrhythmias are classified by their site of origin, ei- rhythm abnormalities or worsen existing ones. Most
ther atrial or ventricular, and by the type of rhythm antidysrhythmic medications are placed into one of
abnormality produced, such as tachycardia, flutter, five classes, based on their mechanisms of action.
or fibrillation. Dysrhythmias are associated with dis- Class I drugs are further subdivided into IA, IB, and
eases such as HTN and heart failure. IC. Nonpharmacologic treatments such as cardiover-
sion or catheter ablation are sometimes preferred over
22.3 The electrical conduction pathway in the myocar- drug therapy.
dium keeps the heart beating in a synchronized
manner. 22.6 Sodium channel blockers slow the rate of impulse
The normal rhythm of the heart is established by conduction through the heart.
the SA node, which ensures that the chambers beat Sodium channel blockers stabilize dysrhythmias by
in a synchronized manner. The central problem slowing the spread of impulse conduction across the
with dysrhythmias is their potential to affect the myocardium. Quinidine, a Class IA drug, is the oldest
function of the heart, reduce cardiac output, and antidysrhythmic drug.
22.7 Beta-adrenergic blockers reduce automaticity and These include reduced automaticity in the SA node,
slow conduction velocity in the heart. slowed impulse conduction through the AV node, and
Beta blockers such as propranolol stabilize dysrhyth- a prolonged refractory period.
mias by slowing the heart rate and decreasing the
22.10 Digoxin and adenosine are used for specific
conduction velocity through the AV node.
ysrhythmias but do not act by blocking ion
d
22.8 Potassium channel blockers prolong the refractory channels.
period of the heart. Digoxin and adenosine are used for specific dysrhyth-
Potassium channel blockers such as amiodarone sta- mias but do not act by the mechanisms of Class I, II,
bilize dysrhythmias by prolonging the duration of the III, or IV drugs. Adenosine is used for short-term,
action potential and extending the refractory period. rapid termination of dysrhythmias.
22.9 Calcium channel blockers are available to treat su-

praventricular dysrhythmias.
Calcium channel blockers such as verapamil have
effects similar to those of beta-adrenergic blockers.
Review Questions
The following questions are written in NCLEX-PN® style. An- 3. Decreased

swer these questions to assess your knowledge of the chapter 4. Doubled
to you. 5. The nurse is monitoring a patient taking an antidysrhyth-
mic drug. What outcome would the nurse expect to see?
1. The nurse is monitoring the electrolytes and ECG of a pa- 1. Decreased heart rate
tient with a cardiac dysthymia because he knows that which 2. Increased heart rate
of the following electrolytes produces depolarization when it 3. Increased renal insufficiency
rushes into cardiac cells? 4. Increased hepatic insufficiency
1. Potassium
2. Magnesium 6. The patient taking an antidysrhythmic is instructed by the
3. Sodium nurse to notify the physician if:
4. Chloride 1. Constipation occurs.
2. The heart rate is less than 60 beats per minute.
2. A patient has been ordered a sodium channel blockers. 3. The heart rate is greater than 90 beats per minute.
In explaining to the patient how this class of drug works, the 4. Blood pressure does not decrease.
nurse says that sodium channel blockers:
1. Increase automaticity 7. A group of patients is being taught about the common
2. Slow impulse conduction adverse effects of antidysrhythmic medications. Some of the
3. Prolong the refractory period adverse effects they are being taught about include: (Select all
4. Increase impulse conduction that apply.)
1. Dizziness
3. The physician has ordered propranolol, 15 mg by mouth 2. Hypotension
(po), three times a day. The pharmacy has propranolol in 3. Weakness
30-mg tablets. How many tablets will the nurse give per dose 4. Anorexia
and how many mg will the patient receive in a day?
1. One-half tablet per dose, 30 mg per day 8. Which of the following would be included in the teaching
2. One-half tablet per dose, 45 mg per day plan for a patient taking an antidysrhythmic medication?
3. One and one-half tablets per dose, 45 mg per day 1. “Take the drug only when you are feeling excessively
4. One and one-half tablets per dose, 35 mg per day tired.”
2. “Take your pulse prior to taking your medication.”
4. When the patient is on amiodarone (Cordarone). What 3. “Do not drink alcohol unless you have spoken with your
changes will the nurse expect to see to the patient’s digoxin physician.”
order? 4. “You will need to increase your sodium and potassium
1. Discontinued intake.”
2. Increased
Chapter Review 345
9. A patient is taking an antidysrhythmic medication and 10. When administering this antidysrhythmic, the nurse also
learns in a patient education session that sometimes this medi- knows that this drug is used to treat hypertension and angina.
cation is also used to treat angina. What medication is the nurse What drug is the nurse administering?
discussing? 1. Diltiazem (Cardizem)
1. Digoxin (Lanoxin) 2. Digoxin (Lanoxin)
2. Verapamil (Calan) 3. Adenosine (Adenocard)
3. Adenosine (Adenocard) 4. Quinidine sulfate
4. Quinidine sulfate
Remember Mrs. Duncan, the patient 3. Have no effect on her hypertension

introduced at the beginning of the 4. First raise her blood pressure, then lower it
the case study. Based on the informa- 3. The physician lowers the dose of propranolol and adds
tion you have learned in this chapter, amiodarone (Cordarone) to the drug regimen. Mrs. Duncan
answer the questions that follow. begins to experience dizziness, fainting spells, and fatigue.
The nurse recognizes that this is most likely caused by which
Mrs. Margaret Duncan, age 72, who has a history of of the following?
hypertension, has arrived in the emergency department with a 1. Mrs. Duncan is not eating enough potassium-rich foods.
life-threatening ventricular dysrhythmia. She is frightened and 2. The drug combination is causing bradycardia or hypertension.
is wondering what is happening. The physician has ordered 3. The drug combination is causing respiratory depression.
that an IV lidocaine infusion be started on Mrs. Duncan. 4. Mrs. Duncan’s hypertension is out of control.
1. The nurse explains to Mrs. Duncan that lidocaine would 4. When taking these medications, Mrs. Duncan is in-
be expected to terminate her dysrhythmia primarily by which structed to:
of the following mechanisms? 1. Check her pulse rate frequently.
1. Speeding up the heart rate 2. Keep a log of weight gain or loss.
2. Lowering blood pressure 3. Eat plenty of foods containing potassium.
3. Increasing the strength of myocardial contractions 4. Avoid taking aspirin, unless instructed to do so by the
4. Slowing the speed of electrical conduction across the physician.
myocardium
2. When Mrs. Duncan is discharged from the hospital, she is
placed on propranolol. The nurse informs the patient that this
drug should:
1. Raise her blood pressure
2. Lower her blood pressure
Pearson Nursing Student Resources Find additional review materials at: nursing.pearsonhighered.com.
C
“Let me see if I understand
H this . . . I need to go to the
A lab and get stuck every other
P day for the next two weeks?”
T Mr. Thomas Hawkins
E
R
23 Drugs for Coagulation Disorders
Core Concepts
23.1 Hemostasis is a complex process involving multiple 23.5 Antiplatelet drugs prolong bleeding time by
steps and many clotting factors. interfering with platelet aggregation.
23.2 Removing a blood clot is essential to restoring 23.6 Thrombolytics are used to dissolve existing clots.
normal circulation. 23.7 Hemostatics are used to promote the formation
23.3 Drugs are used to modify the coagulation process. of clots.
23.4 Anticoagulants prevent the formation and
enlargement of clots.
Drug Snapshot
Anticoagulants heparin 352 Thrombolytics alteplase (Activase) 357
warfarin (Coumadin) 353 Hemostatics aminocaproic acid
(Amicar) 358
Antiplatelet drugs clopidogrel (Plavix) 356
Learning Outcomes
1. Explain the importance of 4. Identify the primary mechanisms 6. For each of the classes in the Drug
hemostasis. by which coagulation modifier Snapshot, identify representative
2. Construct a diagram that illustrates drugs act. drugs and explain their mechanisms
the primary steps of hemostasis and 5. Categorize coagulation modifier of drug action, primary actions, and
fibrinolysis. drugs based on their classifications important adverse effects.
3. Describe the types of disorders for and mechanisms of action.
which coagulation modifier drugs
are prescribed.
Key Terms
activated partial thromboplastin time antiplatelet drugs (ant-eye-PLAY-tuh- coagulation cascade (cass-KADE) 347
(aPTT) (throm-bow-PLAS-tin) 352 let) 350 deep venous thrombosis (DVT) 349
anticoagulant (ANT-eye-co-AG-you- clotting factors 347 embolus (EM-boh-luss) 349
lent) 350 coagulation (co-ag-you-LAY-shun) 347 fibrin (FEYE-brin) 347
fibrinogen (feye-BRIN-oh-jen) 347 low molecular weight heparins thromboembolic disorder (THROM-bow-
fibrinolysis (feye-brin-OL-oh-sis) 349 (LMWHs) 351 EM-bow-lik) 349
glycoprotein IIb/IIIa (GLEYE-koh-proh- plasmin (PLAZ-min) 349 thrombolytics (throm-bow-LIT-iks) 350
teen) 356 plasminogen (plaz-MIN-oh-jen) 349 thrombus (THROM-bus) 349
hemostasis (hee-moh-STAY-sis) 347 prothrombin (PRO-throm-bin) 347 tissue plasminogen activator
hemostatics (hee-moh-STAT-iks) 350 prothrombin time (PT) 352 (tPA) 349
international normalized ratio (INR) 352 thrombin (THROM-bin) 347
E veryone is familiar with the bleeding associated with simple cuts and scrapes, and we take for
granted that bleeding will stop in a few minutes. Hemostasis, or the stopping of blood flow, is an
essential mechanism protecting the body from both external and internal injury. Without efficient
hemostasis, bleeding from wounds would lead to shock and perhaps death. Too much clotting, however,
can be just as deadly as too little. Thus, hemostasis must maintain a delicate balance between blood fluidity
hemo 5 blood
stasis 5 stopping
and coagulation.
Many diseases and conditions affect hemostasis. Some common disorders that often require pharma-
cotherapy with coagulation modifiers are described in Table 23.1 ◆.
Hemostasis is a complex process involving multiple steps

and many clotting factors. core concept 23.1
Hemostasis is complex and involves a number of substances called clotting factors. The clotting fac-
tors are activated in a series of sequential steps, sometimes referred to as a cascade. Drugs can be used to
modify several of these steps.
When an injury occurs, cells lining damaged blood vessels release chemicals that begin the process of
hemostasis. The vessel immediately spasms, which limits blood flow to the injured area. Platelets become
sticky, adhere to the injured area, and aggregate or clump to plug the damaged vessel. Blood flow is fur-
ther slowed, resulting in coagulation, the formation of an insoluble clot. The basic steps of hemostasis are
The coagulation cascade is a complex series of steps that begins when the injured cells release a
chemical called prothrombin activator or prothrombinase. Prothrombin activator converts the clotting fac-
tor prothrombin to an enzyme called thrombin. Thrombin then converts fibrinogen, a plasma protein, to pro 5 before
long strands of fibrin. Thus two of the factors essential to clotting, thrombin and fibrin, are only formed thrombin 5 clot
after injury to the vessels. The fibrin strands form an insoluble web over the injured area to stop blood
loss. Normal blood clotting occurs in about six minutes. The primary steps in the coagulation cascade are
It is important to note that several clotting factors, including thromboplastin and fibrinogen, are pro- thrombo 5 clot
teins made by the liver that are constantly circulating through the blood in an inactive form. Vitamin K is plastin 5 to form
required for the liver to make four of the clotting factors. Because the liver supplies many of the clotting
factors, patients with serious hepatic impairment usually exhibit abnormal coagulation.
Table 23.1 Disorders Commonly Treated with Coagulation Modifier Drugs

Disorder/Condition Description
Angina Pain due to narrowing of the coronary vessels that interferes with
blood flow to cardiac muscle
Deep venous thrombosis (DVT) Clot within a vein in the legs
Indwelling devices Mechanical heart valves, stents
Myocardial infarction Death of cardiac muscle tissue due to blockage of a coronary
artery
Postoperative hemorrhage Bleeding following a surgical procedure
Pulmonary embolus Clot within a pulmonary artery that blocks blood flow to the
lungs
Stroke (cerebrovascular accident) Clot within an artery that blocks blood flow to the brain
Valvular heart disease Disease of heart valves or replacement of a heart valve
348 Chapter 23 Drugs for Coagulation Disorders
Figure 23.1
Basic steps in hemostasis.
Vessel injury
Vessel spasm
Platelets adhere
to injury site and
aggregate to
form plug
Insoluble fibrin
strands form and
coagulate
Figure 23.2
Major steps in the Injured vessel
coagulation cascade.
Platelets and
damaged cells
Factor X
Prothrombin activator (Prothrombinase)
+
Prothrombin Thrombin Injured vessel
+
+
Fibrinogen
Plasma
Liver
Insoluble fibrin
strands
Fast Facts Clotting Disorders

■ More than 60,000–100,000 patients die each year of pulmonary emboli. For 25% of these patients,
sudden death will be the first sign of the condition.
■ Von Willebrand’s disease is the most common hereditary platelet disorder, affecting about
1.4 million Americans.
■ Hemophilia A, or classic hemophilia, is a hereditary condition in which a person lacks clotting factor
VIII; it accounts for 80% of all hemophilia cases.
■ More than 20,000 people in the United States have hemophilia.
Removing a blood clot is essential to restoring normal circulation. Core Concept 23.2
The goal of hemostasis has been achieved once a blood clot is formed, and the body is protected from
excessive hemorrhage. Large clots, however, may prevent adequate blood flow to the affected area; cir-
culation must eventually be restored so that the tissue can resume normal activities. The process of clot
removal is called fibrinolysis. fibrin 5 fiber
Fibrinolysis also involves several sequential steps. When the fibrin clot is formed, nearby blood vessel lysis 5 break apart
cells secrete tissue plasminogen activator (tPA). tPA converts the inactive protein plasminogen, which
is present in the fibrin clot, to its active form called plasmin. Plasmin then digests the fibrin strands to
remove the clot. The body normally regulates fibrinolysis such that unwanted fibrin clots are removed,
whereas fibrin present in wounds is left to maintain hemostasis. The steps of fibrinolysis are shown in
Figure 23.3 ■.
Drugs are used to modify the coagulation process. Core Concept 23.3
There are many types of disorders in which abnormal coagulation might occur. The term thromboem-
bolic disorder is used to describe conditions in which the body forms undesirable clots. Thromboembolic
disorders may occur in either veins or arteries and can place patients in extreme danger. Once a stationary
clot, or thrombus, forms in a vessel, it often grows larger as more fibrin is added. Thrombi in the venous
system usually form in the veins of the legs in patients due to sluggish blood flow, a condition called deep
venous thrombosis (DVT). Pieces of a thrombus may break off and travel in the bloodstream to lodge
in other vessels. A traveling clot is called an embolus. When thrombi or emboli form, drug therapy is
indicated.
Figure 23.3
(a) Primary steps in

Plasminogen fibrinolysis.
activators
Clot in vessel containing Plasminogen converted to

inactive plasminogen plasmin, which digests the clot
Enhanced by
(b)
thrombolytics
• Alteplase
Plasminogen Plasmin
Inhibited by
hemostatics
• Aminocaproic
acid
anti 5 against Drugs can be used to modify hemostasis in a number of ways. Anticoagulants are drugs used to
coagulation 5 clotting prevent excessive clotting, usually by interfering with some aspect of the coagulation cascade. The anti-
platelet drugs, also frequently prescribed to modify hemostasis, act by diminishing the clotting action of
platelets. Regardless of the mechanism, all anticoagulant and antiplatelet drugs will increase the time the
body takes to form clots. These drugs are often referred to as blood thinners, which is an incorrect term,
because they do not change the thickness of the blood.
Once an abnormal clot has formed, it may be critical to quickly remove it in order to restore normal
function. This is particularly important for blood vessels serving the heart, lungs, and brain. A specific
thrombo 5 clot class of drugs, the thrombolytics, is used to dissolve such life-threatening clots.
lytic 5 remove/destroy In some cases, the blood may not clot quickly enough—for example, following surgery. In this case, it
is sometimes desirable to administer medications that make the blood clot more quickly in order to prevent
excessive bleeding. These drugs, called hemostatics, inhibit the normal removal of fibrin, thus keeping the
clot in place for a longer period. Hemostatics are used to speed clot formation, thereby limiting bleeding
from a surgical site (see Figure 23.3).
Concept Review 23.1

■ Which clotting factors are always circulating in the blood? Which are formed only once
coagulation is underway?
Core Concept 23.4 Anticoagulants prevent the formation and enlargement of clots.
Anticoagulants are drugs that inhibit certain clotting factors, thus lengthening clotting time and preventing
thrombi from forming or growing larger. Because thromboembolic disease can be life threatening, therapy
is often begun by administering anticoagulants intravenously or subcutaneously to achieve a rapid onset of
action. As the disease stabilizes, the patient is switched to oral anticoagulants. Anticoagulants act by a number
of different mechanisms, which are illustrated in Figure 23.4 ■. Table 23.2 ◆ lists the primary anticoagulants.
The most frequent, and potentially serious, adverse effect of anticoagulant and antiplatelet drugs is
bleeding. The patient must be observed for signs of hemorrhage, such as bruising, bleeding gums, and
blood in the urine or stools. Patients who have recently experienced a traumatic injury or recent surgery
are especially at risk. Any symptoms of bleeding must be immediately reported to the healthcare provider.
Specific blockers may be administered to reverse the anticoagulant effects: Protamine sulfate is used for
heparin, and vitamin K is administered for warfarin.
Parenteral Anticoagulants
The traditional drug of choice for rapid anticoagulation is heparin. Heparin inactivates thrombin and sev-
eral other clotting factors within minutes after it is given by the IV route. In recent years, the heparin
Figure 23.4
coagulation modifiers.
Inhibition of Aspirin
platelet Abciximab
aggregation
Inhibition of
Inhibition of clotting factors
platelet adhesion and cascade
to injury site
Warfarin
Heparin
Clopidogrel Low molecular
Ticlopidine weight heparins
Lepirudin
Decreased blood
viscosity
Pentoxifylline
Table 23.2 Anticoagulants

antithrombin, recombinant (ATryn) IV infusion; dose is individualized Thrombin inhibitor; for the prevention of perioperative and
based on the patient’s pretreat- peripartum thromboembolic events in hereditary antithrombin
ment AT activity level and body deficient patients
weight
apixaban (Eliquis) PO; 2.5–5 mg bid Factor Xa inhibitor; for prevention of stroke and pulmonary
embolism in patients with atrial fibrillation
argatroban (Acova, Novastan) IV; 2–10 mcg/kg/min Thrombin inhibitor; for prevention of clots in patients with
heparin-induced thrombocytopenia
bivalirudin (Angiomax) IV; 0.75 mg/kg initial bolus followed Thrombin inhibitor; used with aspirin to prevent clots during
by 1.75 mg/kg/hr for 4 hours angioplasty
dabigatran (Pradaxa) PO; 75–150 mg bid Thrombin inhibitor; for prevention of stroke and systemic
desirudin (Iprivask) Subcutaneous; 15 mg bid for Thrombin inhibitor; for DVT prophylaxis in patients undergoing
9–12 days hip replacement surgery
fondaparinux (Arixtra) Subcutaneous; 2.5 mg/daily For prevention of DVT and pulmonary embolism
heparin IV infusion; 5,000–40,000 units/ For prevention and treatment of venous thrombosis and
day subcutaneously; 15,000–20,000 pulmonary edema; therapy begins with a higher dose, which
units/bid is gradually reduced
lepirudin (Refludan) IV; 0.4 mg/kg bolus followed by Thrombin inhibitor; for prevention of clots in patients with
0.15 mg/kg/hr for 2–10 days heparin-induced thrombocytopenia
pentoxifylline (Trental) PO; 400 mg tid Reduces blood viscosity and increases the flexibility of red
blood cells; for intermittent claudication (pain in legs while
walking or exercising)
rivaroxaban (Xarelto) PO; 10 mg once daily Blocks Factor Xa; for prevention of stroke and systemic
warfarin (Coumadin) PO; 2–15 mg/day Same use as heparin but effect is more prolonged; IV form is
available
Low Molecular Weight (Fractionated) Heparins (LMWHs)
dalteparin (Fragmin) Subcutaneous; 2,500–5,000 units/ For prevention and treatment of DVT following knee or hip
day replacement or abdominal surgery, unstable angina, or acute
coronary syndromes
enoxaparin (Lovenox) Subcutaneous; 30 mg bid for
7–10 days
tinzaparin (Innohep) Subcutaneous; 175 units/kg daily for
at least 6 days
molecule has been shortened and modified to create low molecular weight heparins (LMWHs), paren-
teral drugs that possess the same anticoagulant activity as heparin but have several advantages. They pro-
duce a more predictable anticoagulant response than heparin; therefore, less frequent laboratory monitoring
is required. They also exhibit a two to four times longer duration of action than heparin that permits once
daily dosing. Family members or the patient can be taught to give the necessary subcutaneous injections at
home. LMWHs have become preferred drugs for many clotting disorders, including the prevention of DVT
following surgery.
Other parenteral anticoagulants include the direct thrombin inhibitors such as lepirudin (Refludan).
These drugs bind to the active site of thrombin, preventing the formation of fibrin clots. The thrombin in-
hibitors have limited therapeutic uses. Bivalirudin (Angiomax) is administered in combination with aspirin
to prevent thrombi in patients undergoing angioplasty.
Argatroban (Acova, Novastan) and lepirudin are indicated for prevention or treatment of low platelet
counts induced by heparin therapy. Desirudin (Iprivask) is given subcutaneously 15 minutes prior to hip
replacement surgery for prophylaxis of DVT. Dabigatran (Pradaxa) is an oral drug in this class approved to
reduce the risk of stroke and embolism in patients with atrial fibrillation.
To avoid serious adverse effects, drug therapy with coagulation modifier drugs is individualized to
each patient and must be carefully monitored. For heparin, the activated partial thromboplastin time
(aPTT) test is used to monitor the extent of anticoagulation. Baseline values of aPTT range from 25 to
40 seconds. During heparin therapy, the aPTT is maintained at 1.5 to 2 times the baseline level. If the aPTT
rises above 80 seconds, the heparin dosage should be reduced. During the first few days of heparin therapy,
aPTT is measured every four to six hours to avoid abnormal bleeding.
Oral Anticoagulants
The most frequently prescribed oral anticoagulant is warfarin (Coumadin). Often, patients begin anticoagu-
lation therapy with heparin and are switched to warfarin when their condition stabilizes. When transition-
ing, the two drugs are administered concurrently for two to three days because warfarin takes several days
of therapy before it achieves optimum anticoagulation effects.
Warfarin inhibits two enzymes involved in the formation of activated vitamin K, which is required
for the synthesis of several clotting factor. Warfarin inhibits the synthesis of new clotting factors but does
not affect clotting factors that are already circulating in the blood. The result is slowed clot formation and
increased bleeding time.
Oral alternatives to warfarin include pentoxifylline, rivaroxaban, and apixaban. Although not a true
anticoagulant, pentoxifylline (Trental) reduces the viscosity of red blood cells and increases their flex-
ibility. It is given to increase the microcirculation in patients with intermittent claudication. In 2011,
Life Span Fact rivaroxaban (Xarelto) became the first anticoagulant available by the oral route to directly inhibit Factor
Bleeding complications are X in the clotting cascade. Rivaroxaban is indicated for the prophylaxis of DVT in patients undergoing
more likely to occur in older knee or hip replacement surgery and to reduce the risk of stroke and systemic embolism in patients with
adults. Prescribed doses of atrial fibrillation. In 2013, apixaban (Eliquis) was approved as an oral medication to reduce the incidence
anticoagulants are generally of stroke and pulmonary embolism in patients with atrial fibrillation. Patients with artial fibrillation are at
lower for older patients, and increased risk for thrombus formation.
this group receives more fre-
quent assessments and labora-
The laboratory test used during therapy with the oral anticoagulants is prothrombin time (PT).
tory testing to avoid serious Although the normal range for PT is 12 to 15 seconds, this value becomes prolonged with anticoagu-
complications. lant treatment. Daily PT tests may be conducted at the start of pharmacotherapy to ensure optimum
dose levels. The frequency of PT tests is decreased to weekly or monthly as therapy progresses and
the patient’s condition stabilizes. Because the method of performing PT tests varies from labora-
tory to laboratory, clotting time is sometimes reported as an international normalized ratio (INR),
which is the PT multiplied by a correction factor. Recommended post-treatment INR values range
from 2 to 4.
Drug Prototype: Heparin

Therapeutic Class: Anticoagulant Pharmacologic Class: Indirect thrombin inhibitor
Actions and Uses: Heparin is a natural substance found in The patient may experience serious and even life-threatening
the lining of blood vessels. Its normal function is to prevent thrombosis. Although the half-life of heparin is short, it may
excessive clotting within blood vessels. When given as a drug, take a week after the drug is discontinued for platelets to
heparin provides immediate anticoagulant activity. The binding completely recover.
of heparin to a substance called antithrombin III results in an Oral anticoagulants, including warfarin, increase the action
inactivation of some of the clotting factors and an inhibition of heparin. Ibuprofen, ASA, and other drugs that inhibit platelet
of thrombin activity. Heparin must be given either subcutane- aggregation may induce bleeding. Nicotine, digoxin, tetracy-
ously or through IV infusion. The onset of action for IV heparin clines, or antihistamines may inhibit anticoagulation. Herbal
is immediate, whereas subcutaneous heparin may take up to an supplements that may affect coagulation, such as ginger, garlic,
hour for maximum therapeutic effect. green tea, feverfew, or ginkgo, should be avoided because they
may increase the risk of bleeding.
Adverse Effects and Interactions: Abnormal bleeding is
common during heparin therapy. If aPTT becomes prolonged
or toxicity is observed, stopping the heparin infusion will result
in loss of anticoagulant activity within hours. If serious Black Box Warning:
hemorrhage occurs, a specific blocker, protamine sulfate, Epidural or spinal hematomas may occur when heparin or
may be administered to neutralize the anticoagulant activity LMWHs are used in patients receiving spinal anesthesia or
of heparin. Protamine sulfate has an onset time of five minutes lumbar puncture. Because these can result in long-term or
and is also a blocker of the LMWHs. permanent paralysis, frequent monitoring for neurologic
Heparin-induced thrombocytopenia (HIT) is a serious com- impairment is essential.
plication that occurs in up to 30% of patients taking the drug.
Drug Prototype: Warfarin (Coumadin)

Therapeutic Class: Anticoagulant Pharmacologic Class: Vitamin K antagonist
Actions and Uses: Warfarin is used to prevent thrombi and reduced in six hours through the IM or subcutaneous adminis-
emboli formation. Thus it is administered to patients at high tration of its blocker, vitamin K. The therapeutic range of serum
risk for stroke, MI, DVT, and pulmonary embolism. This includes warfarin levels varies from 1 to 10 mcg/mL to achieve an INR
patients undergoing hip or knee surgery, those with long-term value of 2–3.
indwelling central venous catheters or prosthetic heart valves, Extensive protein binding is responsible for numerous
and those who have experienced a recent MI. drug interactions, some of which occur with NSAIDs, diuret-
Unlike heparin, the anticoagulant activity of warfarin can ics, selective serotonin reuptake inhibitors (SSRIs) and other
take several days to reach its maximum effect. This explains antidepressants, steroids, antibiotics and vaccines, and vita-
why heparin and warfarin therapy are overlapped. Warfarin mins (e.g., vitamin K). Use with NSAIDs may increase bleeding
inhibits the action of vitamin K that is essential for the synthesis risk. During warfarin therapy, the patient should not take
of several clotting factors. Because these clotting factors are any other prescription or over-the-counter (OTC) drugs unless
normally circulating in the blood, it takes several days for them approved by the healthcare provider. Use of warfarin with
to clear the plasma and for the anticoagulant effect of warfarin herbal supplements such as green tea, ginkgo, feverfew, gar-
to appear. Another reason for the slow onset is that 99% of lic, cranberry, chamomile, and ginger may increase the risk of
warfarin binds to plasma proteins and is unavailable to produce bleeding.
its effect. This high level of protein binding is responsible for
a significant number of drug–drug interactions that may occur
during warfarin therapy. Black Box Warning:
Warfarin can cause major or fatal bleeding. Regular
Adverse Effects and Interactions: Like all anticoagulants, the monitoring of INR is required. Patients should be instructed
most serious adverse effect of warfarin is abnormal bleeding. about prevention measures to minimize bleeding risk and
On discontinuation of therapy, the activity of warfarin can take to immediately notify healthcare providers of signs and
up to 10 days to diminish. If life-threatening bleeding occurs symptoms of bleeding.
during therapy, the anticoagulant effects of warfarin can be
Nursing Process Focus Patients Receiving Anticoagulant and Antiplatelet Therapy

Prior to administration: ■ Risk for Injury (bleeding) related to adverse effects of anticoagulant
■ Obtain complete health history, including cardiovascular and renal therapy
conditions, surgeries or trauma, allergies, drug history, and possible ■ Ineffective Tissue Perfusion related to altered blood flow
drug interactions. ■ Deficient Knowledge related to a lack of information about drug
signs, height, and weight. ■ Noncompliance related to adverse effects of medications
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, ■ Ineffective Self-Health Maintenance related to insufficient knowledge
clotting factors, and renal and liver function studies. of seriousness of disease and drug therapy regimen
The patient will:

■ Experience therapeutic effects (a decrease in blood coagulability).
Implementation
■ Administer medication correctly and evaluate the patient knowledge Instruct patient and caregivers that:
of proper administration. (Proper medication administration will ■ Correct self-administration of medication is extremely important.
increase effectiveness and help reduce complications and adverse ■ Injections of heparin or LMWH should be administered in the fatty lay-
effects.) ers of the abdomen.
■ Skin is drawn up (pinched) and the needle is inserted at 45-90 degree
angle.
■ Injections are done without aspirating for blood return.
■ Oral medications should be taken at the same time every day.
Monitor for adverse clotting reaction(s): Instruct the patient to:

■ Observe for skin necrosis, blue or purple mottling of the feet that ■ Immediately report to healthcare provider any sudden dyspnea or chest
blanches with pressure or fades when the legs are elevated. (Patients pain, and if temperature or color change occurs in the hands, arms, legs,
on anticoagulant therapy remain at risk for developing emboli result- and feet. (Gangrene may occur between days 3 and 8 of warfarin ther-
ing in cerebrovascular accident or pulmonary embolism. Coumadin apy. Purple toes syndrome usually occurs within weeks 3–10 or later.)
may cause cholesterol microemboli, which result in gangrene, local- ■ Feel pedal pulses daily to check circulation.
ized vasculitis, or “purple toes syndrome.” Heparin can cause throm- ■ Protect feet from injury by wearing loose-fitting socks; avoid going
bus formation with thrombocytopenia, or “white clot syndrome.”) barefoot.
■ Use with caution in patients with GI, renal, and/or liver disease, ■ Advise older adult patients; menstruating women; and those with pep-
alcoholism, diabetes, hypertension, hyperlipidemia, and in older adult tic ulcer disease, alcoholism, or kidney or liver disease that they have
patients and premenopausal women. (Patients with CAD risk factors an increased risk of bleeding.
are at increased risk of developing cholesterol microemboli.) ■ Advise patients with diabetes and those with high blood pressure or
high cholesterol that they are at risk of developing microscopic clots,
despite anticoagulant therapy.
■ Monitor for signs of bleeding: flu-like symptoms, excessive bruising, Instruct the patient to:
pallor, epistaxis, hemoptysis, hematemesis, menorrhagia, hematuria, ■ Immediately report to healthcare provider flu-like symptoms (dizzi-
melena, frank rectal bleeding, or excessive bleeding from wounds or ness, chills, weakness, pale skin), blood coming from a cough, the nose,
in the mouth. (Bleeding is a sign of anticoagulant overdose.) mouth or rectum; menstrual “flooding,” “coffee grounds” vomit;
tarry stools, excessive bruising; bleeding from wounds that cannot be
stopped within 10 minutes, and all physical injuries.
■ Avoid all contact sports and amusement park rides that cause intense
or violent bumping or jostling.
■ Use a soft toothbrush and electric shaver.
■ Keep a “pad count” during menstrual periods to estimate blood losses.
■ Monitor vital signs. (Increase in heart rate accompanied by low blood ■ Instruct the patient to immediately report palpitations, fatigue,
pressure or subnormal temperature may signal bleeding.) or feeling faint, which may signal low blood pressure related to
bleeding.
■ Monitor laboratory values: CBC, especially in premenopausal women; Instruct the patient:
liver function studies, platelets, aPTT, PT, and/or INR for therapeutic ■ About the importance and need of regular laboratory testing.
values. (The aPTT and PT are usually 1.5–2.5 the normal control val- ■ To always inform laboratory and dental personnel of anticoagulant
ues. The value for INR is usually 2–4. Values below the norm indicate therapy when providing samples.
below-therapeutic levels. Values above the norm indicate a high ■ To carry a wallet card or wear medical ID jewelry indicating anticoagu-
potential for bleeding. CBC and platelet levels should remain within lant therapy.
normal limits.) Heparin may also cause significant elevations of liver
function tests because the drug is metabolized by the liver.)
■ Monitor the use of other medications or herbal supplements. ■ Instruct the patient to consult a healthcare provider before taking
any other drugs, including OTC or herbal supplements. Many drugs
decrease the action of anticoagulants.
■ Maintain normal diet, avoiding alcohol and increases in vitamin-K rich ■ Inform the patient to avoid alcohol and increases in vitamin K-rich
foods. (Vitamin K is used in the formation of clots; therefore, ingesting foods such as broccoli, cabbage, dark leafy greens, and asparagus.
high amounts may decrease the effectiveness of warfarin. Alcohol may
also alter the effectiveness of anticoagulants.)
Antiplatelet drugs prolong bleeding time by interfering

Core Concept 23.5 with platelet aggregation.
Antiplatelet medications produce an anticoagulant effect by interfering with platelet aggregation. Un-
like the anticoagulants, which are used primarily to prevent thrombosis in veins, antiplatelet drugs are
used to prevent clot formation in arteries. Doses for antiplatelet medications are listed in Table 23.3 ◆.
Platelets are a key component of hemostasis. Too few platelets or diminished platelet function can
profoundly increase bleeding time. The three primary classes of antiplatelet drugs include the following:
■ Aspirin
■ Adenosine diphosphate (ADP) receptor blockers
■ Glycoprotein IIb/IIIa receptor blockers
Table 23.3 Antiplatelet Drugs

anagrelide (Agrylin) PO; 0.5 mg qid or 1 mg bid (max: Inhibits the production of platelets; for essential
10 mg/day) thrombocythemia (production of too many platelets)
aspirin (acetylsalicylic acid, ASA) (see PO; 80 mg/day–650 mg bid Inhibits platelet aggregation; available without a prescrip-
page 208 for the Drug Prototype box) tion; higher doses are used to treat inflammation or pain
cilostazol (Pletal) PO; 100 mg bid Inhibits platelet aggregation; for intermittent claudication
dipyridamole (Persantine) PO; 75–100 mg qid Platelet inhibitor used to prevent embolism in cardiac
valve replacement; usually used with warfarin
ADP Receptor Blockers
clopidogrel (Plavix) PO; 75 mg daily (300 mg loading Platelet aggregation inhibitor; for prevention of MI and
dose for patients with acute coronary stroke
syndrome)
prasugrel (Effient) PO; 60 mg loading dose followed by Platelet aggregation inhibitor; for prevention of throm-
10 mg/day botic events in patients undergoing PCI
ticagrelor (Brilinta) PO; 90 mg bid Newer drug for prevention of thrombosis in patients
with acute coronary syndrome; given concurrently with
75–100 mg aspirin
ticlopidine (Ticlid) PO; 250 mg bid Platelet aggregation inhibitor; for stroke prevention
Glycoprotein IIB/IIIA Blockers
abciximab (ReoPro) IV; 0.25 mg/kg initial bolus over For prevention of cardiac ischemia during coronary
5 minutes; then 10 mcg/min for 12 angioplasty; effects continue up to 48 hours after infusion
hours is stopped
eptifibatide (Integrilin) IV; 180 mcg/kg initial bolus over For unstable angina and other acute coronary syndromes;
1–2 minutes; then 2 mcg/kg/min for effects continue up to 8 hours after infusion is stopped
24–72 hours
tirofiban (Aggrastat) IV; 0.4 mcg/kg/min for 30 minutes; Similar to eptifibatide; effects continue up to 8 hours after
then 0.1 mcg/kg/min for 12–24 hours infusion is stopped
Aspirin deserves special mention as an antiplatelet drug. Because it is available over-the-counter

(OTC), patients may not consider aspirin a strong medication. However, its anticoagulant activity is
well documented. Aspirin acts by inhibiting thromboxane2, a powerful inducer of platelet aggregation.
The anticoagulant effect of a single dose of aspirin may last for as long as a week. Use of aspirin with
other coagulation modifiers should be avoided unless approved by the prescriber. The primary actions and
adverse effects of aspirin are described in a Drug Prototype feature in Chapter 14.
The ADP receptor blockers are a small group of drugs that irreversibly alter the plasma membrane
of platelets, preventing them from aggregating. Both ticlopidine (Ticlid) and clopidogrel (Plavix) are
CAM Therapy
Garlic for Cardiovascular Health
Garlic (Allium sativum) is one of the best-studied herbs. Several substances have been isolated
from garlic and shown to have pharmacologic activity. Dosage forms include eating prepared
garlic oil or the fresh bulbs from the plant.
Modern claims for garlic uses have focused on the cardiovascular system: treatment of
high blood lipid levels, atherosclerosis, and hypertension. Other modern claims are that garlic
reduces blood glucose levels and has antibacterial and antineoplastic activity.
Like many other supplements, garlic likely has some health benefits, but controlled,
scientific studies are often lacking and the results are mixed. Garlic has been shown to
decrease the aggregation or “stickiness” of platelets, thus producing an anticoagulant effect.
There is some research to show that the herb has a small effect on lowering blood cholesterol,
although the effects seem to be short term.
Garlic is safe for consumption in moderate amounts. Patients taking anticoagulant
medications should limit their intake of garlic to avoid bleeding complications. Patients with
diabetes should monitor their blood glucose levels closely if taking high doses of garlic.
Drug Prototype: Clopidogrel (Plavix)

Therapeutic Class: Antiplatelet drug Pharmacologic Class: ADP receptor blocker
Actions and Uses: Clopidogrel prolongs bleeding time by inhib- cause an acute blood disorder known as thrombotic thrombo-
iting platelet aggregation. It is given orally. Although its only cytopenia purpura, which can be fatal in up to 30% of patients
approved use is to reduce the risk of stroke due to thrombi, who develop the disorder.
it may be given off-label to prevent thrombi formation in pa- Use with anticoagulants, other antiplatelet drugs, throm-
tients with coronary artery stents and to prevent postoperative bolytics, or NSAIDS, including aspirin, will increase the risk of
deep venous thrombosis. Because it is expensive, it is usually bleeding. Barbiturates, rifampin, or carbamazepine may increase
prescribed only for patients unable to tolerate aspirin, which the anticoagulant activity of clopidogrel. The azole antifungals,
has similar anticoagulant activity. Ticlopidine (Ticlid) acts by the protease inhibitors, erythromycin, verapamil, or zafirlukast may
same mechanism as clopidogrel but causes more adverse effects. diminish the antiplatelet actions of clopidogrel.
Adverse Effects and Interactions: Clopidogrel has approximately

the same tolerability as aspirin. The incidence of GI bleeding is Black Box Warning:
less than that for aspirin. Frequent adverse effects include a flu- Because the effectiveness of clopidogrel is dependent on
like syndrome, headache, diarrhea, dizziness, bruising, upper re- its metabolic activation by hepatic enzymes, poor metabo-
spiratory tract infection, and rash or pruritus. Excessive bleeding lizers will exhibit less therapeutic effect and more adverse
is a potential adverse effect, although it only occurs in about cardiovascular events.
1% of patients. The other drug in this class, ticlopidine, can
given orally to prevent thrombi formation in patients who have experienced a recent thromboembolic
event such as a stroke or MI. Clopidogrel is considerably safer and much more widely prescribed,
having adverse effects comparable to those of aspirin. Prasugrel (Effient) and ticagrelor (Brilinta) are
newer drugs in this class, approved to reduce thrombotic events in patients undergoing percutaneous
coronary intervention (PCI).
Glycoprotein IIb/IIIa inhibitors are relatively new additions to the treatment of thromboembolic
disease. Glycoprotein IIb/IIIa is a receptor on the surface of platelets that is necessary for platelet
aggregation. Blocking this receptor has the effect of preventing thrombus formation in patients expe-
riencing a recent MI, stroke, or PCI. These drugs are quite expensive and must be administered by the
IV route.
Core Concept 23.6 Thrombolytics are used to dissolve existing clots.
It is often mistakenly believed that the purpose of anticoagulants such as heparin and warfarin is to digest
and remove preexisting clots. This is not the case: A totally different type of drug is needed for this pur-
pose. These drugs, called thrombolytics, are administered quite differently than the anticoagulants and
produce their effects by different mechanisms. Thrombolytics are prescribed for situations in which a clot
has already formed, including the following:
■ Acute MI
■ Pulmonary embolism
■ Stroke
■ DVT
■ Arterial or coronary thrombosis
■ Clearing thrombi in arteriovenous cannulas and blocked IV catheters
The goal of thrombolytic therapy is to restore blood flow quickly to essential tissues served by the
blocked vessel. Delays in reestablishing circulation may result in permanent tissue damage. The therapeu-
tic effect of thrombolytics is greater when they are administered as soon as possible after clot formation
occurs, preferably within four hours. The role of the thrombolytics in treating MI, and a Nursing Process
for this drug class, is presented in Chapter 20.
Thrombolytics have a narrow margin of safety between dissolving normal and abnormal clots.
Vital signs must be monitored continuously, and signs of bleeding usually call for discontinuation
of therapy. Because these medications are rapidly destroyed in the bloodstream, discontinuation
Drug Prototype: Alteplase (Activase)

Therapeutic Class: Drug for dissolving clots Pharmacologic Class: Thrombolytic
Actions and Uses: Produced through recombinant DNA technol- or with a history of recent trauma. The patient must be
ogy, alteplase is identical to the enzyme human tPA. Like other monitored carefully for signs of bleeding every 15 minutes
thrombolytics, the primary action of alteplase is to convert for the first hour of therapy and every 30 minutes there-
plasminogen to plasmin, which then dissolves clots. Alteplase after. Signs of bleeding such as bruising, hematomas, or
should be given within six hours of the onset of symptoms of nosebleeds should be reported to the healthcare provider
MI and within three hours of thrombotic stroke to be effective. immediately.
Peak effect occurs in 5–10 minutes. Alteplase is a preferred drug Concurrent use with anticoagulants, antiplatelet
for the treatment of acute MI and thrombotic stroke. It is occa- drugs, or NSAIDs, including aspirin, may increase the risk
sionally used to reopen occluded IV catheters. of bleeding. Use with supplements that affect coagulation,
such as feverfew, green tea, ginkgo, fish oil, ginger, or
Adverse Effects and Interactions: Thrombolytics such as al- garlic, should be avoided because they may increase the
teplase are contraindicated in patients with active bleeding risk of bleeding.
n ormally results in the immediate end of thrombolytic activity. After the clot is successfully removed
by the thrombolytic medication, coagulation modifier therapy is initiated to prevent the reformation
of clots.
Concept Review 23.2

■ Both warfarin and heparin are effective anticoagulants. Why would a physician choose
heparin over warfarin?
Hemostatics are used to promote the formation of clots. Core Concept 23.7
Hemostatics, also called antifibrinolytics, have an action opposite to that of anticoagulants: to shorten
bleeding time. The name hemostatics comes from their ability to slow blood flow. They are used to prevent
and treat excessive bleeding following surgical procedures.
All of the hemostatics have very specific indications for use, and none are commonly prescribed.
Aminocaproic acid is administered IV to prevent bleeding in patients who have systemic clotting dis-
orders. A PO form of tranexamic acid (Lysteda) was approved in 2009 for the treatment of heavy men-
strual bleeding. Thrombin (Evithrom, Recothrom, Thrombinar) is approved as a topical drug to prevent
minor oozing and bleeding from surgical sites. Although their mechanisms differ, all drugs in this class
prevent fibrin from dissolving, thus enhancing the stability of the clot. The hemostatics are listed in
Table 23.4 ◆.
Table 23.4 Hemostatics

aminocaproic acid IV; 4–5 g for 1 hour, then 1–1.25 g/hr until For control of excessive bleeding where fibrinolysis contributes
(Amicar) bleeding is controlled to bleeding such as a pathologic condition known as systemic
hyperfibrinolysis or surgical complications following heart
surgery; oral form available
thrombin (Evithrom, Topical; dose varies based on the size of the Used to prevent blood loss following cardiopulmonary bypass
Reothrom, Thrombinar) treated area surgery; considered an investigational new drug
tranexamic acid IV; 10 mg/kg, 3–4 times daily for 2–8 days Used just prior to and following dental surgery in patients with
(Cyklokapron, Lysteda) PO; two 650 mg tablets, three times daily for hemophilia and for women with heavy menstrual bleeding
a maximum of 5 days
Drug Prototype: Aminocaproic Acid (Amicar)

Therapeutic Class: Clot stabilizer Pharmacologic Class: Hemostatic/Antifibrinolytic
Actions and Uses: Aminocaproic acid is prescribed in situa- Adverse Effects and Interactions: Because aminocaproic
tions in which there is excessive bleeding as a result of clots acid tends to stabilize clots, it should be used cautiously in
being dissolved prematurely. The drug acts by inactivating patients with a history of thromboembolic disease. Adverse
plasminogen, the precursor of the enzyme plasmin, which effects are generally mild. The therapeutic serum level is
dissolves the fibrin clot. During acute hemorrhages, it can be 100–400 mcg/mL.
given IV to reduce bleeding in one to two hours. It is most Drug interactions include hypercoagulation when used
commonly prescribed following surgery to reduce postopera- with estrogens and oral contraceptives.
tive bleeding.

Patients treated for coagulation disorders need to know the following:
1. Keep all scheduled appointments for PT, aPTT, and INR laboratory tests. Test results are
used in making decisions about drug dose adjustments.
2. Report unusual bruising or bleeding, such as nosebleeds, bleeding gums, black or red
stool, heavy menstrual periods, or spitting up blood, to healthcare providers.
3. Inform dental hygienists and dentists about the use of anticoagulant medication.
4. Use caution when engaged in activities that can cause bleeding, such as shaving,
brushing teeth, trimming nails, and using kitchen knives. A soft toothbrush and an
electric razor are safe choices. Contact sports, with their high risk for injury, should
be avoided.
5. Take medications on time and as directed. Do not skip a dose, double up on doses, or
discontinue taking medication without guidance from a healthcare provider.
6. Do not eat large or inconsistent amounts of foods high in vitamin K when taking
warfarin because it interferes with clotting time.
7. Speak with the healthcare provider before taking any other drugs, including
OTC drugs or herbal supplements. Many drugs increase or decrease the action of
anticoagulants.
Safety Alert
Medication Label Confusion: Heparin
Medication errors have occurred because of a nurse’s failure to read the information pro-
vided on medication labels properly, such as when the strength of heparin was labeled
only on a per-milliliter basis, and the volume of the vial was stated in another location. To
help prevent these types of errors, the FDA now requires that heparin labels express the
strength of the entire container and milliliters together. However, nurses should not rely on
safety organizations alone to prevent medication errors. It is ultimately the responsibility of
the nurse to read and understand the entire label before preparing and administering any
medication.
Chapter Review 359
Chapter Review
23.1 Hemostasis is a complex process involving multiple coagulation cascade. Heparin is given IV or sub-
steps and many clotting factors. cutaneously to provide immediate anticoagulation
Hemostasis is an essential mechanism protecting the activity, and warfarin is given orally to offer more
body from both external and internal injury; it occurs prolonged action. Protamine sulfate can reverse the
in a sequential series of steps known as the coagu- anticoagulant activity of heparin, and vitamin K can
lation cascade. The final result of coagulation is the reverse the effects of warfarin.
formation of a fibrin clot that protects the body from
23.5 Antiplatelet drugs prolong bleeding time by inter-
excessive blood loss.
fering with platelet aggregation.
23.2 Removing a blood clot is essential to restoring Aspirin, ADP receptor blockers, and glycoprotein IIb/
normal circulation. IIIa receptor blockers prolong bleeding time by inter-
Blood clots are removed by fibrinolysis. Plasmin di- fering with platelet function. They are used to prevent
gests the fibrin strands, thus restoring circulation to thrombus formation in arteries.
the injured area.
23.6 Thrombolytics are used to dissolve existing clots.
23.3 Drugs are used to modify the coagulation process. By dissolving existing clots, thrombolytics restore
Anticoagulants prevent the formation of clots, throm- circulation to an injured area. For maximum effec-
bolytics dissolve existing clots, and hemostatics pro- tiveness, they should be given as soon as possible af-
mote the formation of clots. Coagulation is always ter the thrombus is diagnosed.
carefully monitored through the use of PT or aPTT
23.7 Hemostatics are used to promote the formation
laboratory tests.
of clots.
23.4 Anticoagulants prevent the formation and en- Hemostatics inhibit fibrin in a clot from dissolving
largement of clots. and are used primarily to prevent excessive bleeding
Anticoagulants prolong coagulation time by in- from surgical sites.
hibiting platelets or a specific clotting factor in the
Review Questions
The following questions are written in NCLEX-PN® style. 4. “You will need to be on this medication for a long time
A nswer these questions to assess your knowledge of the before it will break down the clot.”
chapter material, and go back and review any material that is
not clear to you. 3. The patient is on IV heparin, but the nurse informs the pa-
tient that the physician has also ordered warfarin (Coumadin)
to be started because:
1. The patient’s INR is 5.5. The nurse will:
1. Additional medication is needed.
1. Recheck the lab value.
2. Warfarin is much more effective than heparin.
2. Notify the physician.
3. Warfarin is not totally effective for several days after the
3. Administer warfarin (Coumadin).
administration of the first dose.
4. Hold the warfarin (Coumadin) and notify the physician.
4. Heparin has a low molecular weight and is effective only
for a short time.
2. The patient has been started on warfarin (Coumadin) for
DVT. The patient asks when the medication will break up the 4. The patient is receiving enoxaparin (Lovenox) subcutane-
clots. The nurse’s best response would be: ously every 12 hours following knee replacement surgery. The
1. “It will take 7 to 10 days for the clot to break down.” nurse monitors the patient for:
2. “This medication will not break down clots but will make it 1. Gingival hyperplasia
less likely that the clot will get larger.” 2. Signs and symptoms of bruising and bleeding
3. “It will break down the clot within 8 to 12 hours of 3. Clotting at the incision site
administration.” 4. Increased pain
5. The physician prescribes clopidogrel (Plavix) for a pa- 8. The patient on intermittent heparin is found to have he-
tient at risk for a MI. While instructing the patient about the maturia and bleeding from old IV sites. The nurse anticipates
adverse effects and precautions associated with this drug, the what being ordered?
nurse tells him that the following drugs should not be used 1. Protamine sulfate
while on clopidogrel unless the doctor is consulted. (Select all 2. Vitamin K
that apply.) 3. Pentoxifylline (Trental)
1. Coumadin 4. Ardeparin (Normiflo)
2. Ibuprofen
3. Tissue plasminogen activator 9. The physician orders 35,000 units of heparin to be
4. Aspirin given subcutaneously daily after the patient’s aPTT has been
checked. The label on the vial states 10,000 units/mL. How
6. The patient is receiving warfarin (Coumadin). Which of many units should the patient receive daily should the aPTT be
the following laboratory tests should the nurse check to ensure in the recommended range?
that clotting time stays within the therapeutic level? 1. 3.2 mL
1. Prothrombin time (PT) 2. 3.3 mL
2. International normalized ratio (INR) and PT 3. 3 mL
3. Activated partial thromboplastin time (aPTT) 4. 3.5 mL
4. INR
10. A patient is receiving alteplase (Activase), a thrombolytic
7. The physician has ordered that a patient be placed on a drug. The nurse monitors the patient for which of the follow-
hemostatic drug during surgery to prevent blood loss. Which ing possible adverse effects?
of the following medications will the nurse plan to give in this 1. Temperature of 100.8°F
situation? 2. Bruising and epistaxis
1. Aminocaproic acid (Amicar) 3. Skin rash with urticaria
2. Aspirin 4. Wheezing with labored breathing
3. Trombin (Evithrom)
4. Tranexamic acid (Cyklokapron)
emember Mr. Hawkins, the pa-

R 2. Mr. Hawkins is taught by the nurse that the most common
tient introduced at the beginning of adverse effect of heparin therapy is:
the chapter? Now read the remain- 1. Nausea/vomiting
der of the case study. Based on the 2. MI
information you have learned in 3. Bleeding
this chapter, answer the questions 4. Sedation
that follow.
3. In planning for Mr. Hawkins’ discharge from the hospital,
Mr. Thomas Hawkins was recently admitted to the hospital he was switched from heparin to warfarin. When he inquired
with chest pain and suspected pulmonary embolism. He why his drug was switched, the nurse informed him that:
was immediately placed on heparin for two days and then
switched to warfarin. He is now leaving the hospital with in- 1. Warfarin is more effective.
structions to have laboratory testing every other day for the 2. Warfarin is given orally.
next two weeks. 3. Warfarin causes less risk of hemorrhage.
4. Warfarin is less expensive.
1. The nurse understands that the goal of initially placing 4. As part of the discharge instructions, Mr. Hawkins is told
Mr. Hawkins on heparin was to: that he will need to have blood drawn and which of the fol-
1. Dissolve pulmonary emboli. lowing laboratory tests need to be performed during the two
2. Prevent excessive bleeding. weeks after his discharge?
3. Reduce blood viscosity. 1. PT/INR
4. Prevent additional thrombi from forming. 2. Complete blood count (CBC)
3. aPTT
4. White blood cell count

U n i t
4
The Immune System
Unit Contents
Chapter 24 Drugs for Inflammation and Fever / 362
Chapter 25 Drugs for Immune System Modulation / 373
Chapter 26 Drugs for Bacterial Infections / 387
Chapter 27 Drugs for Fungal, Viral, and Parasitic Diseases / 412
Chapter 28 Drugs for Neoplasia / 430

C
“It’s so depressing. My
h hands are swollen all the
a time; and the gardening
p I love so much, I can’t even
do anymore. It’s just too
t painful.”
e Mrs. Emma Greene
r
24 Drugs for Inflammation and Fever
Core Concepts
24.1 Inflammation is a body defense that limits the 24.4 Nonsteroidal anti-inflammatory drugs (NSAIDs)
spread of invading microorganisms and injury. are the primary drugs for the treatment of mild
24.2 The body reacts to injury by releasing chemical inflammation.
mediators that cause inflammation. 24.5 Corticosteroids are effective in treating severe
24.3 Inflammation may be treated with nonpharma- inflammation.
cologic and pharmacologic therapies. 24.6 Antipyretics are drugs used to reduce fever.
Drug Snapshot
Drug Classes Drug ProTOTYPES
NSAIDs aproxen (Naprosyn) and naproxen
n
sodium (Aleve, Anaprox) 366
Corticosteroids prednisone 369
Antipyretics acetaminophen (Tylenol) 369
Learning Outcomes
1. Identify the function of inflammation 4. Outline the general strategies for 7. For each of the classes in the Drug
as part of the body’s normal treating inflammation. Snapshot, identify representative
defenses. 5. Explain the pharmacotherapy of fever. drugs and explain their mechanisms
2. Outline the basic steps in the acute of drug action, primary actions, and
6. Categorize drugs used in the important adverse effects.
inflammatory response. treatment of inflammation and
3. Explain the role of chemical fever based on their classifications
mediators in inflammation. and mechanisms of action.
Key Terms
alternate-day therapy 368 cyclooxygenase (COX) mast cells 363
anaphylaxis (ANN-ah-fah-LAX-iss) 364 (SYE-klo-OK-sah-jen-ays) 366 salicylism (sal-IH-sill-izm) 366
antipyretics 369 histamine (HISS-tuh-meen) 363
Cushing’s syndrome (KUSH-ings) 368 inflammation (IN-flah-MAY-shun) 363
T he pain and redness of inflammation following minor abrasions and cuts is something every-
one has experienced. Although there may be discomfort from such scrapes, inflammation is a
normal and expected part of our body’s defense against injury. For some diseases, however,
inflammation can rage out of control, producing severe pain, fever, and other distressing symptoms.
The purpose of this chapter is to examine these sorts of inflammatory conditions for which drug ther-
apy may be needed.
Fast Facts Inflammatory Disorders

■ Osteoarthritis affects about 27 million people and is the leading cause of disability in the
United States.
■ Inflammatory bowel disease has a peak onset of age 30 and affects about 1.4 million Americans
each year.
■ In the United States, approximately 70 million NSAID prescriptions are written, and 30 billion
over-the-counter (OTC) NSAID tablets are sold each year.
■ More than 1% of the U.S. population uses NSAIDs on a daily basis.
■ It is estimated that NSAIDs cause about 16,000 deaths in the United States annually, largely as
a result of gastrointestinal (GI) complications. This has more mortality than is caused from gastric
cancer.
Inflammation
Inflammation is a body defense that limits the spread of invading

microorganisms and injury. Core Concept 24.1
The human body has developed complex ways to defend itself against physical injury and invasion by
microorganisms. Inflammation is one of these defense mechanisms. Inflammation is a nonspecific pro-
cess that occurs in response to many different stimuli, including physical injury; exposure to toxic chemi-
cals, extreme heat, or invading microorganisms; or death of cells. The central purpose of inflammation is to
contain the injury or destroy the microorganism. By removing cellular debris and dead cells, repair of the
injured area can move at a faster pace. Inflammation proceeds the same regardless of the cause that trig-
gered it. Signs of inflammation include swelling, pain, warmth, and redness of the affected area.
Inflammation may be classified as acute or chronic. Acute inflammation has an immediate onset and
lasts one to two weeks. During acute inflammation, 8–10 days are normally needed for the symptoms to
resolve and for repair to begin. If the body cannot destroy or neutralize the damaging agent, inflamma-
tion may continue for long periods and become chronic. In chronic diseases such as lupus and rheumatoid
arthritis, inflammation may persist for years, with symptoms becoming progressively worse over time.
Other disorders such as seasonal allergy arise at predictable times each year, and inflammation may pro-
duce only minor, annoying symptoms.
The body reacts to injury by releasing chemical mediators that

cause inflammation. Core Concept 24.2
Whether the injury is due to an infection, chemicals, or physical trauma, the damaged tissue releases
chemical mediators that act as “alarms” that notify the surrounding area of the injury. These chemical
mediators initiate the processes and steps of inflammation. Chemical mediators include histamine, leu-
kotrienes, bradykinin, complement, and prostaglandins. Table 24.1 ◆ describes the sources and actions of
these mediators.
Histamine is a key chemical mediator of inflammation. It is primarily stored within mast cells located
in tissue spaces under epithelial membranes such as the skin, in the bronchial tree and digestive tract, and
along blood vessels. Mast cells detect invading microorganisms or injury and respond by releasing hista-
mine, which initiates the inflammatory response within seconds. In addition, histamine directly stimulates
pain receptors.
When released at an injury site, histamine and other mediators dilate nearby blood vessels, caus-
ing the capillaries to become more permeable or leaky. Plasma and components such as complement
364 Chapter 24 Drugs for Inflammation and Fever
Table 24.1 Chemical Mediators of Inflammation

Bradykinin Vasodilator that causes pain; effects are similar to those of histamine
Complement Series of at least 20 proteins that combine in a cascade fashion to neutralize
or destroy an antigen
Histamine Stored and released by mast cells; causes dilation of blood vessels, smooth
muscle constriction, tissue swelling, and itching
Leukotrienes Stored and released by mast cells; effects are similar to those of histamine
Prostaglandins Present in most tissues; stored and released by mast cells; increase capillary
permeability, attract white blood cells to site of inflammation, and cause pain
proteins and phagocytes can then enter the area to neutralize foreign agents. The affected area may
become congested with blood, which can lead to significant swelling and pain. Thrombosis or blood
clotting may result. Figure 24.1 ■ shows the basic steps in acute inflammation.
Rapid release of histamine on a larger scale throughout the body is responsible for anaphylaxis, a
life-threatening allergic response that may result in shock and death. A number of chemicals, insect stings,
foods, and some therapeutic drugs can cause this widespread release of histamine from mast cells. Drug
therapy of anaphylactic shock is discussed in Chapter 21.
Inflammation may be treated with nonpharmacologic

Core Concept 24.3 and pharmacologic therapies.
Because inflammation is a nonspecific process and may be caused by such a diverse variety of causes, it may
occur in nearly any tissue or organ system. When treating inflammation, the following general principles apply:
■ Inflammation is not a disease but a symptom of an underlying disorder. Whenever possible, the
cause of the inflammation is identified and treated.
Figure 24.1
Vasodilation
(redness, heat)
Vascular
permeability
(edema)
Cellular Release of Cellular

injury chemical infiltration
mediators (pus)
• histamine
• bradykinin
• complement Thrombosis
Mast cell
• leukotrienes (clots)
Stimulation of
nerve endings
(pain)
Steps in acute inflammation.

■ Inflammation is a natural process for ridding the body of foreign agents, and it is usually self-
limiting. For mild symptoms, nonpharmacologic therapies such as ice packs and rest should be
used, as appropriate for the condition.
■ When pharmacotherapy is necessary, topical drugs are used when applicable because they cause
fewer adverse effects. Topical sprays, ointments, and creams are often the most effective drugs
for treating inflammation of the skin and mucous membranes of the mouth, nose, rectum, and
vagina. Many of these are available OTC.
The goal of pharmacotherapy with anti-inflammatory drugs is to prevent or decrease the intensity of the
inflammatory response and reduce fever, if present. Most anti-inflammatory medications are nonspecific;
the drug will exhibit the same inhibitory actions regardless of the cause of the inflammation. Diseases that
benefit from anti-inflammatory drugs include allergic rhinitis, anaphylaxis, ankylosing spondylitis, contact rhin 5 nose
dermatitis, Crohn’s disease, glomerulonephritis, Hashimoto’s thyroiditis, peptic ulcer disease, rheumatoid itis 5 inflammation
arthritis, systemic lupus erythematosus, and ulcerative colitis. If the inflammation is the result of an infec-
tion, antibiotic therapy may be necessary.
The two primary drug classes used for inflammation are the NSAIDs and the corticosteroids (also
called glucocorticoids). For mild to moderate pain and inflammation, NSAIDs are the preferred drugs.
Should inflammation become severe, oral corticosteroid therapy is begun. Due to their serious long-term
adverse effects, oral corticosteroids are usually used for only one to three weeks to bring inflammation
under control, and then the patient is switched to NSAIDs.
NSAIDs are the primary drugs for the treatment of mild

inflammation. Core Concept 24.4
NSAIDs such as aspirin and ibuprofen have analgesic, antipyretic, and anti-inflammatory effects. They are
preferred drugs for the treatment of mild to moderate inflammation in most patients. Some of the specific
NSAIDs used for inflammation are listed in Table 24.2 ◆.
Table 24.2 Selected Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

aspirin (acetylsalicylic acid [ASA], PO; 350–650 mg every 4 hours Inhibits the formation of prostaglandins; also for
others) (see page 208 for the Drug (max: 4 g/day) fever, pain, and prevention of stroke and myocardial
Prototype box) PO; 3.6–5.4 g/day in 4–6 divided doses infarction (MI)
for arthritic conditions
celecoxib (Celebrex) PO; 100–200 mg bid (max: 200 mg/day) Selective COX-2 inhibitor
diclofenac (Cataflam, Solaraze, PO; 50 mg bid–qid (max: 200 mg/day) Sustained-release and transdermal forms available
Voltaren)
diflunisal PO; 250–500 mg bid (max: 1,500 mg/day) Similar to ibuprofen
etodolac PO; 200–400 mg tid–qid Extended-release form available
(max: 1,200 mg/day)
fenoprofen (Nalfon) PO; 300–600 mg tid–qid Similar to ibuprofen
(max: 3,200 mg/day)
flurbiprofen (Ansaid) PO; 50–100 tid–qid (max: 300 mg/day) Similar to ibuprofen
ibuprofen (Advil, Motrin, others) PO; 400–800 mg tid–qid Blocks prostaglandin synthesis as well as modulates T-cell
(max: 3,200 mg/day) function; also for dysmenorrhea
ketoprofen PO; 75 mg tid or 50 mg qid Extended-release form available; similar to ibuprofen;
(max: 300 mg/day) also for dysmenorrhea
meloxicam (Mobic) PO: 7.5–15 mg once daily (max: 15 mg/day) Similar to ibuprofen
nabumetone (Relafen) PO; 1,000 mg daily (max: 2,000 mg/day) Similar to ibuprofen
naproxen (Naprosyn) and PO; 250–500 mg bid (max: 1,000 mg/day) Also for dysmenorrhea
naproxen sodium (Aleve, Anaprox)
oxaprozin (Daypro) PO; 600–1,200 mg daily Similar to naproxen; once-a-day dosage
(max: 1,800 mg/day)
piroxicam (Feldene) PO; 10–20 mg once or twice a day Has prolonged half-life
(max: 20 mg/day)
tolmetin (Tolectin) PO; 400 mg tid (max: 2 g/day) Similar to ibuprofen
The analgesic action of NSAIDs is discussed in Chapter 14. Because they are inexpensive and readily
available OTC, NSAIDs such as aspirin and ibuprofen are some of the most widely used drugs. Acetamin-
ophen has no anti-inflammatory action and is thus not classified as an NSAID. It is, however, an effective
analgesic and antipyretic (see Section 24.5).
Aspirin is useful in treating inflammation because it inhibits cyclooxygenase (COX), a key enzyme
in the pathway of prostaglandin synthesis that is found in every tissue. Aspirin causes irreversible inhibi-
tion of both forms of cyclooxygenase, COX-1 and COX-2. Because it is readily available, inexpensive, and
effective, aspirin is sometimes a drug of first choice for treating mild inflammation. The basic pharmacol-
ogy and a drug profile of aspirin are presented in Chapter 14.
Unfortunately, large doses of aspirin are necessary to suppress severe inflammation, and these doses
result in a greater incidence of serious adverse effects. The most common adverse effects observed dur-
ing high-dose therapy relate to the digestive system. By increasing gastric acid secretion and irritating the
stomach lining, aspirin may cause pain, heartburn, and even bleeding due to ulceration. In some patients,
even small doses may cause GI bleeding. Some aspirin formulations are buffered or given an enteric coat-
ing to minimize GI adverse effects. Because aspirin also has an antiplatelet effect (see Chapter 23), the
potential for bleeding must be carefully monitored by the healthcare provider. High doses may produce
salicylism, a syndrome that includes symptoms such as ringing in the ears, dizziness, headache, and sweat-
ing. Patients with preexisting kidney disease should be monitored carefully because aspirin and other
NSAIDs may affect kidney function.
Ibuprofen and ibuprofen-like drugs such as naproxen are available as alternatives to aspirin. Like
aspirin, they exhibit their effects through inhibition of COX-1 and COX-2. Because of their similar mecha-
nisms, they all have similar pharmacologic properties and a relatively low incidence of adverse effects. The
most common adverse effects of these drugs are nausea and vomiting. Although the incidence of gastric
ulceration and bleeding is less than that of aspirin, this can still be a serious problem in patients with peptic
ulcers who are taking high doses of these medications. Most have only a small or insignificant effect on
blood coagulation and are safer to use than aspirin in patients who may be at risk for bleeding.
Selective inhibition of COX-2 produces the analgesic, anti-inflammatory, and antipyretic effects seen
with the NSAIDs without causing some of the serious adverse effects of the older NSAIDs. Because they
have no adverse GI effects and do not affect blood coagulation, these drugs quickly became the treatment
of choice for moderate to severe inflammation.
However, in 2004, research data revealed that one NSAID, rofecoxib (Vioxx), doubled the risk
of heart attack and stroke in patients taking it for extended periods. Based on these reports, the drug
manufacturer voluntarily removed the drug from the market. Shortly afterward, a second COX-2
inhibitor, valdecoxib (Bextra), was also voluntarily withdrawn, leaving celecoxib (Celebrex) the sole
drug in this class.
Drug Prototype: Naproxen (Naprosyn) and Naproxen Sodium (Aleve, Anaprox)

Therapeutic Class: Analgesic, anti-inflammatory drug, antipyretic Pharmacologic Class: Nonsteroidal
anti-inflammatory drug (NSAID)
Actions and Uses: Naproxen is an older NSAID that is prescribed Using naproxen concurrently with oral anticoagulants
for the treatment of mild to moderate pain, fever, and inflam- can prolong bleeding time. Lithium levels may be increased.
mation. Its efficacy at relieving pain and inflammation is similar Bleeding potential increases when used with herbal
to that of aspirin. Common indications include treating the pain supplements such as feverfew, garlic, ginger, and ginkgo
associated with rheumatoid arthritis and osteoarthritis, gout, biloba.
and bursitis. In treating rheumatoid arthritis, the therapeutic
effects may take three to four weeks to appear.
Naproxen inhibits prostaglandin synthesis through the
nonselective inhibition of cyclooxygenase type-1 and type-2 Black Box Warning (prescription forms):
enzymes. It also inhibits platelet aggregation and prolongs NSAIDs may cause an increased risk of MI, and stroke,
bleeding time. which may increase with duration of use. Patients with
cardiovascular disease may be at greater risk. NSAIDs are
Adverse Effects and Interactions: Adverse effects of naproxen contraindicated for the treatment of perioperative pain
are generally not serious and include GI upset, dizziness, and in those undergoing coronary artery bypass graft surgery.
drowsiness. Administration with food will decrease the inci- NSAIDs increase the risk of bleeding, ulceration, and
dence of stomach upset, which is the most common adverse perforation of the stomach or intestines, which can be
effect. Because naproxen may prolong bleeding time, the drug fatal. These events occur more frequently in older adults
should be administered with caution to those with bleeding and can occur at any time during use or without warning
disorders. Patients taking naproxen should notify their dental symptoms.
hygienist before dental procedures are performed.
Nursing Process Focus Patients Receiving NSAID Therapy
Prior to administration: ■ Acute Pain related to injury, disorder, or surgical procedure
■ Obtain a complete health history, including musculoskeletal, GI, renal ■ Chronic Pain related to tissue damage
and liver conditions, infectious diseases, allergies, drug history, and ■ Deficient Knowledge related to a lack of information about drug
■ Evaluate laboratory blood findings: CBC, electrolytes, and renal and ■ Ineffective Health Maintenance related to chronic pain
liver function studies.
■ Determine reasons for analgesic use and patterns of medication usage.
signs, height, and weight.

The patient will:
■ Experience therapeutic effects (pain relief or a reduction in pain intensity).
Implementation
■ Determine need for medication. Record the character, duration, loca- ■ Instruct the patient to report to the healthcare provider any pain and/
tion, and intensity of pain and the presence of inflammation. (NSAIDs or inflammation that remains unresolved.
are usually given to patients who have inflammatory conditions that
cause pain. Monitoring pain and medication use helps to determine
medication effectiveness.)
■ Administer NSAIDs correctly and evaluate the patient’s knowledge of Inform the patient to:
proper administration. (May be administered PO or topical/transdermal. ■ Take only the prescribed amount of NSAIDs to decrease the potential
Overuse may cause severe adverse effects.) for adverse effects.
■ Not cut or crush enteric-coated tablets. Regular tablets may be broken
or pulverized and mixed with food.
■ Take liquid aspirin (ASA) products immediately after mixing because
they break down rapidly.
■ Not take different drugs and formulations, such as ibuprofen and
naproxen, concurrently. Consult the healthcare provider regarding
appropriate OTC analgesics for specific types of pain.
■ Consult the healthcare provider regarding aspirin therapy following
surgery. (ASA also has antiplatelet properties. The body needs time to
manufacture new platelets to make clots that promote wound healing.)
■ Advise laboratory personnel of aspirin therapy when providing urine
samples.
■ Monitor vital signs, especially temperature. (Increased temperature Instruct the patient to:
may indicate infection. Increased pulse and blood pressure may ■ Immediately report the occurrence of a rapid heartbeat, palpitations,
indicate discomfort; if accompanied by pallor and/or dizziness, dizziness, or pallor to the healthcare provider.
may indicate bleeding.) ■ Monitor blood pressure and temperature, ensuring proper use of
home equipment.
■ Monitor for signs of GI bleeding, GI elimination, or hepatic toxicity. Instruct the patient to:
Conduct guaiac stool testing for occult blood and monitor CBC for ■ Report any bleeding, abdominal pain, anorexia, heartburn, nausea,
anemia-related blood loss. (NSAIDs can be a local irritant to the GI vomiting, jaundice, or change in the color or character of stools to the
tract with anticoagulant action that is metabolized in the liver.) healthcare provider.
■ Know the proper method of obtaining stool samples and home testing
for occult blood.
■ Adhere to a regimen of laboratory testing as ordered by the health-
care provider.
■ Take NSAIDs with food to reduce stomach upset.
■ Monitor for hypersensitivity reaction. ■ Advise the patient to monitor for shortness of breath, wheezing,
throat tightness, itching, or hives. If these occur, stop taking ASA
immediately and inform the healthcare provider.
■ Monitor urinary output and edema in feet/ankles. (Medication is excreted ■ Instruct the patient to report changes in urination, flank pain, or
through the kidneys. Long-term use may lead to renal dysfunction.) pitting edema.
■ Monitor serum levels of salicylate. (Monitoring serum levels helps to ■ Advise the patient to return to the healthcare provider for prescribed
monitor for possible toxicity). follow-up appointments.
■ Monitor for sensory changes indicative of drug toxicity. (Signs and ■ Inform patient to immediately report any sensory changes in sight
symptoms of toxicity include tinnitus and blurred vision.) or hearing, especially blurred vision or ringing in the ears, to the
367
Corticosteroids are effective in treating severe

Core Concept 24.5 inflammation.
Corticosteroids or glucocorticoids are natural hormones released by the cortex of the adrenal gland
that have powerful effects on nearly every cell in the body. One of their most useful actions is the
ability to suppress severe inflammation. When used to treat inflammatory disorders, the drug doses
are many times higher than those naturally present in the blood. Corticosteroids have numerous ther-
apeutic applications. The uses of these drugs in treating hormonal imbalances are presented in detail
in Chapter 32. Doses of the corticosteroids used to treat severe inflammatory disease are listed in
Table 24.3 ◆.
Corticosteroids affect inflammation in multiple ways. They suppress the actions of chemical media-
tors of inflammation such as histamine and prostaglandins. In addition, they inhibit the immune system by
suppressing certain functions of phagocytes and lymphocytes. These multiple effects have the ability to
markedly reduce inflammation, making corticosteroids the most effective medications for the treatment of
severe inflammatory disorders.
Unfortunately, medications in the corticosteroid class have several potentially serious adverse effects
that limit their therapeutic usefulness when they are given by the oral or parenteral routes. These include
suppression of the normal functions of the adrenal gland (adrenal insufficiency), elevated blood glucose,
mood changes, cataracts, peptic ulcers, electrolyte imbalances, and osteoporosis. Because of their effec-
tiveness at reducing the signs and symptoms of inflammation, corticosteroids can mask infections that may
be present in the patient. This combination of masking inflammation and suppressing the immune system
creates a potential for existing infections to grow rapidly and undetected. An active infection is usually a
contraindication for corticosteroids therapy.
Because the appearance of these adverse effects is a function of the dose and duration of therapy,
treatment is often limited to the short-term control of acute disease. When longer therapy is indicated,
doses are kept as low as possible and alternate-day therapy is sometimes used; the medication is taken
every other day to encourage the patient’s adrenal glands to function on the days when no drug is taken.
During long-term therapy, the healthcare provider must be alert for signs of overtreatment, a condition
called Cushing’s syndrome. Signs include bruising and a characteristic pattern of fat deposits in the
cheeks (moon face), shoulders (buffalo hump), and abdomen. The body becomes accustomed to the high
doses of corticosteroids, and patients must discontinue the drug gradually because abrupt withdrawal can
result in lack of adrenal function.
The serious adverse effects of the corticosteroids may be prevented by giving the drugs by the intra-
nasal, topical, or intravaginal routes. Although small amounts of the drug are absorbed across the skin
and mucous membranes, the amount reaching the blood is generally small and too low to cause serious
systemic effects.
Table 24.3 Selected Corticosteroids for Severe Inflammation

betamethasone (Celestone, PO; 0.6–7.2 mg/day Topical, intra-articular, IM, and IV forms available
Diprolene, others)
cortisone PO; 20–300 mg/day in divided doses IM form available; also for adrenal insufficiency
dexamethasone PO; 0.25–4 mg bid–qid IM and IV forms available; also for adrenal insufficiency
and immunosuppression
hydrocortisone (Cortef, Topical; 0.5% cream applied 1–4 times Used widely for skin inflammation; IM, PO, rectal, and
Hydrocortone, Solu-Cortef, others) daily IV forms available; may be injected intra-articular
(see page 522 for the Drug PO; 10–320 mg tid–qid
Prototype box)
methylprednisolone (Depo-Medrol, PO; 4–48 mg/day in divided doses Available in IM, IV, and rectal forms; also for neoplasia
Medrol) and adrenal insufficiency
prednisolone (Prelone) PO; 5–60 mg 1–4 times daily Available in IM and IV forms; also for neoplasia and
adrenal insufficiency
prednisone PO; 5–60 mg 1–4 times daily Available in oral form only; also for neoplasia
triamcinolone (Aristospan, PO; 4–48 mg 1–4 times daily Available in IM, subcutaneous, intradermal, intra-
Kenalog) articular, and aerosol forms
Drug Prototype: Prednisone

Therapeutic Class: Anti-inflammatory drug Pharmacologic Class: Corticosteroid
Actions and Uses: Prednisone is a synthetic corticosteroid. Its face, muscle weakness, bruising, and bones that easily fracture.
actions are the result of being metabolized to an active form, Corticosteroids can raise blood glucose levels. Patients with dia-
which is also available as a drug called prednisolone. When betes may require an adjustment in insulin dose. Gastric ulcers
used for inflammation, a 4- to 10-day duration for therapy is may occur with long-term therapy, and an antiulcer medication
common. Alternate-day dosing is used for long-term therapy. may be prescribed prophylactically. Patients must report any
Prednisone is occasionally used to terminate acute broncho- potential infections immediately. This drug should be discontin-
spasm in patients with asthma (see Chapter 29) and for patients ued gradually.
with certain cancers such as Hodgkin’s disease, acute leukemia, Barbiturates, phenytoin, and rifampin increase the metab-
and lymphomas (see Chapter 28)‌. olism of prednisone: Increased doses of prednisone may be
needed. Amphotericin B and diuretics together with prednisone
Adverse Effects and Interactions: When used for short-term can increase potassium loss. Prednisone may inhibit antibody
therapy, prednisone has few adverse effects. Long-term therapy response to vaccines and toxoids. In patients with myasthenia
may result in Cushing’s syndrome, a condition that includes gravis, use of prednisone with ambenonium, neostigmine, or
elevated blood glucose, fat redistribution to the shoulders and pyridostigmine can cause severe muscle weakness.
Fever
Antipyretics are drugs used to reduce fever. Core Concept 24.6
Like inflammation, fever is a natural defense mechanism for neutralizing foreign substances. Many species
of bacteria are killed by high fever. Often, the healthcare provider must determine whether the fever needs
to be dealt with aggressively or allowed to run its course without drug therapy. Drugs used to treat fever are
called antipyretics.
Drug Prototype: Acetaminophen (Tylenol)

Therapeutic Class: Antipyretic, nonopioid analgesic
Pharmacologic Class: Centrally acting prostaglandin inhibitor
Actions and Uses: Acetaminophen reduces fever by direct lethargy, diaphoresis, chills, abdominal pain, and diarrhea.
action at the level of the hypothalamus and causes dilation of Excessive acetaminophen use is the number one cause of acute
peripheral blood vessels, enabling sweating and dissipation of hepatic failure in the United States.
heat. Acetaminophen and aspirin have equal efficacy in reliev- Acetaminophen inhibits warfarin metabolism, causing
ing pain and reducing fever. Acetaminophen is administered warfarin to accumulate to toxic levels. High-dose or long-term
as a substitute for aspirin when NSAIDs are contraindicated acetaminophen usage may result in elevated warfarin levels
due to age, allergy, or gastric irritation. It is not linked with and bleeding. Ingestion of this drug with alcohol is not rec-
Reye’s syndrome, as is aspirin; thus it is safe to administer to ommended due to the possibility of liver failure from hepatic
infants, children, and adolescents who have flu-like symptoms necrosis.
or chickenpox. The patient should avoid taking herbs that have the
Acetaminophen has no peripheral anti-inflammatory potential for liver toxicity, including comfrey, coltsfoot, and
action; therefore, it is not effective in treating arthritis or pain chaparral.
caused by tissue swelling following injury. Acetaminophen is
pregnancy category B.
Black Box Warning:
Adverse Effects and Interactions: At recommended doses, In 2011, the FDA issued a warning that acetaminophen has
acetaminophen is well tolerated and serious adverse effects the potential to cause severe liver injury and may cause
are rare. The risk for adverse effects is dose related and increases serious allergic reactions with symptoms of angioedema,
with long-term use. Acute acetaminophen poisoning is very seri- difficulty breathing, itching, or rash.
ous, and symptoms include anorexia, nausea, vomiting, dizziness,
In most patients, fever is more of a discomfort than a life-threatening problem. Prolonged, high fever
(usually above 102°F or 38.9°C), however, can become dangerous, especially in young children in whom
fever can stimulate seizures. In adults, excessively high fever can break down body tissues, reduce mental
acuity, and lead to delirium or coma, particularly among elderly patients. In rare instances, an elevated
body temperature may be fatal.
The goal of antipyretic therapy is to lower body temperature while identifying and treating the under-
lying cause of the fever, which is often an infection. Aspirin, ibuprofen, and acetaminophen are safe, inex-
pensive, and effective drugs for reducing fever. Many of these antipyretics are marketed for different age
groups, including special, flavored brands for infants and children. For fast delivery and effectiveness,
drugs may come in various forms including gels, caplets, enteric-coated tablets, and suspensions. Aspirin
and acetaminophen are also available as suppositories.

Patients treated for inflammatory disorders or fever need to know the following:
Regarding Anti-Inflammatory Medications and Antipyretics

1. Take NSAIDs with food to decrease stomach irritation.
2. Avoid drinking alcohol when taking high doses of NSAIDs or aspirin because it increases
stomach irritation.
3. If ringing in the ears, dizziness, headache, or signs of bleeding or bruising occur, discon-
tinue aspirin use immediately and report the incident to the healthcare provider.
4. Take corticosteroids exactly as prescribed because improper use may lead to serious
adverse effects.
5. Acetaminophen may be found in many OTC cold and flu products. Be careful not to
take multiple products containing this drug, because additive toxicity may result.
Chapter Review
24.1 Inflammation is a body defense that limits the 24.4 NSAIDs are the primary drugs for the treatment of
spread of invading microorganisms and injury. mild inflammation.
Inflammation is a nonspecific response designed to NSAIDs are drugs that inhibit the enzyme cyclo-
rid the body of invading pathogens or to contain the oxygenase. Nonselective cyclooxygenase inhibitors,
spread of injury. Acute inflammation occurs over a including aspirin, are effective at reducing inflamma-
period of several days, whereas chronic inflammation tion and pain but cause significant GI adverse effects
may continue for months or years. in some patients.
24.2 The body reacts to injury by releasing chemical 24.5 Corticosteroids are effective in treating severe
mediators that cause inflammation. inflammation.
Inflammation is initiated by chemical mediators, the Corticosteroids are hormones that are extremely ef-
most important of which is histamine. Release of fective at reducing inflammation. Because overtreat-
these meditators causes vasodilation, allowing capil- ment with these drugs can cause Cushing’s syndrome,
laries to become leaky, thus causing tissue swelling. corticosteroid therapy for inflammation is generally
Extremely rapid release of histamine throughout the short term.
body can trigger anaphylaxis.
24.6 Antipyretics are drugs used to reduce fever.
24.3 Inflammation may be treated with nonpharmaco- Fever is often self-limiting but when it is elevated or
logic and pharmacologic therapies. prolonged, pharmacotherapy is indicated. Acetamino-
When possible, topical drugs are used because they phen is often a preferred drug for fever, although ibu-
produce fewer adverse effects than oral or parenteral profen is equally effective.
drugs. The two primary drug classes used for inflam-
mation are the NSAIDs and corticosteroids.
Chapter Review 371
Review Questions
The following questions are written in NCLEX-PN® style. An- 6. The nurse is to administer 10 grains of aspirin by mouth.
swer these questions to assess your knowledge of the chapter Available are 325 mg tablets. How many tablets will the nurse
material, and go back and review any material that is not clear administer?
to you. 1. One-half tablet
1. A patient is getting ready to go home from the hospi- 2. One tablet
tal and the nurse and patient are discussing the types of OTC 3. One and one-half tablets
NSAID medications that are available. The nurse states that an 4. Two tablets
OTC medication that is not classified as an NSAID is: 7. While educating a patient about acetaminophen, the nurse
1. Aspirin instructs the patient to report to the healthcare provider if the
2. Ibuprofen following should occur: (Select all that apply.)
3. Acetaminophen 1. Lethargy
4. Motrin 2. Anorexia
2. The patient has been taking aspirin for several days for 3. Tearing of the eyes
a headache. While collecting information from the patient, 4. Difficulty breathing
the nurse discovers that the patient is experiencing ringing 8. The nurse is examining a patient with rheumatoid arthri-
in the ears and dizziness. The most appropriate action by the tis. The patient has been taking prednisone for an extended
nurse is: period of time. During the examination, the nurse observes that
1. To question the patient about history of sinus infection the patient has a very round moon-shaped face, bruising, and
2. To determine if the patient has mixed the aspirin with other shoulder hump. What does the nurse suspect based on these
medications findings?
3. To tell the patient to hold off on taking any more aspirin 1. These are normal reactions based on these findings.
until seen by the physician 2. These are probably birth defects.
4. To tell the patient to take the aspirin with food or milk 3. These are the symptoms of myasthenia gravis.
3. The nurse informs the patient that the most common 4. These are the symptoms of adverse drug effects from
a dverse effect of NSAIDs is: prednisone.
1. Edema 9. A patient has been taking acetaminophen fairly regularly
2. Rash for headaches but has questions regarding food and beverage
3. GI irritation restrictions while taking this medication. The nurse informs the
4. Bleeding patient that taking this drug while regularly drinking alcohol
may cause:
4. The patient is taking corticosteroids, so the nurse moni-
tors for: 1. Liver failure
2. Renal damage
1. Bleeding 3. Thrombosis
2. Respiratory distress 4. Pulmonary damage
3. Dehydration
4. Infection 10. A mother of a 5-year-old asks the nurse why aspirin is
not good for her to give to her child when she has a fever. The
5. A patient with diabetes taking prednisone states that his nurse responds that:
blood sugar is higher than normal. The nurse’s most appropri-
ate response would be: 1. It is not as good an antipyretic as acetaminophen.
2. It may increase fever in children under 10 years.
1. “You must not be following your diet for diabetes.” 3. It may produce nausea and vomiting.
2. “Prednisone can cause blood sugar levels to increase.” 4. It increases the risk of Reye’s syndrome when flu-like
3. “You must be developing an illness.” symptoms are present.
4. “Your diabetes must be getting worse.”
Remember Mrs. Greene, the patient Mrs. Emma Greene, 62 years old, has been experiencing a
introduced at the beginning of the gradual increase in pain and swelling of her hands. Her knuck-
chapter? Now read the remainder of les have also become red and warm to the touch. She enjoys
the case study. Based on the informa- gardening and sewing, but over the past six months she has not
tion you have learned in this chapter, been able to participate in these activities because it is “too
answer the questions that follow. painful.” Mrs. Greene has been treating herself with NSAIDs,
specifically ibuprofen and naproxen.
1. Regarding Mrs. Greene’s use of NSAIDs, what question condition, which of the following drug classes would likely be
should you ask to determine potential adverse effects? prescribed over a 10-day period?
1. “Have you experienced excessive drowsiness?” 1. Biologic response modifiers
2. “Have you experienced GI upset?” 2. Intranasal corticosteroids
3. “Have you experienced excessive dryness or stinging sen- 3. Systemic corticosteroids
sations in your nose?” 4. Sympathomimetics
4. “Have you experienced any rashes or dryness of the skin?”
4. Her healthcare practitioner prescribes prednisone. Mrs.
2. To help Mrs. Greene alleviate the adverse effects of Greene asks why she was given this medication. The office
NSAIDs, the nurse advises her to: nurse tells her that:
1. Take NSAIDs with food. 1. He just wanted to try something different
2. Take NSAIDs on an empty stomach. 2. Prednisone markedly reduces inflammation and is benefi-
3. Take both types of NSAIDs at the same time. It is okay. cial for short-term use
4. There are no adverse effects of most NSAIDs. 3. Prednisone is used only for pain control
4. Prednisone has very few adverse effects, even when used
3. Mrs. Greene is diagnosed with rheumatoid arthritis. She for long periods
experiences a “flare-up” (acute exacerbation) of her disease.
Because Mrs. Greene has experienced a “flare-up” of her

C
“Since I work directly with
so many people, I thought H
it might be a good idea to A
get the hepatitis B vaccine P
series.”
T
Mr. Jose Martel
E
R
Drugs for Immune System

Modulation 25
Core Concepts
25.1 The human body has both innate and adaptive body 25.4 Biologic response modifiers are used to boost the
defenses. immune response.
25.2 The immune response results from activation of the 25.5 Immunosuppressants are used to prevent transplant
humoral and cell-mediated immune systems. rejection and to treat autoimmune disorders.
25.3 Vaccines are biologic agents used to prevent
illness.
Drug Snapshot
Vaccines epatitis B vaccine (Energix-B,
h
Recombivax HB) 378
Biologic response modifiers interferon alfa-2b (Intron a) 380
Immunosuppressants c yclosporine (Gengraf,

Neoral, Sandimmune) 382
Learning Outcomes
1. Compare and contrast innate and 4. Identify indications for their classifications and mechanisms
adaptive body defenses. pharmacotherapy with biologic of action.
2. Compare and contrast the humoral response modifiers. 7. For each of the classes in the Drug
and cell-mediated immune 5. Explain the need for Snapshot, identify representative
responses. immunosuppressant medications drugs and explain their mechanisms
following organ and tissue of drug action, primary actions, and
3. For each of the major vaccines, important adverse effects.
give the recommended dosage transplants.
schedule. 6. Categorize drugs used for
immunomodulation based on
374 Chapter 25 Drugs for Immune System Modulation
Key Terms
active immunity 376 humoral immunity (HYOU-mor-ul passive immunity 376
adaptive body defenses 375 eh-MEWN-uh-tee) 375 plasma cells 375
antibodies (ANN-tee-BOD-ee) 375 immune response 375 T cells 375
antigen (ANN-tih-jen) 374 immunoglobulins (Ig) (ih-MEW-noh- titer (TIE-ter) 376
GLOB-you-lin) 375
B cell 375 toxoid vaccine (TOX-oid vaks-EEN) 376
immunomodulators (ih-mew-no-MOF-
biologic response modifiers 379 transplant rejection 380
you-layter) 374
boosters 376 vaccination (immunization)
immunosuppressants (ih-MEW-noh-suh-
cytokines (SYE-toh-kines) 375 (VAK-sin-AYE-shun/IH-mewn-ize-
PRESS-ent) 380 AYE-shun) 376
cytotoxic T cells 375 innate body defenses 374 vaccines (vaks-EEN) 374
helper T cells 375
O ur bodies come under continuous attack from a host of foreign invaders that include viruses,
bacteria, fungi, and even multicellular organisms. In defending the body, our immune system is
capable of mounting a rapid and effective response against many of these pathogens.
Immunomodulator is a general term referring to any drug that affects body defenses. In some pa-
tients, immunomodulators are used to stimulate body defenses so that microbes or cancer cells can be
more effectively attacked. For example, vaccines (substances given to stimulate the body’s defense so that
disease can be prevented or controlled) are given at various times throughout the lifespan to prevent major
illnesses. On other occasions, it is desirable to suppress body defenses to prevent a transplanted organ from
being rejected by the immune system. The purpose of this chapter is to examine the pharmacotherapy of
drugs that are used to modulate the body’s immune response to disease.
Core Concept 25.1 The human body has both innate and adaptive body defenses.
anti 5 against A foreign substance that is detected by body defenses and elicits a response is called an antigen. Proteins
gen 5 formation such as those present on the surfaces of pollen grains, bacteria, and viruses are the strongest antigens.
When normal cells become damaged, injured, or cancerous, they too can be viewed as antigens by body
defenses. The human body has an elaborate set of body defenses that is able to respond to virtually any
antigen it may encounter. Dozens of different cells and processes are used to battle disease and internal
threats such as cancer cells. These disease-fighting cells and processes are classified into two groups: in-
nate defenses or adaptive defenses.
The first line of protection from pathogens consists of the innate body defenses, which serve as
general barriers to microbes or environmental hazards. The innate defenses are called nonspecific because
they are unable to distinguish one type of threat from another; the response or protection is the same
regardless of the pathogen. These defenses include physical barriers, such as the skin and the lining of
the respiratory and gastrointestinal tracts, which are potential entry points for pathogens. Other innate
defenses are phagocytes, natural killer (NK) cells, the complement system, fever, and interferons. The
purposes of the innate body defenses are to neutralize or destroy the antigen and to alert other components
of body defenses that a threat has arrived. From a pharmacologic perspective, one of the most important of
the innate defenses is inflammation, which was presented in Chapter 24, along with fever, another type of
innate body defense.
Fast Facts Vaccines and Immune Disorders

■ Vaccines lowered the number of measles cases in the United States from more than 503,000 in 1962
to only 100–130 cases annually. Most cases of measles in the United States are due to importation
from other countries.
■ About one-third of the girls in the United States receive the three-dose recommended vaccine for
human papillomavirus (HPV).
■ Severe combined immunodeficiency (SCID) is a very rare disorder, occurring in less than 1,100 births
annually in the United States.
■ Over 23 million Americans suffer from autoimmune disorders, and the frequency is rising.
■ The most common organ transplant is kidney, with over 30,000 people annually waiting for a
transplant.
Figure 25.1
Humoral Immunity Cell-Mediated Immunity Steps in the humoral

and cell-mediated
Inactivated B cell
immune responses.
Inactivated T cell
Activated B cell
with clones Activated T cell
with clones
Memory B cell Helper T cell Memory T cell

Cytokines
Plasma cell Cytotoxic T cell
Cytokines
Antibodies
The body also has the ability to mount a second line of defense known as adaptive body defenses,
which are specific to particular threats. For example, a specific defense may act against only a single spe-
cies of bacteria and be ineffective against all others. Adaptive body defenses are commonly called the
immune response. The primary cells that accomplish most of the functions of the immune response are
the lymphocytes. The two primary divisions of the immune response are antibody-mediated (humoral) im-
munity and cell-mediated immunity. These are illustrated in Figure 25.1 ■.
The immune response results from activation of the humoral

and cell-mediated immune systems. Core Concept 25.2
Humoral immunity is initiated when an antigen encounters a type of lymphocyte known as a B cell. The
antigen activates the B cell, which then divides rapidly to form many copies, or clones, of itself. Most cells
in this clone are called plasma cells. The primary function of the plasma cells is to secrete antibodies, also
called immunoglobulins (Ig), which are specific to the antigen that initiated the immune response. As they
circulate through the body, antibodies physically interact with the antigens to neutralize or target them for
destruction by other cells of the immune response. Peak production of antibodies occurs about 10 days
after an immune response.
After the antigen challenge, memory B cells are formed that will remember the specific antigen–
antibody interaction. Should the body be exposed to the same antigen in the future, the body will be able
to manufacture even higher levels of antibodies in a shorter period, approximately two to three days. For
some antigens, such as those for measles, mumps, or chickenpox, memory can be retained for an entire
lifetime. Vaccines, discussed later in this chapter, are sometimes administered to produce these memory
cells in advance of exposure to the antigen, so that when the body is exposed to the real organism it can
mount a fast, effective response.
The second branch of the immune response involves lymphocytes called T cells. When they en-
counter their specific antigen, T cells become activated and rapidly form clones. Unlike B cells, how-
ever, T cells do not produce antibodies. Instead, T cells produce huge amounts of cytokines, which are cyto 5 cell
chemicals that regulate important aspects of the immune response. Some cytokines kill foreign organisms kine(sis) 5 movement
directly, whereas others act as messengers to the immune system, stimulating T cells, B cells, and other
body defenses to rid the body of the foreign agent. Specific cytokines released by activated T cells include
several interleukins, interferon, colony stimulating factor, and tumor necrosis factor (TNF). Some of these
cytokines have been used to treat certain immune disorders and cancers. This class of medications, called
biologic response modifiers, is discussed later in this chapter. Drugs that block cytokine release are used in
the pharmacotherapy of cancer and rheumatoid arthritis.
The two major types of T cells are helper T cells and cytotoxic T cells. These cells are often named
after a protein receptor on their plasma membrane; the helper T cells have a CD4 receptor, and the cyto-
toxic T cells have a CD8 receptor. Helper T cells are particularly important because they are responsible
Cam Therapy
Echinacea for Boosting the Immune System
Echinacea purpurea, or purple coneflower, is one of the most popular medicinal botanicals.
This plant is native to the midwestern United States and central Canada; its flowers, leaves,
and stems are harvested and dried. Preparations include dried powder, tinctures, fluid ex-
tracts, and teas. No single ingredient seems to be responsible for the herb’s activity; many
active chemicals have been identified from the extracts.
Echinacea was used by Native Americans to treat various wounds and injuries. Echinacea
is claimed to boost the immune system by increasing phagocytosis and inhibiting bacterial
enzymes. Some substances in echinacea appear to have antiviral activity; the herb is sometimes
taken to prevent and treat the common cold and influenza, an indication for which it has
received official approval in Germany. In general, it is used as a supportive treatment for any
disease involving inflammation and to enhance the immune system.
for activating most other immune cells, including B cells. Cytotoxic T cells travel throughout the body,
secreting cytokines that directly kill bacteria, parasites, virus-infected cells, and cancer cells.
Like B cells, some of the activated T cells become memory cells. If the person encounters the same
antigen in the future, the memory T cells will assist in mounting a more rapid immune response.
Immunostimulants
Drugs that enhance the immune response are called immunostimulants. These types of immunomodulators
include vaccines and biologic response modifiers such as interferons and interleukins.
Core Concept 25.3 Vaccines are biological agents used to prevent illness.
Vaccination (immunization) is the process of introducing a foreign substance (a vaccine) into the body to
trigger immune activation before the patient is exposed to the real pathogen. As a result of the vaccination,
memory B cells are formed. When later exposed to the actual infectious organism, these cells will react quickly
by producing large quantities of antibodies that will help to neutralize or destroy the pathogen. Some immu-
nizations require follow-up doses, called boosters, to provide sustained protection. The effectiveness of most
vaccines can be assessed by measuring the amount of antibody produced after the vaccine has been adminis-
tered, a quantity called titer. If the titer falls below a specified protective level over time, a booster is indicated.
The goal of vaccine administration is to induce long-lasting immunity to a pathogen without produc-
ing an illness in an otherwise healthy person. Therefore, the microorganisms and other substances used as
vaccines must be able to strongly trigger the immune response but be modified to pose no significant risk
of disease development. The four methods of producing safe and effective vaccines include the following:
■ Attenuated (live) vaccines contain microbes that are alive but weakened so they are unable to
produce disease. Some attenuated vaccines cause mild symptoms of the disease. An example of
a live attenuated vaccine is the measles, mumps, and rubella (MMR) vaccine.
■ Inactivated (killed) vaccines contain microbes that have been inactivated by heat or chemicals
and are unable to replicate or cause disease. Examples of inactivated vaccines include the
influenza and hepatitis A vaccines.
■ Toxoid vaccines contain bacterial toxins that have been chemically modified to be incapable
of causing disease. When injected, toxoid vaccines induce the formation of antibodies that are
capable of neutralizing the real toxins. Examples include diphtheria and tetanus toxoids.
■ Recombinant technology vaccines are those that contain partial organisms or bacterial proteins
that are generated in the laboratory using biotechnology. The best example of this type is the
hepatitis B vaccine.
The widespread use of vaccines has prevented illness in millions of patients, particularly children.
One disease—smallpox—has been virtually eliminated from the planet through immunization, and others,
such as polio, have diminished to extremely low levels. Table 25.1 ◆ identifies some common vaccines
and their recommended schedules.
Common side effects of vaccine administration include redness and discomfort at the site of injection,
minor aches, and fever. Although severe reactions are rare, anaphylaxis is possible. In the vast majority of
cases, the benefits of disease prevention far outweigh the small risk of adverse effects from the vaccine.
Vaccinations are contraindicated for patients who have a weakened immune system or who are currently
experiencing symptoms such as diarrhea, vomiting, or fever. Most vaccines are pregnancy category C, so
vaccinations are often delayed in pregnant patients until after delivery to avoid any potential harm to the fetus.
There are two types of immunity that can be obtained through the administration of pharmacologic
agents, as illustrated in Figure 25.2 ■. The type of response induced by the real pathogen, or its vaccine,
is called active immunity: The body produces its own antibodies in response to exposure. The active im-
munity induced by vaccines closely resembles that caused by natural exposure to the antigen, including the
generation of memory cells.
Passive immunity occurs when preformed antibodies are transferred or “donated” from one person to
another. Drugs for passive immunity are usually administered when the patient has already been exposed
to a pathogen or is at very high risk to exposure, and there is not sufficient time to develop active immu-
nity. Patients with weakened immune systems may receive these antibodies to prevent infections. Types of
drugs used to provide passive immunity include:
■ Gamma globulin infused to counteract recent exposure to hepatitis or chickenpox
■ Antivenoms administered to treat snake bites
■ Sera used to treat botulism, tetanus, and rabies
Because these medications do not stimulate the patient’s immune system, their protective effects will
disappear within several weeks to several months after the infusions are discontinued.
Table 25.1 Selected Vaccines and Their Schedules

Vaccine Schedule and Age
Adacel and Boostrix (combination of tetanus toxoid and DTaP) IM; single dose as an active booster after age 10 (Boostrix) or between
ages 11 and 64 (Adacel)
Comvax (combination of haemophilus and hepatitis B vaccines) IM; 3 doses at 2, 4, and 2–15 months of age
Diphtheria, tetanus, and pertussis (Daptacel, DTaP, Infanrix, Tripedia) IM; Ages 2 months, 4 months, 6 months, 15–18 months, and 4–6 years
Haemophilus influenza type B conjugate (ActHIB, Hiberix, PedvaxHIB) IM; Ages 2 months, 4 months, 6 months, and 12–15 months
Hepatitis A (Havrix, VAQTA) Children: IM; Age 12 months, followed by a booster 6–12 months later
Adults: 1 mL followed by a booster 6 months to 12 months later
Hepatitis B (Engerix-B, Recombivax HB) Children/Adults: IM; three doses with the second dose 1 month after
the first and the third dose 6 months after the first
Human papilloma virus (Cervarix, Gardasil) Age 9–26 years: IM; with the second dose 2 months after the first and
the third dose 6 months after the first
Influenza vaccine (Afluria, Fluarix, FluLaval, FluMist, Fluvirin, Fluzone): Children: IM; two doses 1 month apart; then annual dose
includes H1N1 influenza protection Adults: IM; single annual dose or intranasal (FluMist)
Measles, mumps, and rubella (MMR II) Subcutaneous; Single dose at ages 12–15 months; second dose at ages
4–6 years
Meningococcal conjugate vaccine (Menactra, Menomune, Menveo) IM; First dose at age 11–12 years and second dose at age 16 years
Pneumococcal, polyvalent (Pneumovax 23), or 7-valent (Prevnar) Adults (Pneumovax 23 or Pnu-Immune 23): subcutaneous or IM;
single dose
Children (Prevnar): IM; four doses at ages 2 months, 4 months,
6 months, and 12–15 months
Poliovirus, inactivated (IPOL, poliovax) Children: subcutaneous; at ages 2 months, 4 months, 6–18 months,
and 4–6 years
Proquad (combination of MMR and varicella vaccines) Subcutaneous; First dose at ages 12–15 months, second dose at ages
4–6 years
Rotavirus (Rotarix, RotaTeq) PO; three doses at ages 2 months, 4 months, and 6 months (Rotarix
does not require a dose at 6 months)
Tetanus toxoid IM; (primary immunization, age 7 or older): three doses; the second
dose is given 4–8 weeks after the first dose; the third dose is given
6–12 months after the second dose
Twinrix (combination of hepatitis A and hepatitis B vaccines) Over age 18: three doses, with the second dose 1 month after the first,
and the third dose 6 months after the first
Varicella (Varivax, Zostavax) Subcutaneous (Varivax); at ages 12–15 months and 4–6 years,
Subcutaneous (Zostavax); single dose at age 50 or older
F i g u re 2 5 . 2
Booster Vaccine
Administered months or years after the initial
vaccine, booster vaccines stimulate the
immune system to maintian enough memory
Antibodies neutralize cells to mount a rapid response to an
or destroy antigens antigen.
A Memory cells provide

long-lived protection
Active immunity
Administration of
vaccine or exposure to
an antigen stimulates
the body to produce
antibodies and
memory cells. Antigen
A
exposure
Passive immunity
Administration of
immunoglobulins (antibodies)
gives passive immunity which
A has a fast onset, but lasts only A
3 to 6 months.
Plasma cell exposed Immunoglobulins

to antigen or vaccine Response from
antibodies
(rapid but short-lived)
Mechanisms of active and passive immunity.
Drug Prototype: Hepatitis B Vaccine (Energix-B, Recombivax HB)

Therapeutic class: Vaccine Pharmacologic class: Vaccine
Actions and Uses: Hepatitis B vaccine is administered IM to pro- Hepatitis B vaccine is sometimes given to patients after
vide prophylaxis against exposure to the hepatitis B virus (HBV). they have been exposed to the virus. In this case, it is often
Following injection, the body produces antibodies against the combined with hepatitis B immune globulin (HBIG), which
virus. It is indicated for infants born to HBV-positive mothers, will provide passive immunity while the body is building its
and those at high risk for exposure to HBV-infected blood, own antibodies to the virus. Once a hepatitis B infection is
including nurses, physicians, dentists, dental hygienists, morti- acquired, it is difficult to eliminate; therefore, prevention is
cians, and paramedics. Because HBV infection is extremely dif- the best treatment.
ficult to treat, it is prudent for all healthcare workers to receive
HBV vaccine before beginning their clinical education, unless Adverse Effects and Interactions: The adverse effects of
contraindicated. The vaccine is also indicated for all persons hepatitis B vaccine are similar to those of other vaccines. Pain
who engage in high-risk sexual practices, such as heterosexual and inflammation may appear at the injection site. A fever
activity with multiple partners, prostitution, or homosexual or may develop, and the patient may feel tired and lethargic.
bisexual practices, or for persons who repeatedly contract sexu- Although anaphylaxis is rare, epinephrine should be kept
ally transmitted infections. The regimen involves three doses of available. The vaccine should be given to pregnant or lactat-
the vaccine, usually followed by a titer to confirm that active ing women only if clearly needed to protect the health of the
immunity has been achieved. mother or child.
Biologic response modifiers are used to boost the immune response. Core Concept 25.4
When challenged by antigens, certain cells in the immune system secrete cytokines that help fight the in-
vading organism. Several of these natural chemicals are now available as medications. Drugs in this class,
the biologic response modifiers, are administered to boost certain functions of the immune system and are
shown in Table 25.2 ◆.
Interferons (IFNs) are cytokines secreted by lymphocytes and macrophages that have been infected
with a virus. IFNs slow the spread of viral infections and enhance the activity of existing leukocytes. In
addition to antiviral properties, these drugs exhibit anticancer and anti-inflammatory actions. Alpha IFNs
have the widest therapeutic application (when used as medications, the spelling is changed to alfa). In-
dications for IFN alpha therapy include cancers, such as hairy cell leukemia and AIDS-related Kaposi’s
sarcoma, and chronic hepatitis virus B or C infections. Interferon alfa-2b (Intron A) is one of the most
common IFNs used in therapy and is featured as a prototype drug. IFN beta is primarily used for treatment
of severe multiple sclerosis (see Chapter 12). Patients receiving IFN therapy must be closely monitored
because drugs in this class can cause serious adverse effects including depression, suicidal ideation, psy-
chosis, cardiovascular disease (including myocardial infarction), pulmonary impairment, hepatic or renal
failure, and a number of other life-threatening disorders.
Interleukins are another class of cytokines secreted by lymphocytes, monocytes, and macrophages.
Although 30 different interleukins have been identified, only a few are available as medications. The inter-
leukins have widespread effects on immune function, and all of them boost the activity of natural defense
mechanisms. Interleukin-2 is available as aldesleukin (Proleukin), which is approved for the treatment of
metastatic renal carcinoma. Interleukin-11, which is derived from bone marrow cells, is a growth factor
with multiple hematopoietic effects. It is marketed as oprelvekin (Neumega) for its ability to stimulate
platelet production in patients with weakened immune systems.
In addition to IFNs and interleukins, a few additional biologic response modifiers are available to
enhance the immune system. Bacillus Calmette–Guérin (BCG) vaccine (Tice, TheraCys) is an attenuated
strain of Mycobacterium bovis used for the pharmacotherapy of certain types of bladder cancer. Colony-
stimulating factors such as filgrastim (Neupogen) and sargramostim (Leukine) promote the production of
white blood cells (WBCs). These drugs are used to shorten the length of neutropenia (reduced leukocyte
count) in patients with cancer and in those who have had a bone marrow transplant.
Table 25.2 Selected Biologic Response Modifiers

aldesleukin (Proleukin): interleukin-2 IV; 600,000 units/kg (0.037 mg/kg) every For metastatic renal cell carcinoma and
8 hours by a 15-minute IV infusion for a total metastatic melanoma
of 14 doses
Bacillus Calmette–Guérin (BCG) vaccine Intradermal (Tice); 0.1 mL as vaccine For bladder cancer
(Tice, TheraCys) Intravesical (TheraCys); bladder instillation
Interferons
interferon alfa-2b (Intron-A) IM/subcutaneous; highly variable depending For hairy cell leukemia, malignant melanoma,
upon indication follicular lymphoma, condylomata acuminata,
Kaposi’s sarcoma, chronic hepatitis B, and
chronic hepatitis C
interferon alfacon-1 (Infergen) Subcutaneous; 9 mcg three times per week For chronic hepatitis C (usually in combination
with ribavirin)
interferon alfa-n3 (Alferon N) Intralesion: 0.05 mL (250,000 international For treatment of genital warts
units) per wart twice per week for up to
8 weeks
interferon beta-1a (Avonex, Rebif) IM (Avonex); 30 mcg/wk For multiple sclerosis
Subcutaneous (Rebif); 44 mcg three times per
week
interferon beta-1b (Betaseron, Extavia) Subcutaneous; 0.25 mg (8 million units) every For multiple sclerosis
other day
peginterferon alfa-2a (Pegasys) Subcutaneous; 180 mcg/wk for 48 weeks For chronic hepatitis B and chronic hepatitis C
Drug Prototype: Interferon alfa-2b (Intron-A)

Therapeutic Class: Immunostimulant Pharmacologic Class: Interferon, biologic response modifier
Actions and Uses: Interferon alfa-2b is a biologic response this usually diminishes as therapy progresses. Headache, nau-
modifier that is prepared by recombinant DNA technol- sea, vomiting, diarrhea, and anorexia are relatively common.
ogy and is approved to treat cancers (hairy cell leukemia, Depression and suicidal ideation have been reported and may
melanoma, non-Hodgkin’s lymphoma, AIDS-related Kaposi’s be severe enough to require discontinuation of the drug. With
sarcoma), as well as viral infections (HPV, chronic hepatitis prolonged therapy, immunosuppression, and serious toxicity
virus B and C). It is available for IV, IM, and subcutaneous such as hepatotoxicity and neurotoxicity may be observed.
administration. Use with ethanol may cause excessive drowsiness and
Rebetron is a combination drug containing interferon dehydration. Zidovudine may increase hematologic toxicity.
alfa-2b and ribavirin, an antiviral agent. Rebetron is indicated
for pharmacotherapy of hepatitis C infection. Peginterferon
alfa-2b (PegIntron) has a molecule of polyethylene glycol (PEG)
attached to the IFN molecule, which gives the drug an extended Black Box Warning:
half-life. Peginterferon alfa-2b is approved to treat chronic IFNs may cause or aggravate fatal or life-threatening neu-
hepatitis C virus infections. ropsychiatric, autoimmune ischemic, or infectious disorders.
Therapy should be discontinued in patients with persistently
Adverse Effects and Interactions: A flu-like syndrome of fever, severe or worsening signs or symptoms of these conditions.
chills, dizziness, and fatigue occurs in 50% of patients, although
Immunosuppressants are used to prevent transplant rejection

Core Concept 25.5 and to treat autoimmune disorders.
The immune system is normally viewed as a lifesaver that protects us from pathogens in the environ-
ment. For those receiving organ or tissue transplants, however, the immune system is the enemy. Despite
careful tissue matching and typing, donated organs and tissues always contain some antigens that trig-
ger the recipient’s immune response. This response, called transplant rejection, is sometimes acute,
with antibodies rushing to destroy the transplanted tissue within a few days. The cell-mediated immune
system reacts more slowly to the transplant, attacking it about two weeks following surgery. Even if the
organ survives these challenges, chronic rejection of the transplant may occur months or even years after
surgery.
Immunosuppressants are medications given to lessen the immune response. One or more of these
drugs are administered at the time of transplantation and continued for several months following surgery.
In some cases, they are continued indefinitely at low doses. Transplantation would be impossible without
the use of effective immunosuppressant drugs.
In addition, these drugs may be prescribed to treat the symptoms of autoimmune disorders, con-
ditions in which the body creates antibodies against its own cells. Over a hundred different disorders
have been found to have some degree of autoimmune involvement. Examples of common autoim-
mune disease include diabetes mellitus (Type I), psoriasis, rheumatoid arthritis, systemic lupus ery-
thematosus (SLE), myasthenia gravis, and Hashimoto’s thyroiditis. Although these disorders affect
different organs, most have in common a hypersensitive immune system that causes symptoms of
acute inflammation. When the disease becomes acute, immunosuppressant pharmacotherapy may be
initiated. Unlike transplant recipients who may receive immunosuppressants indefinitely, patients with
acute inflammation from an autoimmune disorder usually are given these drugs only for brief periods
to control relapses.
Although the various immunosuppressant drugs act by different mechanisms, all suppress some as-
pect of lymphocyte function. Some act nonselectively by inhibiting all aspects of the immune system.
Other, newer drugs suppress only a limited aspect of the immune response. The nonselective agents pro-
vide more widespread immunosuppression but carry a greater risk of adverse effects.
Nearly all the immunosuppresants are toxic to bone marrow. Because the immune system is sup-
pressed, infections are common and the patient must be protected from situations in which exposure to
pathogens is likely. Long-term survivors of transplants are also at increased risk of developing cancers,
especially lymphoma, skin cancer, cervical cancer, and Kaposi’s sarcoma. Doses for these drugs are listed
in Table 25.3 ◆.
Table 25.3 Selected Immunosuppressants

anakinra (Kineret) Subcutaneous; 100 mg once daily For rheumatoid arthritis that has not
responded to safer drugs
azathioprine (Azasan, Imuran) PO/IV; 3–5 mg/kg daily Inhibits DNA, RNA, and protein synthesis; also
for severe rheumatoid arthritis
basiliximab (Simulect) IV; 20 mg times two doses (first dose 2 hours Antibody against the CD25 receptor on
before surgery; second dose 4 days after T cells; approved for use in patients with
transplant) kidney transplant
belatacept (Nulojix) IV; 5–10 mg/kg For prophylaxis of rejection following a kidney
transplant
cyclosporine (Gengraf, Neoral, PO; initial dose 14–18 mg/kg just prior to sur- IV form available; inhibits T cells; also for
Sandimmune) gery; after 2 weeks, then 5–10 mg/kg/day rheumatoid arthritis, severe psoriasis, and
other severe inflammatory disorders
lymphocyte immune globulin or antithymocyte IV; 10–30 mg/kg daily for 1–2 weeks Polyclonal antibodies that reduce T cell
globulin (Atgam) numbers; for prevention of renal transplant
rejection
methotrexate (Rheumatrex, Trexall) PO; 15–30 mg/day for 5 days; repeat every 12 IV, IM, and intrathecal forms available; blocks
(see page 440 for the Drug Prototype box) weeks for three courses metabolism of folic acid; also for neoplasia,
severe psoriasis, and severe rheumatoid
arthritis
muromonab-CD3 (Orthoclone OKT 3) IV; 5 mg/day administered for 10–14 days Antibodies against the CD3 receptor on T cells;
often a treatment of choice to prevent renal
transplant rejection
mycophenolate (CellCept, Myfortic) PO/IV; 720 mg bid IV form available; inhibits B cells, T cells, and
antibody formation; for prevention of kidney,
liver or heart transplant rejection
sirolimus (Rapamune) PO; 6 mg loading dose, then 2 mg/day Suppresses antibody production; for preven-
tion of renal transplant rejection
tacrolimus (Prograf) PO; 0.15–0.3 mg/kg/day in two divided doses IV form available; inhibits T cells; for preven-
every 12 hours tion of kidney, liver, or heart transplant rejec-
tion; ointment is approved to treat atopic
dermatitis
Drug classes that have immunosuppressant activity include corticosteroids (glucocorticoids), anti-
metabolites, antibodies, and calcineurin inhibitors. The corticosteroids are potent inhibitors of inflam-
mation and are often drugs of choice in the short-term therapy of severe inflammation (see Chapter 24).
Antimetabolites such as sirolimus (Rapamune) and azathioprine (Imuran) inhibit aspects of lymphocyte
replication. By binding to the intracellular messenger calcineurin, cyclosporine (Gengraf, Sandimmune,
Neoral), and tacrolimus (Prograf) disrupt T-cell function. The calcineurin inhibitors are of value in treating
psoriasis, an inflammatory disorder of the skin (see Chapter 36).
The final group of immunosuppressants, and the most recently developed, are monoclonal antibodies.
Monoclonal antibodies have been designed that attack very specific targets, usually receptors on T cells. For
example, muromonab-CD3 (Orthoclone OKT3) blocks the function of the CD3 receptor, which is present
on T cells that attack transplanted tissue. Muromonab-CD3 is administered to prevent rejection of kidney,
heart, and liver transplants, and to deplete the bone marrow of T cells prior to marrow transplant. Basilix-
imab (Simulect), belatacept (Nulojix), and daclizumab (Zenapax) are given to prevent acute rejection of
kidney transplants. Infliximab (Remicade) is used to suppress the severe inflammation that often accompa-
nies autoimmune disorders such as Crohn’s disease and rheumatoid arthritis. Belimumab (Benlysta) reduces
abnormal B cells that are a problem in people with severe SLE. Because many drugs in this monoclonal
antibody class are used as antineoplastics, the student should refer to Chapter 28 for additional information.
Concept Review 25.1

■ Why are oral glucocorticoids usually used concurrently with immunosuppressant drugs
following a transplant operation?
Drug Prototype: Cyclosporine (Gengraf, Neoral, Sandimmune)

Therapeutic Class: Immunosuppressant Pharmacologic Class: Calcineurin inhibitor
Actions and Uses: Cyclosporine is a complex chemical obtained counts are necessary to be certain that WBCs do not fall below
from a soil fungus that inhibits helper T cells. It is approved for 4,000 or platelets below 75,000.
the prophylaxis of kidney, heart, and liver transplant rejection, Because cyclosporine is extensively metabolized in the
psoriasis, and xerophthalmia, an eye condition of diminished tear liver, many drug interactions are possible. The following drugs
production caused by ocular inflammation. Cyclosporine is nor- increase the metabolism of cyclosporine, making the drug less
mally administered by the oral route but an IV form is available effective: phenytoin, carbamazepine, TMP–SMZ, and phenobar-
for severe cases of ulcerative colitis or Crohn’s disease. When pre- bital. The following drugs decrease the metabolism of cyclospo-
scribed for transplant recipients, it is usually administered in com- rine, causing the drug to build high concentrations and become
bination with high doses of corticosteroids such as prednisone. potentially toxic: macrolide antibiotics, azole antifungals, and
amphotericin B. Because cyclosporine can damage the kidneys,
Adverse Effects and Interactions: The primary adverse effect of other nephrotoxic drugs such as amphotericin B, NSAIDs, or
cyclosporine occurs in the kidney, with up to 75% of patients aminoglycosides should be administered with great caution.
experiencing reduction in urine output. Frequent laboratory
tests of kidney function, such as BUN and creatinine, are neces-
sary. Other common adverse effects are tremor, hypertension, Black Box Warning:
and elevated hepatic enzyme values. Although opportunistic Therapy with cyclosporine may result in serious infections
infections are common during cyclosporine therapy, they are and increases the risk of malignancies.
fewer than with other immunosuppressants. Periodic blood
NURSING PROCESS FOCUS Patients Receiving Immunosuppressants

Prior to administration: ■ Risk for Infection related to adverse effects of drug therapy
■ Obtain a complete health history, including cardiovascular, ■ Risk for Injury related to adverse effects of drug therapy
neurological, immune, oral, renal and liver conditions, allergies, ■ Risk for Impaired Mucous Membrane related to adverse effects
drug history, and possible drug interactions. of drug therapy
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, ■ Deficient Knowledge related to a lack of information about
and renal and liver function studies. drug therapy
■ Attain history or current cases of cancer, fever, or active infections
(such as herpes and HIV).
■ Acquire the results of a complete physical examination, including
vital signs, height, and weight.

The patient will:
■ Experience therapeutic effects (depending on the reason the drug is being given).
Implementation
■ Administer medications correctly and evaluate the patient’s Inform the patient to:
knowledge of proper administration. (Most immunosuppressants ■ Use enclosed equipment to mix the drug.
are administered either po and/or IV and require specific ■ Use glass; not paper or plastic cups unless package directions indicate
instructions.) they are to be used.
■ Mix drug with milk, chocolate milk or orange juice, stirring well. Take
additional liquid to ensure the drug is taken.
■ Monitor all vital signs and observe for signs and symptoms of infection Advise the patient:
such as fever, elevated pulse, respiration and BP, fatigue, cough, white ■ To immediately report any signs and symptoms of infection such as
patches on mucous membranes, vaginal discharge, itchy blister-like wounds with redness or drainage, increasing cough, fatigue, and fever
vesicles on skin. (Immunosuppressants increase the risk of infection, to the healthcare provider.
especially opportunistic infections such as herpes and yeast infections.) ■ To use proper hand washing techniques.
■ To avoid large crowds and people with known infections or young
children who have higher risk of infection.
■ To cook food thoroughly, allowing others to prepare raw foods and
clean up afterward.
■ Monitor changes in level of consciousness, disorientation/confusion or ■ Instruct the patient to report increasing lethargy, disorientation,
tremors. (Neurological changes may indicate adverse effects of drug confusion, changes in behavior or mood, slurred speech, or tremors to
therapy.) the healthcare provider.
Implementation
■ Continue to monitor serum and urine laboratory tests, specifically Instruct the patient:
noting: CBC, platelets, electrolytes, glucose, liver and renal studies, ■ That it is extremely important to keep scheduled laboratory and doctor
and lipid levels. (Depending on drug, immunosuppressants may cause appointments.
leukopenia, anemia, thrombocytopenia, hyperglycemia, hyperkalemia, ■ To carry a wallet identification or wear medical ID jewelry indicating
and renal failure.) immunosuppressant therapy.
■ Inspect oral mucous membrane and dental health. (Immunospressants Instruct the patient to:
increase the risk of oral candidiasis and gingivitis. Oral antifungal ■ Maintain excellent oral hygiene, inspecting the mouth daily.
medications may be needed.) ■ Keep regular dental visits and consult with dentist about frequency.
■ Determine the patient’s diet and consumption of grapefruit juice. ■ Advise the patient to avoid/eliminate grapefruit and grapefruit juice
(Grapefruit juice significantly increases cyclosporine levels and should from diet while on drug.
be avoided while on immunosuppressant therapy.)
■ Collect information about pregnancy status. (Pregnancy should be ■ Explain the effects of medications on pregnancy and breastfeeding
avoided for up to four months after discontinuing immunosuppressive and the need to delay pregnancy.
therapy.) ■ Discuss options for family planning; alternative contraception methods
may be necessary.
■ Monitor for the development of hirsutism or alopecia. (Hirsutism is ■ Advise patient to notify healthcare provider of changes to hair growth
reversible when drug is discontinued. Alopecia indicates significant or texture.
immunosuppression.)
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Table 25.3
for a list of drugs to which these nursing actions apply.

Patients treated for inflammatory or immune disorders need to know the following:
Regarding Vaccines
1. Maintain an accurate, written record of vaccinations, including the date of the vaccina-
tion, route and site of vaccination, type of vaccine (including manufacturer and lot
number), and the address of the physician’s office where the vaccination occurred.
2. Keep immunizations up to date to prevent illness. Because recommendations can
change, seek current information from a healthcare provider periodically.
3. Vaccines may contain a number of additives, including antibiotics, formaldehyde,
thimersol, and monosodium glutamate. If an allergy is known or suspected to any
of these additives, notify a healthcare provider before getting a vaccination.
Regarding Biologic Response Modifiers

4. Regular laboratory testing is extremely important, especially monitoring complete blood
count (CBC).
5. Immediately report neurological symptoms (depression, suicidal ideations) and cardiovas-
cular effects to healthcare provider.
Regarding Immunosuppressants
6. Never take cyclosporine with grapefruit juice; blood levels of the drug are increased by
this combination.
7. Reduce risk of illness by avoiding crowds, avoiding those with colds/infections, and
washing hands frequently.
8. Keep scheduled laboratory and doctor appointments. Regular laboratory testing is
extremely important, especially monitoring CBC, electrolytes, hormone levels, and urine
studies.
9. Immediately report an elevation in temperature, sore throat, mouth ulcers, and fatigue
to the healthcare provider.
Chapter Review
25.1 The human body has both innate and adaptive 25.3 Vaccines are biologic agents used to prevent illness.
body defenses. Vaccines are usually given to prevent a serious infec-
Innate body defenses are nonspecific, general barriers tious disease. Vaccines may be live, attenuated, or
to disease, such as the skin, inflammation, and phago- toxoids. They are effective when taken according to
cytes. Adaptive body defenses, known as the immune schedule and rarely produce serious adverse effects.
response, involve lymphocytes and are specific to the
particular threats. 25.4 Biologic response modifiers are used to boost the
immune response.
25.2 The immune response results from activation of Several drugs are available to boost a patient’s im-
the humoral and cell-mediated immune systems. mune function. Interleukins, interferons, and other
B cells become plasma cells and secrete large quanti- agents enhance the body’s natural defenses, primarily
ties of antibodies. The antibodies are specific to the in the pharmacotherapy of cancer.
antigen and neutralize the foreign agent or destroy it.
Some B cells remember the antigen for many years. 25.5 Immunosuppressants are used to prevent trans-
T cells also recognize specific antigens, but instead of plant rejection and to treat autoimmune disorders.
producing antibodies, they produce cytokines, some For an organ or tissue transplant to be successful,
of which rid the body of the foreign agent. Memory the patient’s immune system must be suppressed fol-
B and T cells remember the antigen for many years lowing surgery. Immunosuppressants are effective
and mount a faster immune response on subsequent in lessening the immune response but must be moni-
exposures. tored carefully because loss of immune function can
lead to infections and cancer.
Review Questions
The following questions are written in NCLEX-PN® style. An- 3. The physician has ordered oprelvekin (Neumega) for a
swer these questions to assess your knowledge of the chapter patient who has just had chemotherapy. The patient asks the
material, and go back and review any material that is not clear nurse why she needs this drug. The nurse responds:
to you. 1. “You are being given this drug to suppress your immune
1. The nurse is evaluating drug effects in a patient who has system because you are having a hypersensitivity reaction.”
been given interferon alfa-2b (Intron A) for MS. Which of the 2. “You are being given this drug to help reduce any inflam-
following are common adverse effects? (Select all that apply.) mation response you may develop.”
3. “You are being given this drug because it acts as an antivi-
1. Thoughts of suicide ral, helping to reduce infection.”
2. Hepatotoxicity 4. “You are being given this drug to stimulate platelet
3. Hypotension production.”
4. Depression
4. While receiving filgrastim (Neupogen), the nurse should
2. The nurse would question an order for aldesleukin (Pro- monitor for a(n):
leukin) if the patient had which of the following conditions?
(Select all that apply.) 1. Increase in the production of WBC
2. Increase in the production of platelets
1. Liver disease 3. Increase in the production of red blood cells (RBCs)
2. Metastatic lung cancer 4. Decrease in the production of RBCs
3. Metastatic renal cancer
4. Metastatic melanoma
Chapter Review 385
5. A patient who is pregnant with her first child is at the 3. Hypoglycemia

clinic for a checkup and an infant care class. An informational 4. Bleeding
pamphlet on immunizations has been provided and the nurse
begins to review the information with the patient. She informs 8. A patient is to receive tacrolimus (Prograf) 0.15 mg/kg/
the patient that the DTaP vaccine should be given at ages: day to be given in two doses (every 12 hours). She weighs
100 pounds. How many milligrams will the patient receive per
1. 1 months, 4 months, 12 months, 15–18 months, and 4–6 dose?
years
2. 2 months, 6 months, 15–18 months, and 4–6 years 1. 6.82 mg
3. 2 months, 4 months, 6 months, 15–18 months, and 4–6 2. 6.60 mg
years 3. 3.30 mg
4. 2 months, 4 months, 6 months, and 15–18 months 4. 3.41 mg
6. A patient comes to the physician’s office immediately af- 9. Which of the following statements by a patient taking
ter a suspected exposure to hepatitis B. He is to start the hepa- cyclosporine (Neoral, Sandimmune) would indicate the need
titis B vaccine series and also receive the hepatitis B immune for more information?
globulin (HBIG) vaccine injection. He tells the nurse that 1. “I will report any reduction in urine output to my health-
he understands how the hepatitis B vaccine series works but care provider.”
wants to know why he also needs to have the HBIG vaccine. 2. “I will wash my hands frequently.”
The nurse responds the HIBG vaccine is given to: 3. “I will take my blood pressure at home every day.”
1. Enhance the ability of the hepatitis B (Engerix-B) series of 4. “I will take my cyclosporine at breakfast with a glass of
vaccines to provide permanent immunity. grapefruit juice.”
2. Ensure that the hepatitis B (Engerix-B) series eliminates 10. The nurse should monitor a transplant patient for the pri-
the virus. mary adverse effect of cyclosporine (Neoral, Sandimmune)
3. Provide temporary immunity while the body is building its therapy by collecting information on which of the following
own antibodies to the virus. laboratory tests?
4. Provide active immunity by causing the immune system to
1. CBC
form antibodies.
2. BUN and creatinine
7. The nurse evaluates the patient on immunosuppressants for: 3. Liver enzymes
1. Hypotension 4. Electrolytes
2. Infection
Remember Mr. Martel, the patient 1. Mr. Martel asks the nurse how the hepatitis B vaccine
introduced at the beginning of the works. The nurse responds that the vaccine stimulates the im-
chapter? Now read the remainder of mune system to produce antibodies after exposure to compo-
the case study. Based on the informa- nents of the vaccine. This type of vaccine provides ______
tion you have learned in this chapter, immunity.
answer the questions that follow. 1. Passive
2. Attenuated
3. Live
4. Active
2. While providing information about the hepatitis B vac-
cine series, the nurse informs Mr. Martel that:
Mr. Jose Martel, a 32-year-old night club manager, arrives at
the office for his annual check-up. While being interviewed by 1. It is a series of three shots: the first one today, the second
the nurse, he tells her he had called the office in advance and one a month from now, and the last shot six months after
made arrangements to begin the hepatitis B vaccine series. He the first shot.
states, “Since I work directly with so many people, I thought 2. It is a series of two shots: the first one today and then the
it might be a good idea.” He has read about the vaccine from last one a month from now.
some online sites but still has some questions. 3. It is a series of three shots: the first one today, the second
one a month from now, and the last shot six months after
the second shot.
4. It is a series of four shots: the first one today, the second
one a month from now, the third one six months after the
first shot, and the last one a year after the first one.
3. The nurse and Mr. Martel are reviewing his health his- 4. Just prior to administering the first injection of the series,
tory. Which of the following information would cause the the nurse tells Mr. Martel that he might expect which adverse
nurse to withhold the vaccine and check with the healthcare effect(s) to occur? (Select all that apply.)
practitioner? 1. Pain or inflammation at the injection site
1. Mr. Martel smokes cigarettes, one-half pack a day. 2. Nausea
2. Mr. Martel is frightened by needles and injections. 3. Fatigue
3. Mr. Martel is allergic to yeast and yeast products. 4. Fever
4. Mr. Martel drinks several glasses of wine on the weekends.

C
“I don’t know what is
going on. Ever since I had H
my kidney transplant, I’ve A
been experiencing repeated P
bacterial infections and now
I have to wear this mask T
when I’m around people.” E
Ms. Shelly Jackson R
Drugs for Bacterial Infections

26
Core Concepts
26.1 Pathogens are organisms that cause disease by in- 26.8 The tetracyclines have broad spectrums but are
vading tissues or secreting toxins. drugs of choice for few diseases.
26.2 Anti-infective drugs are classified by their chemical 26.9 The macrolides are safe alternatives to penicillin for
structures or by their mechanisms of action. many infections.
26.3 Anti-infective drugs act by selectively targeting a 26.10 The aminoglycosides are narrow-spectrum drugs
pathogen’s metabolism or life cycle. that have the potential to cause serious toxicity.
26.4 Acquired resistance is a major clinical problem that is 26.11 Fluoroquinolones have wide clinical applications
worsened by improper use of anti-infectives. because of their broad spectrum of activity and
26.5 Careful selection of the correct antibiotic is essential relative safety.
for effective pharmacotherapy and to limit adverse 26.12 Sulfonamides and urinary antiseptics are traditional
effects. drugs for urinary tract infections.
26.6 The penicillins are one of the oldest and safest 26.13 A number of additional anti-infectives have distinct
groups of anti-infectives. mechanisms of action and specific indications.
26.7 The cephalosporins are similar in structure and 26.14 The pharmacotherapy of tuberculosis requires
function to the penicillins and are one of the most special dosing regimens and schedules.
widely prescribed anti-infective classes.
Drug Snapshot
Penicillins enicillin G Sodium/
p Fluoroquinolones ciprofloxacin (Cipro) 401
Potassium 395
Sulfonamides trimethoprim–sulfamethoxazole
Cephalosporins cefotaxime (Claforan) 396 (Bactrim, Septra) 402
Tetracyclines t etracycline (Sumycin, Miscellaneous vancomycin (Vancocin) 403
others) 397 antibacterials
Macrolides rythromycin (E-Mycin,
e Antitubercular drugs isoniazid (INH) 406
Erythrocin) 398
Aminoglycosides gentamicin (Garamycin) 400
388 Chapter 26 Drugs for Bacterial Infections
Learning Outcomes
1. Distinguish between the terms 5. Explain the importance of culture 7. Explain how the pharmacotherapy
pathogenicity and virulence. and sensitivity testing to anti- of tuberculosis differs from that of
2. Explain how bacteria are described infective chemotherapy. other infections.
and classified. 6. Identify the mechanism of 8. For each of the classes in the Drug
3. Compare and contrast the terms development and symptoms of Snapshot, identify representative
bacteriostatic and bacteriocidal. superinfections caused by anti- drugs and explain their mechanisms
infective therapy. of drug action, primary actions, and
4. Using an example, explain how important adverse effects.
resistance can develop to an anti-
infective drug.
Key Terms
acquired resistance 392 culture and sensitivity (C&S) testing 393 pathogenicity (path-oh-jen-
antagonism 393 directly observed therapy (DOT) 408 ISS-ih-tee) 389
antibiotic (ann-tie-bye-OT-ik) 390 host flora (host FLOR-uh) 393 photosensitivity 398
anti-infective (ann-tie-in-FEK-tive) 390 mutations (myou-TAY-shuns) 391 plasmids (PLAZ-midz) 392
bacteriocidal (bak-teer-ee-oh-SY-dall) 391 narrow-spectrum antibiotic 393 red-man syndrome 403
bacteriostatic (bak-teer-ee-oh-STAT-ik) 391 nephrotoxicity (NEF-row-toks- superinfections 393
beta-lactam ring (bay-tuh LAK-tam) 393 ISS-ih-tee) 400 toxins (TOX-in) 389
beta-lactamase/penicillinase (bay-tuh- nosocomial infections (noh-soh-KOH- tubercles (TOO-burr-kyouls) 406
LAK-tam-ace/pen-uh-SILL-in-ace) 393 mee-ul) 392 urinary antiseptics 403
broad-spectrum antibiotic 393 ototoxicity (OH-toh-toks-ISS-ih-tee) 400 virulence (VEER-you-lens) 389
chemoprophylaxis (kee-moh-pro- pathogen (PATH-oh-jen) 389
fill-AX-is) 392
T he human body has adapted quite well to living in a world teeming with microorganisms (microbes).
Present in the air, water, food, and soil, microbes are an essential component to life on the planet.
In some cases, microorganisms, such as those in the colon, play a beneficial role in human health.
When in an unnatural environment or when present in unusually high numbers, however, microorganisms
can cause a variety of ailments ranging from mildly annoying to fatal. The development of the first anti-
infective drugs in the mid-1900s was a milestone in the field of medicine. In the past 60 years, pharmacolo-
gists have attempted to keep pace with microbes that rapidly become resistant to therapeutic drugs. This
chapter examines two groups of anti-infectives: the antibacterial drugs and the specialized medications
used to treat tuberculosis (TB).
Fast Facts Bacterial Infections

■ Infectious diseases are the third most common cause of death in the United States and the most
common cause of death worldwide.
■ Foodborne illness is responsible for 76 million illnesses, 300,000 hospitalizations, and 5,000 deaths
each year. About 500 people die of food poisoning each year in the United States.
■ Urinary tract infections (UTIs) are the most common infection acquired in hospitals. Nearly all are
associated with the insertion of a urinary catheter. Hospital-acquired urinary infections add an aver-
age of 3.8 days to a hospital stay and can cost over $3,800 per infection.
■ More than 2 million nosocomial infections are acquired each year. These infections add 1 day to a
hospital stay for UTI, 7–8 days for surgical site infections, and 6–30 days for pneumonia.
■ Up to 30% of all Streptococcus pneumoniae found in some areas of the United States are resistant
to penicillin.
■ Nearly all strains of Staphylococcus aureus in the United States are resistant to penicillin.
■ About 73,000 cases of Escherichia coli (E. coli ) poisoning are reported annually in the United States,
with the most common source being ground beef.
Pathogens are organisms that cause disease by invading

tissues or secreting toxins. Core Concept 26.1
An organism that can cause disease in humans is called a pathogen. Human pathogens include viruses, path 5 disease
bacteria, fungi, unicellular organisms (protozoans), and multicellular animals. Examples of these pathogen 5 producing
gens are illustrated in Figure 26.1 ■. To infect humans, pathogens must bypass a number of elaborate body
defenses, such as those described in Chapter 25. Pathogens may enter through broken skin, or by ingestion,
inhalation, or contact with a mucous membrane such as the nasal, urinary, or vaginal mucosas.
Some pathogens are extremely infectious and life threatening to humans, whereas others simply cause
annoying symptoms or none at all. The ability of an organism to cause infection is called its pathogenicity.
Pathogenicity depends on an organism’s ability to bypass or overcome the body’s immune system. Fortu-
nately for us, only a few dozen pathogens commonly cause disease in humans. Some of these are listed in
Table 26.1 ◆. Another common word used to describe a pathogen is virulence. A highly virulent organism
is one that can produce disease when present in very small numbers.
After gaining entry, pathogens generally cause disease by one of two basic mechanisms. Invasiveness is the
ability of a pathogen to grow extremely rapidly and damage surrounding tissues by their sheer numbers. Because
a week or more may be needed to mount an immune response against the organism, this rapid growth can easily
overwhelm body defenses. A second mechanism is the production of toxins. Even very small amounts of some
bacterial toxins may disrupt normal cellular activity and, in extreme cases, result in death of the individual.
Several methods are used to describe and classify the millions of species of bacteria on the planet. The
three most common methods are shown in Table 26.2 ◆. Healthcare providers must learn these organiza-
tional schemes because anti-infective drugs are often effective only for a specific type of bacteria, such as
gram-positive bacilli or gram-negative anaerobes.
Figure 26.1
Fimbria Chromosome Types of pathogenic
Membranous
Ribosomes envelope organisms: (a) bacte-
Cytoplasm rium, (b) virus, (c) proto-
Capsid
(protein coat)
zoan pathogens,
(d) multicellular para-
Nucleic acid
(DNA or RNA)
sites, and (e) fungi.
Flagellum
Capsule Spikes
or slime (protein)
layer Plasmid
Cell wall
Cell membrane 1 m 0.1 m
A. Bacterium B. Virus
Liver fluke
(Fasciola hepatica)
Trypanosoma;
causes sleeping
sickness
Tapeworm
(Taenia)
1 cm
Amoeba;
10 m causes amoebic
Plasmodium dysentery
(in red blood cell);
causes malaria Ascaris
C. Protozoan pathogens D. Helminths
Candida Pneumocystis Aspergillus

E. Fungi
Table 26.1 Common Bacterial Pathogens

Name of Organism Disease(s) Remarks
Bacillus anthracis Anthrax Appears in cutaneous and respiratory forms
Borrelia burgdorferi Lyme disease Acquired from tick bites
Chlamydia trachomatis Venereal disease, eye infection Most common cause of sexually transmitted disease in the
United States
Enterococcus Wounds, urinary tract infections (UTI), Common opportunistic microbe, part of normal flora of the
endocarditis, bacteremia urogenital and intestinal tracts
Escherichia coli Traveler’s diarrhea, UTI, bacteremia, Part of normal flora of the intestinal tract
meningitis in children
Haemophilus Pneumonia, meningitis in children, Some species are part of the normal host flora of the upper
bacteremia, otitis media, sinusitis respiratory tract
Klebsiella Pneumonia, UTI Common opportunistic microbe
Mycobacterium tuberculosis Tuberculosis Incidence very high in patients infected with HIV
Mycoplasma pneumoniae Pneumonia Most common cause of pneumonia in patients ages 5 to 35
Neisseria gonorrhoeae Gonorrhea and other sexually transmitted Can be part of the normal host flora
diseases, endometriosis, neonatal eye infection
Neisseria meningitidis Meningitis in children Can be part of the normal host flora
Pneumococcus Pneumonia, otitis media, meningitis, Part of normal flora in upper respiratory tract
bacteremia, endocarditis
Proteus mirabilis UTI, skin infections Part of normal flora in the gastrointestinal (GI) tract
Pseudomonas aeruginosa UTI, skin infections, septicemia Common opportunistic microbe
Rickettsia rickettsii Rocky Mountain spotted fever Acquired from tick bites
Salmonella enteritidis Food poisoning From infected animal products, raw eggs, or undercooked
meat or chicken
Staphylococcus aureus Pneumonia, food poisoning, impetigo, wounds, Can be part of the normal host flora on the skin and mucous
bacteremia, endocarditis, toxic shock syndrome, membranes
osteomyelitis, UTI
Streptococcus Pharyngitis, pneumonia, skin infections, Some species are part of the normal host flora of the respira-
septicemia, endocarditis, otitis media tory, genital, and intestinal tracts
Table 26.2 Methods of Describing and Classifying Bacteria

Method Description
Staining Gram positive or gram negative
Shape Bacilli (rods), cocci (spheres), and spirilla (spirals)
Ability to use O2 Aerobic (uses O2) or anaerobic (without O2)
Anti-infective drugs are classified by their chemical structures

Core Concept 26.2 or by their mechanisms of action.
Anti-infective is a general term that applies to any drug that is effective against pathogens. In its broadest
sense, an anti-infective drug may be used to treat bacterial, fungal, viral, or parasitic infections. The most
anti 5 against frequent term used to describe an anti-infective drug is antibiotic. Technically, antibiotic refers to a natural
bio 5 life substance produced by bacteria that can kill other bacteria. In clinical practice, however, the terms antibac-
ic 5 pertaining to terial, anti-infective, antimicrobial, and antibiotic are often used interchangeably.
With more than 300 anti-infective drugs available, it is helpful to group these drugs into classes that have
similar properties. Two means of grouping are widely used: chemical classes and pharmacologic classes.
Chemical class names such as aminoglycosides, fluoroquinolones, and sulfonamides refer to the fun-
damental chemical structure of the anti-infectives. Anti-infectives belonging to the same chemical class
usually share similar antibacterial properties and adverse effects. Although chemical names are often long
and difficult to pronounce, placing drugs into chemical classes will assist the student in mentally organiz-
ing these drugs into distinct therapeutic groups.
Pharmacologic classes are used to group anti-infectives by their mechanism of action. Examples
include cell wall inhibitors, protein synthesis inhibitors, folic acid inhibitors, and reverse trancriptase
inhibitors. These classifications are used in this text, where appropriate.
Anti-infective drugs act by selectively targeting

a pathogen’s metabolism or life cycle. Core Concept 26.3
The primary goal of antimicrobial therapy is to assist the body’s defenses in eliminating a pathogen. Drugs
that accomplish this goal by killing bacteria are called bacteriocidal. Some medications do not kill the bac- bacterio 5 bacteria
teria but instead slow their growth, allowing the body’s natural defenses to eliminate the microorganisms. cidal 5 killing
These growth-slowing drugs are called bacteriostatic. static 5 staying the same
Bacterial cells are quite different from human cells. Bacteria have cell walls and contain certain
enzymes that human cells lack. Antibiotics exert selective toxicity on bacterial cells by targeting these
unique differences. Through this selective action, pathogens can be killed or their growth severely
hampered without major effects on human cells. Of course, there are limits to this selective toxicity,
depending on the specific antibiotic and the dose used, and adverse effects can be expected from all the
anti-infectives. The basic mechanisms of action of antimicrobial drugs are shown in Figure 26.2 ■.
Acquired resistance is a major clinical problem that is worsened

by improper use of anti-infectives. Core Concept 26.4
Microorganisms have the ability to replicate extremely rapidly. For example, under ideal conditions,
E. coli can produce a million cells every 20 minutes. During this rapid replication, bacteria make frequent
errors, or mutations, while duplicating their genetic code. These mutations occur spontaneously and ran-
domly in the bacterial cell. Although most mutations are harmful to the organism, mutations occasionally
result in a bacterial cell that has reproductive advantages over its neighbors. The mutated bacterium may be
able to survive in harsher conditions or perhaps grow faster than surrounding cells. One such mutation of par-
ticular importance to medicine is that which confers drug resistance on a microorganism.
Figure 26.2
5 4
Cell wall synthesis inhibitors DNA synthesis inhibitors
• Carbapenems • Fluoroquinolones
• Cephalosporins
• Isoniazid
• Penicillins
• Vancomycin
DNA
NA
Enzymes
En
Enz yme
yym
me
m es
o essential
or ess
ss
se
ent
nttia
n iial
al
metabolites
metabo
met abolit
abo littes
es
Replication
Rep
R licati
a on
3
Antimetabolites
Proteins
Protei
Proteins
• Sulfonamides
m
mRNA
1
RNA synthesis inhibitors
• Rifampin
2
Protein synthesis inhibitors
• Aminoglycosides
• Ketolides
• Macrolides
• Streptogramins
• Tetracyclines
Mechanisms of action of antimicrobial drugs.

Antibiotics help promote the appearance of drug-resistant bacterial strains by killing the masses of
bacteria that are sensitive to the drug. Consequently, the only bacteria remaining are those microbes that
possess mutations that make them insensitive to the effects of the antibiotic. These drug-resistant bacteria
are then free to grow faster because they are no longer competing for food with neighboring bacteria that
were killed by the antibiotic. Soon the patient develops an infection that is resistant to conventional drug
therapy. This phenomenon, called acquired resistance, is illustrated in Figure 26.3 ■. Bacteria may pass
the resistance gene to other bacteria by transferring small pieces of circular DNA called plasmids.
The widespread and sometimes unwarranted use of antibiotics has led to many resistant strains. For
example, 60% of all Staphylococcus bacteria are now resistant to penicillin. The longer an antibiotic is
used in the population and the more often it is prescribed, the larger will be the percentage of resistant
strains. Infections acquired in a hospital or other healthcare setting, called nosocomial infections, are
often resistant to common antibiotics. Two particularly serious resistant infections are those caused by
methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE).
Healthcare providers play important roles in delaying the emergence of resistance. The following are
four principles recommended by the Centers for Disease Control and Prevention (CDC):
■ Prevent infections whenever possible. It is always easier to prevent an infection than to treat
one. This includes teaching the patient the importance of getting immunizations.
■ Restrict the use of antibiotics to those conditions deemed medically necessary. Antibiotics
should be prescribed only when there is a clear rationale for their use.
■ Advise the patient to take anti-infectives for the full length of therapy, even if symptoms disap-
pear before the regimen is finished. Prematurely stopping antibiotic therapy allows some patho-
gens to survive, thus promoting the development of resistant strains.
■ Prevent transmission of the pathogen by using proper infection control procedures. This in-
cludes the use of standard precautions and teaching patients the methods of proper hygiene for
preventing transmission in the home and community settings.
In most cases, antibiotics are given when there is clear evidence of bacterial infection. Some patients,
however, receive antibiotics to prevent an infection, a practice called prophylactic use, or chemoprophyl
axis. Examples of patients who might receive prophylactic antibiotics include those who have suppressed
immune systems, have experienced deep puncture wounds such as dog bites, and have prosthetic heart
valves and are about to undergo medical or dental surgery.
Figure 26.3
Acquired resistance.
Resistant 1. Infection
organism
Antibotic
2. Antibiotic kills all organisms

except the resistant one.
Time
3. Resistant organism that remained

has rapidly divided to infect the patient.
Antibiotic is no longer effective.
Careful selection of the correct antibiotic is essential for effective

pharmacotherapy and to limit adverse effects. Core Concept 26.5
Selection of an antibiotic that will be effective against a specific pathogen is an important task of the
healthcare provider. Selecting an incorrect drug will delay proper treatment, giving the microorganisms
more time to invade. Prescribing ineffective antibiotics also promotes the development of resistance and
may cause unnecessary adverse effects in the patient.
Ideally, laboratory tests should be conducted to identify the organism prior to beginning anti-infective
therapy. Laboratory tests may include examination of body specimens such as urine, sputum, blood, or pus
for microorganisms. Organisms isolated from the specimens are grown in the laboratory and identified.
The laboratory then tests several antibiotics to determine which is most effective against the identified
pathogen. This process of growing the organism and identifying the effective antibiotic is called culture
and sensitivity (C&S) testing.
Ideally, the pathogen should be identified before anti-infective therapy is begun. However, laboratory
testing and identification may take several days and, in the case of viruses, several weeks. If the infection
is severe, therapy is often begun with a broad-spectrum antibiotic, one that is effective against a wide
variety of different microbial species. After laboratory testing is completed, the drug may be changed to a
narrow-spectrum antibiotic, one that is effective against a smaller group of microbes or only the isolated
species. In general, narrow-spectrum antibiotics have less effect on normal host flora, thus causing fewer
adverse effects.
In most cases, anti-infective therapy uses a single drug, because combining two antibiotics may
actually decrease each drug’s effectiveness. This phenomenon is known as antagonism. Use of multiple
antibiotics also has the potential to promote resistance. However, multidrug therapy is warranted if the
patient’s infection is caused by different organisms or if therapy must be started before C&S testing has
been completed. Multidrug therapy is common in the treatment of TB and HIV infection.
One common adverse effect of anti-infective therapy is the appearance of secondary infections,
called superinfections, which occur when microorganisms normally present in the body are killed by
the drug. These normal microorganisms, or host flora, inhabit the skin and the upper respiratory, uro-
genital, and intestinal tracts. Some of these organisms serve a useful purpose by producing antibacterial
substances and by competing with pathogenic organisms for space and nutrients. Removal of host flora
by an antibiotic gives pathogenic microorganisms space to grow or allows for overgrowth of nonaffected
normal flora. Appearance of a new infection while receiving anti-infective therapy is suspicious of a
superinfection. Signs and symptoms of a superinfection may include diarrhea, bladder pain, painful urina-
tion, or abnormal vaginal discharges. Broad-spectrum antibiotics are more likely to cause superinfections
because they kill so many different species of microorganisms. Figure 26.3 illustrates the production of a
superinfection.
The penicillins are one of the oldest and safest groups of anti-infectives. Core Concept 26.6
Although not the first anti-infective discovered, penicillin was the first mass-produced antibiotic. Iso-
lated from the fungus Penicillium in 1941, penicillin quickly became a miracle drug by preventing
thousands of deaths from what are now considered to be minor infections. The penicillins are listed in
Table 26.3 ◆.
Penicillins kill bacteria by disrupting their cell walls. The chemical structure of penicillin that is re-
sponsible for its antibacterial activity is called the beta-lactam ring. However, some bacteria secrete an
enzyme, called beta-lactamase/penicillinase, which splits the beta-lactam ring. This structural change al-
lows these bacteria to become resistant to the effects of most penicillins. The action of penicillinase is il-
lustrated in Figure 26.4 ■. Since their discovery, large numbers of resistant bacterial strains that limit the
therapeutic usefulness of the penicillins have emerged.
Chemical modifications to the natural penicillin molecule produced drugs offering several advantages.
■ Penicillinase-resistant penicillins Oxacillin and cloxacillin (Cloxapen) are examples of drugs
that are effective against penicillinase-producing bacteria. These are sometimes called antista
phylococcal penicillins.
■ Broad-spectrum penicillins Ampicillin (Principen) and amoxicillin (Amoxil, Trimox) are effec-
tive against a wide range of microorganisms and are called broad-spectrum penicillins. These are
sometimes referred to as aminopenicillins.
■ Extended-spectrum penicillins Carbenicillin (Geocillin) and piperacillin are effective against
even more microbial species than the aminopenicillins, including Pseudomonas, Enterobacter,
Klebsiella, and Bacteroides fragilis.
Several drugs are available that inhibit the bacterial beta-lactamase enzyme. When combined with
penicillin, these drugs protect the penicillin molecule from destruction, extending its spectrum of activity.
Table 26.3 Penicillins

amoxicillin (Amoxil, Trimox) PO; 250–500 mg tid Broad-spectrum penicillin
amoxicillin–clavulanate (Augmentin) PO; 250–500 mg every 8–12 hours Broad-spectrum penicillin with a beta-
lactamase inhibitor
ampicillin (Principen) PO; 250–500 mg qid Broad-spectrum penicillin; IM and IV forms
available
ampicillin–sulbactam (Unasyn) IV/IM; 1.5–3 g qid Broad-spectrum penicillin
dicloxacillin PO; 125–500 mg qid Penicillinase resistant
nafcillin IV/IM; 500 mg–1 g qid (max: 12 g/day) Penicillinase resistant; IM and IV forms
available
oxacillin IV; 250 mg–1 g every 4–6 hours (max: Penicillinase resistant; IV and IM forms
12 g/day) available
penicillin G benzathine (Bicillin) IM; 1.2 million units as a single dose Prolonged duration of action
penicillin G potassium IV/IM; 2–24 million units divided every Ineffective against most forms of S. aureus
4–6 hours
penicillin G procaine (Wycillin) IM; 600,000–1.2 million units daily Prolonged duration of action
penicillin V (Pen-Vee K, Veetids, others) PO; 125–500 mg qid Acid stable
piperacillin IM; 2–4 g tid–qid (max: 24 g/day) Extended-spectrum penicillin
piperacillin–tazobactam (Zosyn) IV; 3.375–4.5 g qid over 30 minutes Extended-spectrum penicillin with a beta-
lactamase inhibitor
ticarcillin–clavulanate (Timentin) IV; 3.1 g qid Extended-spectrum penicillin with a beta-
lactamase inhibitor
Figure 26.4
O
S CH3
C C NH CH CH C
H2 CH3 Penicillin G; b-lactam ring gives
C N CH COOH antibiotic activity
O
b-Lactam ring
Resistant bacteria: Penicillinase/b-lactamase
O
S CH3
C C NH CH HC C
H2 CH3 b-Lactam ring broken, antibiotic activity is lost
O C N CH COOH
H
OH
Action of penicillinase.
CAM THERAPY
The Antibacterial Properties of Goldenseal
Goldenseal (Hydrastis canadensis) was once a common plant found in woods in the eastern
and midwestern United States. As word spread of its medicinal properties, the plant was har-
vested to near extinction. In particular, goldenseal was reported to mask the appearance of
drugs in the urine of patients wanting to hide their drug abuse. This claim has been proven
false.
The roots and leaves of goldenseal are dried and available as capsules, tablets, salves,
and tinctures. One of the primary ingredients in goldenseal is hydrastine, which is reported
to have antibacterial and antifungal properties. When used topically or locally, it is claimed
to be of value in treating bacterial and fungal skin infections and oral conditions such as
gingivitis and thrush. Other possible indications include hypertension, duodenal ulcers, and
conjunctivitis.
Drug Prototype: Penicillin G Sodium/Potassium

Therapeutic Class: Antibacterial Pharmacologic Class: Cell wall inhibitor, natural penicillin
Actions and Uses: Similar to penicillin V, penicillin G is some- Adverse Effects and Interactions: Penicillin G has few adverse
times a drug of first choice against streptococcal, pneumo- effects. Although not serious, diarrhea, nausea, and vomit-
cocci, and staphylococcal organisms that do not produce ing are the most common adverse effects. Anaphylaxis is the
penicillinase and are shown to be susceptible by C&S testing. most serious adverse effect, although its incidence is very low.
It is also a preferred drug for gonorrhea and syphilis caused Pain at the injection site may occur, and superinfections are
by susceptible strains. Penicillin V is more acid stable; over possible.
70% is absorbed after an oral dose compared to the 15% to Penicillin G may decrease the effectiveness of oral
30% from penicillin G. Because of its low oral absorption, contraceptives. Colestipol decreases absorption of penicillin
penicillin G is often given by the IV or IM routes. Penicillinase- G. Potassium-sparing diurectics may cause hyperkalemia with
producing organisms inactivate both penicillin G and penicillin G. Food increases the breakdown of penicillin in the
penicillin V. stomach. Probenecid decreases renal excretion of penicillin G.
The three beta-lactamase inhibitors—clavulanate, sulbactam, and tazobactam—are only available in fixed-
dose combinations with specific penicillins. These include Augmentin (amoxicillin plus clavulanate),
Timentin (ticarcillin plus clavulanate), Unasyn (ampicillin plus sulbactam), and Zosyn (piperacillin plus
tazobactam).
In general, the adverse effects of penicillins are minor, and this has contributed to their widespread
use for more than 60 years. Allergy is the most common adverse effect. Symptoms of penicillin allergy
may include rash, fever, and anaphylaxis. The incidence of anaphylaxis is quite low, ranging from 0.04%
to 2%. Allergy to one penicillin increases the risk of allergy to other drugs in the same class. Other less
common adverse effects of the penicillins include skin rashes and lowered red blood cell, white blood cell,
or platelet counts.
Concept Review 26.1

■ Why does antibiotic resistance become more of a problem when antibiotics are prescribed
too often?
The cephalosporins are similar in structure and function to the penicillins

and are one of the most widely prescribed anti-infective classes. Core Concept 26.7
Isolated shortly after the penicillins, the four generations of cephalosporins comprise the largest antibiotic
class. Like the penicillins, the cephalosporins contain a beta-lactam ring that is primarily responsible for
their antimicrobial activity. The cephalosporins are bacteriocidal and inhibit bacterial cell wall synthesis.
Table 26.4 ◆ lists the cephalosporins and their dosages.
Table 26.4 Selected Cephalosporins

First Generation
cefadroxil (Duricef) PO; 500 mg–1 g once or twice daily Binds to bacterial cell walls; bacteriocidal
(max: 2 g/day)
cefazolin (Ancef, Kefzol) IM; 250 mg–2 g tid (max: 12 g/day) IV form available
cephalexin (Keflex) PO; 250–500 mg qid Binds to bacterial cell walls; bacteriocidal; broad spectrum
Second Generation
cefaclor (Ceclor) PO; 250–500 mg tid Binds to bacterial cell walls; extended-release form available;
bacteriocidal
cefotetan (Cefotan) IM; 1–2 g every 12 hours IV form available
cefprozil (Cefzil) PO; 250–500 mg once or twice daily Binds to bacterial cell walls; bacteriocidal
cefuroxime (Ceftin, Zinacef) PO; 250–500 mg bid Binds to bacterial cell walls; IM and IV forms available;
bacteriocidal
Third to FIFTH Generations
cefdinir (Omnicef) PO; 300 mg bid Third generation; broad spectrum
cefditoren (Spectracef) PO; 400 mg bid for 10 days Third generation
cefepime (Maxipime) IM; 0.5–1 g bid (max: 3 g/day) Fourth generation; IV form available
cefixime (Suprax) PO; 400 mg daily or 200 mg bid Third generation; binds to bacterial cell walls; bacteriocidal
cefotaxime (Claforan) IM; 1–2 g bid–tid (max: 12 g/day) Third generation; binds to bacterial cell walls; bacteriocidal;
IV form available
ceftaroline (Teflaro) IV; 600 mg every 12 hours for 5–14 days Fifth generation; broad spectrum effective against MRSA
ceftriaxone (Rocephin) IM; 1–2 g once or twice daily Third generation; binds to bacterial cell walls; IV form also
(max: 4 g/day) available; bacteriocidal
More than 20 cephalosporins are available, all having similar sounding names that can challenge
even the best memory. They are classified by their “generation.” The first-generation drugs contain a
beta-lactam ring, and bacteria that produce beta-lactamase will normally be resistant to these medications.
The second-generation cephalosporins are more potent and more resistant to beta-lactamase and exhibit
a broader spectrum than the first-generation drugs. The third-generation cephalosporins generally have a
longer duration of action, an even broader spectrum, and are resistant to beta-lactamases. Third-generation
cephalosporins are preferred drugs against infections by Pseudomonas, Klebsiella, Neisseria, Salmonella,
Drug Prototype: Cefotaxime (Claforan)

Therapeutic Class: Antibacterial Pharmacologic Class: Cell wall inhibitor; third-generation cephalosporin
Actions and Uses: Cefotaxime is a third-generation cephalo- Adverse Effects and Interactions: For most patients, cefotaxime
sporin with a broad spectrum of activity against gram-negative and the other cephalosporins are safe medications. Hypersensitiv-
organisms. It is effective against many organisms that have ity is the most common adverse effect, although symptoms may
developed resistance to earlier generation cephalosporins and include only a minor rash and itching. Anaphylaxis is possible;
to other classes of anti-infectives. Cefotaxime exhibits bacte- thus, the healthcare provider should be alert for this reaction.
riocidal activity by inhibiting cell wall synthesis. It is prescribed GI-related adverse effects such as diarrhea, vomiting, and nausea
for serious infections of the lower respiratory tract, central may occur. Some patients experience considerable pain at the
nervous system (CNS), urogenital system, bones, and joints. It injection site.
may also be used for blood infections such as bacteremia or Probenecid decreases elimination by the kidneys. Alcohol
septicemia. Like many of the cephalosporins, cefotaxime is not interacts with cefotaxime to produce a disulfiram-like reaction.
absorbed from the GI tract and must be given by the IM or IV Cefotaxime interacts with nonsteroidal anti-inflammatory drugs
routes. (NSAIDs) to cause an increase in platelet inhibition.
Proteus, and Haemophilus influenzae. Newer, fourth- and fifth-generation drugs are more effective against
organisms that have developed resistance to earlier cephalosporins. There are not always clear distinctions
between the generations.
The primary therapeutic use of the cephalosporins is for gram-negative infections and for patients who
cannot tolerate the less expensive penicillins. Like the penicillins, allergic reactions are the most common
adverse effect. Skin rashes are a common sign of allergy and may appear several days following the initiation
of therapy. GI complaints are common. Earlier generation cephalosporins exhibited kidney toxicity, but this is
diminished with the newer drugs. The nurse must be aware that some patients (5% to 10%) who are allergic to
penicillin will also be allergic to cephalosporins. Despite this small incidence of cross allergy, cephalosporins
offer a reasonable alternative for most patients who are unable to take penicillins. However, cephalosporins
are contraindicated if the patient has previously experienced a severe allergic reaction to a penicillin.
The tetracyclines have broad spectrums but are drugs

of choice for few diseases. Core Concept 26.8
The first tetracyclines were extracted from Streptomyces soil microorganisms in 1948. Their widespread
use in the 1950s and 1960s has resulted in a large number of resistant bacterial strains that now limits their
therapeutic usefulness. Table 26.5 ◆ lists the tetracyclines and their dosages.
Tetracyclines exert a bacteriostatic effect by inhibiting bacterial protein synthesis. They are effective
against a wide range of gram-negative and gram-positive organisms and have one of the broadest spec-
trums of any class of antibiotics. They are drugs of first choice for relatively few diseases, including Rocky
Mountain spotted fever, typhus, cholera, Lyme disease, ulcers caused by Helicobacter pylori, and Chla-
mydia infections. Drugs in this class are occasionally used for the treatment of acne vulgaris, for which
they are given topically or PO at low doses. Minocycline (Arestin) and doxycycline (Atridox, Periostat) are
used to treat periodontal disease. The newest tetracycline, tigecycline (Tygacil) is approved to treat drug-
resistant intra-abdominal infections and complicated skin infections, especially those caused by MRSA.
Table 26.5 Tetracyclines

demeclocycline (Declomycin) PO; 150–300 mg bid–qid (max: 2.4 g/day) Intermediate duration of action; broad spectrum
doxycycline (Vibramycin, PO; 100 mg bid on day 1, then 100 mg daily Long duration of action; IV form available; subgingival form
others) (max: 200 mg/day) available for periodontitis
minocycline (Minocin, others) PO; 200 mg as one dose followed by Long duration of action; IV form available; available as
100 mg bid microsphere powder for periodontitis and as extended-release
tablet for acne
tetracycline (Sumycin) PO; 250–500 mg bid–qid (max: 2 g/day) Short acting; inhibits protein synthesis; bacteriostatic; IM and
topical forms available
tigecycline (Tygacil) IV; 100 mg, followed by 50 mg every Newest tetracycline; very limited indications
12 hours
Drug Prototype: Tetracycline (Sumycin, Others)

Therapeutic Class: Antibacterial Pharmacologic Class: Tetracycline, protein synthesis inhibitor
Actions and Uses: Tetracycline is effective against many dif- oral, and intestinal flora and cause superinfections. Diarrhea
ferent microorganisms, including some protozoans. Its use has may be severe enough to cause discontinuation of therapy.
increased over the past decade due to its effectiveness against Other common adverse effects include nausea, vomiting,
H. pylori in the treatment of peptic ulcer disease. It is given and photosensitivity.
orally and has a short half-life. A topical preparation is available Tetracycline can decrease the effectiveness of oral contra-
for treating acne. When given PO, it should be administered at ceptives, and thus alternative precautions should be taken dur-
least one hour before or two hours after a meal to avoid drug ing therapy to prevent pregnancy. Pregnant patients and those
interactions. who are breastfeeding should not take tetracyclines because
they are pregnancy category D medications.
Adverse Effects and Interactions: As a broad-spectrum
antibiotic, tetracycline has a tendency to affect vaginal,
The tetracyclines cause few serious adverse effects. Gastric distress is relatively common with tetra-
cyclines, so patients tend to take tetracyclines with food. Patients should be urged not to drink milk with
these medications because tetracyclines bind ions such as calcium and iron, thereby decreasing the drug’s
absorption by as much as 50%. Patients should be advised to avoid direct exposure to sunlight because
tetracyclines can cause photosensitivity, which makes the skin particularly susceptible to sunburn. Unless
suffering from a life-threatening infection, patients younger than 9 years are not given tetracyclines because
these drugs may cause permanent yellow-brown teeth discoloration in young children. These drugs are
pregnancy category D drugs; tetracyclines should not be used during pregnancy. Because of their broad
spectrum, the risk for superinfection is relatively high, and nurses should always be observant for signs of
a secondary infection. Outdated tetracycline may deteriorate and become nephrotoxic; therefore, unused
prescriptions should be discarded promptly.
The macrolides are safe alternatives to penicillin for many

Core Concept 26.9 infections.
Erythromycin (E-Mycin, Erythrocin), the first macrolide antibiotic, was isolated from Streptomcyes in a
soil sample in 1952. Macrolides are prescribed for infections that are resistant to penicillins. Commonly
prescribed macrolides are listed in Table 26.6 ◆.
Table 26.6 Macrolides

azithromycin (Zithromax, PO (Zithromax); 500 mg for one dose, then Inhibits protein synthesis; bacteriostatic; IV form available
Zmax) 250 mg daily for 4 days
PO (Zmax): 1–2 g single dose
clarithromycin (Biaxin) PO; 250–500 mg bid Inhibits protein synthesis; bacteriostatic; part of regimen for
Helicobacter pylori infections
erythromycin (E-Mycin, PO; 250–500 mg qid or 333 mg tid Bacteriostatic or bacteriocidal depending on nature of
Erythrocin) organism and drug concentration; IV form available
fidaxomicin (Dificid) PO; 200 mg bid Newer drug in this class for treatment of
pseudomembranous colitis or Clostridium difficile–
associated diarrhea
Drug Prototype: Erythromycin (E-Mycin, Erythrocin)

Therapeutic Class: Antibacterial Pharmacologic Class: Macrolide protein synthesis inhibitor
Actions and Uses: Erythromycin is inactivated by stomach acid vomiting, although these are rarely serious enough to cause dis-
and is thus administered as coated tablets or capsules that discontinuation of therapy. Concurrent administration with food
solve in the small intestine. The drug’s main application is for reduces these symptoms. Its spectrum of activity is similar to
patients who are allergic to penicillins or who may have a that of the penicillins.
penicillin-resistant infection. It is a preferred drug for infections Anesthetics and anticonvulsant drugs may interact to cause
by Bordetella pertussis (whooping cough), Legionella pneu- serum drug levels to rise and result in toxicity. This drug inter-
mophila (Legionnaire’s disease), Mycoplasma pneumoniae, and acts with cyclosporine, increasing the risk for kidney toxicity.
Corynebacterium diphtheriae. It may increase the effects of warfarin. The concurrent use of
erythromycin with lovastatin or simvastatin is not recommended
Adverse Effects and Interactions: The most common adverse because it may increase the risk of muscle toxicity.
effects from erythromycin are nausea, abdominal cramping, and
The macrolide antibiotics inhibit bacterial protein synthesis and may be either bacteriocidal or bac-
teriostatic, depending on the dose and the target organism. Macrolides are considered safe alternatives to
penicillin, although they are drugs of first choice for relatively few infections. Common uses of macrolides
include the treatment of whooping cough, Legionnaire’s disease, and infections by Streptococcus, H. in-
fluenzae, M. pneumoniae, and Chlamydia. Clarithromycin is one of several antibiotics used to treat peptic
ulcer disease.
The macrolides exhibit no serious adverse effects. Mild GI upset, diarrhea, and abdominal pain are
the most common adverse effects. Because macrolides are broad-spectrum drugs, patients should be
observed for signs of superinfection. Like most of the older antibiotics, macrolide-resistant strains are
becoming more common. Other than prior allergic reactions to macrolides, there are no contraindica-
tions to therapy.
The newer macrolides have a longer half-life and cause less GI irritation than erythromycin. For ex-
ample, azithromycin (Zithromax) has such an extended half-life that it can be administered for only 5 days,
rather the 10 days required for most antibiotics. Even shorter durations, often a single dose, are sometimes
used when azithromycin (Zmax) is administered to treat gonorrhea, otitis media, or acute bacterial sinusitis.
The shorter duration of therapy is thought to increase patient adherence.
Concept Review 26.2

■ If penicillins are inexpensive, why might a healthcare provider prescribe a more expensive
cephalosporin or macrolide antibiotic?
The aminoglycosides are narrow-spectrum drugs that have

the potential to cause serious toxicity. Core Concept 26.10
The aminoglycosides, first isolated from soil organisms in 1942, share a common chemical structure of an
amino group (NH2) and a sugar group. Although more toxic than most other antibiotic classes, they have
important therapeutic applications for the treatment of a number of aerobic gram-negative bacteria, myco-
bacteria, and some protozoans. Table 26.7 ◆ lists the aminoglycosides and their dosages.
Aminoglycosides are bacteriocidal and act by inhibiting bacterial protein synthesis. They are normally
reserved for serious aerobic gram-negative infections, including those caused by E. coli, Serratia, Proteus,
Klebsiella, and Pseudomonas. When used for systemic bacterial infections, they are given parenterally
because they are poorly absorbed from the GI tract. They are occasionally given orally to sterilize the
bowel before intestinal surgery. Neomycin is available for topical infections of the skin, eyes, and ears.
Paromomycin (Humatin) is given orally for the treatment of parasitic infections. The first aminoglycoside,
streptomycin, was once widely prescribed, but its use is now limited to the treatment of TB due to the
development of a large number of resistant strains. The student should note the differences in spelling of
some of these drugs, from -mycin to -micin, which reflects the different organisms from which the drugs
were originally isolated.
Table 26.7 Aminoglycosides

amikacin (Amikin) IM; 5–7.5 mg/kg as a loading dose, then Broader spectrum than others in this class; usually
7.5 mg/kg bid bacteriocidal; IV form available
gentamicin (Garamycin) IM; 1.5–2 mg/kg as a loading dose, then IV, topical, and ophthalmic forms available
1–2 mg/kg bid–tid
kanamycin (Kantrex) IM; 5–7.5 mg/kg bid–tid Also used to sterilize the bowel prior to colon surgery; oral,
inhalation, and IV forms available
neomycin PO; 4–12 g/day in divided doses Oral, topical, and IV forms available
paromomycin (Humatin) PO; 7.5–12.5 mg/kg tid For parasitic infections of the intestine; also used to treat
hepatic coma
streptomycin IM; 15 mg/kg up to 1 g as a single dose For tuberculosis, tularemia, and plague
tobramycin (Tobrex) IM/IV; 3 mg/kg tid (max: 5 mg/kg/day) Most effective aminoglycoside against P. aeruginosa
Drug Prototype: Gentamicin (Garamycin)

Therapeutic Class: Antibacterial Pharmacologic Class: Aminoglycoside, protein synthesis inhibitor
Actions and Uses: Gentamicin is a broad-spectrum, bacteriocidal be alert for signs of nephrotoxicity because this may limit drug
antibiotic usually prescribed for serious urinary, respiratory, therapy with gentamicin.
nervous, or GI infections. Activity includes Enterobacter, E. coli, Using this drug together with amphotericin B, cap
Klebsiella, Citrobacter, Pseudomonas, and Serratia. It is often reomycin, cisplatin, polymyxin B, or vancomycin increases
used in combination with other antibiotics or when other anti- the risk of nephrotoxicity. The risk of ototoxicity increases
biotics have proven ineffective. A topical formulation (Genop- if the patient is currently taking amphotericin B, furose
tic) is available for infections of the external eye. mide, aspirin, bumetanide, ethacrynic acid, cisplatin, or
paromomycin.
Adverse Effects and Interactions: As with other aminoglyco-
sides, adverse effects from gentamicin may be severe. Ototox-
icity is possible and may become permanent with continued Black Box Warning:
use. Ringing in the ears, dizziness, and persistent headaches Adverse effects from parenteral gentamicin may be severe
are early signs of ototoxicity. Frequent hearing tests should be and include neurotoxicity, neuromuscular blockade, and
conducted so that gentamicin may be discontinued if early signs nephrotoxicity.
of ototoxicity are detected. The healthcare provider must also
The clinical applications of the aminoglycosides are limited by their potential to cause serious adverse
effects. The degree and types of potential toxicity are similar for all drugs in this class. Of greatest concern
oto 5 ear are their effects on the inner ear and the kidney. Damage to the inner ear, or ototoxicity, causes hearing
toxicity 5 poison impairment, dizziness, loss of balance, persistent headache, and ringing in the ears. Because permanent deaf-
ness may occur, aminoglycosides are usually discontinued when symptoms of hearing impairment first ap-
nephron 5 kidney pear. Kidney damage, or nephrotoxicity, is recognized by abnormal urinary function tests, such as elevated
serum creatinine or blood urea nitrogen (BUN). Nephrotoxicity caused by aminoglycosides is usually revers-
ible. Serum drug levels are sometimes monitored during therapy to prevent toxic doses of these antibiotics.
Fluoroquinolones have wide clinical applications because of their broad

Core Concept 26.11 spectrum of activity and relative safety.
The fluoroquinolones were once reserved only for urinary tract infections (UTIs) because of their toxicity.
However, the newer fluoroquinolones are safer, have a broader spectrum of activity, and are used for a
variety of infections. The fluoroquinolones are listed in Table 26.8 ◆.
Table 26.8 Fluoroquinolones

ciprofloxacin (Cipro) PO; 250–750 mg bid For lung, skin, bone, and joint infections, and for anthrax;
broad spectrum; IV form available
gatifloxacin (Zymar) PO; 400 mg tid For respiratory infections, UTI, and gonorrhea; IV form
available
gemifloxacin (Factive) PO; 320 mg daily For respiratory infections
levofloxacin (Levaquin) PO; 250–500 mg daily For respiratory tract and skin infections; IV form available
moxifloxacin (Avelox, Moxeza, PO/IV; 400 mg daily For sinus and respiratory tract infections; otic drops
Vigamox) available
nalidixic acid (NegGram) PO; acute therapy: 1 g qid; PO; chronic For UTI
therapy: 500 mg qid
norfloxacin (Noroxin) PO; 400 mg bid For UTI; ophthalmic form available
ofloxacin (Floxin) PO; 200–400 mg bid For UTI, respiratory tract infections, and gonorrhea; otic
drops available
Drug Prototype: Ciprofloxacin (Cipro)

Therapeutic Class: Antibacterial Pharmacologic Class: Fluoroquinolone, bacterial DNA synthesis inhibitor
Actions and Uses: Ciprofloxacin (Cipro), a second-generation antacids or mineral supplements because drug absorption will be
fluoroquinolone, is the most widely used drug in this class. diminished. Some patients report headache and dizziness.
Ciprofloxacin inhibits bacterial replication and DNA repair and Using this drug with warfarin may increase warfarin’s
is more effective against gram-negative than gram-positive anticoagulant effects and result in bleeding. Antacids, ferrous
organisms. It is prescribed for respiratory infections, bone and sulfate, and sucralfate decrease the absorption of ciprofloxacin.
joint infections, GI infections, ophthalmic infections, sinusitis, Caffeine should be restricted to avoid excessive nervousness,
and prostatitis. It is rapidly absorbed after oral administration, anxiety, or tachycardia.
and an IV form is available for severe infections. An extended-
release form of the drug, Proquin XR, is administered for only
three days and is approved for bladder infections. Black Box Warning:
Tendinitis and tendon rupture may occur, especially in pa-
Adverse Effects and Interactions: Ciprofloxacin is well toler- tients over age 60; in kidney, heart, and lung transplant
ated by most patients, and serious adverse effects are uncom- recipients; and in those receiving concurrent corticosteroid
mon. Nausea, vomiting, and diarrhea may occur in as many as therapy. Fluoroquinolones may cause extreme muscle weak-
20% of patients. Ciprofloxacin may be administered with food ness in patients with myasthenia gravis.
to lessen adverse GI effects; however, it should not be taken with
The first drug in this class, nalidixic acid (NegGram), was approved in 1962, but its use is restricted to
UTIs. Four generations of fluoroquinolones have since become available. All fluoroquinolones have activ-
ity against gram-negative pathogens; the newer ones are significantly more effective against gram-positive
microbes.
The fluoroquinolones are bacteriocidal and act by inhibiting bacterial DNA synthesis. These antibiot-
ics are extensively used as alternatives to other antibiotics. Clinical applications include infections of the
respiratory, GI, and gynecologic tracts, and some skin and soft-tissue infections.
The most widely used drug in this class, ciprofloxacin (Cipro), is a preferred drug for exposure to
anthrax (Bacillus anthracis), a potential bioterrorist threat. If exposure to anthrax is suspected, 500 mg
of ciprofloxacin is administered by the oral route every 12 hours for 60 days. If exposure is confirmed,
ciprofloxacin is immediately administered IV, 400 mg every 12 hours. Other antibiotics are also ef-
fective against anthrax, including penicillin, vancomycin, ampicillin, erythromycin, tetracycline, and
doxycycline.
A major advantage of the fluoroquinolones is that most are well absorbed orally and may be
administered either once or twice daily. They should not be taken together with multivitamins or
mineral supplements because these interact to reduce the absorption of some fluoroquinolones by as
much as 90%.
Fluoroquinolones are safe for most patients, with nausea, vomiting, and diarrhea being the most fre-
quent adverse effects. The most serious adverse effects are dysrhythmias (for gatifloxacin and moxifloxa-
cin) and potential hepatotoxicity. Fluoroquinolones have been shown to exhibit cartilage toxicity, resulting
in an increased risk of tendonitis and tendon rupture, particularly of the Achilles tendon. The risk of ten-
don rupture is especially increased in patients over age 60 and those receiving concurrent corticosteroids.
Because they may affect cartilage development, these drugs are not approved for children under age 18.
Fluoroquinolones are pregnancy category C and their use should be avoided during pregnancy or in lactat-
ing patients.
Sulfonamides and urinary antiseptics are traditional

drugs for urinary tract infections. Core Concept 26.12
The discovery of the sulfonamides in the 1930s heralded a new era in the treatment of infectious
disease. With their wide spectrum of activity, the sulfonamides significantly reduced deaths due to
infections and earned their discoverer a Nobel Prize in medicine. The sulfonamides are listed in
Table 26.9 ◆. Sulfonamides suppress bacterial growth by inhibiting folic acid, an essential substance
in cellular metabolism.
Table 26.9 Sulfonamides and Urinary Antiseptics

Sulfonamides
silver sulfadiazine Topical; Apply cream 1–2 times per day to For prevention of sepsis in patients with serious burns
thickness of 1.5 mm
sulfadiazine PO; 2–4 g daily in 4–6 divided doses Also for malaria, toxoplasmosis, and prophylaxis of
rheumatic fever
sulfadoxine–pyrimethamine PO; 1 tablet weekly (500 mg sulfadoxine, Also for prevention and treatment of malaria
(Fansidar) 25 mg pyrimethamine)
sulfasalazine (Azulfidine) PO; 1–2 g/day in four divided doses Also for ulcerative colitis and rheumatoid arthritis
(max: 8 g/day)
sulfisoxazole (Gantrisin) PO; 2–4 g initially, followed by 1–2 g qid For UTI; short acting; vaginal form available
trimethoprim-sulfamethoxazole PO; 160 mg TMP/800 mg SMZ bid Combination drug; for UTI, Pneumocystis, and ear
(Bactrim, Septra) infections; IV form available
Urinary antiseptics
fosfomycin (Monurol) PO; 3 g sachet dissolved in 3–4 oz of water Bactericidal; for UTI
as a single dose
methenamine (Mandelamine, Hiprex, PO; hippurate 1 g bid; mandelate 1 g qid For chronic UTI; broad spectrum
Urex)
nalidixic acid (NegGram) PO; acute therapy: 1 g qid; PO; chronic Urinary antiseptic; similar to the fluoroquinolones
therapy: 500 mg qid
nitrofurantoin (Furadantin, Macrobid, PO; 50–100 mg qid For UTI; extended-release form available; interferes
Macrodantin) with bacterial enzymes
Although initially very effective, several factors led to a significant decline in the use of sulfonamides.
Their widespread availability over 70 years produced a substantial number of resistant bacterial strains.
The development of the penicillins, cephalosporins, and macrolides gave healthcare providers greater
choices of safer drugs. Approval of the combination antibiotic trimethoprim–sulfamethoxazole (Bactrim,
Septra) marked a resurgence in the use of sulfonamides in treating UTIs. In communities with high resis-
tance rates, trimethoprim–sulfamethoxazole is no longer a first-line drug, unless C&S testing determines it
to be the most effective drug for the specific pathogen.
Drug Prototype: Trimethoprim–Sulfamethoxazole (Bactrim, Septra)

Therapeutic Class: Antibacterial Pharmacologic Class: Sulfonamide, folic acid inhibitor
Actions and Uses: The combination of sulfamethoxazole (SMZ), Adverse Effects and Interactions: Nausea and vomiting are
a sulfonamide, with the anti-infective trimethoprim (TMP) is the most frequent adverse effects of TMP–SMZ therapy. Hyper-
most frequently used in the pharmacotherapy of UTIs. It is also sensitivity is relatively common and usually manifests as skin
approved for the treatment of Pneumocystis carinii pneumonia, rash, itching, and fever. This medication should be used cau-
Shigella infections of the small bowel, and acute episodes of tiously in patients with preexisting kidney disease, because
bronchitis. sulfonamides can adversely affect renal function. Periodic labo-
Both SMZ and TMP are inhibitors of the bacterial metabo- ratory evaluations are usually performed to identify early signs
lism of folic acid. Combining the two drugs produces a greater of adverse blood effects.
bacterial kill than would be achieved with either drug used TMP and SMZ may increase the effects of oral anticoagu-
separately. Another advantage of the combination is that devel- lants. These drugs may also increase methotrexate toxicity.
opment of resistance is lower than is observed when either of Potassium supplements should not be taken during therapy,
the drugs is used alone. unless directed by the healthcare provider.
Sulfonamides are classified by their route of administration: systemic or topical. Systemic medi-
cations, such as sulfisoxazole (Gantrisin) and trimethoprim–sulfamethoxazole, are readily absorbed
when given PO and excreted rapidly by the kidney. Other sulfonamides such as silver sulfadiazine
(Silvadene) are used only for topical infections. The topical sulfonamides are rarely used because
many patients are allergic to substances containing sulfur. One drug in this class, sulfadoxine–
pyrimethamine (Fansidar), has an exceptionally long half-life and is occasionally prescribed for
malarial prophylaxis.
In general, the sulfonamides are safe medications; however, some adverse effects may be serious.
Adverse effects include the formation of crystals in the urine, allergic reactions, nausea, and vomiting.
Although not common, potentially fatal blood abnormalities, such as aplastic anemia, acute hemolytic ane-
mia, and agranulocytosis, can occur.
Urinary antiseptics are drugs given by the PO route for their antibacterial action in the urinary tract.
The kidney concentrates the drugs; thus, their actions are specific to the urinary system. Urinary antisep-
tics reach therapeutic levels in the kidney tubules, and their anti-infective action continues as they travel
to the urinary bladder. Although not considered first-line drugs for UTI, they serve important roles as
secondary medications, especially in patients who present with infections resistant to TMP–SMZ or the
fluoroquinolones.
A number of additional anti-infectives have distinct mechanisms

of action and specific indications. Core Concept 26.13
Some anti-infectives cannot be grouped into classes, or the class is too small to warrant separate discus-
sion. That is not to diminish their importance in medicine; some of these miscellaneous anti-infectives are
critical drugs for specific infections. For example, clindamycin (Cleocin) is sometimes the drug of choice
for oral infections caused by Bacteroides species. It is considered to be appropriate treatment when less
toxic alternatives are not effective. Vancomycin (Vancocin) is an antibiotic usually reserved for severe
infections from gram-positive organisms such as S. aureus and Streptococcus pneumoniae. It is often used
after bacteria have become resistant to other, safer antibiotics. Vancomycin is the most effective drug for
treating MRSA infections.
Several miscellaneous drugs represent newer classes of antibiotics. Linezolid (Zyvox) is the first
drug in a class called the oxazolidinones. This drug is effective against MRSA infections. Quinupristin–
dalfopristin (Synercid) is a combination drug that is the first in an antibiotic class called streptogramins.
This drug is primarily indicated for treatment of vancomycin-resistant Enterococcus faecalis infec-
tions. Daptomycin (Cubicin) is the first in a newer class of antibiotics called the cyclic lipopeptides. It is
approved for the treatment of serious skin and skin-structure infections such as major abscesses, postsurgi-
cal skin-wound infections, and infected ulcers. Table 26.10 ◆ lists some of these miscellaneous antibiotics
and their dosages.
Drug Prototype: Vancomycin (Vancocin)

Therapeutic Class: Antibiotic Pharmacologic Class: Bacterial cell wall synthesis inhibitor
Actions and Uses: Vancomycin is usually reserved for severe Adverse Effects and Interactions: Frequent, minor side effects
infections from gram-positive organisms such as S. aureus and include flushing, hypotension, and rash on the upper body, some-
Streptococcus pneumoniae. It is often used after bacteria have times called red-man syndrome. More serious adverse effects are
become resistant to other safer antibiotics. It is bacteriocidal, possible with higher doses, including nephrotoxicity and oto-
inhibiting bacterial cell wall synthesis. Because vancomycin toxicity. Some patients experience an acute allergic reaction and
was not used frequently during the first 30 years following its even anaphylaxis.
discovery, the incidence of vancomycin-resistant organisms is Vancomycin adds to toxicity of aminoglycosides, ampho-
smaller than with other antibiotics. Vancomycin is the most tericin B, cisplatin, cyclosporine, polymyxin B, and other ototoxic
effective drug for treating MRSA infections. Vancomycin- and nephrotoxic medications. Cholestyramine and colestipol can
resistant strains of S. aureus, however, have begun to appear in decrease the absorption of vancomycin.
recent years. Vancomycin is normally given IV because it is not
absorbed from the GI tract.
Table 26.10 Miscellaneous Anti-infectives

aztreonam (Azactam) IM; 0.5–2 g bid–qid (max: 8 g/day) Monobactam class; for gram-negative aerobic bacteria; IV form
available
chloramphenicol PO; 50 mg/kg qid Broad spectrum; for typhoid fever and meningitis; IV form
available
clindamycin (Cleocin) PO; 150–450 mg qid Bacteriostatic; effective against anaerobic organisms; topical,
IM, and IV forms available
daptomycin (Cubicin) IV; 4 mg/kg once every 24 hours for 7–14 days Bacteriocidal; for serious skin infections
doripenem (Doribax) IV; 500 mg every 8 hours for 5–14 days IV; Carbapenum class; newer drug approved for the treatment of
500 mg every 8 h for 5–14 days (max: 500 mg serious abdominopelvic and skin infections, pneumonia, and
every 8 h) complicated UTI
ertapenem (Invanz) IV/IM: 1 g/day Carbapenem class; very broad spectrum
imipenem-cilastatin (Primaxin) IV; 250–500 mg tid–qid (max: 4 g/day) Carbapenum class; combination drug; IM form available;
one of the broadest spectrums of any anti-infective
lincomycin (Lincocin) PO; 500 mg tid–qid (max: 8 g/day) Bacteriostatic; effective against anaerobic organisms; IM form
available
linezolid (Zyvox) PO; 600 mg bid (max: 1,200 mg/day) For vancomycin-resistant Enterococcus; IV form available
meropenem (Merrem IV) IV; 1–2 g tid Carbapenum class; for intra-abdominal infections, bacterial
meningitis
metronidazole (Flagyl) (see PO; 7.5 mg/kg qid For serious infections with anaerobic bacteria; also for proto-
page 427 for the Drug zoan infections; IV form available
Prototype box)
quinupristin-dalfopristin IV; 7.5 mg/kg infused over 50 minutes Streptogamins class; for serious infections resistant to
(Synercid) every 8 hours vancomycin
spectinomycin (Trobicin) IM; 2 g as single dose Bacteriostatic; for gonorrhea
telavancin (Vibativ) IV; 10 mg/kg over 60 minutes for 24 hours Approved for treatment of hospital-acquired pneumonia from
gram-positive microbes
telithromycin (Ketek) PO; 800 mg daily Ketolide class; for community-acquired respiratory tract
infections
vancomycin (Vancocin) IV; 500 mg qid–1 g bid For S.aureus-resistant infections
Imipenem (Primaxin), ertapenem (Invanz), and meropenem (Merrem IV) belong to a newer class of
antibiotics called carbapenems. These drugs are bacteriocidal and have some of the broadest antimicrobial
spectrums of any class of antibiotics. Imipenem, the most widely prescribed drug in this small class, is
administered in a fixed-dose combination with cilastatin, which increases the serum levels of the antibiotic.
Meropenem is approved only for peritonitis and bacterial meningitis. Ertapenem is approved for the treat-
ment of serious abdominopelvic and skin infections, community-acquired pneumonia, and complicated
UTI. Diarrhea, nausea, rashes, and thrombophlebitis at injection sites are the most frequent adverse effects
of the carbapenems.
NURSING PROCESS FOCUS Patients Receiving Antibacterial Therapy

Prior to administration: ■ Infection related to inadequate primary defenses
■ Obtain a complete health history, including neurological, GI, renal and ■ Acute Pain related to tissue damage secondary to infection
liver conditions, past infections, allergies, drug history, and possible ■ Risk for Injury related to tissue destruction and adverse effects of drug
drug interactions. therapy
■ Acquire the results of a complete physical examination, including vital ■ Deficient Knowledge related to a lack of information about disease
signs, height, weight, and any signs or symptoms of infection. process, transmission and drug therapy
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, and
■ Obtain specimens for C&S before initiating therapy.

The patient will:
■ Experience therapeutic effects (reduction in symptoms related to the diagnosed infection).
Implementation
■ Monitor signs and symptoms of infection, including vital signs. (Moni- ■ Instruct the patient to notify the healthcare provider if there are
toring of patient signs and symptoms is used to determine antibacte- changes in LOC, if the fever does not return to normal parameters (un-
rial effectiveness or worsening of infection. Another drug or different der 100 oF), or if other symptoms persist or worsen.
dosage may be required.)
of proper administration, especially monitoring for compliance with ■ Take the medication on schedule.
antibiotic therapy. (Partial doses, skipped doses, and shortened length ■ Complete the entire prescription even if feeling better to prevent de-
of treatment encourage the recurrence of infection or development of velopment of resistant bacteria.
resistant organisms.) ■ Follow-up with the healthcare provider after antibiotic therapy is
completed.
■ If drug is being given intravenously, monitor the IV site for signs and ■ Instruct the patient to immediately report pain or other symptoms of
symptoms of tissue irritation, severe pain, and extravasation. discomfort to the healthcare provider during intravenous infusion.
■ Monitor for hypersensitivity reaction. (Immediate hypersensitivity re- ■ Instruct the patient to discontinue the medication and inform the
action may occur within 2–30 minutes; accelerated reaction occurs in healthcare provider if symptoms of hypersensitivity reaction develop
1–72 hours; and delayed reaction after 72 hours.) such as wheezing; shortness of breath; swelling of face, tongue, or
hands; or itching or rash.
■ Monitor for severe diarrhea. (The condition may occur due to superin- Instruct the patient to:
fection or the possible adverse effect of specific antibiotics.) ■ Report any diarrhea that increases in frequency or amount, or that
contains mucus or blood, to the healthcare provider.
■ Consult the healthcare provider before taking antidiarrheal drugs,
which could cause retention of harmful bacteria.
■ Consume cultured dairy products with live active cultures, such as kefir,
yogurt, or buttermilk, to help maintain normal intestinal flora.
■ Monitor for superinfection, especially in elderly, debilitated, or im- Instruct the patient to:
munosuppressed patients. (Increased risk for superinfections is due to ■ Report signs and symptoms of superinfection, such as fever; white
elimination of normal flora.) patches in the mouth; itchy rash; loose, foul-smelling stools or whitish
thick vaginal discharge to the healthcare provider.
■ Use infection control measures such as frequent hand washing.
■ Monitor intake of over-the-counter (OTC) products such as antacids, ■ Advise the patient to consult with the healthcare provider before
calcium supplements, iron products, and laxatives containing magne- using OTC medications or herbal products.
sium. (These products interfere with absorption of many antibiotics.)
■ Monitor for photosensitivity and sensitivity of the skin to the sun. Encourage the patient to:
(Tetracyclines, fluoroquinolones, and sulfonamides can increase the ■ Avoid exposure to direct sunlight during and after therapy.
patient’s sensitivity to ultraviolet light and increase risk of sunburn.) ■ Wear protective clothing, sunglasses, and sunscreen when outdoors.
■ Determine the interactions of the prescribed antibiotics with various Instruct the patient regarding foods and beverages that should be avoided
foods and beverages. (Many antibiotics are associated with significant with specific antibiotic therapies:
GI effects. Food or milk may impair absorption of some antibiotics such ■ No acidic fruit juices with penicillins
as macrolides.) ■ No alcohol intake with cephalosporins
■ No dairy product/calcium products with tetracyclines
■ Monitor for other adverse effects specific to various antibiotic therapies. ■ Instruct the patient to report adverse effects specific to the antibiotic
(See each Core Concept for each antibiotic classification in this chapter.) therapy prescribed.
■ Continue to monitor periodic laboratory work: CBC, liver and renal Inform the patient:
function studies, C & S, peak and trough drug levels as applicable and ■ About the importance and purpose of required laboratory tests.
possibly a urinalysis. (Many antibiotics are renal or hepatic toxic. Pe- ■ To schedule follow-ups with the healthcare provider.
riodic C & S are done to confirm effectiveness of therapy. Drug levels ■ To help with renal function, increase fluid intake to 2,000–3,000 mL/day.
will be monitored with some drugs.)
■ Monitor for symptoms of ototoxicity. (Some antibiotics, such as the Instruct the patient to notify the healthcare provider of:
aminoglycosides and vancomycin, may cause vestibular or auditory ■ Changes in hearing, ringing in the ears, or full feeling in the ears.
nerve damage.) ■ Nausea and vomiting with motion, ataxia, nystagmus, or dizziness.
■ Monitor for symptoms of neurotoxicity. (Penicillins, cephalosporins, ■ Instruct the patient to notify the healthcare provider if dizziness,
sulfonamides, aminoglycosides, and fluoroquinolones have an drowsiness, severe headache changes in LOC, or seizures occur.
increased risk of neurotoxicity.)

Tuberculosis
TB is a highly contagious infection caused by the organism Mycobacterium tuberculosis. Although

M. tuberculosis typically invades the lungs, it may travel to other body systems, particularly bone. The
slow-growing mycobacteria activate cells of the immune response, which attempt to isolate the patho-
gens by creating a wall around them. The mycobacteria usually become dormant, lying inside cavities
called tubercles. They may remain dormant during an entire lifetime, or they may become reactivated if
the immune system becomes suppressed. When active, TB can be quite infectious, being spread by con-
taminated sputum. With the immune suppression characteristic of AIDS, the incidence of TB has greatly
increased: As many as 20% of all patients with AIDS develop active TB.
Two other types of mycobacteria infect humans. Mycobacterium leprae is responsible for leprosy,
a disease rarely seen in the United States and Canada. M. leprae is treated with multiple drugs, usually
beginning with rifampin. Mycobacterium avium complex (MAC) causes an infection of the lungs, most
commonly observed in patients with AIDS. The most effective drugs against MAC are the macrolides
azithromycin (Zithromax) and clarithromycin (Biaxin).
The pharmacotherapy of tuberculosis requires special

Core Concept 26.14 dosing regimens and schedules.
Drug therapy of TB differs from that of most other infections. Mycobacteria have a cell wall that is resis-
tant to penetration by anti-infective drugs. For medications to reach the microorganisms isolated in the
tubercles, therapy must continue for 6–12 months. Although the patient may not be infectious this entire
time and have no symptoms, it is critical that therapy continue the entire period. Some patients develop
multidrug-resistant infections and require therapy for as long as 24 months.
A second feature of the pharmacotherapy of TB is that at least two—and sometimes four or more—
antibiotics must be administered concurrently. During the 6- to 12-month treatment period, different com-
binations of drugs may be used. Multidrug therapy is necessary because the mycobacteria grow slowly,
and resistance is common. Using multiple drugs and switching the combinations during the long treatment
period lowers the potential for resistance and increases therapeutic success. Although many different drug
combinations are used, a typical regimen for patients with no complicating factors includes the following:
■ Initial phase two months of daily therapy with isoniazid (INH), rifampin (Rifadin, Rimactane),
pyrazinamide (PZA), and ethambutol (Myambutol). If laboratory test results show that the strain
is sensitive to the first three drugs, ethambutol is dropped from the regimen.
■ Continuation phase four months of therapy with isoniazid and rifampin, two to three times per week.
There are two broad categories of antitubercular drugs. One category consists of first-line drugs, which
are safer and generally the most effective. Second-line medications, more toxic and less effective than the
first-line drugs, are used when resistance develops. Table 26.11 ◆ lists the first-line drugs for therapy of TB.
Drug Prototype: Isoniazid (INH, Nydrazid)

Therapeutic Class: Antituberculosis drug Pharmacologic Class: Mycolic acid inhibitor
Actions and Uses: Isoniazid is a drug of choice for the treat- Aluminum-containing antacids should not be administered
ment of M. tuberculosis because decades of experience have concurrently because they can decrease the absorption of isonia-
shown it to have a superior safety profile and to be the most zid. When disulfiram is taken with INH, lack of coordination or
effective single drug for the disease. Isoniazid acts by inhibiting psychotic reactions may result.
the synthesis of mycolic acid, an essential cell wall component
of mycobacteria. It is bacteriocidal for actively growing organ-
Black Box Warning:
isms but bacteriostatic for dormant mycobacteria. It is selective
Although rare, hepatotoxicity is a serious and sometimes
for M. tuberculosis. Isoniazid is used alone for chemoprophy-
fatal adverse effect; thus, the patient should be monitored
laxis, or in combination with other antitubercular drugs for
carefully for jaundice, fatigue, elevated hepatic enzymes, or
treating active disease.
loss of appetite. Liver enzyme tests are usually performed
monthly during therapy. Hepatotoxicity usually appears in
Adverse Effects and Interactions: The most common adverse
the first 1–3 months of therapy but may occur at any time
effects of isoniazid are numbness of the hands and feet, rash,
during treatment. Older adults and those with daily alcohol
and fever.
consumption are at greater risk of developing hepatotoxicity.
Table 26.11 First-Line Antitubercular Drugs

ethambutol (Myambutol) PO; 15–25 mg/kg daily Used in combination with other antituberculars
isoniazid (INH, Nydrazid) PO; 15 mg/kg daily Used in combination with other antituberculars; IM form
available
pyrazinamide (PZA) PO; 5–15 mg/kg tid–qid Rifater is a fixed-dose combination of pyrazinamide with
isoniazid and rifampin
rifabutin (Mycobutin) PO; 300 mg once daily (for prophylaxis) Very similar to rifampin and rifapentine
or 5 mg/kg/day (for active TB) (max:
300 mg/day)
rifampin (Rifadin, Rimactane) PO; 600 mg daily as a single dose or Used in combination with other antituberculars; IV form
900 mg twice weekly for 4 months available; also for leprosy, H. influenzae, and meningococcus
infections
rifapentine (Priftin) PO; 600 mg twice a week for 2 months, Used in combination with other antituberculars
then once a week for 4 months
NURSING PROCESS FOCUS Patients Receiving Antitubercular Drugs

Prior to administration: ■ Infection related to inadequate primary defenses, environmental
■ Obtain a complete health history, including respiratory, neurological, exposure
renal and liver conditions, allergies, drug history, past infections, and ■ Risk for Injury related to tissue destruction and adverse effects of drug
■ Evaluate laboratory blood findings: CBC, electrolytes, and renal and ■ Fatigue related to presence of infection; adverse effects of drug
liver function studies. therapy
■ Acquire the results of a complete physical examination, including vital ■ Deficient Knowledge related to a lack of information about drug
signs and any signs or symptoms of infection. therapy
■ Collect information on the presence or history of the following: posi- ■ Noncompliance related to adverse drug effects, deficient knowledge,
tive tuberculin skin test, sputum culture, or smear; close contact with length of treatment or cost of medication
person recently infected with TB; HIV infection, or AIDS; immunosup-
pressant drug therapy; alcohol abuse; cognitive ability to comply with
long-term therapy.

The patient will:
■ Experience therapeutic effects (an absence or reduction in TB symptoms).
Implementation
■ Administer medication correctly and evaluate the patient’s knowledge Explain the importance of complying with the entire therapeutic plan,
of proper administration, especially monitoring the patient’s ability including:
and motivation to comply with therapeutic regimen. (Treatment must ■ Taking all medications as directed by the healthcare provider.
continue for the full-length of therapy to eliminate all M. tuberculosis ■ Not discontinuing medication until so instructed.
organisms.) ■ Wearing a medical alert bracelet.
■ Keeping all appointments for follow-up care.
■ Monitor for hepatic adverse effects. (Antituberculosis ■ Instruct the patient to report yellow eyes and skin, loss of appetite,
drugs, such as isoniazid and rifampin, cause hepatic dark urine, and unusual tiredness.
impairment.)
continued . . .

■ Monitor for neurologic adverse effects such as numbness Instruct the patient to:
and tingling of the extremities. (Antituberculosis drugs, such ■ Report numbness and tingling of extremities.
as isoniazid, cause peripheral neuropathy and depletion of ■ Take supplemental vitamin B6 as ordered to reduce risk of adverse
vitamin B6.) effects.
■ Monitor for dietary compliance when patient is taking isoniazid. ■ Advise patients taking isoniazid to avoid foods containing tyramine,
(Foods high in tyramine can interact with the drug and cause such as aged cheese, smoked and pickled fish, beer and red wine,
palpitations, flushing, and hypertension.) bananas, and chocolate.
■ Monitor for other adverse effects specific to various antituberculosis Instruct the patient to report to the heathcare provider any adverse
drugs. effects specific to the antituberculosis therapy prescribed, such as:
■ Blurred vision or changes in color or vision field (ethambutol).
■ Difficulty in voiding (pyrazinamide).
■ Fever, yellowing of skin, weakness, dark urine (isoniazid,
rifampin).
■ GI system disturbances (rifampin).
■ Changes in hearing (streptomycin).
■ Numbness and tingling of extremities (isoniazid).
■ Red discoloration of body fluids (rifampin).
■ Dark concentrated urine, weight gain, edema (streptomycin).
■ Establish therapeutic environment to ensure adequate rest, nutrition, Instruct the patient:
hydration, and relaxation. (Symptoms of TB are manifested when the ■ About infection control measures, such as frequent handwashing, cov-
immune system is suppressed.) ering the mouth when coughing or sneezing, and proper disposal of
soiled tissues.
■ To incorporate health-enhancing activities, such as adequate rest and
sleep, intake of essential vitamins and nutrients, and intake of six to
eight glasses of water/day.
■ Collect sputum specimens as directed by the healthcare provider. ■ Instruct the patient in technique needed to collect a quality sputum
(This will determine the effectiveness of the antituberculosis specimen.
drug.)
A third feature of anti-TB therapy is that drugs are used extensively for preventing the disease in addi-
tion to treating it. Chemoprophylaxis is common for close contacts or family members of patients recently
infected with TB. Therapy usually begins immediately after a patient receives a positive tuberculin test.
Patients with immunosuppression, such as those with AIDS or those receiving immunosuppressant drugs,
may receive preventive treatment with anti-TB drugs. A short-term therapy of two months, consisting of a
combination treatment with isoniazid and pyrazinamide, is approved for TB prophylaxis in patients posi-
tive for HIV.
Treatment guidelines strongly recommend that directly observed therapy (DOT) be used in
the treatment of TB (CDC, 2010). DOT means that a healthcare worker or other trained individual
administer the medications and watch the patient swallow the dose. This ensures that the medication is
taken exactly as prescribed and decreases the risk for relapse, limits the spread of the infection in the
community, and reduces the development of drug resistance that could result from erratic or partial
treatment.
Concept Review 26.3

■ How does drug therapy of TB differ from that of conventional anti-infective chemother-
apy? What are the rationales for these differences?
Chapter Review 409

Patients treated for bacterial infections need to know the following:
In General
1. Take the entire prescription of anti-infective medication exactly as directed because
partial doses, skipped doses, and shortened length of treatment encourage the develop-
ment of resistant organisms.
2. Some antibiotics may cause GI upset. If this occurs, take the drug with food or milk as
directed. Check prescription label for specific directions.
3. Eating active-culture yogurt or buttermilk may decrease the risks for diarrhea and vagi-
nitis associated with antibiotic destruction of normal flora.
4. Antibiotics are most effective if taken around the clock, rather than just during normal
waking hours.
Regarding Penicillins
5. It may be necessary to stay in the office for at least 30 minutes after receiving an injec-
tion of penicillin so the healthcare providers can monitor for possible allergic reactions.
6. Avoid intake of caffeinated beverages, citrus fruits, and fruit juices for at least one hour
before and two hours after taking oral penicillin to maximize the drug’s absorption.
Regarding Sulfonamides and Tetracyclines
7. Take oral cephalosporins and oral lincomycin with food, and oral sulfonamides with
food or milk, to decrease GI upset. Drink a glass of water with each dose of sulfonamide,
tetracycline, lincomycin, or fluoroquinolone, and drink a total of 2–3 L of fluid a day.
8. Avoid sun/tanning exposure while taking sulfonamides and tetracyclines because these
drugs cause photosensitivity.
9. Antacids, dairy products, iron, baking soda, and kaolin-pectin bind and inactivate tetra-
cycline. Separate intake by two to three hours for full antibiotic effectiveness.
10. Sulfonamides, tetracycline, and other antibiotics may interfere with the effectiveness of
oral contraceptives. Ask a healthcare provider about the advisability of using an addi-
tional form of contraception.
Safety Alert
Allergic Reactions and Antibiotics
After receiving the medication her first dose of levofloxacin (Levaquin), Mrs. Jones reported
itching and a slight swelling of the tongue and lips (angioedema). However, later that day
she had no discomfort or presence of the previous symptoms. Prior to the initial administra-
tion of the drug, the nurse checked Mrs. Jones’ chart for the presence of allergies, but it is
imperative that the nurse now monitor her for an allergic reaction. Hypersensitivity reactions
can worsen with each exposure to an antigen (the antibiotic). The next dose could cause a
life-threatening anaphylactic response.
Chapter Review
26.1 Pathogens are organisms that cause disease by how to classify these drugs because medications in
invading tissues or secreting toxins. the same class exhibit similar pharmacologic activity.
Pathogens can overwhelm natural immune defenses Anti-infective drugs are classified based on similari-
by growing extremely rapidly and invading normal ties in their chemical structures or by their mecha-
tissues or by producing potent toxins. Bacteria are nisms of action.
classified on the basis of their staining ability and
26.3 Anti-infective drugs act by selectively targeting a
structural and functional characteristics.
pathogen’s metabolism or life cycle.
26.2 Anti-infective drugs are classified by their chemical Bacteria multiply rapidly, and drugs have been de-
structures or by their mechanisms of action. signed to take advantage of this characteristic. Anti-
Because of the large number of anti-infectives avail- infectives may be bacteriocidal or bacteriostatic, or
able, it is advantageous for the student to understand both, depending on the organism and dose.
26.4 Acquired resistance is a major clinical problem that 26.9 The macrolides are safe alternatives to penicillin
is worsened by improper use of anti-infectives. for many infections.
Errors during replication result in random mutations The macrolides are generally prescribed when a pa-
of the bacterial DNA. Although rare, an occasional tient is allergic to penicillin or has a penicillin-resis-
mutation may confer antibiotic resistance to a bac- tant infection. They produce few adverse effects.
terium. Therapy with antibiotics kills the affected
26.10 The aminoglycosides are narrow-spectrum drugs
bacteria, leaving the resistant ones to multiply and
that have the potential to cause serious toxicity.
spread within the patient. To limit this problem, an-
tibiotics should be prescribed only when medically The aminoglycosides are usually reserved for severe
necessary. gram-negative infections of the urinary tract because
they have the potential to cause serious adverse
26.5 Careful selection of the correct antibiotic is essen- effects. Most of them are poorly absorbed from the
tial for effective pharmacotherapy and to limit GI tract and must be given parenterally.
adverse effects.
26.11 Fluoroquinolones have wide clinical applications
Culture and sensitivity tests are used to identify the because of their broad spectrum of activity and
type of bacteria present and determine which antibiot- relative safety.
ics are most effective. Until test results are obtained,
Although fluoroquinolones are an older class of antibac-
the patient may be started on a broad-spectrum an-
terials, newer drugs in this class have been developed to
tibiotic. Because broad-spectrum drugs are more
greatly expand their use. They are effective oral alter-
likely to affect the patient’s normal flora, a narrow-
natives to other antibiotics for both gram-negative and
spectrum drug may be prescribed after the organism
gram-positive organisms. Ciprofloxacin (Cipro) is one
is identified.
of the few drugs approved for the treatment of anthrax.
26.6 The penicillins are one of the oldest and safest 26.12 Sulfonamides and urinary antiseptics are tradi-
groups of anti-infectives. tional drugs for urinary tract infections.
Penicillins have been widely used because of their In the 1930s, the sulfonamides revolutionized the treat-
high margin of safety and effectiveness. Some pa- ment of infectious disease. Present-day use of these
tients are allergic to this class of drugs, and many medications is limited by bacterial resistance. The
bacterial species have become resistant to penicillins, fixed combination of trimethoprim–sulfamethoxazole
thus limiting their use. (Bactrim, Septra) is an important drug in the pharma-
cotherapy of UTIs.
26.7 The cephalosporins are similar in structure and
function to the penicillins and are one of the most 26.13 A number of additional anti-infectives have dis-
widely prescribed anti-infective classes. tinct mechanisms of action and specific indications.
The cephalosporins consist of a large class of anti- A number of important antibiotics do not belong to
biotics, classified by generation, that are considered any of the previous classes. The streptogramins and
alternatives to penicillin. In general, they are used for oxazolidinones are small groups of drugs having spe-
serious gram-negative infections and for patients who cific applications. Vancomycin is known as the “last
are resistant to or cannot tolerate the penicillins. chance” antibiotic for use when resistance has devel-
oped to most other anti-infectives.
26.8 The tetracyclines have broad spectrums but are
drugs of choice for few diseases. 26.14 The pharmacotherapy of tuberculosis requires spe-
The tetracyclines have a broader spectrum of action cial dosing regimens and schedules.
and produce more adverse effects than the penicillins. Drug therapy of TB involves taking multiple drugs
Their use is limited to a small number of diseases for prolonged periods. Patients exhibiting a new, pos-
such as Rocky Mountain spotted fever, typhus, chol- itive TB test are often given these drugs prophylacti-
era, Lyme disease, and chlamydial infections. cally, even if no signs of the disease are apparent.
Review Questions
The following questions are written in NCLEX-PN® style. 3. “Before I take my medication, I will avoid orange juice.”
Answer these questions to assess your knowledge of the chap- 4. “I will take the medication until I feel better.”
ter material, and go back and review any material that is not
clear to you. 2. Before administering cefotaxime (Claforan), the nurse
checks for a previous allergic reaction to:
1. The patient is taking amoxicillin (Amoxil). Which of the 1. Yeasts
following statements by the patient demonstrates that she needs 2. Penicillins
additional instruction? 3. Sulfonamides
1. “I will take this medication until it is gone.” 4. Macrolides
2. “I will call my doctor if I develop a fever or a rash.”
Chapter Review 411
3. When assisting with the development of a patient care 7. The patient with tuberculosis is now on isoniazid (INH).
plan, the nurse needs to include what information about Which laboratory test should the nurse monitor?
tetracyclines? 1. PT and PTT
1. To take it with food or milk 2. CBC
2. They are safe for use during pregnancy 3. BUN
3. To take it one to two hours before or after meals 4. Liver enzymes
4. That it has no adverse effects
8. The nurse tells the patient that the most common adverse
4. The nurse monitors the patient on aminoglycosides for: effects of penicillin G include(s): (Select all that apply)
1. Nephrotoxicity 1. Diarrhea
2. Hepatic failure 2. Nausea and vomiting
3. Superinfection 3. Pain at the injection site
4. Hypertension and rash 4. Rash
5. A nurse is instructing a patient about ciprofloxin (Cipro). 9. A patient at a rehabilitation center is prescribed eryth-
The nurse tells him that if this antibiotic is taken with antacids, romycin. The nurse is reviewing the patient’s medication list,
absorption is: checking to see if there are medications that should not be
taken with this antibiotic. One medication is found. What med-
1. Increased ication should not be taken with erythromycin?
2. Decreased
3. Not affected 1. Lisinopril
4. Delayed 2. Ibuprofen
3. Lasix
6. A patient has been diagnosed with MRSA and is pre- 4. Lovastatin
scribed vancomycin. While the patient is on this medication,
10. A patient is to receive Cipro 500 mg po four times a day,
what information should be provided to the patient about pos-
for a week. The pharmacy sends Cipro 250 mg tablets. How
sible adverse effects?
many tablet(s) will the patient receive in 24 hours?
1. Vancomycin may cause flushing.
1. Two tablets
2. Adverse effects are infrequent.
2. Four tablets
3. Vacomycin does not cause rashes.
3. Six tablets
4. During therapy, hypertension may occur.
4. Eight tablets
Remember Ms. Jackson, the patient 2. When speaking with Ms. Jackson about gentamicin, the
introduced at the beginning of the nurse tells her that gentamicin can cause:
chapter? Now read the remainder of 1. Anemia
the case study. Based on the informa- 2. Hearing impairment
tion you have learned in this chapter, 3. Nausea and vomiting
answer the questions that follow. 4. Liver failure
3. Ms. Jackson is showing signs of hearing loss due to gentami-
Ms. Shelly Jackson is a new patient at your clinic. Six months ago, cin therapy and the physician is going to switch her antibiotic. The
she had a kidney transplant and is taking immunosuppressant nurse anticipates which of the following medications being ordered?
drugs. Recently, she has been experiencing repeated bacterial 1. Sulfacetamide (Klaron)
infections due to resistant strains and has been switched to dif- 2. Silver sulfadiazine
ferent antibiotics throughout the past six months. The physician 3. Trimethoprim–sulfamethoxazole (Septra)
suspects a kidney infection. 4. Vancomycin (Vancocin)
1. Ms. Jackson is admitted to the hospital and is adminis- 4. The nurse is educating Ms. Jackson about the adverse
tered gentamicin 300 mg daily by IV infusion. The nurse moni- effects of sulfonamides and tells her that this includes: (Select
tors which of the following tests? all that apply.)
1. Input and output ratio 1. Increased sensitivity of skin to sunlight
2. Serum transaminase levels 2. Liver failure
3. Visual acuity tests 3. Nausea and vomiting
4. Fasting blood glucose levels 4. Hypotension

c
“I’m at the office for my
h annual checkup. If it’s
a not one thing it’s another.
p Earlier in the year, I had
pneumonia. Now I’m having
t problems with itching and
e discharge.”
r Mrs. Martha Davis, 70-year-old retired
auto worker
27 Drugs for Fungal, Viral,

and Parasitic Diseases
Core Concepts
27.1 Fungal infections are classified as superficial or 27.4 Viruses are infectious agents that require a host to
systemic. replicate.
27.2 Systemic antifungal drugs are used for serious 27.5 Antiretroviral drugs do not cure HIV-AIDS, but they
infections of internal organs. do help many patients live longer.
27.3 Superficial infections of the skin, nails, and mucous 27.6 Antiviral drugs are available to treat herpes simplex,
membranes are effectively treated with topical and influenza, and viral hepatitis infections.
oral antifungal drugs. 27.7 Infections caused by helminths and protozoans cause
significant disease worldwide.
Drug Snapshot
Antifungal drugs for mphotericin B (AmBisome,
a
systemic infections Fungizone, others) 416
Antifungal drugs for ystatin (Mycostatin, Nystop,

n
superficial infections others) 416
Antiretroviral drugs for zidovudine (AZT, Retrovir) 421

HIV-AIDS
Antiviral drugs for herpes acyclovir (Zovirax) 425
simplex and influenza
Antiprotozoans and metronidazole (Flagyl) 427
antihelminthics
Learning Outcomes
1. Compare and contrast the 5. Explain the purpose and 8. Categorize drugs used in the
pharmacotherapy of superficial and expected outcomes of HIV treatment of fungal, viral,
systemic fungal infections. pharmacotherapy. protozoan, and helminth infections
2. Identify the types of patients most 6. Define HAART, and explain based on their classifications and
likely to acquire serious fungal why it is commonly used in the mechanisms of action.
infections. pharmacotherapy of HIV infection. 9. For each of the classes listed in the
3. Describe the basic structure of a virus. 7. Identify protozoan and helminth Drug Snapshot, identify representative
infections that may benefit from drugs and explain their mechanisms
4. Identify specific viral infections that of drug action, primary actions, and
benefit from pharmacotherapy. pharmacotherapy.
Key Terms
antiretroviral (an-tie-RET-roh-veye-ral) 420 host 418 reverse transcriptase (ree-VERS
capsid (CAP-sid) 417 influenza (in-flew-EN-zah) 424 trans-CRIP-tace) 420
dysentery (DISS-en-tare-ee) 426 intracellular parasites 418 superficial mycoses 413
fungi (FUN-jeye) 413 malaria (mah-LARE-ee-ah) 426 systemic mycoses 414
helminths (HELL-minthz) 427 mycoses (my-KOH-sees) 413 viruses 417
highly active antiretroviral therapy protozoans (PRO-toh-ZOH-enz) 425 yeasts (YEESTz) 413
(HAART) 420
F ungi, protozoans, and multicellular parasites are exceedingly more complex than bacteria. Most an-
tibacterial drugs are ineffective against these organisms because their structure and biochemistry are
so different from that of bacteria. Although there are fewer medications to treat these diseases, the
available medications are usually effective.
Viruses, on the other hand, are nonliving particles that infect by entering a host cell and using the
host’s internal machinery to replicate itself. Antiviral drugs are the least effective of all the anti-infective
classes. Although the number of antiviral medications has increased dramatically in recent years, they are
relatively ineffective at preventing or treating viral infections.
Antifungal Drugs
Fungal infections are classified as superficial or systemic. Core Concept 27.1
Fungi are single-celled or multicellular organisms that are much more complex than bacteria. Several spe-
cies of fungi grow on skin and mucosal surfaces and are part of the normal host flora. The human body is
remarkably resistant to infection by these organisms; people with healthy immune systems rarely experi-
ence serious fungal diseases. Those with a weakened immune system, however, such as patients infected
with HIV, may acquire frequent fungal infections, some of which may require intensive drug therapy.
Fungal infections are called mycoses. Most exposure to pathogenic fungi occurs through inhalation of
fungal spores or by handling contaminated soil. Thus, many fungal infections involve the respiratory tract, myc 5 fungus
skin, hair, and nails. An additional common source of fungal infections, especially of the mouth or vagina, oses 5 conditions
is overgrowth of normal host flora. Yeasts, which include the common pathogen Candida albicans, are
single-celled fungi. Table 27.1 ◆ lists the most common fungal pathogens.
A simple and useful method of classifying fungal infections is to consider them as either superficial
or systemic. Superficial mycoses typically affect the scalp, skin, nails, and mucous membranes such as the
oral cavity and vagina. Mycoses of this type are often treated with topical drugs because the incidence of
adverse effects is much lower by using this route of administration.
Fast Facts Fungal, Viral, and Parasitic Diseases

■ Ninety percent of human fungal infections are caused by just a few dozen species.
■ Of all human fungal infections, 86% are caused by Candida albicans. The second most common,
about one to two cases per 100,000 people is caused by Aspergillus.
■ About one of every six Americans age 14–49 years are infected with genital herpes.
■ More than 1.1 million Americans are currently living with HIV infections; about 49,000 new
infections occur each year.
■ Approximately 63% of new HIV infections occur in men, with the largest risk category being men
who have sex with other men.
■ Of the new HIV infections in women, 84% are acquired through heterosexual contact.
■ Since the beginning of the AIDS epidemic, more than 636,000 Americans have died of AIDS.
■ About 219 million cases of malaria occur worldwide each year; about 1,500 travelers develop
malaria abroad and return to the United States with the infection.
414 Chapter 27 Drugs for Fungal, Viral, and Parasitic Diseases
Table 27.1 Fungal Pathogens

Name of Fungus Disease and Primary Organ System
SYSTEMIC
Aspergillus fumigatus and others Aspergillosis: opportunistic; most commonly affects the lungs but can spread to other
organs
Blastomyces dermatitidis Blastomycosis: begins in the lungs and spreads to other organs
Candida albicans and others Candidiasis: most common opportunistic fungal infection; may occur in mucous membranes
and nearly any organ
Coccidioides immitis Coccidioidomycosis: begins in the lungs and spreads to the skin and other organs
Cryptococcus neoformans Cryptococcosis: opportunistic; begins in the lungs but is the most common cause of meningitis
in patients with AIDS
Histoplasma capsulatum Histoplasmosis: begins in the lungs and spreads to other organs
Pneumocystis jiroveci Pneumocystis pneumonia: opportunistic; primarily causes pneumonia but can spread to other
organs
SUPERFICIAL
Candida albicans and others Candidiasis: affects the skin, nails, oral cavity (thrush), vagina
Epidermophyton floccosum Athlete’s foot (tinea pedis), jock itch (tinea cruris), and other skin disorders
Microsporum species Ringworm of the scalp (tinea capitus)
Sporothrix schenckii Sporotrichosis: affects primarily the skin and superficial lymph nodes
Trichophyton species Affects the scalp, skin, and nails
Systemic mycoses are those affecting internal organs, typically the lungs, brain, and digestive organs.
Although much less common than superficial mycoses, systemic fungal infections often affect multiple
body systems and are sometimes fatal to patients with suppressed immune systems. Mycoses of this type
require aggressive oral or parenteral medications that produce more adverse effects than the topical drugs.
Systemic antifungal drugs are used for serious infections

Core Concept 27.2 of internal organs.
Systemic or invasive fungal infections require intensive pharmacotherapy for extended periods. Amphoteri-
cin B and fluconazole are the most frequently prescribed drugs for these types of infections. Table 27.2 ◆
lists the primary antifungal drugs.
Serious opportunistic fungal disease can occur in patients whose immune systems are compromised,
such as those with HIV-AIDS. Others who may experience systemic infections include patients receiving
prolonged therapy with corticosteroids (see Chapter 24 and Chapter 32), those with extensive burns, those
receiving antineoplastic drugs (see Chapter 28), and those who have recently received organ transplants
(see Chapter 25). Pharmacotherapy of systemic mycoses may continue for several months to ensure com-
plete removal of the pathogen.
Amphotericin B (AmBisome, Fungizone, others) has been the gold standard for treating systemic fun-
gal infections since the 1960s. However, the newer azole drugs such as fluconazole (Diflucan) and itracon-
azole (Sporanox) are safer and have become preferred drugs for the treatment of some systemic infections.
Ketoconazole has also become a preferred drug for less severe systemic mycoses or for the prophylaxis of
fungal infections. The azole drugs have a spectrum of activity similar to that of amphotericin B, are consid-
erably less toxic, and have the major advantage that they can be administered orally. Several are available
for both superficial and systemic mycoses.
Several other antifungals are available as treatment options for systemic mycoses. These include
caspofungin (Cancidas) for aspergillosis and anidulafungin (Eraxis) and micafungin (Mycamine) for inva-
sive candidiasis. These drugs are usually prescribed when amphotericin B and the systemic azoles have
failed to produce an adequate response.
Concept Review 27.1

■ Why has the number of antifungal and antiviral drugs increased significantly over the
past 20 years?
Table 27.2 Selected Antifungal Drugs

amphotericin B (AmBisome, IV; 0.3–1.5 mg/kg/day, infused over 2–4 hours Cream, lotion, and PO suspension forms available for
Fungizone, others) (max: 1.5 mg/kg/day) topical mycoses; must infuse a test dose first; has
potential for severe adverse effects
butenafine (Mentax) Topical; apply daily for 4 weeks For athlete’s foot
anidulafungin (Eraxis) IV; Loading dose 100 mg on day 1 followed by Newer drug for advanced Candida infections
50 mg/day
caspofungin acetate (Cancidas) IV; 70 mg infused over 1 hour on day 1, followed Newer drug for invasive Candida and Aspergillus
by 50 mg infused over 1 hour qid for 30 days infections
ciclopirox cream, gel, shampoo Topical; apply bid for 4 weeks For skin and nail mycoses
(Loprox) or nail lacquer (Penlac)
flucytosine (Ancobon) PO; 50–150 mg/kg in divided doses For severe systemic infections such as candidiasis or
cryptococcosis; IV form available
griseofulvin (Fulvicin) PO; 500 mg microsize or 330–375 mg For ringworm and other skin and nail infections
ultramicrosize daily
micafungin (Mycamine) IV; 50–150 mg/kg/day Newer drug for advanced Candida infections
naftifine (Naftin) Topical; apply cream daily or gel bid for 4 weeks For skin mycoses
nystatin (Mycostatin, Nystop, PO; 500,000–1,000,000 units tid For candidiasis; vaginal tablet form available
others)
terbinafine (Lamisil) Topical; apply daily or bid for 7 weeks; PO; For skin and nail mycoses
250 mg daily for 6–13 weeks
tolnaftate (Aftate, Tinactin) Topical; apply bid for 4–6 weeks For skin mycoses, ringworm, athlete’s foot
undecylenic acid (Fungi-Nail, Topical; apply once or twice daily For athlete’s foot, diaper rash
Gordochom)
Azole antifungals
butoconazole (Femstat, Topical; one applicator intravaginally at For vaginal mycoses
Gynazole) bedtime for 3 days
clotrimazole (Gyne-Lotrimin, Topical; for skin mycoses apply bid for 4 weeks; For vaginal and skin mycoses, athlete’s foot, and
Mycelex,) for vaginal mycoses, insert one applicatorful candidiasis; oral troche also available for oral
intravaginally at bedtime for 7 days candidiasis
econazole (Spectazole) Topical; apply bid for 4 weeks For skin mycoses
fluconazole (Diflucan) PO; 200–400 mg on day 1, then 100–200 mg For both systemic and superficial mycoses; IV form
daily for 2–4 weeks available for severe mycoses
itraconazole (Sporanox) PO; 200 mg daily; may increase to 200 mg bid For severe systemic lung mycoses and superficial nail
(max: 400 mg/day) mycoses
ketoconazole (Nizoral) PO; 200–400 mg daily For severe systemic mycoses; topical form available
for superficial mycoses
miconazole (Micatin, Topical; apply bid for 2–4 weeks For vaginal and skin mycoses; also available as
Monistat-3) vaginal suppositories and tampons
oxiconazole (Oxistat) Topical; apply daily in the evening for 2 months For skin mycoses
posaconazole (Noxafil) PO; 100–200 mg tid Newer azole; for prevention of invasive Aspergillus
and Candida infections
sertaconazole (Ertaczo) Topical; 2% cream bid for 4 weeks For tinea pedis
sulconazole (Exelderm) Topical; apply once or twice daily for 2–6 weeks Newer azole for skin infections
terconazole (Terazol) Topical; insert one applicator intravaginally For vulvovaginal candidiasis; vaginal suppository
at bedtime for 3–7 days form available
tioconazole (Vagistat) Topical; insert one applicator intravaginally For vulvovaginal candidiasis
at bedtime for 1 day
voriconazole (Vfend) IV; 6 mg/kg every 12 hours on day 1, then For systemic aspergillosis and esophageal
3–4 mg/kg every 12 hours candidiasis; oral form available
Drug Prototype Amphotericin B (AmBisome, Fungizone, Others)

Therapeutic Class: Antifungal (systemic type) Pharmacologic Class: Polyene
Actions and Uses: Amphotericin B has a wide spectrum of activity Adverse Effects and Interactions: Amphotericin B can cause
and is effective against most of the fungi pathogenic to humans; a number of serious adverse effects. Many patients develop
thus, it is a preferred drug for many severe systemic mycoses. It acts fever and chills at the beginning of therapy, which subside as
by binding to fungal cell membranes and causing them to become treatment continues. Phlebitis, or inflammation of the veins,
permeable or leaky. Because amphotericin B is not absorbed from is common during IV therapy. Some degree of nephrotoxicity
the gastrointestinal (GI) tract, it is normally given by IV infusion. is observed in most patients, and laboratory tests of kidney
Topical preparations are available for superficial mycoses. Several function are normally performed throughout the treatment
months of pharmacotherapy may be required for a complete cure. period.
Unlike antibiotics, resistance to amphotericin B is not common. Amphotericin B interacts with many drugs. For example,
To reduce the toxicity of amphotericin B, the original drug therapy with aminoglycosides, vancomycin, carboplatin, and
molecule has been formulated with several lipid molecules. These furosemide, which reduce renal function, is not recommended.
include liposomal amphotericin B (AmBisome), amphotericin B lipid Use with corticosteroids, skeletal muscle relaxants, and
complex (Abelcet), and amphotericin B cholesteryl sulfate complex thiazole may cause hypokalemia. Use with digoxin increases
(Amphotec). These newer forms are very expensive and usually the risk of digoxin toxicity in patients with preexisting
reserved for serious fungal infections. hypokalemia.
Superficial infections of the skin, nails, and mucous membranes are

Core Concept 27.3 effectively treated with topical and oral antifungal drugs.
Superficial fungal infections of the hair, scalp, nails, and the mucous membranes of the mouth and vagina
are rarely medical emergencies. Infections of the nails and skin, for example, may be ongoing for months
or even years before a patient seeks treatment. Unlike systemic fungal infections, superficial infections
may occur in any patient, not just those who have suppressed immune systems.
Antifungal medications applied topically are much safer than their systemic counterparts because only
small amounts are absorbed into the circulation. Many are available as over-the-counter (OTC) creams,
gels, solutions, and ointments. Although a fungal infection may be diagnosed as superficial, oral antifungal
drugs are occasionally prescribed along with topical medications to be certain that the infection is com-
pletely eliminated from the deeper skin layers. The length of pharmacotherapy varies widely among the
different types of superficial mycoses. Vaginal infections are sometimes treated successfully with a single
vaginal tablet of clotrimazole, whereas nail mycoses may require several months of therapy with itracon-
azole or terbinafine.
Adverse effects from topical antifungal therapy are generally minor. If applied to the skin, irritation,
redness, and itching may be experienced. Vaginal administration may result in burning, itching, or irrita-
tion. Antifungal drugs should not be applied to open sores or severely abraded skin because this may result
in undesirable absorption of the drug and additional adverse effects. When applying topical antifungal
medication, gloves should be worn to prevent transmission.
Drug Prototype Nystatin (Mycostatin, Nystop, Others)

Therapeutic Class: Topical antifungal Pharmacologic Class: Polyene
Actions and Uses: Although it belongs to the same chemical often combined with triamcinolone, a corticosteroid that helps
class as amphotericin B, nystatin is available in a wider variety of to reduce inflammation.
formulations, including cream, ointment, powder, tablets, and
lozenges. It is used as a topical drug against Candida infections Adverse Effects and Interactions: When given topically,
of the vagina, skin, and mouth. It may also be used orally to nystatin produces few adverse effects other than minor skin
treat candidiasis of the intestine because it travels through the irritation. When given orally, it may cause diarrhea, nausea,
GI tract without being absorbed. In topical forms, nystatin is and vomiting.
NURSING PROCESS FOCUS Patients Receiving Superficial Antifungal Therapy

Assessment POTENTIAL NURSING DIAGNOSES
Prior to administration: ■ Acute Pain related to tissue damage secondary to infection
■ Obtain a complete health history, including skin, GI, renal and liver ■ Risk for Injury related to adverse effect of drug therapy
conditions, past infections, allergies, drug history, and possible drug ■ Deficient Knowledge related to a lack of information about drug
interactions. therapy
■ Acquire the results of a complete physical examination, including vital ■ Impaired Skin Integrity related to tissue damage and adverse effects of
signs and any signs or symptoms of infection. drug therapy
■ Evaluate laboratory blood findings: CBC, electrolytes, and renal and
liver function studies.

The patient will:
■ Experience therapeutic effects (healing of fungal infection).
Implementation
■ Administer oral medication correctly and evaluate the patient’s Instruct the patient to:
knowledge of proper administration. (Proper administration ■ Complete all medication as prescribed.
increases medication effectiveness.) ■ Swish the oral suspension to coat all mucous membranes, and then
swallow the medication.
■ Spit out the medication instead of swallowing if GI irritation occurs.
■ Allow troche to dissolve completely, rather than chewing or swallow-
ing; it may take 30 minutes for it to dissolve completely.
■ Avoid food or drink for 30 minutes following administration.
■ Remove dentures prior to using the oral suspension.
■ Take ketoconazole with water, fruit juice, coffee, or tea to enhance
dissolution and absorption.
■ Administer topical medication correctly and evaluate the patient’s Instruct the patient to:
knowledge of proper administration. (Proper administration increases ■ Use gloves when applying medication.
medication effectiveness.) ■ Avoid wearing tight-fitting undergarments if using ointment in the
vaginal or groin area.
■ Avoid occlusive dressings. (Dressings increase moisture in the infected
areas and encourage development of additional yeast infections.)
■ Monitor for possible adverse effects or hypersensitivity. Instruct the patient to report any of the following to the healthcare provider:
■ Burning, stinging, dryness, itching, erythema, urticaria, angioedema,
and local irritation (for superficial drugs).
■ Symptoms of hepatic toxicity—jaundice, dark urine, light-colored
stools, and pruritus.
■ Nausea, vomiting, and diarrhea.
■ Signs and symptoms of hypo- or hyperglycemia.
■ Monitor for contact dermatitis with topical formulations. (This is ■ Instruct the patient to report any redness or skin rash.
related to the preservatives found in many of the formulations.)
■ Encourage infection control practices. Ensure that the patient, family Instruct the patient to:
members, and other visitors also practice infection control techniques ■ Clean the affected area daily.
such as handwashing and avoiding the affected area (to prevent the ■ Apply medication while wearing a glove.
spread of infection). ■ Wash hands properly before and after application.
■ Change socks daily if rash is on the feet.
■ Avoid sharing personal care items with family members/guests.

Antiviral Drugs
Viruses are infectious agents that require a host to replicate. Core Concept 27.4
Viruses are nonliving agents that infect bacteria, plants, and animals. Viruses contain none of the vital organ-
elles that are present in the cells of living organisms. In fact, the structure of viruses is primitive compared to
even the simplest cell. Surrounded by a protective protein coat or capsid, a virus contains only a few dozen
Figure 27.1
Structure of the human Glycoproteins

immunodeficiency virus
(HIV).
Protein
coat
Reverse
Core
transcriptase
proteins
Envelope
Viral RNA
(lipid bilayer)
genes—either in the form of ribonucleic acid (RNA) or deoxyribonucleic acid (DNA)—that contain the in-
formation needed for viral replication. Figure 27.1 ■ shows the basic structure of one important virus: HIV.
Although nonliving and structurally simple, viruses are capable of remarkable feats. They infect an or-
ganism (the host), by entering a target cell and using the enzymes inside that cell to replicate. Thus, viruses
intra 5 within are called intracellular parasites, meaning that they must be inside a host cell to cause infection. The host
cellular 5 cell organism and cell are often very specific: It may be a single species of plant, bacteria, or animal, or even a
single type of cell within that species. Most often, viruses that infect one species do not affect others, although
cases have been documented in which viruses can mutate and cross species, as is likely the case for HIV.
Many viral infections, such as the rhinoviruses that cause the common cold, are self-limiting and
require no medical treatment. Although symptoms may be annoying, the virus disappears in 7–10 days
and causes no permanent damage if the patient is otherwise healthy. Other viruses, such as HIV, can cause
serious and ultimately fatal disease and require aggressive drug therapy. Antiviral therapy is extremely
challenging because of the rapid mutation rate of viruses, which can quickly render drugs ineffective. Also
complicating therapy is the intracellular nature of the virus, which makes it difficult for medications to find
their targets without giving excessively high doses that injure normal cells. The antiviral medications are
listed in Tables 27.3 ◆ and 27.4 ◆. Each of the antiviral drugs is specific to one particular virus. The three
basic strategies used for antiviral pharmacotherapy are as follows:
■ Prevent viral infections through the administration of vaccines (see Chapter 25).
■ Treat active infections with drugs that interrupt an aspect of the virus’s replication cycle, such as
acyclovir (Zovirax).
■ For long-term infections, use drugs that boost the patient’s immune response (immunostimu-
lants) so that the virus remains in latency and the patient symptom free.
Antiretroviral drugs do not cure HIV-AIDS, but they

Core Concept 27.5 do help many patients live longer.
Drugs for viral infections may be classified into those used to treat HIV-AIDS and those used for other vi-
ral disorders such as herpes and influenza. Antiviral medications for HIV-AIDS have been developed that
slow the growth of HIV by different mechanisms.
The widespread appearance of HIV infection in 1981 created enormous challenges for public health
and for the development of new antiviral drugs. HIV-AIDS is unlike any other infectious disease because
it is uniformly fatal and demands a continuous supply of new drugs for the patients’ survival. The chal-
lenges of HIV-AIDS have been met by the development of more than 20 antiviral drugs. Unfortunately, the
initial hope of curing HIV-AIDS through antiviral therapy or vaccines has not been realized; none of these
medications produces a cure for this disease. Once begun, antiretroviral therapy continues for the life of the
patient because stopping the therapy results in a rapid rebound in HIV replication. HIV mutates extremely
Table 27.3 Antiretroviral Drugs for HIV-AIDS

NONNUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS (NNRTI)
delavirdine (Rescriptor) PO; 400 mg tid Used in combination with other antivirals
efavirenz (Sustiva) PO; 600 mg daily Used in combination with other antivirals; a once-daily form
is available
etravirine (Intelence) PO; 200 mg bid Less central nervous system (CNS) toxicity and
hepatotoxicity than others
nevirapine (Viramune) PO; 200 mg daily for 14 days, then Used in combination with other antivirals
increase to bid
rilpivirine (Edurant) PO; 25 mg once daily Newer drug in this class that offers convenience of once
daily dosing
NUCLEOSIDE AND NUCLEOTIDE REVERSE TRANSCRIPTASE INHIBITORS (NRTI)
abacavir (Ziagen) PO; 300 mg bid A first-line drug for HIV therapy in combination with other
drugs
didanosine (Videx EC) PO; 125–300 mg bid For use in patients who are intolerant to AZT
emtricitabine (Emtriva) PO; 200 mg daily A first-line drug for HIV therapy in combination with other
drugs
lamivudine (Epivir) PO; 150 mg bid Also used to treat chronic hepatitis B (Epivir-HBV).
stavudine (Zerit) PO; 40 mg bid Usually reserved for advanced HIV infections
tenofovir (Viread) PO; 300 mg/day A nucleotide reverse transcriptase inhibitor; a first-line drug
for HIV therapy in combination with other drugs
zidovudine (AZT, PO; 200 mg every 4 hours for 1 month, For symptomatic or asymptomatic HIV; off-label use:
Retrovir) then 100 mg every 4 hours postexposure chemoprophylaxis; IV form available
PROTEASE INHIBITORS
atazanavir (Reyataz) PO; 400 mg/day A first-line drug for HIV therapy in combination with other
drugs
darunavir (Prezista) PO; 600 mg taken with ritonavir Usually reserved for advanced HIV infections
100 mg bid
fosamprenavir (Lexiva) PO; 700–1400 mg bid in combination A first-line drug for HIV therapy in combination with other
with 100–200 mg ritonavir bid drugs
idinavir (Crixivan) PO; 800 mg tid Has short half-life; administer with a high-fat meal to
increase absorption
lopinavir/ritonavir PO; 400/100 mg (three capsules or 5 mL A first-line drug for HIV therapy in combination with other
(Kaletra) of suspension) bid drugs
nelfinavir (Viracept) PO; 750 mg tid Infrequently used due to adverse effects and three doses per
day
ritonavir (Norvir) PO; 600 mg bid Always used in small doses to boost the effectiveness of
other PIs
saquinavir (Invirase) PO; 1,000 mg bid Usually a second-line drug
tipranavir (Aptivus) PO; 500 mg taken with 200 mg of Usually a second-line drug; administer with a high-fat meal
ritonavir bid to increase absorption
MISCELLANEOUS DRUGS FOR HIV
enfuvirtide (Fuzeon) Subcutaneous; 90 mg bid Fusion inhibitor; usually reserved for advanced HIV infections
maraviroc (Selzentry) PO; 150–600 mg bid CCR5 receptor inhibitor; newer drug usually reserved for
advanced HIV infections
raltegravir (Isentress) PO; 400 mg bid Integrase inhibitor; newer drug usually reserved for advanced
HIV infections
rapidly, and resistant strains develop so quickly that the creation of novel approaches to antiretroviral drug
therapy must remain an ongoing process.
After initial exposure, HIV may remain dormant for several months to many years. During this latent
phase, patients are asymptomatic and may not even realize they are infected. Once diagnosis is established,
however, a decision must be made as to when to begin pharmacotherapy. The advantage of beginning the
therapy during the latent stage is that early treatment may delay the onset of acute symptoms and the devel-
opment of AIDS.
Unfortunately, the decision to begin treatment during the latent phase has some negative conse-
quences. Medications for HIV-AIDS are expensive; treatment with some of the newer drugs may cost
more than $30,000 per year. These drugs produce uncomfortable and potentially serious adverse effects.
Therapy over many years promotes viral resistance; when the acute stage eventually develops, the medica-
tions may no longer be effective.
The decision to begin therapy during the acute phase is much easier because the severe symptoms of
AIDS can rapidly lead to death. Thus, therapy is nearly always initiated during this phase, when the CD4
T-cell count falls below 200 cells/mcL or when AIDS-defining symptoms become apparent.
The therapeutic goals for the pharmacotherapy of HIV-AIDS include the following:
■ Reduce HIV-related morbidity and prolong survival
■ Improve the quality of life
■ Restore and preserve natural functions of the immune system
■ Suppress the viral load to the extent possible
■ Prevent the transmission from mother to child in pregnant patients infected with HIV
Although drug therapy for HIV-AIDS has not produced a cure, it has resulted in a number of thera-
peutic successes. For example, many patients with HIV are able to live symptom free with their disease for
a much longer time because of antiviral therapy. Furthermore, the transmission of the virus from a mother
infected with HIV to her offspring has been reduced dramatically because of drug therapy of the mother
prior to delivery and of the baby immediately following birth. These two factors have resulted in a signifi-
cant decline in the death rate due to HIV-AIDS in the United States.
Antiviral medications used for HIV-AIDS are called antiretrovirals because they block the repli-
cation cycle of HIV, which is classified as a retrovirus. The standard treatment for HIV-AIDS includes
aggressive treatment with three to four drugs at a time, a regimen called highly active antiretroviral
therapy (HAART). The goal of HAART is to reduce the amount of HIV in the plasma to its lowest pos-
sible level. It must be understood, however, that HIV is harbored in locations other than the blood, such as
in lymph nodes; therefore, elimination of the virus from the blood is not a cure.
The replication of HIV is illustrated in Figure 27.2 ■. Antiretroviral drugs are classified into groups
based on how they inhibit HIV replication.
■ Nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs and NtRTIs) The oldest
antiretroviral drug, zidovudine, belongs to the NRTI class. Drugs in this group are structurally
similar to nucleosides, the building blocks of DNA. NRTIs inhibit the action of reverse
transcriptase, the viral enzyme that converts viral RNA into viral DNA.
■ Nonnucleoside reverse transcriptase inhibitors (NNRTIs) This class also inhibits the viral en-
zyme reverse transcriptase, but these drugs are not structurally similar to the building blocks of
DNA. Instead, these drugs bind directly to the reverse transcriptase molecule and inhibit its abil-
ity to build viral DNA.
■ Protease inhibitors These drugs block the final assembly of the HIV particle. They are effective
at reducing plasma HIV to very low levels, although resistance develops quickly.
■ Miscellaneous drugs for HIV infection Newer drugs are being developed as scientists discover
more about the HIV replication cycle. Enfuvirtide (Fuzeon) blocks the fusion of HIV to the CD4
receptor on the lymphocyte. Raltegravir (Isentress) is classified as an integrase inhibitor. This
drug prevents HIV from inserting its genes into the human chromosome.
Research into HIV-AIDS is constantly evolving as clinicians strive to determine the most effective
combinations of antiretroviral drugs. In current clinical practice, the following regimens have been shown
to be the most successful choices for the initial therapy of HIV infection (Panel on Antiretroviral Guide-
lines for Adults and Adolescents, 2011):
■ NNRTI-based regimen: efavirenz +tenofovir+emtricitabine
■ PI-based regimens
■ atazanavir (ritonavir-boosted) + tenofovir+emtricitabine
■ darunavir (ritonavir-boosted) + tenofovir+emtricitabine
■ Integrase inhibitor–based regimen: raltegravir + tenofovir + emtricitabine
Figure 27.2
Host
DNA
Viral RNA Viral DNA Viral DNA
Viral
Viral
Integrated mRNA
proteins
Reverse viral DNA
Integrase
transcriptase
2 3 4
Reverse transcriptase Integrase Protease
inhibitors (NNRTIs inhibitors inhibitors
and NRTIs)
1
Entry
inhibitors
CD4 Cytoplasm
receptor
CCR5
coreceptor
Reverse transcriptase
Envelope
Core Coat
Viral RNA
Replication of HIV.
Drug Prototype Zidovudine (AZT, Retrovir)

Therapeutic Class: Antiretroviral Pharmacologic Class: Nucleoside reverse transcriptase inhibitor (NRTI)
Actions and Uses: Zidovudine was first discovered in the 1960s, Adverse Effects and Interactions: Zidovudine can result in
and its antiviral activity was demonstrated prior to the AIDS severe toxicity to blood cells at high doses. Many patients
epidemic. As the HIV reverse transcriptase enzyme begins to report GI symptoms such as anorexia, nausea, and diarrhea.
synthesize viral DNA, it mistakenly uses zidovudine as one of Patients may experience fatigue and report generalized weak-
the building blocks, thus creating a defective DNA strand. Once ness. Headache will occur in the majority of patients taking
incorporated, zidovudine slows synthesis of HIV, thereby reduc- zidovudine, and more serious CNS effects have been reported.
ing symptoms associated with this infection. Zidovudine interacts with many drugs. Acetaminophen
Because of its widespread use over the past 25 years, and ganciclovir may worsen bone marrow suppression. The fol-
strains of HIV resistant to zidovudine are common. It is usually lowing drugs may increase the risk of AZT toxicity: atovaquone,
used in combination with other antiretrovirals because this amphotericin B, aspirin, doxorubicin, fluconazole, methadone,
slows the development of resistance and allows HIV to be and valproic acid.
attacked by several mechanisms. Combination products con- Use with caution with herbal supplements such as St. John’s
taining zidovudine include Combivir (zidovudine and lamivu- wort, which may cause a decrease in antiretroviral activity.
dine) and Trizivir (zidovudine, lamivudine, and abacavir).
Zidovudine is one of the few HIV-AIDS drugs that can
prevent HIV infection. By administering zidovudine to a mother Black Box Warning:
infected with HIV starting at 14 weeks of gestation and to the Rare cases of fatal lactic acidosis with hepatomegaly and
newborn for six weeks following delivery, the risk of transmis- steatosis have been reported with zidovudine use. Bone
sion of the virus to the child can be significantly reduced. Zidovu- marrow suppression may result in neutropenia or severe
dine is also administered as prophylaxis to healthcare providers anemia. Myopathy may occur with long-term use.
following an accidental needlestick or other exposure to HIV.
Although no drug or drug combination has yet been found to cure HIV-AIDS, some progress has been
made on its prevention. In addition, manufacturers have compounded multiple drugs into single tablets for
ease of use. Approved in 2011, Complera combines emtricitabine, rilpirivine, and tenofovir into a tablet
taken once daily. Truvada (emtricitabine + tenofovir) has been found to reduce the risk of acquiring HIV
infection and may be recommended for people at very high risk for the disease. In 2012, the FDA also ap-
proved Stribild for preventing HIV infection. Stribild combines four medications into a single daily tablet:
emtricitabine, tenofovir, elvitegravir, and cobicistat. Newly approved for this combination, elvitegravir is
an integrase inhibitor and cobicistat is an enzyme that prolongs the action of elvitegravir. It is important for
patients to be taught, however, that no drug combination is 100% effective and that established methods for
HIV prevention such as abstinence, condoms, or other safe sex measures should always be implemented.
Concept Review 27.2

■ Why are viral infections difficult to treat with current drugs?
Nursing Process Focus Patients Receiving Pharmacotherapy for HIV-AIDS

Prior to administration: ■ Infection related to compromised immune system
■ Obtain a complete health history, including cardiovascular, GI, neuro- ■ Decisional Conflict related to therapeutic regimen
logical, skin, renal and liver conditions, past infections, allergies, ■ Fear related to HIV diagnosis and a lack of knowledge about thera-
sexual and drug history, and possible drug interactions. peutic regimen
■ Acquire the results of a complete physical examination, including vital ■ Risk for Injury related to adverse effects of drug therapy
signs, height, weight, lung sounds, LOC, ECG, echocardiogram, and ■ Deficient Knowledge related to a lack of information about disease
any signs of a current infection. process, transmission, and drug therapy
■ Evaluate laboratory blood findings: CBC, electrolytes, renal and liver ■ Ineffective Therapeutic Regimen Management related to the complex-
function studies, amylase, glucose, and HIV viral load/CD4 count. ity of therapies (medications, counseling, diet)
■ Obtain specimens for C&S before initiating therapy for possible
bacterial infections.

The patient will:
■ Experience therapeutic effects (a decrease in viral load and an increase in CD4 counts).
Implementation

■ Administer medication correctly and evaluate the patient’s knowledge Inform the patient:
of proper administration, especially monitoring the patient’s ability ■ That treatment for HIV-AIDS is a life-long, ongoing process. Stopping
and motivation to comply with treatment regimen. (Antiretroviral therapy will result in a rebound in the HIV viral replication.
therapy continues for the life of the patient. Stopping the therapy re- ■ Not to stop taking the drug regimen when “feeling better.”
sults in a rapid rebound in HIV replication.) ■ To take according to drug schedule.
■ Not to share doses with others.
■ To return to healthcare provider if adverse effects make adherence to
therapy difficult to continue.
■ Monitor for symptoms of hypersensitivity reactions. (Zalcitabine may ■ Instruct the patient to discontinue the medication and inform the
cause anaphylactic reaction.) healthcare provider if symptoms of hypersensitivity reaction develop,
such as wheezing; shortness of breath; swelling of face, tongue, or
hands; or itching or rash.
■ Monitor vital signs, especially temperature, and for symptoms of in- Instruct the patient:
fection. Monitor white blood cell count. (Antiretroviral drugs such as ■ To report symptoms of infections such as fever, chills, sore throat, and
delavirdine may cause neutropenia.) cough to the healthcare provider.
■ On methods to minimize exposure to infection, such as frequent
handwashing; avoiding crowds and people with colds, flu, and other
infections; limiting exposure to children and animals; increasing fluid
intake; emptying the bladder frequently; and coughing and deep
breathing several times per day.
■ Monitor the patient for signs of stomatitis. (Immunosuppression may ■ Inform the patient to be alert for mouth ulcers and to report their
result in the proliferation of oral bacteria.) appearance to the healthcare provider.
■ Monitor blood pressure. (Antiviral drugs such as abacavir may cause Instruct the patient to:
significant decrease in blood pressure.) ■ Rise slowly from lying or sitting position to minimize effects of pos-
tural hypotension.
■ Report changes in blood pressure.

■ Monitor HIV RNA assay, CD4 counts, liver function, kidney function, Instruct the patient:
CBC, blood glucose, and serum amylase and triglyceride levels. (Moni- ■ On the purpose of required laboratory tests and scheduled follow-ups
toring labs will aid in determining effectiveness and/or drug toxicity.) with the healthcare provider.
■ To monitor weight and presence of swelling.
■ To keep all appointments for laboratory tests.
■ Determine potential drug–drug and drug–food interactions. (Antiret- Instruct the patient:
roviral medications have multiple drug–drug interactions and must be ■ When to take the specific medication in relationship to food intake.
taken as prescribed.) ■ About foods or beverages to avoid when taking medication; some an-
tiretrovirals should not be taken with acidic fruit juice.
■ To take medication exactly as directed; do not skip any doses.
■ To consult with the healthcare provider before taking any OTC medica-
tions or herbal supplements.
■ Monitor for symptoms of pancreatitis, including severe abdominal ■ Instruct the patient to report the following immediately: fever, severe
pain, nausea, vomiting, and abdominal distention. (Antiretroviral abdominal pain, nausea/vomiting, and abdominal distention.
drugs such as didanosine may cause pancreatitis.)
■ Monitor the skin for rash; withhold medication and notify the physi- ■ Advise the patient to check the skin frequently and to notify the
cian at the first sign of rash. (Several antiretroviral drugs may cause healthcare provider at the first sign of any rash.
Stevens–Johnson syndrome, which may be fatal.)
■ Establish therapeutic environment to ensure adequate rest, nutrition, Advise the patient to incorporate the following health-enhancing activities:
hydration, and relaxation. (Support of the immune system is essential ■ Adequate rest and sleep
in patients with HIV to minimize opportunistic infections.) ■ Proper nutrition that provides essential vitamins and nutrients
■ Intake of six to eight glasses of water per day
■ Monitor blood glucose levels. (Antiretroviral drugs may cause hyper- ■ Instruct the patient to report excessive thirst, hunger, and urination to
glycemia, especially in patients with type 1 diabetes.) the healthcare provider.
■ Instruct patients with diabetes to monitor blood glucose levels regularly.
■ Monitor for neurologic adverse effects such as numbness and tingling Instruct the patient to:
of the extremities. (Many NRTI drugs cause peripheral neuropathy.) ■ Report numbness and tingling of extremities.
■ Use caution when in contact with heat and cold due to possible pe-
ripheral neuropathy.
■ Determine the effect of the prescribed antiretroviral drugs on ■ Instruct the patient to use an alternate form of birth control while tak-
oral contraceptives. (Many drugs reduce the effectiveness of oral ing antiretroviral medications.
contraceptives.)
■ Provide resources for medical and emotional support. (Medications for ■ Advise the patient on community resources and support groups.
the treatment of HIV-AIDS can be expensive.)
■ Determine the patient’s understanding of the effect of the medication Advise the patient:
and impact on lifestyle activities. (Antiviral medications used for HIV- ■ That the medication may decrease the level of HIV infection in the
AIDS do not “cure” the disease therefore patients need to understand blood but will not prevent transmission of the virus.
that lifestyle changes still need to occur.) ■ To use barrier protection during sexual activity.
■ To avoid sharing needles.
■ To not donate blood.

lists of drugs to which these nursing actions apply.
Antiviral drugs are available to treat herpes simplex,

influenza, and viral hepatitis infections. Core Concept 27.6
Other than the drugs used to treat HIV, only a few antivirals are available to treat serious viral infections.
These include drugs to treat infections with the herpesviruses, the influenza virus, and the hepatitis virus.
Treatment of herpesvirus infection
Herpes simplex viruses (HSVs) are a family of viruses that cause repeated, blisterlike lesions on the skin,
genitals, and other mucosal surfaces. Herpesviruses are acquired through sexual intercourse or other direct
physical contact with an infected person. The herpesvirus family includes the following:
■ HSV-type 1—primarily causes infections of the eye, mouth, and lips, although the incidence of
genital infections is increasing
■ HSV-type 2—primarily genital infections
■ Cytomegalovirus (CMV)—affects multiple body systems, usually in patients with
immunosuppression
■ Varicella-zoster virus—shingles (zoster) and chickenpox (varicella)

■ Epstein-Barr virus—infectious mononucleosis and Burkitt’s lymphoma (a form of cancer)
Following its initial entrance into the human host, HSV may remain in a latent, nonreplicating state in
nerve cells for many years. Immunosuppression, physical challenge, or emotional stress can activate the vi-
rus and cause the characteristic lesions to reappear. Initial HSV-1 and HSV-2 infections are usually treated
with oral antiviral therapy for 5 to 10 days. Topical drugs are available for application on active lesions, but
they are not as effective as oral medications. Although recurrent herpes lesions are often mild and require
no drug therapy, patients who experience frequent or severe recurrences may benefit from low doses of pro-
phylactic antiviral therapy. It should be noted that the antiviral drugs used to treat herpesviruses do not cure
the patient; the virus remains in the patient for life. Drugs for treating herpesviruses are listed in Table 27.4.
Treatment of Influenza Virus Infection

Influenza is a viral infection characterized by acute symptoms that include sore throat, sneezing, cough-
ing, fever, and chills. The virus is easily spread via airborne droplets. In patients with compromised im-
mune systems, an influenza infection may be fatal.
The best approach to influenza infection is prevention through annual vaccination. Those who benefit
greatly from vaccinations include residents of long-term care facilities, those with chronic cardiopulmo-
nary disease, women who will be in their second or third trimester during the peak flu season, and healthy
adults older than age 50. Adequate immunity is achieved about two weeks after vaccination and lasts for
several months to a year. The CDC recommends that people get vaccinated as soon as the vaccine becomes
available in their community. Additional details on vaccines are presented in Chapter 25.
Antivirals may be used to prevent influenza or decrease the severity of influenza symptoms. The drug
amantadine (Symmetrel) has been available to prevent and treat influenza for many years. Amantadine or riman-
tadine is indicated for unvaccinated high-risk patients after a confirmed outbreak of influenza type A. Therapy
with these antivirals is sometimes started at the same time as vaccination; the antiviral offers protection during
the period before antibody titers are achieved from the vaccine. Antivirals for influenza are shown in Table 27.4.
The neuroamidase inhibitors are used to treat active infections. If given within 48 hours of the onset
of symptoms, oseltamivir (Tamiflu) and zanamivir (Relenza) are reported to shorten the normal seven-
day duration of influenza symptoms to five days. Because these influenza antivirals produce only modest
benefits for patients with an active infection, prevention through vaccination remains the best alternative.
Table 27.4 Antiviral Drugs for Herpes and Influenza Infections

HERPES VIRUS DRUGS
acyclovir (Zovirax) PO; 400 mg tid For HSV-1, HSV-2, and varicella-zoster; topical and IV forms available
cidofovir (Vistide) IV; 5 mg/kg once weekly for 2 consecutive For cytomegalovirus retinitis in patients with AIDS; must give proben-
weeks ecid before and after infusion
docosanol (Abreva) Topical; 10% cream applied to lesion up to five For herpes simplex lesions on the face and lips
times/day
famciclovir (Famvir) PO; 500 mg tid for 7 days For HSV-2 and varicella-zoster
foscarnet (Foscavir) IV; 40–60 mg/kg infused over 1–2 hours tid For cytomegalovirus retinitis; for the treatment of
acyclovir-resistant herpes virus
ganciclovir (Cytovene) PO; 1 g tid IV; 5 mg/kg infused over 1 hour bid Preferred drug for cytomegalovirus; oral form available
penciclovir (Denavir) Topical; 0.5 inch of ointment to each eye For herpes simplex lesions on the face and lips
every 3 hours
trifluridine (Viroptic) Topical; one drop in each eye every 2 hours For herpes eye infections
during waking hours (max: nine drops/day)
valacyclovir (Valtrex) PO; 1 g tid For HSV-1, HSV-2, and varicella-zoster
INFLUENZA DRUGS
amantadine (Symmetrel) PO; 100 mg bid For treatment and prevention of influenza A; also for Parkinson’s
disease
oseltamivir (Tamiflu) PO; 75 mg bid for 5 days For treatment of influenza
rimantadine (Flumadine) PO; 100 mg bid For treatment and prevention of influenza
zanamivir (Relenza) Inhalation; two inhalations per day for 5 days For treatment of influenza
Drug Prototype Acyclovir (Zovirax)

Therapeutic Class: Antiviral for herpesviruses Pharmacologic Class: Nucleoside analog
Actions and Uses: The antiviral activity of acyclovir is limited Adverse Effects and Interactions: There are few adverse effects to
to the herpesviruses, for which it is the preferred drug. It is acyclovir when administered topically or orally. When given IV,
most effective against HSV-1 and HSV-2 and effective only the drug may cause painful inflammation of vessels at the site of
at high doses against CMV and varicella-zoster. By inhibit- infusion. Because nephrotoxicity is possible, especially when the
ing viral DNA synthesis, acyclovir decreases the duration and drug is given by the IV route, kidney function should be carefully
severity of herpes episodes. Resistance has developed to the monitored.
drug, particularly in patients with HIV-AIDS. When given for Acyclovir interacts with several drugs. For example, proben-
prophylaxis, it may decrease the frequency of active herpes ecid decreases acyclovir elimination, and zidovudine may cause
episodes, but it does not cure the patient. It is available in increased drowsiness and lethargy.
topical form for placing directly on active lesions, in oral form
for prophylaxis, and as an IV for particularly severe disease.
Treatment of Viral Hepatitis Infection

Viral hepatitis is a common infection caused by several different viruses: hepatitis A, hepatitis B, and hepatitis
C. Although each has its own unique features, all hepatitis viruses cause inflammation and death of liver cells
and produce similar symptoms. Acute symptoms include fever, chills, fatigue, anorexia, nausea, and vomiting.
Chronic hepatitis may result in prolonged fatigue, jaundice, liver cirrhosis, and, ultimately, hepatic failure.
Hepatitis A Hepatitis A virus (HAV) infection in the United States is usually caused by eating food
contaminated with the virus. The best treatment for HAV is prevention by the administration of HAV vac-
cine (Havrix, VAQTA). Because acute HAV infection is self-limiting, there is no specific therapy for the
condition. Unlike the other hepatitis viruses, HAV infection is not considered to have a chronic component.
Hepatitis B Hepatitis B virus (HBV) is transmitted primarily through exposure to contaminated blood
and body fluids. Major risk factors for HBV include injected drug abuse, sex with a partner infected with
HBV, and sex between men. Healthcare workers are at risk because of accidental exposure to HBV-
contaminated needles or body fluids.
Treatment of acute HBV infection is symptomatic because 90% of these infections resolve with com-
plete recovery and do not progress to chronic disease. Symptoms of chronic HBV, however, may develop
as long as 10 years following exposure. The final stage of the infection is hepatic cirrhosis. In addition,
chronic HBV infections are associated with an increased risk of hepatocellular carcinoma.
The best treatment for HBV infection is prevention through vaccination with HBV vaccine (Recom-
bivax HB, Engerix-B). Once chronic hepatitis becomes active, three different therapies are approved for
pharmacotherapy:
■ Interferon alfa-2B (Intron A) or peginterferon alfa-2A (Pegasys) or 2B (PEG-Intron): these
drugs are natural proteins that suppress viral replication and enhance body defenses
■ Lamivudine (Epivir): resembles a building block for DNA; inhibits viral DNA synthesis
■ Adefovir (Hepsera): blocks viral DNA synthesis; primarily used for patients with viruses resis-
tant to lamivudine.
Hepatitis C Transmitted primarily through exposure to infected blood or body fluids, hepatitis C virus
(HCV) is more common than HBV. HCV is the most common cause of liver transplants. Current pharmaco-
therapy for chronic HCV infection includes interferon (or peginterferon) and the antiviral ribavirin. In 2011, two
new antivirals bocepprevir (Victrelis) and telaprevir (Incivek) were approved for chronic hepatitis C infection.
ANTIPARASITIC Drugs
Infections caused by helminths and protozoans cause
significant disease worldwide. Core Concept 27.7
Other pathogens that may infect humans include single-celled organisms, or protozoans, and multicellular proto = first
animals such as mites, ticks, and worms. Some of these parasites thrive in conditions in which sanitation zoans = animals
and personal hygiene are poor and population density is high. Although many of these diseases are rare in
Table 27.5 Selected Drugs for Helminth and Protozoan Infections

ANTIHELMINTHICs
albendazole (Albenza) PO; 400 mg bid (max: 800 mg/day) Only antihelminthic drug active against all stages
of the helminth life cycle
ivermectin (Stromectol) PO; 150–200 mcg/kg for one dose Preferred drug for many helminth infections
mebendazole (Vermox) PO; 100 mg for one dose or 100 mg bid for For the treatment of whipworm, roundworm,
3 days hookworm, and pinworm
praziquantel (Biltricide) PO; 5 mg/kg for one dose or 25 mg/kg tid For all stages of schistosomiasis; bitter tablet
pyrantel (Antiminth, Ascarel, Pin-X, PO; 11 mg/kg for one dose (max: 1 g) For the treatment of hookworm and roundworm
Pinworm Caplets)
ANTIMALARIALS
artemether and lumefantrine Oral; 3–6 doses for 3 days (20 mg of arte- Newer drug for patients with chloroquine-resistant
(Coartem) mether and 120 mg of lumefantrine per dose) malaria.
atovaquone and proguanil (Malarone) PO; for prophylaxis; one tablet/day starting Also for Pneumocystis
1–2 days before travel, and continuing until
7 days after return
chloroquine (Aralen) PO; 600 mg initial dose, then 300 mg weekly Preferred drug for malaria; also for amebiasis
and rheumatoid arthritis; IM form available; if
administered IV, oral medication is ineffective
hydroxychloroquine (Plaquenil) (see PO; 620 mg initial dose, then 310 mg weekly Also for rheumatoid arthritis and lupus
page 575 for the Drug Prototype box) erythematosus
pyrimethamine (Daraprim) PO; 25 mg once per week for 10 weeks Also antiprotozoan; drug of choice for
toxoplasmosis
ANTIPROTOZOANS (NONMALARIAL)
doxycycline (Vibramycin) PO; 100 mg/day For traveler’s diarrhea; used also for malaria
prophylaxis; a tetracycline antibiotic
metronidazole (Flagyl) PO; 250–750 mg tid For many parasitic infections; IV form available
paromomycin (Humatin) PO; 25–35 mg/kg divided in three doses for For acute and chronic amebiasis; an aminoglycoside
5–10 days antibiotic
pentamidine (NebuPent, Pentam) IV; 4 mg/kg daily for 14–21 days; infuse over For Pneumocystis active infections and prophylaxis;
60 minutes IM and inhalation forms available
tinidazole (Tindamax) PO; 2 grams per day for 3 days Newer drug for amebiasis, giardiasis, or trichomoniasis
the United States and Canada, travelers to Africa, Asia, and South America may acquire infections over-
seas and return home with them. Table 27.5 ◆ lists selected antiparasitics. Scabicides and pediculicides are
covered in Chapter 36.
With a few exceptions, antibiotics, antifungal, and antiviral drugs are ineffective against these com-
plex organisms. Drugs prescribed for parasitic diseases may be classified as antimalarials, antiprotozoans
(other than antimalarial drugs), antihelminthics, and scabicides/pediculicides.
Malaria is a disease caused by four species of the protozoan Plasmodium. Although rare in the United
States and Canada, malaria is the second most common fatal infectious disease in the world, with 300 to
500 million cases occurring annually. The Centers for Disease Control and Prevention (CDC) recommends
that travelers to infected areas receive prophylactic antimalarial drugs prior to and during their visit and
for one week after leaving. Chloroquine (Aralen) is the traditional drug of choice, however, most regions
of the world have developed chloroquine-resistant strains of Plasmodium. Many of the newer drugs used
in high malaria regions have not been approved by the FDA. Healthcare providers planning travel to these
regions should consult the CDC website for the most current information on pharmacotherapy.
Other species of protozoans that cause significant disease worldwide include Entamoeba, Giardia,
Leishmania, Pneumocystis, Toxoplasma, and Trypanosoma. Amebiasis is a disease caused by Entamoeba
histolytica, commonly found in Africa, Latin America, and Asia, where it frequently causes serious dis-
ease. Although primarily an intestinal disease, E. histolytica can invade the liver, where it causes abscesses.
dys = difficult or painful The primary sign of amebiasis is a severe form of diarrhea known as amebic dysentery. Drugs used to treat
enter = intestine amebiasis include those that act directly on amebas in the intestine and those that are administered for their
systemic effects on the liver and other organs.
Helminths consist of various species of parasitic worms, including hookworms, pinworms, round-
worms, tapeworms, and flukes. Many of these worms attach to the mucosa of the human intestinal tract.
Helminth diseases are quite common in areas of the world lacking high standards of sanitation. Helminth
infections in the United States and Canada are generally neither common nor fatal, although drug therapy
may be indicated. The most common helminth disease worldwide is caused by the roundworm Ascaris;
however, infection by the pinworm Enterobius is more common in the United States. For ascariasis, oral
mebendazole (Vermox) for three days is the standard treatment. Pharmacotherapy of enterobiasis includes
a single dose of mebendazole, albendazole (Albenza), or pyrantel (Antiminth). To prevent the spread of
these parasites, good handwashing techniques must be practiced.
Concept Review 27.3

■ How do most patients in the United States and Canada acquire protozoan infections?
Drug Prototype Metronidazole (Flagyl)

Therapeutic Class: Anti-infective, antiprotozoan Pharmacologic Class: Drug that disrupts nucleic acid synthesis
Actions and Uses: Metronidazole is a preferred drug for Adverse Effects and Interactions: Although adverse effects
amebiasis because it is effective against amebas in the are relatively common, most are not serious enough to cause
intestine and in other organs. Metronidazole is also a drug discontinuation of therapy. The most common adverse effects
of choice for two other protozoan infections: giardiasis from of metronidazole are anorexia, nausea, diarrhea, dizziness, and
Giardia lamblia and trichonomiasis due to Trichomonas headache. Dryness of the mouth and an unpleasant metallic
vaginalis. taste may be experienced.
Metronidazole is somewhat unique in that it also has Metronidazole interacts with several drugs. For example, oral
antibiotic activity against anaerobic bacteria and thus is anticoagulants increase hypoprothombinemia. In combination with
used to treat a number of respiratory, bone, skin, and CNS alcohol and medications that contain alcohol, metronidazole may
infections. Topical forms are used to treat rosacea, a disease cause a disulfiram reaction. It may also elevate lithium levels.
characterized by reddening of the sebaceous glands in the
skin around the nose and face. It is used in combination
Black Box Warning:
with bismuth and tetracycline to eradicate H. pylori
infection, which is associated with peptic ulcer disease. Metronidazole (oral and injection) causes cancer in laboratory
animals and should be used only for approved indications.
Patients treated for fungal, viral, or parasitic infections need to know the following:
Regarding Antifungals
1. Avoid alcohol and other drugs toxic to the liver while taking azole-type antifungals.
2. Griseofulvin, used to treat superficial mycoses, can decrease the effectiveness of oral
contraceptives. An alternative method of contraception is advised.
3. Older children and adult patients should swish oral antifungal drugs around in their
mouths and swallow them. Caregivers should swab the mouths of infants and toddlers.
Wait at least 10 minutes after antifungal treatment to put anything else in the mouth.
4. Rinse the mouth after use of corticosteroid inhalers to avoid a decrease in local immune
defenses against oral candidiasis.
5. While taking antifungal drugs for a vaginal infection, refrain from sexual intercourse
until the infection is resolved.
6. Wear gloves when applying topical medications.
Regarding Antivirals
7. When taking antivirals, it is important to report symptoms of hypersensitivity reactions.
8. When taking drugs for HIV-AIDS, avoid crowds and those with infections because many
of these medications will suppress your immune system.
Regarding Helminths and Protozoans
9. Course of treatment depends on the nature of the infection/infestation, and treatment
plan is to be followed completely as prescribed.
10. Take showers instead of baths. Change underwear, linens, and towels daily.
11. Good handwashing practices are a must in the prevention of pinworms/roundworms.
Chapter Review
27.1 Fungal infections are classified as superficial or 27.5 Antiretroviral drugs do not cure HIV-AIDS, but
systemic. they do help many patients live longer.
Fungi are multicellular organisms. Because most are Drugs used to treat HIV infections include the nucle-
unaffected by antibiotics, they require different classes oside and nonnucleoside reverse transcriptase inhibi-
of medications. Fungal infections are usually a serious tors, protease inhibitors, and fusion inhibitors. These
problem only in patients with compromised immune sys- drugs may produce significant toxicity. Although
tems. Mycoses are classified as superficial or systemic. they are not able to cure the disease, they may extend
the symptom-free period.
27.2 Systemic antifungal drugs are used for serious in-
fections of internal organs. 27.6 Antiviral drugs are available to treat herpes sim-
Systemic mycoses affect the internal organs and may re- plex, influenza, and viral hepatitis infections.
quire prolonged and aggressive drug therapy. Systemic Drug therapy is used to extend the latent period of
antifungal drugs may cause serious adverse effects. genital herpes and to speed the recovery from ac-
tive lesions. A few antivirals are available to pre-
27.3 Superficial infections of the skin, nails, and mucous vent influenza, and these are most useful when
membranes are effectively treated with topical combined with vaccines. New drugs have been de-
and oral antifungal drugs. veloped to shorten the discomfort period for influ-
Superficial mycoses of the hair, skin, nails, and mu- enza symptoms, although these drugs have limited
cous membranes are very common, though rarely effectiveness.
serious. Antifungals given topically as powders, tro-
ches, and ointments produce few adverse effects. 27.7 Infections caused by helminths and protozoans
cause significant disease worldwide.
27.4 Viruses are infectious agents that require a host to Malaria is one of the most common infections in the
replicate. world, and a significant number of drugs are available
Viruses take over the cellular machinery of host cells to disrupt the Plasmodium life cycle. Similarly, am-
and use it to replicate themselves. Although most vi- ebiasis is a common protozoan disease requiring in-
ral infections require no pharmacotherapy, patients tensive drug treatment. Diseases caused by helminths
with infections by HIV, herpesviruses, and the influ- are common in areas of the world lacking adequate
enza virus may benefit from drug treatment. sanitation.
Review Questions
The following questions are written in NCLEX-PN® style. Answer 3. The patient with a fungal infection of her toenails asks
these questions to assess your knowledge of the chapter material, how long treatment must occur. The nurse’s best response
and go back and review any material that is not clear to you. would be:
1. The nurse would expect that the patient on amphotericin 1. “Treatment is very quick, requiring only one tablet of
B must be monitored for: clotrimazole.”
2. “Treatment will occur daily for three days.”
1. Ototoxicity 3. “Treatment will last for several months.”
2. Hepatic toxicity 4. “You will need to speak to your physician.”
3. Nephrotoxicity
4. Anoxia
4. When instructing a patient on zidovudine (AZT), the
2. The patient has oral candidiasis. Which of the following nurse would include:
medications does the nurse expect to be ordered? 1. The importance of taking the medication every four hours
1. Terbinafine (Lamisil) for a month
2. Clotrimazole (Mycelex) 2. That the medication is taken daily for one month only
3. Ketoconazole (Nizoral) 3. That if taken correctly, AZT will cure the disease.
4. Nystatin (Mycostatin) 4. That the medication is used to treat symptoms of influenza
Chapter Review 429
5. A patient has just been diagnosed with genital herpes and 8. When applying topical antifungals, which of the follow-
has been prescribed acyclovir (Zovirax). The patient asks how ing statements should be included in a patient teaching plan?
this drug will help his condition. The nurse replies: (Select all 1. No other antifungals should be administered.
that apply.) 2. Gloves should be worn to prevent transmission.
1. “It can be given to reduce the frequency of herpes episodes.” 3. Antifungals should not be applied to open areas.
2. “If taken correctly, this medication will cure the disease.” 4. Vital signs should be checked prior to administration.
3. “It decreases the duration and severity of herpes episodes.”
4. “In addition to treating herpes, it also can be used to treat 9. A patient on an antiretroviral for HIV has developed
HPV.” anemia. The nurse suspects that this condition could indicate
which of the following?
6. The patient complains of flu-like symptoms that started 1. The patient is most likely being abused.
24 hours ago. Which of the following class of medications 2. The patient is experiencing minor adverse reactions.
would the nurse anticipate being ordered? 3. The patient is not taking the medications as ordered.
1. Protease inhibitors 4. The patient may be experiencing severe toxicity due to
2. Nonnucleoside reverse transcriptase inhibitors high doses of the drug.
3. Nucleoside reverse transcriptase inhibitors
4. Neuroamidase inhibitors 10. The nurse is providing education to a mother of a young
patient about pinworms and roundworms. Which of the follow-
7. A patient has started taking metronidazole (Flagyl) for ing should be included in this educational session?
the treatment of Trichomonas vaginalis. The nurse knows to 1. Good handwashing practices are a must in preventing the
monitor her for which of the following adverse effects? (Select spread of pinworms and roundworms.
all that apply.) 2. Play habits do not contribute to the transmission of pin-
1. Vomiting worms and roundworms.
2. Anorexia 3. It is not important that children wear shoes when playing
3. A metallic taste outside.
4. Dryness of the mouth 4. Once the child has had worms, reinfection cannot occur.
Remember Mrs. Davis, the patient 3. Receive a flu vaccination as soon as it becomes available.
introduced at the beginning of the 4. Take acyclovir (Zovirax) during the flu season.
the case study. Based on the informa- 2. Mrs. Davis states, “If I get the vaccine today, when will it
tion you have learned in this chapter, start working?” The nurse tells her that immunity is achieved:
answer the questions that follow. 1. In about a day or two
2. Within a week after the vaccination
Mrs. Martha Davis is a 70-year-old 3. About two weeks after the vaccination
retired auto worker who is frail and in 4. About three to four weeks after the vaccination
ill health and comes to the healthcare
3. Mrs. Davis also reported vaginal itching and abnormal
provider’s office for her annual fall
discharge, and the physician diagnoses vaginal candidiasis.
check-up. Her arthritis is getting
Which of the following medications does the nurse expect to be
worse so she “can’t get around” like she used to do. Although she
ordered?
is not demonstrating any respiratory difficulties at the time of the
visit, she had pneumonia earlier in the year and she states she is 1. Amphotericin B (Fungizone)
“still tired all the time.” In addition, she complains that she started 2. Clotrimazole (Gyne-Lotrimin)
having problems with itching and discharge in the vaginal area. 3. Acyclovir (Zovirax)
4. Tinidazole (Tindamax)
1. The office nurse gives her an informational pamphlet on
the flu vaccine. The information contained in the pamphlet 4. The nurse advises Mrs. Davis that she may experience
states that the best way to avoid a potential life-threatening what adverse effect when taking clotrimazole? (Select all that
bout with the flu is to: apply.)
1. Begin taking oseltamivir (Tamiflu) one month before the 1. Burning
flu season begins. 2. An increase in discharge
2. Take zanamavir (Relenza) within 48 hours of the onset of 3. Itching
flu symptoms. 4. Irritation

C
“I know they are helping
H with my cancer, but four
A different drugs? I guess it
P could be worse.”
T Ms. Patricia Novak
E
R
28 Drugs for Neoplasia
Core Concepts
28.1 Cancer is characterized by rapid, uncontrolled 28.9 Antimetabolites disrupt critical cellular pathways in
growth of cells. cancer cells.
28.2 The causes of cancer may be chemical, physical, or 28.10 A few cytotoxic antibiotics are used to treat cancer
biological. rather than infections.
28.3 Personal risk of cancer may be lowered by a number 28.11 Some natural products kill cancer cells by preventing
of lifestyle factors. cell division.
28.4 The three primary goals of chemotherapy are cure, 28.12 Some hormones and hormone antagonists are
control, and palliation. effective against prostate and breast cancer.
28.5 To achieve a total cure, every malignant cell must be 28.13 Targeted therapies and some miscellaneous
removed or killed. antineoplastic drugs are effective against specific
28.6 Use of multiple drugs and special dosing schedules tumors.
improves the success of chemotherapy. 28.14 Adjunct medications are sometimes necessary
28.7 Serious toxicity limits therapy with most of the to treat cancer symptoms and to reduce the
antineoplastic drugs. intensity of adverse effects from antineoplastic
drugs.
28.8 Alkylating drugs act by changing the structure of
DNA in cancer cells.
Drug Snapshot
Alkylating drugs cyclophosphamide (Cytoxan) Natural products vincristine (Oncovin)
438 443
Antimetabolites ethotrexate (Rheumatrex,

m Hormones and hormone tamoxifen 444
Trexall) 440 antagonists
Antitumor antibiotics doxorubicin (Adriamycin) Adjunct drugs for cancer poetin alfa (Epogen,
e
441 patients Procrit) 446
Learning Outcomes
1. Explain differences between normal 3. Describe the lifestyle factors 4. Differentiate among the terms
cells and cancer cells. associated with a reduced risk of neoplasm, benign, malignant,
2. Identify the factors associated with acquiring cancer. and carcinoma.
an increased incidence of cancer.
5. Identify the three primary increase the effectiveness of 10. For each of the classes listed in
treatments for cancer. chemotherapy. the Drug Snapshot, explain their
6. Explain why cancer is difficult 8. Describe the general adverse effects mechanisms of drug action,
to cure. of antineoplastic drugs. primary actions, and important
adverse effects.
7. Explain how combination therapy 9. Categorize anticancer drugs
and special dosing schedules based on their classifications and
mechanisms of action.
Key Terms
adenomas (AH-den-OH-mahz) 432 gliomas (glee-OH-muhz) 432 purines (PYUR-eenz) 439
adjuvant chemotherapy (AD-ju-vent) 433 leukemia (lew-KEE-mee-ah) 432 pyrimidines (peer-IM-uh-deenz) 439
alkylation (AL-kill-AYE-shun) 437 lipomas (lip-OH-mahz) 432 targeted therapies 445
alopecia (AL-oh-PEESH-ee-uh) 436 liposomes (LIP-oh-sohms) 441 taxanes (TAKS-ane) 442
anemia (ah-NEE-mee-ah) 446 lymphomas (lim-FOH-mahz) 432 topoisomerase (TOH-poh-eye-SOM-
benign (bee-NINE) 432 malignant (mah-LIG-nent) 432 er-ase) 442
cancer (KAN-sir) 431 metastasis (mah-TAS-tah-sis) 432 tumor (TOO-more) 432
carcinogens (kar-SIN-oh-jenz) 432 neoplasm (NEE-oh-PLAZ-um) 432 tumor suppressor genes 432
chemotherapy 433 nitrogen mustards 437 vinca alkaloids (VIN-ka AL-kah-
loids) 442
folic acid (FOH-lik) 440 palliation (PAL-ee-AYE-shun) 433
C ancer is one of the most feared diseases for a number of valid reasons. It may be silent, producing
no symptoms until it is too advanced for a complete cure. It sometimes requires painful and disfig-
uring surgery. It may strike at an early age—even during childhood—depriving people of a normal
lifespan. Perhaps worst of all, the medical treatment of cancer often cannot offer a cure, and progression to
death is sometimes psychologically difficult for patients and their loved ones.
Despite its feared status, many advances have been made in the diagnosis, understanding, and treat-
ment of cancer. Modern treatment methods result in a cure for nearly two of every three cancer patients
and the five-year survival rate has steadily increased for many types of cancer. This chapter examines the
role of drugs in the treatment of cancer. Medications used to treat this disease are called anticancer drugs,
antineoplastics, or cancer chemotherapeutic agents.
Cancer is characterized by rapid, uncontrolled growth of cells. Core Concept 28.1
Cancer is a disease characterized by abnormal, uncontrolled cell division. Cell division is a normal process
occurring extensively in most body tissues from conception to late childhood. At some point in time, how-
ever, most cells stop dividing at such a rapid rate. Indeed, some adult cells such as muscle cells and brain cells
have a total lack of ability to divide. In other cells, the genes controlling growth can be turned back on when-
ever it is necessary to replace worn-out cells, as is the case for blood cells and cells lining the digestive tract.
Fast Facts Cancer

■ It is estimated that more than 1,660,000 new cancer cases occur each year, in the United States,
with about 580,300 deaths (almost 1,600 people every day).
■ Although cancer occurs most frequently in older adults, over 11,600 new cases of childhood
cancer occur annually.
■ Leukemia is the most common childhood cancer and is responsible for one quarter of all cancers
occurring before age 20.
■ Lung cancer has the highest mortality rate in both women and men, being responsible for about
29% of all cancer deaths.
■ Death rates for breast cancer have steadily decreased in women since 1989, with larger decreases
in younger than in older women.
■ Pancreatic cancer has the lowest five-year survival rate at 6%. About 65% of patients with pancre-
atic cancer have either diabetes or prediabetes at the time of diagnosis.
■ The highest five-year survival rates are for cancers of the prostate, testes, and thyroid. The lowest
survival rates are for pancreatic, lung, and liver cancers.
■ Among ethnic groups, African Americans have the highest incidence and death rates for most types
of cancers.
432 Chapter 28 Drugs for Neoplasia
Figure 28.1
Invasion and metastasis Cancer cells

by cancer cells. Blood vessels traveling to
distant sites
Motile
cancer
cells
Primary
invasive
cancer
Brain metastases
Lymphatic
ducts
Breast cancer Lung metastases
Cancer is thought to result from the damage to genes controlling cell growth. Once damaged, the cell
becomes unresponsive to normal chemical signals checking its growth. The cancer cells lose their normal
functions, divide rapidly, and invade surrounding cells. The abnormal cells often travel to distant sites, where
they populate new tumors, a process called metastasis. Figure 28.1 ■ illustrates the metastasis of cancer cells.
neo 5 new The word tumor means swelling, abnormal enlargement, or mass. Neoplasm is often used inter-
plasm 5 thing formed changeably with tumor. The suffix -oma signifies tumor. Tumors may be either benign or malignant.
Benign tumors grow slowly, do not metastasize, and rarely require drug treatment. Although they
do not kill patients, their growth may cause pressure on nerves, blood vessels, or other tissues. When this
adeno 5 gland occurs, they may be surgically removed; they do not normally grow back. Examples include adenomas,
oma 5 tumor which are benign tumors of glandular tissue, and lipomas, which are tumors of adipose tissue.
lip 5 fat
Malignant tumors are called cancer. The word malignant refers to a disease that grows rapidly worse,
becomes resistant to treatment, and normally results in death. The two major divisions of malignant neo-
plasms are carcinomas and sarcomas. Other types include cancer of the blood-forming cells in bone mar-
leuk 5 white row (leukemia), cancers of lymphatic tissue (lymphomas), and cancers of the central nervous system
emia 5 blood condition (CNS) (gliomas).
Core Concept 28.2 The causes of cancer may be chemical, physical, or biological.
A large number of factors have been found to cause cancer or to be associated with a higher risk for acquir-
ing the disease. These factors are known as carcinogens.
Many chemical carcinogens have been identified. For example, chemicals in tobacco smoke are
responsible for about one-third of all cancers in the United States. Some chemicals, such as asbestos and
benzene, have been associated with a higher incidence of cancer in the workplace. The actual site of the
cancer may be distant from the site of exposure, as is the case of bladder cancer caused by the inhalation of
certain industrial chemicals.
A number of physical factors are also associated with cancer. For example, exposure to large amounts
of x-rays is associated with a higher risk of leukemia. Ultraviolet (UV) light from the sun is a known cause
of skin cancer.
Viruses are associated with about 15% of all human cancers. Examples include herpes simplex viruses
types I and II, Epstein-Barr virus, human papillomavirus (HPV), cytomegalovirus, and human T-lymphotrophic
viruses. Factors that suppress the immune system, such as HIV or drugs given after transplant surgery, may
encourage the growth of cancer cells.
Some cancers have a strong genetic component. The fact that close relatives may acquire the same
type of cancer suggests that the patient may have certain genes that predispose him or her to the condition.
These abnormal genes interact with chemical, physical, and biological agents to promote cancer forma-
tion in the patient. Other genes, called tumor suppressor genes, may inhibit the formation of tumors. The
BRCA gene is an example of a tumor suppressor gene that, once damaged, results in a significantly higher
incidence of breast cancer. About 40% to 65% of women who have the BRCA mutation will develop
breast cancer before age 70.
Concept Review 28.1

■ What is the fundamental feature that makes a cancer cell different from a normal cell?
Personal risk of cancer may be lowered by a number

of lifestyle factors. Core Concept 28.3
Fortunately, adopting healthy lifestyle habits such as those shown in the following list may reduce the risk
of acquiring cancer. Eliminating tobacco use is the most important means of reducing cancer risk. Limiting
exposure to exhaled, or secondhand, smoke is also thought to be important. Intake of alcoholic beverages
and saturated fats should be limited, and body weight kept within medically recommended ranges. The fol-
lowing list indicates some actions that healthcare providers can recommend to their patients to reduce their
risk of cancer:
■ Eliminate tobacco use and exposure to secondhand tobacco smoke.
■ Maintain a healthy diet low in fat and high in fresh vegetables and fruit.
■ Choose most of the foods from plant sources; increase fiber in the diet.
■ Exercise regularly and keep body weight within optimum guidelines.
■ Self-examine your body monthly for abnormal lumps and skin lesions.
■ Avoid chronic or prolonged exposure to direct sunlight and/or wear protective clothing
or sunscreen.
■ For women, have periodic mammograms, according to the schedule recommended by their
■ For men, receive prostate screening, as recommended by their healthcare provider.
■ Receive screening colonoscopy, as recommended by the healthcare provider.
■ For women who are sexually active or have reached age 18, have an annual Pap test and pelvic
examination.
■ For girls, receive the HPV vaccine (Cervarix, Gardasil) according to the schedule recommended
by the Centers for Disease Control and Prevention.
The three primary goals of chemotherapy are cure,

control, and palliation. Core Concept 28.4
Pharmacotherapy of cancer is sometimes simply referred to as chemotherapy. Because oral and parenteral
drugs are transported through the blood, chemotherapy has the potential to reach cancer cells in virtually
any location. Chemotherapy has three general goals: cure, control, or palliation.
When diagnosed with cancer, the primary goal desired by most patients is to achieve a complete cure:
permanent removal of all cancer cells from the body. The possibility for cure is much greater if a cancer
is identified and treated in its early stages, when the tumor is small and localized to a well-defined region.
Examples in which chemotherapy has been used successfully as curative treatments include Hodgkin’s
lymphoma, certain leukemias, and choriocarcinoma.
When cancer has progressed and cure is not possible, a second goal of chemotherapy is to control or
manage the disease. Although the cancer is not eliminated, preventing the growth and spread of the tumor may
extend the patient’s life. Essentially, the cancer is managed as a chronic disease, as is hypertension or diabetes.
In its advanced stages, cure or control of the cancer may not be achievable. For these patients, chemo-
therapy is used as palliation. Chemotherapy drugs are administered to reduce the size of the tumor, easing
the severity of pain and other tumor symptoms, thus improving the quality of life.
Chemotherapy may be used alone or in combination with surgery or radiation therapy. Surgery is espe-
cially useful for removing solid tumors that are localized. Surgery lowers the number of cancer cells in the body
so that radiation therapy and pharmacotherapy can be more successful. Surgery is not an option for tumors of
blood cells or when it would not be expected to extend a patient’s life span or to improve the quality of life.
Approximately 50% of patients with cancer receive radiation therapy as part of their treatment. Radi-
ation therapy is most successful for cancers that are localized. Radiation treatments are frequently pre-
scribed postoperatively to kill cancer cells that may remain following an operation. Radiation is sometimes
given as palliation for inoperable cancers to shrink the size of a tumor that may be pressing on vital organs
and to relieve pain, difficulty breathing, or difficulty swallowing.
Adjuvant chemotherapy is the administration of antineoplastic drugs after surgery or radiation
therapy. The purpose of adjuvant chemotherapy is to rid the body of any cancerous cells that were not
removed during the surgery or to treat any microscopic metastases that may be developing. In a few cases,
drugs are given as chemoprophylaxis with the goal of preventing cancer from occurring. For example,
some patients who have had a primary breast cancer removed may receive tamoxifen, even if there is no
evidence of metastases, because there is a high likelihood that the disease will recur. Chemoprophylaxis
of cancer is uncommon, because most of these drugs have potentially serious adverse effects.
To achieve a total cure, every malignant cell must be removed

Core Concept 28.5 or killed.
To cure a patient, it is believed that every single cancer cell must be eliminated from the body. Leaving
even a single malignant cell could result in regrowth of the tumor. Eliminating every cancer cell, however,
is a very difficult task.
Consider that a 1-cm breast tumor may contain 1 billion cancer cells before it is detected. A drug that
kills 99% of these cells would be considered a very effective drug. Yet even with this fantastic achieve-
ment, 10 million cancer cells would still remain, any one of which could cause the tumor to return and kill
the patient. The relationship between cell kill and chemotherapy is shown in Figure 28.2 ■.
It is likely that no antineoplastic drug (or combination of drugs) will kill 100% of the tumor cells. The
large burden of cancer cells, however, may be lowered sufficiently to permit the patient’s immune system
to control or eliminate the remaining cancer cells. Because the immune system is able to eliminate only a
relatively small number of cancer cells, it is important that as many cancerous cells as possible be elimi-
nated during treatment. This example reinforces the need to diagnose and treat tumors at an early stage,
when the number of cancer cells is smaller.
Figure 28.2
Cell kill and

chemotherapy.
Primary tumor
1,000,000,000 cells
First round of
chemotherapy
Reduced tumor
99% kill
10,000,000 cells
Second round of
chemotherapy
Reduced tumor
99.9% kill
1,000,000 cells
T cells
removing
remaining
cancer cells
CAM THERAPY
Selenium’s Role in Cancer Prevention
Selenium is an essential trace element that is necessary to maintain healthy immune function.
It is a vital antioxidant, especially when combined with vitamin E. It protects the immune sys-
tem by preventing the formation of free radicals, which can damage cells.
Selenium can be found in meat and grains, Brazil nuts, brewer’s yeast, broccoli, brown rice,
dairy products, garlic, molasses, and onions. The amount of selenium in food, however, has
a direct correlation to the selenium content of the soil. The soil of much American farmland
is low in selenium, resulting in selenium-deficient produce. Low dietary intake of s elenium is
associated with increased incidence of several cancers, including lung, colorectal, skin, and
prostate cancers. Selenium supplementation has resulted in increased natural killer cell activ-
ity, and studies have shown its promise as protection against prostate and colorectal c ancers,
especially among smokers.
Use of multiple drugs and special dosing schedules improve

the success of chemotherapy. Core Concept 28.6
Because of their rapid cell division, tumor cells express a high mutation rate. This causes the tumor to
change its genetic make-up as it grows, resulting in hundreds of different clones with different growth
rates and physiologic properties. An antineoplastic drug may kill only a small portion of the tumor, leaving
some clones unaffected. Complicating the chances for a cure is that cancer cells often develop resistance
to antineoplastic drugs. Thus a therapy that was very successful in reducing the tumor mass at the start of
chemotherapy may become less effective over time.
A number of treatment strategies have been found to increase the effectiveness of anticancer
drugs. In most cases, multiple medications from different antineoplastic classes are given concurrently
during a course of chemotherapy. Multiple classes will affect different stages of the cancer cell’s life
cycle, as illustrated in Figure 28.3 ■. This allows the tumor to be attacked through several mechanisms
of action, thus increasing the cell kill percentage. Using multiple drugs also allows the dosages of each
individual medication to be lowered, thereby reducing toxicity and slowing the development of resis-
tance. Examples of common therapies include cyclophosphamide-methotrexate-fluorouracil (CMF)
Figure 28.3
Antineoplastic drugs
• Methotrexate
and the cell cycle.
• Fluorouracil
• Mercaptopurine
• Asparaginase • Cytarabine
• Pegaspargase • Topotecan
G1 S
Early protein DNA synthesis G2
synthesis RNA
G0 synthesis
Resting phase • Bleomycin
• Etoposide
• Paclitaxel
Telophase MITOSIS
Prophase
Nonspecific to
phase of cell cycle Prometaphase
• Alkylating agents Anaphase

• Antitumor antibiotics
• Hormones Metaphase • Vincristine
• Hormone inhibitors • Vinblastine
for breast cancer, cyclophosphamide-doxorubicin-vincristine (CAV) for lung cancer, and cyclo-
phosphamide-doxorubicin-vincristine-prednisone (CHOP) for non-Hodgkin’s lymphoma. Each type
of cancer requires its own individual protocol, which is continually being revised based on recent
research.
Specific dosing schedules or cycles have been found to increase the effectiveness of antineoplastic
drugs. For example, some anticancer drugs are given as single doses or perhaps a couple of doses over a
few days. Several weeks may pass before the next series of doses. This gives normal cells time to recover
from the adverse effects of the drugs, especially bone marrow suppression. It also allows tumor cells that
may not have been replicating at the time of the first dose to begin dividing and become more sensitive to
the next round of chemotherapy. The specific dosing schedule depends on the type of tumor, stage of the
disease, and the patient’s overall condition.
Concept Review 28.2

■ Why is it important to kill or remove 100% of the cancer cells to achieve a cure?
Serious toxicity limits therapy with most of

Core Concept 28.7 the antineoplastic drugs.
Almost all anticancer drugs have the potential to cause serious toxicity. These drugs are often pushed to
their maximum possible dosages so that the greatest cell kill can be obtained. Such high dosages always
result in adverse effects in the patient. A list of typical adverse effects of anticancer drugs is given in
Table 28.1 ◆.
Normal tissues that are rapidly dividing in the adult are most susceptible to adverse effects. Hair
follicles are damaged, resulting in hair loss or alopecia. The lining of the digestive tract is affected,
sometimes resulting in bleeding, difficulty eating, or severe diarrhea. The vomiting center in the
medulla is triggered by many antineoplastics, resulting in severe nausea and vomiting. Vomiting is
often so severe that patients may be treated with antiemetic drugs such as prochlorperazine (Com-
pazine) or odansetron (Zofran) just prior to the start of antineoplastic therapy. Blood cells in the
bone marrow may be destroyed, causing a reduction in the number of red blood cells (RBCs), white
blood cells (WBCs), and platelets. Severe effects on blood cells often cause discontinuation of chemo-
therapy. Efforts to minimize this toxicity may include therapy with growth factors such as filgrastim
(Neupogen) or sargramostim (Leukine). These drugs stimulate the production of WBCs within the
bone marrow.
Antineoplastic drugs act by many mechanisms, most of which involve cell killing, or cytotoxicity.
Classification is quite variable because some drugs kill cancer cells by several mechanisms and have char-
acteristics from more than one class. Furthermore, the mechanisms by which some of these medications
act are not completely understood. A simple method of classifying this complex class of drugs includes the
following groups:
■ Alkylating drugs
■ Antimetabolites
■ Antitumor antibiotics
■ Natural products
■ Hormones and hormone blockers
■ Targeted therapies and miscellaneous drugs
Table 28.1 Adverse Effects of Anticancer Drugs

Blood Toxicity GI Toxicity Other Effects
Anemia (low red blood cell count) Anorexia (loss of appetite) Alopecia (loss of hair)
Leukopenia (low white blood cell count) Bleeding Fatigue
Thrombocytopenia (low platelet count) Diarrhea Fetal birth defects
Nausea and vomiting Opportunistic infections
Ulceration and bleeding of the lips and gums
Alkylating drugs act by changing the structure of DNA

in cancer cells. Core Concept 28.8
Alkylating drugs act by chemically binding to DNA and inhibiting cell division. They are some of the most
widely used antineoplastic drugs. Table 28.2 ◆ lists the alkylating drugs and their dosages.
The first alkylating drugs, the nitrogen mustards, were developed in secrecy as chemical warfare
agents during World War II. Although the drugs in this class have very different chemical structures, all
have the common characteristic of being able to form bonds or linkages with DNA. These agents physi-
cally attach to DNA, a process called alkylation. Alkylation changes the shape of DNA and prevents it
from functioning normally. Although each alkylating drug attaches to DNA in a different manner, col-
lectively they have the effect of inducing cell death, or at least slowing the replication of tumor cells. The
alkylation may occur in any cancer cell; however, the killing action does not occur until the affected cell
attempts to divide. Figure 28.4 ■ illustrates the process of alkylation.
Because blood cells are particularly sensitive to alkylating drugs, bone marrow suppression is the
primary dose-limiting toxicity of these drugs. Within days of administration, the numbers of RBCs, WBCs,
and platelets begin to decline. Cells lining the gastrointestinal (GI) tract are also damaged, resulting in nau-
sea, vomiting, and diarrhea. Alopecia is expected from most of the alkylating drugs. As a delayed adverse
effect, some patients treated with alkylating agents will develop acute leukemia four years or more after
chemotherapy has been completed.
Table 28.2 Alkylating Drugs

Nitrogen Mustards
bendamustine (Treanda) IV; 90–120 mg/m2 (variable schedule) Newer antineoplastic drug; for chronic lymphocytic
leukemia and non-Hodgkin’s lymphoma
busulfan (Busulflex, Myleran) PO; 4–8 mg daily For chronic myelogenous leukemia; also available IV, prior to
stem cell transplant
chlorambucil (Leukeran) PO; initial dose 0.1–0.2 mg/kg daily; For chronic lymphocytic leukemia; non-Hodgkin’s
maintenance dose 4–10 mg daily lymphoma, and cancer of the breast and ovary
cyclophosphamide PO; initial dose 1–5 mg/kg daily; For Hodgkin’s disease, non-Hodgkin’s lymphoma, leukemias,
(Cytoxan) maintenance dose 1–5 mg/kg every multiple myeloma, and cancer of the
7–10 days breast, ovary, and lung; IV form available
estramustine (Emcyt) PO; 14 mg/kg/day in 3–4 divided doses For palliative treatment of advanced prostate
cancer
ifosfamide (Ifex) IV; 1.2 g/m2 daily for five consecutive days For testicular cancer
mechlorethamine (Mustargen) IV; 6 mg/m2 on days 1 and 8 of a 28-day For Hodgkin’s disease, non-Hodgkin’s lymphoma,
cycle and lung cancer
melphalan (Alkeran) PO; 6 mg daily for 2–3 weeks For multiple myeloma
Nitrosoureas
carmustine (BiCNU, Gliadel) IV; 200 mg/m2 every 6 weeks For Hodgkin’s disease, malignant melanoma, multiple
myeloma, and brain cancer
lomustine (CeeNU) PO; 130 mg/m2 as a single dose For Hodgkin’s disease and brain cancer
streptozocin (Zanosar) IV; 500 mg/m2 for five consecutive days For pancreatic cancer
OTHER Alkylating Drugs
carboplatin (Paraplatin) IV; 360 mg/m2 every 4 weeks For cancer of the ovary
cisplatin (Platinol) IV; 20 mg/m2 daily for 5 days For testicular, bladder, ovarian, uterine, head, and neck
carcinomas
dacarbazine (DTIC-Dome) IV; 2–4.5 mg/kg daily for 10 days For Hodgkin’s disease and malignant melanoma
oxaliplatin (Eloxatin) IV; 85 mg/m2
infused over 120 minutes once For metastatic colorectal cancer
every 2 weeks
temozolomide (Temodar) PO; 150 mg/m2 daily for five For brain cancer
consecutive days
thiotepa (Thioplex) IV; 0.3–0.4 mg/kg every 1–4 weeks For Hodgkin’s disease and breast and ovarian cancer
Figure 28.4
C
alkylating drugs. G
T A
C
C G G
T A
C G
A T
A T
X Cross-link between DNA strands

G C
G C
C G
C G
T
A
T A
C
G
C G X
A T A
T
T A T
A
G X C G
C
C G X = Alkylating drug C G
DNA DNA
(a) Alkylation occurring during G0 (b) Strand breaks occurring

(resting) phase of cell cycle when DNA replicates
during S phase of cell cycle
Drug Prototype: Cyclophosphamide (Cytoxan)

Therapeutic Class: Antineoplastic Pharmacologic Class: Alkylating drug
Actions and Uses: Cyclophosphamide is a commonly prescribed observed. Nausea, vomiting, and diarrhea are frequently
nitrogen mustard. It is used alone or in combination with other experienced. Fifty percent of patients will develop total
drugs against a wide variety of cancers, including Hodgkin’s baldness, although this effect is usually reversible. Unlike
disease, lymphoma, multiple myeloma, breast cancer, and ovar- other nitrogen mustards, cyclophosphamide causes little
ian cancer. Cyclophosphamide acts by attaching to DNA and neurotoxicity.
disrupting cell replication, particularly in rapidly dividing cells. Cyclophosphamide interacts with many drugs. For
It is one of only a few anticancer drugs that are well absorbed example, immunosuppressant agents may increase the
when given orally. risk of infections and promote the development of neo-
Cyclophosphamide is a powerful immunosuppressant. plasms. There is an increased chance of bone marrow
Although this is considered an adverse effect during cancer toxicity if cyclophosphamide is used together with allopu-
chemotherapy, the drug is sometimes used to intentionally rinol. There is an increased risk of bleeding if given with
cause immunosuppression for the prophylaxis of organ trans- anticoagulants.
plant rejection and to treat severe rheumatoid arthritis and If used with digoxin, decreased serum levels of digoxin
systemic lupus erythematosus (SLE). occur. Using it with insulin may lead to increased hypoglyce-
mia. Phenobarbital, phenytoin, or glucocorticoids may lead
Adverse Effects and Interactions: Bone marrow suppression to an increased rate of cyclophosphamide metabolism by the
is a potentially life-threatening adverse reaction that occurs liver. Thiazide diuretic use with cyclophosphamide may lead
during days 9–14 of therapy; the patient is at dangerous risk to leukopenia.
for severe infection and sepsis during this period. Throm- St. John’s wort may increase the toxic effects of
bocytopenia is common; thus bleeding and bruising may be cyclophosphamide.
Antimetabolites disrupt critical cellular pathways

in cancer cells. Core Concept 28.9
Rapidly growing cancer cells require large amounts of nutrients to build proteins and nucleic acids. Anti-
metabolites are drugs that chemically resemble essential building blocks of the cell. When cancer cells
attempt to construct proteins or DNA, they use the antimetabolite drugs instead of the normal building
blocks. By disrupting metabolic pathways in this manner, antimetabolites can kill cancer cells or slow
their growth. For example, methotrexate interferes with the synthesis of folate. Folate is required for the
synthesis of DNA, RNA, and protein in rapidly dividing cancer cells. The antimetabolites are listed in
Table 28.3 ◆.
Several of these antimetabolites resemble purines and pyrimidines, chemicals that are the building
blocks of DNA and RNA. These antimetabolites are called purine or pyrimidine analogs. For example,
floxuridine (FUDR) and fluorouracil (Adrucil) are able to block the formation of thymidylate, an essential
chemical needed to make DNA. After becoming activated and incorporated into DNA, cytarabine (Cyto-
sar) blocks DNA synthesis. Figure 28.5 ■ illustrates the similarities of some of these analogs to their natu-
ral counterparts.
Table 28.3 Antimetabolites

Folic Acid Antagonists
methotrexate PO; 10–30 mg/day for 5 days For acute lymphoblastic leukemia, choriocarcinoma, lymphoma,
(Rheumatrex, Trexall) head and neck cancer, testicular cancer, bone cancer; IV and IM
forms available
pemetrexed (Alimta) IV; 500 mg/m2 on day 1 of each 21-day cycle For malignant mesothelioma and non–small cell lung cancer
pralatrexate (Folotyn) IV; 30 mg/m2 administered over 3–5 minutes For refractory T-cell lymphoma
Pyrimidine and purine Analogs
capecitabine (Xeloda) PO; 2,500 mg/m2 daily for 2 weeks For metastatic breast cancer and colon cancer
cladribine (Leustatin) IV; 0.09 mg/m2 For hairy cell leukemia
clofarabine (Clolar) IV; 52 mg/m2 over 2 hours for five For childhood acute lymphoblastic leukemia
consecutive days
cytarabine (Cytosar, Cytosine IV; 200 mg/m2 as a continuous infusion over For leukemias and lymphomas; subcutaneous and intrathecal
arabinoside, Depot-Cyt) 24 hours forms available
fludarabine (Fludara) IV; 25 mg/m2 daily For chronic lymphocytic leukemia
floxuridine (FUDR) Intra-arterial; 0.1–0.6 mg/kg daily For metastasis from the GI tract to the liver
as a continuous infusion
fluorouracil (5-FU, Adrucil, IV; 12 mg/kg daily for four consecutive days For cancer of the breast, colon, rectum, stomach, and pancreas;
Efudex, Fluorodex) topical form available for basal cell carcinoma
gemcitabine (Gemzar) IV; 1,000 mg/m2 every week For advanced cancers of the pancreas, breast, ovaries,
and lung
mercaptopurine (6-MP, PO; 2.5 mg/kg daily For childhood acute leukemia
Purinethol)
nelarabine (Arranon) IV; 1,500 mg/m2 on days 1, 3, and For leukemias and lymphomas
5; repeat every 21 days
pentostatin (Nipent) IV; 4 mg/m2 every other week For hairy cell leukemia
thioguanine (Tabloid) PO; 2 mg/kg daily For remission induction in adult acute leukemia
Figure 28.5
Normal metabolite
OH COOH
N O
N CH2 NH CO NH CH O
HN
CH2 N
H2N N N H N
CH2 O N
H 2N N N
CO NH H H
Folic acid Guanine Uracil
Antimetabolite
S O
H2N N N CH3 O H F
COOH N
N HN
N H N C CH
N C N CH2 CH2 COOH
H H H 2N N N O N
NH2 H H
Methotrexate Thioguanine Fluorouracil
Structural similarities between antimetabolites and their natural counterparts.
Drug Prototype: Methotrexate (Rheumatrex, Trexall)

Therapeutic Class: Antineoplastic Pharmacologic Class: Antimetabolite, folic acid analog
Actions and Uses: Methotrexate blocks folic acid metabolism in Aspirin may interfere with excretion of methotrexate, leading to
rapidly growing tumor cells. Folic acid is a water-soluble vitamin increased serum levels and toxicity. Administration with live oral
found in eggs, veal, liver, whole grains, and dark green vegeta- vaccine may result in decreased antibody response and increased
bles. Folic acid is part of a coenzyme essential to the synthesis of adverse reactions to the vaccine. Use with caution with herbal sup-
nucleic acids. plements, such as echinacea, which may interfere with the drug’s
Methotrexate is prescribed alone or in combination with immunosuppressant effects.
other drugs for choriocarcinoma, bone cancers, leukemias,
head and neck cancers, breast carcinoma, and lung carcinoma.
It is occasionally used to treat non-neoplastic disorders such Black Box Warnings:
as severe psoriasis, rheumatoid arthritis, and lupus that are Methotrexate combined with nonsteroidal anti-inflam-
unresponsive to safer medications. matory drugs (NSAIDs) may cause severe and sometimes
fatal bone marrow suppression, which is the primary dose-
Adverse Effects and Interactions: Methotrexate has many limiting toxicity of this drug. The drug is hepatotoxic and
adverse effects, some of which can be life threatening and may cause liver cirrhosis. Ulcerative stomatitis and diarrhea
which are described in the black box warning. In addition, require suspension of therapy because they may lead to
hemorrhage and bruising due to low platelet counts are intestinal bleeding or perforation. Potentially fatal opportu-
often observed. Nausea, vomiting, and anorexia are common. nistic infections may occur during therapy. Pulmonary toxic-
Methotrexate is a pregnancy category X drug. ity may result in acute or chronic interstitial pneumonitis at
Methotrexate interacts with several drugs. Bone marrow sup- any dose level. Severe, sometimes fatal, dermatologic reac-
pressants such as other antineoplastic drugs may cause increased tions such as toxic epidermal necrolysis and Stevens–Johnson
effects; the patient will require a lower dose of methotrexate. syndrome (SJS) have been reported.
When used with NSAIDs, severe methotrexate toxicity may occur.
Core Concept 28.10 A few cytotoxic antibiotics are used to treat cancer rather than infections.
Antitumor antibiotics are drugs obtained from bacteria that have the ability to kill cancer cells. Although
they are not widely prescribed, they are very effective against certain tumors. Table 28.4 ◆ lists the pri-
mary antitumor antibiotics.
Table 28.4 Antitumor Antibiotics

bleomycin (Blenoxane) IV; 0.25–0.5 units/kg every 4–7 days For squamous cell carcinoma, Hodgkin’s disease, lymphomas,
and testicular cancer
dactinomycin (Cosmegen) IV; 500 mcg/day for a maximum of 5 days For Wilms’ tumor and rhabdomyosarcoma
daunorubicin (Cerubidine) IV; 30–60 mg/m2 daily for 3–5 days For leukemias and lymphomas
daunorubicin liposomal IV; 40 mg/m2 every 2 weeks For Kaposi’s sarcoma
(DaunoXome)
doxorubicin IV; 60–75 mg/m2 as a single dose For lymphomas, sarcomas, acute leukemia, and cancer of the
(Adriamycin) breast, lung, testes, thyroid, and ovary
doxorubicin liposomal IV; 20 mg/m2 every 3 weeks For Kaposi’s sarcoma, refractory ovarian cancer and refractory
(Doxil, Evacet) multiple myeloma
epirubicin (Ellence) IV; 100–120 mg/m2 as a single dose For breast cancer
idarubicin (Idamycin) IV; 8–12 mg/m2 daily for 3 days For acute myelogenous leukemia
mitomycin (Mutamycin) IV; 2 mg/m2 as a single dose For cancer of the colon, stomach, lung, head and neck,
rectum, bladder, pancreas, and breast; also for malignant
melanoma
mitoxantrone (Novantrone) IV; 12 mg/m2 daily for 3 days For acute nonlymphocytic leukemia
Several substances isolated from bacteria have been found to possess antitumor properties. These
chemicals are more toxic than the traditional antibiotics; thus, their use is restricted to treating specific can-
cers. All the antitumor antibiotics interact with DNA in a manner similar to the alkylating drugs. Because
of this, their general actions and adverse effects are similar to those of the alkylating drugs. Unlike the
alkylating drugs, however, all the antitumor antibiotics must be administered intravenously or through
direct instillation into a body cavity using a catheter. A major dose-limiting adverse effect of drugs in this
class is bone marrow suppression.
Drug Prototype: Doxorubicin (Adriamycin)

Therapeutic Class: Antineoplastic Pharmacologic Class: Antitumor antibiotic
Actions and Uses: Doxorubicin attaches to DNA, causing the doxorubicin and decreased effectiveness. Using doxorubicin
double strands to be distorted, thus preventing cancer cell divi- with phenytoin may lead to decreased phenytoin levels
sion. It is prescribed for solid tumors of the lung, breast, ovary, and possible seizure activity. Liver toxicity may occur if mer-
and bladder, and for certain types of leukemias and lymphomas. captopurine is taken at the same time. Using with verapamil
It is structurally similar to daunorubicin (Cerubidine). Doxo- may increase serum doxorubicin levels, leading to doxorubicin
rubicin is one of the most effective single drugs against solid toxicity.
tumors.
A novel delivery method has been developed for both
doxorubicin and daunorubicin. The drug is enclosed in small
sacs, or vesicles, of lipids called liposomes. The liposomal vesicle Black Box Warning:
opens and releases the antitumor antibiotic when it reaches a Severe bone marrow suppression may occur, which is the
cancer cell. The goal is to deliver a higher concentration of drug major dose-limiting toxicity with doxorubicin. It may mani-
directly to the cancer cells, thus sparing normal cells. Doxoru- fest as seriously low blood cell counts. Doxorubicin exhibits
bicin liposomal is approved for use in patients with Kaposi’s significant cardiotoxicity, which may be either acute or
sarcoma, refractory ovarian tumors, and relapsed multiple chronic. Cardiac adverse effects can be life threatening and
myeloma. may include sinus tachycardia, bradycardia, delayed heart
failure, acute left ventricular failure, and myocarditis. Heart
Adverse Effects and Interactions: Doxorubicin has many adverse failure may occur months or years after the termination
effects, some of which can be life threatening and which are of therapy. Acute, IV infusion–related reactions may occur,
described in the black box warning. In addition, nausea, vomit- including anaphylaxis. Severe local necrosis may result if
ing, diarrhea, and hair loss are common. extravasation occurs. Secondary malignancies, especially
Doxorubicin interacts with many drugs. If digoxin is taken acute myelogenous leukemia, may occur one to three years
at the same time, the patient will have decreased serum digoxin following therapy.
levels. Phenobarbital leads to increased plasma clearance of
Core Concept 28.11 Some natural products kill cancer cells by preventing cell division.
Natural products are substances with anticancer properties that have been extracted from plants. The natu-
ral products used as antineoplastics are listed in Table 28.5 ◆.
Chemicals with antineoplastic activity have been isolated from a number of plants, including the com-
mon periwinkle (Vinca rosea), the Pacific yew, the mandrake plant (May apple), and the shrub Campothe-
cus acuminata. Although structurally very different, drugs in this class have the common ability to arrest
cell division; thus they are sometimes called mitotic inhibitors.
The vinca alkaloids, vincristine (Oncovin) and vinblastine (Velban), are older medications derived
from the periwinkle plant. Their biological properties were described in folklore for many years in various
parts of the world prior to their use as anticancer drugs.
Native Americans described uses of the May apple long before teniposide (Vumon) and etoposide
(VePesid) were isolated from this plant and used for chemotherapy. These drugs are called topoisomerase
inhibitors because they block the enzyme topoisomerase, whose natural function is to help repair DNA
damage. Bone marrow suppression is a serious adverse effect of most natural product drugs. More
recently isolated topoisomerase inhibitors include topotecan (Hycamtin), which is used to treat meta-
static ovarian cancer and lung cancer, and irinotecan (Camptosar), which is indicated for metastatic
cancer of the colon.
The taxanes, which include cabazitaxel (Jevtana), paclitaxel (Abraxane, Taxol), and docetaxel
(Taxotere), were isolated from the Pacific yew, an evergreen found throughout the Western United
States. Paclitaxel is approved for metastatic ovarian and breast cancer and for Kaposi’s sarcoma; how-
ever, off-label uses include many other cancers. Bone marrow toxicity is usually the dose-limiting factor
for the taxanes.
Table 28.5 Natural Products

Vinca Alkaloids
vinblastine (Velban) IV; 3.7–18.5 mg/m2 every week For cancer of the breast and testes; Hodgkin’s disease
vincristine (Oncovin, IV; 1.4 mg/m2 every week (max: 2 mg/m2) For acute leukemias, Hodgkin’s disease, lymphosarcoma,
Vincasar) neuroblastoma, Wilms’ tumor, lung and breast cancer, reticular
cell carcinoma, and osteogenic sarcomas
vincristine liposome IV; 2.25 mg/m2 once every week For acute lymphoblastic leukemia
(Marquibo)
vinorelbine IV; 30 mg/m2 every week For lung cancer
(Navelbine)
Taxanes
cabazitaxel (Jevtana) IV: 25 mg/m2 every 3 weeks For prostate cancer
docetaxel (Taxotere) IV; 60–100 mg/m2 every 3 weeks For ovarian cancer, metastatic breast and prostate cancer,
advanced stomach cancer, and lung cancer
paclitaxel (Abraxane, IV; 135–175 mg/m2 every 3 weeks For Kaposi’s sarcoma, ovarian cancer, metastatic breast cancer,
Taxol) lung cancer, and certain other solid tumors
Topoisomerase Inhibitors and other natural products
eribulin (Halaven) IV; 1.4 mg/m2 on days 1 and 8 of For metastatic breast cancer
a 21-day cycle
etoposide (VePesid) IV; 50–100 mg/m2 daily for 5 days For testicular and lung cancer; choriocarcinomas; PO form
available
irinotecan (Camptosar) IV; 125 mg/m2 every week for For colorectal cancer
4 weeks
teniposide (Vumon) IV; 165 mg/m2 every 3–4 days for For acute lymphocytic leukemia
4 weeks
topotecan (Hycamtin) IV; 1.5 mg/m2 daily for 5 days For ovarian cancer
Drug Prototype: Vincristine (Oncovin)

Therapeutic Class: Antineoplastic Pharmacologic Class: Vinca alkaloid, plant extract
Actions and Uses: Vincristine affects rapidly growing cells by Vincristine interacts with many drugs. Asparaginase used
inhibiting their ability to complete mitosis. Although it must together with or before vincristine may cause increased neu-
be given IV, a major advantage of vincristine is that it causes rotoxicity secondary to decreased liver clearance of vincristine.
minimal immunosuppression. It is usually prescribed in combina- Doxorubicin or prednisone may increase bone marrow sup-
tion with other antineoplastics for the treatment of lymphoma, pression. Calcium channel blockers may increase vincristine
leukemias, Kaposi’s sarcoma, Wilms’ tumor, bladder carcinoma, accumulation in cells. When used with digoxin, the patient may
and breast carcinoma. A newer form of vincristine (Marquibo), need an increased digoxin dose. When vincristine is given with
encased in a liposomal carrier, was approved in 2012 for acute methotrexate, the patient may need lower doses of methotrex-
lymphoblastic leukemia. ate. Vincristine may decrease serum phenytoin levels, leading to
increased seizure activity.
Adverse Effects and Interactions: Vincristine has many adverse
effects, some of which can be life threatening and which are
described in the black box warning. In addition, the major Black Box Warnings:
dose-limiting adverse effect of vincristine is neurotoxicity. Myelosuppression may be severe and predispose to oppor-
Symptoms include numbness and tingling in the limbs, muscular tunistic infections. Extravasation can cause intense pain,
weakness, loss of neural reflexes, and pain. CNS effects may inflammation, and tissue necrosis. If extravasation occurs,
include seizures, depression, hallucinations, and coma. Severe treatment with warm compresses and hyaluronidase is
constipation is common. Reversible alopecia occurs in most recommended; cold compresses will significantly increase
patients. the toxicity of vinca alkaloids.
Some hormones and hormone antagonists are effective against

prostate and breast cancer. Core Concept 28.12
Use of hormones or hormone antagonists is a strategy used to slow the growth of hormone-dependent
tumors. Most hormone therapies are limited to treating hormone-sensitive tumors of the breast or prostate.
The major hormones and hormone antagonists prescribed for cancer are given in Table 28.6 ◆.
The growth of certain tumors of reproductive tissues is greatly stimulated by natural hormones.
Administering high doses of specific hormones or hormone antagonists can block these receptors and slow
tumor growth. For example, administering the male hormone testosterone or the antiestrogen drug tamoxi-
fen can slow specific types of breast cancer that depend on estrogen for growth. Tamoxifen is one of the
most widely used drugs for this type of cancer. Administration of the female sex hormone estrogen slows
the growth of prostate cancer. The other major class of hormones used for chemotherapy is the corticoste-
roids. When used for chemotherapy, the doses of these hormones are much higher than the levels normally
found in the body. Additional indications for hormone pharmacotherapy are discussed in Chapter 32.
As a group, hormones and hormone antagonists are the least toxic of the antineoplastic classes. They
can, however, cause serious adverse effects when given at high doses for prolonged periods. Because they
rarely produce cancer cures when used singly, these drugs are normally given for palliation.
Concept Review 28.3

■ Would a patient with breast cancer be given estrogen, or an estrogen antagonist? Explain
your answer.
Table 28.6 Hormones and Hormone Antagonists

Hormones
dexamethasone (Decadron, others) PO; 0.25 mg bid–qid For palliative treatment of leukemias and lymphomas
diethylstilbestrol (DES, PO; for treatment of prostate cancer, For cancer of the prostate and breast
Stilbestrol) 500 mg tid; for palliation, 1–15 mg daily
ethinyl estradiol PO; for treatment of breast cancer, 1 mg tid For cancer of the prostate and breast, and
(Estinyl, others) for 2–3 months; for palliation of prostate contraception
cancer, 0.15–3 mg/day
fluoxymesterone (Halotestin) PO; 10 mg tid For breast cancer
(continued )
Table 28.6 Hormones and Hormone Antagonists (continued )

methoxyprogesterone IM; 400–1,000 mg every week For uterine and renal cancer, dysfunctional uterine
(Depo-Provera, Depo-SubQ-Provera, bleeding, and contraception
Provera) (see page 552 for the
Drug Prototype box)
megestrol (Megace) PO; 40–160 mg bid–qid For advanced cancer of the prostate and breast
prednisone (see page 369 for PO; 20–100 mg/m2 daily For acute leukemia, Hodgkin’s disease, lymphomas,
the Drug Prototype box) and many inflammatory conditions
testolactone (Teslac) PO; 250 mg qid For breast cancer
testosterone (Andro 100, IM; 200–400 mg every 2–4 weeks For breast cancer and replacement therapy in men
Histerone, Testred, Delatest)
Hormone Antagonists
abiraterone (Zytiga) PO: 1 g once daily in combination with prednisone For prostate cancer
anastrozole (Arimidex) PO; 1 mg daily For advanced breast cancer
bicalutamide (Casodex) PO; 50 mg daily For metastatic prostate cancer
degarelix (Firmagon) Subcutaneous; 240 mg loading dose followed by For advanced prostate cancer
80 mg every 28 days
enzalutamide (Xtandi) PO; 160 mg once daily For metastatic prostate cancer
exemestane (Aromasin) PO; 25 mg daily after a meal For advanced breast cancer
flutamide (Eulexin) PO; 250 mg tid For prostate cancer
goserelin (Zoladex) Subcutaneous; 3.6 mg every 28 days For prostate and breast cancer, dysfunctional uterine
bleeding, and endometriosis
histrelin (Vantas) Implant; one implant every 12 months (50 mg) For palliation of advanced prostate cancer
letrozole (Femara) PO; 2.5 mg daily For advanced breast cancer
leuprolide (Eligard, Lupron, Subcutaneous; 1 mg daily For palliation of advanced prostate cancer, endometriosis,
Viadur) and precocious puberty; IM depot form available
nilutamide (Nilandron) PO; 300 mg/daily for 30 days, then 150 mg daily For metastatic prostate cancer
raloxifene (Evista) (see page 571 PO; 60 mg once daily For prophylaxis of breast cancer; treatment of
for the Drug Prototype box) osteoporosis in postmenopausal women;
tamoxifen PO; 10–20 mg bid For breast cancer
toremifene (Fareston) PO; 60 mg daily For metastatic breast cancer
triptorelin (Trelstar) IM; 3.75 mg once monthly For palliation of advanced prostate cancer
Drug Prototype: Tamoxifen

Therapeutic Class: Antineoplastic Pharmacologic Class: Hormone, estrogen receptor blocker
Actions and Uses: Because it blocks estrogen receptors in cancer Tamoxifen interacts with several drugs. For example,
cells, tamoxifen is sometimes classified as an antiestrogenic. nticoagulants may increase the risk of bleeding. Using this
a
Tamoxifen is effective against breast tumors that require estro- drug with cytotoxic drugs may increase the risk of blood clots.
gen for their growth. These susceptible cancer cells are known
as estrogen receptor (ER)-positive cells. Tamoxifen is given orally Black Box Warnings:
and is a preferred drug for treating breast cancer.
The most serious problem associated with tamoxifen use
A unique feature of tamoxifen is that it is the only antineo-
is the increased risk of endometrial cancer. The benefits of
plastic that is approved for prophylaxis of breast cancer—for high-
tamoxifen outweigh the risks in women who are taking
risk patients who are at risk of developing the disease. In addition,
tamoxifen to treat breast cancer. The benefit versus risk is
it is approved as adjunctive therapy in women following mastec-
not as clear in women who are taking tamoxifen to prevent
tomy to decrease the potential for cancer in the other breast.
breast cancer. There is also a slightly increased risk of throm-
Adverse Effects and Interactions: Other than nausea and vomit- boembolic disease, including stroke, pulmonary embolism,
ing, tamoxifen produces little of the serious toxicity observed with and deep venous thrombosis (DVT) with the use of tamoxi-
other antineoplastics. Hot flashes, fluid retention, venous blood fen. The risk of a thromboembolic event is believed to be
clots, and abnormal vaginal bleeding are relatively common. about the same as for oral contraceptives.
Targeted therapies and some miscellaneous antineoplastic drugs

are effective against specific tumors. Core Concept 28.13
Although they originated from normal cells, cancer cells are clearly different. Scientists have been quite
productive in finding ways that cancer cells differ, and in developing drugs that take advantage of these
differences. Dozens of new antineoplastic drugs are now available that target specific aspects of cancer cell
physiology. These drugs, appropriately called targeted therapies, were developed with the hope that they
would be more selective in their cell killing than existing drugs and thus cause fewer adverse effects in
normal cells. Unfortunately, this has not always been the case.
Monoclonal antibodies (MABs) are a type of targeted therapies that are engineered to attack only
one specific type of tumor cell. Once the MAB binds to its target cell, the cancer cell dies or is marked for
destruction by other cells of the immune response. For example, rituximab (Rituxan) is a MAB that binds
to CD20, a surface protein present on cancerous B lymphocytes. Once bound, rituximab shatters the tumor
cells. The largest group of targeted therapies attack tyrosine kinase, a key enzyme for cell growth. The
development of new targeted therapies for cancer is progressing at a rapid rate. These drugs, along with
some miscellaneous antineoplastics, are shown in Table 28.7 ◆.
Table 28.7 Selected Targeted Therapies and Miscellaneous Anticancer Drugs*

alemtuzumab (Campath) IV; 3–30 mg/day For chronic lymphocytic leukemia
altretamine (Hexalen) PO; 65 mg/m2/day For ovarian cancer
arsenic trioxide (Trisenox) IV; 0.15 mg/kg/day For acute promyelocytic leukemia
axitinib (Inlyta) PO; 5 mg bid For advanced renal cancer
bevacizumab (Avastin) IV; 5 mg/kg every 14 days For metastatic colorectal cancer
cetuximab (Erbitux) IV; 400 mg/m2 over 2 hours, then 250 mg/m2 For metastatic colorectal cancer
over 1 hour weekly
erlotinib (Tarceva) PO; 150 mg once daily For metastatic non–small cell lung cancer
gefitinib (Iressa) PO; 250–500 mg/day For advanced or metastatic lung cancer
gemtuzumab (Mylotarg) IV; 9 mg/m2 for 2 hours For acute myeloid leukemia
imatinib (Gleevec) PO; 400–600 mg daily For chronic myeloid leukemia after failure with interferon alfa therapy
interferon alfa-2 Subcutaneous or IM; 2–3 million units For hairy cell leukemia, Kaposi’s sarcoma non-Hodgkin’s lymphoma,
(Intron A) daily for leukemia; 36 million units daily for and malignant melanoma; also for chronic hepatitis B and C viral
Kaposi’s sarcoma infections
levamisole (Ergamisol) PO; 50 mg tid for 3 days For colon cancer
mitotane (Lysodren) PO; 3–4 mg tid–qid For adrenal cortex cancer
ofatumumab (Arzerra) IV; 300 mg initial dose followed by 2,000 mg Newer antineoplastic drug; for chronic lymphocytic leukemia
weekly for 7 doses
pazopanib (Votrient) PO; 800 mg once daily Newer antineoplastic drug; for advanced renal carcinoma
pegaspargase (Oncaspar, IV; 2,500 international units/m2 every For acute lymphocytic leukemia; IM form available
PEG-L-asparaginase) 14 days
pertuzumab (Perjeta) IV; 840 mg followed every 3 weeks thereafter For metastatic breast cancer
by 420 mg
procarbazine (Matulane) PO; 2–4 mg/kg daily For Hodgkin’s disease
rituximab (Rituxan) IV; 375 mg/m2 daily as a continuous infusion For non-Hodgkin’s lymphomas
scinitinib (Sutent) PO; 50 mg once daily for 4 weeks followed by For gastrointestinal and advanced renal carcinoma
2 weeks off
sunitinib (Sutent) PO; 37.5–50 mg once daily for 4 weeks For gastrointestinal, advanced renal and pancreatic tumors
trastuzumab (Herceptin) and IV (Herceptin); 4 mg/kg as a single dose, For metastatic breast cancer
ado-trastuzumab (Kadcycla) then 2 mg/kg every week
IV (Kadcycla); 3.6 mg/kg every 3 weeks
vismodegib (Erivedge) PO; 150 mg once daily For advanced or metastatic basal cell carcinoma
zoledronic acid (Zometa) IV; 4 mg over at least 15 minutes For multiple myeloma, severe hypercalcemia caused by malignancy,
and Paget’s disease
*This table includes a selected sample of drugs in this class. For a complete listing, see Adams & Urban, Pharmacology: Connections to Nursing Practice, 2nd ed., 2013. Upper Saddle River, NJ: Pearson.
All targeted therapies, including the MABs, are very specific: They are designed to affect only cells
with certain antibodies or proteins. The key point about targeted therapies is that the tumor cells must pos-
sess the specific antibody or protein; otherwise, the drug will be ineffective.
Adjunct medications are sometimes necessary to treat cancer

symptoms and to reduce the intensity of adverse effects from
Core Concept 28.14 antineoplastic drugs.
Antineoplastic drugs are only part of the arsenal of medications used to treat cancer patients. Adjunctive
medications are those used to supplement the primary therapies. The three primary groups of drugs used as
adjunctive therapy are opioid analgesics, antiemetics, and hematopoietic drugs.
Many types of cancer produce extreme pain, which affects the patient’s quality of life. Indeed,
pain management is one of the primary concerns of both patients and healthcare providers. Pain man-
agement proceeds up a ladder, starting with NSAIDs to the weak opioid analgesics (codeine, tramadol)
and eventually to the strongest opioids (morphine, fentanyl, hydromorphone). Drug combinations may
be used to achieve optimum pain control. At high levels, opioids produce significant adverse effects
(see Chapter 14).
Chemotherapy-induced nausea and vomiting (CINV) can be debilitating for patients. CINV
can occur in the first few hours after the initiation of chemotherapy, or be delayed more than 24
hours. Antineoplastics are classified as their emetogenic potential and those with the highest potential
require adjunctive therapy with antiemetics. The most effective drug class used for this purpose are
called serotonin receptor antagonists. Examples include palonosetron (Alxi) and ondansetron (Zofran,
Zuplenz), which can be given as an orally disintegrating tablet. The antiemetic drugs are presented in
Chapter 30.
Many antineoplastic drugs are toxic to bone marrow and can produce serious blood abnormalities.
Some drugs are given during chemotherapy to limit or counteract this toxicity. Oprelvekin (Neumega)
stimulates platelet production and helps to prevent severe thrombocytopenia. Epoetin alfa (Epogen,
Procrit) stimulates RBC production and is used to limit anemia, the loss of RBCs, caused by certain anti-
neoplastics. Administration of filgrastim (Neupogen) increases neutrophil production in patients with can-
cer whose bone marrow has been suppressed by antineoplastic drugs. Low WBC counts (neutropenia)
often result in severe bacterial and fungal infections in patients during chemotherapy or following organ
transplants.
Drug Prototype: Epoetin Alfa (Epogen, Procrit)

Therapeutic Class: Drug for anemia Pharmacologic Class: Hematopoietic growth factor, erythropoietin
Actions and Uses: Epoetin alfa is made through recombinant The effectiveness of epoetin alfa will be greatly reduced in
DNA technology and functions like human erythropoietin. patients with iron deficiency or other vitamin-depleted states
Because of its ability to stimulate red blood cell formation, because erythropoiesis cannot be enhanced without these vital
epoetin alfa is effective in treating specific disorders caused nutrients. There are no clinically significant drug interactions
by a deficiency in the number of red blood cells. Patients with with epoetin alfa.
chronic renal failure often cannot secrete enough erythropoi-
etin and thus will benefit from epoetin administration. Epoetin
is sometimes given to patients undergoing cancer chemother-
apy to counteract the anemia caused by antineoplastic drugs. Black Box Warning:
It is occasionally prescribed for patients prior to blood transfu- The risk of serious cardiovascular events is increased with
sions or surgery and to treat anemia in patients infected with epoetin alfa therapy. Transient ischemic attacks (TIAs),
HIV. Epoetin alfa is usually administered three times per week myocardial infarctions (MIs), and strokes have occurred
until a therapeutic response is achieved. in patients who are on dialysis and being treated with
epoetin alfa. Epoetin increased the rate of deep venous
Adverse Effects and Interactions: Epoetin alfa has some serious thrombosis (DVT) in patients not receiving concurrent
adverse effects which are described in the black box warning. anticoagulation. The lowest dose possible should be used
The most common adverse effect of epoetin alfa is hyperten- in patients with cancer because the drug can promote
sion, which may occur in as many as 30% of patients receiving tumor progression and shorten overall survival in some
the drug. Blood pressure should be monitored during therapy, patients.
and an antihypertensive drug may be indicated.
Nursing Process Focus Patients Receiving Antineoplastic Therapy

Prior to administration: ■ Infection related to compromised immune system secondary to

■ Obtain a complete health history, including GI, renal and liver adverse effects of antineoplastic drugs and disease process
conditions, allergies, drug history, past infections, and possible drug ■ Imbalanced Nutrition: Less than Body Requirements related to nausea,
interactions. vomiting, diarrhea, and anorexia secondary to adverse effects of drug
■ Evaluate laboratory blood findings: CBC, platelets, electrolytes, uric therapy
acid, glucose, and renal and liver function studies. ■ Impaired Skin Integrity related to extravasation of antineoplastic drug
signs, height, weight, and any diagnostic test dependent on type of ■ Risk for Disturbed Body Image related to physical changes from the
antineoplastic therapy (audiology, cardiac, electromyography). adverse effects of drug therapy or other treatment regimens
■ Determine neurologic status, including level of consciousness (LOC), ■ Fatigue related to adverse effects of drug therapy
mood, and/or sensory impairment. ■ Fear related to lack of knowledge of disease process and effects of
■ Collect information about previous immunization and a history or treatment regimen
presence of herpes zoster or chickenpox. ■ Deficient Knowledge related to a lack of information about drug
therapy
The patient will:

■ Experience therapeutic effects (a reduction in tumor mass and/or progression of abnormal cell growth).
■ Experience minimal adverse effects from drug therapy.
Implementation
■ Monitor immune status. Observe for signs and symptoms for potential Instruct the patient to:
and actual infections and monitor laboratory tests such as CBC, ■ Immediately report profound fatigue, fever, sore throat,
specifically WBC and neutrophil counts. (Most antineoplastic drugs epigastric pain, coffee-grounds vomit, bruising, tarry stools,
cause immunosuppression neutropenia.) or frank bleeding to the healthcare provider.
■ Avoid crowded indoor places and persons with active infections.
■ Monitor vital signs daily, ensuring proper use of home
equipment.
■ Take temperature every four hours, if symptoms indicate a need,
and to notify the healthcare provider if it goes above approved
parameters.
■ Not use antipyretics unless approved by oncology provider.
■ Not eat raw foods. Cook foods thoroughly, allowing family
members to prepare raw foods.
■ Anticipate fatigue and balance daily activities to prevent
exhaustion.
■ Monitor cardiac and respiratory status, including vital signs, heart and Instruct the patient:
breath sounds, presence of edema, ECG, and laboratory testing. (Many ■ To report immediately any problems with dyspnea; pain in the
antineoplastic agents, such as alkylating drugs, antimetabolites, and chest, arm, neck, or back; tachycardia; cough; frothy sputum; swell-
antitumor antibodies, have adverse effects that cause problems with ing; or activity intolerance to the healthcare provider.
the cardiac and respiratory systems.) ■ To adhere to laboratory testing regimen for serum blood level
tests (CBC, clotting factors, chemistry panel), as directed. Alert
lab personnel of chemotherapy use.
■ That heart changes may be a sign of drug toxicity; heart failure may
not appear for up to six months after completion of doxorubicin
therapy.
■ Monitor nutritional status. Administer antiemetics 30–45 minutes Instruct the patient to:
prior to antineoplastic administration or at the first sign of nausea. ■ Report loss of appetite, nausea/vomiting.
(Profound nausea, dry heaves, and/or vomiting are common with ■ Consume frequent small, high calorie, and nutrient dense meals.
antineoplastic therapy. Dry mouth can also occur. Dietary consultation Nutritional supplements may help.
may be needed.) ■ Avoid highly scented, spicy foods; high-roughage and very hot or
cold foods.
■ Avoid carbonated and acidic beverages, alcohol, and caffeine.
■ Monitor for mucositis. (Antineoplastic drugs may cause significant Instruct the patient to:
mucositis because of its effects on rapidly dividing cells.) ■ Examine mouth daily for changes and report the presence of mouth
redness, soreness, or ulcers.
■ Maintain regular dental exams.
■ Encourage frequent oral hygiene, use of lip balm, and avoid alcohol-
based mouthwash, which can be drying to the mucosa.
■ Use a soft toothbrush; avoid toothpicks.
continued . . .
■ Monitor for diarrhea and constipation. (An adverse effect of many Instruct the patient to:
antineoplastic drugs is diarrhea although severe constipation may ■ Report changes in bowel habits to the healthcare provider.
occur with vincristine use, especially among older adults.) ■ Report excessive diarrhea, especially if it contains blood or
mucus.
■ Increase fluid intake 2–3 L a day to prevent constipation.
■ Monitor liver function tests. (Antineoplastics are metabolized by the Instruct the patient to:
liver, increasing the risk of hepatotoxicity.) ■ Report nausea, vomiting, jaundice, abdominal pain, tenderness or
bloating, or light or clay-colored stool to the healthcare provider.
■ Adhere to laboratory testing regimen for serum blood level tests of
liver enzymes, as directed.
■ Monitor DTRs, neurologic/sensory status, and LOC. (Antineoplastics Instruct the patient to:
such as cyclophosphamide and natural product antineoplastics such as ■ Report any changes in skin color, vision, hearing; numbness or tingling;
vincristine have neurological adverse effects. Such neurologic changes staggering gait; changes in consciousness; or depressed mood to the
may be irreversible.) healthcare provider.
■ Monitor genitourinary status: intake and output, daily weights, and Instruct the patient:
renal function tests. (Antineoplastic drugs may cause significant renal ■ To report the following immediately: diminished urinary output,
toxicity. Hormones, and especially tamoxifen, increase the risk of changes in thirst; changes in color, quantity, and character of
endometrial cancer and may alter menstrual cycles in women and may urine (e.g., “cloudy,” with odor or sediment); joint, suprapubic,
produce impotence in men.) abdominal, flank, or lower back pain; difficult urination; and
weight gain to the healthcare provider.
■ That doxorubicin will turn urine red-brown for one to two days after
administration; blood in the urine may occur several months after
cyclophosphamide has been discontinued.
■ To increase fluid intake to 2–3 L a day.
■ To report changes in menstruation, sexual functioning, and/or
vaginal discharge.
■ To recognize the risk of endometrial cancer before taking
tamoxifen.
■ Monitor for hypersensitivity or other adverse reactions. (Antineoplastic ■ Instruct the patient to immediately report chest or throat tightness,
drugs may cause significant hypersensitivity and allergic responses.) difficulty swallowing, swelling (especially facial), abdominal pain,
headache, or dizziness to the healthcare provider.
■ Monitor hair and skin status. (Alopecia is associated with most Instruct the patient to:
antineoplastic drugs. Alkylating and antimetabolites may cause ■ Immediately report desquamation of skin on hands and feet, rash,
significant skin reactions including SJS.) pruritus, acne, or boils to the healthcare provider.
■ Wear a cold gel cap during chemotherapy to minimize hair loss.
■ Monitor for conjunctivitis. (Doxorubicin may cause conjunctivitis.) ■ Instruct the patient or caregiver to immediately report eye redness,
stickiness, or pain or weeping.
■ Administer with caution to patients with diabetes mellitus. Instruct the patient to:
(Hypoglycemia may occur secondary to combination of ■ Report any signs and symptoms of hypoglycemia (e.g., sudden
cyclophosphamide and insulin.) weakness, tremors) to the healthcare provider.
■ Monitor blood glucose daily; consult the healthcare provider
regarding reportable results (e.g., less than 70 mg/dL).
■ Be aware of specific policies and procedures related to antineoplastic ■ Provide the patient, family, and caregiver education and support
administration. (Intense education programs are usually required prior when giving antineoplastic (chemotherapy) drugs.
to administering chemotherapy drugs.)
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”). See Tables 28.2–28.7
for lists of drugs to which these nursing actions apply.
Chapter Review 449

Patients treated for cancer need to know the following:
1. If hair loss is expected, cut long hair and be fitted for a wig or hairpiece before starting
treatment. Select hats, scarves, or turbans. Use mild shampoo and conditioner.
2. Limit sun exposure; wear sunscreen, sunglasses, and long sleeves when outdoors. When
hair is lost, protect the scalp from sunburn with sunscreen or a hat.
3. Eat foods that appeal in small amounts at frequent intervals if appetite is decreased. A
healthcare provider may provide an appetite stimulant such as megestrol (Megace).
4. Discuss drugs to control nausea with a healthcare provider if nausea is a problem. Drink
liquids between meals rather than with food.
5. Because the mouth may become irritated or ulcerated, avoid alcohol-based mouthwash,
and use plain water or mild salt solution instead. Use a soft toothbrush. Avoid spicy
foods and very hot or very cold food and drink. Ask about a mouth rinse to coat, soothe,
and numb, such as Benadryl, Maalox, and Xylocaine.
6. Because chemotherapy may decrease sperm production or increase the risk of genetic
damage to sperm, consider sperm banking prior to receiving chemotherapy.
7. Increase fluid intake to decrease the risk of kidney damage and uric acid crystal
formation.
8. Avoid exposure to crowds and individuals with infections or recent vaccinations because
the immune system may be less able to protect you. Report temperatures of 101ºF (38ºC)
or higher.
9. Follow a neutropenic diet if WBC count is significantly reduced. Avoid raw fruits and
vegetables, peppercorns, and raw fish and meat.
10. Report easy bruising, blood in the stool or urine, vomiting, severe fatigue, epigastric
pain, and difficulty clotting. Many chemotherapeutic drugs reduce production platelets
needed for clot formation.
Chapter Review
28.1 Cancer is characterized by rapid, uncontrolled 28.4 The three primary goals of chemotherapy are cure,
growth of cells. control, and palliation.
Cancer cells grow rapidly, seemingly unaffected by Surgery, radiation, and chemotherapy are the thera-
their host surroundings. Cancer cells continue divid- pies used for treating cancer. The three primary goals
ing until they invade normal tissues and eventually of chemotherapy are cure, control, and palliation.
metastasize. Benign neoplasms grow slowly and Antineoplastic drugs may also be administered as
rarely result in death. Malignant neoplasms, also adjuvant or neoadjuvant chemotherapy, prophylaxis,
known as cancer, are fast growing and often fatal. or myeloablation.
28.2 The causes of cancer may be chemical, physical, or 28.5 To achieve a total cure, every malignant cell must
biological. be removed or killed.
Many factors have been found to cause or promote A single cancer cell may be able to divide rapidly
cancer. These include industrial chemicals, x-rays, enough to kill its host. Therefore, to achieve a com-
UV light, and viruses. The genetic make-up of the plete cure, every single cancer cell must be elimi-
patient plays an important role in whether or not can- nated by surgery, radiation, drugs, or the patient’s
cer will develop after exposure to carcinogens. immune system.
28.3 Personal risk of cancer may be lowered by a num- 28.6 Use of multiple drugs and special dosing schedules
ber of lifestyle factors. improve the success of chemotherapy.
Eliminating tobacco use and limiting the intake Combinations of antineoplastic drugs are often used
of saturated fats and alcohol are important factors to attack cancer cells through several mechanisms
in reducing the risk of developing cancer. Peri- and to allow lower doses than if a single drug were
odic self-examinations and physician checkups are used. The schedule of drug administration is critical
important in catching cancer at an early, more treat- to the success of the chemotherapy.
able stage.
28.7 Serious toxicity limits therapy with most of the drugs. Drugs in this class also include the topoisomer-
antineoplastic drugs. ase inhibitors.
Antineoplastic drugs are among the most toxic medi-
28.12 Some hormones and hormone antagonists are
cations available. Adverse effects are expected and
effective against prostate and breast cancer.
may be severe. Whereas each drug has somewhat
different toxicities, common adverse effects include A number of estrogens, androgens, corticosteroids,
thrombocytopenia, anemia, leukopenia, alopecia, and hormone inhibitors have antitumor activ-
severe nausea, vomiting, and diarrhea. ity and are most often given for palliation. They
are usually reserved for tumors of the breast or
28.8 Alkylating drugs act by changing the structure of prostate.
DNA in cancer cells.
28.13 Targeted therapies and some miscellaneous anti-
Alkylating drugs are some of the oldest and most
neoplastic drugs are effective against specific
reliable of the antineoplastic drugs. By attaching to
tumors.
DNA, they prevent cancer cells from replicating.
Targeted therapies include monoclonal antibodies
28.9 Antimetabolites disrupt critical cellular pathways that have been designed to affect some specific aspect
in cancer cells. of cancer cell physiology. While a large number of
Antimetabolites block a specific step in cancer cell new targeted therapies have been marketed, they are
metabolism. By blocking the synthesis of critical only effective against specific cancers and most have
cellular molecules, the drugs can slow the growth of significant adverse effects.
cancer cells.
28.14 Adjunct medications are sometimes necessary
28.10 A few cytotoxic antibiotics are used to treat cancer to treat cancer symptoms and to reduce the
rather than infections. intensity of adverse effects from antineoplastic
drugs.
Antitumor antibiotics attach to the DNA of cancer cells,
thereby inhibiting their growth. Their properties and Adjunct medications are needed to reduce the intense
adverse effects resemble those of the alkylating drugs. pain, nausea, and drug adverse effects that can occur
during cancer treatment. Adjuncts include opioid anal-
28.11 Some natural products kill cancer cells by prevent- gesics, antiemetics, and drugs to reduce bone marrow
ing cell division. toxicity.
Natural products of the periwinkle plant and the Pacific
yew have provided several important antineoplastic
Review Questions
The following questions are written in NCLEX-PN® style. Answer 3. Acetaminophen

these questions to assess your knowledge of the chapter material, 4. Nonsteroidal anti-inflammatory drugs (NSAIDs)
and go back and review any material that is not clear to you.
4. The patient with breast cancer has been receiving IV
1. The nurse administers antiemetic drugs to a patient doxorubicin (Adriamycin). The patient is now complaining of
receiving chemotherapy: severe pain at the IV site. The nurse understands that the fol-
1. Only when vomiting occurs lowing most likely occurred:
2. Once the treatment regimen is completed 1. An allergic reaction
3. Just prior to treatment 2. Leaking at the IV site
4. Only if the patient requests to be medicated 3. Loss of neural reflexes
4. Development of a blood clot
2. The patient with testicular cancer is receiving cisplatin
(Platinol) IV. The nurse plans to monitor for: 5. A patient has started on tamoxifen as a treatment for cancer.
1. Irreversible heart failure The physician orders 20 mg, po, daily but it is only available in
2. Bone marrow suppression 10 mg tablets. How many tablets will the patient receive in a day?
3. Cardiac toxicity How many tablets in a week?
4. Peripheral neuropathy 1. 1 tablet a day, 7 tablets a week
2. 2 tablets a day, 14 tablets a week
3. Before a patient begins drug therapy with methotrexate, the 3. 2 tablets a day, 10 tablets a week
nurse collects information regarding the use of other medications. 4. 4 tablets a day, 14 tablets a week
What medication(s) would be of concern if the patient were to
take it along with the methotrexate? (Select all that apply.)
1. Aspirin
2. Iron supplement
Chapter Review 451
6. The patient on cyclosphosphamide (Cytoxan) is taught: 2. Binds to surface proteins present on cancer cells and
1. That alopecia is not irreversible shatters them
2. About signs and symptoms of neurotoxicity 3. Blocks a specific step in cancer cell metabolism
3. About signs and symptoms of renal toxicity 4. Attaches to the DNA of cancer cells, inhibiting their growth
4. That nausea, vomiting, and diarrhea frequently occur 9. The nurse informs a patient with a decreased white blood
7. The nurse monitors a patient taking methotrexate for cell count that he should:
which adverse effect(s)? (Select all that apply.) 1. Use alcohol-based mouthwash for mouth sores.
1. Cardiac dysthymias 2. Increase liquid intake with meals.
2. Bruising 3. Avoid raw foods.
3. Decreased urinary output 4. Ask his physician about ordering megestrol (Megace).
4. Diarrhea 10. The patient on tamoxifen must be checked for:
8. A patient is about to start his chemotherapy treatments. 1. Flu-like symptoms
He will be taking rituximab (Rituxan), a type of monoclonal 2. Uterine cancer
antibody. He asks the nurse how it works. The nurse tells him 3. Alopecia
that this type of monoclonal antibody: 4. Thrombocytopenia
1. Changes the structure of cancer cell’s DNA, preventing
them from replicating
Remember Ms. Novak, the patient intro- 2. Asked why she is taking epoetin alfa (Epogen), the nurse
duced at the beginning of the chapter? Now responds that it is being administered to:
read the remainder of the case study. Based 1. Boost Ms. Novak’s immune system.
on the information you have learned in this 2. Boost the number of her red blood cells.
chapter, answer the questions that follow. 3. Reduce possible neurotoxicity.
4. Kill her cancer cells.
3. During vincristine (Oncovin) therapy, the nurse must
Ms. Patricia Novak has arrived at the cancer center in her r egularly monitor for:
community. She is being treated for an invasive type of cancer. 1. Blood glucose levels
She is getting really tired of all the drugs she has to take, stat- 2. Signs of peripheral neuropathy
ing, “I know they are helping but four different drugs? I guess 3. Ototoxicity
it could be worse.” Ms. Novak is receiving the following drugs: 4. Signs of confusion
1. vincristine (Oncovin) 4. Because of the type of cancer she has and the type of
2. interferon alfa-2b (Intron A) antineoplastic drug she is taking, Ms. Novak complains of
3. tamoxifen (Soltamox) pain. The physician orders a pain medication. Understanding
4. epoetin alfa (Epogen) the pain management protocols, the nurse may expect to use
1. Ms. Novak knows that one of her medications boosts her what type of medication to achieve optimum pain control for
immune system but can’t remember which one. The nurse tells Ms. Novak?
her that the medication she is referring to is: 1. Combination drugs such as an NSAID and codeine
1. Vincristine (Oncovin) 2. A strong opioid such as fentanyl
2. Epoetin alfa (Epogen) 3. A weak opioid such as codeine
3. Interferon alfa-2b (Intron A) 4. A nonsteroidal anti-inflammatory drug
4. Tamoxifen

U n i t
5
The Respiratory and
Digestive Systems
Unit Contents
Chapter 29 Drugs for Respiratory Disorders / 454
Chapter 30 Drugs for Gastrointestinal Disorders / 476
Chapter 31 Vitamins, Minerals, and Nutritional Supplements / 496

c
“I can’t sleep at night with
h this cough, and I can hardly
a work without getting short
p of breath.”
t Mr. Michael Thomas
e
r
29 Drugs for Respiratory Disorders
Core Concepts
29.1 The respiratory system supplies oxygen for the 29.7 Antitussives and expectorants are used to treat
body and provides protection against inhaled symptoms of the common cold.
organisms. 29.8 Asthma is a chronic inflammatory disease
29.2 The inhalation route of drug administration characterized by bronchospasm.
quickly delivers medications directly to their 29.9 Beta-adrenergic agonists are the most effective
sites of action. drugs for relieving acute bronchospasm.
29.3 Allergic rhinitis is characterized by sneezing, 29.10 Corticosteroids are the most effective drugs for
watery eyes, and nasal congestion. the long-term prophylaxis of asthma.
29.4 Antihistamines are widely used to treat allergic 29.11 Mast cell stabilizers and leukotriene modifiers
rhinitis and other minor allergies. are alternative anti-inflammatory drugs for the
29.5 Intranasal corticosteroids are first-line drugs prophylaxis of asthma.
for treating allergic rhinitis. 29.12 Chronic obstructive pulmonary disease is a
29.6 Decongestants are used to reduce nasal progressive disorder treated with multiple
congestion caused by allergic rhinitis and drugs.
the common cold.
Drug Snapshot
Antihistamines diphenhydramine Beta-adrenergic drugs
(H1-receptor blockers) (Benadryl, others) 460
Anticholinergics
Intranasal f luticasone (Flonase,
corticosteroids Veramyst) 463 Inhaled corticosteroids
Decongestants xymetazoline (Afrin,

o Xanthines
(sympathomimetics) others) 464 Mast cell stabilizers cromolyn (Intal) 471
Antitussives, Leukotriene modifiers
expectorants, and
mucolytics
Learning Outcomes
1. Identify major structures and 2. Explain why inhalation is an effective 3. Describe the types of devices used
functions associated with the route of drug administration for to deliver medications via the
respiratory system. respiratory medicines. inhalation route.
4. Describe some common causes and 6. Identify the drugs that are used to 8. For each of the classes in the Drug
symptoms of allergic rhinitis, asthma, bring symptomatic relief from the Snapshot, identify representative
and chronic obstructive pulmonary common cold. drugs and explain their mechanisms
disease. 7. Categorize drugs used in the of drug action, primary actions, and
5. Explain the pharmacologic treatment of respiratory disorders important adverse effects.
management of allergic rhinitis, based on their classifications and
asthma, and chronic obstructive mechanisms of action.
pulmonary disease.
Key Terms
aerosol (AIR-oh-sol) 456 bronchodilation (BRON-koh-dye- metered-dose inhalers (MDIs) 456
allergen 458 LAY-shun) 467 mucolytics 465
allergic rhinitis (rye-NYE-tis) 458 bronchospasm (bron-koh-SPAZ-um) 466 nebulizers (NEB-you-lyes-urz) 456
alveoli (al-VEE-oh-lie) 455 chronic bronchitis (KRON-ik bron- perfusion (purr-FEW-shun) 455
KEYE-tis) 472
antitussive (anti-TUSS-ive) 465 rebound congestion 463
dry powder inhaler (DPI) 456
asthma (AZ-muh) 465 respiration (res-purr-AY-shun) 455
dyspnea 466
bronchi (BRON-ky) 455 status asthmaticus (STAT-us az-MAT-
emphysema (em-fuss-EE-muh) 472 ik-us) 467
bronchioles (BRON-key-oles) 455
expectorants (eks-PEK-tor-entz) 465 ventilation (ven-tah-LAY-shun) 455
bronchoconstriction (BRON-koh-
kun-STRIK-shun) 466 H1-receptor blocker 458
T he respiratory system is one of the most important organ systems; a mere five to six minutes with-
out breathing may result in death. When functioning properly, the respiratory system filters incom-
ing air and provides the body with the oxygen critical for all cells to function. The respiratory
system also provides a means by which the body can rid itself of excess acids and bases, a topic that is
covered in Chapter 17. The first portion of this chapter examines drugs used to treat conditions associated
with the upper respiratory tract: allergic rhinitis, nasal congestion, and cough. The second portion presents
the pharmacotherapy of asthma and conditions that affect the lower respiratory tract.
The respiratory system supplies oxygen for the body and provides
protection against inhaled organisms. Core Concept 29.1
The primary function of the respiratory system is to bring oxygen into the body and to remove carbon diox-
ide. The process by which gases are exchanged is called respiration. The basic structures of the respiratory
system are shown in Figure 29.1 ■. This system is sometimes divided into two anatomic divisions: the
upper and lower respiratory tracts.
Upper Respiratory Tract

The upper respiratory tract (URT) consists of the nose, nasal cavity, pharynx, and paranasal sinuses. These
passageways warm, humidify, and clean the air before it enters the lungs. The URT traps and removes par-
ticulate matter and many pathogens before they reach the lower portions of the lungs, where they would be
able to access the capillaries of the systemic circulation.
The nasal mucosa is a dynamic structure, richly supplied with vascular tissue, under the control of
the autonomic nervous system. For example, certain drugs can reduce the thickness of the mucosal layer,
thus relieving nasal congestion (see Core Concept 29.5). The nasal mucosa is also the first line of immune
defense. Up to a quart of nasal mucus is produced daily, and this fluid is rich with substances that are able
to neutralize airborne pathogens. Unfortunately, these cells can overreact to some substances and cause
symptoms typical of seasonal allergies, such as nasal congestion, watery eyes, and sneezing.
Lower Respiratory Tract

The lower respiratory tract (LRT) consists of the lungs and associated structures. Air leaving the URT travels
into the trachea and bronchi, which divide into smaller and smaller passages called bronchioles. The bron-
chial tree ends in dilated sacs called alveoli. Although they have no smooth muscle, the alveoli are abundantly
rich in capillaries. An extremely thin membrane in the alveoli allows gases to readily move between the inter-
nal environment of the blood and the inspired air. As oxygen crosses this membrane, it is exchanged for carbon
dioxide, a cellular waste product that travels from the blood to the air. The lung is richly supplied with blood.
Blood flow through the lung is called perfusion. The process of gas exchange is depicted in Figure 29.1.
Ventilation is the process of moving air into and out of the lungs. As the muscular diaphragm contracts
and lowers in position, it creates a negative pressure that draws air into the lungs. This process, known as
inspiration, requires energy to produce the contraction. During expiration, the diaphragm relaxes and air
456 Chapter 29 Drugs for Respiratory Disorders
Figure 29.1
Pharynx Nasal cavity
Vocal cord Tongue
Esophagus Larynx
Trachea Expired air

Right lung
Left lung
Right bronchus
Left bronchus
Alveolus
O2
Oxygenated CO2 Deoxygenated

blood circulated blood from
back to the heart the heart
Alveoli
Diaphragm
The respiratory system and the process of gas exchange.
leaves the lung passively, with no energy expenditure required. Ventilation is a purely mechanical process
that occurs approximately 12–18 times per minute in adults, a rate determined by neurons in the brainstem.
This rate may be modified by a number of factors, including emotions, fever, stress, and the pH of the blood.
Concept Review 29.1

■ What is the difference between ventilation and perfusion?
The inhalation route of drug administration quickly delivers

Core Concept 29.2 medications directly to their sites of action.
The respiratory system offers a rapid and efficient mechanism for delivering drugs. The enormous surface
area of the bronchioles and alveoli, and the rich blood supply to these areas, results in an almost instanta-
neous onset of action for inhaled substances.
Medications are delivered to the respiratory system by aerosol therapy. An aerosol is a suspension of
very small liquid droplets or fine solid particles suspended within a gas. Aerosol therapy can give imme-
diate relief for bronchospasm. Drugs may also be given to loosen thick mucus in the bronchial tree. The
major advantage of aerosol therapy is that it delivers the medications to their immediate site of action, thus
reducing systemic adverse effects. To produce the same therapeutic action, an oral medication would have
to be given at higher doses and would be distributed to all body tissues.
It should be clearly understood that drugs delivered by inhalation can produce systemic effects because there
is always some degree of absorption across the respiratory membrane. For example, anesthetics such as nitrous
oxide and isoflurane (Forane) are delivered via the inhalation route and are rapidly distributed to cause central
nervous system (CNS) depression, as presented in Chapter 15. Solvents such as paint thinners and glues are some-
times intentionally inhaled and can cause serious adverse effects on the nervous system and even death. In general,
however, drugs administered by the inhalation route for respiratory conditions produce minimal systemic toxicity.
Several devices are used to deliver medications via the inhalation route. Nebulizers are small
machines that vaporize a liquid drug into a fine mist that can be inhaled, often using a facemask. If the
drug is a solid, it may be administered using a dry powder inhaler (DPI). A DPI is a small device that is
activated by the process of inhalation to deliver a fine powder directly to the bronchial tree. Turbohalers
and rotahalers are types of DPIs. Metered-dose inhalers (MDIs) are a third type of device commonly used
to deliver respiratory medicines. MDIs use a propellant to deliver a measured dose of drugs to the lungs
during each breath. The patient times the inhalation to the puffs of drug emitted from the MDI. Patients
must be carefully instructed on the correct use of these devices because drug dose depends on their correct
use. Patients should be advised to rinse their mouth thoroughly following drug use to reduce the potential
for absorption of the drug across the oral mucosa because swallowing medication that has been deposited
Figure 29.2
Devices used to deliver respiratory drugs.
in the oral cavity may cause the drug to be absorbed in the gastrointestinal (GI) tract, causing potential
adverse effects. Devices used to deliver respiratory drugs are shown in Figure 29.2 ■.
The primary goal of drug therapy for many respiratory disorders is to keep the airways open. Drugs
include bronchodilators, which directly open the airways, and anti-inflammatory drugs, which prevent their
closure. Drugs may be used to act on excessive mucus blocking the airways, either by causing it to become
thinner or by breaking up thick mucus plugs. These and other types of drugs used to treat respiratory disor-
ders are illustrated in Figure 29.3 ■.
Figure 29.3
Antitussives
Medullary cough center
• Suppress cough
Topical decongestants
• Dry nasal mucosa

Mucolytics
• Loosen mucus
Inhaled corticosteroids
Mucus
• Suppress inflammation
Expectorants
• Produce thinner mucus
Mast cell stabilizers

Antihistamines
• Inhibit histamine release
Alveoli
Bronchodilators = Mast cell
= Histamine
• Dilate bronchi
Drugs used to treat respiratory disorders.

Concept Review 29.2

■ Name the three types of devices used to deliver drugs by the inhalation route. What are
the differences among them?
Allergic Rhinitis
Allergic rhinitis, or hay fever, is inflammation of the nasal mucosa due to exposure to allergens.
Although not life threatening, allergic rhinitis is a condition affecting millions of patients, and pharma-
cotherapy is frequently necessary to control symptoms and to prevent secondary complications.
Allergic rhinitis is characterized by sneezing, watery eyes,

Core Concept 29.3 and nasal congestion.
Allergic rhinitis is a common disorder affecting millions of people annually. Symptoms resemble those
of the common cold: tearing eyes, sneezing, nasal congestion, postnasal drip, and itching of the throat. In
addition to the acute symptoms, complications of allergic rhinitis may include loss of taste or smell, sinus-
itis, chronic cough, hoarseness, and middle ear infections in children.
As with other allergies, the cause of allergic rhinitis is exposure to an antigen. An antigen, or allergen,
may be defined as anything that is recognized as foreign by the body’s defense system. The specific
allergen is often difficult to pinpoint; however, common agents include pollen from weeds, grasses, and
trees; molds; dust mites; certain foods; and animal dander. Nonallergenic factors such as chemical fumes,
tobacco smoke, or air pollutants such as ozone may contribute to the symptoms. Although some patients
experience symptoms at specific times of the year, when pollen and mold are at high levels in the environ-
ment, others are bothered throughout the year.
The fundamental problem of allergic rhinitis is inflammation of the mucous membranes in the nose,
throat, and airways. Chemical mediators such as histamine are released and initiate the distressing symp-
toms. The pathophysiology of allergic rhinitis is illustrated in Figure 29.4 ■.
The therapeutic goals of treating allergic rhinitis are to prevent its occurrence and to relieve
symptoms. Drugs used to treat allergic rhinitis may thus be grouped into two basic categories: pre-
venters and relievers. Preventers are used for prophylaxis and include antihistamines, intranasal
corticosteroids, and mast cell stabilizers. Relievers are used to provide immediate, though tempo-
rary, relief for allergy symptoms once they have occurred. Relievers include the oral and intranasal
sympathomimetics.
Fast Facts Allergies

■ The odds that a child with two allergic parents will develop allergies is 70%.
■ A person is more likely to have a severe allergic reaction to food if he or she also has asthma
or has had a previous anaphylactic reaction.
■ Most children outgrow milk, egg, soy, and wheat allergies by the teenage years.
Antihistamines are widely used to treat allergic rhinitis and other

Core Concept 29.4 minor allergies.
Antihistamines are drugs that selectively block the actions of histamine at the H1-receptor, thus alleviating
allergic symptoms. Also called H1-receptor blockers, they are available over the counter (OTC) and fre-
quently used for relief of allergy symptoms, motion sickness, and insomnia. Common H1-receptor blockers
used to treat allergies and other disorders are listed in Table 29.1 ◆.
Figure 29.4
Pathophysiology of
1
Exposure to pollen allergic rhinitis.
2
Plasma cell
releases
antibodies
Plasma cell
IgE antibodies
Vesicle
containing
histamine
3
antibodies
Binding site
bind to mast cells
for “allergy
antibodies”
Mast cell Inflamed
4
Pollen binds to
antibodies and
causes histamine
release
5
Histamine
causes
allergy
symptoms
Table 29.1 H1-Receptor Blockers (Antihistamines)

First-Generation Drugs
azelastine (Astelin, Intranasal; one or two sprays daily per First-generation antihistamine; for nonallergic rhinitis
Astepro) nostril
brompheniramine PO; 4–8 mg tid–qid (max: 40 mg/day) Less sedative effect than diphenhydramine; combined with
(Dimetapp, others) other drugs for OTC use
chlorpheniramine (Chlor- PO; 2–4 mg tid–qid (max: 24 mg/day) Usually combined with a decongestant to treat cold, flu,
Trimeton, others) and allergy symptoms; available for OTC use
clemastine (Tavist) PO; 1.34–2.68 mg bid (max: 8.04 mg/day) Central sedative effects are generally mild
dexchlorpheniramine PO; 2 mg every 4–6 hours (max: For seasonal rhinitis and other allergy disorders
(Dexchlor, Poladex, others) 12 mg/day)
dimenhydrinate PO; 50–100 mg every 4–6 hours Primarily for motion sickness and treatment of nausea and
(Dramamine) vomiting; IV / IM form available
diphenhydramine PO; 25–50 mg tid–qid (max: 300 mg/day) Topical, IV, IM, and subcutaneous forms available; also for
(Benadryl, others) motion sickness, Parkinson’s disease, vertigo, and as an OTC
sleep aid
promethazine (Phenergan) PO; 12.5–25 mg/day (max: 100 mg/day) IV, IM, and rectal suppository forms available; also for
preoperative sedation, motion sickness, nausea, and vertigo
(continued )
Table 29.1 H1-Receptor Blockers (Antihistamines) (continued )

Second-Generation Drugs
acrivastine with PO; One capsule daily (8 mg acrivastine/ For allergic rhinitis
pseudoephedrine 60 mg pseudoephedrine)
(Semprex-D)
cetirizine (Zyrtec) PO; 5–10 mg/day (max: 10 mg/day) Nonsedating; available OTC
desloratadine (Clarinex) PO; 5 mg/day (max: 5 mg/day) Nonsedating; the active metabolite of loratadine
fexofenadine (Allegra) PO; 60 mg twice daily or 180 mg once Once-a-day dosing; nonsedating
daily
levocetirizine (Xyzal) PO; 5 mg (1 tablet or 2 teaspoons) once Very similar to cetirizine; also for chronic idiopathic urticaria
daily
loratadine (Claritin) PO; 10 mg daily Nonsedating; became available OTC in 2001
olopatadine (Patanase) Intranasal; two sprays per nostril twice Newer drug, approved in 2007; the first second-generation
daily nasal spray for allergic rhinitis
Because the term antihistamine is nonspecific and does not specify which of the two histamine recep-
tors is affected, H1-receptor blocker is the more accurate term. Although a large number of H 1-recep-
tor blockers are available for use, their effectiveness, therapeutic uses, and adverse effects are similar.
A simple classification of these drugs is based on their ability to cause sedation. Older, first-generation
H1-receptor blockers have the potential to cause significant drowsiness, whereas the newer, second-genera-
tion drugs lack this effect in most patients. Care must be taken to avoid alcohol and other CNS depressants
when taking antihistamines because their sedating effects may be additive.
The most common therapeutic use of H1-receptor blockers is for the treatment of allergies. These
drugs provide relief from the characteristic sneezing; runny nose; and itching of the eyes, nose, and throat
of allergic rhinitis. Many H1-receptor blockers are used in OTC cold and sinus medicines, often in combi-
nation with decongestants and antitussives. Some common OTC antihistamine combinations used to treat
allergies are listed in Table 29.2 ◆.
Antihistamines are most effective when taken to prevent allergic symptoms; their ability to treat
allergy symptoms after they are present is limited. Their effectiveness may diminish with long-term use. It
should be noted that during severe allergic reactions such as anaphylaxis, histamine is just one of several
chemical mediators released; thus, H1-receptor blockers are not very effective in treating this disorder.
Although most antihistamines are given orally, two are available by the intranasal route. Azelastine
(Astelin, Astepro) is approved for nonallergic rhinitis. Although a first-generation drug, azelastine causes
less drowsiness than others in its class because it is applied locally to the nasal mucosa, and limited sys-
temic absorption occurs. Dymista is a newer combination that includes azelastine with fluticasone, an
intranasal corticosteroid. Olopatadine (Patanase) is a newer second-generation intranasal antihistamine
approved for allergic rhinitis.
Drug Prototype: Diphenhydramine (Benadryl, Others)

Therapeutic Class: Drug to treat allergies Pharmacologic Class: H1-receptor blocker, antihistamine
Actions and Uses: Diphenhydramine is a first-generation Adverse Effects and Interactions: First-generation H1-receptor
H1-receptor blocker whose primary use is to treat symptoms blockers such as diphenhydramine cause significant drowsiness,
of allergy and the common cold such as sneezing, runny although this usually diminishes with long-term use. Occasion-
nose, and tearing of the eyes. Diphenhydramine is often com- ally, a patient will exhibit CNS stimulation and excitability rather
bined with an analgesic, a decongestant, or an expectorant in than drowsiness. Excitation is more frequent in children than in
OTC cold and flu products. Diphenhydramine is also used as a adults. Anticholinergic effects such as dry mouth, tachycardia,
topical drug to treat rashes, and IM/IV forms are available and mild hypotension are seen in some patients.
for severe allergic reactions. Other indications for diphen- Use of diphenhydramine with alcohol, CNS depressants, or
hydramine include Parkinson’s disease, motion sickness, monoamine oxidase (MAO) inhibitors may cause additive CNS
and insomnia. depression. Use with other OTC cold preparations may increase
anticholinergic adverse effects.
Table 29.2 Selected OTC Antihistamine Combinations

Brand Name Antihistamine Decongestant Analgesic
Actifed Cold and Allergy tablets chlorpheniramine phenylephrine —
Benadryl Allergy/Cold caplets diphenhydramine phenylephrine acetaminophen
Chlor-Trimeton Allergy/Decongestant tablets chlorpheniramine pseudoephedrine —
Dimetapp Children’s Cold and Allergy brompheniramine phenylephrine —
Sudafed PE Nighttime Cold diphenhydramine phenylephrine acetaminophen
Sudafed PE Sinus and Allergy tablets chlorpheniramine phenylephrine —
Tavist Allergy tablets clemastine — —
Triaminic Cold/Allergy chlorpheniramine phenylephrine —
Tylenol Allergy Multisystem gels chlorpheniramine phenylephrine acetaminophen
Tylenol PM gelcaps diphenhydramine — acetaminophen
H1-receptor blockers have been used to treat a number of other disorders. Motion sickness responds
well to these medications. It is also one of the few classes of drugs available to treat vertigo, a form of
dizziness that causes significant nausea. Some of the older antihistamines are marketed as OTC sleep
aids, taking advantage of their ability to cause drowsiness. A few are used to treat tremors associated with
Parkinson’s disease.
Concept Review 29.3

■ Why are the antihistamines most effective if given before inflammation occurs?
Nursing Process Focus Patients Receiving Antihistamine Therapy

Prior to administration: ■ Ineffective Airway Clearance related to difficulty swallowing and

■ Obtain a complete health history including respiratory, cardiovascular, coughing
renal, liver, thyroid, and skin conditions; experiences with anaphylaxis, ■ Ineffective Breathing Pattern related to retained secretions and
asthma, or other allergies; drug history; and possible drug interactions. discomfort
■ Evaluate laboratory blood levels: CBC, renal, and liver function studies. ■ Disturbed Sleep Pattern related to somnolence or agitation
■ Acquire the results of a complete physical examination including vital ■ Deficient Knowledge related to a lack of information about
signs, ECG, pulmonary function tests, breathing patterns, and neuro- drug therapy
logical status (LOC).
The patient will:

■ Experience therapeutic effects (relief from allergic symptoms such as congestion, itching, or postnasal drip).
Implementation
■ Auscultate breath sounds before administering drug therapy. Use ■ Instruct the patient to immediately report wheezing or difficulty
with extreme caution in patients with asthma or chronic obstructive breathing.
pulmonary disease (COPD). Keep resuscitative equipment accessible. ■ Advise patients with asthma to consult the nurse regarding the use
(Anticholinergic effects of antihistamines may trigger bronchospasm.) of injectable epinephrine in emergency situations.
of proper administration. (Proper administration helps increase ■ Begin taking antihistamines before allergy season begins or at the
effectiveness of drugs. Mixing antihistamines with other medication earliest possible appearance of symptoms for best effects.
may increase adverse effects such as drowsiness.) ■ Follow directions on specific medication label.
■ Avoid mixing OTC antihistamines; always consult the healthcare
provider before taking any OTC drugs or herbal supplements.
continued . . .
■ Monitor vital signs (including ECG) before administering drug therapy. Instruct the patient to:
Use with extreme caution in patients with a history of cardiovascular ■ Immediately report dizziness, palpitations, headache, or chest, arm,
disease. (Anticholinergic effects can increase heart rate and lower or back pain accompanied by nausea/vomiting and/or sweating to
blood pressure. Fatal dysrhythmias and cardiovascular collapse have the healthcare provider.
been reported in some patients receiving antihistamines.) ■ Monitor vital signs daily, ensuring proper use of home equipment.
■ Monitor thyroid function. Use with caution in patients with a history ■ Instruct the patient to report immediately any nervousness or restless-
of hyperthyroidism. (Antihistamines exacerbate CNS-stimulating ness, insomnia, fever, profuse sweating, thirst, and mood changes to
effects of hyperthyroidism and may trigger thyroid storm.) healthcare provider.
■ Monitor for vision changes. Use with caution in patients with Instruct the patient to:
narrow-angle glaucoma. (Antihistamines can increase intraocular ■ Report head or eye pain and visual changes immediately to healthcare
pressure and cause photosensitivity.) provider.
■ Wear dark glasses, use sunscreen, and avoid excessive sun exposure.
■ Monitor neurologic status, especially LOC. Use with caution in Instruct the patient to:
patients with a history of seizure disorder. (Drugs may cause ■ Avoid driving or performing hazardous activities until the effects
sedation, especially in older adults. Antihistamines can also lower of the drug are known.
the seizure threshold.) ■ Immediately report to the healthcare provider any seizure activity,
including any changes in character and pattern of seizures.
■ Observe for signs of renal toxicity. Measure intake and output. Use ■ Instruct the patient to immediately report flank pain, difficulty
with caution in patients with a history of kidney or urinary tract urinating, reduced urine output, and changes in the appearance of
disease. (Antihistamines promote urinary retention.) urine (cloudy, with sediment, odor, etc.) to the healthcare provider.
■ Use with caution in patients with diabetes mellitus. Monitor serum Instruct the patient to:
glucose levels with increased dosing frequency. (Antihistamines ■ Immediately report symptoms of hypoglycemia.
decrease serum glucose levels.) ■ Consult the healthcare provider regarding timing of glucose
monitoring and reportable results (e.g., “less than 70 mg/dL”).
■ Monitor for GI adverse effects. Use with caution in patients with Instruct the patient to:
a history of GI disorders, especially peptic ulcers or liver disease. ■ Immediately report nausea, vomiting, anorexia, bleeding, chest or
(Antihistamines block H1-receptors, altering the mucosal lining of abdominal pain, heartburn, jaundice, or a change in the color or
the stomach. These drugs are metabolized in the liver, increasing character of stools to the healthcare provider.
the risk of hepatotoxicity.) ■ Avoid substances that irritate the stomach, such as spicy foods,
alcoholic beverages, and nicotine; take drug with food to avoid
stomach upset.
■ Monitor for anticholinergic-related effects such as dry mouth, thick- Instruct the patient to:
ened mucus, and nasal drying. (Mild anticholinergic effects are com- ■ Immediately report fever or flushing accompanied by difficulty
mon and are usually treated symptomatically.) swallowing (“cotton mouth”) to the healthcare provider.
■ Suck on hard candy to relieve dry mouth and maintain adequate
fluid intake.
Intranasal corticosteroids are first-line drugs for treating

Core Concept 29.5 allergic rhinitis.
Corticosteroids, also known as glucocorticoids, are applied directly to the nasal mucosa to prevent symptoms
of allergic rhinitis. When applied consistently, they decrease the secretion of inflammatory mediators, reduce
tissue edema, and cause mild vasoconstriction. They have largely replaced antihistamines as preferred drugs
in the treatment of chronic allergic rhinitis. The intranasal corticosteroids are listed in Table 29.3 ◆. All have
equal effectiveness and can require two to three weeks of therapy before optimum benefits are attained. When
delivered by oral inhalation (not intranasal) some of these medications are also used to treat asthma.
Intranasal corticosteroids are administered with a metered-spray device that delivers a consistent dose
of drug per spray. One to three weeks may be required to achieve peak response. Because of this delayed
effect, intranasal corticosteroids are most effective when taken in advance of expected allergen exposure.
Intranasal corticosteroids produce none of the potentially serious adverse effects that are observed when
these hormones are given orally. The most frequently reported adverse effects are an intense burning sen-
sation in the nose immediately after spraying and drying of the nasal mucosa.
Table 29.3 Intranasal Corticosteroids

beclomethasone (Beconase Intranasal; 1–2 sprays in each nostril Oral inhaler available (Beclovent) for asthma
AQ, Qnasl, QVAR) bid–qid
budesonide (Rhinocort Aqua) Intranasal; two sprays in each nostril bid Oral inhaler available (Pulmicort) for asthma
ciclesonide (Omnaris) Intranasal; two sprays in each nostril once Newer drug approved in 2006; less likely to cause steroid
daily (max: 200 mcg/day) adverse effects than others in this class
flunisolide (Aerospan) Intranasal; two sprays in each nostril bid Oral inhaler available (Aerospan) for asthma
fluticasone (Flonase, Intranasal; one spray in each nostril once Oral inhaler available (Flovent) for asthma; topical form
Flovent, Veramyst) (Veramyst) or twice (Flonase) daily available (Cutivate) for dermatologic use
mometasone (Nasonex) Intranasal; two sprays in each nostril daily Topical form available (Elocon) for dermatologic use
triamcinolone (Nasacort AQ) Intranasal; 2–4 sprays in each nostril qid Oral inhaler available (Nasacort) for asthma; also available
in IM, subcutaneous, intradermal, and intra-articular forms
Drug Prototype: Fluticasone (Flonase, Veramyst)

Therapeutic Class: Drug for allergic rhinitis Pharmacologic Class: Intranasal corticosteroid
Actions and Uses: Fluticasone is typical of the intranasal corti- Adverse Effects and Interactions: Adverse effects of fluticasone
costeroids used to treat allergic rhinitis. Therapy usually begins are rare. Small amounts of the intranasal corticosteroids are
with two sprays in each nostril twice daily and decreases to one sometimes swallowed, which increases their potential for caus-
dose per day. Fluticasone acts to decrease local inflammation in ing systemic adverse effects. Nasal irritation and bleeding occur
the nasal passages, thus reducing nasal stuffiness. in a few patients.
Decongestants are used to reduce nasal congestion caused by

allergic rhinitis and the common cold. Core Concept 29.6
Decongestants are drugs that relieve nasal congestion. They are administered by either the oral or intrana-
sal routes and are often combined with antihistamines in the pharmacotherapy of allergies or the common
cold. Most decongestants are sympathomimetics—drugs that activate the sympathetic nervous system.
Doses for the decongestants are given in Table 29.4 ◆.
Sympathomimetics are effective at relieving the nasal congestion associated with allergic rhini-
tis and the common cold. Both oral and intranasal preparations are available. The intranasal drugs
such as oxymetazoline (Afrin, others) are available OTC as sprays or drops and produce an effec-
tive response within minutes. Because of their local action, intranasal sympathomimetics produce few
systemic effects. The most serious, limiting adverse effect of the intranasal preparations is rebound
congestion, a condition characterized by hypersecretion of mucus and worsened nasal congestion once
the drug effects wear off. This rebound effect sometimes leads to a cycle of increased drug use as the
condition worsens. Because of rebound congestion, intranasal sympathomimetics should be used for
no longer than three to five days. Patients with allergic rhinitis who develop tolerance to the effects
of decongestants should be gradually switched to intranasal corticosteroids because they do not cause
rebound congestion.
When administered orally, sympathomimetics do not produce rebound congestion. Their onset of
action by this route, however, is much slower than the intranasal preparations, and they are less effec-
tive at relieving severe congestion. The possibility of systemic adverse effects is also greater with the
oral drugs. Potential adverse effects include hypertension and CNS stimulation that may lead to insom-
nia or anxiety.
Prior to 2000, pseudoephedrine was the most common decongestant found in oral OTC cold and
allergy medicines. Pseudoephedrine, however, is the starting chemical for the synthesis of illegal metham-
phetamine by drug traffickers. Although pseudoephedrine is still available without a prescription, pharma-
cists are required to monitor its distribution by keeping a log of patients’ names and addresses and checking
the photo identification of the buyer. Most manufacturers have reformulated their OTC cold medicines to
contain phenylephrine rather than pseudoephedrine. A drug prototype feature for phenylephrine is included
in Chapter 8.
Table 29.4 Decongestants

ipratropium (Atrovent) Nasal spray; two sprays in each nostril Anticholinergic drug; also available by the inhalation
3–4 times per day up to 4 days route for asthma
naphazoline (Privine) Intranasal; two drops in each nostril Also available as spray
every 3–6 hours
oxymetazoline (Afrin Intranasal (0.05%); 2–3 sprays in each Also available as drops
12 hour, Neo-Synephrine nostril bid for up to 3–5 days
12 hour, others)
phenylephrine (Afrin 4–6 hours, Intranasal (0.25–0.5%); one or two sprays Also available as drops, chewable tablets, and
Neo-Synephrine 4–6 hours, in each nostril every 3–4 hours hemorrhoidal cream; also available by the subcutaneous,
others) (see page 98 for the Drug IM and IV routes for severe hypotension and shock
Prototype box)
pseudoephedrine (Sudafed, PO; 60 mg every 4–6 hours (max: Produces little congestive rebound or irritation; also
others) 120 mg/day) available as drops and in extended-release form
tetrahydrozoline (Tyzine) Intranasal (0.1%); 2–4 drops in each Ophthalmic solution is available for allergic reactions
nostril every 3 hours of the eye
xylometazoline (Otrivin) Intranasal (0.1%); one or two sprays in Also available as drops
each nostril bid (max: 3 doses/day)
Because sympathomimetics relieve only nasal congestion, they are often combined with antihista-
mines to control the sneezing and tearing of allergic rhinitis. It is interesting to note that some OTC drugs
having the same basic name (Neo-Synephrine, Afrin, Visine) may contain different sympathomimetics.
For example, Neo-Synephrine preparations with a 12-hour duration contain the drug oxymetazoline, while
those with a 4- to 6-hour duration contain phenylephrine.
Ipratropium (Atrovent) is an anticholinergic drug sometimes used for the symptomatic relief of
runny nose due to the common cold or allergic rhinitis. Given by the intranasal route, ipratropium has
no serious adverse effects. Its actions are limited to runny nose; it does not stop the sneezing, postnasal
drip, or itchy throat or eyes. A more common indication for ipratropium is for the pharmacotherapy of
asthma.
Concept Review 29.4

■ The sympathomimetics are the most effective drugs for relieving nasal congestion,
but physicians often prefer to prescribe antihistamines or intranasal corticosteroids.
Why?
Drug Prototype: Oxymetazoline (Afrin, Others)

Therapeutic Class: Decongestant Pharmacologic Class: Sympathomimetic
Actions and Uses: Oxymetazoline activates alpha-adrenergic Adverse Effects and Interactions: Rebound congestion is com-
receptors of the sympathetic nervous system. This stimulation mon when oxymetazoline is used for longer than three to five
causes arterioles in the nasal passages to constrict, producing days. Minor stinging and dryness in the nasal mucosa may be
a drying of the mucous membranes. Relief from the symptoms experienced. Systemic adverse effects are unlikely, unless a
of nasal congestion occurs within minutes and lasts for considerable amount of the medicine is swallowed. Patients
10–12 hours. The drug is administered with a metered-spray with thyroid disorders, hypertension, diabetes, or heart disease
device or by nose drops. should use sympathomimetics only on the direction of their
Oxymetazoline (Visine LR) is also available as eyedrops. healthcare provider.
It causes vasoconstriction of vessels in the eye and is used to No clinically significant interactions have been found.
relieve redness and provide relief from dryness and minor eye
irritations.
Antitussives and expectorants are used to treat symptoms of the

common cold. Core Concept 29.7
In addition to congestion, cough is a symptom that causes patients to take OTC remedies or to seek medical
attention. Cough is a reflex mechanism controlled by neurons in the cough center, located in the medulla
oblongata of the brain. In diseases such as emphysema and bronchitis, or when liquids have been aspirated
into the bronchi, it is not desirable to suppress the normal cough reflex. Because cough is merely a symp-
tom, the therapeutic goal is to identify and treat the underlying disorder whenever possible.
There are many possible causes of cough, ranging from the acute cough of an upper respiratory infec-
tion to the chronic cough of tobacco smoking. Some drugs, such as the angiotensin-converting enzyme
(ACE) inhibitors and beta-adrenergic blockers, can trigger persistent cough. In many cases, keeping the
throat moist with sugar-free candy, “cough drops,” or frequent sips of water is sufficient to suppress cough.
However, a dry, hacking, nonproductive cough can be irritating to the membranes of the throat and can
deprive a patient of much-needed rest. It is these types of conditions in which therapy with drugs that con-
trol cough, or antitussives, may be warranted. anti 5 against
Opioids, the most effective class of antitussives, act by raising the cough threshold in the cough center, tussive 5 pertaining to a
thereby decreasing both the frequency and the intensity of cough. Hydrocodone and codeine are effective opi- cough
oid antitussives. Doses needed to suppress the cough reflex are low; thus there is minimal potential for depen-
dence. Most codeine cough mixtures are classified as Schedule III, IV, or V drugs and are reserved for more
serious cough conditions. The amount of codeine in cough mixtures is low and rarely causes serious adverse
effects. However, care must be taken not to give these mixtures to patients allergic to codeine or other opi-
oids. In addition, the drug must be kept secure from children because accidental overdose of opioids in infants
can cause severe respiratory depression and even death. Opioids may be combined with other drugs such as
antihistamines, decongestants, and nonopioid antitussives in the therapy of severe cold or flu symptoms.
The most frequently used OTC antitussive is dextromethorphan, which is included in most severe cold
and flu preparations. Dextromethorphan is chemically similar to the opioids and also acts on the CNS to raise
the cough threshold. Although it does not have the high abuse potential of opioids, dextromethorphan can cause
slurred speech, dizziness, drowsiness, euphoria, and lack of motor coordination when taken in high amounts.
Benzonatate (Tessalon) is a nonopioid antitussive that does not act on the cough center. Instead, ben-
zonatate has a local anesthetic-like effect on stretch receptors in the lung, which essentially interrupts the
cough message. The patient must be instructed not to chew the soft capsules because they will cause numb-
ness of the throat and tongue.
Expectorants are drugs that reduce the thickness or viscosity of bronchial secretions. They stimulate
mucus flow, which thins bronchial secretions, allowing them to be removed with less forceful coughing.
The most effective OTC expectorant is guaifenesin. Like dextromethorphan, guaifenesin produces few
adverse effects and is a common ingredient in many OTC cold and flu preparations. Higher doses of guai-
fenesin are available by prescription. Nonprescription cough and cold products (including those containing
guaifenesin) should not be used in children under six years of age.
Acetylcysteine (Mucomyst) is one of the few drugs available to directly loosen thick, viscous bron-
chial secretions by breaking down the chemical structure of mucus molecules. Drugs of this type are called
mucolytics. Acetylcysteine is delivered by the inhalation route and is not available OTC. It is used in muco 5 mucus
patients who have cystic fibrosis or other diseases that produce large amounts of thick bronchial secretions. lytic 5 destruction or
Acetylcysteine (Acetadote) is also given as a 5% oral solution for acetaminophen overdose. When given disintegration
within 24 hours of the overdose, acetylcysteine prevents acute liver damage by blocking the formation of
toxic metabolites of acetaminophen.
Asthma
Asthma is a chronic pulmonary disease that has both inflammatory and bronchospasm components. Drugs
are given to either decrease the frequency of asthmatic attacks or terminate attacks in progress. Asthma is
one of the most common chronic conditions in the United States, affecting about 24 million Americans.
Asthma is a chronic inflammatory disease characterized by

bronchospasm. Core Concept 29.8
Asthma is characterized by chronic inflammation that occurs when potent mediators of the immune and
inflammatory responses are released by mast cells lining the bronchi. The result of this inflammation is
increased mucus secretion, which narrows the airways and makes breathing more difficult.
Figure 29.5
Changes in bronchioles
during an asthma NORMAL BRONCHIOLE
attack: (a) normal Mucous membrane
bronchiole, (b) inflam-
mation obstructing the
airway, and
(c) constricted
bronchiole in Airway
asthma attack.
(a) Smooth muscle
(b) Inflammatory cells

and debris fill the
airway
Asthma attack n
Inflammatio
Bronch
oconstr (c) Smooth muscle
iction
contraction
constricts the airway
The second component of asthma is acute bronchoconstriction or bronchospasm during which

bronchiolar smooth muscle contracts and the airway diameter narrows. This condition is illustrated in
Figure 29.5 ■. The inflammatory conditions in the airway make the smooth muscle hyperresponsive to
a variety of stimuli. Stimuli such as breathing smoke, pollutants, or cold air may trigger acute broncho-
spasm. Specific triggers are listed in Table 29.5 ◆. Some patients experience bronchospasm on exertion,
a condition called exercise-induced asthma.
dys 5 painful or difficult The patient with asthma will exhibit symptoms such as evening cough, dyspnea (shortness of breath),
pnea 5 breathing chest tightness, and wheezing. Intervals between symptoms may vary from days to weeks to months.
Table 29.5 Common Triggers of Asthma

Air pollutants Tobacco smoke
Ozone
Nitrous and sulfur oxides
Fumes from cleaning fluids or solvents
Burning leaves
Allergens Pollen from trees, grasses, and weeds
Animal dander
Household dust
Mold
Chemicals and food Drugs such as aspirin, ibuprofen, and beta blockers
Sulfite preservatives
Food such as nuts, monosodium glutamate (MSG), shellfish, and dairy products
Respiratory infections Bacterial, fungal, and viral
Stress Emotional stress or anxiety
Exercise in dry, cold climates
Figure 29.6
Drug classes used in the

pharmacotherapy of
asthma.
ASTHMA
Termination of Prevention of
acute bronchospasm acute bronchospasm
• Short-acting beta- • Inhaled corticosteroids

adrenergic drugs • Anticholinergics
• Anticholinergics • Long-acting beta-
• Xanthines adrenergic drugs
• Mast cell stabilizers
• Leukotriene modifiers
tatus asthmaticus is a severe, prolonged form of asthma that is unresponsive to drug treatment and may
S
lead to respiratory failure.
Because asthma has both a bronchoconstriction component and an inflammatory component, drug
therapy of the disease focuses on one or both of these mechanisms. The goals of drug therapy are twofold:
to terminate acute bronchospasms in progress and to reduce the frequency of acute asthma attacks. Differ-
ent drugs are usually needed to achieve each of these goals. The various classes of drugs used for asthma
are shown in Figure 29.6 ■.
Beta-adrenergic agonists are the most effective drugs for relieving

acute bronchospasm. Core Concept 29.9
Recall from Chapter 8 that the smooth muscle lining the bronchioles is under the control of the auto-
nomic nervous system. Changes in the airway diameter are made possible by the contraction or relax-
ation of the bronchiolar smooth muscle. During the fight-or-flight response, beta2-adrenergic receptors
of the sympathetic nervous system are stimulated, the bronchiolar smooth muscle relaxes, and bron-
chodilation results. This allows more air to enter the alveoli, thus increasing the oxygen supply to the
body during periods of stress or exercise. In practical terms, drugs that enhance bronchodilation will
cause the patient to breathe more easily; these are some of the most common medications for treating
pulmonary disorders.
Bronchodilators are medications from several drug classes that are used to rapidly relieve the acute
bronchospasm characteristic of an asthmatic attack. Although the beta-adrenergic drugs are the most com-
monly prescribed types of bronchodilators, theophylline and ipratropium may also be used. Bronchodila-
tors used for asthma are listed in Table 29.6 ◆.
Beta-adrenergic drugs, or sympathomimetics, are the most effective drugs for the treatment of acute
bronchospasm. In most cases, the drugs used for pulmonary disease are selective for beta2-receptors in the
lung; thus, they produce fewer cardiac adverse effects than the nonselective beta drugs. There are two basic
classes of beta-adrenergic drugs, and each has different indications.
Fast Facts Asthma

■ According to the Asthma and Allergy Foundation of America, every day in America:
■ 44,000 people have an asthma attack.
■ 36,000 children miss school due to asthma.
■ 27,000 adults miss work due to asthma.
■ 4,700 people visit the emergency room due to asthma.
■ 1,200 people are admitted to the hospital due to asthma.
■ 9 people die from asthma.
Table 29.6 Bronchodilators

Beta-Adrenergic Drugs
albuterol (Proventil, Ventolin, MDI; two inhalations every 4–6 hours as needed Relaxes smooth muscle of the bronchial tree;
VoSpire) (max: 12 inhalations/day) nebulizer form available
Nebulizer; 1.25–5 mg every 4–8 hours as needed
PO; 2–4 mg tid-qid (max: 32 mg/day); Extended-release
tablets: 8 mg every 12 hours (max: 32 mg/day divided)
arformoterol (Brovana) Nebulizer; 15 mcg twice daily (max: 30 mcg/day) Newer drug for COPD; long acting; similar to
formoterol
formoterol (Foradil, DPI; 12 mcg inhalation capsule every 12 hours Long acting; used for asthma prophylaxis
Perforomist) (max: 24 mcg/day)
Nebulizer; 20 mcg bid (max: 40 mcg/day)
indacaterol (Arcapta neohaler) Inhalation: one 75 mcg capsule daily using the Newer drug used as a maintenance bronchodilator
Neohaler for COPD
levalbuterol (Xopenex) Nebulizer; 0.63 mg tid–qid Short acting; similar to albuterol
MDI; two inhalations every 4–6 hours
pirbuterol (Maxair) MDI; two inhalations four times a day Short acting; similar to albuterol
(max: 12 inhalations/day)
salmeterol (Serevent) DPI; two aerosol inhalations bid or one Long acting; used for asthma prophylaxis
powder diskus bid
terbutaline (Brethine) PO; 2.5–5 mg tid (max: 15 mg/day) Also used to delay premature labor
Subcutaneous; 250 mcg (may be repeated in 15 min)
Inhalation; two inhalations (200 mcg/spray) every
4–6 hours
Xanthines
aminophylline (Truphylline) PO; 380 mg/day in divided doses every 6–8 hours IV form available
(max: 928 mg/day)
theophylline (Theo-dur) PO; 300–600 mg/day in divided doses IV and extended-release form available
(max: 900 mg/day)
Anticholinergics
aclidinium (Tudorza Pressair) Inhalation: 400 mcg bid Newer drug for acute bronchospasm
ipratropium (Atrovent, MDI; two inhalations qid (max: 12 inhalations/day) Combivent is a combination of ipratropium
Combivent) Nebulizer; 500 mcg every 6–8 hours as needed and albuterol
tiotropium (Spiriva) DPI; one capsule inhaled/day Handihaler device is used to puncture capsule
■ Short-acting beta drugs Short-acting beta agonists are the most frequently prescribed drugs
for aborting or terminating an acute asthma attack because they begin to act within minutes.
Their effects, however, last only two to six hours.
■ Long-acting beta drugs Because long-acting beta drugs take 20 to 60 minutes to act, they are
not used to terminate bronchospasm. They should only be used in combination with inhaled
corticosteroids for the prophylaxis of severe, persistent asthma.
Inhaled beta-adrenergic drugs produce little systemic toxicity because only small amounts of the
drugs are absorbed. When given orally, a longer duration of action is achieved, but adverse effects such as
tachycardia and tremor are more frequently experienced. Tolerance may develop to the therapeutic effects
of the beta-adrenergic drugs; therefore, the patient must be instructed to seek medical attention if the drugs
prove to be less effective with continued use.
As discussed in Chapter 8, blocking the parasympathetic nervous system produces similar effects to stim-
ulation of the sympathetic nervous system. It is predictable then, that anticholinergic drugs would cause bron-
chodilation and have potential use in the pharmacotherapy of asthma and other pulmonary diseases. The most
widely used drug in this class, ipratropium (Atrovent), is taken via inhalation to rapidly relieve bronchospasm.
Because it is not readily absorbed from the lungs, it produces few adverse effects, although it is considered
less effective than beta-adrenergic drugs. Inhaled anticholinergics are more effective when used with other
bronchodilators; Combivent is a combination of ipratropium and albuterol in a single MDI canister. Tiotro-
pium (Spiriva) is a newer anticholinergic with a long duration of action that allows for once-daily dosing.
The third class of bronchodilators is the xanthines (sometimes called methylxanthines). Chemically
related to caffeine, theophylline (Theo-dur) and aminophylline (Truphylline) were drugs of choice for bron-
choconstriction 20 years ago. Theophylline, however, has a narrow margin of safety and interacts with a
large number of other drugs. Adverse effects such as nausea, vomiting, and CNS stimulation are relatively
common, and dysrhythmias may occur at high doses. Having been largely replaced by safer and more effec-
tive drugs, theophylline is now primarily used for the long-term oral prophylaxis of persistent asthma.
Nursing Process Focus Patients Receiving Bronchodilators

Prior to administration: ■ Impaired Gas Exchange related to bronchial constriction

■ Obtain a complete health history, including respiratory, cardiovascular, ■ Anxiety related to difficulty in breathing
renal and liver conditions, drug history, and possible drug interactions. ■ Deficient Knowledge related to a lack of information about drug
■ Obtain information about experiences with anaphylaxis, asthma, al- therapy
lergies and exposure to environmental irritants; effects of respiratory ■ Ineffective Therapeutic Regimen Management related to noncompli-
difficulties on sleep, eating, and performance of ADLs. ance with medication regimen, presence of adverse effects, and need
■ Evaluate laboratory blood findings: CBC, ABGs, and renal and liver for long-term medication use
function studies. In addition, evaluate information regarding results of
pulmonary function tests (peak expiratory flowmeter).
signs, pulse oximetry, and symptoms related to respiratory deficiency,
such as dyspnea, orthopnea, cyanosis, nasal flaring, adventitious lung
sounds (wheezing), and weakness.
The patient will:

■ Experience therapeutic effects (adequate oxygenation, improved lung sounds, and improved pulmonary function values).
Implementation

■ Continue to monitor vital signs (including pulse and blood pressure) Instruct the patient to:
respiratory pattern, pulse oximetry, and lung sounds. Monitor periodic ■ Use medication as directed even if asymptomatic to prevent the onset
pulmonary function tests: peak expiratory flow meter and arterial of respiratory difficulties.
blood gas. (Monitoring is necessary to determine drug effectiveness.) ■ Instruct the patient to report symptoms of deteriorating respiratory
status such as increased dyspnea, breathlessness with speech, and/or
orthopnea to the healthcare provider.
of proper use of the inhaler. (Proper administration techniques and ■ Recognize the difference between long- and short-acting inhalers.
use of equipment ensures correct dosage.) ■ Use a spacer between MDI and mouth.
■ Shake or load the inhaler with tablet or powder.
■ If using a bronchodilator inhaler with a corticosteroid inhaler: Use the
bronchodilator first to open the airway, wait 5 to 10 minutes,
then take the corticosteroid.
■ Use the medication strictly as prescribed; do not “double up” on doses.
■ Rinse the mouth thoroughly following use.
■ Rinse inhaler and spacer with water daily.
■ Observe for adverse effects specific to the medication used. (An ■ Instruct the patient regarding adverse effects and to report spe-
increase in pulse rate, changes in blood pressure or sensations of cific drug adverse effects such as palpitations or fast heart rate and
palpitations may occur with beta-adrenergic drugs.) respirations.
■ Maintain the environment free of respiratory contaminants such as Instruct the patient to:
dust, dry air, flowers, and smoke. (These substances may exacerbate ■ Avoid respiratory irritants.
bronchial constriction.) ■ Maintain a “clean air environment.”
■ Stop smoking and avoid secondhand smoke, if applicable.
■ Maintain dietary intake adequate in essential nutrients and vitamins. Instruct the patient to:
(Dyspnea interferes with proper nutrition.) ■ Maintain nutrition with foods high in essential nutrients.
■ Consume small frequent meals to prevent fatigue.
■ Ensure that the patient maintains adequate hydration of 3 to 4 L /day Instruct the patient to:
(to liquefy pulmonary secretions). ■ Consume 3 to 4 L of fluid per day if not contraindicated.
■ Avoid caffeine (increases CNS irritability).
continued . . .
■ Provide emotional and psychosocial support during periods of ■ Instruct the patient in relaxation techniques and controlled
shortness of breath. (Providing support and remaining calm helps breathing techniques.
to reduce the anxiety brought on by respiratory difficulties.)
■ Monitor patient compliance. (Maintaining therapeutic drug levels ■ Inform the patient of the importance of ongoing medication
is essential to effective therapy.) compliance and follow-up.
Corticosteroids are the most effective drugs for the long-term

Core Concept 29.10 prophylaxis of asthma.
The role of intranasal corticosteroids as first-line drugs in the treatment of allergic rhinitis is discussed in
Core Concept 29.5. When given by the inhalation route, corticosteroids are also prime drugs for the man-
agement of asthma.
Because asthma has a major inflammatory component, several classes of anti-inflammatory drugs
are used for asthma prophylaxis. The inhaled corticosteroids are most commonly used for this purpose,
although mast cell stabilizers and leukotriene inhibitors are also effective. Doses of the anti-inflammatory
drugs used for asthma are given in Table 29.7 ◆.
Corticosteroids are the most effective drugs available for the prevention of acute asthmatic episodes.
When inhaled on a daily schedule, corticosteroids suppress inflammation without producing major adverse
effects. Mucus production and edema are diminished, thus reducing airway obstruction. Patients should
Table 29.7 Anti-Inflammatory Drugs for Asthma

Inhaled Corticosteroids
beclomethasone MDI; one or two inhalations tid or qid Intranasal form available for allergic rhinitis
(Beconase AQ, Qvar) (max: 20 inhalations/day)
budesonide (Pulmicort DPI; one or two inhalations (200 mcg/ Intranasal form available for allergic rhinitis
Turbuhaler, Rhinocort) inhalation) daily (max: 800 mcg/day)
ciclesonide (Alvesco) MDI; one or two inhalations/day (max: Newer drug; for asthma prophylaxis, not for acute
320–640 mcg/day) bronchospasm
flunisolide (Aerospan) MDI; two or three inhalations bid or tid Intranasal form available for allergic rhinitis
(max: 12 inhalations/day)
fluticasone (Flovent) MDI (44 mcg); two inhalations bid (max: Intranasal form available for allergic rhinitis; also
10 inhalations/day) available in 110 and 120 mcg inhalers
mometasone (Asmanex) DPI; one inhalation daily (max: two Intranasal form available for allergic rhinitis and
inhalations daily) topical form for skin inflammation
triamcinolone (Azmacort) MDI; two inhalations tid or qid (max: Also available in IM, subcutaneous, intradermal,
16 inhalations/day) topical, and oral forms
Mast Cell Stabilizers
cromolyn (Intal) MDI; one inhalation qid Intranasal form available OTC for allergic rhinitis;
also for ophthalmic use
nedocromil (Tilade) MDI; two inhalations qid Topical form available for ophthalmic use
Leukotriene Modifiers
montelukast (Singulair) PO; 10 mg/day in evening Not for acute bronchospasm; also for allergic rhinitis
roflumilast (Daliresp) PO; 500 mcg once daily Newer drug for COPD
zafirlukast (Accolate) PO; 20 mg bid 1 hour before or Not for acute bronchospasm; also for allergic rhinitis
2 hours after meals
zileuton (Zyflo) PO; 1,200 mg bid Not for acute bronchospasm
be informed that inhaled corticosteroids must be taken daily to produce their therapeutic effect and that
these medications are not effective at terminating episodes in progress. Although symptoms will improve
in the first one to two weeks of therapy, four to eight weeks may be required for maximum benefit. For
some patients, a beta-adrenergic drug may be prescribed along with an inhaled corticosteroid because this
permits the dose of the corticosteroid to be reduced by as much as 50%.
For severe, persistent asthma that is unresponsive to other treatments, oral corticosteroids may be
prescribed. Treatment time is limited to the shortest length possible, usually five to seven days. If taken for
longer than 10 days, oral corticosteroids may produce significant adverse effects such as adrenal gland sup-
pression, peptic ulcers, and hyperglycemia. Other uses and adverse effects of corticosteroids are presented
in Chapters 24 and 31.
Mast cell stabilizers and leukotriene modifiers are alternative

anti-inflammatory drugs for the prophylaxis of asthma. Core Concept 29.11
Two mast cell inhibitors play a limited though important role in the prophylaxis of asthma. These drugs act
by inhibiting the release of histamine from mast cells.
Cromolyn (Intal) is an anti-inflammatory drug that is useful in preventing asthma attacks. When
administered via an MDI or a nebulizer, cromolyn is a safe alternative to the corticosteroids. Patients must
be informed that cromolyn should be taken on a daily basis and should not be used to terminate acute
attacks. An intranasal form of cromolyn (Nasalcrom) is used in the treatment of seasonal allergies. The
second mast cell stabilizer, nedocromil (Tilade), has actions and uses similar to cromolyn. The drug is used
for asthma prophylaxis and has an unpleasant taste.
The leukotriene modifiers reduce inflammation and ease bronchoconstriction by modifying the action
of leukotrienes, which are mediators of the inflammatory response in patients with asthma. Leukotriene
modifiers are alternative drugs used for the management of persistent asthma that cannot be controlled with
inhaled corticosteroids or short-acting beta drugs.
The leukotriene modifiers are approved for the prophylaxis of chronic asthma; they are ineffective
in relieving acute bronchospasm. They are all given orally. Zileuton and roflumilast have a rapid onset of,
whereas the other two leukotriene modifiers take as long as a week to provide therapeutic benefit. Adverse
effects associated with the leukotriene modifiers include headache, cough, nasal congestion, GI upset, and
psychiatric effects such as depression and suicidal thinking.
Concept Review 29.5

■ Distinguish the classes of drugs that prevent asthma attacks from those that can terminate
an attack in progress. Name at least one drug in each class.
Drug Prototype: Cromolyn (Intal)

Therapeutic Class: Anti-inflammatory drug for asthma and allergic rhinitis Pharmacologic Class: Mast cell
stabilizer
Actions and Uses: Cromolyn prevents the inflammation that conjunctiva. Gastrocrom is a PO dosage form of cromolyn that
is characteristic of asthma and COPD. For asthma therapy the is the only FDA-approved drug to treat systemic mastocytosis,
drug is administered via oral inhalation. An intranasal over the which is a rare condition in which the patient has an excessive
counter (OTC) formulation (NasalCrom) is available for allergic number of mast cells.
rhinitis. Cromolyn is considered an alternate drug for the treat-
ment of mild to moderate asthma when inhaled corticosteroids Adverse Effects and Interactions: Adverse effects are uncom-
have not proven effective. mon when the drug is administered by oral inhalation. The
Cromolyn is only effective for preventing asthma and most common effects are bronchospasm, cough, and pharyn-
should not be used to terminate an asthma attack. Several geal irritation. Intranasal and ophthalmic administration may
weeks of therapy are needed for optimum benefit. An ophthal- cause local burning and stinging. There are no significant drug
mic solution (Crolom) is used to treat allergic disorders of the interactions.
Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) includes progressive lung disorders primarily caused by
tobacco smoking. COPD is a major cause of death and disability. Drugs may bring symptomatic relief but
do not cure the disorders.
Chronic obstructive pulmonary disease is a progressive disorder

Core Concept 29.12 treated with multiple drugs.
The two primary disorders classified as COPD are chronic bronchitis and emphysema. Both are strongly
bronch 5 bronchus associated with smoking tobacco products and, secondarily, air pollutants. In chronic bronchitis, excess
itis 5 inflammation mucus is produced in the respiratory tree due to inflammation and irritation from smoke or pollutants. The
airway becomes partially obstructed with mucus, resulting in the classic signs of dyspnea and coughing.
Because microbes enjoy the mucus-rich environment, pulmonary infections are common. Gas exchange
may be impaired.
COPD is a progressive disease, with the terminal stage being emphysema. After years of
chronic inflammation, the bronchioles lose their elasticity, and the alveoli dilate to maximum size to
get more air into the lungs. The patient suffers from extreme dyspnea from even the slightest physi-
cal activity.
Patients with COPD may receive a number of pulmonary drugs for symptomatic relief of their dis-
order. The goal of pharmacotherapy is to control cough and bronchospasm. Typical drugs considered in
COPD therapy include the following:
■ Long-acting beta-adrenergic drugs such as salmeterol
■ Anticholinergic bronchodilators such as ipratropium or tiotropium
■ Inhaled corticosteroids such as budesonide
■ Mucolytics and expectorants to reduce the thickness of the bronchial mucus and to aid in its
removal
■ Oxygen therapy may be used in patients with emphysema.
Patients should be taught to avoid taking any drugs that have beta-blocking activity or that otherwise
cause bronchoconstriction. Respiratory depressants should be avoided. It is important to note that none of
the pharmacotherapies offer a cure for COPD; they only treat the symptoms of a progressively worsening
disease.

Patients treated for pulmonary disorders need to know the following:
In General
1. Because tolerance to some medications may occur, if medication is no longer effective,
report this tolerance to a healthcare provider. Do not take extra medication without
notifying a healthcare provider.
Regarding Inhaled Medications

2. When using MDIs or DPIs, allow an interval of at least one minute to pass between
puffs.
3. When taking more than one respiratory medicine, take the bronchodilator first. This
opens the airways and increases the effectiveness of the second medication.
4. Rinse the mouth thoroughly following inhaler use to reduce the oral absorption of
inhaled medicines.
5. Take inhaled corticosteroids on a regular basis—not as needed. These medications are
not used to stop acute asthma attacks.
6. Do not use decongestant nasal sprays for more than two or three days unless instructed
to do so by a healthcare provider.
Regarding Bronchodilators
7. Avoid caffeine-containing foods and beverages
8. Immediately report any abnormalities in pulse rate, changes in blood pressure, or sensa-
tions of palpitations when taking beta-adrenergic stimulators.
Regarding Antihistamines and Decongestants

9. If taking antihistamines for the first time, avoid operating machinery or performing
other tasks requiring alertness because drowsiness may occur.
10. Use hard candies, chewing gum, or ice chips to reduce the dry mouth caused by some
decongestants and antihistamines.
11. Stop taking antihistamines and notify a healthcare provider if excessive sedation,
wheezing, chest tightness, or bleeding/bruising occurs.
12. Do not take OTC cold or allergy medicines containing antihistamines at the same time
as prescription antihistamines.
Chapter Review 473
Chapter Review
29.1 The respiratory system supplies oxygen for the 29.7 Antitussives and expectorants are used to treat
body and provides protection against inhaled symptoms of the common cold.
organisms. Antitussives are effective at inhibiting the cough
The URT warms the incoming air and reacts to par- reflex. Although opioids are the most effective, there
ticles or pathogens that attempt to enter the body. is some risk of physical dependence. Guaifenesin is
The LRT brings needed oxygen into the body and an OTC drug used to increase bronchial secretions
removes carbon dioxide through expiration. The pro- so that cough may be more productive. Mucolytics
cess of moving air into and out of the lungs, or ven- loosen mucus so that it may be more easily removed
tilation, is distinct from the process of gas exchange from the bronchial tree.
across the alveoli, a process known as respiration.
29.8 Asthma is a chronic inflammatory disease charac-
29.2 The inhalation route of drug administration terized by bronchospasm.
quickly delivers medications directly to their sites Asthma is a common disease characterized by bron-
of action. chospasm and chronic airway inflammation. Expo-
Inhalation is frequently used as a route of drug admin- sure to a number of factors, including allergens, can
istration for those medications targeted for the respi- cause an acute episode.
ratory system. Nebulizers, DPIs, and MDIs are used
to deliver drugs via the inhalation route. 29.9 Beta-adrenergic agonists are the most effective
drugs for relieving acute bronchospasm.
29.3 Allergic rhinitis is characterized by sneezing, Inhaled beta2-adrenergic drugs are preferred medica-
watery eyes, and nasal congestion. tions for relieving bronchospasm. Anticholinergics
Allergic rhinitis, also known as hay fever, is a chronic are sometimes used for bronchodilation, but fewer
allergy triggered by a wide variety of antigens. The are available because of their incidence of adverse
release of chemicals mediating the immune response effects. Xanthines, once widely used in pulmonary
can result in seasonal symptoms for some patients, medicine, are now second-choice drugs for relieving
and chronic, continuous symptoms for others. bronchospasm because of their higher potential for
adverse effects.
29.4 Antihistamines are widely used to treat allergic
rhinitis and other minor allergies. 29.10 Corticosteroids are the most effective drugs for the
The H1-receptor blockers, or antihistamines, are used long-term prophylaxis of asthma.
to treat allergies, motion sickness, and insomnia. Inhaled corticosteroids are the drugs of choice for
Newer drugs in this class are nonsedating and offer asthma prophylaxis. The inhaled corticosteroids, even
the advantage of once-a-day dosing. when used on a long-term basis, produce few adverse
effects compared to oral corticosteroids.
29.5 Intranasal corticosteroids are first-line drugs for
treating allergic rhinitis. 29.11 Mast cell stabilizers and leukotriene modifiers are
Intranasal corticosteroids are the treatment of choice alternative anti-inflammatory drugs for the pro-
for allergic rhinitis because of their high effective- phylaxis of asthma.
ness and wide margin of safety. When used by this Mast cell stabilizers such as cromolyn are sometimes
route, they do not produce the serious adverse effects used for asthma prophylaxis, although they are not
observed when they are given orally or parenterally. as effective as the corticosteroids. The leukotriene
modifiers offer another option for the prophylaxis of
29.6 Decongestants are used to reduce nasal conges- chronic asthma.
tion caused by allergic rhinitis and the common
cold. 29.12 Chronic obstructive pulmonary disease is a pro-
Oral and intranasal sympathomimetics are effective gressive disorder treated with multiple drugs.
at relieving nasal congestion. The intranasal drugs Chronic bronchitis and emphysema are two dis-
act more rapidly and are more effective. Use of the orders of COPD that often require multiple drug
intranasal preparations, however, is usually limited to therapy. Bronchodilators, expectorants, mucolyt-
three to five days because of the potential for rebound ics, antibiotics, and oxygen may offer symptomatic
congestion. relief.
Review Questions
The following questions are written in NCLEX-PN® style. 3. “The terms are interchangeable.”
Answer these questions to assess your knowledge of the chap- 4. “Both types of drugs work to loosen and remove secretions.”
clear to you. 6. A patient with asthma states that it has become worse
over the past few months. He continues to say that when an
1. The patient is having an acute asthma attack. The nurse acute asthma attack occurs, budesonide (Pulmicort Turbuhaler)
would expect which of the following drugs to be most appropriate? does not stop the episode. The nurse should advise the patient:
1. Pirbuterol (Maxair) 1. To use four inhalations of budesonide instead of two
2. Budesonide (Pulmicort) 2. That budesonide must be taken on a regular schedule to work
3. Fluticasone (Flovent) 3. To request a tablet form of corticosteroid, rather than an
4. Zafirlukast (Accolate) inhaler
4. To always clear his nose gently just prior to using budesonide
2. Salmeterol (Serevent) has been added to your patient’s
treatment regimen for asthma. Which of the following would 7. The patient complains of numbness of the throat and
be of highest priority for patients to know? tongue after taking benzonatate (Tessalon). The nurse instructs
1. Nausea and vomiting may be adverse effects. the patient:
2. It is important to take this medication every day in order to 1. To swallow, not chew, the medication
prevent an asthma attack. 2. To decrease the dosage of medication
3. The drug causes tremors. 3. To stop taking the medication immediately
4. Avoid caffeine-containing foods and beverages. 4. That this is a common adverse effect and that will subside
over time
3. A 24-year-old patient has just started taking Benadryl be-
cause of an allergic reaction. The nurse knows to monitor the 8. The healthcare practitioner ordered albuterol 4 mg, three
patient for: (Select all that apply.) times a day. The available concentration is 2 mg in 5 mL. How
1. Drowsiness many milliliters would be given per dose?
2. Dry mouth 1. 2 mL
3. Tachycardia 2. 5 mL
4. Nausea 3. 10 mL
4. 20 mL
4. The physician has ordered montelukast (Singulair). As the
nurse begins to administer the medication, the patient asks how 9. The nurse informs patients taking intranasal corticosteroids
soon the medication will begin working. The nurse responds by that they may experience which of the following adverse effects?
answering: 1. Rebound congestion
1. “The medication has a rapid onset—within 2 hours.” 2. Intense burning sensation
2. “It will take about a week to become effective.” 3. Drowsiness
3. “This medication is used to treat acute bronchospasms only.” 4. Nervousness
4. “Therapeutic benefits may take several weeks.”
10. While planning an educational session for patients using
5. The patient asks what the difference is between antitus- Afrin, the nurse would include:
sives and mucolytics. The nurse replies: 1. Not to use it for longer than three to five days to prevent
1. “Antitussives loosen bronchial secretions, and mucolytics rebound congestion from occurring
stimulate removal of bronchial secretions.” 2. The importance of monitoring for hypertension
2. “Antitussives suppress cough, whereas mucolytics loosen 3. To notify the physician if nervousness occurs
bronchial secretions.” 4. Not to take it with any other medications
Remember Mr. Thomas, who was fever and shortness of breath when walking. He is 60 years old,
introduced at the beginning of the smokes a pack of cigarettes daily, and has a history of emphysema,
chapter? Now read the remainder of although he doesn’t usually take any medications. For his upper
the case study. Based on the informa- respiratory infection, the physician prescribes hydrocodone, guai-
tion you have learned in this chapter, fenesin, acetaminophen, and an ipratropium (Atrovent) inhaler.
answer the questions that follow.
1. Before leaving the doctor’s office, Mr. Thomas asks the
Mr. Michael Thomas arrives at the office with what appears to nurse which of his prescribed drugs will directly help him with
be an acute upper respiratory tract infection. He tells the nurse, his shortness of breath. The nurse tells him that it is:
“I can’t sleep at night with this cough, and I can hardly work with- 1. Hydrocodone
out getting short of breath.” Upon examination, he has low-grade 2. Acetaminophen
Chapter Review 475
3. Guaifenesin 3. Guaifenesin
4. Ipratropium 4. Ipratropium
2. He also wants to know which of his prescriptions will 4. Mr. Thomas also has emphysema. The physician plans to
help him “get the mucus up that’s stuck in the back of my continue him on guaifenesin and ipratropium. He also wants
throat.” The nurse tells him that _________ will help thin bron- him to take an inhaled corticosteroid. The nurse expects that
chial secretions, allowing them to be removed more easily. Mr. Thomas will be given a prescription for:
1. Hydrocodone 1. Salmeterol
2. Acetaminophen 2. Tiotropium
3. Guaifenesin 3. Budesonide
4. Ipratropium 4. Olopatadine
3. Mr. Thomas calls the office the next day, complaining that
he is unable to drive his car because of excessive drowsiness.
The nurse suspects that __________ is most likely causing this
drowsiness.
1. Hydrocodone
2. Acetaminophen

C
“An ulcer . . . this is the
h last thing I need right
a now. My job is stressful
p enough.”
t Mr. Jeffery Han, stockbroker
e
r
30 Drugs for Gastrointestinal Disorders
Core Concepts
30.1 The digestive system breaks down food, absorbs 30.8 Several miscellaneous drugs are also beneficial in
nutrients, and eliminates wastes. treating peptic ulcer disease.
30.2 Peptic ulcer disease is caused by an erosion of the 30.9 Laxatives are used to promote defecation.
mucosal layer of the stomach or duodenum. 30.10 Opioids are the most effective drugs for controlling
30.3 Peptic ulcer disease is treated by a combination of severe diarrhea.
lifestyle changes and pharmacotherapy. 30.11 Antiemetics are prescribed to treat nausea, vomit-
30.4 Proton-pump inhibitors are effective at reducing ing, and motion sickness.
gastric acid secretion. 30.12 Anorexiants and lipase inhibitors are used for the
30.5 H2-receptor blockers reduce the secretion of gastric short-term management of obesity.
acid. 30.13 Pancreatic enzymes are administered as replacement
30.6 Antacids rapidly neutralize stomach acid and reduce therapy for patients with pancreatitis or malabsorp-
the symptoms of peptic ulcer disease and GERD. tion syndromes.
30.7 Antibiotics are administered to eliminate Helico-
bacter pylori, the cause of many peptic ulcers.
Drug Snapshot
Proton-pump omeprazole (Prilosec) 483 Antidiarrheals diphenoxylate with
inhibitors atropine (Lomotil) 488
H2-receptor blockers ranitidine (Zantac) 483 Antiemetics ondansetron (Zofran,
Zuplenz) 490
Antacids
Antiobesity drugs
Antibiotics for H. pylori
Pancreatic enzyme
Laxatives syllium mucilloid
p replacements
(Metamucil, others) 487
Chapter 30 Drugs for Gastrointestinal Disorders 477
Learning Outcomes
1. Describe the major anatomic 5. Explain the conditions in which the 10. Describe the pharmacotherapy of
structures of the digestive system. drug treatment of constipation is pancreatic insufficiency.
2. Identify common causes, signs, and warranted. 11. Categorize drugs used in the
symptoms of peptic ulcer disease 6. Identify the major classes of laxatives. treatment of digestive system
and gastroesophageal reflux 7. Explain the conditions in which disorders based on their classifications
disease (GERD). the drug treatment of diarrhea is and mechanisms of action.
3. Identify classes of drugs used to warranted. 12. For each of the classes listed in the
treat peptic ulcer disease and GERD. 8. Identify the major classes of antiemetics. Drug Snapshot, identify representative
4. Explain why two or more drugs and explain their mechanisms
9. Describe the types of drugs used of drug action, primary actions, and
antibiotics are used concurrently in in the short-term management of
the treatment of H. pylori. important adverse effects.
obesity and their effectiveness.
Key Terms
alimentary canal (AL-uh-MEN-tare-ee) diarrhea 488 inflammatory bowel disease (IBD) 480
478 dietary fiber 486 pancreatic insufficiency 492
anorexia (AN-oh-REX-ee-uh) 480 digestion (dye-JES-chun) 478 peptic ulcer 479
anorexiant (AN-oh-REX-ee-ant) 491 emesis (EM-eh-sis) 489 peristalsis (pair-ih-STAL-sis) 478
antacid (an-TASS-id) 485 emetics (ee-MET-ikz) 490 proton-pump inhibitors (PPIs) 482
antiemetic (AN-tie-ee-MET-ik) 489 gastroesophageal reflux disease (GERD) triple therapy 481
antiflatulent (an-tie-FLAT-u-lent) 485 (GAS-troh-ee-SOF-ah-JEEL REE-flux) 480 ulcerative colitis (UL-sir-ah-tiv koh-LIE-
cathartic (kah-THAR-tik) 486 H+, K+-ATPase 482 tuss) 480
constipation (kon-stah-PAY-shun) 486 H2-receptor blocker 483 Zollinger–Ellison syndrome (ZOLL-in-jer
Crohn’s disease (KROHNS) 480 Helicobacter pylori (hee-lick-oh-BAK-tur ELL-ih-sun) 483
defecation (def-ah-KAY-shun) 486 py-LOR-eye) 479
V ery little of the food we eat is directly available for use as energy to our body. Food must be broken
down, absorbed, and chemically modified before it is in a form useful to cells. The digestive sys-
tem performs these functions and more. Some disorders of the digestive system are mechanical in
nature, slowing or speeding up the transit of substances through the gastrointestinal tract. Other disorders
are metabolic, affecting the secretion of digestive enzymes and fluids or the absorption of essential nutri-
ents. Many signs and symptoms are nonspecific and may be caused by any number of different disorders.
This chapter examines the drug therapy of common conditions affecting the digestive system.
Fast Facts Gastrointestinal Tract Disorders

■ Sixty to seventy million Americans are affected by a digestive disease.
■ Thirteen percent of all hospitalizations are for digestive disorders.
■ Over a million people experience pancreatitis each year, and about 3,000 die from the disorder.
■ More than 480,000 new cases of peptic ulcer disease are diagnosed each year.
■ Colorectal cancer is the second leading cause of cancer deaths, killing more than 55,000 Americans
annually.
■ Irritable bowel syndrome affects 10% to 20% of adults.
■ Americans spend more than $33 billion annually on weight-reduction products and services.
478 Chapter 30 Drugs for Gastrointestinal Disorders
The digestive system breaks down food, absorbs nutrients,

Core Concept 30.1 and eliminates wastes.
The digestive system consists of two basic anatomic divisions: the alimentary canal and the accessory or-
gans. The alimentary canal, or gastrointestinal (GI) tract, is a long, continuous, hollow tube that extends
from the mouth to the anus. The accessory organs of digestion include the liver, gallbladder, and pancreas.
The structure of the digestive system is shown in Figure 30.1 ■.
Digestion is the process by which the body breaks down ingested food into small molecules that can
be absorbed. The primary functions of the GI tract are to physically transport ingested food and to provide
the necessary enzymes and surface area for chemical digestion and absorption. The inner surface is lined
with a mucosa layer that secretes acids, bases, mucus, and enzymes important to digestion. The mucosa of
the small intestine is lined with tiny projections called villi and microvilli that provide a huge surface area
for the absorption of food and medications.
Substances are propelled along the GI tract by the contractions of several layers of smooth muscle, a pro-
peri 5 around cess known as peristalsis. The speed of transit is critical to the absorption of nutrients and water and for the
stalsis 5 contraction removal of wastes. If peristalsis is too fast, substances will not have sufficient contact with the mucosa to be
absorbed. In addition, the large intestine will not have enough time to absorb water, and diarrhea may result.
Abnormally slow transit times may result in constipation or even obstructions in the small or large intestine.
To chemically break down ingested food, a large number of enzymes and other substances are re-
quired. Digestive enzymes are secreted by the salivary glands, stomach, small intestine, and pancreas. The
liver makes bile, which is stored in the gallbladder until needed for lipid digestion. Because these digestive
substances are not common targets for drug therapy, their discussion in this chapter is limited, and the stu-
dent should refer to anatomy and physiology texts for additional information.
Figure 30.1
The digestive system.
Parotid gland
Tongue Parotid duct
Salivary Sublingual Pharynx
glands Submandibular
Esophagus
Fundus of
stomach
Spleen
Left lobe
of liver
Right lobe of liver
Body of stomach
Gallbladder
Left colic flexure
Pylorus Pancreas
Right colic flexure Transverse colon
Ascending colon Descending colon
Small intestines
Cecum (duodenum, jejunum,
and ileum)
Appendix
Rectum
Peptic Ulcer Disease
An ulcer is a sore or erosion of the mucosa of the GI tract. Although ulcers may occur in any portion of the
GI tract, the duodenum is the most common site.
Peptic ulcer disease is caused by an erosion of the mucosal layer of the

stomach or duodenum. Core Concept 30.2
The term peptic ulcer refers to a lesion located in either the stomach (gastric) or small intestine (duode- pept = to digest
nal). The disorder is very common, affecting about 10% of the population at some point during their life ic = pertaining to
span. Peptic ulcer disease (PUD) is associated with lifestyle factors such as cigarette smoking, stress, alco-
hol consumption, caffeine, and the use of drugs such as corticosteroids and nonsteroidal anti-inflammatory
drugs (NSAIDs).
One to three liters of hydrochloric acid are secreted each day by cells in the stomach mucosa. Al-
though this strong acid aids in the chemical breakdown of food and helps to protect the body from ingested
microbes, it may be quite damaging to stomach cells. A number of natural defenses protect the stomach lin-
ing against this extremely acidic fluid. Certain cells lining the surface of the stomach secrete a thick mucus
layer and bicarbonate, a basic ion that neutralizes acid and provides a protective function. On reaching the
duodenum, the stomach contents are further neutralized by bicarbonate from pancreatic and biliary secretions.
These natural defenses are depicted in Figure 30.2 ■.
The primary cause of peptic ulcers is infection by the bacterium Helicobacter pylori. In noninfected
patients, the most common cause is therapy with NSAIDs. Secondary factors that contribute to ulcer and
the subsequent inflammation include secretion of excess stomach acid and hyposecretion of adequate mu-
cous protection. Figure 30.3 ■ illustrates the mechanism of peptic ulcer formation.
The characteristic symptom of duodenal ulcer is a gnawing or burning upper abdominal pain that oc-
curs one to three hours after a meal. The pain is worse between meals when the stomach is empty and it
often disappears following ingestion of food. Nighttime pain, nausea, and vomiting are uncommon. If the
erosion progresses deeper into the mucosa, bleeding will occur, and this may be evident as bright red blood
in vomit or black, tarry stools. Many duodenal ulcers heal spontaneously, although they often recur after
months of remission.
Figure 30.2
Gastric juice pH ~ 2 Stomach lumen
Bicarbonate barrier
HCO3- neutralizes acid. HCO3-
Mucus layer
pH ~ 7 at cell surface
Mucus
droplets
Gastric
mucosa
Gastric
mucosa
cell
Capillary
Natural defenses against stomach acid.

Figure 30.3
Mechanism of peptic
ulcer formation.
Gastric juices
(acidic)
Gastric juices are

released into the
stomach
H. pylori infection
causes inflammation
in mucosa
Acid secretions further

Duodenal break down the lining
ulcer of the stomach,
forming an ulcer
Gastric
ulcer
Gastric ulcers are less common than the duodenal type and have different symptoms. Although re-
an = not or without lieved by food, pain may continue even after a meal. Loss of appetite (known as anorexia), weight loss,
orexia = appetite and vomiting are more common. Remissions may be infrequent or absent. Medical follow-up of gastric
ulcers sometimes proceeds for many years because a small percentage of the erosions become cancerous.
The most severe ulcers may penetrate through the wall of the stomach and cause death. Whereas duodenal
ulcers occur most frequently in the 30- to 50-year-old age group, gastric ulcers are more common in those
older than age 60.
Gastroesophageal reflux disease (GERD) is a common condition in which the acidic contents
of the stomach move upward into the esophagus. This causes an intense burning known as heartburn
and may lead to ulcers in the esophagus. The cause of GERD is usually a loosening of the sphincter
located between the esophagus and the stomach. GERD is strongly associated with obesity, and losing
weight may eliminate the symptoms. Many of the drugs prescribed for peptic ulcers are also used to
treat GERD.
Ulceration in the lower small intestine is known as Crohn’s disease, and erosions in the large intes-
tine are called ulcerative colitis. These diseases are called inflammatory bowel disease (IBD). Patients
with these disorders experience abdominal cramping, diarrhea, and weight loss. Pharmacotherapy of IBD
is usually with anti-inflammatory medications such as sulfasalazine (Azulfidine) or mesalamine (Asacol,
Lialda, others). Severe cases may require immunosuppressant drugs such as corticosteroids, or immuno-
modulators such as infliximab (Remicade). A newer approach is to administer budesonide (Entocort EC,
Uceris), a corticosteroid that is taken orally but is not absorbed. Budesonide produces its anti-inflammatory
actions directly on the intestine, with few or no systemic side effects.
Concept Review 30.1

■ What are the similarities and differences between duodenal ulcers and gastric ulcers?
Peptic ulcer disease is treated by a combination of lifestyle

changes and pharmacotherapy. Core Concept 30.3
Before starting drug therapy, patients are usually advised to change lifestyle factors that contribute to PUD.
For example, eliminating tobacco, alcohol, and caffeine consumption, and reducing stress often allow heal-
ing of the ulcer, causing it to go into remission.
For patients requiring drug therapy, a wide variety of both prescription and over-the-counter (OTC)
medications are available. These drugs fall into four primary classes, plus one miscellaneous group:
■ Proton-pump inhibitors
■ H2-receptor blockers
■ Antacids
■ Antibiotics
■ Miscellaneous drugs
The treatment goals for pharmacotherapy are to provide immediate relief from symptoms, promote
healing of the ulcer, and prevent recurrence of the disease. The choice of medication depends on the source
of the disease (infectious versus inflammatory), the severity of symptoms, and the convenience of OTC
versus prescription drugs. The most common therapy for the management of PUD is a combination of a
proton-pump inhibitor plus two antibiotics. This approach, referred to as triple therapy, eliminates the
cause of most peptic ulcers (H. pylori) while also reducing acid secretion. The mechanisms of action of the
four major classes of drugs used to treat PUD are depicted in Figure 30.4 ■.
Figure 30.4
Proton pump H2-receptor

Mechanisms of action
inhibitors blockers of antiulcer drugs:
(a) Proton-pump inhibi-
tors act by blocking acid
secretion by the HCl
pump; (b) H2-receptor
blockers act by decreas-
ing acid secretion;
(c) antibiotics act by
removing H. pylori;
Proton pump H2-receptor (d) antacids act by
neutralizing acids.
(a) Proton pump inhibitors bind to (b) H -receptor antagonists occupy
2
the enzyme H1, K1-ATPase and the histamine receptors and
prevent acid from being secreted. prevent acid secretion.
Acid secretion
Parietal cell with K1 Parietal cell with

proton pump H2-receptor
Ulcer with H. pylori
Antacid
Antibiotic 1 HCL water 1 salt
(c) Antibiotics eradicate H. pylori, the (d) Alkaline antacids chemically combine
primary cause of peptic ulcers. with acids to raise stomach pH.
Core Concept 30.4 Proton-pump inhibitors are effective at reducing gastric acid secretion.
Proton-pump inhibitors act by blocking the enzyme responsible for secreting hydrochloric acid in the stom-
ach. The proton-pump inhibitors are listed in Table 30.1 ◆.
Proton-pump inhibitors (PPIs) are the most effective medications available for reducing acid secre-
tion and thus are preferred drugs for the treatment of PUD and GERD. These drugs reduce acid secretion
by binding irreversibly to the enzyme H+, K+-ATPase. In the mucosal cells of the stomach, this enzyme
acts as a pump to release acid (also called H+, or protons) onto the surface of the GI mucosa. PPIs reduce
acid secretion to a greater extent than do the H2-receptor blockers and have a longer duration of action.
In addition to PUD, the PPIs are also indicated for GERD and for acid hypersecretory conditions such
as Zollinger–Ellison syndrome. They may also be prescribed to prevent PUD in patients taking high doses
of NSAIDs. As a component of triple therapy, PPIs are usually continued for one to two weeks. In refrac-
tory cases, therapy may continue for four to eight weeks. The beneficial effects of PPIs last three to five
days after therapy is stopped.
Adverse effects from short-term therapy with PPIs are uncommon. Headache, abdominal pain, diar-
rhea, nausea, and vomiting are the most frequently reported adverse effects. If taken for prolonged periods,
PPIs may interfere with calcium absorption and cause osteoporosis and fractures.
Table 30.1 Drugs for Peptic Ulcer Disease

H2-Receptor Blockers
cimetidine (Tagamet) PO; 300 mg every 6 hours or 800 mg at Also for GERD and hypersecretory disorders; IM and IV forms
bedtime or 400 mg bid with food available
famotidine (Pepcid) PO; 20 mg bid or 40 mg at bedtime Also for GERD and hypersecretory disorders; IV form available
nizatidine (Axid) PO; 150–300 mg at bedtime Newest drug in this class; rapid onset with few adverse effects
ranitidine (Zantac) PO; 100–150 mg bid or 300 mg at Also for GERD and hypersecretory disorders; IM and IV forms
bedtime available
Proton-Pump Inhibitors
esomeprazole (Nexium) PO; 20–40 mg/day Also for GERD and hypersecretory disorders; IV form available
lansoprazole (Prevacid) PO; 15–60 mg/day Also for GERD and hypersecretory disorders; Prevpac combines
lansoprazole, amoxicillin, and clarithromycin
omeprazole (Prilosec) PO; 20–60 mg once or twice daily Often used in combination with antibiotics for Helicobacter
infections; also for GERD
pantoprazole (Protonix) PO; 40 mg/day Primarily for GERD and hypersecretory disorders; IV form available
rabeprazole (AcipHex) PO; 20 mg/day Also for GERD and hypersecretory disorders
Antacids
aluminum hydroxide PO; 600 mg tid–qid Not absorbed; may cause constipation
(AlternaGEL, others)
calcium carbonate (Titralac, PO; 1–2 g bid–tid Also for calcium replacement therapy; may cause constipation
Tums)
calcium carbonate with PO; two to four capsules or tablets prn Common OTC therapy
magnesium hydroxide (max: 12 tablets/day)
(Mylanta Gel-caps, Rolaids)
magaldrate (Riopan) PO; 540–1080 mg (5–10 mL suspension or Lower incidence of bowel adverse effects than magnesium or
one or two tablets) daily (max: 20 tablets aluminum antacids
or 100 mL/day)
magnesium hydroxide (Milk PO; 5–15 mL or two to four tablets as Also used as a laxative; may cause diarrhea
of Magnesia) needed up to four times daily
magnesium hydroxide and PO; 10–20 mL prn (max: 120 mL/day) or two Common OTC therapy
aluminum hydroxide with to four tablets prn (max: 24 tablets/day)
simethicone (Mylanta,
Maalox Plus)
sodium bicarbonate (NaHCO3) PO; 325 mg–2 g one to four times per day IV form available to treat metabolic acidosis and cardiac arrest
(see page 261 for the Drug
Prototype box)
Drug Prototype: Omeprazole (Prilosec)

Therapeutic Class: Antiulcer drug Pharmacologic Class: Proton-pump inhibitor
Actions and Uses: Omeprazole was the first proton-pump inhib- Adverse Effects and Interactions: Adverse effects are generally
itor approved for PUD; both prescription and OTC forms are minor and include headache, nausea, diarrhea, and abdominal
available. Although this drug may take 2 hours to reach thera- pain. Long-term therapy can interfere with calcium absorption
peutic levels, its effects last up to 72 hours. It is used for the and result in fractures due to weakened bones.
short-term therapy of peptic ulcers and GERD. Most patients are Omeprazole interacts with several drugs. For example, us-
symptom-free after two weeks of therapy. It is used for longer ing it together with diazepam, phenytoin, and central nervous
periods in patients who have chronic hypersecretion of gastric system (CNS) depressants will cause increased blood levels of
acid, a condition known as Zollinger–Ellison syndrome. Omepra- these drugs. Concurrent use with warfarin may increase the risk
zole is available in oral form only. Zegerid is a combination drug of bleeding.
containing omeprazole and the antacid sodium bicarbonate.
H2-receptor blockers reduce the secretion of gastric acid. Core Concept 30.5
The discovery of the H2-receptor blockers in the 1970s marked a major breakthrough in the treatment
of PUD. Since then they have become available OTC and are widely used in the treatment of PUD and
GERD. Doses of the H2-receptor blockers are given in Table 30.1.
Histamine has two types of receptors: H1 and H2. Activation of H1-receptors produces the classic
symptoms of allergy, whereas the H2-receptors are responsible for increasing acid secretion in the stomach.
Cimetidine (Tagamet), the first H2-receptor blocker, and other drugs in this class are quite effective at
suppressing the volume and acidity of stomach acid. These drugs are also used to treat the symptoms of
GERD.
Adverse effects of the H2-receptor blockers are minor and rarely cause discontinuation of therapy.
Patients taking high doses, or those with renal or hepatic disease, may experience confusion, restlessness,
hallucinations, or depression. Patients should be advised not to take antacids at the same time as H2-receptor
blockers because the absorption of these drugs will be lessened.
Concept Review 30.2

■ Explain the following statement: All H2-receptor blockers are antihistamines, but not all
antihistamines are H2-receptor blockers.
Drug Prototype: Ranitidine (Zantac)

Therapeutic Class: Antiulcer drug Pharmacologic Class: H2-receptor blocker
Actions and Uses: Ranitidine has become one of the most Adverse Effects and Interactions: Adverse effects are uncom-
frequently used drugs in the treatment of PUD and GERD. It mon and mild. Ranitidine does not cross the blood–brain barrier
has a higher potency than cimetidine, which allows it to be to any appreciable extent, so the confusion and CNS depres-
administered once daily, usually at bedtime. Adequate healing sion observed with cimetidine does not occur with ranitidine.
of the ulcer takes four to eight weeks. Patients with persistent Ranitidine has fewer drug–drug interactions than cimetidine.
disease may continue on drug maintenance for long periods to Although rare, severe reductions in the number of red and
prevent recurrence. Gastric ulcers heal more slowly than duo- white blood cells and platelets are possible.
denal ulcers and require longer drug therapy. IV and IM forms Ranitidine exhibits fewer drug–drug interactions than
are available for the treatment of acute stress-induced bleed- cimetidine. Ranitidine may reduce the absorption of cefpo-
ing ulcers. Ranitidine is available in a dissolving tablet form doxime, ketoconazole, and itraconazole. Antacids should not
(EFFERdose) for treating GERD in children and infants older be given within one hour of H2-receptor antagonists because
than one month of age. effectiveness may be decreased due to reduced absorption.
NURSING PROCESS FOCUS Patients Receiving Drug Therapy for Peptic Ulcer Disease

■ Obtain a complete health history, including GI and liver therapy
conditions, nutrition, allergies, drug history, and possible drug ■ Acute Pain related to tissue damage of the gastric mucosa or gastric
interactions. inflammation and/or to ineffective drug therapy
■ Evaluate laboratory blood findings: CBC, electrolytes, renal, and liver ■ Imbalanced Nutrition: Less than Body Requirements related to adverse
function studies. effects of drug
vital signs, height and weight, pain, signs of bleeding, and LOC.
The patient will:

■ Experience therapeutic effects (diminished or absent gastric pain and bloating).
Implementation
■ Administer medications correctly and evaluate the patient’s knowl- Inform the patient to:
edge of proper administration. (Following guidelines with regard to ■ Take PPIs before meals, preferably before breakfast.
meals and other medications will result in improved outcomes.) ■ Shake liquid antacids well before pouring.
■ Take H2-receptor antagonists and other medications at least one hour
before antacids. Patients taking antacids should avoid taking other
medications for at least two hours.
■ Monitor level of abdominal pain or discomfort (to assess effectiveness Advise the patient:
of drug therapy; it may take days to weeks before pain is controlled). ■ That pain relief may not occur for several days after beginning
therapy
■ To immediately report episodes of severe or increasing pain to the
■ Monitor patient use of alcohol. (Alcohol can increase gastric irritation.) ■ Instruct the patient to avoid alcohol use.
■ Discuss and monitor for possible drug interactions, including OTC Instruct the patient to:
drugs like antacids. (Antacids can decrease the effectiveness of other ■ Consult with the healthcare provider before taking other medications
drugs taken concurrently.) or herbal products.
■ Avoid drugs that may cause stomach irritation such as aspirin or
NSAIDs.
■ Institute effective safety measures regarding falls. (Drowsiness may ■ Instruct the patient to avoid driving or performing hazardous
occur when starting H2-receptor blockers.) activities until drug effects are known.
■ Explain need for lifestyle changes. Provide consultation for dietitian Encourage the patient to:
and information on smoking cessation programs. (Smoking and ■ Adopt a healthy lifestyle: eliminate alcohol and smoking, increase
certain foods increase gastric acid secretion.) exercise, and choose low-fat foods.
■ Keep a food diary in order to identify foods that trigger discomfort.
Avoid foods that cause stomach discomfort.
■ Observe the patient for signs of GI bleeding. (Drugs used to treat PUD ■ Instruct the patient to immediately report to the healthcare provider
decrease gastric acidity making the gastric environment less favorable any episodes of blood in the stool or vomitus, increase in abdominal
for ulcer development, but they do not heal existing ulcers. Blood discomfort, or diarrhea.
in the stool or emesis and abdominal pain may indicate a worsening
condition.)
■ Monitor CBC, electrolytes, liver function, and serum gastrin during ■ Inform the patient of the importance of keeping all scheduled doctor
long-term use of medications for PUD. (Abnormal liver function tests and laboratory visits.
may indicate adverse effect of drug therapy. Long-term therapy with
PPIs can lead to decreased calcium absorption. H2 receptors can af-
fect CBC values. Antacids may affect electrolytes such as sodium and
phosphorus.)
■ Monitor for pregnancy or breastfeeding. (Women who are breastfeed- ■ Instruct the patient to report possible pregnancy and plans for breast-
ing should not take these medications.) feeding to the healthcare provider.

Antacids rapidly neutralize stomach acid and reduce the symptoms

of peptic ulcer disease and GERD. Core Concept 30.6
Antacids are alkaline substances that have been used to neutralize stomach acid for hundreds of years.
Doses of the antacids are listed in Table 30.1.
Prior to the development of H2-receptor blockers and PPIs, antacids were the mainstay of peptic ulcer
and GERD pharmacotherapy. Indeed, many patients still use these inexpensive and readily available OTC
medications. Antacids, however, are no longer recommended as the sole medication for PUD because they
do not promote healing of the ulcer.
Antacids are alkaline, inorganic compounds of aluminum, magnesium, or calcium. Combinations of
aluminum hydroxide and magnesium hydroxide are the most common type. Both aluminum hydroxide and
magnesium hydroxide are bases that are capable of rapidly neutralizing stomach acid. A few products com-
bine antacids and H2-receptor blockers into a single tablet; for example, Pepcid Complete contains calcium
carbonate, magnesium hydroxide, and famotidine.
Simethicone is sometimes added to antacid preparations because it reduces gas bubbles that cause
bloating and discomfort. For example, Mylanta contains simethicone, aluminum hydroxide, and magne-
sium hydroxide. Simethicone is classified as an antiflatulent because it reduces gas. It also is available by anti 5 against
itself in OTC products such as Gas-X and Mylanta. flatus 5 gas in the GI tract
Self-medication with antacids is safe when taken in doses directed on the labels. Although they act
within 10 to 15 minutes, their duration of action is only 2 hours. Therefore, they must be taken often dur-
ing the day. Products containing sodium, calcium, or magnesium can result in absorption of these minerals
to the general circulation. When given in high doses, aluminum compounds may interfere with phosphate
metabolism and cause constipation. Magnesium compounds may cause diarrhea. Patients should follow the
label instructions very carefully and not take more than the recommended dosages.
Antibiotics are administered to eliminate Helicobacter pylori,

the cause of many peptic ulcers. Core Concept 30.7
The bacterium H. pylori is associated with 80% of all duodenal ulcers and 70% of all gastric ulcers. This
organism has adapted well as a human pathogen by devising ways to neutralize the high acidity surround-
ing it and by making substances that allow it to stick tightly to the GI mucosa. H. pylori causes inflamma-
tion of the stomach mucosa by both increasing acid secretion and reducing bicarbonate secretion.
Because H. pylori infections can remain active for life if not treated, treatment for this infection is a
primary goal of PUD management. Elimination of this organism causes ulcers to heal more rapidly and to
remain in remission longer. The following antibiotics are commonly used for this purpose:
■ amoxicillin (Amoxil)
■ clarithromycin (Biaxin)
■ metronidazole (Flagyl)
■ tetracycline (Sumycin)
Two or more antibiotics are given concurrently (usually with a PPI) to increase the effectiveness of
therapy and to lower the potential for bacterial resistance. Clarithromycin and amoxicillin are the preferred
drugs. Antibiotic therapy generally continues for 7 to 14 days. Bismuth compounds (Pepto-Bismol, Tritec)
are sometimes added to the antibiotic regimen. Although not antibiotics, bismuth compounds do inhibit
bacterial growth and prevent H. pylori from adhering to the surface of the gastric mucosa. Dosages and ad-
ditional information for these anti-infectives can be found in Chapter 26.
Several miscellaneous drugs are also beneficial in treating

peptic ulcer disease. Core Concept 30.8
Three additional drugs are beneficial in treating PUD. Sucralfate (Carafate) consists of sucrose (a sugar)
plus aluminum hydroxide (an antacid). The drug produces a thick, gel-like substance that coats the ulcer,
protecting it against further erosion and promoting healing. Very little of the drug is absorbed from the GI
tract. Other than constipation, adverse effects are minimal. A major disadvantage of sucralfate is that it
must be taken four times a day.
Misoprostol (Cytotec) is a prostaglandin-like substance that inhibits gastric acid secretion and stimu-
lates the production of protective mucus. Its primary use is for the prevention of peptic ulcers in patients
taking high doses of NSAIDs. Diarrhea and abdominal cramping are relatively common. Classified as a
pregnancy category X drug, misoprostol is contraindicated during pregnancy. In fact, misoprostol is some-
times used to terminate pregnancies, as discussed in Chapter 34.
Metoclopramide (Reglan) is occasionally used for the short-term therapy of PUD in patients who fail
to respond to first-line drugs. It is also approved to treat nausea and vomiting associated with surgery or
cancer chemotherapy. Metoclopramide is available for the oral, IM, or IV routes. CNS adverse effects such
as drowsiness, fatigue, confusion, and insomnia may occur in a significant number of patients.
Concept Review 30.3

■ Is peptic ulcer disease considered an infection, an inflammation, or both?
Constipation
Life Span Fact A major function of the large intestine is to reabsorb water from stools. If the waste material remains in the
colon for an extended period, however, too much water will be reabsorbed, leading to small, hard stools.
Constipation occurs more fre- The normal frequency of bowel movements varies widely among individuals, from two to three per day to
quently in older adults because
as few as one per week. Difficult or infrequent bowel movements, known as constipation, is a common
fecal transit time through the
colon slows with aging; this
problem with a large number of different causes that include lack of exercise, insufficient food or fluid
population also exercises less intake, and lack of sufficient insoluble dietary fiber. Certain medications such as opioids, antihistamines,
and has more chronic disorders certain antacids, and iron supplements promote constipation. Dietary adjustments and increased physical
that cause constipation. activity should be considered before drugs are used to treat constipation.
Core Concept 30.9 Laxatives are used to promote defecation.
Occasional constipation is common and does not require drug therapy. However, chronically infrequent
and painful bowel movements accompanied by severe straining may justify pharmacotherapy. Also, phar-
macotherapy may be indicated following surgical procedures to prevent the patient from straining or bear-
ing down when attempting a bowel movement. Drugs are given to cleanse the bowel prior to surgery or for
diagnostic procedures of the colon, such as a colonoscopy or barium enema.
laxat 5 to loosen Laxatives are drugs that promote emptying of the bowel, or defecation. Cathartic is a related term
ive 5 nature of, quality of that implies a stronger and more complete bowel emptying. When taken in prescribed amounts, laxatives
have few adverse effects. Selected medications used to treat constipation are listed in Table 30.2 ◆. These
drugs are often classified into four primary groups and a miscellaneous category.
Life Span Fact ■ Bulk-forming absorb water, thus adding size to the fecal mass. These are preferred drugs for the
prevention and treatment of chronic constipation. They have a slow onset of action and are not
Because of their reduced food used when a rapid and complete bowel evacuation is necessary.
intake and diminished physi-
cal activity, elderly patients ■ Stimulants promote peristalsis by irritating the bowel. Although drugs in this class are effective
are most prone to laxative and act rapidly, they are more likely to cause diarrhea and cramping than the other types of laxa-
misuse. Healthcare providers tives. They should only be used occasionally because they may cause laxative dependence and
should advise these patients
depletion of fluid and electrolytes.
to increase their fluid intake,
fiber consumption, and level ■ Saline/osmotic cause water to be retained in the fecal mass, causing a more liquid stool. These
of exercise. drugs produce a bowel movement in one to six hours, and they should not be used on a regular
basis because of the possibility of fluid and electrolyte depletion.
■ Stool softeners/surfactants cause more water and fat to be absorbed into the stools. They
are most often used to prevent constipation, especially in patients who have undergone recent
surgery.
■ Miscellaneous act by mechanisms other than those just described.
Although laxatives are safe drugs, there are several conditions and potential adverse effects that must
be monitored carefully. Laxatives are contraindicated in any patient with a suspected bowel obstruction
because their use could cause the bowel to perforate. If acute abdominal cramping or diarrhea occurs, laxa-
tives should be discontinued. Patients should be advised not to overuse laxatives because the smooth mus-
cle in the colon can lose its tone and cause chronic constipation.
Concept Review 30.4

■ Bismuth compounds are used to treat several digestive disorders. Describe these drugs
and their uses.
Table 30.2 Laxatives

bisacodyl (Correctol, Dulcolax, others) PO; 10–15 mg daily prn Stimulant type; also available as a rectal suppository
calcium polycarbophil (Equalactin, PO; 1 g/day Bulk-forming type
FiberCon, others)
castor oil (Emulsoil, Neoloid) PO; 15–60 mL daily Stimulant type; the only laxative to act on the small intestine
docusate (Colace, Surfak) PO; 50–500 mg daily Stool softener/surfactant type
lubiprostone (Amitiza) PO; 24 mcg bid Stool softener type; used for constipation-dominant irritable
bowel syndrome
magnesium hydroxide (Milk of Magnesia) PO; 20–60 mL daily Saline type
methylcellulose (Citrucel) PO; 5–20 mL tid in 8–10 oz water Bulk-forming type
mineral oil PO; 45 mL bid Miscellaneous type; lubricates the stools
psyllium mucilloid (Metamucil, others) PO; 1–2 tsp in 8 oz water daily Bulk-forming type; also used for diarrhea and as an aid in
lowering blood cholesterol
senna (Ex Lax, Senokot, others) PO; 8.6–17.2 mg/day Stimulant type; considered an herbal product
Drug Prototype: Psyllium Mucilloid (Metamucil, Others)

Therapeutic Class: Drug for constipation Pharmacologic Class: Bulk-type laxative
Actions and Uses: Like other bulk-forming laxatives, psyllium Adverse Effects and Interactions: Psyllium is a safe laxative
is an insoluble fiber that is indigestible and not absorbed from and rarely produces adverse effects. It causes less cramping
the GI tract. When taken with plenty of water, psyllium swells than the stimulant-type laxatives and produces a more natural
and increases the size of the fecal mass by drawing water into bowel movement. If taken with insufficient water, it may cause
the intestine. The larger the size of the fecal mass, the more the obstructions in the esophagus or intestine.
defecation reflex will be stimulated to promote bowel move- Psyllium may decrease absorption and the clinical
ments. Several doses of psyllium may be needed to produce a effects of antibiotics, warfarin, digoxin, nitrofurantoin,
therapeutic effect. More frequent doses of psyllium (7 g/day) and salicylates.
may cause a small reduction in blood cholesterol level.
Nursing Process Focus Patients Receiving Laxative Therapy

Prior to administration: ■ Diarrhea related to adverse effect of drug therapy

■ Obtain a complete health history, including GI and liver conditions, ■ Deficient Knowledge related to a lack of information about drug
nutrition, allergies, drug history, and possible drug interactions. therapy
■ Evaluate laboratory blood findings: CBC, electrolytes, and liver ■ Acute Pain related to intestinal irritation or adverse effect of drug
function studies. therapy
signs, height, weight, bowel elimination patterns, and bowel sounds.
The patient will:

■ Experience therapeutic effects (relief from constipation).
Implementation
■ Administer medications correctly and evaluate the patient’s Instruct the patient to:
knowledge of proper administration. (Following guidelines will ■ Take medication as prescribed.
result in improved outcomes.) ■ Expect results from medication within two to three days of the initial dose.
■ Increase fluids and dietary fiber, such as whole grains, fibrous fruits, and
vegetables.
continued . . .
■ Determine the patient’s ability to swallow. (Bulk laxatives can swell ■ Instruct the patient to discontinue the medication and notify the
and cause obstruction in the esophagus.) healthcare provider if having difficulty swallowing.
■ Monitor the patient’s fluid intake. (Adequate fluid intake helps to Instruct the patient to:
prevent constipation or intestinal obstruction.) ■ Drink six 8-oz glasses of fluid per day.
■ Mix medication in a full 8 oz of liquid.
■ Drink at least 8 oz of additional fluid.
■ Monitor frequency, volume, and consistency of bowel movements. Advise the patient to:
(Changes in bowel habits can indicate a serious condition.) ■ Discontinue laxative use if diarrhea occurs.
■ Notify the healthcare provider if constipation continues.
Diarrhea
Occasionally, the colon does not reabsorb enough water from the fecal mass, and stools become watery.
dia 5 through/between Diarrhea is an increase in the frequency and fluidity of bowel movements. Like constipation, occasional
rrhea 5 flow/discharge diarrhea is a common, self-limiting disorder that does not require drug therapy. When prolonged or severe,
especially in children, diarrhea can result in significant loss of body fluids, and medications may be indi-
cated. Prolonged diarrhea may lead to acid–base or electrolyte disorders, as discussed in Chapter 17.
Diarrhea is not a disease; it is a symptom of an underlying disorder. Diarrhea may be caused by certain
medications, infections of the bowel, inflammatory bowel disease such as Crohn’s disease or u lcerative
colitis, and substances such as lactate. Superinfections occurring during anti-infective therapy are common
causes of diarrhea because they disrupt the normal microbial flora in the colon.
Core Concept 30.10 Opioids are the most effective drugs for controlling severe diarrhea.
Drug therapy of diarrhea depends on the severity of the condition and whether or not a specific cause can
be identified. If the cause is an infectious disease, then an antibiotic or antiparasitic drug such as metroni-
dazole (Flagyl) is indicated. If the cause is inflammatory, anti-inflammatory drugs are needed. If the cause
appears to be drug induced, the medication should be discontinued and another substituted.
Antidiarrheals act by relaxing the colon’s smooth muscle, thus relieving cramping. Slower transit
through the large intestine allows for better-formed stools. The selection of a particular drug depends on
the severity of the diarrhea. Some antidiarrheals are listed in Table 30.3 ◆.
Drug Prototype: Diphenoxylate with Atropine (Lomotil)

Therapeutic Class: Antidiarrheal Pharmacologic Class: Opioid
Actions and Uses: The primary antidiarrheal ingredient in low potential for abuse. The drug is well tolerated at normal
Lomotil is diphenoxylate. Like other opioids, diphenoxylate doses. Some patients experience dizziness or drowsiness, and
slows peristalsis, resulting in additional water being reabsorbed care should be taken not to operate machinery until the effects
from the colon and formation of more solid stools. It is effective of the drug are known. At higher doses, the anticholinergic
for moderate to severe diarrhea. The atropine in Lomotil is not effects of atropine may be observed, which include drowsiness,
added for its anticholinergic effect; it is added to discourage dry mouth, and tachycardia.
patients from taking too much of the drug. Diphenoxylate is Other CNS depressants, including alcohol, will cause addi-
discontinued as soon as the diarrhea symptoms resolve. tive CNS depressant/sedative effects. Monoamine oxidase
(MAO) inhibitors may cause hypertensive crisis. Alcohol and
Adverse Effects and Interactions: Unlike most opioids, other CNS depressants may enhance CNS effects.
diphenoxylate has no analgesic properties and has an extremely
Table 30.3 Antidiarrheals

bismuth salts (Pepto-Bismol) PO; two tablets or 30 mL prn OTC adsorbent
camphorated opium tincture PO; 5–10 mL one to four times daily Contains morphine: Schedule III drug; also used to
(Paregoric) prevent severe opioid withdrawal symptoms in neonates
difenoxin with atropine (Motofen) PO; one to two mg after each diarrhea Opioid; Schedule IV drug
episode (max: 8 mg/day)
diphenoxylate with PO; one or two tablets or 5–10 mL tid–qid Opioid; Schedule V drug
atropine (Lomotil)
loperamide (Imodium) PO; 4 mg as a single dose, then 2 mg after Opioid with no physical dependence; abuse is so low,
each diarrhea episode (max: 16 mg/day) it is not classified as a controlled substance
octreotide (Sandostatin) Subcutaneous/IV; 100–600 mcg/day in For severe diarrhea associated with cancer
two to four divided doses
Acute or long-lasting diarrhea can lead to serious and even life-threatening conditions. The opioids
are drugs of choice for this type of diarrhea because of their rapid onset and effectiveness. At doses used
for diarrhea, opioids do not produce dependence or serious adverse effects. The most common opioid an-
tidiarrheal is diphenoxylate (Lomotil), which is a Schedule V controlled substance. Loperamide (Imodium)
is an opioid that carries no risk for dependence and is available OTC.
Nonopioid antidiarrheals include bismuth subsalicylate (Pepto-Bismol), which acts by binding and
absorbing toxins. The psyllium and pectin preparations slow diarrhea by absorbing large amounts of fluid
to form bulkier stools. Intestinal flora modifiers are supplements that help to correct the altered GI flora; a
good source of healthy bacteria is yogurt with active cultures.
Nausea and Vomiting
Nausea is an uncomfortable, subjective sensation that is sometimes accompanied by dizziness and an urge
to vomit. Vomiting, or emesis, is a reflex primarily controlled by the vomiting center, which is located
in the medulla oblongata of the brain. Nausea and vomiting are commonly associated with a wide variety
of conditions such as food poisoning, early pregnancy, extreme pain, migraines, trauma to the head or
abdominal organs, inner ear disorders, and emotional disturbances. Some drugs cause nausea or vomiting
as an adverse effect. The most extreme example of this is the antineoplastic drugs, almost all of which
cause some degree of nausea or vomiting. In treating nausea or vomiting, an important therapeutic goal is
to remove the cause whenever feasible.
Antiemetics are prescribed to treat nausea, vomiting,

and motion sickness. Core Concept 30.11
Drugs from several pharmacologic classes are prescribed to prevent or treat nausea and vomiting. As
shown in Table 30.4 ◆, Antiemetic drugs belong to a number of different classes, including the following:
■ Antipsychotics
■ Antihistamines
■ Serotonin-receptor blockers
■ Corticosteroids (glucocorticoids)
■ Benzodiazepines
Therapy with antineoplastic drugs is one of the most common reasons why antiemetic medications are pre- anti 5 against
scribed. When cancer chemotherapy is initiated, it is common for a patient to receive three or more antiemetics. emetic 5 vomit
To avoid losing antiemetic medication due to vomiting, many of these drugs are available through the
IM, IV, transdermal, and suppository routes, as well as orally disintegrating tablets and soluble films. The
most effective antiemetics for serious nausea and vomiting are serotonin-receptor blockers such as ondan-
setron (Zofran, Zuplenz).
Motion sickness is a disorder that affects a portion of the inner ear known as the vestibular apparatus
that is associated with significant nausea. The most common drug used for motion sickness is scopolamine,
which is administered as a transdermal patch placed behind the ear. Antihistamines such as dimenhydrinate
Table 30.4 Selected Antiemetics

cyclizine (Marezine) PO; 50 mg every 4 hours–qid Antihistamine; for prevention of motion sickness and
postoperative nausea and vomiting; IM form available
dexamethasone (Decadron) IV; 10–20 mg before chemotherapy Corticosteroid; IM, inhalation, and IV forms available; also for
inflammatory disorders, severe allergies, acute asthma, and neoplasia
dimenhydrinate PO; 50–100 mg every 4 hours–qid (max: Antihistamine; also used for allergies and cold/flu symptoms;
(Dramamine, others) 400 mg/day) IM and IV forms available
diphenhydramine (Benadryl, PO; 25–50 mg tid–qid (max: 300 mg/day) Antihistamine; IM, IV, and topical forms available; also for
others) (see page 460 for allergies, Parkinson’s disease, and anaphylaxis
dolasetron (Anzemet) PO; 100 mg 1 hour before chemotherapy Serotonin-receptor blocker; IV form available
doxylamine (Diclegis) PO; 2 tablets daily at bedtime Newer formulation that contains pyridoxine (vitamin B6) for
the nausea and vomiting of pregnancy
granisetron (Kytril) IV; 10 mcg/kg 30 minutes before Serotonin-receptor blocker; oral form available
chemotherapy
hydroxyzine (Atarax, PO; 25–100 mg tid or qid Antihistamine; IM form available; also for anxiety and as a
Vistaril) preoperative medication
meclizine (Antivert, PO; 25–50 mg/day, 1 hour before travel Antihistamine; for motion sickness and nausea associated
Bonine) with vertigo
methylprednisolone IV; two doses of 125–500 mg 6 hours Corticosteroid; IM and IV forms available; also for inflammatory
(Medrol, Solu-Medrol) apart before chemotherapy disorders, severe allergies, acute asthma, and neoplasia
metoclopramide (Reglan) PO; 2 mg/kg 1 hour before chemotherapy Phenothiazine-like; IV and IM forms available; also for GERD,
facilitation of small-bowel intubation, and gastric stasis
ondansetron (Zofran) IV; 4 mg tid prn Serotonin-receptor blocker; IM and PO forms available
perphenazine (Phenazine, PO; 8–16 mg bid–qid Phenothiazine; IM and IV forms available; also for psychoses
Trilafon)
prochlorperazine PO; 5–10 mg tid or qid Phenothiazine; IM, IV, and suppository forms available; also
(Compazine) for treatment of psychoses
promethazine (Phenergan) PO; 12.5–25 mg every 4 hours–qid Both a phenothiazine and an antihistamine; IM, IV, and
suppository forms available; also for allergic disorders and
as an adjunct to anesthesia and surgery
scopolamine (Isopto Transdermal patch; 0.5 mg every 72 hours Anticholinergic; oral, IV, IM, and subcutaneous forms
hyoscine, Transderm Scop) available
(Dramamine) and meclizine (Antivert) are also effective but may cause significant drowsiness in some patients.
Drugs used to treat motion sickness are most effective when taken 20 to 60 minutes before travel is expected.
On some occasions, it is desirable to stimulate the vomiting reflex with drugs called emetics. Indica-
tions for emetics include ingestion of poisons and overdoses of oral drugs. Ipecac syrup, given orally, or
apomorphine, given subcutaneously, will induce vomiting in about 15 minutes. Drugs used to stimulate
emesis should be used only in emergency situations under the direction of a healthcare provider.
Drug Prototype: Ondansetron (Zofran, Zuplenz)

Therapeutic Class: Antiemetic Pharmacologic Class: Serotonin (5-HT) receptor blocker
Actions and Uses: Ondansetron and other drugs in the sero- for nausea and vomiting. It is available by the PO, IV, IM, oral
tonin-receptor blocker class have replaced other, older drugs disintegrating tablet, and oral soluble film routes.
for the treatment of serious nausea and vomiting. To prevent
chemotherapy-induced nausea and vomiting the medication is Adverse Effects and Interactions: The most common adverse effects
started at least 30 minutes prior to chemotherapy and contin- are headache, dizziness, drowsiness, and diarrhea. Caution must
ued for several days after. be used when treating patients with cardiac abnormalities because
Ondansetron acts by blocking serotonin receptors in the ondansetron can prolong the QT interval and cause dysrhythmias.
chemoreceptor trigger zone, an area of the brain responsible Ondansetron exhibits few drug interactions.
Weight Loss
Hunger occurs when the hypothalamus in the brain responds to the levels of certain chemicals (glu-
cose) or hormones (insulin) in the blood. Hunger is a normal physiologic response that drives people to
seek nourishment. Appetite is somewhat different than hunger. Appetite is a psychological response that
drives food intake based on associations and memory. For example, people often eat not because they
are experiencing hunger, but because it is a particular time of day or they find the act of eating pleasur-
able or social.
Anorexiants and lipase inhibitors are used for the short-term

management of obesity. Core Concept 30.12
Despite the public’s desire for effective drugs to promote weight loss, there are few such drugs available.
The approved drugs used for the treatment of obesity produce only modest weight loss.
Obesity may be defined as being more than 20% above ideal body weight or having a body mass
index of 30 kg/m2 or higher. Because of the prevalence of obesity in society and the difficulty that most
patients experience when following weight-reduction plans for extended periods, drug manufacturers have
long sought to develop safe drugs that cause weight loss. In the 1970s, amphetamine and dextroamphet-
amine (Dexedrine) were widely prescribed as anorexiants to reduce appetite. These drugs, however, are
addictive, and amphetamines are rarely prescribed for this purpose today. In the 1990s, the combination
of fenfluramine and phenteramine, known as fen-phen, was widely prescribed until fenfluramine was re-
moved from the market for causing heart valve defects. Sibutramine (Meridia), once the most widely pre-
scribed anorexiant for the short-term control of obesity, was removed from the market in 2010 due to an
increased risk for heart attacks and strokes. Current pharmacologic strategies for weight management focus
on two mechanisms: lipase inhibitors and anorexiants.
Orlistat (Xenical) acts by inhibiting the enzyme lipase in the GI tract. This blocks the absorption of
fats in the small intestine. Unfortunately, orlistat may also decrease absorption of other substances, includ-
ing fat-soluble vitamins and warfarin (Coumadin). Orlistat produces only a small decrease in weight com-
pared to placebos.
A second strategy to reduce weight is to block parts of the nervous system responsible for hunger
with anorexiants, also called appetite suppressants. Phentermine, once part of the combination fen-
phen, was approved in 2012 as a fixed dose combination with topiramate (Qysmia). Phenteramine
decreases appetite but the precise mechanism of antiobesity action of topiramate (an antiepileptic) drug
is unknown. Side effects of Qysmia include paresthesia, dizziness, dysgeusia, insomnia, constipation,
and dry mouth.
Also approved in 2012, lorcaserin (Belviq) is one of the newest anorexiants that is believed to act
by activating serotonin receptors in the hypothalamus, causing a feeling of fullness or satiety. The drug is
well tolerated, with headache and upper respiratory tract infection being the most common side effects.
Like other antiobesity drugs, it should be combined with a regimen of diet and exercise for optimum
weight loss.
Cam Therapy
Ginger for Nausea
Ginger is obtained from the roots of the herb Zingiber officinale, which grows in a wide vari-
ety of places across the world. Active ingredients include aromatic oils that give the herb its
characteristic scent and antiemetic activity. Because of its widespread use as a spice in Asian
cooking, ginger is widely available in a number of forms, including tincture, tea, dried and
fresh root, and capsules. Commercial products that use ginger as a flavoring include ginger
cookies, gingerbread, and ginger ale. Consumers should check the product ingredients to be
certain that the item truly contains ginger extract, rather than artificial ginger flavoring.
Ginger has been used in Chinese medicine for thousands of years. Indications relating to
the digestive system include nausea, vomiting, morning sickness, and motion sickness. Studies
have shown its effectiveness to be comparable to OTC medications.
Ginger is purported to have other significant benefits. The herb is said to have anti-
inflammatory properties that are of benefit to patients with arthritis. It is sometimes given to
patients with flu symptoms to help coughs and lower fever. Because of a possible effect on
blood clotting, patients taking anticoagulants should avoid ginger unless otherwise directed
by their healthcare provider.
Pancreatic Enzymes
In addition to secreting insulin, the pancreas is also responsible for the producing essential digestive
enzymes. Lack of secretion, or pancreatic insufficiency, will result in malabsorption disorders. Replace-
ment therapy with pancreatic enzymes is sometimes necessary.
Pancreatic enzymes are administered as replacement therapy for

Core Concept 30.13 patients with pancreatitis or malabsorption syndromes.
The pancreas secretes more than 1 L of pancreatic juice daily, which contains enzymes that split proteins,
fats, and carbohydrates. Because these nutrients must be broken down into simpler molecules before they
can be absorbed, lack of sufficient pancreatic juice can cause malabsorption syndromes. Lipase, the en-
zyme that digests fats, is most affected. The most common cause of pancreatic insufficiency is chronic
pancreatitis, which is most often associated with alcoholism.
Symptoms of chronic pancreatitis include upper abdominal pain, loss of appetite, nausea, vomiting,
steato 5 fat and weight loss. Steatorrhea, the passing of bulky, foul-smelling fatty stools, occurs because dietary fats
rrhea 5 flow or discharge are passing through the GI tract without being broken down.
Pancrelipase (Cotazym, Pancrease, others) is a pancreatic enzyme supplement obtained from pigs
that contains the necessary enzymes to digest fats, carbohydrates, and proteins. To avoid destruction by
stomach acid, capsules are made with an enteric coating. Dosing is individualized to the degree of pan-
creatic insufficiency in each patient. Administration of the drug is timed to coincide with meals so that
the enzymes are available when food reaches the duodenum. Overtreatment can cause nausea, vomiting,
and diarrhea.

Patients treated for digestive disorders need to know the following:
Regarding Antiulcer Medications

1. Do not smoke tobacco when taking H2-receptor blockers because this interferes with the
drug action.
2. Because drowsiness may occur when starting therapy with H2-receptor blockers or pro-
ton-pump inhibitors, monitor operating equipment and the use of alcohol or other CNS
drugs carefully.
3. When taking medications for peptic ulcer, avoid drugs that may cause stomach irritation
such as aspirin or NSAIDs.
4. Shake liquid antacids well before pouring. Chewable tablets should be thoroughly
chewed before swallowing.
Regarding Laxatives
5. Because bulk-forming laxatives and stool softeners may take several days for results, be
patient and do not take more than prescribed.
6. Take bulk-forming laxatives with at least two full glasses of water because this aids in
forming larger stools.
7. If constipation is a frequent problem, try drinking more fluids and adding fiber to the
diet rather than taking laxatives on a continual basis. Foods rich in fiber include all fruits
and vegetables, bran cereals, and whole grain breads.
Regarding Antiemetics
8. Before taking antiemetic medications, try other methods of relieving nausea, such as
drinking flat carbonated beverages or weak tea or eating small amounts of crackers or
dry toast.
9. When taking phenothiazines or antihistamines as antiemetics, use sugarless candy, gum,
or ice chips to minimize dry mouth.
10. Recall that medications taken to suppress hunger produce only modest weight loss and
are not effective without a reduced-calorie diet. True, sustained weight loss can only be
achieved by modification of exercise and dietary habits.
Chapter Review 493
Chapter Review
30.1 The digestive system breaks down food, absorbs 30.7 Antibiotics are administered to eliminate Helico-
nutrients, and eliminates wastes. bacter pylori, the cause of many peptic ulcers.
The alimentary canal provides a large surface area for Elimination of H. pylori using combination therapy
the absorption of nutrients and drugs. Substances are with different antibiotics has been found to promote
propelled through the GI tract by peristalsis. Abnor- more rapid ulcer healing and longer remissions.
mally fast or slow peristalsis can affect nutrient, drug,
and water absorption. 30.8 Several miscellaneous drugs are also beneficial in
treating peptic ulcer disease.
30.2 Peptic ulcer disease is caused by an erosion of the Sucralfate produces a gel-like substance that provides
mucosal layer of the stomach or duodenum. a protective coating for ulcers. Misoprostol inhibits
Infection with H. pylori and therapy with NSAIDs gastric acid secretion and promotes the secretion of
are the most common causes of peptic ulcers. A protective mucus. Pirenzepine inhibits acid secretion
gnawing pain in the upper abdomen that is relieved by blocking cholinergic receptors.
by eating is the most common symptom of duode-
nal ulcer. Though less common, gastric ulcers may 30.9 Laxatives are used to promote defecation.
be more serious and require longer treatment and Laxatives are given to promote emptying of the
follow-up. GERD has symptoms similar to those of colon. Laxatives act by stimulating peristalsis or by
peptic ulcers and is treated with some of the same adding more bulk or water to the fecal mass.
medications.
30.10 Opioids are the most effective drugs for control-
30.3 Peptic ulcer disease is treated by a combination of ling severe diarrhea.
lifestyle changes and pharmacotherapy. Diarrhea is treated by addressing its cause, which may
Before beginning drug therapy, the patient should include anti-inflammatory drugs or anti-infectives. Opi-
eliminate tobacco and alcohol use and reduce stress oids are the most effective drugs for relieving severe
levels because these changes will favor remission of diarrhea, but they have some abuse potential. OTC bis-
peptic ulcer disease. Goals of drug therapy include muth compounds can help with simple diarrhea.
relief of symptoms, promotion of ulcer healing, and
prevention of recurrences. 30.11 Antiemetics are prescribed to treat nausea, vomit-
ing, and motion sickness.
30.4 Proton-pump inhibitors are effective at reducing Symptomatic treatment of nausea and vomiting involves
gastric acid secretion. drugs from many different classes, including phenothi-
Proton-pump inhibitors diminish gastric acid secre- azines, antihistamines, corticosteroids, benzodiazepines,
tion by interfering with the enzyme H+, K+-ATPase, and serotonin-receptor blockers. Motion sickness can
which is present in the mucosal cells in the stomach. be controlled through medications such as transdermal
Although very effective, use is usually limited to scopolamine or dimenhydrinate (Dramamine).
two months because of the possibility of long-term
adverse effects. 30.12 Anorexiants and lipase inhibitors are used for the
short-term management of obesity.
30.5 H2-receptor blockers reduce the secretion of gastric Only a few drugs are available for the short-term
acid. management of obesity, and these drugs produce only
H2-receptor blockers reduce the volume and acid- modest weight loss. The anorexiant sibutramine and
ity of stomach acid. Healing of duodenal ulcers the lipase inhibitor orlistat are used to help obese
occurs in four to eight weeks, and adverse effects are patients lose weight.
uncommon.
30.13 Pancreatic enzymes are administered as replace-
30.6 Antacids rapidly neutralize stomach acid and ment therapy for patients with pancreatitis or mal-
reduce the symptoms of peptic ulcer disease and absorption syndromes.
GERD. Pancreatic insufficiency leads to lack of breakdown
Once drugs of choice for treating peptic ulcer dis- and absorption of sufficient quantities of fats, carbo-
ease, antacids are now primarily used to give imme- hydrates, and proteins. This can lead to malabsorption
diate relief for the heartburn associated with GERD syndromes. Pancrelipase and pancreatin are used to
or peptic ulcers. restore the deficient enzymes.
Review Questions
The following questions are written in NCLEX-PN® style. 3. Neuropathy

Answer these questions to assess your knowledge of the chap- 4. Respiratory disorders
clear to you. 6. The nurse instructs patients using laxatives to:
1. Use daily for best results.
1. A nurse is providing information about peptic ulcers to 2. Not overuse them because they can cause chronic
a group at a senior residential facility. She tells them that the constipation
primary cause of peptic ulcers is: 3. Decrease fluid intake.
1. Stress 4. Decrease food intake.
2. Smoking
3. H. pylori bacteria 7. A patient about ready to receive chemotherapy has an
4. Family history order for ondansetron (Zofran). When should the nurse admin-
ister the ondansetron?
2. The patient with a gastric ulcer has been started on raniti- 1. Every time the patient complains of nausea
dine (Zantac). The nurse should include what instructions: 2. Thirty to sixty minutes before starting chemotherapy
(Select all that apply.) 3. Only if the patient complains of nausea
1. Drug therapy will extend over several weeks or months. 4. When the patient begins to experience vomiting during the
2. Information about the signs and symptoms of CNS depression. chemotherapy
3. Drug therapy will extend over a few days.
4. Antacids should not be given within one hour of taking 8. A patient, newly diagnosed with a peptic ulcer, needs
H2-receptor antagonists. more education when he states:
1. “It’s OK for me take aspirin if I get a headache.”
3. A patient has been experiencing acute diarrhea. In order 2. “Good thing I can eat raw foods. I love to go to the salad
to control this condition, the physician initially orders Lomotil bar.”
10 mL (2 teaspoons), four times a day. Every 5 mL (1 tea- 3. “If I need to take an appetite suppressant, I should be able
spoon) contains 2.5 mg of medication. How many milligrams to.”
of medication will the patient receive a day? 4. “Right now, I’m not feeling sick but if I do feel nauseous,
1. 20 mg I can take an antiemetic.”
2. 15 mg
3. 10 mg 9. The patient on topiramate (Qysmia) must be monitored
4. 2.5 mg for: (Select all that apply.)
1. Constipation
4. The nurse understands that it is important that the teach- 2. Dizziness
ing plan for a patient on omeprazole (Prilosec) should include 3. Hypertension
which of the following? 4. Diarrhea
1. This drug is safe for long-term use.
2. This drug should not be taken for a prolonged period of time. 10. The patient demonstrates understanding about the medi-
3. Therapeutic effects may take weeks. cation pancrelipase (Cotazym) when she states:
4. This drug must be used with antacids to be effective. 1. “I will take this medication with meals.”
2. “I will take this medication on an empty stomach.”
5. After administering magnesium hydroxide (Mylanta) to a 3. “I will only take this medication when I am eating
patient, the nurse monitors for: carbohydrates.”
1. Diarrhea 4. “If I develop nausea, vomiting, or diarrhea, I will increase
2. Peripheral disease my dosage.”
Remember Mr. Han, who was intro- “all this pain,” he is not happy to learn he has an ulcer and
duced at the beginning of the chap- states, “This is the last thing I need right now. My job is stress-
ter? Now read the remainder of the ful enough.” The physician prescribed omeprazole (Prilosec),
case study. Based on the informa- clarithromycin, and amoxicillin, with OTC antacids as needed.
tion you have learned in this chapter,
answer the questions that follow. 1. Mr. Han is a little confused about the function of each
one of his new drugs. He asks the nurse about how each drug
Mr. Jeffery Han is a 32-year-old stockbroker with a very is going to help him “overcome” the ulcer. The nurse begins
stressful job. He has just been diagnosed with a peptic ulcer. by explaining that part of the pain he is experiencing is due to
Although he is relieved to find out what has been causing inflammation caused by both the hydrochloric acid produced
Chapter Review 495
in his stomach and the presence of H. pylori, a bacteria. She 3. In the treatment of H. pylori, the nurse explains that the use
also tells him that the medication responsible for blocking acid of two or more antibiotics is essential to: (Select all that apply.)
secretion is: 1. Lower the potential for bacterial resistance
1. Omeprazole 2. Increase the effectiveness of therapy
2. Antacid 3. Guarantee that the bacteria will be totally destroyed
3. Clarithromycin 4. Decrease the cost of future drug therapy
4. Amoxicillin
4. Mr. Han had already been taking aluminum-based antacids
2. The nurse explains to Mr. Han that __________ was pre- for his pain but explains that he has started to experience con-
scribed to eradicate the bacteria H. pylori. (Select all that stipation. In order to promote bowel movements, which of the
apply.) following OTC medications would be beneficial for Mr. Han?
1. Omeprazole 1. Methylcellulose (Citrucel)
2. Clarithromycin 2. Famotidine (Pepcid)
3. Amoxicillin 3. Omeprazole (Prilosec)
4. Antacid 4. Bismuth salts (Pepto-Bismol)

C
“I’m so busy, I don’t eat
h very much so I take lots
a of vitamins and minerals.
p I figure it’s better to take
more than not enough.”
t
Ms. Mei Chin
e
r
31 Vitamins, Minerals, and

Nutritional Supplements
Core Concepts
31.1 Vitamins are needed to promote growth and 31.4 Vitamin therapy is indicated for specific conditions.
maintain health. 31.5 Minerals are inorganic substances needed in
31.2 Vitamins are classified as fat soluble or water very small amounts to maintain normal body
soluble. metabolism.
31.3 Recommended dietary allowances (RDAs) for 31.6 Enteral and total parenteral nutrition are therapies
vitamins have been established for the average that deliver essential nutrients to patients with
healthy adult. deficiencies.
Drug Snapshot
Vitamins cyanocobalamin
(Crystamine, others) 499
Minerals f errous sulfate (Feosol,
Feostat, others) 501
Enteral nutrition
Total parenteral nutrition
Learning Outcomes
1. Identify the characteristics that 4. Describe the role of vitamin and 6. Compare and contrast the functions
differentiate vitamins from other mineral therapies in the treatment of major minerals and trace minerals.
nutrients. of deficiency disorders. 7. Compare and contrast the enteral
2. Describe the functions of vitamins 5. Identify drug–vitamin and drug– and parenteral methods of providing
and minerals. mineral interactions. nutrition.
3. Explain the rationale behind
recommended dietary allowances
(RDAs).
Key Terms
enteral nutrition 504 pernicious (megaloblastic) anemia total parenteral nutrition (TPN) 505
hypervitaminosis 499 (pur-NISH-us ah-NEE-mee-ah) 499 trace mineral 500
intrinsic factor 499 provitamin 497 undernutrition 504
major mineral (macromineral) 500 recommended dietary allowance (RDA) 498 vitamins 497
M ost people are able to obtain all necessary nutrients their body requires through a balanced diet.
There are some conditions, however, in which dietary supplementation is necessary and will
benefit the patient’s health. This chapter focuses on these conditions and explores the role of
vitamins, minerals, and nutritional supplements in pharmacology.
Vitamins are needed to promote growth and maintain health. Core Concept 31.1
Vitamins are organic compounds required by the body in small amounts for growth and for the maintenance
of normal metabolic processes. Since the discovery of thiamine in 1911, over a dozen vitamins have been
identified. Because scientists did not know the chemical structures of the vitamins when they were discov-
ered, they were assigned letters and numbers such as A, B12, and C. These names are still widely used today.
An important characteristic of vitamins is that, with the exception of vitamin D, human cells cannot
synthesize them. They or their precursors—known as provitamins—must be supplied in the diet. A sec- pro 5 before
ond important characteristic is that if the vitamin is not present in adequate amounts, the body’s metabo- vitamin 5 essential substance
lism will be disrupted and disease will result. Furthermore, the symptoms of the deficiency can be reversed
by the administration of the missing vitamin.
Vitamins serve diverse and important roles in human physiology. For example, the B complex vita-
mins are coenzymes essential to many metabolic pathways. Vitamin A is a precursor of retinal, a pigment
needed for normal vision. Calcium metabolism is regulated by a hormone that is derived from vitamin D.
Without vitamin K, abnormal prothrombin is produced, and blood clotting is affected. Patients having a
low or unbalanced dietary intake, those who are pregnant, and those experiencing a chronic disease may
benefit from vitamin therapy.
Fast Facts Vitamins, Minerals, and Dietary Supplements

■ About 33% of Americans take a multivitamin supplement daily.
■ There is no difference between the chemical structure of a natural vitamin and a synthetic vitamin,
yet consumers pay much more for the natural type.
■ Because vitamin B12 is present only in animal products, vegetarians must obtain this vitamin in
fortified cereals, nutritional supplements, or yeast.
■ Administration of folic acid during pregnancy has been found to reduce birth defects in the
nervous system of the baby.
■ Patients who never receive sun exposure may need vitamin D supplements.
■ Heavy menstrual periods may result in considerable iron loss.
■ Technically, vitamins and minerals cannot increase a patient’s energy levels. Energy can be
provided only by adding calories in carbohydrates, proteins, and fats.
Vitamins are classified as fat soluble or water soluble. Core Concept 31.2
A simple way to classify vitamins is by their ability to mix with water. Those that dissolve easily in water
are called water-soluble vitamins. Examples include vitamin C and the B vitamins. Those that dissolve in
lipids are called fat soluble or lipid soluble and include vitamins A, D, E, and K.
The difference in solubility affects the way the vitamins are absorbed by the gastrointestinal (GI) tract
and stored in the body. The water-soluble vitamins are absorbed along with water in the digestive tract and
readily dissolve in blood and body fluids. When excess water-soluble vitamins are ingested, they cannot Life Span Fact
be stored for later use and are simply excreted in the urine. Because they are not stored to any significant Infancy and childhood are
degree, they must be ingested daily; otherwise deficiencies will quickly develop. times of potential vitamin defi-
Fat-soluble vitamins, however, cannot be absorbed in sufficient quantity in the small intestine unless ciency due to the high growth
they are ingested with other fats. These vitamins can be stored in large quantities in the liver and fat. demands placed on the body.
498 Chapter 31 Vitamins, Minerals, and Nutritional Supplements
Should the patient not ingest sufficient quantities, fat-soluble vitamins are removed from storage depots in
the body as needed. Unfortunately, this storage can lead to dangerously high levels of the fat-soluble vita-
mins if they are taken in excessive amounts.
Recommended dietary allowances (RDAs) for vitamins have been

Core Concept 31.3 established for the average healthy adult.
Based on scientific research on humans and animals, the Food and Nutrition Board of the National
Academy of Sciences has established levels for the intake of vitamins and minerals, called recom-
mended dietary allowances (RDAs). The RDA values represent the minimum amount of a vitamin or
mineral needed to prevent a deficiency in a healthy adult. The RDAs are revised periodically to reflect
the latest scientific research. Current RDAs for vitamins are listed in Table 31.1 ◆. A newer stan-
dard, the Dietary Reference Index (DRI), is sometimes used to represent the optimum level of nutrient
needed to ensure wellness.
Vitamin, mineral, or nutritional supplements should never substitute for a balanced diet. Sufficient
intake of proteins, carbohydrates, and fats is needed for proper health. Furthermore, although the label on
a vitamin supplement may indicate that it contains 100% of the RDA for a particular vitamin, the body
may absorb as little as 10% to 15% of the amount ingested. With the exception of vitamins A and D,
Table 31.1 Vitamins

RDA
Vitamin Function(s) Men Women Common Cause(s) of Deficiency
A Visual pigments, 1,000 RE* 800 RE Prolonged dietary deprivation, particularly when
epithelial cells rice is the main food source; pancreatic disease;
cirrhosis
B complex: Biotin (B7) Coenzyme in metabolic 30 mcg 30 mcg Deficiencies are rare.
reactions
Cyanocobalamin (B12) Coenzyme in nucleic 2 mcg 2 mcg Lack of intrinsic factor, inadequate intake of
acid metabolism foods from animal origin
Folic acid/folate (B9) Coenzyme in amino 200 mcg 160–180 mcg Pregnancy, alcoholism, cancer, oral
acid and nucleic acid contraceptive use
metabolism
Niacin (B3) Coenzyme in metabolic 15–20 mg 13–15 mg Prolonged dietary deprivation, particularly when
reactions Indian corn (maize) or millet is the main food
source; chronic diarrhea; liver disease; alcoholism
Pantothenic acid (B5) Coenzyme in metabolic 5 mg 5 mg Deficiencies are rare.
reactions
Pyridoxine (B6) Coenzyme in amino acid 2 mg 1.5–1.6 mg Alcoholism; oral contraceptive use;
metabolism malabsorption diseases
Riboflavin (B2) Coenzyme in metabolic 1.4–1.8 mg 1.2–1.3 mg Inadequate consumption of milk or animal products;
reactions chronic diarrhea; liver disease; alcoholism
Thiamine (B1) Coenzyme in metabolic 1.2–1.5 mg 1.0–1.1 mg Prolonged dietary deprivation, particularly when
reactions rice is the main food source; hyperthyroidism,
pregnancy, liver disease; alcoholism
C Coenzyme and 60 mg 60 mg Inadequate intake of fruits and vegetables;
antioxidant pregnancy; chronic inflammatory disease; burns;
diarrhea; alcoholism
D Calcium and phosphate 5–10 mcg 5–10 mcg Low dietary intake; inadequate exposure to
metabolism sunlight
E Antioxidant 10 TE** 8 TE Premature infants; malabsorption diseases
K Cofactor in blood 65–80 mcg 55–65 mcg Newborns; liver disease; long-term parenteral
clotting nutrition; certain drugs such as cephalosporins
and salicylates
*RE = retinoid equivalents
**TE = alpha-tocopherol equivalents
it is not harmful for most patients to consume two to three times the recommended levels of vitamins. In
cases where there is an increase in dietary needs, such as during pregnancy and growth periods, the RDAs
will need adjustment and supplements may be needed to achieve optimum wellness.
Vitamin therapy is indicated for specific conditions. Core Concept 31.4
Most people who eat a normal, balanced diet obtain all the necessary nutrients without vitamin supple-
mentation. Indeed, megavitamin therapy is not only expensive but may be harmful to health if taken for
long periods. Hypervitaminosis, or toxic levels of vitamins, has been reported for vitamins A, C, D, E, B6, hyper 5 above
niacin, and folic acid. In the United States, it is actually more common to observe syndromes of vitamin vitamin 5 vitamin
excess than those of vitamin deficiency. Most patients are unaware that taking too much of a vitamin or osis 5 condition
mineral can cause serious adverse effects.
Vitamin deficiencies may have a number of causes. Table 31.1 lists the functions of the vitamins
and some common causes of deficiencies. In the United States, deficiencies are most often the result of
poverty, fad diets, chronic alcoholism, or prolonged parenteral feeding. Infants, pregnant women, nursing
mothers, older adults, and those eating a vegan or vegetarian diet often require larger amounts of vitamins
and minerals to maintain optimal health. Men and women can have different vitamin and mineral needs,
as do persons who participate in vigorous exercise. Vitamin deficiencies in patients with chronic liver and Life Span Fact
kidney disease are well documented. Patients with alcohol or serious drug dependency are often deficient
in the quality and quantity of their nutritional intake. In cases in which dietary needs are increased, the Elderly patients who have
less exposure to direct sun-
RDAs will need adjustment, and supplements are indicated to achieve optimum wellness.
light may need vitamin D
Certain drugs affect vitamin metabolism. Alcohol is well known for its ability to inhibit the absorption supplements.
of thiamine and folic acid; alcohol abuse is the most common cause of thiamine deficiency in the United
States. Folic acid levels may be reduced in patients taking phenothiazines, oral contraceptives, phenytoin
(Dilantin), or barbiturates. Vitamin D deficiency can be caused by therapy with certain anticonvulsants.
Inhibition of vitamin B12 absorption has been reported with a number of drugs, including trifluoperazine,
alcohol, and oral contraceptives.
One of the most common and clinically important vitamin syndromes is deficiency of vitamin B12.
The most obvious consequence of B12 deficiency is a type of anemia called pernicious or megaloblastic megalo 5 large
anemia. Insufficient vitamin B12 creates a lack of activated folic acid, which is essential for DNA synthesis blastic 5 embryonic state
and cell division. Lack of vitamin B12 also affects the nervous system, causing tingling or numbness in the an 5 lack of
emia 5 blood condition
limbs, mood disturbances, and even hallucinations in severe deficiencies.
Treatment of vitamin B12 deficiency is most often accomplished by weekly or biweekly intra-
muscular (IM) or subcutaneous injections. Although oral supplements are available, they are effective
only in patients who have sufficient intrinsic factor and normal absorption in the small intestine (see
Drug Prototype for cyanocobalamin). Parenteral administration rapidly reverses most signs and symp-
toms of B12 deficiency. If the disease has been prolonged, symptoms may take longer to resolve, and
some neurologic damage may be permanent. Treatment may need to continue for the remainder of the
patient’s life. Life Span Fact
Vitamins are indicated for several additional conditions. Vitamin K is administered to patients with
Infants fed only breast milk
certain clotting disorders and as an antidote to warfarin (Coumadin) overdose. B complex vitamins such as receive insufficient amounts
folic acid, thiamine, and riboflavin are commonly administered to patients with chronic alcoholism. The of vitamin D, which can result
role of vitamin D therapy in the pharmacotherapy of bone disorders is discussed in Chapter 33. in rickets.
Drug Prototype: Cyanocobalamin (Crystamine, Others)

Therapeutic Class: Drug for anemia Pharmacologic Class: Vitamin supplement
Actions and Uses: Cyanocobalamin is a purified form of vitamin Cyanocobalamin is available by the PO, IM, and intranasal
B12 that is administered in deficiency states. Vitamin B12 is not routes. The intranasal spray and gel formulations (Nascobal)
synthesized by either plants or animals; only bacteria perform provide for once-weekly dosage. Intranasal formulations are
this function. Because only miniscule amounts of vitamin B12 used for maintenance therapy after normal vitamin B12 levels
are required, deficiency of this vitamin is not usually caused have been restored by IM preparations.
by insufficient dietary intake. The most common cause of vita-
min B12 deficiency is lack of intrinsic factor, which is secreted Adverse Effects and Interactions: Adverse effects from cyano-
by stomach cells. Intrinsic factor is required for vitamin B12 cobalamin are uncommon. Hypokalemia is possible; thus, serum
to be absorbed from the intestine. Figure 31.1 ■ illustrates potassium levels are monitored periodically.
the metabolism of vitamin B12. Inflammatory diseases of the Alcohol, aminosalicylic acid, neomycin, and colchicine may
stomach or surgical removal of the stomach may result in decrease absorption of oral cyanocobalamin. Chloramphenicol
deficiency of intrinsic factor. may interfere with therapeutic response to cyanocobalamin.
Figure 31.1
Metabolism of Dietary vitamin B12 (from meat)

vitamin B12.
Free B12 IF = Intrinsic factor
IF
B12 - IF Parietal cells
Ileum B12 can be absorbed

only in last 60 cm of
B12 - IF the small intestine
Liver
B12
B12 storage
To (3–5 yr supply)
storage
Excretion
Blood
vessel
To growing cells B12 to bile

(recycled)
Concept Review 31.1

■ What are some conditions in which the RDA for a vitamin may not be sufficient?
Minerals are inorganic substances needed in very small amounts to

Core Concept 31.5 maintain normal body metabolism.
Minerals are inorganic substances that constitute about 4% of body weight. The most common minerals are
the bone salts, calcium and phosphorus, which make up about 75% of the total mineral content in the body.
Minerals are classified as major minerals (macrominerals) or trace minerals, depending on how much
is needed in the diet. The seven major minerals must be obtained daily from dietary sources in amounts of
100 mg or higher. Required daily amounts of the nine trace minerals are 20 mg or less. These minerals are
Life Span Fact Minerals serve many important and diverse functions in the body. Some minerals, such as sodium and
magnesium, appear primarily as ions in body fluids. Others, such as iron and cobalt, are usually bound to
For each decade after age 40, organic molecules. The functions of many of the minerals in human physiology, such as calcium, sodium,
bone mass decreases approxi- and potassium, are well known. The functions of some of the trace minerals, such as aluminum, silicon,
mately 3% to 5%. To avoid
arsenic, and nickel, are less understood.
bone fractures, older adults
must ensure a substantial di- Because minerals are needed in very small amounts for human metabolism, a balanced diet will
etary intake of calcium or take supply the necessary quantities for most patients. Like vitamins, excess amounts of minerals can lead
calcium supplements. to toxicity, and patients should be advised not to exceed recommended doses. For example, arsenic,
Table 31.2 Minerals

Major Minerals Recommended Daily Intake Trace Minerals Recommended Daily Intake
Calcium 800–1,200 mg Chromium 0.05–2 mg
Chloride 750 mg Cobalt 0.1 mcg
Magnesium Men: 350–400 mg Copper 1.5–3 mg
Women: 280–300 mg
Phosphorus 700 mg Fluoride 1.5–4 mg
Potassium 2g Iodide 150 mcg
Sodium 500 mg Iron Men: 10–12 mg
Sulfur Not established Women: 10–15 mg
Manganese 2–5 mg
Molybdenum 75–250 mg
Selenium Men: 50–70 mcg
Women: 50–55 mcg
Zinc 12–15 mg
chromium, and nickel have been implicated as human carcinogens, and excess sodium intake can lead to
water retention and hypertension.
Mineral therapy is indicated for certain disorders. Iron-deficiency anemia is the most common nutri-
tional deficiency in the world and is a primary indication for iron supplements. Women at high risk for
osteoporosis are advised to consume extra calcium, either in their diet or as a supplement (see Chapter 35). osteo 5 bone
Magnesium deficiencies are promptly treated with oral or IV magnesium salts because lack of sufficient por 5 passage
amounts of this electrolyte can lead to weakness, dysrhythmias, and hypertension. Iodine-based drugs osis 5 condition
serve a number of functions, including use as topical antiseptics, as contrast drugs in radiologic procedures
of the urinary and cardiovascular systems, and the treatment of thyroid abnormalities (see Chapter 32).
Selected minerals used in pharmacotherapy are shown in Table 31.3 ◆.
Certain drugs affect mineral metabolism. For example, loop or thiazide diuretics can cause significant
urinary potassium loss. Corticosteroids, oral contraceptives, and a number of other drugs can cause sodium reten-
tion. The uptake of iodine by the thyroid gland can be impaired by certain oral hypoglycemics and lithium (Eska-
lith). Oral contraceptives have been reported to lower the plasma levels of zinc and increase those of copper.
Concept Review 31.2

hemo 5 blood
■ What is the difference between a vitamin and a mineral? globin 5 protein
Drug Prototype: Ferrous Sulfate (Feosol, Feostat, Others)

Therapeutic Class: Drug for anemia Pharmacologic Class: Iron supplement
Actions and Uses: Ferrous sulfate is an iron supplement. Iron is a Adverse Effects and Interactions: The most common adverse
mineral essential to the function of several biological molecules, effect of iron sulfate is GI upset. Although taking iron with
the most significant of which is hemoglobin. Each molecule of meals will lessen GI upset, food can decrease the absorption of
hemoglobin in a red blood cell contains four iron atoms, each iron by as much as 70%. It is recommended that iron prepara-
of which can bind reversibly to an oxygen atom. Sixty to eighty tions be administered one hour before or two hours after a
percent of all iron in the body is associated with hemoglobin. meal. However, if major gastric irritation is experienced, the
After red blood cells die, nearly all of the iron in their iron may be taken with juice or small meals. Patients should be
hemoglobin is recycled for later use. Because of this recycling, advised that iron preparations may darken stools and that this is
very little iron is excreted; thus, dietary iron requirements in a harmless adverse effect. Excessive doses of iron are very toxic,
most individuals are small. and patients should be advised to take their medication exactly
Iron deficiency is a common cause of anemia. The usual as directed.
cause of iron-deficiency anemia is blood loss, such as may occur Antacids and food decrease the absorption of iron. Vitamin
during menstruation or from peptic ulcers. Certain patients C increases the absorption of iron, whereas calcium (including
have an increased demand for iron, including those who are dairy products) and bran block its absorption. Vitamin C may
pregnant and those undergoing intensive athletic training. Fer- increase the absorption of ferrous sulfate.
rous sulfate is available in a wide variety of dosage forms to
prevent or rapidly reverse symptoms of iron-deficiency anemia.
Table 31.3 Selected Minerals Used for Pharmacotherapy

potassium chloride (KCl) PO; 10–100 mEq/hr in divided doses Drug should be discontinued immediately if
(see page 260 for the Drug IV; 10–60 mEq/hr diluted to at least hyperkalemia is suspected.
Prototype box) 10–20 mEq/100 mL of solution (max:
200–400 mEq/day)
sodium bicarbonate (NaHCO3 ) PO; 0.3–2 g once or twice daily or 1 tsp For treatment of metabolic acidosis, to enhance
(see page 261 for the Drug of powder in a glass of water renal excretion of certain drugs, and as an antacid
Prototype box)
CALCIUM
calcium acetate (PhosLo) PO; two to four tablets with each meal (each To prevent high blood phosphate levels in patients
tablet contains 169 mg) who are on dialysis
calcium carbonate (Rolaids, PO; 1–2 g bid–tid For calcium supplementation and as an antacid
Tums, Os-Cal, others)
calcium citrate (Citracal) PO; 1–2 g bid–tid For calcium supplementation
calcium gluconate (Kalcinate) PO; 1–2 g bid–qid For calcium supplementation and to reverse cardiac
signs of hyperkalemia
calcium lactate (Cal-Lac) PO; 325 mg–1.3 g tid with meals To correct mild hypokalemia
Iron
ferrous fumarate (Feostat, PO; 200 mg tid–qid For iron supplementation
others)
ferrous gluconate (Fergon, PO; 325–600 mg qid; may be gradually increased For iron supplementation
others) to 650 mg qid as needed and tolerated
ferrous sulfate (Feosol, PO; 750–1,500 mg/day in one to three divided For iron supplementation
others) doses
iron dextran (Dexferrum, IM/IV; dose is individualized and determined For iron supplementation when oral administration is
others) from a table in the package insert (max: 100 mg not indicated
[2 mL] of iron dextran within 24 hours)
Magnesium
magnesium chloride PO; 270–400 mg/day For magnesium supplementation
(Chloromag, Slow-Mag)
magnesium hydroxide (Milk PO; 5–15 mL or two to four tablets up to four For constipation, hyperacidity, or magnesium
of Magnesia) times per day supplementation
magnesium oxide (Mag-Ox, PO; 400–1,200 mg/day in divided doses For constipation, hyperacidity, or magnesium
Maox, others) supplementation
magnesium sulfate (Epsom IV/IM; 0.5–3 g/day For constipation, to control seizures, or for
salt) magnesium supplementation
Phosphorus
potassium/sodium PO; 250–1,000 mg /day For correction of phosphate deficiency and to lower
phosphates (K-Phos original, urinary calcium concentration
K-Phos MF, K-Phos neutral,
Neutra-Phos-K, Uro-KP
neutral)
Zinc
zinc gluconate PO; 20–100 mg (20-mg lozenges may be taken For correction of zinc deficiency
to a max of six per day)
zinc sulfate (Orazinc, PO; 15–220 mg/day For correction of zinc deficiency
Zincate, others)
Nursing Process Focus Patients Receiving Iron Supplements

Prior to administration: ■ Risk for Imbalanced Nutrition related to inadequate iron intake
■ Obtain a complete health history, including GI, renal and liver ■ Risk for Injury (weakness, dizziness, syncope) related to anemia
conditions; problems with anemia; prophylaxis during infancy, ■ Deficient Knowledge related to a lack of information about drug
childhood, and pregnancy; allergies, drug history, and possible therapy
drug interactions.
■ Evaluate laboratory blood findings: CBC (specifically
hematocrit and hemoglobin levels), electrolytes, and liver
function studies.
■ Acquire the results of a complete physical examination including
The patient will:

■ Experience therapeutic effects (an increase in hematocrit level and improvement in anemia-related symptoms).
Implementation
■ Monitor vital signs, especially pulse. (Increased pulse is an indicator ■ Instruct the patient to monitor pulse rate and report irregularities
of decreased oxygen content in the blood.) and changes in rhythm to the healthcare provider.
■ Monitor CBC to evaluate effectiveness of treatment. (Increases in Instruct the patient:

hematocrit and hemoglobin values indicate increased red blood cell ■ On the need for initial and continuing laboratory blood
[RBC] production.) monitoring.
■ To keep all laboratory appointments.
■ Monitor changes in stool. (Supplement may cause constipation, Instruct the patient:
change stool color, and cause false positives when stool is tested ■ That stool color may change, and that this is no cause for
for occult blood.) alarm.
■ On measures to relieve constipation, such as including fruits
and fruit juices in the diet and increasing fluid intake and
exercise.
■ Plan activities and allow for periods of rest to help the patient Instruct the patient to:
conserve energy. (Diminished iron levels result in decreased ■ Rest when he or she is feeling tired and avoid overexertion.
formation of hemoglobin, leading to weakness.) ■ Plan activities to avoid fatigue.
■ Administer oral forms of ferrous sulfate (iron) one hour before or Instruct the patient:
two hours after meals with a full glass of water or juice for better ■ Not to crush or chew sustained-release preparations; take with a
absorption. full glass of water or juice.
■ That medication may cause GI upset and may be taken with food
if this becomes a problem.
■ Administer liquid iron preparations through a straw or place on Instruct the patient to:
the back of the tongue (to avoid staining the teeth). ■ Dilute liquid medication before using and to use a straw to take
the medication.
■ Rinse the mouth after swallowing to decrease the chance of
staining the teeth.
■ Monitor dietary intake to ensure adequate intake of foods high in ■ Instruct the patient to increase intake of iron-rich foods such as
iron. liver, egg yolks, brewer’s yeast, wheat germ, and muscle meats.
■ Monitor for potential for child access to the medication. (Iron ■ Advise the parent to store iron-containing vitamins out of reach
poisoning can be fatal to young children.) of children and in childproof containers.
Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”).
Cam Therapy
Sea Vegetables
Sea vegetables, or seaweeds, are a form of marine algae that grow in the upper levels of the
ocean, where sunlight can penetrate. Examples of these edible seaweeds include spirulina,
kelp, chlorella, arame, and nori, many of which are used in Asian cooking. Sea vegetables
are found in coastal locations throughout the world. Kelp, or Laminaria, is found in the cold
waters of the North Atlantic and Pacific oceans.
Sea vegetables contain a multitude of vitamins as well as protein. Their most notable
nutritional aspect, however, is their mineral content. Plants from the sea contain more
minerals than most other food sources, including calcium, magnesium, phosphorus, iron,
potassium, and all essential trace elements. Because they are so rich in minerals, seaweeds
act as alkalizers for the blood, helping to rid the body of acid conditions (acidosis). Spirulina,
kelp, and chlorella are available in capsule or tablet form.
Enteral and total parenteral nutrition are therapies that deliver

Core Concept 31.6 essential nutrients to patients with deficiencies.
When a patient is eating or drinking fewer nutrients than required for normal body growth and mainte-
nance, undernutrition occurs. Undernutrition can also occur in certain malabsorption disorders of the
intestinal tract. The two primary goals in treating undernutrition are to identify the specific type of defi-
ciency and supply the missing nutrients. Nutritional supplements may be needed for short-term therapy or
for the remainder of a patient’s life.
Causes of undernutrition range from simple to complex and include the following:
■ Advanced age
■ HIV-AIDS
■ Alcoholism
■ Severe burns
■ Cancer
■ Chronic inflammatory bowel disease
■ Eating disorders
The most obvious cause for undernutrition is low dietary intake. Reasons for the inadequate intake
Life Span Fact must be carefully assessed. Patients may have no resources to purchase food and may be suffering from
Elderly patients may have starvation. Clinical depression leads many patients to shun food. Older adults may have poorly fitting den-
poor-fitting dentures or dif- tures or difficulty chewing or swallowing after a stroke. In terminal disease, patients may be comatose or
ficulty chewing or swallowing otherwise unable to take food orally. Although the causes differ, patients with insufficient intake exhibit a
following a stroke. similar pattern of general weakness, muscle wasting, and loss of subcutaneous fat.
Many different types of nutritional supplements are available to assist patients suffering from under-
nutrition. Products administered via the GI tract, either orally or through a feeding tube, are called enteral
nutrition. Oral feeding allows natural digestive processes to occur and requires less nursing care. Tube
feeding is necessary when the patient has difficulty swallowing or is otherwise unable to take meals orally
(Figure 31.2 ■ ). An advantage of tube feeding is that the amount of enteral nutrition the patient is receiv-
ing can be precisely measured and recorded.
Figure 31.2
Nurse administering
enteral nutrition
through a feeding
tube.
The particular enteral product is chosen to address the specific nutritional needs of the patient. For
example, some contain mixtures of amino acids and protein, whereas others contain primarily carbohy- Life Span Fact
drates or fats. There are many different formulations of enteral products available, each designed to meet a The absorption of food dimin-
specific nutrient need. Examples of enteral products include Vivonex T.E.N., Peptamen, Sustacal, Ensure- ishes with age, and often the
Plus, Casec, Polycose, Microlipid, and MCT Oil. quantity of ingested food is
Patients sometimes exhibit vomiting, nausea, or diarrhea when first receiving enteral nutrition. Ther- reduced, leading to vitamin
apy is often started slowly, with small quantities so that adverse effects can be assessed. deficiencies in elderly patients.
When the metabolic needs of the patient cannot be met through enteral nutrition, total
parenteral nutrition (TPN) is indicated. For short-term therapy, peripheral vein TPN may be
used. Because of the risk of phlebitis, however, long-term therapy often requires central vein TPN.
Because the GI tract is not being used, patients with severe malabsorption disease may be success-
fully treated with TPN.
TPN is able to provide all the patient’s nutritional needs with solutions containing amino acids, fats,
carbohydrate (as dextrose), electrolytes, vitamins, and minerals. The particular formulation may be specific
to the disease state, such as products for renal failure or hepatic failure. TPN is administered through an
infusion pump so that nutrition can be precisely monitored. Patients in various settings such as acute care,
long-term care, and home health care often benefit from TPN therapy.

Patients treated with vitamins, minerals, or herbs need to know the following:
In General
1. If receiving regular monthly injections of vitamin B12, do not take additional oral supple-
ments of vitamin B12 or folic acid without the advice of a healthcare provider.
2. Do not take more than the recommended doses of any vitamin or mineral without first
checking with a healthcare provider. Although small amounts of these substances are
beneficial, large amounts may be dangerous.
3. Ensure that diet is nutritionally adequate, adding foods that naturally supply the
needed vitamins and minerals before taking supplements. See a dietician for advice,
particularly for special needs such as pregnancy or diabetes.
4. Avoid foods with high zinc or oxalate content if a calcium supplement is being taken
because these may interfere with absorption. These foods include nuts, peas, beans,
spinach, and soy products.
5. Know that niacin, or vitamin B3, is also effective at lowering lipid levels. The dose for
lowering cholesterol, however, is 2–3 g per day, whereas the vitamin dose is only 25
mg per day.
6. When providing a medical or drug history to the physician or dentist, always report
vitamins, minerals, herbs, or dietary supplements being taken. If allergies to any dietary
supplements are known, be sure to report these also.
7. Because liquid iron preparations can stain teeth, dilute these solutions with juice or
water and rinse the mouth after taking the medication to reduce staining.
8. Take oral forms of ferrous sulfate (iron) one hour before or two hours after meals for
better absorption. Take with a full glass of water or juice.
Safety Alert
Accidental Overdose of Vitamins and Other Medications
Accidental overdose of vitamins or other medications are of special concern in children. They
have the ability to cause injury and death. Medications used for children, such as vitamins and
cough medicine, may be appealing to children because of their candy-like appearance. To
avoid tragedy, nurses should teach caregivers not to refer to any medications as “candy” and
to store all medications in a secure place; out of the reach and sight of children even if the
containers have child-resistant caps.
Chapter Review
31.1 Vitamins are needed to promote growth and 31.4 Vitamin therapy is indicated for specific conditions.
maintain health. Most people do not need vitamin supplementation, and
With the exception of vitamin D, vitamins cannot be excess intake may lead to hypervitaminosis. Indications
synthesized by the body and must be provided in the for vitamin therapy include alcoholism, pregnancy or
diet. Although only very small amounts of vitamins breast-feeding, chronic kidney or liver disease, therapy
are needed, lack of sufficient quantity will result in with certain drugs that affect vitamin metabolism, and
disease. reduced food intake in elderly patients.
31.2 Vitamins are classified as fat soluble or water 31.5 Minerals are inorganic substances needed in
soluble. very small amounts to maintain normal body
Water-soluble vitamins include vitamins C and B. metabolism.
Fat-soluble vitamins include vitamins A, D, E, and Like vitamins, most people receive all the minerals
K. Water-soluble vitamins cannot be stored and must they need through a balanced diet. Certain conditions,
be ingested daily, whereas excess fat-soluble vita- such as osteoporosis or iron-deficiency anemia, do
mins can be stored for later use. warrant mineral therapy.
31.3 Recommended dietary allowances (RDAs) for 31.6 Enteral and total parenteral nutrition are therapies
vitamins have been established for the average that deliver essential nutrients to patients with
healthy adult. deficiencies.
RDA values represent the minimum amount of vita- Enteral nutrition supplies patients all the essential
min or mineral needed to prevent a deficiency in a nutrients via the oral route or through feeding tube.
healthy adult. These values must be adjusted for For patients who cannot take oral supplements, nutri-
changes in health status, such as athletic training, ents are supplied parenterally by way of total paren-
pregnancy, or chronic disease. teral nutrition.
Review Questions
The following questions are written in NCLEX-PN® style. 3. This medication should never be taken on an empty
Answer these questions to assess your knowledge of the chap- stomach.
ter material, and go back and review any material that is not 4. Blood pressure must be monitored closely.
clear to you.
4. The nurse monitors patients with a history of alcohol
1. The nurse knows that Vitamin B12 is indicated for which abuse for a ______ deficiency.
of the following conditions? 1. Biotin
1. Liver disease 2. Thiamine
2. Chronic inflammatory bowel disease 3. Niacin
3. Pernicious anemia 4. Riboflavin
4. Inadequate exposure to sunlight
5. The patient on a thiazide or loop diuretic, such as Lasix,
2. The nurse administers which vitamin for a patient experi- is monitored for which electrolyte?
encing warfarin (Coumadin) overdose? 1. Selenium
1. Vitamin A 2. Calcium
2. Vitamin D 3. Potassium
3. Vitamin E 4. Magnesium
4. Vitamin K
6. The nurse instructs the patient taking liquid iron to:
3. For the patient taking ferrous sulfate, the nurse will pro- 1. Swish medication in his mouth for one minute.
vide what instructions? 2. Take medication with food.
1. Do not take antacids with this medication. 3. Avoid foods with high iron content.
2. This medication can cause severe diarrhea. 4. Rinse his mouth with water after swallowing.
Chapter Review 507
7. The patient is exhibiting weakness, hypertension, 9. The patient’s GI tract is not functioning. Which type of
and dysrhythmias. Which of the following will the nurse feeding technique does the nurse expect to use to ensure the
check? patient is receiving adequate nutrition?
1. Calcium levels 1. Oral
2. Magnesium levels 2. Enteral
3. Aluminum levels 3. TPN
4. Chromium levels 4. GI
8. The nurse understands that which of the following is a 10. The patient has hypomagnesemia and is to receive and IV
common indication for vitamin or mineral pharmacotherapy? infusion of 350 mg of magnesium in 250 mL over four hours.
(Select all that apply.) How many milliliters per hour will the patient receive?
1. Chronic alcoholism 1. 65.5 mL
2. Liver failure 2. 50.5 mL
3. Anemia 3. 62.5 mL
4. Pregnancy 4. 55.5 mL
Remember Ms. Chin, who was intro- 3. “It is the amount of nutrient needed by an average
duced at the beginning of the chap- person.”
ter? Now read the remainder of the 4. “It is the minimum amount of nutrient needed to prevent a
case study. Based on the informa- deficiency in healthy adults.”
tion you have learned in this chapter,
answer the questions that follow. 3. Ms. Chin asks if she should be taking the multivitamins.
The nurse collects what information before responding? (Select
Ms. Mei Chin, a young woman, has come to the office for a all that apply.)
routine check-up. While reviewing her medications, Ms. Chin 1. Weight
tells the nurse that she has been taking multivitamins with min- 2. Diet
erals for the last year, and that lately, she has been taking four 3. Presence of any chronic diseases
times the label dose because she doesn’t eat very much and 4. Use of alcohol
figures that “it’s better to take more than not enough.”
4. Ms. Chin wants to continue to take the multivitamins,
1. While teaching Ms. Chin about multivitamins, the nurse convinced that it is helping her. She states that sometimes she
identifies which of the following as a water-soluble vitamin? just doesn’t feel like eating. The nurse tells Ms. Chin to:
1. A 1. Stop taking the multivitamins, her diet is good enough.
2. B complex 2. Continue taking four times the label dose until she starts to
3. D feel sick.
4. E 3. Not take more than the recommended dose until she
speaks to the doctor about the problems associated with
2. While continuing the discussion on the topic of multivi- her diet
tamins and minerals, Ms. Chin asks the nurse the meaning of 4. Discontinue taking four times the recommended dose,
RDA. The nurse responds: instead take two times the recommended dose because she
1. “It is the amount of nutrient required by all people.” hasn’t been eating well.
2. “It is the maximum amount of nutrient needed to prevent
a deficiency in healthy adults.”
Pearson Nursing Student Resources Find additional review materials at: nursing.pearsonhighered.com.
U n i t
6
The Endocrine and
Reproductive Systems
Unit Contents
Chapter 32 Drugs for Endocrine Disorders / 510
Chapter 33 Drugs for Diabetes Mellitus / 528
Chapter 34 Drugs for Disorders and Conditions of the Reproductive System / 542
c
“I don’t know why I’m so
h tired all the time. I’ve gained
a a lot of weight and am cold
p all the time too. Maybe it’s
just hormones.”
t
Mrs. Helen Brookfield
e
r
32 Drugs for Endocrine Disorders
Core Concepts
32.1 The endocrine system maintains homeostasis by 32.6 Thyroid disorders may be treated by administering
using hormones as chemical messengers. thyroid hormone or by decreasing the activity of
32.2 The hypothalamus and the pituitary gland secrete the thyroid gland.
hormones that control other endocrine organs. 32.7 Corticosteroids are released during periods of stress
32.3 Hormones are used as replacement therapy, as and influence carbohydrate, lipid, and protein
antineoplastics, or as “antihormones” to block metabolism in most cells.
endogenous actions. 32.8 Corticosteroids are prescribed for adrenocortical
32.4 Of the many pituitary and hypothalamic hormones, insufficiency and to dampen inflammatory and
several have clinical applications as drugs. immune responses.
32.5 The thyroid gland controls the basal metabolic rate
and affects virtually every cell in the body.
Drug Snapshot
Hypothalamic and desmopressin (DDAVP) 514
Pituitary Drugs
Thyroid Drugs levothyroxine (Synthroid) 518
Antithyroid Drugs propylthiouracil (PTU) 519
Adrenal Drugs ydrocortisone (Cortef, Hydrocortone,
h
Solu-Cortef, others) 522
Learning Outcomes
1. Describe the general structure and 4. Explain the primary functions of the based on their classifications and
functions of the endocrine system. adrenal cortex. mechanisms of action.
2. Explain the primary functions of the 5. Describe the signs and symptoms 7. For each of the drug classes listed
thyroid gland. of Addison’s disease and Cushing’s in the Drug Snapshot, identify
3. Identify the signs and symptoms syndrome. representative drugs and explain their
of hypothyroidism and 6. Categorize drugs used in the mechanisms of drug action, primary
hyperthyroidism. treatment of endocrine disorders actions, and important adverse effects.
Key Terms
Addison’s disease (ADD-iss-uns) 521 diabetes insipidus (die-uh-BEE-tees in- mineralocorticoids (min-ur-al-oh-KORT-
adrenal atrophy (AT-troh-fee) 521 SIP-uh-dus) 514 ik-oyds) 520
adrenocorticotropic hormone (ACTH) dwarfism 515 myxedema (mix-uh-DEEM-uh) 516
(uh-dreen-oh-kor-tik-o-TRO- follicular cells (fo-LIK-yu-lur) 516 parafollicular cells (par-uh-fo-LIK-u-
pik) 520 glucocorticoids (glu-ko-KORT-ik- lur) 516
anterior pituitary 511 oyds) 520 pituitary gland (pit-TOO-it-air-
antidiuretic hormone (ADH) (ANT-eye- gonadocorticoids (go-NAD-oh-KORT-ik- ee) 511
DYE-yure-EH-tick) 514 oyds) 521 posterior pituitary 511
corticosteroid (KORT-ik-ko-STARE- Graves’ disease 516 releasing hormones 511
oyd) 520 hormones 511 somatotropin (so-mat-oh-TROH-
cretinism (KREE-ten-izm) 516 hypothalamus (hi-po-THAL-ih- pin) 515
Cushing’s syndrome (KUSH-ings) 522 mus) 511 vasopressin (vaz-oh-PRESS-in) 514
L ike the nervous system, the endocrine system is a major controller of homeostasis. Whereas a nerve
may exert instantaneous control over a single muscle or gland, a hormone from the endocrine sys-
tem may affect thousands of body cells and take as long as several days to produce an optimal
response. Hormonal balance must be maintained within a narrow range. Too little or too much of a hor-
mone may produce profound changes in the body. This chapter examines common endocrine disorders and
endo 5 within
crine 5 to secrete
their pharmacotherapy. Drugs for diabetes mellitus are covered in Chapter 33. The reproductive hormones
are covered in Chapter 34
The endocrine system maintains homeostasis by using hormones

as chemical messengers. Core Concept 32.1
The endocrine system consists of various glands that secrete hormones, chemical messengers released in
response to a change in the body’s internal environment. For example, whenever body temperature falls,
the thyroid gland secretes thyroid hormone. When levels of calcium in the bloodstream fall, the parathyroid
glands secrete parathyroid hormone (PTH). The various endocrine glands and their locations in body are
In the endocrine system, it is common for one hormone to control the secretion of another hor-
mone. In addition, it is common for the last hormone or action in the pathway to provide feedback to
turn off the action of the first hormone. For example, as serum calcium level falls, PTH is released.
PTH causes an increase in serum calcium level, which provides feedback to the parathyroid glands
to shut off PTH secretion. This is a common feature of endocrine homeostasis known as negative
feedback.
The hypothalamus and the pituitary gland secrete hormones

that control other endocrine organs. Core Concept 32.2
Two endocrine structures in the brain deserve special recognition because they control many other
endocrine glands. The hypothalamus secretes chemicals called releasing hormones that travel via
blood vessels a short distance to an area immediately below, called the pituitary gland. These releas-
ing factors tell the pituitary which hormone to release. After the pituitary releases the appropriate
hormone, it travels to its target organ to cause its effect. For example, the hypothalamus secretes thy-
rotropin-releasing hormone, which travels to the pituitary gland with the message to secrete thyroid-
stimulating hormone (TSH). TSH then travels to its target organ—the thyroid gland—to stimulate the
release of thyroid hormone.
The pituitary gland comprises two distinct areas, the anterior pituitary or adenohypophysis and adeno 5 glandular tissue
the posterior pituitary or neurohypophysis. The majority of hormones are released by glandular neuro 5 neural tissue
tissue of the adenohypophysis. Only a few hormones are released from neural tissue of the neuro- hypo 5 under
physis 5 growth
hypophysis. Selected hormones associated with the hypothalamus and pituitary gland are shown in
Figure 32.2 ■.
512 Chapter 32 Drugs for Endocrine Disorders
Figure 32.1
The endocrine system.
Pineal gland
Hypothalamus
Pituitary gland
Parathyroid Thyroid gland

glands
Thymus
Adrenal
glands Pancreas
Gonad
(ovary)
Hormones are used as replacement therapy, as antineoplastics,

Core Concept 32.3 or as “antihormones” to block endogenous actions.
The goals of hormone pharmacotherapy vary widely. In many cases, the hormone is administered simply
endo 5 within as replacement therapy for patients who are unable to secrete sufficient quantities of their own endogenous
genous 5 generated from hormones. Examples of replacement therapy include the administration of thyroid hormone after the thy-
roid gland has been surgically removed or supplying insulin to a patient whose pancreas is not functioning.
Replacement therapy usually supplies the same physiologically low-level amounts of the hormone that
would normally be present in the body. A summary of selected endocrine disorders and their drug therapy
is given in Table 32.1 ◆.
Some hormones are used in cancer chemotherapy to shrink the size of hormone-sensitive tumors.
Examples include testosterone for breast cancer and estrogen for testicular cancer. Exactly how these hor-
mones produce their antineoplastic action is unknown. When used as antineoplastics, the doses of these
hormones far exceed those levels normally present in the body (see Chapter 28).
Another goal of hormone therapy may be to produce an exaggerated response that is part of the nor-
mal action of the drug. Administering hydrocortisone to suppress inflammation takes advantage of the
Figure 32.2
CRH Corticotropin-releasing hormone

GHIH Growth hormone-inhibiting hormone
PIH Prolactin-inhibiting hormone
MSH-IH Melanocyte-stimulating hormone
inhibiting hormone
GnRH Gonadotropin-releasing hormone
HYPOTHALAMUS GHRH Growth hormone-releasing hormone
Direct release
of hormones TRH Thyrotropin-releasing hormone
ACTH Adrenocorticotropic hormone
TSH Thyroid-stimulating hormone
Indirect control through release of regulatory factory GH Growth hormone
PRL Prolactin
CRH TRH GHIH PIH GHRH FSH Follicle-stimulating hormone
Adrenocorticosteroids LH Luteinizing hormone
GnRH MSH-IH
MSH Melanocyte-stimulating hormone
ADH Antidiuretic hormone
Anterior lobe
of pituitary Posterior lobe
of pituitary
Kidneys
ACTH
Adrenal ADH
gland
TSH
Oxytocin
GH
Uterine
smooth
PRL MSH muscle
FSH LH
Thyroid
gland
Thyroid
hormones
Melanocytes
Breast Testis Ovary

Peripheral
tissues
Testosterone Estrogen Progesterone
Hormones associated with the hypothalamus and pituitary gland.
normal action of the corticosteroids but to a greater extent than would normally occur in the body. Sup-
plying small amounts of estrogen or progesterone at specific times during the menstrual cycle can prevent
ovulation and pregnancy.
Endocrine pharmacotherapy also involves the use of “antihormones.” These hormones block the
actions of endogenous hormones. For example, propylthiouracil (PTU) is given to block the effects of an
overactive thyroid gland. Tamoxifen (Nolvadex) is given to block the actions of estrogens in estrogen-
dependent breast cancers (see Chapter 34).
Table 32.1 Endocrine Disorders and Their Drug Treatment

Gland Hormone(s) Disorder Drugs
Adrenal Cortex Corticosteroids Hypersecretion: Cushing’s syndrome Antiadrenal drugs
Hyposecretion: Addison’s disease Corticosteroids
Pancreas (Islets Insulin Hyposecretion: diabetes mellitus Insulin and antidiabetic drugs
of Langerhans)
Pituitary Growth hormone Hyposecretion: dwarfism somatotropin (Genotropin, others)
Hypersecretion: acromegaly (adults) octreotide (Sandostatin)
Antidiuretic hormone Hyposecretion: diabetes insipidus vasopressin, desmopressin, and
lypressin
Thyroid Thyroid hormone (T3 and T4 ) Hypersecretion: Graves’ disease propylthiouracil (PTU) and I-131 thyroid
hormone
Hyposecretion: myxedema (adults) levothyroxine (T4)
and cretinism (children)
hypothalamic and pItuitary disorders
Of the many pituitary and hypothalamic hormones, several have

Core Concept 32.4 clinical applications as drugs.
diabetes 5 siphon (urine Of the hormones secreted by the pituitary and the hypothalamus, only a few are used in pharmacotherapy.
passing through) There are valid reasons why they are not widely used. Some of these hormones can be obtained only from
mellitus 5 sweetened natural sources and can be quite expensive when used in therapeutic quantities. Furthermore, it is usually
insipidus 5 tasteless more effective to give drugs that directly affect secretion at the target organs. Hypothalamic and pituitary
(watered down)
en 5 in
agents are listed in Table 32.2 ◆. Hypothalamic and pituitary agents used for conditions of the male and
uresis 5 to urinate female reproductive systems are presented in Chapter 34.
Antidiuretic hormone (ADH) is one of the most important means the body uses to maintain fluid
homeostasis. As its name implies, ADH conserves water in the body. ADH is secreted from the posterior
osmolality 5 concentration pituitary gland when the hypothalamus senses that plasma volume has decreased or that the osmolality
of the blood has become too high. ADH is also called vasopressin, because it has the ability to constrict
blood vessels and raise blood pressure. A deficiency in ADH results in diabetes insipidus (DI), a rare
vaso 5 blood vessel condition characterized by the production of large volumes of very dilute urine, usually accompanied by
pressin 5 tension increased thirst. Two ADH preparations are available for the treatment of DI: desmopressin (DDAVP) and
Drug Prototype: Desmopressin (DDAVP, Stimate)

Therapeutic Class: Antidiuretic hormone replacement; retains fluid in the body
Pharmacologic Class: Antidiuretic hormone; vasopressin
Actions and Uses: Desmopressin is a synthetic analog of human Desmopressin can cause symptoms of water intoxication:
ADH that acts on the kidneys to increase the reabsorption of edema, weight gain, hypertension, drowsiness, headache, and list-
water. It is used to control the acute symptoms of DI in patients lessness, progressing to convulsions and coma. Patients are advised
who have insufficient ADH secretion. The oral route is preferred, to weigh themselves daily. Other adverse effects include transient
although intranasal and parenteral forms are available. It has a headache, nausea, mild abdominal pain and cramping, facial
duration of action of up to 20 hours, whereas vasopressin has a flushing, hypertension (HTN), pain, or swelling at the injection site.
duration of only 2–8 hours. Desmopressin is available as a nasal Intranasal forms can cause nasal congestion, rhinitis, and epistaxis.
spray (Stimate) to treat von Willebrand’s disease, a disorder of Desmopressin is contraindicated in patients with DI that
blood clotting. is caused by kidney disease because the drug can worsen fluid
retention and overload. It is used with caution in patients with
Adverse Effects and Interactions: Desmopressin causes contrac- coronary artery disease and HTN and in patients at risk for
tion of smooth muscle in the vascular system, uterus, and GI hyponatremia or thrombi.
tract. It also is used for the management of bleeding in patients Increased antidiuretic action can occur with carbamaze-
with hemophilia A. When taken an hour prior to bedtime, pine, chlorpropamide, clofibrate, and nonsteroidal anti-inflam-
desmopressin lowers the production of urine during the night matory drugs (NSAIDs). Decreased antidiuretic action can occur
and thus is useful in the management of nocturnal enuresis with lithium, alcohol, heparin, and epinephrine.
(bed-wetting).
Table 32.2 Selected Hypothalamic and Pituitary Drugs

hypothalamic drug
bromocriptine (Cycloset, PO (Cycloset); 0.8 mg daily, increased weekly to Blocks the release of prolactin; for treatment of
Parlodel) achieve 1.6–4.8 mg daily acromegaly (overproduction of GH) and pituitary
PO; 1.25–2.5 mg/day for 3 days, then increase dose tumors; for signs and symptoms of Parkinson’s
every 3–7 days to 30–60 mg/day disease and type 2 diabetes mellitus
pituitary drugs
Posterior Pituitary – ADH Drugs
desmopressin (DDAVP, IV/subcutaneous; 2–4 mcg in two divided doses To control symptoms of diabetes insipidus; in
Stimate) PO; 0.2–0.4 mg/day children under 6 years old, for bed-wetting
(enuresis); also used to treat von Willebrand’s
disease
vasopressin IM/subcutaneous; 5–10 units aqueous solution two Human antidiuretic hormone; reduces urine output
to four times per day by targeting renal collecting tubules
IV: 0.2–0.4 units/min up to 1 unit/min
Anterior Pituitary – GH and TSH Drugs
lanreotide (Somatuline Subcutaneous; 60–100 mg every 4 weeks For long-term treatment of patients with
Depot) acromegaly who cannot be treated with surgery
or radiation
mecasermin (Increlex) Subcutaneous; 0.04–0.08 mg/kg twice daily. Must be Synthetic version of insulin-like growth factor
administered within 20 min of a meal or snack (IGF-1); suppresses liver glucose production and
(max: 0.12 mg/kg given twice daily) stimulates glucose uptake in the body; for long-
term treatment of growth failure in children with
antibodies that neutralize GH
octreotide (Sandostatin) Subcutaneous/IV; 100–600 mcg/day in two to four For treatment of acromegaly due to too much GH
divided doses; after 2 weeks may switch to IM depot, in the body; may be used to treat severe diarrhea
20 mg every 4 weeks and other symptoms that occur with intestinal
tumors or metastatic carcinoid tumors (tumors
already spread in the body)
pegvisomant (Somavert) Subcutaneous; 40 mg loading dose, then 10 mg/day Growth hormone receptor antagonist (blocker)
(max: 30 mg/day) used in the treatment of patients with acromegaly
who cannot be treated with surgery or radiation
somatropin (Genotropin, Humatrope: Subcutaneous; 0.006 mg/kg daily (max: Growth hormone; protein-based peptide
Humatrope, Norditropin, 0.0125 mg/kg/day) prescribed in human growth hormone therapy
Nutropin, Saizen, Serostim, Serostim: Subcutaneous; Weight more than 55 kg:
Zorbtive) 6 mg at bedtime; 45–55 kg: 5 mg at bedtime;
35–45 kg: 4 mg at bedtime; less than 35 kg:
0.1 mg/kg at bedtime
Child: Genotropin: Subcutaneous; 0.16–0.24 mg/kg/
week in six to seven divided doses
Norditropin: 0.024–0.034 mg/kg six to seven times
per week
vasopressin. Desmopressin is the most common drug for treating DI. Details regarding this drug are found
in the Prototype Drug feature.
Growth hormone (GH), also called somatotropin, stimulates the growth and metabolism of nearly somato 5 cells of the body
every cell in the body. Deficiency of this hormone in children can cause short stature, a condition charac- tropin 5 attraction toward
terized by significantly decreased physical height compared with the norm of a specific age group. Severe
deficiency results in dwarfism. Short stature is caused by many conditions other than GH deficiency, and dwarfism 5 small stature
often a specific cause cannot be identified. Treatment of this condition usually involves the administration
of the growth hormone. It is given subcutaneously, several times a week during periods of active growth
and may continue until adulthood. The earlier the condition is treated, the better the chance that a child will
grow to be a near-normal adult height. When hormone therapy is first initiated, the gain in growth is very
rapid but then slows over time.
acro 5 extremeties Excess secretion of GH in adults is known as acromegaly. Acromegaly is a rare disorder caused by
megaly 5 enlarged a GH-secreting tumor of the pituitary gland. Because the epiphyseal plates are closed in adults, bones
become deformed rather than elongated with this disorder. The onset is gradual, with enlargement of
the small bones of the hands and feet, face, and skull; broad nose, protruding lower jaw; and slanting
forehead.
Treatment of acromegaly consists of a combination of surgery, radiation therapy, and pharmaco-
therapy to suppress GH secretion or block GH receptors. Pharmacotherapy is generally attempted only in
patients who are unable to undergo surgical removal of the tumor. Octreotide (Sandostatin) is a synthetic
GH antagonist (blocker) structurally related to GH–inhibiting hormone (somatostatin). Other choices to
treat acromegaly include pegvisomant (Somavert), bromocriptine (Cycloset, Parlodel), and lanreotide
(Somatuline Depot).
Thyroid Disorders
The thyroid gland controls the basal metabolic rate and affects
Core Concept 32.5 virtually every cell in the body.
The thyroid gland secretes hormones that affect nearly every cell in the body. Thyroid hormone increases
basal metabolic rate, which is the baseline speed at which cells perform their functions. By increasing cel-
lular metabolism, this hormone increases body temperature. Adequate secretion of thyroid hormone is also
necessary for the normal growth and development in infants and children. Cretinism is the abnormal stunt-
ing of growth due to the lack of thyroid hormone. The thyroid strongly affects cardiovascular, respiratory,
gastrointestinal, and neuromuscular function.
The thyroid gland lies in the neck, just below the larynx and in front of the trachea. Follicular
cells in the gland secrete thyroid hormone, which is actually a combination of two different hormones:
thyroxine (tetraiodothyronine or T4) and triiodothyronine (T3). Iodine is essential for the synthesis of
these hormones and is provided through the dietary intake of common iodized salt. T3 is named for
the three iodine atoms that make up its chemical structure; T 4 has four iodine atoms. Parafollicular
cells in the thyroid gland secrete calcitonin, a hormone that is involved with calcium homeostasis (see
Chapter 35).
Thyroid function is regulated in various ways. Thyroid-releasing hormone (TRH) from the hypo-
thalamus stimulates the pituitary gland to secrete TSH. TSH then stimulates the thyroid gland to release
thyroid hormone. As blood levels of thyroid hormone increase, negative feedback suppresses the secre-
tion of TRH and TSH. High levels of iodine can also cause a temporary decrease in thyroid activity
that can last for several weeks. One of the strongest stimuli for increased thyroid hormone production
is exposure to cold temperatures. The negative feedback mechanism for the thyroid gland is shown in
Figure 32.3 ■.
Thyroid disorders may be treated by administering thyroid hormone

Core Concept 32.6 or by decreasing the activity of the thyroid gland.
Disorders of the thyroid result from hypofunction or hyperfunction of the thyroid gland. Abnormal thyroid
hormone levels could occur due to disease within the thyroid gland itself or be caused by abnormalities
of the pituitary gland or hypothalamus. Thyroid disorders are quite common, and drug therapy is often
indicated.
Hypothyroidism is a common disease caused by insufficient secretion of either TSH or thyroid hor-
mone. Symptoms of hypothyroidism in adults, also known as myxedema, include slowed body metab-
olism, fatigue, slurred speech, bradycardia, weight gain, low body temperature, and intolerance to cold
environments. Low or absent thyroid function may be a consequence of autoimmune disease, surgical
removal of the gland, or aggressive treatment with antithyroid drugs. Hypothyroidism is treated with natu-
ral or synthetic thyroid hormone.
Hypersecretion of thyroid hormone results in symptoms that are the opposite of hypothyroidism and
are the result of increased body metabolism. The symptoms include nervousness, irritability, insomnia,
tachycardia, palpitations, weight loss, hyperthermia, and heat intolerance. A particularly severe form of
hyperthyroidism is called Graves’ disease. If the cause of the hypersecretion is found to be a tumor, the
disease is corrected through surgical removal of the thyroid gland, or thyroidectomy. In less severe condi-
tions, the patient may receive antithyroid medications or ionizing radiation to kill or inactivate some of the
hyperactive thyroid cells. Antithyroid drugs are sometimes given 10 to 14 days prior to thyroidectomy to
decrease bleeding during surgery.
Figure 32.3
Cold
Feedback mechanisms
1
Stress of the thyroid gland.
5 Neurosecretory
cells of hypothalamus
Blood
Releasing
Endocrine cells of hormone
anterior pituitary
2 Thyroid-stimulating
hormone
Negative
feedback
Thyroid
Thyroxine
4 Increased metabolic rate

in most body cells
Fast Facts Thyroid Disorders

■ Hypothyroidism is 10 times more common in women than men; hyperthyroidism is 5–10 times more
common in women.
■ The two most common thyroid disorders, Graves’ disease and Hashimoto’s thyroiditis, are autoim-
mune diseases and may run in families.
■ One of every five women older than age 75 has Hashimoto’s thyroiditis.
■ One of every 4,000 babies is born without a working thyroid gland.
■ About 15,000 new cases of thyroid cancer are diagnosed each year.
■ Postpartum thyroiditis occurs in 5–9% of women after giving birth and may recur in future pregnancies.
■ Both hyperthyroidism and hypothyroidism can affect a woman’s ability to become pregnant; both
also can cause miscarriages.
Table 32.3 Thyroid and Antithyroid Drugs

Thyroid drugs
levothyroxine (Levothroid, PO; 100–400 mcg/day Synthetic T4; IV form available
Synthroid, others)
liothyronine (Cytomel, Triostat) PO; 25–75 mcg/day Synthetic T3
liotrix (Thyrolar) PO; 12.5–30 mcg/day Mixture of synthetic T3 and synthetic T4 in a 1:4 ratio
thyroid dessicated (Armour PO; 60–100 mg/day Obtained from animal thyroid glands
Thyroid, Thyrar, Thyroid USP)
Antithyroid drugs
methimazole (Tapazole) PO; 5–15 mg tid Ten times more potent than propylthiouracil
potassium iodide and iodine PO; 0.1–1.0 mL tid IV form available; Lugol’s is a mixture of 5% elemental
(Lugol’s solution, Thyro-block) iodine and 10% potassium iodide
propylthiouracil (PTU) PO; 100–150 mg tid May take 6–12 months for full therapeutic effect
radioactive iodide (I-131) PO; 0.8–150 mCi (based on May take 2–3 months for full therapeutic effect
radiation quantity)
The thyroid is the organ most susceptible to nuclear and radiation exposure (see Chapter 1). Symp-
toms of radiation exposure remain some of the most difficult to treat pharmacologically. Apart from the
symptomatic treatment of acute radiation syndrome, taking potassium iodide (KI) tablets after an incident
or an attack is the only recognized therapy.
Following a nuclear explosion, one of the resultant radioisotopes is iodine-131 (I-131). Because
iodine is naturally concentrated in the thyroid gland, I-131 will immediately enter the thyroid and dam-
age thyroid cells. If taken prior to, or immediately following, a nuclear incident, KI can prevent up to
100% of the radioactive iodine from entering thyroid tissue. Unfortunately, KI only protects the thyroid
gland from I-131. It has no protective effects on other body tissues, and it offers no protection against
the dozens of other harmful radioisotopes generated by a nuclear blast. Interestingly, I-131 is also a
medication used to shrink the size of overactive thyroid glands. The thyroid and antithyroid medications
are listed in Table 32.3 ◆.
Concept Review 32.1

■ If thyroid hormone is secreted by the thyroid gland, how can a deficiency in this hormone
be caused by disease in the hypothalamus or pituitary gland?
Drug Prototype: Levothyroxine (Levothroid, Synthroid, Others)

Therapeutic Class: Thyroid hormone replacement; metabolic enhancer Pharmacologic Class: Thyroid hormone
Actions and Uses: Levothyroxine is a synthetic form of thyroxine adverse effects is quite narrow. Adverse effects of levothy-
(T4) used for replacement therapy in patients with low thyroid roxine resemble symptoms of hyperthyroidism and include
function. Actions are those of thyroid hormone and include loss tachycardia, anxiety, insomnia, weight loss, and heat
of weight, improved tolerance to environmental temperature, intolerance. Menstrual irregularities may occur in women.
increased activity, and increased pulse rate. Blood levels of thy- Long-term use of levothyroxine has been associated with
roid hormone are monitored carefully until the patient’s symp- osteoporosis in women.
toms stabilize. In order to closely approximate the body’s own Levothyroxine interacts with many other drugs; for exam-
hormone level, levothyroxine should be taken in the morning, ple, cholestyramine and colestipol decrease the absorption of
ideally at the same time each day. To achieve the proper level levothyroxine. Using it with epinephrine and norepinephrine
of thyroid function, doses may require periodic adjustments for increases the risk of cardiac insufficiency. Oral anticoagulants
several months or longer. may increase hypoprothrombinemia.
High fiber foods may affect absorption. Herbal supple-
Adverse Effects and Interactions: The difference between ments such as lemon balm should be used cautiously. Lemon
a therapeutic dose of levothyroxine and one that produces balm may interfere with thyroid hormone function.
Drug Prototype: Propylthiouracil (PTU)

Therapeutic Class: Drug for hyperthyroidism Pharmacologic Class: Antithyroid drug
Actions and Uses: Propylthiouracil is administered to patients a small percentage of patients display blood changes such as
with hyperthyroidism, sometimes prior to surgery. It acts by decreased platelet and white blood cell counts, which may
interfering with the synthesis of T3 and T4. Because it does not increase the risk of infection. Periodic laboratory blood counts
affect thyroid hormone that has already been secreted, its action and thyroid hormone values are necessary to establish the
may be delayed from several days to as long as 6 to 12 weeks. proper dosage.
Effects include a return to normal thyroid function: weight gain, Antithyroid medications interact with many other drugs.
reduction in anxiety, less insomnia, and slower pulse rate. For example, propylthiouracil can reverse the effectiveness
of drugs such as aminophylline, anticoagulants, and cardiac
Adverse Effects and Interactions: Overtreatment with propyl- glycosides.
thiouracil produces symptoms of hypothyroidism. In addition,
Nursing Process Focus Patients Receiving Thyroid Hormone Replacement

Prior to administration: ■ Activity Intolerance related to decrease in levels of thyroid hormones

■ Obtain a complete health history, including cardiovascular, neurologi- ■ Fatigue related to impaired metabolic status
cal, renal and liver conditions; pregnancy, allergies, drug history, and ■ Deficient Knowledge related to a lack of information about drug
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, renal ■ Infective Health Maintenance related to adverse effects of drug
and liver function studies, T4, T3, and TSH levels. therapy
■ Acquire the results of a complete physical examination, including vital ■ Risk for Infection related to adverse effects of drug therapy
signs, height, weight, and ECG.
The patient will:

■ Experience therapeutic effects of drug regimen (normal thyroid levels).
Implementation
■ Administer medication correctly and evaluate the patient’s knowl- ■ Instruct the patient about the disease, the importance of taking the
edge of proper administration. In addition, monitor the patient for medication regularly each day, and the importance of follow-up care.
signs of decreased compliance with therapeutic regimen. (Proper
administration and compliance helps to ensure adequate thyroid
hormone levels and a decrease in adverse effects.)
■ Monitor vital signs. (Changes in metabolic rate will be manifested Instruct the patient to:
as changes in blood pressure, pulse, and body temperature.) ■ Take and record pulse rate two to three times a week.
■ Report to the healthcare provider any dizziness, palpitations, and an
intolerance to temperature changes.
■ Monitor for symptoms related to hypothyroidism, such as fatigue, ■ Instruct the patient about the signs of hypothyroidism and to report
constipation, cold intolerance, lethargy, depression, and menstrual symptoms to the healthcare provider.
irregularities. (Decreasing symptoms will help determine effectiveness
of hormone replacement hormone.)
■ Monitor for symptoms related to hyperthyroidism, such as nervous- ■ Instruct the patient about the signs of hyperthyroidism and to report
ness, irritability, insomnia, tachycardia, palpitations, weight loss, symptoms to the healthcare provider.
hyperthermia, and heat intolerance. (Symptoms of hyperthyroidism
may indicate overuse or adverse effect of hormone replacement
medication.)
■ Monitor T3, T4, and TSH levels. (This helps to determine need or Instruct the patient:
effectiveness of drug therapy.) ■ About the importance of ongoing monitoring of thyroid hormone
levels.
■ To keep all laboratory appointments.
continued . . .
■ Monitor blood glucose levels, especially in individuals with diabetes ■ Instruct the patient with diabetes to monitor blood glucose levels
mellitus. (Thyroid hormones increase metabolic rate and may alter and adjust insulin doses as directed by the healthcare provider.
glucose utilization.)
■ Provide supportive nursing care to cope with symptoms of hypothy- Instruct the patient to:
roidism such as constipation, cold intolerance, and fatigue until the ■ Increase fluid and fiber intake, as well as activity, to reduce
drug has achieved therapeutic effect. (Providing care will ensure constipation.
patient comfort and enable the nurse to monitor sign/symptoms.) ■ Wear additional clothing and maintain a comfortable room
environment for cold intolerance.
■ Plan activities and include rest periods to avoid fatigue.
■ Monitor weight at least weekly. (Weight loss or gain may indicate Instruct the patient to:
disease process and helps to determine the effectiveness of drug ■ Take and record weight weekly.
therapy.) ■ Report significant changes in weight to the healthcare provider.
■ Unless approved by the healthcare provider, avoid iodine-containing ■ Provide dietary instruction on foods to avoid.
foods such as soy sauce, tofu, milk, eggs, yogurt, and some fish.
(Increasing or decreasing normal intake of these foods may result
in adverse drug effects.)
Adrenal disorders
Corticosteroids are released during periods of stress and influence

Core Concept 32.7 carbohydrate, lipid, and protein metabolism in most cells.
Though small, the adrenal glands secrete hormones that affect almost every body tissue. Adrenal disor-
ders include those resulting from either excess hormone production or deficient hormone production. The
specific pharmacotherapy depends on which portion of the adrenal gland is being affected. There are two
mineralo 5 minerals major portions of the adrenal glands: the outer cortex and the inner medulla. The outer cortex releases three
(i.e., sodium, potassium) important classes of hormones: the mineralocorticoids, glucocorticoids, and androgens. Collectively, these
hormones are referred to as corticosteroids or adrenocortical hormones.
cortic/cortico 5 cortex
Control of corticosteroids begins with corticotropin-releasing factor (CRF), secreted by the hypothala-
tropin/tropic 5 attraction
toward mus. CRF travels to the pituitary, where it causes the release of adrenocorticotropic hormone (ACTH).
adreno 5 adrenal glands ACTH then travels through the bloodstream and reaches the adrenal cortex, causing the adrenal gland to
release cortisol and other important corticosteroids. When the level of corticosteroids in the bloodstream
rises, it provides negative feedback to the hypothalamus and pituitary to shut off further release of cortico-
steroids. This negative feedback mechanism is shown in Figure 32.4 ■.
Aldosterone accounts for most of the mineralocorticoids secreted by the adrenal glands. Mineralo-
corticoids regulate the extracellular concentrations of mineral salts, particularly sodium and potassium, in
the body. Aldosterone is the principle mineralocorticoid. The primary function of aldosterone is to regulate
plasma volume by promoting sodium reabsorption and potassium secretion by the renal tubules. When
hyper 5 elevated plasma volume falls, the kidney secretes renin, which results in the production of angiotensin II. Angio-
natri 5 sodium tensin II then causes aldosterone secretion, which promotes sodium retention (hypernatremia) and water
emia 5 blood levels retention. Attempts to modify this pathway led to the development of the angiotensin-converting enzyme
tension 5 blood pressure (ACE) inhibitor class of medications, which are often preferred drugs for treating hypertension and heart
failure (see Chapters 18 and 19).
gluco/glyc 5 sugar Cortisol is one of numerous glucocorticoids secreted from the outer portion, or cortex, of the adrenal
al/oid 5 resembling gland. Glucocorticoids affect the metabolism of nearly every cell in the body. During long-term stress,
these hormones increase the level of blood glucose (hyperglycemia) and promote the breakdown of pro-
neo 5 new teins and lipids for energy (gluconeogenesis). They have a potent anti-inflammatory effect and they sup-
press the immune response (Chapters 24 and 29).
Figure 32.4
Circadian rhythms Stress Feedback control of the

adrenal cortex.
Hypothalamus
CRF
2
1
Anterior pituitary
Negative
ACTH feedback
1
2
Adrenal cortex
Corticosteroids
1 Stimulation
Negative
Biological effects feedback
The gonadocorticoids secreted by the adrenal cortex are mostly androgens (male sex hormones), gonado 5 gonads (e.g., sex
though small amounts of estrogens (female sex hormones) are also produced. The amounts of these hor- organs)
mones are far less than the levels secreted by either the testes or ovaries. The physiological effects of andro 5 male hormones
androgens and estrogens are detailed in Chapter 34. estro 5 female hormones
gens/genesis 5 synthesized
Corticosteroids are prescribed for adrenocortical insufficiency

and to dampen inflammatory and immune responses. Core Concept 32.8
Symptoms of adrenocortical insufficiency include hypoglycemia, unusual fatigue, orthostatic hypotension,

darkening skin pigmentation, joint pain, and GI disturbances such as anorexia, vomiting, and diarrhea.
Low plasma levels of cortisol, accompanied by high plasma levels of ACTH indicate that the adrenal
gland is not responding to ACTH stimulation. Primary adrenocortical insufficiency, known as Addison’s
disease, is quite rare and includes a deficiency of both glucocorticoids and mineralocorticoids. Secondary
adrenocortical insufficiency is more common than primary and can occur when corticosteroids are sud-
denly withdrawn during pharmacotherapy.
When corticosteroids are taken as medications for prolonged periods, they provide negative feedback
to the pituitary to stop secreting ACTH. Without stimulation by ACTH, the adrenal cortex shrinks and
stops secreting endogenous corticosteroids, a condition known as adrenal atrophy. If the corticosteroid a 5 without
medication is abruptly discontinued, the shrunken adrenal glands will not be able to secrete sufficient cor- trophy 5 nourishment
ticosteroids, and symptoms of adrenocortical insufficiency will appear. Gradual withdrawal of cortico-
steroids allows adrenal glands to resume normal function. The goal of replacement therapy is to achieve
the same physiologic level of corticosteroids in the blood that would be present if the adrenal glands were
functioning properly. Patients requiring replacement therapy must take corticosteroids their entire lifetime,
and concurrent therapy with a mineralocorticoid such as fludrocortisone (Florinef) is essential. Selected
corticosteroids are listed in Table 32.4 ◆.
Table 32.4 Selected Corticosteroids

short acting
cortisone PO; 20–300 mg/day IM form available; has mineralocorticoid activity
hydrocortisone (Cortef, PO; 10–320 mg/day in three to four divided doses Topical form available; has both glucocorticoid and
Solu-Cortef) IV/IM; 15–800 mg/day in three to four divided mineralocorticoid activity
doses (max: 2 g/day)
Intermediate Acting
methylprednisolone (Depo- PO; 2–60 mg one to four times per day IV and IM forms available; has little mineralocorticoid
Medrol, Medrol, others) activity
prednisolone PO; 5–60 mg one to four times per day IV and IM forms available; has little mineralocorticoid activity
prednisone (see page 369 PO; 5–60 mg one to four times per day Has little mineralocorticoid activity
for the Prototype Drug box)
triamcinolone (Aristospan, PO; 4–48 mg one to two times per day IV, intra-articular, subcutaneous, topical, inhalation, and
Kenalog) IM forms available; has little mineralocorticoid activity
Long Acting
betamethasone (Celestone, PO; 0.6–7.2 mg/day IV, topical, and IM forms available; has little
Diprolene, others) IM; 0.5–9 mg/day mineralocorticoid activity
dexamethasone IM; 8–16 mg bid–qid IV, ophthalmic, topical, intranasal, inhalation, and IM
PO; 0.25–4 mg bid–qid forms available; has little mineralocorticoid activity
fludrocortisone (Florinef) PO; 0.1–0.2 mg/day Has strong mineralocorticoid activity
In addition to treating adrenal insufficiency, corticosteroids are prescribed for a large number of nonen-
docrine disorders. Their ability to suppress inflammatory and immune responses quickly and effectively gives
them tremendous therapeutic utility to treat a diverse set of conditions including shock, swelling, post-transplant
surgery, some cancers, allergies, asthma, inflammatory bowel disease, and some rheumatic and skin disorders.
Cushing’s syndrome occurs when high levels of corticosteroids are present in the body over a prolonged
period. Although hypersecretion of these hormones can be due to pituitary (due to excess ACTH) or adrenal
tumors, the most common cause of Cushing’s syndrome is long-term therapy with high doses of systemic
corticosteroids. Signs and symptoms include adrenal atrophy, behavioral changes, changes in vision, osteo-
porosis, hypertension, increased risk of infections, delayed wound healing, acne, peptic ulcers, fluid retention,
weight gain, and a redistribution of fat around the face (moon face) and shoulders and neck (buffalo hump).
Concept Review 32.2

■ Why does administration of corticosteroids for extended periods result in adrenal atrophy?
Drug Prototype: Hydrocortisone (Cortef, Hydrocortone, Others)

Therapeutic Class: Adrenal hormone replacement; drug for moderate to severe asthma and allergies, and
antineoplastic therapy Pharmacologic Class: Systemic corticosteroid
Actions and Uses: Structurally identical to the natural hormone of Cushing’s syndrome, which can develop with high doses. If
cortisol, hydrocortisone is a synthetic corticosteroid that is the taken for longer than two weeks, hydrocortisone should be
drug of choice for treating adrenocortical insufficiency. When discontinued gradually.
used for replacement therapy, it is given at physiologic doses. Hydrocortisone interacts with many drugs. For example,
Once proper dosing is achieved, its therapeutic effects should barbiturates, phenytoin, and rifampin may increase liver metab-
mimic those of natural corticosteroids. Hydrocortisone is also olism, thus decreasing hydrocortisone levels. Estrogens increase
available for the treatment of inflammation, allergic disorders, the effects of hydrocortisone. Nonsteroidal anti-inflammatory
and many other conditions. Intra-articular injections may be drugs (NSAIDs) increase the risk of ulcers. Cholestyramine and
given to decrease severe inflammation in affected joints. colestipol decrease hydrocortisone absorption. Diuretics and
amphotericin B increase hypokalemia. Anticholinesterase drugs
Adverse Effects and Interactions: When used at physiologic may produce severe weakness. Hydrocortisone may cause a
doses for replacement therapy, adverse effects of hydrocorti- decrease in immune response to vaccines and toxoids.
sone should not be evident. The patient and the healthcare Herbal supplements, such as aloe and buckthorn (a laxative),
professional must be vigilant, however, in observing for signs may cause potassium deficiency.
Nursing Process Focus Patients Receiving Systemic Corticosteroid Therapy

Prior to administration: ■ Risk for Infection related to immunosuppression

■ Obtain a complete health history, including cardiovascular, respiratory, ■ Risk for Injury related to adverse effects of drug therapy
neurological, renal, and liver conditions; pregnancy, allergies, drug ■ Deficient Knowledge related to a lack of information about drug
history, and possible drug interactions. therapy
■ Evaluate laboratory blood findings: CBC, electrolytes, glucose, lipid ■ Risk for Fluid Volume Excess related to fluid retention properties
panel, renal and liver function studies. of corticosteroids
■ Acquire the results of a complete physical examination, including ■ Risk for Electrolyte Imbalance related to adverse drug effects of
vital signs, height, and weight. drug therapy
■ Risk for Impaired Blood Glucose related to adverse effects of drug
therapy
The patient will:

■ Experience therapeutic effects (decreased signs and symptoms of inflammation or allergic response).
Implementation
of proper administration. Do not stop drug abruptly; tamper off over ■ Not stop taking corticosteroids abruptly and to notify the healthcare
a one- to two-week period. Monitor the patient’s compliance with the provider if unable to take drug for more than one day
drug regimen. (Improper use can cause an increase in adverse effects. ■ Use the self-administering tapering dose pack properly.
Sudden discontinuation of these drugs can precipitate an adrenal ■ Take oral medications with food.
crisis/insufficiency.)
■ Monitor vital signs. (Corticosteroids may cause increase in blood pres- Instruct the patient:
sure and tachycardia because of increased blood volume and potential ■ To report tachycardia, blood pressure over 140/90, dizziness,
vasoconstriction effect.) palpitations, or headaches to the healthcare provider.
■ How to use blood pressure monitoring equipment properly.
■ Monitor for infection. Protect the patient from potential infections. Instruct the patient to:
(Corticosteroids increase susceptibility to infections by suppressing ■ Avoid people with infections.
the immune response.) ■ Report signs of infection: fever, cough, sore throat, joint pain,
increased weakness, rash, white patches in mouth, and malaise to the
■ Consult with the healthcare provider before taking any
immunizations.
■ Monitor for symptoms of Cushing’s syndrome, such as moon face, Instruct the patient:
“buffalo hump” contour of shoulders, weight gain, muscle wasting, ■ To weigh self daily.
and increased deposits of fat in the trunk. (Symptoms may indicate ■ That initial weight gain is expected; provide the patient with
excessive use of corticosteroids.) weight-gain parameters that warrant reporting.
■ That there are multiple adverse effects to therapy and that changes
in health status should be reported to the healthcare provider.
■ Monitor blood glucose levels. (Corticosteroids cause an increase in glu- Instruct the patient to:
cose formation [gluconeogenesis] and a decrease in glucose utilization ■ Report symptoms of hyperglycemia, such as excessive thirst, copious
causing hyperglycemia.) urination, and insatiable appetite to the healthcare provider.
■ Adjust insulin dose based on blood glucose level, as directed by the
■ Monitor skin and mucous membranes for lacerations, abrasions, or Instruct the patient to:
breaks in integrity. (Corticosteroids impair wound healing.) ■ Examine skin daily for cuts and scrapes and to cover any injuries with
sterile bandage.
■ Watch for symptoms of skin infection such as redness, swelling, and
drainage.
■ Notify the healthcare provider of any nonhealing wound or
symptoms of infection.
■ Monitor GI status: evidence of ulcers, GI bleeding. (Corticosteroids Instruct the patient to

decrease gastric mucus production and predispose patients to peptic ■ Report GI adverse effects such as heartburn, dizziness, abdominal
ulcers.) pain, blood in emesis, or tarry stools to the healthcare provider.
■ Take drug with food or milk to decrease GI irritation.
■ Avoid or eliminate alcohol.
continued . . .
■ Continue to monitor periodic laboratory work: CBC, electrolytes Instruct the patient to:
glucose, lipid panel, liver and renal function studies. (Corticosteroids ■ Consume a diet high in protein, calcium, and potassium but low in
can cause hypernatremia and hypokalemia.) fat and concentrated simple carbohydrates.
■ Keep all laboratory appointments.
■ Monitor changes in the musculoskeletal system. (Corticosteroids Instruct the patient:

decrease bone density and strength and cause muscle atrophy and ■ That the drug may cause weakness in bones and muscles; avoid
weakness.) strenuous activity that may cause injury.
■ To participate in weight-bearing exercise or physical activity to help
maintain bone and muscle strength.
■ To maintain adequate calcium in diet.
■ Monitor emotional status. (Corticosteroids may produce mood and ■ Instruct the patient that mood changes may be expected and to report
behavior changes such as depression or feeling of invulnerability.) excessive mood swings or unusual changes in mood to the healthcare
provider.
■ Monitor vision periodically. (Corticosteroids may cause increased Inform the patient to:
intraocular pressure and an increased risk of glaucoma and cataracts.) ■ Have regular eye exams twice a year.
■ Immediately report any eye pain, halos, inability to focus, or
diminished or blurring vision to the healthcare provider.
■ Weigh patient daily and report increasing peripheral edema. (Daily ■ Instruct the patient to weigh self daily at the same time every day
weight is an accurate measure of fluid status.) and to report a gain of two pounds per day or presence of or
increase in edema.

Patients treated for endocrine disorders need to know the following:
Regarding Hypothalamic and Pituitary Drugs

1. Patients taking GH should record height and weight weekly. Records should be brought
to the healthcare provider each visit.
2. A diary of nighttime sleep habits and any bed-wetting should be kept and provided to
3. Patients should be aware of drug costs, especially when taking ADH and GH drugs.
Regarding Thyroid Medications

4. Pulse rates should be taken regularly because they are a good indicator of the effec-
tiveness of thyroid medications. If the pulse rate consistently exceeds 100 or any other
significant change is noted, contact the healthcare provider.
5. Because finding the correct dosage of thyroid hormone often takes several months,
do not change the prescribed dose without being advised to do so by a healthcare
provider.
Regarding Corticosteroids
6. When taking oral corticosteroids for more than two weeks, do not miss doses or discon-
tinue the drug without consulting a healthcare provider.
7. See a physician if any infections, cuts, or injuries appear to be healing too slowly while
on corticosteroids.
8. If taking hydrocortisone for replacement therapy, take the medication between 6:00 a.m.
and 9:00 a.m. because this is the time when natural corticosteroids are released.
Chapter Review 525
Chapter Review
32.1 The endocrine system maintains homeostasis by thyroid hormone, which is essential for normal growth
using hormones as chemical messengers. and development. Adequate hormone levels are neces-
Hormones are secreted by endocrine glands in sary for infants, children, and adults. Thyroid hormone
response to changes in the internal environment. The is a combination of two different hormones, thyroxine
hormones act on their target cells to return the body and triiodothyronine, both of which require iodine for
to homeostasis. Negative feedback prevents the body their synthesis.
from overresponding to internal changes.
32.6 Thyroid disorders may be treated by administering
32.2 The hypothalamus and the pituitary gland secrete thyroid hormone or by decreasing the activity of
hormones that control other endocrine organs. the thyroid gland.
The hypothalamus secretes releasing hormones that Hypothyroidism produces symptoms such as slowed
signal the anterior pituitary gland to release its hor- body metabolism, slurred speech, bradycardia, weight
mones. Pituitary hormones travel throughout the gain, low body temperature, and intolerance to cold
body to affect many other organs. environments. Administration of thyroid hormone
reverses these effects. Hyperthyroid patients exhibit
32.3 Hormones are used as replacement therapy, as the opposite symptoms. Hyperthyroidism may be
antineoplastics, or as “antihormones” to block treated with drugs that kill or inactivate thyroid cells.
endogenous actions.
Hormones are often given as replacement therapy to 32.7 Corticosteroids are released during periods of
patients who are not able to secrete sufficient quanti- stress and influence carbohydrate, lipid, and pro-
ties of endogenous hormones. In high doses, several tein metabolism in most cells.
hormones may be used as antineoplastics. Hormones The adrenal cortex secretes corticosteroids in response
may also be used therapeutically to block natural to stimulation by ACTH from the pituitary gland.
physiologic effects. Corticosteroids affect the metabolism of nearly every
cell in the body and have potent anti-inflammatory
32.4 Of the many pituitary and hypothalamic hor- effects.
mones, several have clinical applications as drugs.
Growth hormone, or somatotropin, is used to increase 32.8 Corticosteroids are prescribed for adrenocortical
the height of children with growth hormone deficien- insufficiency and to dampen inflammatory and
cies. ADH, or vasopressin, increases water reabsorp- immune responses.
tion in the kidney and is used to treat diabetes insipidus. Corticosteroids are given to patients whose adrenal
glands are unable to produce adequate amounts of
32.5 The thyroid gland controls the basal metabolic rate these hormones and for a wide variety of other condi-
and affects virtually every cell in the body. tions. When used at high doses, oral therapy is limited
TSH released from the pituitary gland stimulates because of the potential for producing Cushing’s syn-
release of thyroid hormone. The thyroid gland secretes drome and adrenal atrophy.
Review Questions
The following questions are written in NCLEX-PN® style. Answer 2. The nurse is assisting a patient with chronic adrenal insuf-
these questions to assess your knowledge of the chapter material, ficiency to make a medication plan for an upcoming camping
and go back and review any material that is not clear to you. trip. He is taking hydrocortisone (Cortef) and fludrocortisones
(Florinef) as replacement therapy. Which detail does this
1. The patient, who has been diagnosed with adrenal insuf- patient need to remember?
ficiency, has been started on corticosteroids. The nurse explains
that at high doses, and for long periods of time, these drugs 1. Take his blood pressure once or twice a day.
may cause symptoms like those seen in ________________. 2. Avoid crowded indoor areas to avoid infections.
3. Have his vision check before he leaves.
1. Cushing’s syndrome 4. Make sure to carry extra medication in case there is a delay
2. Graves’ disease in getting home.
3. Diabetes insipidus
4. Diabetes mellitus
3. A patient is being treated with propylthiouracil (PTU) for 7. A patient will be started on desmopressin (DDAVP) for
hyperthyroidism while awaiting a thyroidectomy. While the treatment of diabetes insipidus. Which instruction should the
patient is taking this drug, what symptoms will the nurse tell nurse include in the patient teaching plan?
the patient to report to the healthcare provider? 1. Drink plenty of fluids, especially those high in calcium.
1. Tinnitus, altered taste, thickened saliva 2. Avoid close contact with children or pregnant women for
2. Insomnia, nightmares, night sweats one week after administration of the drug.
3. Sore throat, chills, low-grade fever 3. Obtain and record your weight daily.
4. Dry eyes, decreased blinking, reddened conjunctiva 4. Wear a mask if around children and pregnant women.
4. The physician ordered Vasopressin 5 units subcuta- 8. The patient has been started on desmopressin (DDAVP).
neously, bid, for a patient. The pharmacy has Vasopressin The nurse understands the medication is effective when the
20 units/mL. How many milliliters will the nurse administer patient’s:
per dose? 1. Urinary output increases.
1. 0.5 mL 2. Blood pressure falls below 90/60.
2. 0.25 mL 3. Blood sugar level is between 80 and 120 mg/dL.
3. 0.75 mL 4. Urinary output decreases.
4. 1 mL
9. The nurse will be talking with the parents of a child who
5. The patient has been on methylprednisolone (Medrol) for has been prescribed somatropin (Humatrope). The nurse should
an exacerbation of asthma. Which of the following instructions inform the parents that:
to the patient is of the highest priority? 1. The drug must be given by injection.
1. “This medication may cause weight gain.” 2. The drug must be given regularly to prevent mental
2. “Do not stop taking this medication abruptly.” deficiencies.
3. “This medication can cause sleeplessness.” 3. If the drug is given during late adolescence, it could add
4. “This medication may cause restlessness.” 6 to 8 inches to the child’s height.
4. Daily laboratory monitoring will be required during the
6. An older adult with chronic bronchitis has been taking first weeks of therapy.
a low dose of dexamethasone for several months. In order to
reduce the risk of osteoporosis, an adverse effect, the nurse 10. A nurse is helping to prepare a teaching plan for a patient
informs the patient to: (Select all that apply.) who will be discharged on methylprednisolone (Medrol
1. Perform weight-bearing exercises at least three to four Dosepak) after a significant response to poison ivy. The nurse
times a week. includes which of the following information about the adverse
2. Increase dietary intake of calcium and vitamin D enriched effects of this medication: (Select all that apply.)
foods. 1. Tinnitus
3. Remain sedentary except during periods of exercise. 2. Edema
4. Increase fluid intake, including carbonated sodas, but avoid 3. Visual changes
alcohol. 4. Lower abdominal pain
Remember Mrs. Brookfield, the indicate that she has hypothyroidism. She is prescribed levo-
patient introduced at the beginning of thyroxine (Synthroid) 100 mcg/day.
the chapter? Now read the remainder
of the case study. Based on the infor- 1. The nurse explains to Mrs. Brookfield that the adverse
mation you have learned in this chap- effects of levothyroxine (Synthroid) are: (Select all that apply.)
ter, answer the questions that follow. 1. Constipation
2. Weight gain
Mrs. Helen Brookfield is a 42-year-old mother of two children 3. Tachycardia
who works full time at a department store. She has been feeling 4. Insomnia
very tired, gaining weight, and says she feels cold all the time.
Because of this, she saw the doctor several weeks ago. At that 2. The nurse also instructs Mrs. Brookfield:
visit, the physician ordered some laboratory tests including T3, 1. To take the pill in the afternoon with a high fiber snack to
T4, and TSH. She has returned to the office today to discuss her prevent stomach upset
continuing symptoms and lab results. Her vital signs are 94/60, 2. To eat plenty of fruits and vegetables to replace nutrients
58 (pulse), and a temperature of 36.3°C (97.4°F). Her weight 3. To take the dose in the morning before breakfast, as close
has increased 30 pounds over the past 6 months, but she says to the same time each day as possible
that her appetite has decreased. The symptoms and lab results 4. That the drug may be taken every other day if diarrhea occurs
Chapter Review 527
3. Mrs. Brookfield has been on levothyroxine (Synthroid) 1. Mrs. Brookfield is still experiencing symptoms of hypothy-
100 mcg/day. The nurse recognizes the medication is being roidism and the dose may need to be increased.
effective when the: 2. Mrs. Brookfield’s thyroid is now functioning normally and
1. Patient sleeps more hours per day. levothyroxine is no longer needed.
2. Patient’s weight increases. 3. Mrs. Brookfield has developed diabetes and needs further
3. Patient’s pulse rate increases. evaluation.
4. Patient states she feels tired. 4. Mrs. Brookfield is experiencing symptoms of hyperthy-
roidism and the drug dosage needs to be decreased.
4. A month later, Mrs. Brookfield reports feeling nervous
and is having occasional palpations and tremors. The nurse rec-
ognizes that these symptoms may indicate that:

C
“I’ve always felt OK but
h recently I’ve been feeling
a sluggish. Now I learn that
p my sugar levels are high.”
t Mr. Brian Jones
e
r
33 Drugs for Diabetes Mellitus
Core Concepts
33.1 The pancreas is responsible for the regulation of 33.4 Type 2 diabetes is the most common form of the
blood glucose levels. disorder.
33.2 Type 1 diabetes is caused by a deficiency in insulin. 33.5 Antidiabetic drugs are prescribed after diet and
33.3 Insulin replacement therapy is required for exercise have failed to reduce blood glucose to
type 1 diabetes. normal levels.
Drug snapshot
Insulin r egular insulin (Humulin R,
Novolin R) 532
Antidiabetic drugs for etformin (Fortamet,

m
Type 2 diabetes Glucophage, Glumetza,
others) 537
Learning Outcomes
1. Explain how blood glucose levels are 4. Describe the signs and symptoms of 7. For each of the classes listed
maintained within narrow limits by insulin overdose and underdose. in the Drug Snapshot, identify
insulin and glucagon. 5. Explain the cause of type 2 diabetes representative drug examples
2. Explain the cause of type 1 diabetes mellitus. and explain their mechanisms of
mellitus. drug action, primary actions, and
6. Compare and contrast the drug classes important adverse effects.
3. Compare and contrast types of insulin. used to treat type 2 diabetes mellitus.
Key Terms
diabetic ketoacidosis (DKA) (KEY-toe- hypoglycemic effect (hi-po-gli- insulin resistance 534
assi-doh-sis) 530 SEEM-ik) 529 islets of Langerhans (EYE-lits of LANG-
diabetic ketoacids (KEY-toe-ass-ids) 530 incretin–glucose control mechanism 537 gur-hans) 529
glucagon (GLUE-kah-gon) 529 incretins (EN-kreh-tenz) 537 type 1 diabetes mellitus (die-uh-BEE-tees
hyperglycemic effect (hi-pur-gli- insulin (IN-sule-in) 529 MEL-uh-tiss) 530
SEEM-ik) 529 insulin analogs (ANNAH-logs) 531 type 2 diabetes mellitus 534
D iabetes is one of the leading causes of death in the United States. Mortality due to diabetes has
been steadily increasing, causing concern among public health officials and the general public.
Diabetes can lead to serious complications, including heart disease, stroke, blindness, kidney fail-
ure, and amputations. Since healthcare providers frequently care for patients with diabetes, it is imperative
that its treatment and possible complications are well understood.
The pancreas is responsible for the regulation of blood glucose levels. Core Concept 33.1
Located behind the stomach and between the duodenum and spleen, the pancreas is an organ that is
essential to function of both the digestive and the endocrine systems. It is responsible for the secretion of
enzymes that assist in the chemical digestion of nutrients in the duodenum. This is the exocrine function of exo 5 out/away from
the pancreas. Clusters of cells in the pancreas, called islets of Langerhans, are responsible for the secre- crine 5 to secrete
tion of hormones, glucagon, and insulin. This is the pancreas’ endocrine function (Figure 33.1 ■). endo 5 within
Glucose is one of the body’s most essential molecules. The body prefers to use glucose as its primary
energy source: The brain relies almost exclusively on glucose for its energy needs. Because of this need,
blood levels of glucose must remain relatively constant throughout the day. Although many factors con-
tribute to maintaining a stable blood glucose level, the two pancreatic hormones play major roles: insulin
acts to decrease blood glucose levels and glucagon acts to increase blood glucose levels (Figure 33.2 ■). gluco 5 glucose
Following a meal, the pancreas recognizes the rising blood glucose level and releases insulin. Without
insulin, glucose stays in the bloodstream and is not able to enter cells of the body. Cells may be virtually
surrounded by glucose but they are unable to use it until insulin arrives. Insulin acts like a gateway for the
entry of glucose into the cell. Thus, insulin is said to have a hypoglycemic effect, because its presence hypo 5 lowered
causes glucose to leave the bloodstream, and therefore blood glucose falls. Some of the glucose is stored as glyc 5 sugar
glycogen in the liver, where it can be converted back to glucose between meals. emic 5 blood
The pancreas also secretes glucagon, which has the opposite effect of insulin. When levels of blood
glucose fall, glucagon is secreted. Glucagon’s primary function is to maintain adequate blood levels of glu-
cose between meals. Thus, glucagon has a hyperglycemic effect, because it causes glucose in the blood- hyper 5 elevated
stream to rise. The physiological actions of glucagon are essentially opposite of insulin.
Type 1 Diabetes Mellitus
Type 1 diabetes is caused by a deficiency in insulin. Core Concept 33.2
Diabetes mellitus (DM) is a metabolic disorder in which there is deficient insulin secretion or decreased
sensitivity of insulin receptors on target cells. Without insulin present, glucose is prevented from entering
the cells and builds to high levels in the blood; thus, hyperglycemia is the hallmark characteristic of DM.
The causes of DM include a combination of genetic and environmental factors. The recent increase in the
frequency of the disease is probably the result of trends toward more inactive and stressful lifestyles and
increasing consumption of foods with higher calories. According to the International Diabetes Federation,
diabetes and obesity are among the biggest public health challenges of the 21st century.
Figure 33.1
Microscopic view of
glucagon- and insulin-
secreting cells in the
islets of Langerhans.
ALPHA CELL
Glucagon-
secreting
cell
BETA CELL Islet of

Insulin- Langerhans
secreting in pancreas
cell
Glucagon—raises blood glucose level

Insulin—lowers blood glucose level
530 Chapter 33 Drugs for Diabetes Mellitus
Figure 33.2
Insulin, glucagon, and
blood glucose levels. High blood glucose Low blood glucose
Pancreas releases Pancreas releases

insulin glucagon
Liver produces Liver breaks

Cells take glycogen down glycogen
up glucose
from blood
Blood glucose falls Blood glucose rises
(a) (b)
Fast Facts Diabetes Mellitus

■ Of the 26 million Americans over age 20 who have diabetes, 7 million are unaware that they have
the disease.
■ Gestational diabetes affects about 5% to 10% of all pregnant women in the United States each
year.
■ Diabetes is the seventh leading cause of death; the risk of death among people with diabetes is
twice that of people of similar age without diabetes.
■ Diabetes is the leading cause of blindness in adults.
■ Diabetes is responsible for 60% of nontraumatic lower-limb amputations; over 65,000 amputations
are performed each year on patients with diabetes.
dia 5 through (e.g., siphon) Type 1 diabetes mellitus is one of the most common diseases of childhood. Type 1 DM was pre-
betes 5 to go viously called juvenile-onset diabetes. It is often diagnosed in children between the ages of 11 and 13.
mellitus 5 sweet Because approximately one-fourth of patients with type 1 DM develop the disease in adulthood, this is
not the most accurate name for this disorder. This type of diabetes is also sometimes referred to as insulin-
dependent diabetes mellitus because with this disorder the pancreas does not produce insulin.
The signs and symptoms of type 1 DM are consistent from patient to patient. The typical signs and
symptoms are fasting blood glucose greater than 126 mg/dL on at least two separate occasions, polyuria
poly 5 excessive (excessive urination), polyphagia (increased hunger), polydipsia (increased thirst), glucosuria (high levels
phagia 5 hunger of glucose in the urine), weight loss, and fatigue.
dipsia 5 thirst When glucose is unable to enter cells, lipids are used as the primary energy source and ketoacids
glucos 5 glucose are produced as waste products. These ketoacids can give the patient’s breath an acetone-like, fruity odor.
uria 5 urination More importantly, high levels of ketoacids lower the pH of the blood, causing diabetic ketoacidosis
keto 5 ketone chemical (DKA). Untreated DM produces long-term damage to arteries, which leads to heart disease, stroke, kidney
compound (e.g., acetone) disease, and blindness. Lack of adequate circulation to the feet may cause gangrene of the toes, requiring
acids/acidosis 5 state of amputation. Nerve degeneration, or neuropathy, is common, with symptoms ranging from tingling in the
lowered pH fingers or toes to complete loss of sensation of a limb.
Insulin replacement therapy is required for type 1 diabetes. Core Concept 33.3
Patients with type 1 DM are severely deficient in insulin production; thus, insulin replacement therapy is
required in normal physiological amounts. Insulin is also required for those with type 2 diabetes who are
unable to manage their blood glucose levels with diet, exercise, and antidiabetic drugs.
Because normal insulin secretion varies greatly in response to daily activities such as eating and
exercise, glucose monitoring and insulin administration must be carefully planned along with proper
meal planning and lifestyle habits. The desired outcome of insulin therapy is to prevent the long-term
consequences of the disorder by strictly maintaining blood glucose levels within the normal range.
Poor compliance (not properly monitoring glucose levels or skipping insulin injections) can lead to
continuing hyperglycemia and even death. Illness and stress can also cause an increase in blood glu-
cose levels.
Many types of insulin are available, differing in their source, time of onset and peak effect, and dura-
tion of action. Until the 1980s, the source of all insulin was beef or pork pancreas. Almost all insulin today,
however, is human insulin obtained through recombinant DNA technology because it is more effective,
causes fewer allergies, and has a lower incidence of resistance. Pharmacologists have modified human
insulin to create forms that have a more rapid onset of action or a more prolonged duration of action. These
modified forms are called insulin analogs. All the different types of insulin are administered by the subcu-
taneous route and are listed in Table 33.1 ◆.
Doses of insulin are highly individualized for the precise control of blood glucose levels in each
patient. Some patients require two or more injections daily for proper diabetes management. If mixing
insulin, such as rapid or short acting with an intermediate acting, the rapid or short-acting insulin is always
drawn into the syringe first. For ease of administration, some of these combinations are marketed in car-
tridges containing premixed solutions:
■ Humulin 70/30 and Novolin 70/30: contain 70% NPH insulin and 30% regular insulin
■ Humulin 50/50: contains 50% NPH insulin and 50% regular insulin
■ NovoLog Mix 70/30: contains 70% insulin aspart protamine and 30% insulin aspart
■ Humalog Mix 75/25: contains 75% insulin lispro protamine and 25% insulin lispro
Some patients may have an insulin pump (Figure 33.3 ■). This pump is usually abdominally anchored
and is programmed to release small subcutaneous doses of insulin into the abdomen at predetermined inter-
vals, with larger amounts administered manually at mealtime if necessary. Most pumps contain an alarm
that sounds to remind patients to take their insulin.
Adverse effects of insulin may include allergic reactions, redness at the site of injection, and changes
in fat tissue (lipodystrophy) in the areas of body where injections are given more frequently. However, the
most common adverse effect of insulin therapy is overtreatment: when insulin removes too much glucose
Table 33.1 Types of Insulin: Actions and Administration
Drug Action Onset Peak Duration Administration

insulin aspart (NovoLog) Rapid 15 minutes 1–3 hours 3–5 hours Subcutaneous; 5–10 minutes
before a meal
insulin lispro (Humalog) Rapid 5–15 minutes 0.5–1 hours 3–4 hours Subcutaneous; 5–10 minutes
before a meal
insulin glulisine (Apidra) Rapid 15–30 minutes 1 hours 3–4 hours Subcutaneous; 15 minutes before a meal
or within 20 minutes after starting a meal
insulin regular Short 30–60 minutes 2–4 hours 5–7 hours Subcutaneous; 30–60 minutes
(Humulin R, Novolin R) before a meal; IV in emergencies
insulin isophane (NPH, Intermediate 1–2 hours 4–12 hours 18–24 hours Subcutaneous; 30 minutes before first
Humulin N, Novolin N, ReliOn N) meal of the day and 30 minutes before eve-
ning meal, if necessary
insulin detemir (Levemir) Long Gradual: over 6–8 hours To 24 hours Subcutaneous; with evening meal or
24 hours at bedtime
insulin glargine (Lantus) Long Gradual; over N/A To 24 hours Subcutaneous; once daily, given at the
24 hours same time each day
Figure 33.3
Insulin pump pro-

grammed to release
insulin at prede-
termined intervals
throughout the day.
from the blood resulting in hypoglycemia. This occurs when a patient with type 1 diabetes has more insulin
in the blood than is needed to balance the amount of glucose in the blood. Hypoglycemia may occur when
insulin levels peak, during exercise, when the patient receives too much insulin due to medication error, or
if the patient skips a meal. Signs and symptoms of hypoglycemia include the sudden onset of pale, cool,
and moist skin; confusion; mild tremors; and dizziness, usually with blood glucose of less than 50 mg/dL.
Giving food or drinks containing glucose (sugar) can reverse mild to moderate hypoglycemia symp-
toms. Patients are encouraged to routinely carry candy or other readily absorbable carbohydrates, such as
crackers, to take at the first signs of a drop in blood glucose. For serious hypoglycemia, glucose can be
administered via the intravenous (IV) route. In addition, the hormone glucagon is also used in emergency
treatment. Glucagon can be administered IV, IM, or subcutaneously.
Drug Prototype: Regular Insulin (Humulin R, Novolin R)

Therapeutic Class: Drug for diabetes mellitus Pharmacologic Class: Hypoglycemic drug
Actions and Uses: Regular insulin is prepared as human insulin carbohydrates must be in the blood when insulin is injected;
through recombinant DNA technology. It is classified as short- otherwise the drug will remove too much glucose, and signs of
acting insulin, with an onset of action of 30 to 60 minutes, a hypoglycemia—tachycardia, confusion, sweating, and drowsiness—
peak effect at 2 to 3 hours, and a duration of 5 to 7 hours. Its will result. If severe hypoglycemia is not quickly treated with
primary action is to promote the entry of glucose into cells. For glucose, convulsions, coma, and death may follow.
the emergency treatment of acute ketoacidosis, it may be given Regular insulin interacts with many drugs. For example,
subcutaneously or IV. Regular insulin is also available as Humu- the following substances may increase hypoglycemic effects:
lin 70/30 (a mixture of 30% regular insulin and 70% isophane alcohol, salicylates, monoamine oxidase inhibitors (MAOIs),
insulin) or as Humulin 50/50 (a mixture of 50% of both regular and anabolic steroids. The following substances may decrease
and isophane insulin). hypoglycemic effects: corticosteroids, thyroid hormones, and
epinephrine. Serum glucose levels may be increased with furo-
Adverse Effects and Interactions: The most serious adverse semide or thiazide diuretics. Symptoms of hypoglycemic reac-
effect from insulin therapy is hypoglycemia. Hypoglycemia may tion may be hidden if beta blockers are used at the same time.
result from taking too much insulin, not properly timing the Use cautiously with herbal supplements such as garlic and
insulin injection with food intake, or skipping a meal. Dietary ginseng, which may increase the hypoglycemic effects of insulin.
Nursing Process Focus Patients Receiving Insulin Therapy

Prior to administration: ■ Risk for Unstable Blood Glucose Level related to lack of diabetes
■ Obtain a complete health history, including cardiovascular, vision, skin, management, unhealthy diet, inadequate glucose monitoring, or
neurological, renal, and liver conditions; allergies; drug history; and improper use of medication
possible drug interactions. ■ Risk for Injury related to blood glucose elevations, impaired
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, liver circulation, or adverse effects of drug therapy
and renal function studies, glucose, and HbA1C. ■ Deficient Knowledge related to a lack of information about the
■ Acquire the results of a complete physical examination, including vital disease process, medications, and need for lifestyle changes
signs, height, and weight; presence of paresthesia of hands or feet; ■ Risk for Imbalanced Nutrition related to adverse effects of drug
ulceration of lower extremities; and condition of skin at insulin therapy
injection sites. ■ Risk for Infection related to blood glucose elevations and impaired
■ Obtain a dietary history including caloric intake if on ADA diet, circulation
number of meals and snacks, fluid type, and amount of intake. ■ Ineffective Therapeutic Regimen Management related to noncompliance
■ Determine knowledge of diabetic medications, adverse effects, with medication regimen, presence of adverse effects, and lifelong need
self-administration, and blood glucose monitoring. for medication
■ Noncompliance related to the complexity of the medication regimen,
lifestyle changes, and adverse effects of drug therapy

The patient will:
■ Experience therapeutic effects (stable blood glucose levels).
■ Demonstrate an understanding of lifestyle modifications necessary for successful maintenance of drug therapy.
Implementation

■ Monitor blood glucose at least several times a day, usually before ■ Instruct the patient how to monitor blood glucose, including use of
meals. Hold or provide insulin per healthcare provider’s protocols. equipment, and when to notify the healthcare provider.
(Daily glucose levels will assist in maintaining stable blood glucose.)
■ Administer insulin as prescribed, planning administration around meal Inform patient or caregivers the:
or insulin peak times. In addition, evaluate the patient’s knowledge of ■ Correct administration techniques for type of insulin ordered. Have
proper administration. (Maintaining levels of insulin with meal times patient return demonstration.
or peak times will assist in maintaining stable blood glucose levels.) ■ Peak insulin levels and proper food sources needed to prevent both
hyper/hypoglycemia. Provide written materials for future reference.
■ Need to rotate insulin injection sites on a weekly basis to prevent
tissue damage.
■ Increase frequency of blood glucose monitoring if the patient is expe- Instruct the patient to:
riencing fever, nausea, vomiting, or diarrhea. (Illness usually requires ■ Increase blood glucose monitoring when experiencing fever, nausea,
adjustments in insulin doses.) vomiting, or diarrhea.
■ Notify the healthcare provider if unable to eat normal meals for a
possible change in insulin dose.
■ Continue to monitor periodic laboratory work: CBC, electrolytes, glu- Inform the patient:
cose, HbA1C, lipid profile, liver and renal function studies. (Insulin can ■ About the need to keep laboratory appointments.
cause potassium to move into the cell and may cause hypokalemia. ■ To report to the healthcare provider the first sign of heart irregularity.
Periodic monitoring assists in determining glucose control, need for
medication changes, and any indicators of complications.)
■ Monitor weight on a routine basis. (Changes in weight will alter ■ Instruct the patient to weigh self on a routine basis at the same time
insulin needs.) each day and to report to the healthcare provider any significant
changes (e.g., plus or minus 10 lb).
■ Monitor vital signs. (Increased pulse and blood pressure are early ■ Ensure that the patient knows how to take blood pressure and pulse
signs of hypoglycemia. Patients with diabetes may have circulatory and to report significant changes.
problems and/or impaired kidney function that can increase blood
pressure.)
■ Check for signs of hypoglycemia, especially around the time of insulin Advise the patient:
peak activity. If symptoms occur, provide quick-acting carbohydrate ■ To always carry a quick-acting carbohydrate source in case symptoms
source (juice or simple sugar) and then recheck blood glucose. (Using a of hypoglycemia occur.
simple sugar will raise blood sugar immediately.) ■ If unsure whether symptoms are hypo or hyper, treat as hypoglycemia,
wait 10–15 minutes then check glucose level.
■ If symptoms are not relieved or glucose is below 70 mg/dL, notify the
continued . . .

■ Encourage patient to increase physical activity gradually but continue Inform the patient:
to monitor blood glucose level before and after exercise. (Exercise ■ About the benefit of exercise.
assists muscle cells to use glucose more efficiently, lowering blood ■ To check blood glucose before and after exercise and to keep a simple
glucose. Effects may last up to 48 hours after activity, increasing risk of sugar on his or her person while exercising.
hypoglycemia.) ■ To eat some form of simple sugar or complex carbohydrate before
strenuous exercise as prophylaxis against hypoglycemia.
■ Ensure the proper storage of insulin to maintain potency. (Unopened ■ Inform the patient about proper storage of insulin.
vials may be stored at room temperature, avoiding direct sunlight and
heat. Opened vials may be stored at room temperature for up to one
month. Discard if any changes in solution are noted.)

Type 2 Diabetes Mellitus
Core Concept 33.4 Type 2 diabetes is the most common form of the disorder.
Type 2 diabetes mellitus is the more common form of the disorder. Because type 2 DM first appeared in
middle-aged adults, it has been referred to as adult-onset diabetes or maturity-onset diabetes. These are
inaccurate descriptions of this disorder, however, because increasing numbers of children are being diag-
nosed with type 2 DM. Type 2 is more common in patients who are overweight and those with low HDL-
asymptomatic 5 without cholesterol and high triglyceride levels. Patients with type 2 DM are often asymptomatic and may have the
having symptoms condition for years before their diagnosis.
Unlike patients with type 1 diabetes, some patients with type 2 are capable of secreting insulin,
although in amounts that are too small. However, the fundamental problem in type 2 is that insulin recep-
tors in the target tissues have become unresponsive to the hormone, a phenomenon called insulin resist-
ance. Essentially, the pancreas produces sufficient amounts of insulin, but target cells do not recognize it.
Whereas patients with type 1 diabetes must take insulin, those with type 2 diabetes are usually controlled
with antidiabetic drugs. In severe, unresponsive cases, insulin may also be necessary for patients with type
2 diabetes.
Cam Therapy
Omega-3 Fatty Acids and Diabetes
Omega-3 fatty acids are unsaturated fats found in fatty fish such as salmon, mackerel, and
tuna; vegetables oils such as canola and soybean; and nuts, green leafy vegetables, and beans.
Omega-3 fatty acids are essential to the body and necessary for regulating muscle function,
blood clotting, digestion, cell growth, and other functions.
Research has clearly shown that omega-3 fatty acids reduce inflammation and lower the
risk for cardiovascular disease. The research on type 2 diabetes is not as clear. Fish oils (which
contain high amounts of omega-3 fatty acids) lower triglyceride levels and decrease some
inflammatory markers that signal a risk for diabetes. Some studies suggest insulin sensitivity
may be increased. Other research, however, suggests that supplementation with omega-3
fatty acids does not improve the risk of developing cardiovascular disease in diabetic patients.
Because fish oils have the potential to raise blood sugar levels, all diabetic patients should
check with their healthcare provider before taking these supplements.
In many people as they get older, cells become more resistant to insulin, blood glucose levels rise,
and the pancreas responds by secreting even more insulin. Eventually, the hypersecretion of insulin causes
beta cell exhaustion and ultimately leads to beta cell death. As type 2 DM progresses, it becomes a disorder
characterized by insufficient insulin levels as well as insulin resistance. The long-term consequences of
untreated type 1 and type 2 diabetes are the same.
The activity of insulin receptors can be increased by physical exercise and lowering the level of circu-
lating insulin. In fact, adhering to a healthy diet and a regular exercise program has been shown to reverse
insulin resistance and delay or prevent the development of type 2 DM. Many patients with type 2 diabetes
are obese and need a medically supervised plan to help them reduce weight gradually and exercise safely.
This is an important lifestyle change for such patients; they will need to maintain these changes for the
remainder of their lives.
Antidiabetic drugs are prescribed after diet and exercise have

failed to reduce blood glucose to normal levels. Core Concept 33.5
Type 2 DM is usually controlled with noninsulin antidiabetic drugs. These drugs are sometimes referred
to as oral hypoglycemic drugs but this is an inaccurate name because some are given by the subcutaneous
route and some do not cause hypoglycemia.
The primary groups of antidiabetic drugs for type 2 DM are classified by their chemical struc-
tures and their mechanisms of action. These include alpha-glucosidase inhibitors, biguanides, incre- incretin 5 gut-derived
tin enhancers, meglitinides, sulfonylureas, and thiazolidinediones (or glitazones). Therapy with type
2 antidiabetic drugs is not effective for persons with type 1 DM. Antidiabetic drugs for type 2 DM are
Table 33.2 Antidiabetic Drugs for Type 2 Diabetes

Drug Route and Adult Dose DRUG Class Remarks
Alpha-Glucosidase Inhibitors
acarbose (Precose) PO; 25–100 mg tid (max: 300 mg/day), taken These drugs block an intestinal enzyme that breaks down com-
with the first bite of each meal plex carbohydrates into simple sugars. Avoid use in patients
miglitol (Glyset) PO; 25–100 mg tid (max: 300 mg/day), taken with chronic intestinal diseases; use cautiously in patients with
with the first bite of each meal renal impairment.
Biguanide
metformin PO; 500 mg two times per day or 850 mg Immediate-release forms and extended-release forms are
Immediate release (Gluco- once daily; increase to 1,000–2,550 mg in available. Lactic acidosis is a potential complication with this
phage, Riomet) two to three divided doses per day (max: medication.
2.55 g/day)
Extended release (Fortamet,
Glucophage XR, Glumetza) Fortamet: 1,000 mg once daily
(max: 2.5 g/day)
Glumetza: 1,000–2,000 mg once daily
(max: 2 g/day)
Glucophage XR: 500 mg once daily
(max: 2 g/day)
Incretin Enhancers
exenatide (Byetta) Subcutaneous; 5–10 mcg one to two times These drugs target a chemical called glucagon-like peptide
per day 60 minutes prior to a meal (GLP). Insulin release is stimulated and glucagon release is
linagliptin (Tradjenta) PO: 5 mg once daily inhibited. Nausea, diarrhea, headaches, and dizziness are com-
mon symptoms due to falling blood glucose levels. These drugs
liraglutide (Victoza) Subcutaneous: 0.6–1.8 mg once daily decrease appetite and promote weight loss. These drugs should
saxagliptin (Onglyza) PO: 2.5–5 mg once daily be taken or injected prior to meals.
sitagliptin (Januvia) PO; 100 mg once daily
(continued )
Table 33.2 Antidiabetic Drugs for Type 2 Diabetes (continued)

Drug Route and Adult Dose DRUG Class Remarks
Meglitinides
nateglinide (Starlix) PO; 60–120 mg tid, 1–30 minutes prior to These drugs stimulate the release of insulin from pancreatic
meals islet cells similar to sulfonylurea drugs.
repaglinide (Prandin) PO; 0.5–4 mg bid–qid, 1–30 minutes prior to
meals (max: 16 mg/day)
Sodium-glucose co-transporter 2 (SGLT2) inhibitor
canagliflozin (Invokana) PO; 100 mg taken before the first meal of SGLT2 is an enzyme in the kidney tubule that causes glucose to
the day; for additional glycemic control, may be reabsorbed from urine; this drug blocks the action of SGLT2
increase to 300 mg every day (patients who leading to more excretion of glucose in the urine.
have an effective glomerular filtration rate of
60 mL/min/1.73 m²)
Sulfonylureas, First Generation
chlorpropamide (Diabinese) PO; 100–250 mg/day (max: 750 mg/day) These drugs stimulate the release of insulin from pancreatic is-
tolazamide (Tolinase) PO; 100–500 mg one to two times per day let cells. Symptoms are hypoglycemia, weight gain, GI distress,
(max: 1 g/day) and liver toxicity.
tolbutamide (Orinase) PO; 250–1,500 mg one to two times per day

(max: 3 g/day)
Sulfonylureas, Second Generation
glimepiride (Amaryl) PO; 1–4 mg/day (max: 8 mg/day) Symptoms are similar to first-generation sulfonylureas except
glipizide (Glucotrol) PO; 2.5–20 mg one to two times per day that there are fewer drug–drug interactions. These drugs should
(max: 40 mg/day) be taken 30 minutes before breakfast.
glyburide (DiaBeta, Micronase) PO; 1.25–10 mg one to two times per day
(max: 20 mg/day)
glyburide micronized (Glynase) PO; 0.75–12 mg one to two times per day
(max: 12 mg/day)
Thiazolidinediones
pioglitazone (Actos) PO; 15–30 mg/day (max: 45 mg/day) Have been under review since 2007, due to the increased risk of
rosiglitazone (Avandia) PO; 2–4 mg one to two times per day heart failure with drugs in this class.
(max: 8 mg/day)
Miscellaneous Drug
bromocriptine (Cycloset) PO; 0.8–4.8 mg/day upon awakening Approved for Parkinson’s disease, pituitary adenoma, acro-
megaly, for women with amenorrhea, and infertility caused by
prolactin secretion.
The first oral hypoglycemics available, sulfonylureas are divided into first- and second-generation cat-
egories. Although drugs from both generations are equally effective at lowering blood glucose, the second-
generation drugs exhibit fewer drug–drug interactions. The sulfonylureas act by stimulating the release of
insulin from pancreatic islet cells and by increasing the sensitivity of insulin receptors on target cells.
Metformin (Glucophage) is the only drug in the biguanide drug class. Information on this drug is pre-
sented in the prototype feature box in this chapter.
The alpha-glucosidase inhibitors, which include acarbose (Precose) and miglitol (Glyset), act by
blocking enzymes in the small intestine that are responsible for breaking down complex carbohydrates into
monosaccharides. Because carbohydrates must be in the monosaccharide form to be absorbed, digestion of
glucose is delayed.
The thiazolidinediones, or glitazones, reduce blood glucose by decreasing insulin resistance and by
inhibiting hepatic production of glucose. Optimal lowering of blood glucose may take three to four months
of therapy. Liver function should be monitored, because thiazolidinediones may be hepatotoxic. Drugs in
this class contain black box warnings. In the summer of 2013, Food and Drug Administration (FDA) panel
experts voted to modify or remove measures that limited patient access to rosiglitazone. Under the FDA’s
risk-evaluation management strategy (REMS), this drug remains under close scrutiny due to the risk of
fluid retention and heart problems observed in some patients.
The meglitinides, repaglinide (Prandin) and nateglinide (Starlix), act by stimulating the release of
insulin from the pancreas in a manner similar to that of the sulfonylureas. Both drugs in this class have
short durations of action of two to four hours, and they are well tolerated.
Drug Prototype: Metformin (Fortamet, Glucophage, Glumetza, Others)

Therapeutic Class: Antidiabetic drug Pharmacologic Class: Hypoglycemic drug; biguanide
Actions and Uses: Metformin is a preferred antidiabetic drug Metformin is contraindicated in patients with impaired
for managing type 2 DM because of its effectiveness and safety. renal function. It is also contraindicated in patients with heart
It is used alone or in combination with other oral hypoglycemics failure, liver failure, history of lactic acidosis, or concurrent seri-
or insulin. It is approved for use in children age 10 or above. It is ous infection. It is contraindicated for two days prior to and two
available as immediate release and extended release. days after receiving IV radiographic contrast.
Metformin reduces glucose levels by decreasing the hepatic Alcohol increases the risk for lactic acidosis. Captopril,
production of glucose and reducing insulin resistance. It does furosemide, and nifedipine may increase the risk for hypoglyce-
not promote insulin release from the pancreas. A major advan- mia. The following drugs may decrease renal excretion of met-
tage of the drug is that it does not cause hypoglycemia. The formin: amiloride, cimetidine, digoxin, dofetilide, midodrine,
drug’s actions do not depend on stimulating insulin release, morphine, procainamide, quinidine, ranitidine, triamterene,
so it is able to lower glucose levels in patients who no longer trimethoprim, and vancomycin. Acarbose may decrease blood
secrete insulin. In addition to lowering blood glucose levels, it levels of metformin. Use with other antidiabetic drugs potenti-
lowers triglyceride and total and low-density lipoprotein (LDL) ates hypoglycemic effects. Metformin decreases the absorption
cholesterol levels, and it promotes weight loss. of vitamin B12 and folic acid. Garlic and ginseng may increase
Metformin is used off-label to treat women with polycystic hypoglycemic effects.
ovary syndrome. Women with this syndrome have insulin resis-
tance and high serum insulin levels. Black Box Warning:
Lactic acidosis is a rare, though potentially fatal, adverse
Adverse Effects and Interactions: The most common adverse effect of metformin therapy. The risk for lactic acidosis is
effects are GI related and include nausea, vomiting, abdominal increased in patients with renal insufficiency or any condi-
discomfort, metallic taste, diarrhea, and anorexia. It may also tion that puts them at risk for increased lactic acid produc-
cause headache, dizziness, agitation, and fatigue. Unlike the tion, such as liver disease, severe infection, excessive alcohol
sulfonylureas, metformin rarely causes hypoglycemia or weight intake, shock, or hypoxemia.
gain.
Several new drugs have been approved that act by the incretin–glucose control mechanism. Incretins hypox 5 lowered oxygen
are hormones secreted by the mucosa of the small intestine following a meal, when blood glucose is ele- emia 5 blood levels
vated. Incretins signal the pancreas to increase insulin secretion and the liver to stop producing glucagon.
Both of these actions lower blood glucose levels. In addition, these drugs decrease food intake by increas-
ing the feeling of satiety (fullness), and they also delay gastric emptying, which slows glucose absorption. satiety 5 state of fullness
Exenatide (Byetta) and liraglutide (Victoza) are injectable incretin enhancers that accomplish their
actions by activating a receptor called GLP-1. Activation of the GLP-1 receptor causes the same types of
effects as the natural incretin hormone: lowering blood glucose by increasing the secretion of insulin, slow-
ing the absorption of glucose, and inhibiting glucagon.
The second group of incretin enhancers are given orally. Linagliptin (Tradjenta), saxagliptin (Ong-
lyza), and sitagliptin (Januvia) prevent the breakdown of incretins, allowing hormone levels to rise. These
drugs are effective at lowering blood glucose with few adverse effects. They work well with other antidia-
betic drugs and do not cause hypoglycemia.
Combinations of antidiabetic drugs have been developed to maximize the therapeutic effects and min-
imize adverse effects. Examples of selected drug combinations are listed below:
■ ACTOplus pioglitazone/metformin
■ Avandamet rosiglitazone/metformin
■ Avandaryl rosiglitazone/glimepiride
■ Duetact pioglitazone/glimepiride
■ Glucovance glyburide/metformin
■ Janumet sitagliptin/metformin
■ Jentadueto linagliptin/metformin
■ Juvisync sitagliptin/simvastatin
■ Metaglip glipizide/metformin
■ PrandiMet repaglinide/metformin
Concept Review 33.1

■ Why are noninsulin antidiabetic drugs ineffective for treating type 1 diabetes?
NURSING PROCESS FOCUS Patients Receiving Pharmacotherapy for Type 2 Diabetes

Same as for patients receiving insulin (see page 533), so abbreviated here. Same as for patients receiving insulin (see page 533), so abbreviated here.
Prior to administration: ■ Risk for Unstable Blood Glucose Level
■ Obtain a complete health history. ■ Risk for Injury
■ Evaluate laboratory blood findings. ■ Deficient Knowledge
■ Acquire the results of a complete physical examination. ■ Risk for Imbalanced Nutrition
■ Obtain a dietary history. ■ Risk for Infection
■ Determine knowledge of diabetic medications and blood glucose ■ Ineffective Therapeutic Regimen Management
monitoring. ■ Noncompliance

The patient will:
■ Experience therapeutic effects (stable blood glucose levels).
■ Demonstrate an understanding of lifestyle modifications necessary for successful maintenance of drug therapy.
Implementation

■ Monitor blood glucose at least daily. (Daily glucose levels will assist in ■ Instruct the patient how to monitor blood glucose, including use of
maintaining stable blood glucose.) equipment, and when to notify the healthcare provider.
■ Administer medication correctly (at appropriate time according to Inform patient or caregivers about:
type of medication ordered) and evaluate the patient’s knowledge of ■ Correct administration time for type of medication ordered.
proper administration. (Most oral antidiabetic medications are given ■ Peak medication levels and proper food sources needed to prevent
at or around meal times. Maintaining levels of medication will assist in both hyperglycemia and hypoglycemia. Provide written materials for
maintaining stable blood glucose levels.) future reference.
■ Monitor for signs of lactic acidosis if the patient is receiving a bigu- ■ Instruct the patient to report signs of lactic acidosis such as hyperven-
anide. (Mitochondrial oxidation of lactic acid is inhibited, and lactic tilation, muscle pain, fatigue, and increased sleeping to the healthcare
acidosis may result.) provider.
■ Continue to monitor periodic laboratory work: CBC, electrolytes, glu- Instruct the patient:
cose, HbA1C, lipid profile, liver and renal function studies. (Periodic ■ On sulfonylureas to immediately report any nausea, vomiting, yellow
monitoring assists in determining glucose control, need for medication skin, pale or clay colored stools, abdominal pain, or dark urine to the
changes and any indicators of complications. These drugs are metabo- healthcare provider.
lized in the liver and may cause elevations in AST and LDH.) ■ Taking biguanides to immediately report any drowsiness, malaise, de-
creased respiratory rate, or general body aches to the healthcare provider.
■ About the need to keep laboratory appointments.
■ Ensure dietary needs are met based on weight and current glucose lev- ■ Advise the patient to abstain from alcohol and to avoid liquid over-
els. Avoid alcohol. (Patients taking sulfonylurea or biguanides should the-counter (OTC) medications, which may contain alcohol.
avoid alcohol entirely to prevent an antabuse-like reaction.)
■ Monitor for edema, blood pressure, and lung sounds in patients ■ Instruct the patient to immediately report to the healthcare provider
taking thiazolidiones. (These drugs may cause edema and worsening any signs of edema of the hands or feet, dyspnea or excessive fatigue.
heart failure.)
■ Increase frequency of blood glucose monitoring if the patient is expe- ■ Instruct the patient to report the first signs of fatigue, muscle weak-
riencing fever, nausea, vomiting, or diarrhea. (Illness may affect blood ness, and nausea.
glucose levels and usually requires adjustments in medication) ■ Discuss the importance of adequate rest and healthy routines.
■ Check for signs of hypoglycemia, especially around the time of insulin Inform the patient:
peak activity. If symptoms occur, provide quick-acting carbohydrate ■ Signs and symptoms of hypoglycemia, such as hunger, irritability, sweating.
source (juice or simple sugar) and then recheck blood glucose. (Using ■ At first sign of hypoglycemia, to check blood glucose and eat a simple
a simple sugar will raise blood sugar immediately.) Also monitor care- sugar; if symptoms do not improve, call 911.
fully patients who also take beta blockers, because early signs of hypo- ■ If necessary, to monitor blood glucose before breakfast and supper.
glycemia may not be apparent. ■ Not to skip meals and to follow a diet specified by the healthcare provider.
■ Monitor weight, weighing at the same time of day each time. (Changes in ■ Instruct the patient to weigh each week, at the same time of day, and
weight will affect the amount of drug needed to control blood glucose.) report any significant loss or gain.
■ Encourage patient to increase physical activity gradually but continue Inform the patient:
to monitor blood glucose level before and after exercise. (Exercise ■ About the benefit of exercise.
assists muscle cells to use glucose more efficiently, lowering blood ■ To check blood glucose before and after exercise and to keep a simple
glucose.) sugar on his or her person while exercising.
■ To eat some form of simple sugar or complex carbohydrate before
strenuous exercise as prophylaxis against hypoglycemia.
■ Monitor hypersensitivity and allergic reactions. (Anaphylactic reactions ■ Advise the patient of the importance of immediately reporting
are possible.) symptoms such as skin rashes, itching, swelling of the tongue or face,
flushing, dizziness syncope wheezing, throat tightness, or shortness of
breath to the healthcare provider.
continued . . .
Chapter Review 539

■ Determine pregnancy status. (Some oral antidiabetic medications are ■ Advise female patients of childbearing age to inform the healthcare
category C and must be stopped during pregnancy. Due to increasing provider if pregnancy is suspected.
the metabolic needs of pregnancy, insulin therapy may be needed.)


Patients treated for DM need to know the following:
1. When administering insulin, meals should not be skipped. If self-injecting insulin, carefully
follow all instructions provided by the healthcare provider to avoid injury or infection.
Store unopened vials of insulin in the refrigerator. Do not use after the expiration date.
2. Check with a healthcare provider before beginning a vigorous exercise program. Often,
insulin doses should be reduced or extra food should be ingested just prior to intense
exercise.
3. Know the time of peak action of any insulin, because that is when the risk for hypogly-
cemic adverse effects is greatest.
4. The right amount of insulin must be available to cells when glucose is available in the
blood. Without insulin present, glucose from a meal can build up to high levels in the
blood, causing hyperglycemia and possible coma.
5. When taking antidiabetic drugs, report to your healthcare provider immediately any
signs of hypoglycemia, such as weakness, sweating, dizziness, tremor, anxiety, or tachy-
cardia. Mild symptoms may be treated with small amounts of sugar in the form of
candy or fruit juice.
6. Always take antidiabetic drugs the same time each day. When self-monitoring blood
glucose, recall that normal values are 80–120 mg/dL before meals and 100–140 mg/dL
before bedtime.
7. Read the directions for all medications very carefully because many drug–drug interac-
tions are possible. Medications such as corticosteroids, thiazide diuretics, and sympa-
thomimetics can raise blood glucose levels and inhibit the effects of insulin.
Safety Alert
Expiration Dates on Multidose Vials
Multidose vials, such as insulin, can be kept for a specific period of time depending institu-
tional policy and manufacturers recommendations. When a vial is punctured, it is imperative
that the nurse not forget to document either the expiration date or the date it was opened
on the vial label. If this is not done, the vial may not be discarded appropriately, allowing the
use of a medication that may no longer be safe or effective.
Source: Institute for Safe Medication Practices
Chapter Review
33.1 The pancreas is responsible for the regulation of 33.2 Type 1 diabetes is caused by a deficiency in insulin.
blood glucose levels. Type 1 DM is caused by an absolute lack of insulin
The pancreas is both an endocrine and an exocrine secretion due to autoimmune destruction of pan-
gland. The islets of Langerhans are responsible for creatic islet cells. If untreated, it results in serious,
secretion of insulin and glucagon. Insulin is released chronic conditions affecting the cardiovascular and
when blood glucose increases, and glucagon is nervous systems.
released when blood glucose decreases.
33.3 Insulin replacement therapy is required for type 1 2 DM are older adults; more obese children and ado-
diabetes. lescents are being diagnosed.
Type 1 DM is treated by dietary restrictions, exercise,
33.5 Antidiabetic drugs are prescribed after diet and ex-
and insulin therapy. The many types of insulin prepa-
ercise have failed to reduce blood glucose to nor-
rations vary as to their onset of action, time to peak
mal levels.
effect, and duration. Doses of insulin are highly indi-
vidualized in each patient. Type 2 DM is controlled through lifestyle changes
and oral hypoglycemic drugs. Various classes of
33.4 Type 2 diabetes is the most common form of the drugs are available for the pharmacotherapy of type
disorder 2 DM: alpha-glucosidase inhibitors, biguanides,
Type 2 DM is caused by a lack of sensitivity of insu- incretin enhancers, meglitinides, sulfonylureas, and
lin receptors at the target cells and a deficiency in thiazolidinediones (or glitazones). Combinations of
insulin secretion. If untreated, the same chronic con- antidiabetic drugs maximize therapeutic effects and
ditions result as in type 1 DM. Most people with type minimize adverse effects.
Review Questions
The following questions are written in NCLEX-PN® style. Answer 2. “My insulin needs may increase when I have an infection.”
these questions to assess your knowledge of the chapter material, 3. “I must draw the NPH insulin first if I am mixing it with
and go back and review any material that is not clear to you. regular insulin.”
4. “If my blood glucose levels are above 140 mg/dL, I should
1. While collecting information from a patient, the nurse
notify my healthcare provider.”
notes which of the following symptoms of type I diabetes?
(Select all that apply.) 6. The physician starts a patient on 500 mg, po, twice a day.
1. Polyphagia The pharmacy provides him or her with scored 1,000 mg tab-
2. Polyuria lets. How many tablets will he or she take in a day?
3. Polydipsia 1. One tablet
4. Weight gain 2. Two tablets
3. One and one-half tablets
2. When giving insulin, the nurse plans on administering it
4. One-half tablet
by what route?
1. Oral 7. The patient with diabetes has decided to start an exercise
2. Intradermal program. He remembers that the nurse told him that exercise:
3. Subcutaneous 1. Increases glucose in the blood thus increasing the need for
4. Intramuscular insulin just after exercise.
3. A patient, who has just been prescribed an incretin enhancer 2. Decreases glucose in the blood thus decreasing the need for
(oral hypoglycemic medication), asks the nurse how it works. The more insulin just after exercise.
nurse informs the patient that these types of medications: 3. Does not affect glucose or the need for insulin.
4. Decreases glucose in the blood thus increasing the need for
1. Decrease the uptake of glucose by body cells. insulin after exercise.
2. Stimulate insulin release from the pancreas.
3. Increase insulin production by the pancreas. 8. The nurse informs a group of patients, newly diagnosed with
4. Decrease the amount of insulin produced by the pancreas. type 1 DM, that the following factors can influence the amount of
insulin needed to control blood glucose levels: (Select all that apply.)
4. A patient receives NPH and regular insulin every morn-
ing. The nurse, verifying that the patient understands that there 1. Exercise
are two different peak times to be aware of for this insulin com- 2. Diet
bination, questions the patient because: 3. Illness
4. Sleep
1. The patient needs to plan the next insulin injection around
the peak times. 9. The nurse administers glipizide (Glucotrol):
2. Additional insulin may be needed at peak times to avoid 1. Subcutaneously only
hyperglycemia. 2. After meals
3. It is best to plan exercise or other activities around the peak 3. At bedtime
insulin activity. 4. Just before breakfast
4. The risk for hypoglycemia is greatest around the peak of
insulin activity. 10. The nurse plans to administer glargine (Lantus) to a
patient with type 1 diabetes:
5. The nurse is evaluating the patient’s knowledge about the
use and effects of insulin. Which of the following statements 1. Before meals
indicates that the patient needs additional information? 2. With meals
3. Only at bedtime
1. “If I experience hypoglycemia, I should drink half a cup of
4. Same time each day.
apple juice.”
Chapter Review 541
Remember Mr. Jones, the patient 2. Mr. Jones is told that he has the symptoms of type 2 DM.
introduced at the beginning of the He wants to know how it can be controlled. The nurse tells him
chapter? Now read the remainder of that it can be controlled by: (Select all that apply.)
the case study. Based on the informa- 1. Regular exercise
tion you have learned in this chapter, 2. Oral antidiabetic medications
answer the questions that follow. 3. Maintaining current weight
Mr. Brian Jones is a 45-year-old fire- 4. Better coping skills to deal with stress
fighter who smokes and is somewhat
overweight. Over the past five years, he 3. Mr. Jones is started on metformin. As part of the infor-
has begun to develop slightly elevated mation packet given to newly diagnosed patients with diabetes,
blood pressure as determined by annual physical exams. He knows there is a section on antidiabetic medications. Mr. Jones starts
he should lose weight and is concerned about his energy level. He to read it but instead asks the nurse about adverse effects. The
has always felt “OK” despite the fact that he smokes, but recently he nurse states that some of the adverse effects of metformin are:
has begun to feel sluggish and wonders what’s going on. He thinks (Select all that apply.)
to himself, “Maybe I’m just getting older.” At this current visit to 1. Constipation
the doctor, laboratory results reveal a fasting blood glucose level of 2. Diarrhea
136 mg/dL. His blood pressure is 150/90 mmHg. Mr. Jones has not 3. Abdominal discomfort
been taking medications for any reported disorders. 4. Headaches
1. Mr. Jones is told that his blood glucose level is above the 4. Mr. Jones also has high blood pressure and is going to
normal range, a condition known as hyperglycemia. In helping be prescribed medication. The nurse understands that several
to determine factors that influenced his test results, the nurse blood pressure drugs, captopril, furosemide, and nifedipine,
asks him about: (Select all that apply.) may cause a(n):
1. His daily diet 1. Increased risk for hypoglycemia
2. His level of stress 2. Decreased renal excretion
3. How long he has smoked 3. Increased renal excretion
4. How long he has had hypertension 4. Decreased risk for hypoglycemia

C
“I can’t wait until all this
h stops. My periods hurt so
a bad and last so long. It just
p makes me tired.”
t Ms. Marge Philips
e
r
34 Drugs for Disorders and Conditions

of the Reproductive System
Core Concepts
34.1 The hypothalamus, pituitary, and gonads control re- 34.5 Oxytocin and tocolytics are drugs that influence
productive function in both men and women. uterine contractions and labor.
34.2 Oral contraceptives are drugs used in low doses to 34.6 Androgens are used to treat hypogonadism in males.
prevent pregnancy. 34.7 Erectile dysfunction is a common disorder success-
34.3 Hormone replacement therapy provides estrogen to fully treated with drug therapy.
treat postmenopausal symptoms, but benefits may 34.8 In its early stages, benign prostatic hyperplasia is
not outweigh risks. successfully treated.
34.4 Conjugated estrogens and progestins are prescribed
for dysfunctional uterine bleeding, endometrial can-
cer, and postmenopausal symptoms.
Drug Snapshot
Oral contraceptives stradiol with noreth-

e Uterine stimulants and oxytocin (Pitocin) 553
(OCs) indrone (Ortho-Novum, relaxants
others) 547 Androgens testosterone 554
Hormone replacement strogen, conjugated
e Drugs for erectile sildenafil (Viagra) 556
therapy (HRT) (Cenestin, Enjuvia, dysfunction
Premarin) 551
Drugs for benign finasteride (Proscar) 558
Drugs for dysfunc- ethoxyprogesterone
m prostatic hyperplasia
tional uterine bleeding (Depo-Provera, Depo-SubQ-
Provera, Provera) 552
Learning Outcomes
1. Describe the roles of the hypothalamus, 2. Explain the mechanisms by which 3. Describe the role of drug therapy in
pituitary, and sex organs in maintaining estrogens and progestins prevent the treatment of menopausal and
female and male reproductive function. conception. postmenopausal symptoms.
4. Discuss the uses of progestins in the the treatment of patients giving 9. Describe the pharmacotherapy of
therapy of dysfunctional uterine birth and after delivery of the benign prostatic hyperplasia.
bleeding. baby. 10. For each of the classes listed
5. Identify the role of the female 7. Identify the reasons for in the Drug Snapshot, identify
sex hormones in the treatment of pharmacotherapy with representative drugs and explain
endometrial cancer. androgens. their mechanisms of drug action,
6. Compare and contrast the use of 8. Describe the pharmacotherapy primary actions, and important
uterine stimulants and relaxants in of erectile dysfunction. adverse effects.
Key Terms
amenorrhea (ah-men-oh-REE-ah) 550 follicle-stimulating hormone (FSH) 543 ovulation (ov-you-LAY-shun) 543
androgens (AN-droh-jens) 554 gonadotropin-releasing hormone (GnRH) oxytocics (ox-ee-TOH-sicz) 552
benign prostatic hyperplasia (BPH) (bee- (go-NAD-oh-TROPE-en) 543 oxytocin (ox-ee-TOH-sin) 552
NINE pros-TAT-ik hy-PURR-plays-she-ah) hormone replacement therapy postmenopausal bleeding (POST-men-oh-
557 (HRT) 549 pause-ahl) 550
breakthrough bleeding 550 hypogonadism (hy-poh-GO-nad-izm) 554 premenstrual syndrome (PMS) (PREE-
corpora cavernosa (KORP-us kav-ver- impotence (IM-poh-tense) 555 men-stroo-ahl) 550
NOH-sah) 555 libido (lih-BEE-do) 554 progesterone (pro-JESS-ter-own) 544
corpus luteum (KORP-us LUTE-ee-uhm) 544 luteinizing hormones (LH) (LEW-ten- prolactin (pro-LAK-tin) 552
dysfunctional uterine bleeding 549 iz-ing) 543 prostaglandins (pros-tah-GLAN-
endometrial carcinoma (en-doh-MEE- menopause (MEN-oh-paws) 549 dins) 552
tree-ahl CAR-sin-OH-mah) 550 menorrhagia (men-oh-RAGE-ee-uh) 550 testosterone (test-AHST-erh-own) 544
endometriosis (en-doh-MEE-tree-oh-sis) 550 oligomenorrhea (ol-ego-men-oh- tocolytics (toh-koh-LIT-ikz) 552
estrogen (ES-troh-jen) 544 REE-uh) 550 virilization (veer-you-lih-ZAY-shun) 554
H ormones from the pituitary gland and the sex organs provide for the growth and continued
maintenance of the male and female reproductive systems. Reproductive hormones impact
virtually every body system, including coagulation, blood vessels, bone, muscles, overall
body growth, and behavior. Hormonal therapy of the female reproductive system is used to achieve
a variety of therapeutic goals, ranging from replacement therapy after menopause to prevention of
pregnancy to milk production. The pharmacologic treatment of reproductive disorders in men is less
complex because hormonal secretion in men is relatively constant throughout the adult life span. This
chapter examines hormones and drugs used to treat disorders and conditions associated with the repro-
ductive system.
The hypothalamus, pituitary, and gonads control reproductive

function in both men and women. Core Concept 34.1
Regulation of the reproductive system is achieved by hormones from the hypothalamus, pituitary
gland, and the sex organs. The hypothalamus secretes gonadotropin-releasing hormone (GnRH), gonads/gonado 5 sex organs
which travels a short distance to the pituitary to stimulate the secretion of follicle-stimulating tropin 5 attraction toward
hormone (FSH) and luteinizing hormone (LH). Both of these pituitary hormones act at the levels of
luteum/luteinizing 5
the reproductive organs. The hormonal changes that occur during the ovarian and uterine cycles are yellowing (color of
illustrated in Figure 34.1 ■. developing structures)
During a woman’s reproductive years and under the influence of FSH and LH, several ovarian fol-
licles begin the maturation process each month. On approximately day 14 of the ovarian cycle, a surge
of LH secretion causes one follicle to expel its oocyte, a process called ovulation. The ruptured follicle,
544 Chapter 34 Drugs for Disorders and Conditions of the Reproductive System
Figure 34.1
Hormonal changes
FEMALE REPRODUCTIVE CYCLE
during the ovarian and Gonadotropic
uterine cycles. hormone LH
cycle
hormone levels
FSH
Ovarian
cycle
Follicle growth Ovulation Corpus luteum degeneration
Progestins
hormone levels
Ovarian
hormone
cycle
Estrogens
menstruation
thickness of uterine lining
Menstrual
(uterine)
cycle
Menstrual flow Proliferative

Secretory phase
phase phase
Days: 0 7 14 28
corpus 5 body minus its oocyte, remains in the ovary and is transformed into the hormone-secreting corpus luteum. The
oocyte 5 egg cell expelled oocyte begins its journey through the uterine tube and eventually reaches the uterus. If conception
does not occur, the outer lining of the uterus degenerates and is shed to the outside during menstruation.
estro 5 desire As ovarian follicles mature, they secrete the female sex hormones estrogen and progesterone. Estro-
gen 5 forming gen is responsible for the maturation of the female reproductive organs and for the appearance of second-
pro 5 before ary sex characteristics. In addition, estrogen has numerous metabolic effects on nonreproductive tissues in
gest 5 gestation the body. When women enter menopause at about age 50 to 55, the ovaries stop secreting estrogen.
In the last half of the monthly cycle, the corpus luteum secretes progesterone. In combination with
estrogen, progesterone promotes breast development and regulates the monthly changes in the uterus.
Under the influence of estrogen and progesterone, the uterine lining thickens in preparation for receiving
a fertilized egg. High progesterone and estrogen levels in the final part of the uterine cycle provide neg-
ative feedback to shut off GnRH, FSH, and LH secretion. This negative feedback loop is illustrated in
Figure 34.2 ■.
The same pituitary hormones that control reproductive function in women also affect men. FSH regu-
lates sperm production. LH regulates the production of testosterone. If the level of testosterone in the blood
rises above normal, negative feedback to the pituitary shuts off the secretion of LH and FSH.
testo 5 testis Testosterone is the primary male sex hormone responsible for male secondary sex characteristics.
erone/sterone 5 sterol Unlike the 28-day cyclic secretion of estrogen and progesterone in women, testosterone secretion is rela-
chemical compound
tively constant. Beginning in puberty, testosterone production increases rapidly and is maintained at a high
level until late adulthood, after which it slowly declines.
Figure 34.2
GnRH
– –
– –
LH FSH LH FSH
Negative Negative
feedback feedback
+ + + +
Ovulation
Ovaries Testes
Maturation of follicles
• Secretion of estrogens • Increased testosterone secretion
Development of corpus luteum • Stimulation of spermatogenesis
• Secretion of progestins
Uterus
Stimulation
of endometrium
Hormonal control over male and female reproductive hormones.

ORAL Contraceptives
Core Concept 34.2 Oral contraceptives are drugs used in low doses to prevent pregnancy.
The most widespread pharmacologic use of the female sex hormones is for the prevention of pregnancy.
When used appropriately, they are nearly 100% effective. Most oral contraceptives (OCs) contain a combi-
nation of estrogen and progestin, although a few contain only progestin. The most common estrogen used
in these preparations is ethinyl estradiol, and the most common progestin is norethindrone.
The estrogen–progestin oral contraceptives prevent ovulation, which is required for conception to
occur. These hormones act by providing negative feedback to the pituitary gland that shuts down secre-
tion of LH and FSH. Without these pituitary hormones, the egg cannot mature, and ovulation is pre-
vented. The estrogen–progestin agents also make the lining of the uterus less favorable to receiving an
embryo.
mono 5 single There are four types of estrogen–progestin OCs: monophasic, biphasic, triphasic, and quadriphasic
bi 5 two version. The monophasic delivers a constant dose of estrogen and progestin throughout the 21-day treat-
tri 5 three ment cycle. With biphasic formulations, the amount of estrogen in each pill remains constant, but the
phasic 5 dosing level(s)
amount of progestin is increased toward the end of the treatment cycle to better nourish the uterine lining.
In triphasic formulations, the amounts of both estrogen and progestin vary in three distinct phases during
the treatment cycle. In 2010, the first quadriphasic OC, called Natazia, was introduced. Natazia contains a
synthetic estrogen called estradiol valerate and a progestin called dienogest; it is the first drug containing
this specific combination. All four types of OC formulations are equally effective, although a common
dys 5 abnormal or unhealthy problem, and most likely the most common reason for treatment failure (pregnancy), is forgetting to take
a 5 without the medication daily. Selected OCs are listed in Table 34.1 ◆.
meno 5 monthly The most common adverse effects of estrogen–progestin OCs are nausea, breast tenderness, weight
rrhea 5 flow
gain, and breakthrough bleeding. Less common serious effects include edema, gallbladder disease, abdom-
inal cramps, changes in urinary function, dysmenorrhea, fatigue, skin rash, headache, and vaginal candi-
thrombo 5 stationary
blood clot diasis. Cardiovascular adverse effects, the most serious of all, include hypertension and thromboembolic
embolytic 5 circulating disorders. The estrogen component of the pill can lead to venous and arterial thrombosis, which can result
blood clot in pulmonary, myocardial, and thrombotic strokes.
Table 34.1 Selected Oral Contraceptives

Trade Name Estrogen Progestin
Monophasic
Desogen ethinyl estradiol; 30 mcg desogestrel; 0.15 mg
Loestrin 1.5/30 Fe ethinyl estradiol; 30 mcg norethindrone; 1.5 mg
Ortho-Cyclen-28 ethinyl estradiol; 35 mcg norgestimate; 0.25 mg
Yasmin ethinyl estradiol; 30 mcg drospirenone; 3 mg
Zovia 1/50E-21 and 28 ethinyl estradiol; 50 mcg ethynodiol diacetate 1 mg
Biphasic
Mircette ethinyl estradiol 20 mcg for 21 days; desogestrel; 0.15 mg for 21 days
10 mcg for 5 days
Triphasic
Ortho-Novum 7/7/7-28 ethinyl estradiol; 35 mcg norethindrone; 0.50, 0.75, 0.1 mg
Ortho Tri-Cyclen-28 ethinyl estradiol; 35 mcg norgestimate; 0.18, 0.215, 0.25 mg
Trivora-28 ethinyl estradiol; 30, 40, 30 mcg levonorgestrel; 0.05, 0.075, 0.125 mg
Progestin Only
Micronor None norethindrone; 0.35 mg
Nor-Q.D. None norethindrone; 0.35 mg
The progestin-only OCs, sometimes called minipills, prevent pregnancy primarily by producing a
thick, viscous mucus at the entrance to the uterus that prevents penetration by sperm. A thicker muco-
sal lining inhibits implantation of a fertilized egg. Progestin-only agents are less effective than estrogen–
progestin combinations and produce a higher incidence of menstrual irregularities. Because of this, they
are generally reserved for women who are at high risk for adverse effects from estrogen. When women
taking estrogen also smoke, they have an increased chance of developing blood clots which may be fatal.
Several long-term hormonal formulations of contraception are available. These extended-duration for-
mulations are equally effective in preventing pregnancy and have the same basic safety profile as OCs.
Examples of alternative formulations are:
■ Depot injections: Depo-Provera (IM injection of medroxyprogesterone), Depo-SubQ-Provera
(subcutaneous injection of medroxyprogesterone)
■ Implants: Implanon (single rod containing the progestin etonogestrel inserted under the skin of
the upper arm)
■ Transdermal patches: Ortho Evra (transdermal patch containing ethinyl estradiol and norelge-
stromin), Minivelle (transdermal patch containing estradiol)
■ Vaginal route: NuvaRing (2-inch-diameter ring containing estrogen and progestin inserted into
the vagina)
■ Intrauterine route: Mirena (polyethylene cylinder placed in the uterus and releases levonorg-
estrel), Skyla (levonorgestrel release may last up to three years)
■ Extended-regimen OCs: Seasonale consists of tablets containing levonorgestrel and ethi-
nyl estradiol that are taken for 84 consecutive days, followed by 7 inert tablets (without
hormones).
Emergency contraception (EC) is the prevention of pregnancy following unprotected intercourse. The
treatment goal for EC is to provide effective and immediate contraception. Two different medications are
approved for EC: Levonorgestrel (Plan B) and ulipristal (Ella).
Plan B is approved for purchase over the counter (OTC). Dosing for Plan B involves taking 0.75 mg
of levonorgestrel in two doses, 12 hours apart. Plan B One Step includes a single 1.5 mg dose. The
drug acts in a manner similar to OCs; it prevents ovulation and also alters the lining of the uterus so
that implantation does not occur. If implantation has already occurred, Plan B will not terminate the
pregnancy. Plan B must be taken as soon as possible after unprotected intercourse; if taken more than
120 hours later, it becomes less effective. Adverse effects are mild and may include nausea, vomiting,
abdominal pain, fatigue, headache, menstrual changes, diarrhea, dizziness, and breast tenderness. In 2010,
ulipristal (Ella) was approved as a single-dose product for EC. Unlike Plan B, which is available OTC,
ulipristal requires a prescription. One advantage of ulipristal is that it retains its effectiveness for five days
following unprotected sex.
Drug Prototype: Estradiol with Norethindrone (Ortho-Novum, Others)

Therapeutic Class: Oral Contraceptive Pharmacologic Class: Estrogen/Progestin
Actions and Uses: Ortho-Novum is typical of the monophasic pressure. Bleeding in the early or mid-menstrual cycle is rela-
oral contraceptives, containing fixed amounts of estrogen and tively common.
progesterone for 21 days followed by placebo tablets for 7 days. Ethinyl estradiol interacts with many drugs. For exam-
It is nearly 100% effective at preventing conception. If a dose ple, rifampin, some antibiotics, barbiturates, anticonvulsants,
is missed, the patient should take the dose as soon as possible, and antifungals decrease efficacy of oral contraceptives,
or take two tablets the next day. If two consecutive doses so the risks of breakthrough bleeding and pregnancy are
are missed, conception is possible, and the patient should use higher
other birth control methods until the regular dosing schedule
is reestablished.
Adverse Effects and Interactions: Like most oral contracep- Black Box Warning:
tives, Ortho-Novum can increase the risks of thromboembolic Cigarette smoking increases the risk of serious cardiovascu-
disease: the potential for blood clots, hemorrhage, pulmonary lar adverse effects in women who are taking OCs containing
embolism, or stroke. It should be used with caution in women estrogen.
with hypertension because it has the potential to raise blood
NURSING PROCESS FOCUS Patients Receiving Oral Contraceptive Therapy

■ Obtain a complete health history, including genitourinary (GU), sexual, therapy
cardiovascular (especially hypertension or thromboembolic), thyroid, ■ Infective Health Maintenance related to noncompliance with medica-
renal and liver conditions; pregnancy (or lactating); allergies; drug tion regimen or adverse drug effects
history; and possible drug interactions. ■ Risk for Ineffective Peripheral Tissue Perfusion related to adverse
■ Gather information about lifestyle such as pain, cigarette smoking, drug effects
and diet. ■ Risk of Excess Fluid Volume related to adverse drug effects
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel,

The patient will:
■ Experience therapeutic effects (effective birth control).
Implementation

of proper administration. (Incorrect use may lead to pregnancy.) ■ Take the pill at the same time every day.
■ Not omit, increase, or decrease doses without consulting health-
care provider: omitting or decreasing doses increases the chance of
pregnancy.
■ Take medication according to the specific type of hormone being
taken. For estrogen–progestin combinations: take a missed dose as
soon as remembered. If two consecutive doses are missed, take
the two missed pills on the day remembered and next two pills on
the following day. Then follow the remaining schedule of pills but use
additional birth control until the regular schedule is reestablished.
■ Contact the healthcare provider if two consecutive periods are missed
because pregnancy may have occurred.
■ Monitor for the occurrence of breakthrough bleeding. (Spotting may ■ Inform the patient that spotting may occur with low-dose hormone
occur, especially with low-dose hormone therapy, at mid-cycle. Any therapy, at mid-cycle but to report any unusual changes in the amount
continuous, unusual, or heavy bleeding may indicate adverse effects, of bleeding or if bleeding continues.
pregnancy loss, or disease and should be reported.)
■ Monitor for thrombophlebitis or other thromboembolic disease. ■ Instruct the patient to immediately report to the healthcare provider
(Estrogen predisposes to thromboembolic disorders by increasing any pain in the calves, limited movement in the legs, dyspnea, sudden
levels of clotting factors.) severe chest pain, headache, seizures, anxiety, or fear.
■ Monitor for cardiac disorders: take vital signs, especially pulse and Instruct the patient to:
blood pressure. (These drugs can increase blood levels of angiotensin ■ Report immediately signs of possible cardiac problems such as chest
and aldosterone, which increase blood pressure.) pain, dyspnea, edema, tachycardia or bradycardia, and palpitations.
■ Have blood pressure monitored regularly.
■ Report to the healthcare provider any symptoms of hypertension such
as headache, flushing, fatigue, dizziness, palpitations, tachycardia, and
nosebleeds.
■ Encourage the patient not to smoke. (Smoking increases risk Instruct the patient to:
of thromboembolic disease.) ■ Be aware that the combination of oral contraceptives and smoking
greatly increases risk of cardiovascular disease, especially MI.
■ Be aware that the risk increases with age (>35) and with number of
cigarettes smoked (15 or more per day).
■ Monitor liver function tests, lipid profile studies, and thyroid studies Instruct the patient to:
periodically. (These drugs are associated with an increased risk of ■ Return periodically for laboratory tests.
gallbladder disease and a rare risk of liver toxicity.) ■ Report any symptoms of abdominal or right upper quadrant discom-
fort, yellowing of the skin or sclera, fatigue, anorexia, darkened urine,
or clay-colored stools to the healthcare provider.
■ Monitor for the development of breast or other estrogen-dependent ■ Instruct the patient to immediately report to the healthcare provider
tumors. (Estrogen may cause tumor growth or proliferation.) if a first-degree relative is diagnosed with any estrogen-dependent
tumor.
continued . . .

■ Encourage compliance with follow-up treatment. (Follow-up is Instruct the patient to:
necessary to avoid serious adverse effects.) ■ Schedule annual Pap smears.
■ Perform breast self-exams (BSEs) monthly and obtain routine mammo-
grams as recommended by the healthcare provider.

Cam Therapy
Dong Quai for Premenstrual Syndrome
Since antiquity, dong quai has been recognized as an important herb for women’s health in
Chinese medicine. Obtained from Angelica sinensis, a small plant that grows in China, dong
quai, contains a number of active substances that are said to exert analgesic, antipyretic, anti-
inflammatory, and antispasmodic activity. The dried root is available as capsules, tablets, teas,
and tinctures.
The reproductive effects of dong quai may be due to active substances that have
estrogenic activity. These estrogenic ingredients act as a “uterine tonic” to improve the overall
hormonal balance of the female reproductive system. Dong quai is used to treat the symptoms
of premenstrual syndrome, as well as other disorders such as irregular menstrual periods or
painful menstruation.
Dong quai has also been used for its cardiovascular effects. It is claimed to increase
circulation by dilating blood vessels. Because some of the active ingredients of dong quai
may have anticoagulant activity, patients taking warfarin (Coumadin) or high doses of aspirin
should not take the herb without notifying their healthcare practitioner.
Menopause
Hormone replacement therapy provides estrogen to treat postmeno-

pausal symptoms, but benefits may not outweigh risks. Core Concept 34.3
Menopause is the permanent cessation of menses, resulting in a lack of estrogen secretion by the ovaries. post 5 after
Menopause is neither a disease nor a disorder, but a natural consequence of aging that is often accompa- meno 5 monthly
nied by unpleasant symptoms that include hot flashes, night sweats, irregular menstrual cycles, vaginal pause/pausal 5 stopping
dryness, and bone mass loss.
Over the past 50 years, healthcare providers have commonly prescribed hormone replacement therapy
(HRT) for menopause. HRT supplies physiological doses of estrogen, sometimes combined with a progestin,
to treat unpleasant symptoms of menopause and to prevent the long-term consequences of estrogen loss.
Studies have raised questions regarding the safety of HRT for menopause. Data suggest that patients
may have an increased risk of coronary artery disease, stroke, and venous thromboembolism. Women are
now encouraged to discuss alternatives with their healthcare provider. Undoubtedly, research will continue to
provide valuable information on the long-term effects of HRT. Until then, the choice of HRT to treat meno-
pausal symptoms will remain a highly individualized one between the patient and her healthcare provider.
Uterine Abnormalities
Conjugated estrogens and progestins are prescribed for dysfunctional

uterine bleeding, endometrial cancer, and postmenopausal symptoms. Core Concept 34.4
Conjugated estrogens are combined estrogens, and these, along with progestins, treat a variety of condi-
tions. Dysfunctional uterine bleeding is a condition in which hemorrhage occurs on a noncyclic basis or
in abnormal amounts. It is the most frequent health problem reported by women and is a common reason
hyster 5 womb or uterus for hysterectomy. Other types of uterine abnormalities include the following:
ectomy 5 excision
■ Amenorrhea—absence of menstruation
endo 5 inside (e.g., uterus ■ Endometriosis—abnormal location of endometrial tissues
lining)
metri/metrial 5 measure
■ Oligomenorrhea—infrequent menstruation
osis 5 abnormal ■ Menorrhagia—prolonged or excessive menstruation
oligo 5 scanty
■ Breakthrough bleeding—hemorrhage between menstrual periods
meno 5 month ■ Premenstrual syndrome (PMS)—symptoms develop during the luteal phase
rrhagia 5 excessive
rrhea 5 flow ■ Postmenopausal bleeding—hemorrhage following menopause
■ Endometrial carcinoma—cancer of the endometrium
Dysfunctional uterine bleeding is often caused by a hormonal imbalance between estrogen and pro-
gesterone. Poor estrogen levels cause the uterine lining to remain thin. Progestins (progesterone-like hor-
mones) limit and stabilize growth of the uterine lining.
The primary indication for conjugated estrogens has been to treat moderate to severe symptoms of
menopause, which include irregular menstrual cycles and extreme uterine bleeding. Progestins are the
drugs most commonly used for treating uterine abnormalities. Administration of a progestin in a pattern
starting 5 days after the onset of menses and continuing for the next 20 days can sometimes reestablish a
normal, monthly cyclic pattern. OCs may also be prescribed for this disorder. Progestins are also occasion-
ally prescribed for the treatment of metastatic endometrial carcinoma. In cases like this, progestins are used
for total patient care, usually in combination with other antineoplastics. Conjugated estrogens and selected
progestins with their dosages are listed in Table 34.2 ◆.
Concept Review 34.1

osteo 5 bone ■ Why is a progestin usually prescribed along with estrogen in oral contraceptives and
porosis 5 porous condition when treating postmenopausal symptoms?
Table 34.2 Drugs for Hormone Replacement Therapy and Uterine Abnormalities
Drug Route and Adult Dose Drug Class Remarks
Estrogens
estradiol (Alora, Climara, PO (Estrace); 0.5–2 mg daily Systemic estrogens come in pill form, skin patches, gels,
Divigel, Elestrin, Estraderm, Transdermal patch; 1 patch either once creams, and sprays. Low-dose vaginal preparations of estrogen
Estrace, others) weekly (Climara) or twice weekly (Alora, are available in cream, tablet, and ring form. Estradiol valerate
Estraderm) (0.025–0.1 mg/day) injection is provided as a long-acting estrogen dissolved in
sterile oil solution for intramuscular use.
Topical gel (Divigel, Elestrin);
0.25–1 g/day applied to the skin of the
upper thigh or arm
Intravaginal cream (Estrace); Insert 2–4 g/
day for 2 weeks, then reduce to one-half the
initial dose for 2 weeks, then use 1 g one to
three times per week
estradiol valerate IM; 10–20 mg every 4 weeks
(Delestrogen)
estrogen, conjugated PO; 0.3–1.25 mg/day for 21 days each month
(Cenestin, Enjuvia, Premarin)
estropipate (Ogen) PO; 0.75–6 mg/day for 21 days each month
Intravaginal cream (Ogen): Insert 2–4 g/day
(continued )
Table 34.2 Drugs for Hormone Replacement Therapy and Uterine Abnormalities (continued )
Progestins
medroxyprogesterone PO; 5–10 mg daily on days 1–12 of the Synthetic versions of progestin are generally provided as
(Depo-Provera, Depo-SubQ- menstrual cycle high-dose pills or birth control pills. Injectable forms are also
Provera, Provera) IM (Depo-Provera); 150 mg daily for available. Treatments help restore hormonal balance.
3 months. Give the first dose during the first
5 days of the menstrual period or within the
first 5 days postpartum if not breastfeeding
Subcutaneous (Depo-SubQ-Provera); 104 mg
daily for 3 months. Give the first dose during
the first 5 days of the menstrual period or at the
sixth week postpartum if not breastfeeding
norethindrone (Micronor, PO (for amenorrhea); 5–20 mg/day on days
Norlutin, Nor-Q.D.) 5–25 of the menstrual cycle
progesterone (Crinone, Amenorrhea or functional uterine bleeding:
Endometrin, Prochieve, IM; 5–10 mg/day
Prometrium) Assisted reproductive technology: Intravagi-
nal; 90 mg gel once daily or 100 mg tablets
two to three times per day
Estrogen–Progestin Combinations
Conjugated estrogens with PO; Premphase: estrogen 0.625 mg/daily on Conjugated estrogens combined with progestins are prescribed
medroxyprogesterone days 1–28; add 5 mg medroxyprogesterone to help women treat symptoms of menopause. Preparations are
(Premphase, Prempro) daily on days 15–28 also used to treat certain menstrual disorders and to prevent
PO; Prempro: estrogen 0.3 mg and medroxy- osteoporosis (bone loss) in women.
progesterone 1.5 mg daily
Intravaginal cream: insert 1/2 to 2 g daily for
3–6 months
estradiol with norgestimate PO; 1 tablet of 1 mg estradiol for 3 days, fol-
(Prefest) lowed by 1 tablet of 1 mg estradiol combined
with 0.09 mg norgestimate for 3 days. Regimen
is repeated continuously without interruption
ethinyl estradiol with norethin- PO; 1 tablet daily, which contains 0.5–0.1 mg
drone acetate (Activella) of estradiol and 0.5–1 mg norethindrone
Transdermal patch; 1 patch, twice weekly
Drug Prototype: Estrogen, conjugated (Cenestin, Enjuvia, Premarin)

Therapeutic Class: Hormone replacement therapy Pharmacologic Class: Estrogen
Actions and Uses: Conjugated estrogens (Premarin) contain a mix- Drug interactions include a decreased effect of tamoxifen
ture of different natural estrogens. Conjugated estrogen A (Cenes- and anticoagulants. The effects of estrogen may be decreased if
tin) and conjugated estrogen B (Enjuvia) contain a mixture of 9–10 taken with barbiturates, and there is a possible increased effect
different synthetic plant estrogens. Conjugated estrogens exert of tricyclic antidepressants.
several positive metabolic effects, including an increase in bone
density and a reduction in LDL cholesterol. It may also lower the
risk of coronary artery disease and colon cancer in some patients.
Black Box Warning:
Adverse Effects and Interactions: Adverse effects of conjugated Estrogens, when used alone, have been associated with
estrogens include nausea, fluid retention, edema, breast tender- a higher risk of endometrial cancer in postmenopausal
ness, abdominal cramps, and bloating. Conjugated estrogens women. Although adding a progestin may exert a protec-
are contraindicated in pregnant patients and in women with tive effect by lowering the risk of uterine cancer, studies
breast cancer. Caution should be used when treating patients suggest that progestin may increase the risk of breast cancer
with a history of thromboembolic disease, hepatic impairment, following long-term use.
or abnormal uterine bleeding.
Drug Prototype: Medroxyprogesterone (Depo-Provera, Depo-SubQ-Provera, Provera)

Therapeutic Class: Drug for endometriosis and dysfunctional uterine bleeding and endometriosis
Pharmacologic Class: Progestin
Actions and Uses: Medroxyprogesterone is a synthetic progestin dysmenorrhea, and vaginal candidiasis may also occur. The
with a prolonged duration of action. As with its natural coun- most serious adverse effect is an increased risk for thrombo-
terpart, the primary target tissue for medroxyprogesterone is embolic disease.
the endometrium of the uterus. It inhibits the effect of estrogen Medroxyprogesterone is contraindicated during preg-
on the uterus, thus restoring normal hormonal balance. Indica- nancy and in women with known or suspected carcinoma of
tions include dysfunctional uterine bleeding, secondary amenor- the breast. Caution should be used when treating patients with
rhea, and contraception. a history of thromboembolic disease, hepatic impairment, or
Medroxyprogesterone may also be given by sustained undiagnosed vaginal bleeding.
release IM (Depo-Provera) or subcutaneous (Depo-SubQ-
Provera) depot injection. This is available in two doses: a lower
dose for contraception and a higher dose for the alleviation of
inoperable metastatic uterine or renal carcinoma. Black Box Warning:
Progestins combined with conjugated estrogens may in-
Adverse Effects and Interactions: The most frequent adverse crease the risk of stroke, deep venous thrombosis (DVT),
effects of medroxyprogesterone are breast tenderness, myocardial infarction (MI), pulmonary emboli, and invasive
breakthrough bleeding, and other menstrual irregularities. breast cancer.
Weight gain, depression, hypertension, nausea, vomiting,
Labor and Breastfeeding
Oxytocin and tocolytics are drugs that influence uterine

Core Concept 34.5 contractions and labor.
oxytocic 5 oxytocin-related Several drugs are used to manage uterine contractions and to stimulate lactation. Oxytocics are drugs that
toco 5 contraction stimulate uterine contractions to promote the induction of labor. Tocolytics are used to inhibit uterine con-
lytic 5 arrested
tractions during premature labor. These drugs are listed in Table 34.3 ◆.
The most widely used oxytocic is the natural hormone oxytocin, which is secreted by the posterior
portion of the pituitary gland. The target organs for oxytocin are the uterus and the breast. As the growing
fetus distends the uterus, oxytocin is secreted in increasingly larger amounts, thus promoting labor and the
delivery of the baby. This process is referred to as positive feedback.
post 5 after In postpartum women, oxytocin is released in response to suckling, which causes milk to be
partum 5 childbirth ejected (let down) from the mammary glands. Oxytocin does not increase the volume of milk produc-
tion. This function is provided by the pituitary hormone prolactin, which increases the synthesis
of milk.
preterm 5 before term Several prostaglandins including dinoprostone (Cervidil, Prepidil, Prostin E2) and carboprost (Hema-
bate) are also used as uterine stimulants. Unlike most hormones, which travel through the blood to affect
distant tissues, prostaglandins are local hormones that act directly at the site where they are secreted.
These drugs are used to initiate labor, dilate the cervix prior to delivery, and control hemorrhage following
delivery.
Tocolytics are given as uterine relaxants to suppress preterm labor. This option is carefully weighed
against harm to the mother and the baby. Risks to the baby involve an elevated heart rate, circulatory
collapse, and respiratory paralysis. Risk to the mother is elevated blood pressure. Of the tocolytics listed
in Table 34.3, only hydroxyprogesterone (Makena) is approved for this indication: the others are used
off-label.
Concept Review 34.2

■ What is the difference between the effects of prolactin and oxytocin on the breast?
Table 34.3 Uterine Stimulants and Relaxants

Oxytocics
oxytocin (Pitocin) To control postpartum bleeding: 10–40 units Rapidly causes uterine contractions and in-
per infusion pump in 1,000 mL of IV fluid duces labor; postpartum bleeding is partially
To induce labor: IV 0.5–2 milliunits/min, controlled due to the stimulatory effect that
gradually increasing the dose no greater than oxytocin has on uterine smooth muscle
1–2 milliunits/min at 30–60 minute intervals
until contraction pattern is established
Ergot Alkaloid
methylergonovine (Methergine) PO; 0.2–0.4 mg bid–qid Ergot alkaloids help to prevent and control
bleeding after delivery of the baby
Prostaglandins
carboprost (Hemabate) IM; initial: 250 mcg (1 mL) repeated at 1½- Prostaglandins make uterine muscles contract;
and 3½-hour intervals if indicated by uterine during the uterine cycle, they naturally help
response the uterus shed its lining; clinically, these drugs
dinoprostone (Cervidil, Prepidil, Prostin E2) Intravaginal; 10 mg are for refractory postpartum uterine bleeding
Tocolytics
magnesium sulfate IV; 1–4 g in 5% dextrose by slow infusion These drugs inhibit uterine contractions in
(initial max dose = 10–14 g/day, then no more pregnant women at risk for preterm labor.
than 30–40 g/day at a max rate of 1–2 g/hour) Drugs are from different classes: magnesium
hydroxyprogesterone (Makena) IM; 250 mg once weekly, beginning at 16 week sulfate (mineral supplement), hydroxyproges-
gestation and continuing until week 37 terone (progestin), nifedipine (calcium channel
blocker), and terbutaline (beta-adrenergic drug)
nifedipine (Adalat, Procardia) PO; Initial dosage of 20 mg, followed by
20 mg orally after 30 minutes
If contractions persist, therapy can be continued
with 20 mg orally every 3–8 hours for 48–72
hours with a maximum dose of 160 mg/day
After 72 hours, if maintenance is still required,
long-acting nifedipine 30–60 mg daily can be used
terbutaline (Brethine) IV; 2.5–10 mcg/min; increase every 10–20
minutes; duration of infusion: 12 hours
(max: 17.5–30 mcg/min)
PO; maintenance dose: 2.5–10 mg every
4–6 hours
Drug Prototype: Oxytocin (Pitocin)

Therapeutic Class: Drug to induce labor; uterine stimulant Pharmacologic Class: Oxytocic
Actions and Uses: Oxytocin (Pitocin), identical to the complications in the mother may include uterine rupture,
natural hormone secreted by the posterior pituitary gland, seizures, or coma. Risk of uterine rupture increases in women
is a preferred drug for inducing labor. It is timed to the who have delivered five or more children.
final stage of pregnancy, after the cervix has dilated,
membranes have ruptured, and presentation of the fetus
has occurred. Black Box Warning:
Oxytocin is not indicated for the elective induction of labor
Adverse Effects and Interactions: The most common adverse (the initiation of labor in a pregnant patient who has no
effects of oxytocin are elevated blood pressure, rapid, pain- medical reason for induction).
ful uterine contractions and fetal tachycardia. Serious
Hypogonadism
Core Concept 34.6 Androgens are used to treat hypogonadism in males.
andro 5 male Androgens are male sex hormones. Testosterone is the primary androgen. Lack of sufficient testosterone
gen 5 forming secretion by the testes can result in male hypogonadism. Hypogonadism is the reduced function of gonads
or sex organs in the body. Hypogonadism may be congenital or acquired later in life. When the condition is
hypo 5 reduced
gonadism 5 sex hormone caused by a testicular disorder, it is called primary hypogonadism. Without sufficient FSH and LH secre-
function tion by the pituitary, the testes will lack their stimulus to produce testosterone. This condition is known as
secondary hypogonadism. Lack of FSH and LH secretion may have a number of causes, including Cush-
ing’s syndrome (negative feedback from corticosteroids), thyroid disorders, and estrogen-secreting tumors.
Symptoms of male hypogonadism include a diminished appearance of the secondary sex characteris-
tics of men: sparse axillary (armpit) hair, less facial and pubic hair; increased subcutaneous fat; and small
testicular size. In adult men, lack of testosterone can lead to erectile dysfunction, low sperm counts, and
libido 5 sexual desire decreased libido or interest in sex. In young men, lack of sufficient testosterone secretion may lead to
delayed puberty.
Pharmacotherapy of hypogonadism includes replacement therapy with testosterone or other andro-
gens. Within days or weeks of initiating therapy, androgens improve libido and correct erectile dysfunction
resulting from low testosterone levels. Male sex characteristics reappear, a condition called masculini-
virilization 5 appearance zation or virilization. Therapy with androgens is targeted to return serum testosterone to normal levels.
of male characteristics Above-normal levels serve no therapeutic purpose and increase the risk of adverse effects. High levels
of androgens may cause abnormal growth of body hair, testicular shrinkage, altered sex drive, develop-
ment of breasts, infertility, severe acne on the face and back, and possible mood swings involving rage or
depression.
Testosterone is available in a variety of formulations to better meet individual patient preferences and
lifestyles:
■ Implantable pellets (subcutaneous): Testopel one to six pellets are implanted on the anterior
abdominal wall.
■ Intramuscular (IM): Testosterone cypionate (Depo-Testosterone) and testosterone enanthate
(Delatestryl).
■ Testosterone buccal system: Striant tablet is applied to the gum area just above the front teeth
producing a continuous supply of testosterone in the bloodstream.
■ Transdermal testosterone gel: Androgel, Fortesta, and Testim are applied once daily to the upper
arms, shoulders, or abdomen. The drug is absorbed across the skin and into the bloodstream.
■ Transdermal testosterone patch: Androgen patch is applied directly to the upper arm, thigh,
back, or abdomen.
Selected androgens with indications for men are listed in Table 34.4 ◆.
Drug Prototype: Testosterone

Therapeutic Class: Male hypogonadism drug Pharmacologic Class: Androgen
Actions and Uses: The primary therapeutic use of testosterone is Testosterone base interacts with many drugs. For example,
for the treatment of hypogonadism in men. The administration when taken with oral anticoagulants, testosterone base may
of testosterone to young men who have an abnormally delayed increase hypoprothrombinemia. Insulin requirements may de-
puberty will stimulate normal secondary sex characteristics crease, and the risk of liver toxicity may increase when used
to appear, including enlargement of the sexual organs, facial with echinacea.
hair, and a deepening of the voice. In adult men, testosterone
administration will increase interest in sexual activity, or libido,
and restore masculine characteristics that may be deficient.
Black Box Warning:
Adverse Effects and Interactions: An obvious adverse effect of tes- Virilization in women and children may occur following sec-
tosterone therapy is virilization or appearance of masculine char- ondary exposure. Signs of virilization may include any of the
acteristics. Salt and water are often retained, causing edema. following; deepening of the voice, hirsutism, oily skin, and
Liver damage is a rare, although potentially serious, adverse male-pattern baldness.
effect. Acne and skin irritation is common during therapy.
Table 34.4 Selected Androgens and Anabolic Steroids

danazol (Danocrine) PO; 200–400 mg bid for 3–6 months Prevention of attacks of angioedema of all types (cutaneous,
abdominal, laryngeal)
fluoxymesterone (Halotestin) PO; 5 mg one to four times per day Replacement therapy for deficiency or absence of endogenous
testosterone, primary and secondary hypogonadism, or delayed
puberty
methyltestosterone (Android, PO; 10–50 mg/day Primary hypogonadism, testicular failure, hypogonadotropic
Testred, Virilon) Buccal: 5–25 mg/day hypogonadism, and delayed puberty
nandrolone (Durabolin, IM; 50–200 mg/week Management of anemia due to renal insufficiency, to increase
Hybolin) hemoglobin and red cell mass, and for patients who have had
kidney surgery with symptoms of swelling and inflammation
oxandrolone (Oxandrin) PO; 2.5–20 mg/day divided two to four times Adjunctive therapy to offset the protein breakdown associated
per day for 2–4 weeks with prolonged administration of corticosteroids, and for the
relief of the bone pain accompanying osteoporosis
oxymetholone (Anadrol-50) PO; 1–5 mg/kg/day Treatment of anemias caused by deficient red cell production,
aplastic anemias, and myelofibrosis; drugs should not replace
other supportive measures such as transfusion, correction of
iron, folic acid, vitamin B12 or pyridoxine deficiency, antibacte-
rial therapy, and the appropriate use of corticosteroids.
testosterone (buccal: Buccal; 30 mg/12 hours Primary therapy is for delayed puberty and hypogonadism; other
Striant); (transdermal patch: Transdermal; apply 1–2 patches daily indications are described in the Prototype drug feature
Androderm); (topical gels: (max: 5 mg/day)
Androgel, Fortesta, Testim);
(implantable pellets: Testopel) Gel; apply 5 g daily (max 10 g)
IM; 50–400 mg every 2–4 weeks
Pellets: 150–450 mg every 6 months (each
pellet is 75 mg)
testosterone cypionate IM; 50–400 mg every 2–4 weeks For replacement therapy in conditions associated with symp-
(Depo-Testosterone) toms of deficiency or absence of endogenous testosterone
testosterone enanthate IM; 50–400 mg every 2–4 weeks For replacement therapy in conditions associated with a defi-
(Delatestryl) ciency or absence of endogenous testosterone, primary hypogo-
nadism, secondary hypogonadism, and delayed puberty
Erectile Dysfunction
Erectile dysfunction is a common disorder successfully

treated with drug therapy. Core Concept 34.7
Penile erection has both neuromuscular and vascular components. Autonomic nerves dilate arterioles lead-
ing to the major erectile tissues of the penis, called the corpora cavernosa. The corpora have vascular corpora 5 bodies
spaces that fill with blood to cause rigidity. In addition, constriction of veins draining blood from the cor- cavernosa 5 cavernous
pora allows the penis to remain rigid long enough for successful penetration. After ejaculation, the veins
dilate, blood leaves the corpora, and the penis quickly loses its rigidity. Organic causes of erectile dysfunc-
tion may include damage to the nerves or blood vessels involved in the erection reflex.
Erectile dysfunction, or impotence, is a common disorder in men. The defining characteristic of this
condition is the consistent inability to either obtain an erection or to sustain an erection long enough to
achieve successful intercourse.
The incidence of erectile dysfunction increases with age, although it may occur in an adult male of
any age. Certain diseases, most notably atherosclerosis, diabetes, kidney disease, stroke, and hypertension,
are associated with a higher incidence of the condition. Smoking increases the risk of erectile dysfunction.
Psychogenic causes may include depression, fatigue, guilt, or fear of sexual failure. A number of com- psycho 5 the mind
mon drugs cause impotence as an adverse effect, including thiazide diuretics, phenothiazines, selective genic 5 generated from
Table 34.5 Drugs for Erectile Dysfunction

avanafil (Stendra) PO; 100 mg approximately 30 minutes The PDE-5 inhibitors do not cause an erection; they merely
before intercourse (max: 200 mg once enhance the erection by increasing blood flow and maintaining
per day) relaxation of the smooth muscle in the penis.
sildenafil (Viagra) PO; 50 mg approximately 30–60 minutes be- These drugs alter the body’s response to sexual stimulation by
fore intercourse (max: 100 mg once per day) enhancing the effect of the nitric oxide, a chemical that is nor-
mally released during stimulation. Nitric oxide causes relaxation
tadalafil (Cialis) PO; 10 mg approximately 30 minutes before
of the muscles in the penis, which allows for better blood flow
intercourse (max: 20 mg once per day)
to the penile area.
Once-daily dosing: 2.5–5 mg daily
vardenafil (Levitra) PO; 10 mg approximately 1 hour before
intercourse (max: 20 mg once per day)
serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), beta- and alpha-adrenergic block-
ers, and angiotensin-converting enzyme (ACE) inhibitors. Low testosterone secretion can cause an inabil-
ity to develop an erection due to loss of libido.
The development of sildenafil (Viagra), an inhibitor of the enzyme phosphodiesterase-5 (PDE-5),
revolutionized the medical therapy of erectile dysfunction. The PDE-5 inhibitors do not cause an erection;
they merely enhance the erection resulting from physical contact or other sexual stimuli by increasing
blood flow and maintaining relaxation of the smooth muscle in the penis.
Three other PDE-5 inhibitors have been approved by the Food and Drug Administration (FDA). Var-
denafil (Levitra) acts by the same mechanism as sildenafil but has a faster onset and slightly longer dura-
tion of action. Tadalafil (Cialis) acts within 30 minutes and has a prolonged duration lasting from 24 to 36
hours. In 2011, the indications for tadalafil were extended to include a daily dosing for the treatment of
benign prostatic hyperplasia (BPH). The newest of the drugs in this class, avanafil (Stendra), has the same
properties of the others but is claimed to have a faster onset of action. Drugs for erectile dysfunction are
Life Span Fact

Concept Review 34.3
Erectile dysfunction affects
about 1 in 4 men older than ■ Why do you think that sildenafil is used to treat erectile dysfunction instead of
age 65. testosterone?
Drug Prototype: Sildenafil (Viagra)

Therapeutic Class: Drug for erectile dysfunction Pharmacologic Class: Phosphodiesterase-5 inhibitor
Actions and Uses: Sildenafil acts by dilating blood vessels (vaso- of these drugs causes a marked increase in vasodilation, causing
dilation) and relaxing the erectile tissues in the penis, called the a drop in blood pressure and decreased blood flow to the heart,
corpora cavernosa, which allows increased blood flow into the possibly causing a heart attack. Minor adverse effects include
organ. The increased blood flow results in a firmer and longer- headache, flushing, and nasal congestion.
lasting erection in about 70% of men taking the drug. Cimetidine, erythromycin, and ketoconazole increase
serum levels of sildenafil and require lower drug doses.
Adverse Effects and Interactions: The most serious adverse Protease inhibitors (ritonavir, amprenavir, and others) will
effects with sildenafil occur in men who are concurrently cause increased sildenafil levels, which may lead to toxicity.
taking organic nitrates, common drugs that also dilate blood Rifampin may decrease sildenafil levels, leading to decreased
vessels and are used in the therapy of angina. The combination effectiveness.
Benign Prostatic Hyperplasia
In its early stages, benign prostatic hyperplasia is successfully treated. Core Concept 34.8
Benign prostatic hyperplasia (BPH) is the most common benign neoplasm in men. It is character- benign 5 mild
ized by enlargement of the prostate gland. This decreases the outflow of urine by obstructing the ure- hyper 5 over
thra, causing difficult urination. Symptoms include increased urinary frequency (usually with small plasia 5 growth
amounts of urine), increased urgency to urinate, excessive nighttime urination (nocturia), decreased noct 5 nighttime
force of the urine stream, and a sensation that the bladder is not completely empty. BPH is illustrated uria 5 urine
in Figure 34.3 ■.
Early in the course of the disease, drug therapy may relieve some symptoms. Only a few drugs are
available for the treatment of BPH. These drugs are listed in Table 34.6 ◆.
Life Span Fact
BPH affects 50% of men older
than age 60 and 90% of men
older than age 80.
Figure 34.3
Urinary bladder
Ureteral
opening
Prostate
gland
Urethra
Urinary
Openings of bladder
bulbourethral Hypertrophied
glands tissue True prostate
Corpus tissue
spongiosum Narrowed
urethra
Corpus
cavernosum penis
(b)
Glans
penis
(a)
Benign prostatic hyperplasia (BPH): (a) normal prostate with penis; (b) benign prostatic hyperplasia.
Table 34.6 Drugs for Benign Prostatic Hyperplasia

Alpha1-Adrenergic Blockers
alfuzosin (Uroxatral) PO; 10 mg/day (max: 10 mg/day) When activated, the alpha1-adrenergic receptors compress the
doxazosin (Cardura) PO (Regular-release); 1–8 mg/day urethra and provide resistance to urine outflow from the blad-
(max: 8 mg/day) der. Alpha1blockers counter urethral compression.
doxazosin (Cardura XL) PO (Extended-release); 4–8 mg/day

(max: 8 mg/day)
silodosin (Rapaflo) PO; 8 mg once daily with a meal
tamsulosin (Flomax) PO; 0.4 mg 30 minutes after a meal

(max: 0.8 mg/day)
terazosin (Hytrin) PO; start with 1 mg at bedtime, then
1–5 mg/day (max: 20 mg/day)
5-Alpha-Reductase Inhibitors
dutasteride (Avodart) PO; 0.5 mg once daily 5-Alpha-reductase inhibitors block the action of the enzyme
that converts testosterone into dihydrotestosterone, a pro-
finasteride (Proscar) PO; 5 mg once daily moter of prostate growth. The size of the prostate is therefore
reduced.
Drug Prototype: Finasteride (Proscar)

Therapeutic Class: Drug for benign prostatic hyperplasia (BPH)
Pharmacologic Class: 5-Alpha-reductase enzyme inhibitor
Actions and Uses: Finasteride acts by inhibiting 5-alpha reduc- Adverse Effects and Interactions: Finasteride causes
tase, the enzyme responsible for converting testosterone to various types of sexual dysfunction in some patients,
one of its metabolites. This metabolite causes growth of pros- including impotence, diminished libido, and ejaculatory
tate cells and promotes enlargement of the gland. Finasteride dysfunction.
shrinks enlarged prostates and helps to restore urinary function. No clinically significant drug interactions have been estab-
It is most effective in patients with larger prostates. This drug is lished. Use with caution with herbal supplements. For example,
also marketed as Propecia, which is prescribed to promote hair saw palmetto may increase the effects of finasteride.
regrowth in patients with male-pattern baldness. Doses of finas-
teride are five times higher when prescribed for BPH than when
prescribed for baldness.

Patients treated for reproductive disorders need to know the following:
Regarding Oral Contraceptives

1. If taking oral contraceptives, schedule frequent medical checkups. Take blood pressure
periodically and report any persistent changes to a healthcare provider.
2. Discontinue oral contraceptives, estrogen, or progestins immediately if pregnancy is sus-
pected. Continued use may injure the fetus.
3. Be certain to inform the healthcare provider if oral contraceptives are being taken. Some
drugs decrease the effectiveness of oral contraceptives and could result in pregnancy.
These drugs include several common antibiotics and antiseizure medications.
4. A balanced diet is important when taking oral contraceptives, because these drugs may
lower levels of folic acid and vitamin B6.
Chapter Review 559
Regarding Hormone Replacement Therapy

5. Before beginning HRT, a baseline mammogram should be performed. Monthly breast self-
examinations should be conducted in addition to an annual exam by a healthcare provider.
Regarding Erectile Dysfunction Medications

6. If taking antihypertensive drugs, monitor blood pressure carefully when taking sildenafil.
An increased risk of hypotension is possible.
Regarding Androgens
7. When taking androgens, expect virilization to occur. Prolonged erections, known as
priapisms, should be reported to a healthcare provider immediately. This is a sign of
overdose, and permanent damage to the penis may result.
Chapter Review
34.1 The hypothalamus, pituitary, and gonads control secretion. Administration of progestins may rees-
reproductive function in both men and women. tablish a normal cyclic menstrual pattern. Progestins
Estrogens are secreted by ovarian follicles and are are also used to treat endometrial cancer. Conjugated
responsible for maturation of the sex organs and the estrogens treat postmenopausal symptoms.
secondary sex characteristics of the female. Proges- 34.5 Oxytocin and tocolytics are drugs that influence
tins are secreted by the corpus luteum and prepare uterine contractions and labor.
the endometrium for implantation. Testosterone is
Oxytocics are drugs that stimulate uterine contrac-
secreted by the testes and is responsible for the growth
tions and induce labor. Oxytocin, methylergonovine
and maintenance of the male reproductive system. The
(ergot alkaloid), and prostaglandins are examples of
sex hormones are controlled by GnRH from the hypo-
uterine stimulants. Tocolytics slow uterine contrac-
thalamus and FSH and LH from the pituitary gland.
tions to delay labor.
34.2 Oral contraceptives are drugs used in low doses to 34.6 Androgens are used to treat hypogonadism
prevent pregnancy. in males.
OCs contain low doses of estrogens and progestins. Administration of testosterone promotes the appear-
Nearly 100% effective, these drugs prevent concep- ance of masculine characteristics, a desirable action
tion by blocking ovulation. Long-term formulations in men with hypogonadism. Anabolic steroids are tes-
offer greater flexibility of administration. OCs are tosterone-like drugs which may produce serious and
safe for the large majority of women, but they have permanent adverse effects.
some potentially serious adverse effects. Antibiotics,
antifungals, barbiturates, and antiseizure medications 34.7 Erectile dysfunction is a common disorder success-
can interfere with the effectiveness of OCs. fully treated with drug therapy.
Erectile dysfunction is a common disorder with many
34.3 Hormone replacement therapy provides estrogen
possible physiologic and psychogenic causes. Silde-
to treat postmenopausal symptoms, but benefits
nafil is effective at promoting more rigid and longer-
may not outweigh risks.
lasting erections. It is contraindicated in patients
Estrogen–progestin combinations are used for hor- taking organic nitrates.
mone replacement therapy during and after meno-
pause. Their long-term use may have serious adverse 34.8 In its early stages, benign prostatic hyperplasia is
effects including increased risk of MI, stroke, breast successfully treated.
cancer, and blood clots. BPH results in urinary difficulties that may be treated
by drug therapy or surgery. Alpha1-blockers relax
34.4 Conjugated estrogens and progestins are pre- smooth muscle in the urethra to promote urine flow.
scribed for dysfunctional uterine bleeding, endo- 5-Alpha-reductase inhibitors reduce the size of the
metrial cancer, and postmenopausal symptoms. prostate to reduce pressure on the urethra. Goals are
Dysfunctional uterine bleeding is often the result of to minimize urinary obstruction, increase urine flow,
an imbalance between progesterone and estrogen and to minimize complications.
Review Questions
The following questions are written in NCLEX-PN® style. 3. Fetal dysrhythmias

Answer these questions to assess your knowledge of the chap- 4. Hypotension
clear to you. 6. A patient, seeking information about testosterone replace-
ment therapy, asks the nurse about its application and possible
1. A nurse is discussing the various types of birth control complications. The nurse informs him that complications of
with a new patient at the clinic. The nurse tells the patient that testosterone therapy may include:
the type of birth control where the estrogen level remains con- 1. Renal failure
stant throughout the cycle but the progestin level increases to- 2. Hepatic failure
ward the end of the menstrual cycle is called: 3. Decreased cholesterol levels
1. Monophasic 4. Maturation of male sex organs
2. Biphasic
3. Triphasic 7. Your patient states that she has forgotten to take her birth
4. Quadriphasic control pills for the last 2 days. You should instruct her to:
1. Take her missed pills immediately.
2. Before a patient begins taking sildenafil (Viagra), the 2. Get back on schedule as soon as possible.
nurse asks which of the following questions? 3. Use additional birth control measures until a regular sched-
1. “Are you currently taking any medications for angina?” ule is established with the birth control pills.
2. “Do you have a history of diabetes?” 4. Get a home pregnancy kit.
3. “Have you ever had an allergic reaction to dairy products?”
4. “Have you ever been treated for migraine headaches?” 8. The physician ordered danazol (Danocrine) 100 mg,
po, twice a day. The pharmacy has 200 mg tablets. How many
3. When planning patient care, the nurse understands that milligrams will the nurse administer in a day?
medroxyprogesterone (Prempro) would be contraindicated for 1. 100 mg
which of the following patients? 2. 400 mg
1. A 37-year-old woman with dysfunctional uterine bleeding 3. 300 mg
2. A 65-year-old woman diagnosed with metastatic uterine 4. 200 mg
cancer
3. A 40-year-old woman with a history of deep vein thrombosis 9. A patient states that she is experiencing menopausal
4. A healthy 21-year-old who needs birth control symptoms and asks the nurse for advice regarding hormone re-
placement therapy (HRT). The nurse’s best response is:
4. The patient states she had sexual intercourse yesterday 1. “HRT is dangerous and should never be prescribed.”
and is concerned she may be pregnant. She is requesting emer- 2. “HRT is perfectly safe, with no risks.”
gency prevention. The nurse knows that which of the following 3. “You are not a candidate for HRT.”
drugs may be ordered? 4. “You need to discuss risks versus benefits of HRT with
1. Oxytocin your physician.”
2. Levonorgestrel
3. Medroxyprogesterone 10. Your patient with benign prostatic hyperplasia (BPH) is
4. Magnesium sulfate complaining of feeling like he “cannot empty his bladder.” You
suspect that the physician will order which of the following?
5. The patient is being given oxytocin (Pitocin). The nurse 1. Finasteride (Propecia)
evaluates her response to the drug, looking specifically for the 2. Sildenafil (Viagra)
possibility of: (Select all that apply.) 3. Estrogen
1. Uterine rupture 4. Finasteride (Proscar)
2. Seizures
Remember Ms. Philips, the patient bleeding with prolonged menstruation. Blood pressure and
introduced at the beginning of the pulse are slightly elevated. She states that she has had prob-
chapter? Now read the remainder of lems with frequently being tired. Other than her current
the case study. Based on the informa- complaint, she has no other health problems or concerns.
tion you have learned in this chapter, Ms. Philips’ last physical exam was one year ago. She is di-
answer the questions that follow. agnosed with dysfunctional uterine bleeding and is prescribed
Depo-Provera.
Ms. Marge Philips, a 42-year-old female, enters the clinic with
complaints of lower abdominal pain and irregular menstrual
Chapter Review 561
1. After the diagnosis is confirmed, the nurse knows that 3. Ms. Philips is to begin the oral contraceptive, Depo-
__________ is a common method of treating dysfunctional uter- Provera, as a means to control the uterine bleeding. The nurse
ine bleeding. informs her: (Select all that apply.)
1. Use of condoms 1. That smoking increases the risk of serious cardiovascular
2. Visiting the doctor only when the pain gets really bad adverse effects
3. Possible use of oral contraceptives 2. That it is OK to miss taking the medication for several days
4. Screening of sexual partner in a row
3. To notify her healthcare provider if two or more consecu-
2. In order to determine if Ms. Philips is a good candidate tive periods are missed
for the medication, Depo-Provera, the nurse asks Ms. Philips 4. That caffeine will actually be beneficial
if she:
1. Has diabetes 4. The nurse also informs Ms. Philips that the adverse
2. Is planning on losing weight effects of Depo-Provera are: (Select all that apply.)
3. Has a diet high in protein 1. Weight loss
4. Is planning on becoming pregnant 2. Breast tenderness
3. Loss of appetite
4. Breakthrough bleeding

U n i t
7
Integumentary System,
and Eyes and Ears
Unit Contents
Chapter 35 Drugs for Bone and Joint Disorders / 564
Chapter 36 Drugs for Skin Disorders / 582
Chapter 37 Drugs for Eye and Ear Disorders / 598

c
“I can’t even work in the
h garden anymore. My joints
a ache so badly and I don’t
p understand what’s going on
with my big toe.”
t
Mr. Steven Hurtt
e
r
35 Drugs for Bone and Joint Disorders
Core Concepts
35.1 Adequate levels of calcium, vitamin D, parathyroid 35.5 Treatment for Paget’s disease includes bisphospho-
hormone, and calcitonin are necessary for bone and nates and calcitonin.
body homeostasis. 35.6 Analgesics and anti-inflammatory drugs are
35.2 Hypocalcemia is a serious condition that requires important components of pharmacotherapy
immediate therapy. for osteoarthritis.
35.3 Osteomalacia and rickets are successfully treated 35.7 Immunosuppressants and disease-modifying drugs
with calcium salts and vitamin D supplements. are additional therapies used to treat rheumatoid
35.4 Treatment for osteoporosis includes calcitonin, arthritis.
selective estrogen-receptor modulators, and 35.8 Pharmacotherapy for gout requires drugs that
bisphosphonates. control uric acid levels.
Drug Snapshot
Calcium supplements calcium salts 569 Disease-modifying hydroxychloroquine
antirheumatic drugs (Plaquenil) 575
Vitamin D therapy c alcitriol (Calcijex,
(DMARDs)
Rocaltrol) 569
Uric acid inhibitors llopurinol (Lopurin,
a
Selective estrogen- raloxifene (Evista) 571
for gout Zyloprin) 578
receptor modulators
Bisphosphonates alendronate (Fosamax) 572
Learning Outcomes
1. Identify the role of calcium and calcium and vitamin D deficiency and 6. Explain drug treatments for
vitamin D in maintaining bone health. disorders related directly to bones osteoarthritis, rheumatoid arthritis,
2. Identify the symptoms or disorders and joints. and gout.
associated with an imbalance of 4. Discuss drug treatments for 7. For each of the classes listed in the
calcium, vitamin D, parathyroid hypocalcemia, osteomalacia, and rickets. Drug Snapshot, identify representative
hormone, and calcitonin. 5. Identify important disorders drugs and explain their mechanisms of
3. Describe the pharmacologic characterized by weak and fragile drug action, primary drug actions, and
management of disorders caused by bones. important adverse effects.
Key Terms
acute gouty arthritis (ah-CUTE GOW-ty calcitonin (kal-sih-TOH-nin) 565 osteomalacia (OSS-tee-oh-muh-LAY-
are-THRYE-tis) 577 calcitriol (kal-si-TRY-ol) 565 shee-uh) 566
autoantibodies (AW-tow-ANN-tee-BAH- cholecalciferol (KOH-lee-kal-SIF- osteoporosis (OSS-tee-oh-poh-ROH-sis) 569
dees) 575 er-ol) 565 Paget’s disease (PAH-jets) 573
bisphosphonates (bis-FOSS-foh-nayts) disease-modifying antirheumatic (ANTY- rheumatoid arthritis (RA) (ROO-mah-toyd
572 roo-MAT-ik) drugs (DMARDs) 575 are-THRYE-tis) 575
bone deposition 565 gout (GOWT) 576 selective estrogen-receptor modulators
bone resorption (ree-SORP-shun) 565 osteoarthritis (OA) (OSS-tee-oh-are- (SERMs) 570
calcifediol (kal-SIF-eh-DYE-ol) 565 THRYE-tis) 574 uricosurics (YOUR-ik-cose-youriks) 577
T he skeletal system and joints are at the core of movement and must be free from any defect that
would destabilize the other body systems. For nerves, muscles, and bones to function well, the body
needs adequate levels of calcium. Disorders associated with bones and joints affect a patient’s abil-
ity to fulfill daily activities and lead to immobility.
This chapter focuses on the pharmacotherapy of skeletal disorders such as osteomalacia, osteoporosis,
arthritis, and gout and stresses the importance of calcium balance and the action of vitamin D as they relate
to the proper structure and function of bones and joints. Drugs are important because major mobility prob-
lems would occur without intervention.
Adequate levels of calcium, vitamin D, parathyroid hormone,

and calcitonin are necessary for bone and body homeostasis. Core Concept 35.1
As shown in Figure 35.1 ■, calcium levels in the bloodstream are controlled by two endocrine glands: the
parathyroid glands and the thyroid gland. The parathyroid glands secrete parathyroid hormone (PTH), and
the thyroid gland secretes calcitonin. PTH stimulates bone cells called osteoclasts. Osteoclasts break down
bone tissue into its mineral components, a process called bone resorption. Once the bone is broken down,
calcium is released for transport in the bloodstream and is used elsewhere in the body. The opposite of
this process is bone deposition, or bone building. Calcitonin stimulates the building of bones by adding
calcium to bone tissue.
Vitamin D is unique among vitamins in that the body is able to synthesize it from precursor mol-
ecules. The inactive form of vitamin D, called cholecalciferol, is synthesized in the skin from cholesterol.
Exposure of the skin to sunlight or ultraviolet light increases the level of cholecalciferol in the blood-
stream. Cholecalciferol can also be obtained from dietary products such as milk or other foods fortified
with vitamin D. Figure 35.2 ■ illustrates the metabolism of vitamin D.
Once cholecalciferol is absorbed or formed in the body, it is converted to an intermediate vitamin
form called calcifediol. Enzymes in the kidneys metabolize calcifediol to calcitriol, the active form of
vitamin D. Patients with extensive kidney disease are unable to synthesize adequate levels of calcitriol. The
primary function of calcitriol is to increase calcium absorption from the gastrointestinal (GI) tract. Dietary
calcium is absorbed better in the presence of PTH and active vitamin D.
The importance of proper calcium balance in the body cannot be overstated. Calcium ions influence
the excitability of all neurons. When calcium concentrations are too high (hypercalcemia), sodium per- hyper 5 elevated
meability decreases across cell membranes. This is dangerous because nerve conduction depends on the
proper influx of sodium into cells. When calcium levels in the bloodstream are too low (hypocalcemia), hypo 5 lowered
cell membranes become hyperexcitable. If hypocalcemia becomes severe, seizures or muscle spasms may calc 5 calcium
emia 5 blood level
result. Calcium is also important for the normal functioning of other body processes such as blood coagula-
tion, neurotransmitter release, and stability of the entire skeletal system.
Hypocalcemia
Hypocalcemia is a serious condition that requires immediate therapy. Core Concept 35.2
Hypocalcemia, or lowered levels of calcium in the blood, is associated with a range of conditions, includ-
ing poor nutrition, seizures, muscle spasms, and endocrine and bone disorders. Hypocalcemia is not a
disease, but a sign of underlying pathology; therefore, diagnosis of the cause of hypocalcemia is essential.
One common cause is hyposecretion of PTH, which occurs when the thyroid and parathyroid glands are
566 Chapter 35 Drugs for Bone and Joint Disorders
Figure 35.1
(a) Parathyroid hormone Parathyroid glands

(PTH); (b) calcitonin
action.
1 Release of calcium from bone
Parathyroid glands cause: 2 Increased calcium reabsorption

PTH release from kidneys
3 Increased absorption of calcium
in small intestine (with help of
calcitriol or vitamin D)
Lower levels of calcium Higher levels of calcium

in the bloodstream in the bloodstream
(a)
Thyroid gland
Thyroid gland causes: 1 Addition of calcium to bone

Calcitonin release
2 Decreased absorption of
calcium in small intestine
Higher levels of calcium

in the bloodstream
Lower levels of calcium
in the bloodstream
(b)
surgically removed. Digestive-related malabsorption disorders and vitamin D deficiencies also result in
hypocalcemia. In cases of hypocalcemia, healthcare providers should assess for the adequate intake of
calcium-containing foods. With hypocalcemia, numbness and tingling of the extremities may occur, and
convulsions are possible. Symptoms of hypocalcemia are nerve and muscle excitability. Muscle twitching,
tremor, or cramping may be evident. A patient may be confused or behave abnormally.
Therapies for calcium disorders involve calcium salts, vitamin D supplements, bisphosphonates, and/
or miscellaneous drugs. Severe hypocalcemia requires IV administration of calcium salts, whereas less
severe hypocalcemia can often be reversed with oral supplements.
Osteomalacia and Rickets
Osteomalacia and rickets are successfully treated with calcium

Core Concept 35.3 salts and vitamin D supplements.
Osteomalacia, referred to as rickets in children, is a disorder characterized by softening of bones without

alteration of basic bone structure. The cause of osteomalacia and rickets is a lack of vitamin D and calcium
in the diet, usually as a result of kidney failure or malabsorption of calcium from the GI tract.
Figure 35.2
Pathway for vitamin D

activation.
Cholecalciferol
(inactive vitamin D)
Skin
Diet
Liver
Calcifediol
(intermediate form)
PTH
Kidney
Parathyroid glands
Calcitriol
(active vitamin D)
Increased absorption
of calcium in
the small intestine
Signs and symptoms of osteomalacia include hypocalcemia, muscle weakness, muscle spasms, and
diffuse bone pain, especially in the hip area. Patients may also experience pain in the arms, legs, and spi-
nal column. Classic signs of rickets in children include bowlegs and a pigeon breast. Children may also
develop a slight fever and become restless at night.
Tests performed to verify osteomalacia include bone biopsy; bone radiographs; computerized tomog-
raphy (CT) scan of the vertebral column and other bone density tests; and determination of serum calcium,
phosphate, and vitamin D levels. Many of these tests are routine for bone disorders and are performed as
needed to determine the extent of bone health.
Drug therapy for osteomalacia consists of calcium salts and vitamin D supplements. Drugs used for treat-
ing metabolic bone disorders including hypocalcemia, osteomalacia, and rickets are shown in Table 35.1 ◆.
In extreme cases, surgical correction of disfigured limbs may be required.
Most calcium salts are in the form of complexed calcium. These products are often compared on the
basis of their ability to release elemental calcium into the bloodstream. The supplement is more potent
when the complexed calcium has a greater ability to release elemental calcium. Milliequivalence (mEq)
Table 35.1 Calcium Salts and Vitamin D Therapy

Calcium Salts (The higher the mEq, the more potent the calcium salt)
calcium acetate (PhosLo) PO; 1–2 g bid–tid One gram calcium acetate equals 250 mg (12.6 mEq) elemental
calcium; phosphate binder used to treat hypophosphatemia in
dialysis patients
calcium carbonate (Rolaids, PO; 1–2 g bid–tid One gram calcium carbonate equals 400 mg (20 mEq) elemental
Tums, others) calcium
calcium chloride IV; 0.5–1 g by slow infusion (1 mL/min) One gram calcium chloride equals 272 mg (13.6 mEq) elemental
calcium; may be irritating to body tissues
calcium citrate (Citracal) PO; 1–2 g bid–tid One gram calcium citrate equals 210 mg (12 mEq) elemental
calcium
calcium gluconate (Kalcinate) PO; 1–2 g bid–tid One gram calcium gluconate equals 90 mg (4.5 mEq) elemental
IV; 0.5–4 g by slow infusions (1 g/hour) calcium
calcium lactate (Cal-Lac) PO; 100–200 mg tid with meals One gram calcium lactate equals 130 mg (6.5 mEq) elemental
calcium
calcium phosphate tribasic PO; 1–2 g bid–tid One gram calcium phosphate equals 390 mg (19.3 mEq)
(Posture) elemental calcium
Vitamin D Supplements
calcitriol (Calcijex, PO; 0.25 mcg/day For hypocalcemia in chronic renal failure and with
Rocaltrol) IV; 0.5 mcg three times per week at the hypoparathyroidism
end of dialysis
doxercalciferol (Hectorol) PO; 10 mcg, three times per week For hyperparathyroidism in patients with chronic kidney disease
(max: 60 mcg/week) or in patients on dialysis
IV; 4 mcg, three times per week at the
end of dialysis (max: 18 mcg/week)
ergocalciferol (Calciferol, PO; 25–125 mcg/day for 6–12 weeks For osteomalacia; also used for vitamin D–dependent rickets
Drisdol) and hypoparathyroidism
paricalcitol (Zemplar) PO; 1 mcg/day or 4 mcg three times per For the prevention and treatment of hyperparathyroidism in
week patients with chronic kidney disease
IV; 0.04–0.1 mcg/kg, every other day during
dialysis (max: 24 mcg/kg)
is the unit used to describe the amount of electrolyte available to the bloodstream. Therefore, the higher
the mEq, the more potent the calcium salt. Elemental calcium may be obtained from dietary sources
such as dark green vegetables, canned salmon, and fortified products, including tofu, orange juice,
and milk.
Inactive, intermediate, and active forms of vitamin D are also available. The amount of vitamin D a
patient needs will often vary depending on how much he or she is exposed to sunlight. After age 70, the
average recommended intake of vitamin D increases from 400 to 600 units per day. Because vitamin D
is needed to absorb calcium from the GI tract, many supplements combine vitamin D and calcium into a
single tablet.
Concept Review 35.1

■ Identify the major drug therapies used for hypocalcemia, osteomalacia, and rickets.
Drug Prototype: Calcium salts

Therapeutic Class: Calcium supplement for hypoparathyroidism, osteoporosis, and rickets
Pharmacologic Class: Reverses hypocalcemia
Actions and Uses: Calcium salts are used to correct hypocalcemia by taking too much of these supplements. Symptoms include
and to treat osteoporosis and rickets. The objective of calcium drowsiness, lethargy, weakness, headache, anorexia, nausea and
therapy is to return serum levels of calcium to normal. People at vomiting, increased urination, and thirst. IV administration of
high risk for developing these conditions include postmenopausal calcium may cause hypotension, bradycardia, dysrhythmia, and
women; those with little physical activity over a prolonged period; cardiac arrest.
and patients taking certain medications such as corticosteroids, Using calcium salts with cardiac glycosides increases the
immunosuppressive drugs, and some antiseizure medications. risk of dysrhythmias. Magnesium antacids or supplements may
compete for GI absorption. Calcium decreases the absorption of
Adverse Effects and Interactions: The most common adverse tetracyclines.
effect of calcium salts is hypercalcemia, which is brought on
Drug Prototype: Calcitriol (Calcijex, Rocaltrol)

Therapeutic Class: Drug for osteoporosis, osteomalacia, and rickets
Pharmacologic Class: Vitamin D, reverses hypocalcemia
Actions and Uses: Calcitriol is the active form of vitamin D and Adverse Effects and Interactions: Common adverse effects
is available in both oral and IV formulations. It promotes the include hypercalcemia, headache, weakness, dry mouth, thirst,
intestinal absorption of calcium and elevates serum levels of increased urination, and muscle or bone pain. Thiazide diuretics
calcium. This medication is used when patients have impaired may increase the effects of vitamin D, causing hypercalcemia.
kidney function or have hypoparathyroidism. Calcitriol reduces Too much vitamin D may cause dysrhythmias in patients who
bone resorption and is useful in treating rickets. The effective- are receiving cardiac glycosides. Magnesium antacids or
ness of calcitriol depends on the patient receiving an adequate supplements should not be given together with calcitriol
amount of calcium; therefore, it is usually prescribed in combi- because of the increased risk of hypermagnesemia.
nation with calcium supplements.
Osteoporosis
Treatment for osteoporosis includes calcitonin, selective

estrogen-receptor modulators, and bisphosphonates. Core Concept 35.4
Osteoporosis is the most common metabolic bone disorder. This disorder is usually asymptomatic until
the bones become brittle enough to fracture or a vertebra collapses. In some cases, a lack of dietary cal-
cium and vitamin D contribute to bone deterioration. In other cases, osteoporosis is due to disrupted bone
homeostasis.
Simply stated, the homeostatic imbalance with osteoporosis is that bone resorption outpaces bone
deposition, and patients begin to develop weak bones. This is generally considered an aging disorder. Fol-
lowing are the risk factors for osteoporosis:
■ Postmenopausal status
■ High alcohol or caffeine consumption
■ Anorexia nervosa
■ Tobacco use
■ Physical inactivity
■ Testosterone deficiency, particularly in elderly men
■ Lack of adequate vitamin D or calcium in the diet
■ Drugs such as corticosteroids, some anticonvulsants, and immunosuppressants that lower cal-
cium levels in the bloodstream
Figure 35.3
Calcium metabolism in (a) Normal calcium intake

osteoporosis: (a) bone Bone
deposition equals bone Deposition
resorption; (b) bone re-
sorption outpaces bone
deposition).
Intestine Normal bone
homeostasis:
Deposition =
resor ption
Blood n
R e s o r p ti o
To body
(b) Low calcium intake

Bone
No deposition
Osteoporotic bone:
Intestine Resorption exceeds
deposition. Bone
becomes fragile.
Blood
E xcess
R e s o r p ti o n
To body
The most common risk factor associated with the development of osteoporosis is the onset of meno-
pause. When women reach menopause, estrogen secretion declines and bones become weak and fragile.
One theory to explain this occurrence is that normal levels of estrogen may limit the life span of osteo-
clasts, the bone cells that resorb bone. When estrogen levels become low, osteoclast activity is no longer
controlled, and bone demineralization accelerates, resulting in loss of bone density. In women with osteo-
porosis, fractures often occur in the hips, wrists, forearms, or spine. The metabolism of calcium in osteopo-
rosis is illustrated in Figure 35.3 ■.
Many drug therapies are available for osteoporosis. These include calcium and vitamin D therapy,
hormone therapy with estrogen, estrogen-receptor modulators, calcitonin, statins, slow-release sodium
fluoride, and bisphosphonates. Many of these drug classes are also used for other bone disorders or condi-
tions unrelated to the skeletal system. Selected drugs for osteoporosis and related bone disorders are listed
in Table 35.2 ◆.
Selective Estrogen-Receptor Modulators

Selective estrogen-receptor modulators (SERMs) bind to estrogen receptors and comprise a class of
drugs used in the prevention and treatment of osteoporosis. SERMs may be estrogen agonists or antago-
nists, depending on the specific drug and the tissue involved. In the uterus and breasts, raloxifene (Evista)
blocks estrogen receptors; thus, it has no estrogen-like proliferative effects on these tissues that might
promote cancer. It is one of the few drugs available for the prevention of breast cancer in postmenopausal
women at high risk for the disease. Evista decreases bone resorption, thus increasing bone density and
making fractures less likely. Like estrogen, it has a cholesterol-lowering effect.
Table 35.2 Bone Resorption Inhibitors and Selected Drugs

Hormonal (Biologic) and Selected Drugs
calcitonin–salmon (Fortical, Hypercalcemia: subcutaneous/IM; salmon, Calcium regulating hormone; used commonly for hypercalcemia
Miacalcin) 4 units/kg bid and postmenopausal osteoporosis
Osteoporosis: intranasal; 1 spray/day
(200 international units) in one nostril,
alternating nostrils each day
cinacalcet (Sensipar) PO; start with 30 mg once daily; may For secondary hyperparathyroidism
increase every 2–4 weeks until target PTH
of 150–300 mg/mL (max: 300/day)
denosumab (Prolia, Xgeva) Subcutaneous (Prolia); 60 mg every For postmenopausal osteoporosis in women at high risk for
6 months fracture (Prolia) or prevention of skeletal-related adverse events
in patients with bone metastases (Xgeva)
raloxifene (Evista) PO; 60 mg daily Selective estrogen-receptor modulator; for prevention and
treatment of osteoporosis in postmenopausal women and
breast cancer prophylaxis
teriparatide (Forteo) SC; 20 mcg/day Parathyroid hormone (rDNA origin); for osteoporosis in
postmenopausal women; for male patients with high risk of
fractures
Bisphosphonates
alendronate (Fosamax) Osteoporosis treatment: PO; 10 mg daily For osteoporosis in men and women; for Paget’s disease
Osteoporosis prevention: PO; 5 mg daily
Paget’s disease: PO 40 mg daily for 6 months
etidronate (Didronel) PO; 5–10 mg/kg daily for 6 months or For Paget’s disease
11–20 mg/kg daily for 3 months
ibandronate (Boniva) PO; 2.5 mg daily or 150 mg once monthly For treatment and prevention of postmenopausal osteoporosis
pamidronate (Aredia) IV; 30–90 mg infused over 4–24 hours For Paget’s disease and hypercalcemia of malignancy
risedronate (Actonel) PO; 5 mg daily or 35 mg once weekly or For prevention and treatment of osteoporosis and Paget’s
75 mg daily for two consecutive weeks disease
tiludronate (Skelid) PO; 400 mg daily taken with 6–8 ounces For Paget’s disease
of water 2 hours before or after food for
3 months
zoledronate (Reclast, Zometa): IV; 4–5 mg, may be repeated in 7 days For hypercalcemia of malignancy; treatment of steroid-induced
also called zoledronic acid osteoporosis, postmenopausal osteoporosis, bone metastases,
and Paget’s disease
Drug Prototype: Raloxifene (Evista)

Therapeutic Class: Treatment of postmenopausal osteoporosis in women
Pharmacologic Class: Bone resorption inhibitor, selective estrogen-receptor modulator
Actions and Uses: Raloxifene is a SERM. It decreases bone disorder, breast pain, and vaginal bleeding. Patients should
resorption and increases bone mass and density by acting not take cholesterol-lowering drugs or estrogen replacement
through the estrogen receptor. Raloxifene is primarily used for therapy concurrently with this medication.
the prevention of osteoporosis in postmenopausal women. It Absorption is reduced by cholestyramine. Patients taking
is also one of the few drugs used for the prevention of breast raloxifene, along with warfarin, should have their PT/INR tested
cancer in women at high risk for invasive breast cancer. This when starting or stopping this medication
drug also reduces serum total cholesterol and low-density
lipoprotein (LDL) without lowering high-density lipoprotein Black Box Warning:
(HDL) or triglycerides. Raloxifene increases the risk of venous thromboembolism
and death from strokes. Women with a history of venous
Adverse Effects and Interactions: Common adverse effects are thromboembolism should not take this drug.
hot flashes, migraine headache, flu-like symptoms, endometrial
Calcitonin
Calcitonin is a naturally occurring hormone secreted by the thyroid gland when blood calcium becomes
elevated. It is involved in the process of bone building by opposing the effects of the PTH and inhibiting
osteoclast activity in the bone. As a medication, calcitonin is obtained from salmon and is approved for the
treatment of osteoporosis in women who are more than five years postmenopausal. It is available by nasal
spray or subcutaneous injection. Calcitonin increases bone density and reduces the risk of vertebral frac-
tures. Adverse effects are generally minor; the nasal formulation may irritate the nasal mucosa and aller-
gies are possible. Parenteral forms may produce nausea and vomiting. In addition to treating osteoporosis,
calcitonin is indicated for Paget’s disease and hypercalcemia.
Bisphosphonates
The most common drug class used to treat osteoporosis is the bisphosphonates. These drugs are very
similar to pyrophosphate, a natural inhibitor of bone resorption. Bisphosphonates inhibit bone resorption
by suppressing osteoclast activity, thereby increasing bone density and reducing the incidence of frac-
tures. Examples include alendronate (Fosamax), etidronate (Didronel), ibandronate (Boniva), pamidronate
(Aredia), risedronate (Actonel, Atelvia), tiludronate (Skelid), and zoledronate (Reclast, Zometa). Although
primarily used to treat osteoporosis in postmenopausal women, drugs in this class are also used to treat
Paget’s disease, osteoporosis in men, hypercalcemia of malignancy and metastases due to bone cancer,
multiple myeloma or breast cancer. Adverse effects include GI problems such as nausea, vomiting, abdom-
inal pain, and esophageal irritation; therefore, patients are advised to remain in an upright position for 30
minutes after taking these medications. Because these drugs are poorly absorbed, they should be taken on
an empty stomach, as tolerated by the patient. Once-weekly dosing may give the same bone-density ben-
efits as daily dosing because of these drugs’ extended duration of action.
Concept Review 35.2

■ What are the major drug therapies used for the treatment of osteoporosis and related
bone disorders?
Drug Prototype: Alendronate (Fosamax)

Therapeutic Class: Drug for osteoporosis Pharmacologic Class: Bone resorption inhibitor, bisphosphonate
Actions and Uses: Alendronate is approved for the following Adverse Effects and Interactions: Common adverse effects of
indications: prevention of osteoporosis in postmenopausal alendronate are diarrhea, nausea, vomiting, esophageal irrita-
women, treatment of glucocorticoid-induced osteoporosis tion, and a metallic or altered taste perception. Pathologic frac-
in both women and men, to increase bone mass in men with tures may occur if the drug is taken longer than three months.
osteoporosis, and treatment of symptomatic Paget’s disease in Calcium supplements may decrease absorption of alendronate;
both women and men. Alendronate is also used off-label for therefore, use of these drugs together should be avoided.
treating hypercalcemia due to malignancy. Therapeutic effects Food–drug interactions are common. Milk and other dairy
may take from one to three months to appear and may con- products and medications, such as calcium, iron, antacids, and
tinue for several months after therapy is discontinued. All doses other mineral supplements, must be reviewed before beginning
must be taken on an empty stomach, preferably in a fasting bisphosphonate therapy because they have the potential to
state two hours before breakfast. decrease the effectiveness of bisphosphonates. Blood levels of
the enzyme alkaline phosphatase are lowered with this drug.
Nursing Process Focus Patients Receiving Pharmacotherapy for Osteoporosis

■ Obtain a complete health history, including musculoskeletal, GI, therapy
cardiovascular, neurological, thyroid/parathyroid, renal, and liver ■ Infective Health Maintenance related to lifestyle changes or adverse
conditions; allergies; drug history; and possible drug interactions. drug effects
■ Evaluate laboratory blood findings: CBC, electrolytes, lipid panel, ■ Risk for Injury related to disease process and adverse drug effects
T3, T4 and TSH, and renal and liver function studies. ■ Risk of Falls related to disease process and adverse drug effects
■ Collect a dietary history, noting adequacy of essential vitamins,
minerals, and nutrients obtained through food sources.
■ Obtain a history of current symptoms and effect on activities of
daily living (ADLs).
continued . . .

The patient will:
■ Experience therapeutic effects (a gain or maintenance of adequate bone density).
■ Verbalize understanding of the drug’s use, adverse effects, and required precautions.
Implementation
of proper administration. (Incorrect use may decrease absorption of ■ About the proper administration method guidelines.
medication.) ■ Bisphosphonates should be taken on an empty stomach, and to
remain in a sitting position after taking medication.
■ Review dietary history and discuss food source options, correcting Inform the patient:
any calcium and vitamin D deficiencies. (Adequate amounts of ■ To eat adequate amounts of calcium, vitamin D, and magnesium
calcium, vitamin D and magnesium are needed for bone health. If from food.
taking bisphosphonates, a review of foods and medications should be ■ That milk and other calcium rich foods and medications (such as ant-
done because calcium rich foods, medication, and supplements may acids and calcium supplements) must be reviewed before beginning
decrease absorption of bisphosphonates.) bisphosphonate therapy because they may decrease absorption of drug.
■ Monitor for adverse effects of medications. Bisphosphonates may Inform the patient:
cause GI irritation. SERMs increase the risk of venous thromboembo- ■ Bisphosphonates may cause esophageal and gastric irritation,
lism and death from strokes. (Women with a history of thrombosis abdominal pain, and nausea; to report immediately the onset of
should not take this medication.) nausea or abdominal pain to the healthcare provider.
■ SERMs may cause hot flashes, migraines, flu-like symptoms endome-
trial problems, breast pain and increase the risk of forming blood clots.
Discontinue three days prior to surgery.
■ That intranasal administration of calcitonin may cause nasal irritation.
Allergies are also possible.
■ Review and monitor the use of other medications. (Concurrently using Instruct the patient:
some medications with those used for osteoporosis may cause adverse ■ Not to take cholesterol-lowering drugs or estrogen replacement
effects or impact absorption.) therapy concurrently with SERMs.
■ If taking raloxifene along with warfarin, PT/INR should be tested
when starting or stopping.
■ Calcium supplements should not be used with bisphosphonates.
■ Continue to monitor periodic laboratory tests, especially calcium, Instruct the patient to:
magnesium, phosphorus, and creatinine. Assess for sign or symptoms ■ Return periodically for laboratory tests.
of hypo/hypercalcemia. (These electrolytes should remain or return to ■ Report any symptoms of hypocalcemia (muscle spasms, facial grimac-
normal limits. Increased creatinine levels may require discontinuation ing, irritability hyper-reflexes) or hypercalcemia (increased bone pain,
of medication.) anorexia, nausea, vomiting, constipation, thirst, lethargy, fatigue) to
■ Increase fluid intake, avoiding caffeine, soda, and alcohol. (Some Instruct the patient to:
kidney stones are composed of calcium; increasing fluid intake ■ Increase fluid intake to 2 L/day.
decreases the risk of kidney stones formation. Caffeine diminishes ■ Avoid excessive caffeine because it diminishes the absorption of calcium.
the absorption of calcium.) ■ Limit or eliminate alcohol.
■ Monitor for adherence to recommended lifestyle, for example, diet, Inform the patient:
exercise, and medication regimen. (Bone remodeling occurs over ■ To engage in weight-bearing exercises, three to five times a week.
several months. The patient may discontinue the drug because of ■ To acquire a limited amount of daily sun exposure (15–20 minutes) for
perceived lack of results.) vitamin D synthesis.
■ That the therapeutic effects of the medication(s) may take one to three
months and to continue taking the drug as prescribed to ensure full effect.

Paget’s Disease
Treatment for Paget’s disease includes bisphosphonates and calcitonin. Core Concept 35.5
Paget’s disease, or osteitis deformans, is a chronic, progressive condition characterized by enlarged and
abnormal bones. With this disorder, the processes of bone resorption and bone formation occur at a high
rate. Excessive bone turnover causes the new bone to be weak and brittle, which may result in deformity
and fractures. The patient may be asymptomatic or have only vague, nonspecific complaints for many
years. Symptoms include pain of the hips and femurs, joint inflammation, headaches, facial pain, and hear-
ing loss if bones around the ear cavity are affected. Nerves along the spinal column may be pinched in the
compressed vertebrae.
Paget’s disease is sometimes confused with osteoporosis because some of the symptoms are similar.
In fact, medical treatments for osteoporosis are similar to those for Paget’s disease. The cause of Paget’s
disease, however, is quite different. Blood levels of the enzyme alkaline phosphatase are elevated because
of the extensive bone turnover. Detection of this enzyme in the blood often provides early confirmation
of the disease. Calcium blood levels are also increased. The symptoms of Paget’s disease can be treated
successfully when diagnosis is made early. If the diagnosis is made late in the disease’s progression, per-
manent skeletal abnormalities may develop, and other disorders may appear, including arthritis, kidney
stones, and heart disease.
Bisphosphonates are the preferred pharmacotherapy for Paget’s disease. Therapy is usually cyclic:
Bisphosphonates are administered until serum alkaline phosphatase levels return to normal; then a drug-
free period of several months follows. When serum alkaline phosphatase levels become elevated, therapy
is begun again. The pharmacologic goals are to slow the rate of bone reabsorption and encourage the depo-
sition of strong bone. Calcitonin nasal spray is used as an option for patients who cannot tolerate bisphos-
phonates. Surgery may be indicated in cases of severe bone deformity, degenerative arthritis, or fracture.
Patients with Paget’s disease should receive adequate daily dietary intake of calcium and vitamin D.
Sufficient exposure to sunlight is also important.
Concept Review 35.3

■ Identify two important disorders characterized by weak and fragile bones. What are the
major drug therapies used in their treatments?
Osteoarthritis
Analgesics and anti-inflammatory drugs are important

Core Concept 35.6 components of pharmacotherapy for osteoarthritis.
Arthritis is a general term meaning inflammation of a joint. There are several types of arthritis, each having
somewhat different characteristics based on the etiology. Because joint pain is common to both arthritic
and joint disorders, analgesics and/or anti-inflammatory drugs are important components of pharmaco-
therapy. A few additional drugs are specific to the particular pathologies.
osteo 5 bone Osteoarthritis (OA) is a degenerative disease in which the cartilage at articular joint surfaces wears
arthr 5 joint away. Like osteoporosis, this condition is considered to be an aging disorder. It is not accompanied by the
itis 5 associated disease, degree of inflammation associated with other forms of arthritis. Signs are localized pain and stiffness, joint
often linked with
and bone enlargement, and limitations in movement. The cause of OA is thought to be excessive wear and
inflammation
tear of weight-bearing joints; the knee, spine, and hip are particularly affected.
The goals of pharmacotherapy for OA include reduction of pain and inflammation. The initial treat-
ment of choice is acetaminophen. For patients whose pain is unrelieved by acetaminophen, nonsteroidal
anti-inflammatory drugs (NSAIDs), including naproxen and ibuprofen-like drugs, are usually given. Tra-
madol (Ultram) is a non-NSAID option for the treatment of moderate to severe pain. Although classified
as an opioid, tramadol does not have abuse potential and is not a scheduled drug. Opioids such as codeine
may be combined with acetaminophen for severe pain.
Many patients with OA use over-the-counter (OTC) topical creams, gels, sprays, patches, or oint-
ments that include salicylates (Aspercreme and Sportscreme), capsaicin (Capzasin), and counterirritants
(Ben-Gay and Icy Hot). These therapies are well tolerated and produce few adverse effects. Pennsaid is a
prescription, topical form of the NSAID diclofenac that is rubbed on the knee for symptoms of OA.
A newer approach to treating patients with moderate OA who do not respond adequately to analge-
sics includes sodium hyaluronate (Hyalgan), a chemical normally found in high amounts within syno-
vial fluid. Administered by injection directly into the knee joint, this drug replaces or supplements the
body’s natural hyaluronic acid that deteriorated because of the inflammation of OA. By coating the
articulating cartilage surface, Hyalgan helps provide a barrier that prevents friction and further inflam-
mation of the joint.
Rheumatoid Arthritis
Immunosuppressants and disease-modifying drugs are additional

therapies used to treat rheumatoid arthritis. Core Concept 35.7
Rheumatoid arthritis (RA) is a systemic autoimmune disorder that causes disfigurement and inflamma- rheuma 5 watery discharge
tion of multiple joints and usually occurs at an earlier age than OA. RA is the second most common form toid 5 associated
of arthritis and has an autoimmune etiology. In RA, autoantibodies, called rheumatoid factors, activate auto 5 self-directed
other inflammatory substances called complement proteins and draw leukocytes into an area where they anti 5 against
attack normal cells. This results in ongoing injury and formation of inflammatory fluid within the joints. bodies 5 things
Joint capsules, tendons, ligaments, and skeletal muscles may also be affected. Unlike OA, which causes
local pain in affected joints, patients with RA may develop systemic manifestations that include infections,
pulmonary disease, pericarditis, abnormal numbers of blood cells, and symptoms of metabolic dysfunction
such as fatigue, anorexia, and weakness.
The goals for the pharmacotherapy of RA include management of pain and inflammation and slowing
the progress of the disease. The same classes of analgesics and anti-inflammatory drugs used to treat OA
are used to manage RA. If inflammation is especially severe, short-term therapy with corticosteroids may
be indicated (see Chapter 32).
Additional drugs are sometimes prescribed to manage the immune aspects of RA. Research has shown
that the progression of tissue damage can be slowed by the use of disease-modifying antirheumatic drugs
(DMARDs). DMARDs may require several months of treatment before maximum therapeutic effects are
achieved. Because many of these drugs can be toxic, patients should be closely monitored. Adverse effects vary
depending on the type of drug. There are many DMARDs available, and these drugs are listed in Table 35.3 ◆.
The newest types of DMARDs are called biologic therapies. These drugs are used to block specific steps in
the inflammatory process. Examples of biologic agents include adalimumab (Humira), etanercept (Enbrel), and
golimumab (Simponi). Biologic agents are very effective and some are also prescribed to treat other disease with
inflammatory components, such as Crohn’s disease, psoriasis, ulcerative colitis, and ankylosing spondylitis.
Concept Review 35.4

■ Identify the major types of arthritis. What are the general differences between these disorders?
Drug Prototype: Hydroxychloroquine (Plaquenil)

Therapeutic Class: Disease-modifying antirheumatic drug (DMARD)
Pharmacologic Class: Protein synthesis inhibitor, inhibitor of DNA and RNA polymerase, rheumatoid drug
Actions and Uses: Hydroxychloroquine is prescribed for RA mood and mental changes. Hydroxychloroquine has pos-
and lupus erythematosus in patients who have not responded sible ocular effects that include blurred vision, photophobia,
well to other anti-inflammatory drugs. This drug relieves the diminished ability to read, and blacked out areas in the
severe inflammation characteristic of these disorders. For full visual field.
effectiveness, hydroxychloroquine is most often prescribed with Antacids with aluminum and magnesium may prevent
salicylates and glucocorticoids. This drug has also been used for absorption. This drug interferes with the patient’s response to
prophylaxis and treatment of malaria. the rabies vaccine. Hydroxychloroquine may increase the risk of
liver toxicity when administered with drugs that are toxic to the
Adverse Effects and Interactions: Adverse symptoms include liver. Alcohol use should be eliminated during therapy. It also
blurred vision, GI disturbances, loss of hair, headache, and may lead to increased digoxin levels.
Fast Facts Arthritis and Joint Disorders

■ Between 20 million and 40 million patients in the United States are affected by OA.
■ After age 40, more than 90% of the population has symptoms of OA in major weight-bearing joints.
After 70 years of age, almost all patients have symptoms of OA.
■ Of the world’s population, 1% has RA, which most often affects patients between 30 and 50 years
of age. Women are three to five times more likely to develop RA than men.
■ Between 1% and 3% of the U.S. population is affected by gout. Most of the patients are men
between the ages of 30 and 60. Women are more likely to be affected after menopause.
Table 35.3 Disease-Modifying Antirheumatic Drugs (DMARDs) and Biologic Therapies

abatacept (Orencia) IV; 500–1,000 mg given on 0, 2, and Immune modulating drug; inhibits T lymphocyte activation
4 weeks, then every 4 weeks thereafter
adalimumab (Humira) Subcutaneous; 40 mg every other week; Tumor necrosis factor blocker
without methotrexate, dose can be increased
up to 40 mg every week
anakinra (Kineret) Subcutaneous; 100 mg per day Interleukin-1 receptor blocker
azathioprine (Azasan, Imuran) PO; 1 mg/kg/day once or in divided doses Immunosuppressant and anti-inflammatory; may cause bone
bid for 6–8 weeks (max: 2.5 mg/kg/day); marrow depression
maintenance dose: 1–2.5 mg/kg/day as a
single dose or divided
certolizumab pegol (Cimzia) Subcutaneous; 400 mg initially and at weeks Tumor necrosis factor blocker
2 and 4, followed by 200 mg every other week
etanercept (Enbrel) Subcutaneous; 25 mg twice weekly; or 0.08 Tumor necrosis factor blocker
mg/kg or 50 mg once weekly
golimumab (Simponi) Subcutaneous; 50 mg once monthly Injectable man-made protein that binds to tumor necrosis factor
and blocks its action
hydroxychloroquine PO; 400–600 mg/day for 4–12 weeks, then Has been used for acute malaria and malaria suppression
(Plaquenil) 200–400 mg once daily; maintenance dose:
10–20 mg/day
infliximab (Remicade) IV; 3 mg/kg followed by 3 mg/kg 2 weeks Tumor necrosis factor-alpha blocker, used in combination with
and 6 weeks after initial dose and then methotrexate
every 8 weeks
leflunomide (Arava) PO; loading dose: 100 mg/day for 3 days; Immunomodulator with anti-inflammatory effects; may cause
maintenance dose: 10–20 mg daily Stevens–Johnson syndrome
methotrexate (Rheumatrex, PO; 7.5 mg once/wk or 2.5–5 mg every 12 Folic acid blocker; antineoplastic and immunosuppressant;
Trexall) (see page 440 for the hours for three doses each week (max 20 may cause liver toxicity, sudden death, and pulmonary
Drug Prototype box) mg/week) fibrosis
rituximab (Rituxan) IV; 1,000 mg every 2 weeks for a total of Also indicated for the treatment of non-Hodgkin’s lymphoma
two doses (give a corticosteroid 30 minutes (NHL)
prior to treatment)
sulfasalazine (Azulfidine) PO; 1–2 g daily in four divided doses Also for ulcerative colitis
(max: 8 g/day)
tocilizumab (Actemra) IV; 4–8 mg/kg every other week Interleukin-6 receptor blocker
Gout
Core Concept 35.8 Pharmacotherapy for gout requires drugs that control uric acid levels.
Gout, a form of acute arthritis, is a metabolic disorder caused by the accumulation of uric acid in
the bloodstream or joint cavities. This disorder is extremely painful. Gout occurs when excretion of
uric acid by the kidneys is reduced. One metabolic step important to the pharmacotherapy of this dis-
ease is the conversion of hypoxanthine (part of the chemical structure of the genes found with the
body’s cells) to uric acid by the enzyme xanthine oxidase. An elevated blood level of uric acid is called
hyper 5 elevated hyperuricemia.
uric 5 uric acid Gout may be classified as primary or secondary. Primary gout, caused by genetic errors in uric
emia 5 blood level acid metabolism, is most commonly observed in Pacific Islanders. Secondary gout is caused by diseases
or drugs that increase the metabolic turnover of nucleic acids or that interfere with uric acid excretion.
Examples of drugs that may cause gout include thiazide diuretics, aspirin, cyclosporine, and alcohol (when
ingested on a chronic basis). Conditions that can cause secondary gout include diabetic ketoacidosis, kid-
ney failure, and diseases associated with a rapid cell turnover, such as leukemia, hemolytic anemia, and
polycythemia.
Acute gouty arthritis occurs when needle-shaped uric acid crystals accumulate in joints, resulting in
red, swollen, and inflamed tissue. Attacks have a sudden onset; often occur at night; and may be triggered
by diet, injury, or other stresses. Gouty arthritis most often occurs in the big toes, heels, ankles, wrists, fin-
gers, knees, and elbows. About 90% of patients with gout are men.
NSAIDs are the preferred drugs for treating the pain and inflammation associated with acute gout
attacks (Table 35.4 ◆). The use of colchicine (Colcrys) has declined, although it may still be prescribed
for patients whose symptoms cannot be controlled with NSAIDs. Low doses may be prescribed for gout
prophylaxis.
Most patients with acute gout will experience subsequent attacks within one to two years after the first
attack. Thus, long-term prophylactic therapy with drugs that lower serum uric acid is often initiated. This
can be accomplished through three strategies.
One strategy to prevent hyperuricemia is to use uricosurics, drugs that increase the excretion of uric uricos 5 uric acid excretion
acid by blocking its reabsorption in the kidney. The uricosuric drugs used for gout prophylaxis include urics 5 impact on urination
probenecid (Probalan) and sulfinpyrazone (Anturane).
A second strategy for preventing hyperuricemia is to reduce the formation of uric acid. The tradi-
tional drug for gout prophylaxis, allopurinol (Lopurin, Zyloprim), blocks the enzyme xanthine oxidase,
thus reducing the formation of uric acid. A newer antigout drug, febuxostat (Uloric), acts by the same
mechanism as allopurinol but is safer for patients with renal impairment because it is not excreted by the
kidneys.
A third strategy for preventing hyperuricemia is to convert uric acid to a less toxic form. Two drugs
are available that act by this mechanism. Rasburicase (Elitek) is an enzyme produced through recombinant
DNA technology that is used to reduce uric acid levels in patients who are receiving cancer chemotherapy.
Approved in 2010, pegloticase (Krystexxa) is a synthetic enzyme that metabolizes uric acid to an inert
substance. It is used to lower uric acid levels in patients with chronic gout who have not responded to con-
ventional therapies.
Concept Review 35.5

■ Identify drug therapies used to treat the major arthritic and joint disorders.
Table 35.4 Uric Acid–Inhibiting Drugs for Gout and Gouty Arthritis
allopurinol (Lopurin, PO (primary); 100 mg daily; may increase by For primary hyperuricemia, secondary hyperuricemia, and
Zyloprim) 100 mg/week (max: 800 mg/day) prevention of gout flare-up
PO (secondary); 200–800 mg daily for 2–3
days or longer
colchicine (Colcrys) PO; 0.5–1.2 mg followed by 0.5–0.6 mg For acute gouty attack; may cause gastric upset at higher doses;
every 1–2 hours until pain relief IV form available
(max: 1.2 mg/day)
febuxostat (Uloric) PO; 40–80 mg once daily For chronic management of hyperuricemia in patients with gout
pegloticase (Krystexxa) IV; 8 mg every 2 weeks by IV infusion For chronic gout; enzyme that metabolizes uric acid
probenecid (Benemid, PO; 250 mg bid for 1 week; then 500 mg bid For gout; also used as an adjunctive drug for penicillin or
Probalan) (max: 3 g/day) cephalosporin therapy
rasburicase (Elitek) IV; 0.2 mg/kg over 30 minutes for up to For management of plasma uric acid levels in pediatric patients
5 days with leukemia; recombinant urate-oxidase produced by a
genetically modified Saccharomyces cerevisiae (yeast) strain;
may cause hypersensitivity reactions
sulfinpyrazone (Anturane) PO; 100–200 mg bid for 1 week; then For gout; also used for inhibition of platelet aggregation
increase to 200–400 mg bid
Cam Therapy
Glucosamine and Chondroitin for Osteoarthritis
Glucosamine sulfate is a natural substance that is an important building block of cartilage.
With aging, glucosamine is lost with the natural thinning of cartilage. As cartilage wears down,
joints lose their normal cushioning ability, resulting in the pain and inflammation of OA. Glu-
cosamine sulfate is available as an OTC dietary supplement. Some studies have shown it to be
more effective than a placebo in reducing mild arthritis and joint pain. It is claimed to promote
cartilage repair in the joints. Although reliable long-term studies are not available, glucosamine
is marketed as a safe and inexpensive alternative to prescription anti-inflammatory drugs.
Chondroitin sulfate is another dietary supplement claimed to promote cartilage repair.
It is a natural substance that forms part of the matrix between cartilage cells. Chondroitin is
usually combined with glucosamine in specific arthritis formulas.
Drug Prototype: Allopurinol (Lopurin, Zyloprim)

Therapeutic Class: Antigout drug Pharmacologic Class: Inhibitor of uric acid formation, xanthine
oxidase blocker
Actions and Uses: Allopurinol reduces the production of uric epidermal necrolysis and Stevens–Johnson syndrome. Other
acid, controlling the buildup of uric acid that causes severe gout possible adverse effects include drowsiness, headache, vertigo,
and it reduces the risk of acute gout attacks. It is also approved nausea, vomiting, abdominal discomfort, malaise, diarrhea,
to prevent recurrent kidney stones in patients with elevated retinopathy, and thrombocytopenia.
uric acid levels. It may be used prophylactically to reduce the Alcohol may inhibit the renal excretion of uric acid. Ampi-
severity of the elevated uric acid blood levels associated with cillin and amoxicillin may increase the risk of skin rashes. An
antineoplastic and radiation therapies, both of which increase enhanced anticoagulant effect may be seen with the use of
blood uric acid levels by promoting nucleic acid degradation. warfarin. The risk of ototoxicity is increased when allopurinol is
This drug takes one to three weeks to bring blood uric acid used with thiazides and angiotensin-converting enzyme (ACE)
levels to within the normal range. inhibitors. Aluminum antacids taken concurrently with allopu-
rinol may decrease its effects. An increased effect may be seen
Adverse Effects and Interactions: The most frequent and seri- with phenytoin and anticancer drugs, necessitating the need for
ous adverse effects are skin rash and rare cases of fatal toxic altered doses of these medications.

Patients taking drugs for bone or joint disorders need to know the following:
In General
1. W
hen receiving treatment for problems with mobility, it often takes several weeks for
effectiveness to begin. Follow the advice of a healthcare provider in order to achieve
full therapeutic effect.
Regarding Calcium and Bone-Regulating Medications

2. When taking calcium or vitamin D supplements, be aware of the signs and symptoms of
hypercalcemia. Check with the healthcare provider or pharmacist before taking supple-
ments of any kind. In some cases, only proper diet and sunshine are needed for successful
therapy.
3. Calcium may react with some foods or interfere with the absorption of iron and
bisphosphonates.
4. Be familiar with the risks and long-term effects of vitamin D therapy, corticosteroids,
hormone therapy involving estrogen, and estrogen-receptor modulators. Major
undesirable adverse effects could occur in some cases.
5. Know how to use a nasal pump if taking calcitonin by this method.
6. Be aware that some vitamins may interfere with the pharmacologic effects of calcitonin.
7. Some medications cause GI discomfort. Most drugs like these can be taken after meals
or with milk to minimize discomfort.
Regarding Arthritic and Joint-Related Medications

8. Report any unfavorable symptoms such as bone pain, restricted mobility, inflammation,
or fracture to a healthcare provider. Report any muscle pain because muscles that have
not been moved for a while may feel stiff and tender.
9. When taking some antigout medications, drink plenty of fluids to avoid kidney stones.
To ensure proper fluid balance, monitor intake and output of fluids.
10. When taking probenecid, avoid taking aspirin for pain because it interferes with the
drug’s action. Take acetaminophen instead.
Chapter Review 579
Safety Alert
Soundalike Drug Names
Nurses need to counsel patients about ways to avoid a self-medication error when taking
medications that are “soundalike” drugs, such as Celebrex and Celexa. Confusing drugs with
similar names accounts for about approximately 10% of all medication errors, according to
the U.S. Food and Drug Administration (FDA). Patients could ask the pharmacist to package
the “soundalikes” in distinctly different containers or to label the bottles with large letters
describing the drug’s use, like PAIN PILL and ANTIDEPRESSANT.
Chapter Review
35.1 Adequate levels of calcium, vitamin D, parathyroid therapy, estrogen therapy, estrogen-receptor modula-
hormone, and calcitonin are necessary for bone tors, statins, slow-release sodium fluoride, bisphos-
and body homeostasis. phonates, and calcitonin.
One of the most important minerals in the body
35.5 Treatment for Paget’s disease includes bisphos-
responsible for proper nerve conduction, muscle
phonates and calcitonin.
contractions, and bone formation is calcium. Cal-
cium homeostasis is controlled by two important Paget’s disease is a chronic progressive condi-
hormones, PTH and calcitonin. These hormones tion characterized by enlarged and abnormal bones.
influence major body targets: the bones, kidneys, and Although the cause of Paget’s disease is different
GI tract. They direct the processes of bone resorption from that of osteoporosis, medical treatments are
and bone deposition. Active vitamin D increases cal- similar. Bisphosphonates are drugs of choice for the
cium absorption from the GI tract and helps to keep pharmacotherapy of Paget’s disease.
proper calcium balance in the body.
35.6 Analgesics and anti-inflammatory drugs are
35.2 Hypocalcemia is a serious condition that requires important components of pharmacotherapy for
immediate therapy. osteoarthritis.
Hypocalcemia, or lowered calcium levels in the Arthritis is a general term meaning inflammation
bloodstream, is a sign of an underlying disorder; of the joints. The initial pharmacotherapy goals for
therefore, identifying its cause is essential. Signs of osteoarthritis are to reduce pain and inflammation.
hypocalcemia are nerve and muscle excitability, mus-
35.7 Immunosuppressants and disease-modifying drugs
cle twitching, tremor, or cramping. These conditions
are additional therapies used to treat rheumatoid
are often reversed with calcium salts. Calcium salts
arthritis.
consist of complexed and elemental calcium. Ele-
mental calcium is also obtained from dietary sources. Rheumatoid arthritis (RA) is the second most com-
mon form of arthritis and has an autoimmune etiology.
35.3 Osteomalacia and rickets are successfully treated Pharmacotherapy for RA includes the same classes of
with calcium salts and vitamin D supplements. analgesics and anti-inflammatory drugs, plus disease-
Osteomalacia, called rickets in children, is a disorder modifying antirheumatic drugs (DMARDs), immu-
characterized by softening of bones without alteration nosuppressants, and biologic drugs.
of basic bone structure. Drug therapy for children and
35.8 Pharmacotherapy for gout requires drugs that
adults consists of calcium supplements and vitamin D.
control uric acid levels.
35.4 Treatment for osteoporosis includes calcitonin, Gout is caused by an accumulation of uric acid in the
selective estrogen-receptor modulators, and bloodstream. Gout may be classified as a primary
bisphosphonates. or secondary condition. Acute gouty arthritis occurs
Osteoporosis, or weak bones caused by disrupted when needle-shaped uric acid crystals accumulate in
bone homeostasis, is the most common metabolic the joints. The goals of gout pharmacotherapy include
bone disease. The onset of menopause is the most fre- termination of acute attacks and prevention of future
quent risk factor. Many drug therapies are available attacks with several approaches to control uric acid
for this disorder, including calcium and vitamin D levels.
Review Questions
The following questions are written in NCLEX-PN® style. 6. A patient is about to begin taking calcitonin and asks the
Answer these questions to assess your knowledge of the chap- nurse if this drug has any adverse effects. The nurse tells the
ter material, and go back and review any material that is not patient that it may cause:
clear to you. 1. Nasal irritation
1. The nurse is explaining to a group of women that there 2. Headaches
are many brand names of certain medications. The brand 3. Watery eyes
name of a medication that lowers serum alkaline phospha- 4. Sinus infection
tase is: 7. A patient has been taking hydroxychloroquine (Plaquenil)
1. Azulfidine for rheumatoid arthritis. Which of the following symptoms
2. Fosamax may alert the nurse to an adverse effect?
3. Colchicine 1. Cardiac dysrhythmias
4. Benemid 2. Joint stiffness
2. The patient on raloxifene (Evista) has had warfarin (Cou- 3. Blurred vision
madin) ordered. The nurse incorporates what laboratory test 4. Decreased muscle strength
into the plan of care? 8. The nurse is speaking with a group of women at the local
1. Platelets community center about vitamin and mineral supplements.
2. WBC She tells them that milliequivalence (mEq) is the unit used to
3. Sodium describe the amount of electrolyte available to the bloodstream;
4. INR/PT the higher the mEq, the more potent the calcium salt. To demon-
strate their new knowledge, the nurse has the group choose the
3. The patient taking calcitriol should be monitored for: calcium salts with the greatest potency. Which do they choose?
1. Dysrhythmias 1. Calcium chloride
2. Hypercalcemia 2. Calcium citrate
3. Fluid overload 3. Calcium phosphate
4. Flu-like symptoms 4. Calcium gluconate
4. For the patient diagnosed with gout, the nurse would most 9. The nurse would include calcitonin in the plan of care for
likely administer which medication? patients with: (Select all that apply.)
1. Calcitriol (Calcijex, Rocaltrol) 1. Paget’s disease
2. Azathioprine (Imuran) 2. Hypercalcemia
3. Allopurinol (Lopurin, Zyloprim) 3. Hypocalcemia
4. Raloxifene (Evista) 4. Osteoporosis
5. Because esophageal irritation can occur, the nurse 10. The doctor has ordered tocilizumab (Actemra), 5 mg/kg of
instructs the patient to remain in an upright position for 30 min- weight, to be given IV. The patient weighs 121 pounds and is to
utes after what medication? receive 275 mg in a 250 mL bag of solution to be delivered over
1. Allopurinol (Lopurin) 4 hours. How many milliliters will the patient receive in one hour?
2. Calcitonin 1. 60 mL
3. Alendronate (Fosamax) 2. 62 mL
4. Raloxifene (Evista) 3. 61.5 mL
4. 62.5 mL
Remember Mr. Hurtt, the patient Mr. Steven Hurtt is a 67-year-old white male. In an office visit,
introduced at the beginning Mr. Hurtt complains of joint pain in the knees, ankles, toes,
of the chapter? Now read the and shoulders. Over the last several years, he has taken aspirin
remainder of the case study. for overall pain. Laboratory and physical examination yield
Based on the information you the following information: small nodules found sporadically
have learned in this chapter, under the skin, acute swelling of the knees, redness of the big
answer the questions that follow. toe and elevated uric acid and white blood cell (WBC) count
Chapter Review 581
in the blood. Mr. Hurtt is diagnosed with gouty arthritis and is 3. Toxic epidermal necrolysis
prescribed allopurinol (Lopurin). 4. Skin rash
1. Mr. Hurtt asks how allopurinol works. The nurse explains 3. Mr. Hurtt asks why he should avoid drinking alcohol
that it works by: while he is taking allopurinol. The nurse responds by telling
1. Decreasing the deposits of uric acid in the joint spaces him that alcohol:
2. Reducing the pain associated with joint inflammation by 1. Significantly increases the drug levels of allopurinol
uric acid crystals 2. Interferes with the absorption of antigout medications
3. Increasing renal excretion of uric acid 3. Raises uric acid levels
4. Reducing the production of uric acid 4. Causes the urine to become more alkaline
2. Since Mr. Hurtt is starting on allopurinol, the nurse 4. Which of the following statements demonstrates that
informs him that this medication has several possible adverse Mr. Hurtt needs additional instructions?
effects that he needs to know about. These effects include: 1. “I will take my allopurinol as prescribed by my physician.”
(Select all that apply.) 2. “I will stop having alcoholic beverages.”
1. Headache 3. “I will avoid high purine foods.”
2. Vertigo 4. “I will continue taking my aspirin.”

c
“I don’t think I can go to
h the game this weekend. Can
a anything be done to get rid
p of these zits by Friday?”
t Burt Nicholson
e
r
36 Drugs for Skin Disorders
Core Concepts
36.1 Layers of skin provide protection to the body. 36.5 Acne and rosacea are treated by a combination of
36.2 The major causes of skin disorders are injury, aging, over-the-counter (OTC) and prescription drugs.
inherited factors, and other medical conditions. 36.6 Topical corticosteroids are used mainly to treat
36.3 Scabicides and pediculicides treat parasitic mite dermatitis and related symptoms.
and lice infestations. 36.7 Several topical and systemic medications are used to
36.4 The goal of drug therapy for sunburn is to eliminate treat psoriatic symptoms.
discomfort until healing occurs.
Drug Snapshot
Drugs for skin parasites
Scabicides and ermethrin (Acticin,
p
pediculicides Elimite, Nix) 587
Drugs for sunburn and enzocaine (Americaine,
b
minor skin irritations Anbesol, others) 589
Drugs for acne and t retinoin (Avita, Retin-A,
rosacea Tretin-X) 591
Drugs for dermatitis
and eczema
Drugs for psoriasis
Learning Outcomes
1. Identify important skin layers and 3. Identify the major actions of 4. Describe popular treatments used
explain how superficial skin cells the following types of drugs as in conjunction with available drug
must be replaced after they become they pertain to treatment of skin therapies for skin disorders.
damaged or lost. disorders: scabicides, pediculicides, 5. For each of the classes in the Drug
2. Describe major symptoms associated topical anesthetics, antibiotics, Snapshot, identify representative
with stress and injury to the skin retinoids, keratolytic agents, drugs and explain their mechanisms
versus those associated with a corticosteroids, emollients, and of drug action, primary actions, and
patient’s changing age or health. psoralens. important adverse effects.
Key Terms
closed comedones (KOME-eh-dones) 589 open comedones 589 retinoids (RETT-ih-noydz) 590
dermatitis (dur-mah-TIE-tiss) 591 papules (PAP-yools) 589 retinol (RETT-in-nall) 591
eczema (ECK-zih-mah) 591 pediculicides (puh-DIK-you-lih-sides) 587 rosacea (roh-ZAY-shee-uh) 589
emollients 593 pruritus (proo-RYE-tus) 583 scabicides (SKAY-bih-sides) 587
erythema (ear-ih-THEE-mah) 584 psoralens (SOR-uh-lenz) 594 scabies (SKAY-beez) 586
keratinization (keh-RAT-en-eye- psoriasis 593 seborrhea (seb-oh-REE-ah) 589
zay-shun) 589 pustules (PUSS-chools) 589 urticaria (EHR-tik-air-ee-ah) 583
keratolytic agents (keh-RAT-oh-lih-tik) 590
T he integumentary system consists of the skin, hair, nails, sweat glands, and oil glands. The largest
of all organs in the body is the skin. Because of its large surface area, the skin provides an effective
barrier between extreme conditions in the outside environment and the body’s internal tissues. At
times, however, changes in external and internal conditions can damage the skin. When this happens, drug
therapy may be provided to improve the skin’s condition. The relationship between the integumentary sys-
tem and other systems in the body is shown in Figure 36.1 ■.
The purpose of this chapter is to examine the broad scope of skin disorders and the medications used
for skin therapy. Particular attention is given to drugs that are of direct benefit to lice and mite infestations,
sunburn, acne, inflammation, and dry, scaly skin.
Layers of skin provide protection to the body. Core Concept 36.1
The integument has three major layers: the epidermis, dermis, and a subcutaneous layer called the hypodermis. epi 5 on top of
Studies in healthcare often describe the skin as having two major layers with the hypodermis underneath. hypo 5 below
Each layer of the integument is distinct in form and function and determines how drugs are injected or dermis 5 the skin
applied to the surface of the skin (see Chapter 3). sub 5 underneath
The most superficial skin layer is the epidermis. Depending on its thickness, the epidermis has either cutaneous 5 skin-related
four or five sublayers. The strongest and outermost sublayer is the stratum corneum, or horny layer. It is
called this because of the abundance of the protein keratin, also found in the hair, hooves, and horns of
many vertebrate mammals. Not every part of the skin has a large amount of keratin—only those areas that
are subject to mechanical stress—for example, the soles of the feet and the palms of the hands.
The deepest sublayer of the epidermis is the stratum germinativum. It supplies the epidermis with
new cells after older superficial cells have been damaged or lost by normal wear. Cells must migrate over
their lifetime to the outermost layers of the skin, where they eventually fall off. As these cells are pushed
to the surface, they are flattened and covered with a water-insoluble material, forming a protective seal.
The average time it takes for a cell to move from the germinativum layer to the outer body surface is about
three weeks. Specialized cells called melanocytes within the deeper layers of the epidermis secrete the dark
pigment melanin, which offers a degree of protection from the sun’s ultraviolet rays.
The next major layer of skin, the dermis, is made up of dense, irregular connective tissue, named this
way because of its irregular arrangement of thick collagen fibers. The dermis provides a foundation for the
epidermis and appendages such as hair and nails. Most receptor nerve endings, sweat glands, oil glands,
and blood vessels are found within the dermis.
Below the dermis is the subcutaneous layer, or hypodermis. This layer is composed mainly of adipose
tissue or fat that cushions, insulates, and provides a source of energy for the body. The hypodermis is
involved with the maintenance of body homeostasis, temperature regulation, and metabolism.
The major causes of skin disorders are injury, aging, inherited factors,
and other medical conditions. Core Concept 36.2
Skin that is dry, cracked, scaly, or inflamed represents a disturbance in the outermost skin layer. Pruritus, prur 5 itching
or itching, is a general symptom often associated with dry, scaly skin, or it may be a symptom of infestation itus 5 condition
with mites and lice. Urticaria, commonly referred to as hives, is recognized as raised, red, itchy bumps. Most
commonly, urticaria is caused by an allergic reaction. Many drugs, especially antibiotics, can cause urticaria
and pruritus as side effects. Although most drug allergies of the skin require only symptomatic treatment with
over-the-counter (OTC) medications, some are severe. Toxic epidermal necrolysis (TEN) is a life-threatening
drug reaction that results in massive death of skin cells and separation of the epidermis from the dermis.
Burns are a unique type of stress that may affect all layers of the skin. They are classified according to
the degree of skin damage. First-degree burns affect only the outer layers of the epidermis, are characterized
by redness, and are analogous to sunburn. Second-degree burns affect most of the epidermis and part of the
584 Chapter 36 Drugs for Skin Disorders
Figure 36.1
The integumentary
Endocrine system Nervous system
system
Hormones influence Emotions affect skin
glandular activity, calcium coloration. The skin is a
homeostasis, and skin health. sensory organ.
Cardiovascular system
The blood carries oxygen
Muscular system and carbon dioxide, factors
The skin and muscles are that influence skin health
important for proper body and coloration.
movement and expression.
Respiratory system
The lungs provide
oxygen to all cells
Lymphatic system in the body.
Helps fight diseases and
infections of the skin.
Skeletal system
The bones are a storage site
for calcium, an important
mineral connected with
Digestive system vitamin D function.
Proper nutrition is important
for healthy skin.
Reproductive system
Urinary system The skin covers external
The accumulation of toxic genitalia. Sex hormones
For all systems influence skin health.
substances in the
The skin forms a protective
bloodstream will affect the
barrier against hazardous
skin adversely.
conditions.
The integumentary system (skin) and how the other body systems affect it.
dermis, resulting in inflammation and blisters. Third-degree burns are full-thickness burns; all layers of the
skin are damaged. With full-thickness burns, the skin cannot regenerate, and skin grafting is required.
Inflammation, a characteristic of burns and other traumatic disorders, occurs when damage to the skin
eryth 5 red is extensive. Signs accompanying inflammation include erythema or redness, irritation, and pain. Symp-
ema 5 appears toms including bleeding, bruises, and infections may accompany trauma to deeper tissues.
Not all skin disorders are associated with injury or infection. Many common skin disorders are related
to inherited factors or the normal aging process. Sometimes the skin may appear unhealthy because of a
disease process occurring in a different organ system, such as yellowing of the skin (jaundice) that occurs
from liver damage. In many cases, the cause of the skin condition may be unknown. Common symptoms
associated with a range of conditions are presented in Table 36.1 ◆. Although the causes and symptoms of
skin conditions are very diverse, a simple method of classifying them is shown in Table 36.2 ◆.
Most skin conditions are not debilitating and require only intermittent drug therapy. A few irritating
disorders are of particular importance to patients who require treatment on an outpatient basis. Examples
Table 36.1 Signs and Symptoms of Skin Conditions Associated with a Patient’s
Changing Health, Age, or Weakened Immune System
Symptom Description
Delicate skin, wrinkles, and hair loss Many degenerative changes occur in the skin; some are found in
elderly patients; others are genetically related (fragile epidermis,
wrinkles, reduced activity of oil and sweat glands, male pattern
baldness, poor blood circulation); hair loss may also be linked to
some medical procedures, such as radiation and chemotherapy.
Discoloration of the skin Discoloration is often a useful sign of another medical disorder
(for example, anemia, cyanosis, fever, jaundice, or Addison’s
disease); some medications have photosensitive properties,
making a patient’s skin sensitive to the sun and causing erythema.
Scales, patches, and itchy areas Some symptoms may be related to a combination of genetics,
stress, and immunity; other symptoms may be related to a fast
turnover of skin cells; some symptoms develop for unknown
reasons.
Seborrhea/oily skin and bumps This condition is usually associated with a younger age group;
examples include cradle cap in infants and an oily face, chest,
arms, and back in teenagers and young adults; pustules, cysts,
papules, and nodules represent lesions connected with oily skin.
Tumors Tumors may be genetic or may occur because of exposure to
harmful agents or conditions.
Warts, skin marks, and moles Some skin marks are congenital; others are acquired or may be
linked to environmental factors.
Table 36.2 Classification of Skin Disorders

Disorder Example
Infectious disorders Bacterial infections: boils, impetigo, and infected hair follicles
Fungal infections: ringworm, athlete’s foot, jock itch, and nail
infections
Parasitic infections: ticks, mites, and lice
Viral infections: cold sores, fever blisters (herpes simplex),
chickenpox, warts, shingles (herpes zoster), measles (rubeola),
and German measles (rubella)
Inflammatory disorders Injury and exposure to the sun
Combination of overactive glands, increased hormone production,
or infection such as acne and rosacea
Disorders marked by itching, cracking, and discomfort, such as
atopic dermatitis, contact dermatitis, seborrheic dermatitis, stasis
dermatitis, and psoriasis.
Neoplastic Malignant skin cancers: squamous cell carcinoma, basal cell
carcinoma, and malignant melanoma.
Malignant melanoma is the most dangerous. Benign neoplasms:
include keratosis and keratoacanthoma.
include lice infestation, minor sunburn, and acne. Eczema, dermatitis, and psoriasis are more serious dis-
orders requiring therapy for a longer time. Figure 36.2 ■ shows examples of regions of the body where
irritating symptoms most likely appear.
Concept Review 36.1

■ Identify the skin layers protecting the body. Give examples of layers specifically affected
by minor or major external stresses. What skin disorders are not related to the external
environment? How would you categorize most skin disorders?
Figure 36.2
Anatomical distribution
of common skin
disorders: (a) contact
dermatitis due to
footwear, (b) cosmetics,
(c) seborrheic dermati-
tis, (d) acne, (e) scabies,
(f) sunburn.
(a) (b)
(c) (d)
(e) (f)
Skin Parasites
Common skin parasites include mites and lice. Mites cause a skin disorder called scabies, based on their
scientific name, Sarcoptes scabiei. Scabies is an eruption of the skin caused by the female mite burrowing
into the skin and laying eggs. This causes intense itching, most commonly between the fingers, extremities,
and around the trunk and pubic area. Scabies is readily spread among family members and sexual partners.
Lice, scientific name Pediculus, are another type of skin parasite readily passed on by infected clothing
or close personal contact. Lice often infest the pubic area or the scalp and lay eggs that attach to body hairs.
Fast Facts Skin Disorders

■ An estimated three million people with new cases of lice infestation are treated each year in the
United States.
■ Nearly 17 million people in the United States have acne, making it the most common skin disease.
■ More than 15 million people in the United States have symptoms of dermatitis.
■ Ten percent of infants and young children experience symptoms of dermatitis. Roughly 60% of
these infants continue to have symptoms into adulthood.
■ Psoriasis affects 1% to 2% of the U.S. population. This disorder occurs in all age groups—adults
mainly—affecting about the same number of men as women.
Scabicides and pediculicides treat parasitic mite and lice infestations. Core Concept 36.3
Scabicides are pharmacologic agents that kill mites; pediculicides kill lice. Either treatment may be effec-
tive for both types of parasites. The preferred drug often depends on where the infestation has occurred.
The preferred drug for lice infestation is permethrin, a chemical derived from chrysanthemum flowers
and formulated as a 1% liquid (Nix). This drug is considered the safest agent, especially for infants and
children. Pyrethrin (RID, others) is a related product also obtained from the chrysanthemum plant. Perme-
thrin and pyrethrins, which are also widely used as insecticides on crops and livestock, kill lice and their
eggs on contact. Malathion (Ovide) is an alternative for resistant organisms.
Permethrin is also a preferred drug for scabies. The 5% permethrin cream (Elimite) is applied to the
entire skin surface and allowed to remain for 8 to 14 hours before bathing. Itching may continue for several
weeks as the dead mites are removed from the skin. Crotamiton (Eurax) is an alternative scabicide avail-
able by prescription as a 10% cream. Approved in 2012, ivermectin (Sklice) is a lotion that is left on the
scalp for 10 minutes and does not require a nit comb following treatment. Because lindane (Kwell) has the
potential to cause serious nervous system toxicity, it is now prescribed only after other less toxic drugs
have failed to produce a therapeutic response.
All scabicides and pediculicides must be used strictly as directed, because excessive use has the
potential to cause serious systemic effects and skin irritation. Drugs for the treatment of lice or mites must
not be applied to the mouth, open skin lesions, or eyes, because this will cause severe irritation.
Lice lay eggs called nits. Fine-toothed nit combs are useful in removing nits after the lice have been
killed. Patients should comb the infested area after the hair has been dried. To ensure that drug therapy
is effective, patients should inspect hair shafts daily for at least 1 week after treatment. Because nits may
be present in bedding and other upholstery material, all material coming in close contact with the patient
should be washed or treated with the medication.
Concept Review 36.2

■ Name examples of medications used to treat mite and lice infestations. What precautions
should be taken when using these medications?
Drug Prototype: Permethrin (Acticin, Elimite, Nix)

Therapeutic Class: Antiparasitic drug Pharmacologic Class: Scabicide, pediculicide
Actions and Uses: Nix is marketed as a cream or shampoo to Adverse Effects and Interactions: Permethrin causes few sys-
kill head and crab lice. It will also kill mites and eradicate their temic effects. Local reactions may occur and include pruritus,
ova. A 1% lotion is approved for lice and 5% lotion for mites. rash, transient tingling, burning, stinging, erythema, and
The medication should be allowed to remain on the hair and edema of the infested area.
scalp 10 minutes before removal. Patients should be aware that Contraindications include hypersensitivity to pyrethrins,
itching may last up to two or three weeks even after parasites chrysanthemums, sulfites, or other preservatives. Permethrin
have been killed. Successful elimination of parasitic infestations should be used cautiously on inflamed skin, in those with
should include removing the nits with a comb, washing bed- asthma, or in lactating women. No significant clinical drug
ding, and cleaning or removing objects that have been in interactions have been documented.
contact with the head or hair.
NURSING PROCESS FOCUS Patients Receiving Pharmacotherapy for Lice or Mite Infestation
Prior to drug administration: ■ Deficient Knowledge related to a lack of information about condition
■ Obtain a complete health history, including age, dermatological and drug therapy regimen
conditions, social history and close contacts, allergies, drug history, ■ Impaired Health Maintenance related to treatment regimen
and possible drug interactions. ■ Risk for Impaired Skin Integrity related to infestation or adverse
■ Examine skin areas to be treated for signs of infestation (e.g., lice effects of drug therapy
or nits in hair, reddened track areas between web of fingers, around ■ Risk for Poisoning related to adverse effects of drug therapy
the belt or elastic lines), irritation, excoriation, or drainage.

The patient will:
■ Experience therapeutic effects (free of lice or mites).
■ Verbalize an understanding of how lice and mites are spread; proper administration of medication; necessary household hygiene; and the need to
notify household members, sexual partners, and other close contacts (such as classmates) about infestation.
Implementation

■ Apply medication correctly and evaluate the patient and caregiver’s Instruct the patient and family members:
knowledge of proper administration. (Everyone in the household with ■ That all skin lotions, creams, and oil-based hair products should be
mites or lice should be treated at the same time. Proper application is removed completely before applying medication.
critical to elimination of infestation.) ■ To apply the drug per package directions and allow it to remain in the
hair or on the skin for the prescribed length of time (approximately
10 minutes).
■ To use a fine-toothed comb to comb affected hair to remove any
remaining dead lice or mites.
■ That eyelashes can be treated with the application of petroleum jelly
once a day for one week. Use a fine-toothed comb to remove mites.
■ To recheck affected hair or skin daily for at least one to two weeks
after treatment.
■ Monitor the skin/head areas for infestation over the next 1 to 2 weeks. Instruct the patient and family members to:
Reinfestations may reappear within 1 week and retreatment may be ■ Monitor for nits on hair shafts; lice on skin or clothes, inner thigh
necessary. (Monitoring helps to determine proper medication adminis- areas, and seams of clothes that come in contact with axilla, neckline,
tration technique and adherence to prevention protocols.) or beltline.
■ Monitor for mites between the fingers, on the extremities, in the
axillary and gluteal folds, around the trunk, and in the pubic area.
■ Monitor household for signs of infestation. Inform the patient and Instruct the patient and family members to:
others living in the home about proper care of clothing and equip- ■ Wash all bedding and clothing in hot water, and to dry-clean all
ment. (Contaminated articles can cause reinfestation.) nonwashable items that came in close contact with the patient.
■ Vacuum furniture or fabric that cannot be cleaned and seal children’s
toys in plastic bags for two weeks.
■ Not share personal care items such as combs, brushes, and towels
■ Clean combs and brushes and rinse thoroughly after every use.

Evaluate the effectiveness of drug therapy by confirming that patient goals and expected outcomes have been met (see “Planning”).
Sunburn and Minor Skin Irritation
The goal of drug therapy for sunburn is to eliminate

Core Concept 36.4 discomfort until healing occurs.
Sunburn, a common problem among the general public, is associated with factors such as light skin com-
plexion and lack of proper sun protection. Nonpharmacologic approaches to sun protection include the
appropriate use of sunscreens, sunglasses, and sufficient clothing. Limiting the amount of time spent
directly in the sun is essential to avoiding sunburn. Many dangers result from sun exposure, including eye
injury and skin cancer. Some of these disorders may not appear until years after the exposure.
Pharmacologic treatments for sunburn may not be necessary. Remaining calm until the minor irri-
tation passes is one common approach to mild sunburn. In cases in which pharmacologic intervention
is necessary, drugs for sunburn and minor irritation include mild lotions and topical anesthetics such as
Drug Prototype: Benzocaine (Americaine, Anbesol, Others)

Therapeutic Class: Agent for sunburn pain and minor skin irritations
Pharmacologic Class: Local anesthetic, sodium channel blocker
Actions and Uses: Benzocaine provides temporary relief for pain Adverse Effects and Interactions: Benzocaine should not be
and discomfort in cases of sunburn, pruritus, minor wounds, and used for treatment of patients with open lesions, traumatized
insect bites. Its pharmacologic action is caused by local anesthe- mucosal areas, or a history of drug sensitivity. Benzocaine may
sia of skin receptor nerve endings. Preparations are also avail- interfere with the activity of some antibacterial sulfonamides.
able to treat the skin and other areas such as the ear, mouth, Patients should use preparations only in areas of the body for
throat, rectal, and genital areas. which the medication is intended.
benzocaine (Solarcaine, others), dibucaine (Nupercainal), and tetracaine (Pontocaine). These are used to
provide temporary relief of painful symptoms. Some of these medications may also provide minor relief
from insect bites and pruritus. In cases of more lengthy sun exposure, more potent pain medications may
be administered (see Chapters 14 and 24), or tetanus toxoid might be administered to prevent infection (see
Chapter 26).
Concept Review 36.3

■ What is the major purpose of drugs used to treat sunburn, insect bites, and related inju-
ries? What major class of drugs would be used for this purpose?
Acne And Rosacea
Acne, sometimes called acne vulgaris, is a common condition found most often in adolescents and young
adults. The disorder usually begins one or two years before puberty and is caused by overproductive oil
glands or seborrhea. Acne is also caused by abnormal keratinization or development of the horny layer sebor 5 oil
of the epithelial tissue of skin. This activity results in blocked oil glands. Administration of androgens or rhea 5 flow
testosterone-like hormones may cause extensive acne by increasing keratinization and the production of
sebum (oil). Following this, the bacterium Propionibacterium acnes grows within gland openings and
modifies the sebum into an acidic and irritating substance. As a result, small inflamed bumps appear on the
surface of the skin.
Blackheads, or open comedones, are a type of acne in which sebum has plugged the oil gland, caus-
ing it to become black because of the presence of melanin granules. Whiteheads, or closed comedones,
are a type of acne that develops just beneath the surface of the skin and appears white rather than black. In
more severe cases of acne, deeper bumps called nodules may appear and become very painful because of
the intense inflammation and pus found within pore pockets.
Another skin disorder characterized by inflammation but without pus is rosacea. Unlike pimples or
pustules—the technical name given to pus-filled bumps—rosacea is characterized by small papules or
inflammatory bumps that swell, thicken, and become very painful. Characteristic of rosacea is its swelling
just beneath the surface of the skin. The face of a patient with rosacea may take on a flushed appearance,
particularly around the nose and cheek area. Rosacea is exacerbated by many factors, including sunlight,
stress, increased temperature, and agents that dilate facial blood vessels such as alcohol, spicy foods, and
warm beverages.
Acne and rosacea are treated by a combination of OTC

and prescription drugs. Core Concept 36.5
Most acne drugs slow down the turnover of skin cells, especially those surrounding pore openings. Some
inhibit bacterial growth because they are combined with antibiotics such as doxycycline and tetracy-
cline (see Chapter 26). Some drugs must be used carefully because of their ability to dramatically reduce
oil gland activity and skin cell turnover. Important medications for acne and rosacea are summarized in
Table 36.3 ◆.
Table 36.3 Drugs for Acne and Rosacea

Drug Remarks
OTC Medication—Topical Preparation
benzoyl peroxide (Clearasil, Fostex, others) Often combined with erythromycin or clindamycin to fight bacterial
infection (see Chapter 26)‌
Prescription Medications—Topical
adapalene (Differin) Retinoid-like compound used to treat acne formation
azelaic acid (Azelex, Finacea, others) For mild to moderate inflammatory acne and rosacea
metronidazole (Metrogel, MetroCream) For inflammatory papules and pustules of rosacea
sulfacetamide sodium (Cetamide, Klaron, others) For sensitive skin; sometimes combined with sulfur to promote
peeling, as in rosacea; also used for conjunctivitis
tazarotene (Avage, Tazorac) A retinoid drug that may also be used for plaque psoriasis; has
antiproliferative and anti-inflammatory effects
tretinoin (Avita, Retin-A, others) A retinoid used to prevent clogging of pore follicles associated with
acne; the oral form (Vesanoid) is used for the treatment of acute
promyelocytic leukemia and wrinkles
Prescription Medications—Oral
doxycycline (Vibramycin, others) Antibiotic (see Chapter 26)‌
ethinyl estradiol Oral contraceptives are sometimes used for acne treatment; combina-
tion drugs may be helpful, for example, ethinyl estradiol plus
norgestimate (see Chapter 34)‌
isotretinoin (Accutane) A retinoid used for severe acne with cysts or acne formed in small,
rounded masses; pregnancy category X
minocycline (Minocin, others) Antibiotic (see Chapter 26)‌
tetracycline (Sumycin, others) (see page 397 for the Antibiotic (see Chapter 26)‌
Drug Prototype box)
Benzoyl peroxide (Clearasil, Fostex, others) is one of the primary OTC medications used to treat
acne. This medication may be dispensed as a lotion, cream, or gel and is available in various concentra-
tions. Benzoyl peroxide decreases symptoms of acne by inhibiting bacterial growth and suppressing the
turnover of skin cells at the pore’s opening. Applied directly to affected skin, it is relatively safe, with red-
ness, irritation, and drying being the most common adverse effects. Patients usually see some improvement
with the first week but it make take weeks even a month, or longer to notice the full effect. Sometimes ben-
zoyl peroxide is combined with antibiotics to directly fight bacterial infections. When acne is particularly
severe, resorcinol, salicylic acid, or sulfur may be used as additional treatments to promote shedding of old
kerato 5 horny layer skin. These are called keratolytic agents.
lytic 5 loosening Retinoids are vitamin A–like compounds used for acne. Vitamin A provides improved resistance
to bacterial infection by reducing oil production and the occurrence of clogged pores. Retinoids are not
recommended during pregnancy because of possible harmful effects to the fetus. A common reaction to
retinoids is sensitivity to sunlight.
Some drugs may be taken in combination with or in lieu of other acne medications, including doxycy-
cline, tetracycline, and ethinyl estradiol. Doxycycline and tetracycline are antibiotics used to inhibit bacte-
rial growth (see Chapter 26). Oral contraceptive medications containing ethinyl estradiol may be used to
help clear the skin of acne by suppressing oil production (see Chapter 34).
The two most effective treatments for rosacea are topical metronidazole (Metrogel, MetroCream)
and azelaic acid (Azelex, Finacea). Alternative medications include topical clindamycin (Cleocin-T, Clin-
daMax) and sulfacetamide. Tetracycline antibiotics are beneficial to patients with rosacea with multiple
pustules or with ocular involvement. Severe, resistant cases may respond to isotretinoin (Accutane).
Concept Review 36.4

■ What is the major purpose of drugs used to treat acne and related skin conditions? Give
examples of both topical and systemic medications. Which medications are OTC, and
which are prescription medications?
Drug Prototype: Tretinoin (Avita, Retin-A, Others)

Therapeutic Class: Antiacne drug Pharmacologic Class: Retinoid receptor drug, vitamin derivative
Actions and Uses: This drug is indicated for the early treatment bone and joint pain, and photosensitivity. Additive photo-
and control of mild to moderate acne vulgaris. Symptoms take 4 toxicity can occur if tretinoin is used concurrently with other
to 8 weeks to improve, and maximum therapeutic benefit may phototoxic drugs such as tetracyclines, fluoroquinolones, or
take up to 5 or 6 months. This drug is most often reserved for sulfonamides.
cystic acne or severe keratinization disorders. Using tretinoin together with hypoglycemic agents may
The principal action of tretinoin is regulation of skin lead to loss of glycemic control as well as increased risk of
growth and cell turnover. As cells from the germinativum grow cardiovascular disease due to elevated triglyceride levels.
toward the skin’s surface, skin cells are lost from the pore open-
ings, and their replacement is slowed down. Tretinoin also
decreases oil production by reducing the size and number of oil
glands. Black Box Warning:
Patients with acute promyelocytic leukemia (APL) are at
Adverse Effects and Interactions: Tretinoin is a natural deriva- high risk for serious adverse effects: fever, weakness, fa-
tive of retinol or vitamin A. Thus, vitamin A supplements, which tigue, dyspnea, weight gain, peripheral edema, respiratory
increase toxicity, should be avoided. insufficiency, pneumonia, and rapidly evolving leukocytosis,
Common adverse effects are skin irritation (such as a which is associated with a high risk of life-threatening com-
burning or stinging sensation, redness, and crusting), conjunc- plications. There is a high risk that infants will be severely
tivitis (visual disturbance), dry mouth, inflammation of the deformed if this drug is administered during pregnancy.
lip, dry nose, increased serum concentrations of triglycerides,
Dermatitis and Eczema
Dermatitis is a general term that refers to superficial inflammatory disorders of the skin. Eczema, also dermat 5 skin
called atopic dermatitis, is a skin disorder with symptoms resembling an allergic reaction, including itis 5 inflammation
inflammation, itching, and rash. Long-term itching and scaling may cause the skin to appear thickened and atopic 5 out of place
leathery. Exposure to environmental irritants may make these symptoms worse. Other conditions, includ-
ing stress, too little or too much moisture, and extreme temperature fluctuations, may worsen symptoms.
Blisters and other lesions may also develop. In infants and small children, lesions usually begin on the face
and progress to other parts of the body. The skin may become raw and infected from scratching.
Contact dermatitis is a delayed type of allergic reaction resulting from exposure to specific allergens—
for example, perfume, cosmetics, detergents, latex, or jewelry. Accompanying the allergic reaction may be
various degrees of cracking, bleeding, or small blisters.
Seborrheic dermatitis is a disorder caused by overactive oil glands. This condition is sometimes seen
in newborns and in teenagers after puberty. Oily and scaly patches of skin appear in areas of the face, scalp,
chest, back, or pubic area. Bacterial infection or dandruff may accompany these symptoms.
Stasis dermatitis is seen more commonly in older women. It is found primarily in the lower extremi-
ties. Redness and scaling may be observed in areas where venous circulation is impaired or where deep
venous blood clots have formed.
Topical corticosteroids are used mainly to treat dermatitis

and related symptoms. Core Concept 36.6
Topical corticosteroids are used in cases of dermatitis and eczema to treat symptoms of inflammation,
burning, and pruritus. In conjunction with other medical therapies, topical corticosteroids are also used for
the treatment of psoriasis.
Topical corticosteroids are the most effective treatment for dermatitis. As seen in Table 36.4 ◆, there
are many varieties of corticosteroids supplied at different levels of potency. Creams, lotions, solutions,
gels, and pads are specially formulated to cross skin membranes. These medications are especially intended
for the relief of local inflammation and itching. In cases of long-term use, however, adverse effects such
as irritation, redness, and thinning of the skin membranes may occur. If absorption occurs, topical cortico-
steroids may produce undesirable systemic effects, including adrenal insufficiency, mood changes, serum
imbalances, and bone defects, as discussed in Chapter 24.
Table 36.4 Selected Topical Corticosteroids for Dermatitis and Related Symptoms
Generic Name Trade Names
Highest Potency
betamethasone dipropionate Diprolene
clobetasol Temovate
diflorasone Maxiflor
halobetasol Ultravate
High Potency
amcinonide Cyclocort
fluocinonide Lidex
halcinonide Halog
Medium Potency
betamethasone benzoate Uticort
betamethasone valerate Valisone
clocortolone Cloderm
desoximetasone, cream Topicort
fluocinolone acetonide Synalar
flurandrenolide, cream Cordran
fluticasone propionate, cream Cutivate
hydrocortisone valerate Westcort
mometasone furoate Elocon
prednicarbate Dermatop
triamcinolone acetonide Aristocort, Kenalog
betamethasone benzoate Uticort
Lower Potency
alclometasone dipropionate Aclovate
desonide Desonate, DesOwen, Verdeso
dexamethasone Decaspray
hydrocortisone Cortizone, Hycort
Cam Therapy
Aloe Vera for Skin Conditions
Aloe vera is derived from the gel inside the leaf of the aloe plant, which is a member of the
lily family. Used medicinally for thousands of years aloe vera contains over 70 active sub-
stances, including amino acids, minerals, vitamins, and enzymes. Aloe vera is best known for
its ability to sooth and heal minor skin irritations, cuts, and burns. For the most part, scientific
studies have confirmed its benefit for these conditions. It can be found as an ingredient in
many products, including soaps, lotions, creams, and sunblocks. Some evidence suggests it
may be useful in treating genital herpes lesions and moderate plaque psoriasis. Although
oral formulations can be found, these are not recommended because they can cause serious
gastrointestinal (GI) side effects.
Psoriasis
Psoriasis is a chronic, noninfectious inflammatory skin disorder that affects 1% to 2% of the population.
Psoriasis is characterized by red patches of skin covered with flaky, silver-colored scales called plaques.
The reason for the appearance of plaques is an extremely fast skin turnover rate. The skin reacts as if it has
been injured, but skin cells reach the surface much more quickly than usual, in about four days, or six to
seven times faster than usual. The reason for this kind of reaction is not known, although scientists believe
that it may be a genetic immune reaction. Plaques are ultimately shed from the skin’s surface, while the
underlying skin becomes inflamed and irritated.
Several topical and systemic medications are used

to treat psoriatic symptoms. Core Concept 36.7
Because psoriatic symptoms may be extreme, numerous drugs are employed to soothe the patient’s symp-
toms, including emollients, topical corticosteroids, and immunosuppressant medications. Drugs used in emolli 5 to soften
the treatment of psoriasis are provided in Table 36.5 ◆. ent 5 causing
Table 36.5 Drugs for Psoriasis and Related Disorders

Topical Medications
anthralin Topical; apply to lesions daily or as directed Second-line therapy after tolerance to corticosteroids has
developed
calcipotriene (Dovonex) Topical; apply to lesions once or twice daily Synthetic form of vitamin D3; may raise the level of calcium in
up to 8 weeks the body to unhealthy levels
coal tar (Balnetar, Cutar, Topical; apply to lesions daily or as directed Second-line therapy after tolerance to corticosteroids has
others) developed
salicylic acid (Salax, Neutro- Topical; apply to lesions (concentrations Wide range of delivery: creams, foams, gels, lotions, ointments,
gena, others) ranging from 2–10%) as directed pads, plasters, shampoos, soaps, and skin solutions
tazarotene (Tazorac) Acne: topical; apply thin film to clean, dry Topical retinoid; less toxic than corticosteroids; also approved
area daily for facial wrinkles and acne
Plaque psoriasis: topical; apply a thin film
daily in the evening
Systemic Medications
acitretin (Soriatane) PO; 10–50 mg/day with the main meal Retinoid; pregnancy category X drug
adalimumab (Humira) Subcutaneous; 40–80 mg every other week Tumor necrosis factor blocker; also for rheumatoid arthritis and
Crohn’s disease
alefacept (Amevive) IM; 15 mg once weekly for 12 weeks Engineered immunosuppressant drug
cyclosporine (Gengraf, Neoral, PO; 1.25 mg/kg bid (max: 4 mg/kg/day) Immunosuppressant drug; also to prevent transplant rejection
Sandimmune) (see page 382 and rheumatoid arthritis
for Drug Prototype box)
etanercept (Enbrel) Subcutaneous; 50 mg twice weekly (given 3–4 Also for rheumatoid arthritis
days apart); maintenance dose 50 mg/week
infliximab (Remicade) IV; 5 mg/kg with additional doses 2 and 6 Tumor necrosis factor blocker; also for rheumatoid arthritis,
weeks after the initial infusion, then every 8 Crohn’s disease and ulcerative colitis
weeks thereafter
hydroxyurea (Hydrea) PO; 80 mg/kg every 3 days or 20–30 mg/kg daily Off-label use for psoriasis; also used for sickle cell anemia
methotrexate (Rheumatrx, PO; 2.5–5 mg bid × 3 doses each week For rheumatoid arthritis and neoplasia
Trexall) (see page 440 for the (max: 25–30 mg/week)
Drug Prototype box)
ustekinumab (Stelara) Subcutaneous; 45–90 mg initially and 4 weeks Interleukin blocker
later, followed by 45–90 mg every 12 weeks
Topical corticosteroids, such as betamethasone or hydrocortisone, are the primary, initial treat-
ment for psoriasis because they are effective, safe, and inexpensive. Topical corticosteroids reduce the
inflammation associated with fast skin turnover. Therapy usually begins with the high potency cor-
ticosteroids and switches to moderate- and low-potency agents after the initial symptoms have been
controlled.
Other topical drugs are retinoid-like compounds such as calcipotriene (Dovonex) and tazarotene
(Tazorac). These drugs provide the same benefits as topical corticosteroids, but they exhibit fewer side
effects. Calcipotriene produces elevated levels of calcium in the bloodstream, so this medication is not
used on an extended basis.
Some patients have severe psoriasis that is resistant to topical drugs, so systemic therapy must be
used. Systemic medications for psoriasis include acitretin (Soriatane), adalimumab (Humira), alefacept
(Amevive), etanercept (Enbrel), infliximab (Remicade), and ustekinumab (Stelara). These drugs are
taken orally to inhibit skin cell growth. Methotrexate (Rheumatrex, Trexall), an anticancer drug taken in
tablet form, produces similar effects in the body (see Chapter 28). Other medications that have been used
for different disorders but may provide relief of severe psoriatic symptoms are hydroxyurea (Hydrea)
and cyclosporine (Sandimmune, Neoral). Cyclosporine is an immunosuppressive agent, discussed in
Chapter 24.
Other skin therapy techniques may be used with or without psoriasis medications. These include vari-
ous forms of tar treatment (coal tar) and a material called anthralin. Both substances are applied to the
skin’s surface and are not considered first-line therapies. Tar and anthralin inhibit DNA synthesis and
arrest abnormal cell growth.
Ultraviolet B (UVB) and ultraviolet A (UVA) phototherapy are techniques used in cases of severe
psoriasis. UVB therapy is less hazardous than UVA therapy. UVB light has a wavelength similar to sun-
light; it reduces widespread lesions that normally resist topical treatments. With close supervision, this
type of phototherapy can be administered at home. Keratolytic pastes are often applied between treat-
ments. The second type of phototherapy is often referred to as PUVA (psoralen plus ultraviolet light)
therapy because psoralens are often administered in conjunction with phototherapy. Psoralens are oral
or topical agents that, when exposed to UV light, produce a photosensitive reaction. This reaction seems
to provide benefit to the patient by reducing the number of lesions, but unpleasant adverse effects such as
headache, nausea, and skin sensitivity may occur, limiting the effectiveness of this therapy. Immunosup-
pressant drugs such as cyclosporine are not used in conjunction with PUVA therapy because they increase
the risk of skin cancer.
Concept Review 36.5

■ In most cases, which drug category is used to treat symptoms of dermatitis and psoriasis?
What other drug therapies and techniques are used to provide a measure of relief for
these symptoms?

Patients taking medications for skin disorders need to know the following:
1. Inform family members, sexual partners, school personnel, and any other persons with
whom close contact has occurred about skin infestations. Treat clothes, bed linens, and
personal items properly to avoid reinfestation.
2. Be informed and understand the proper way to apply medication or to remove nits if
necessary. Scabicides and pediculicides should not be applied to the face, mouth, open
skin lesions, or the eyes.
3. For acne and related disorders, apply medication only to areas where it is supposed to be
applied. Follow instructions in package inserts and do not deviate from the precautions
communicated by the healthcare provider.
4. Do not share skin medications with family or friends. Be familiar with medication adverse
effects, especially those of retinoids, retinoid-like products, or medications used to treat
severe skin disorders.
5. Use medications only during the time for which they are intended. With extended use,
some medications (e.g., corticosteroids) may cause adverse effects. Take a medication suit-
able for the disorder; avoid those that are too potent or not potent enough.
6. Give medications a chance to work. Some systemic medications must be taken exactly as
prescribed without skipping or stopping early.
7. Avoid contact with objects or drugs that are known to cause allergy or dermatitis. Try to
avoid scratching, if possible. For severe skin disorders, see a dermatologist.
Chapter Review 595
Chapter Review
36.1 Layers of skin provide protection to the body. 36.5 Acne and rosacea are treated by a combination of
Two layers of skin and one underlying layer protect OTC and prescription drugs.
the body: the epidermis, dermis, and hypodermis. The Blackheads, whiteheads, and rosacea are disorders in
most superficial layer is the epidermis, in which skin which pores become blocked, inflamed, or infected
cells are replenished every three weeks. New cells because of accelerated skin processes. Topical drugs
arise from the bottom layer of the epidermis, called for acne are those that inhibit bacterial growth (anti-
the germinativum, and are pushed to the outermost biotics) or promote shedding of old skin (keratolytic
layer. agents). Vitamin A–like compounds (retinoids) pro-
vide an improved resistance to bacterial infections
36.2 The major causes of skin disorders are injury, aging, by reducing oil production and the occurrence of
inherited factors, and other medical conditions. clogged pores.
Many symptoms are associated with skin stress and
injury. Others are associated with a patient’s chang- 36.6 Topical corticosteroids are used mainly to treat
ing age or health. Skin disorders fit into three main dermatitis and related symptoms.
categories: infectious, inflammatory, and cancerous Dermatitis is treated by agents that reduce symptoms
disorders. of inflammation, itchiness, flaking, cracking, bleed-
ing, and lesions. Topical corticosteroids are the pri-
36.3 Scabicides and pediculicides treat parasitic mite mary drug treatment for dermatitis. Potency depends
and lice infestations. on the type of drug formulation and whether it is
Mites affect the skin and hair, whereas lice remain packaged as a cream, lotion, solution, gel, or pad.
localized in hairy regions of the body. Both condi-
tions are treatable with medications. Scabicides kill 36.7 Several topical and systemic medications are used
mites; pediculicides kill lice. to treat psoriatic symptoms.
Psoriasis is a chronic disorder characterized by
36.4 The goal of drug therapy for sunburn is to elimi- extreme discomfort and flaky areas called plaques.
nate discomfort until healing occurs. The treatments for psoriasis include topical corticoste-
Local anesthetics are the primary medication used to roids, retinoid-like compounds, drugs that arrest skin
treat mild sunburn and irritation. Often drugs are used cell growth, and immunosuppressants. Skin therapy
for temporary relief of minor discomfort; in some techniques are also used, including keratolytic agents,
cases, drugs may not be needed at all. coal tar, anthralin, psoralens, and phototherapy.
Review Questions
The following questions are written in NCLEX-PN® style. 3. Worsening of acne

Answer these questions to assess your knowledge of the chap- 4. Skin irritation and redness in the application area
clear to you. 3. The nurse and a patient are discussing how to eliminate
lice. The patient is given a shampoo-like medication that is ap-
1. The nurse informs a patient taking benzocaine for a minor plied and rinsed from the body within 10 minutes after applica-
skin irritation that benzocaine: tion. This medication is:
1. Cannot be used for sunburns 1. Lindane
2. Should not be used on open lesions 2. Crotamiton
3. Causes blisters 3. Cortizone
4. Can be used on open sores 4. Permethrin
2. The nurse is helping to create a teaching plan for a patient 4. The patient is complaining of discomfort related to mi-
prescribed desoximetasone (Topicort) for atopic dermatitis. nor sunburn. Which of the following medications would be in-
The nurse will include which adverse effect in that plan? cluded in a plan of care for someone who has minor sunburn?
1. Localized pruritus and hives 1. Benzocaine (Solarcaine)
2. Hair loss in the application area 2. Cortizone
3. Benzoyl peroxide 3. Acitretin (Soriatane)

4. Doxycycline 4. Cyclosporine (Sandimmune, Neoral)
5. The nurse is providing information at a high school health 8. Some patients with acne may need medications that
fair. Many of the students ask for information on acne treat- promote the shedding of old skin. These medications are
ment. The nurse tells them that ___________ is available but known as:
it is extremely important that women who are pregnant should 1. Pediculicides
not take this medication. 2. Keratolytic agents
1. Hydrocortisone 3. Retinoids
2. Tretinoin 4. Corticosteroids
3. Benzoyl peroxide
4. Benzocaine 9. A nurse is caring for a newly diagnosed patient with psoria-
sis. The skin on her elbow is covered with red plaques and scales.
6. The patient is using topical corticosteroids. The nurse will She finds it very embarrassing. Even though she doesn’t have much
need to monitor for which of the following systemic effects of money, she wants to know what medication can help her. The nurse
the medication? (Select all that apply.) understands that the initial and inexpensive medication is:
1. Mood changes 1. Betamethasone
2. Bone defects 2. Doxycycline
3. Liver toxicity 3. Cyclosporine
4. Adrenal insufficiency 4. Benzocaine
7. A patient with rosacea is being seen at the doctor’s office 10. A patient is to receive the initial infused dose of inflix-
with concerns about her skin. She has been trying to deal with imab (Remicade), 5 mg/kg. The patient weighs 198 pounds.
her condition by using over-the-counter medications, but they How many milligrams will the patient receive?
seemed to have made her condition worse. The nurse under- 1. 40 mg
stands the patient may need: 2. 90 mg
1. Calcipotriene (Dovonex) 3. 450 mg
2. Metronidazole (Metrogel) 4. 990 mg
Remember Burt Nicholson, the 1. Burt said that he had tried a lot of over-the-counter
patient introduced at the begin- medications so the nurse asks him what medications he
ning of the chapter? Now read the tried. He says that he can’t remember all of them but he’s
remainder of the case study. Based sure he tried benzoyl peroxide but stopped using it after a
on the information you have learned week because his acne was still visible. The nurse responds
in this chapter, answer the questions by saying:
that follow. 1. “The cream should have worked within that first week.”
2. “Improvements begin in the first week but the full effects
may take several weeks to a month or longer.”
Burt Nicholson is a 16-year-old white male with a family history 3. “Acne is very difficult to treat. It may take several months
of various allergy disorders. He is complaining of general irri- before you see improvements.”
tation and sores around the face, neck, and upper back. Upon 4. “If your acne isn’t gone by now, you may need an antibiotic.”
examination, a severe case of acne and moderate erythema are
observed on the chin, cheeks, and forehead. No excessive oil 2. Right now the physician wants Burt to try the benzoyl
is noted. Although areas around the neck and upper back are peroxide again, but because Burt’s skin is red and inflamed, the
inflamed, these do not appear to be infected. Burt states that he nurse suspects that a(n) __________ will also be prescribed.
is so embarrassed about his skin, it’s impacting his social life. 1. Metronidazole
He also says that he has tried a lot of different over-the-counter 2. Benzocaine
medications to help his acne but nothing seems to work. Burt is 3. Corticosteroid
diagnosed with acne vulgaris. 4. Antibiotic
Chapter Review 597
3. Other medication options are discussed. Burt is informed 4. The nurse continues to tell Burt that tretinoin may cause
that he could also take tretinoin, a retinoid antiacne medication. the following adverse effects: (Select all that apply.)
When asked how the medication works, the nurse responds that 1. Swelling around the lips
tretinoin: 2. Dry mouth and nose
1. Sheds the outer layer of the skin 3. Photosensitivity (sensitivity to light)
2. Decreases oil production by reducing the size and number 4. Skin irritation such as burning and redness
of oil glands
3. Inhibits bacterial growth
4. Reduces inflammation
Pearson Nursing Student Resource Find additional review materials at nursing.pearsonhighered.com.

c
“Moving is so stressful, and
h it’s worse because I haven’t
a had any help. I’m not even
p sure where I packed my
medication so I’ve been
t having problems seeing.”
e Ms. Mary Saunders
r
37 Drugs for Eye and Ear Disorders
Core Concepts
37.1 Knowledge of basic eye anatomy is essential for an 37.5 Other antiglaucoma medications decrease the
understanding of eye disorders and drug therapy. formation of aqueous humor.
37.2 Glaucoma is one of the leading causes of blindness. 37.6 Drugs provide relief for minor eye conditions and
37.3 Glaucoma therapy focuses on adjusting the are used for eye exams.
circulation of aqueous humor. 37.7 Otic preparations treat infections, inflammation,
37.4 Some antiglaucoma medications increase the and earwax buildup.
outflow of aqueous humor.
Drug Snapshot
Drugs for glaucoma that latanoprost (Xalatan) 601
increase the outflow of
aqueous humor
Drugs for glaucoma that t imolol (Betimol,
decrease the formation Timoptic, others) 604
of aqueous humor
Drugs for eye examinations and minor eye conditions
Drugs for ear conditions
Learning Outcomes
1. Describe important eye anatomy 5. Explain the two major mechanisms 8. Identify examples of drugs for
relevant to glaucoma development. by which drugs reduce intraocular treating ear infections, earaches, or a
2. Identify the major risk factors pressure. buildup of earwax.
associated with glaucoma. 6. Identify examples of important drugs 9. For each of the classes listed
3. Explain how intraocular pressure is for treating glaucoma, and explain in the Drug Snapshot, identify
related to nerve damage in the eye. their basic actions and adverse effects. representative drugs and explain
7. Identify examples of drugs that their mechanisms of drug action,
4. Compare and contrast the two primary actions, and important
principal types of glaucoma, dilate or constrict pupils, relax ciliary
muscles, constrict ocular blood adverse effects.
and explain their reasons for
development. vessels, or moisten eye membranes.
Key Terms
closed-angle glaucoma (glaw-KOH-mah) mastoiditis (mass-toy-DYE-tuss) 606 open-angle glaucoma
601 miosis (my-OH-sis) 601 (glaw-KOH-mah) 601
cycloplegia (sy-kloh-PLEE-jee-ah) 602 mydriasis (mih-DRY-uh-siss) 601 otitis media (oh-TYE-tuss
cycloplegic drugs (sy-kloh-PLEE-jik) 605 MEE-dee-ah) 606
mydriatic drugs (mih-
external otitis (oh-TYE-tiss) 606 DRY-atik) 605 tonometry (toh-NAHM-uh-tree) 601
T he senses of vision and hearing provide the primary means for us to communicate with the world
around us. Disorders affecting the eye and ear can result in problems with self-care, mobility,
safety, and communication. The eye is vulnerable to a variety of conditions, many of which can
be prevented, controlled, or reversed with proper pharmacotherapy. The first part of this chapter covers
drugs used for the treatment of glaucoma and those used routinely by ophthalmic healthcare providers. The
remaining part of the chapter presents drugs used for treatment of common ear disorders, including infec-
tions, inflammation, and the buildup of earwax.
Knowledge of basic eye anatomy is essential for an understanding

of eye disorders and drug therapy. Core Concept 37.1
To understand eye disorders and drug action, a firm knowledge of basic ocular anatomy is required. As
shown in Figure 37.1 ■, a watery fluid called aqueous humor is found in the anterior cavity of the eye. The
anterior cavity has two divisions: the anterior chamber and the posterior chamber. In the posterior chamber
(Figure 37.2 ■), aqueous humor originates from an important muscle structure called the ciliary body.
From there, aqueous humor flows through the pupil and into the anterior chamber. Within the anterior
chamber and around the periphery is a network of spongy connective tissue called trabecular meshwork. trabecular 5 strut-like
Connected with trabecular meshwork is an opening called the canal of Schlemm, the location where aque-
ous humor drains from the anterior cavity.
Figure 37.1
Internal structures
of the eye.
Fovea
Anterior Central artery
cavity and vein
Cornea
Edge of Optic nerve
pupil
Orbital fat
Visual axis Posterior

cavity
Lens
Retina
Iris
Sclera
Conjunctiva
Bony orbit
600 Chapter 37 Drugs for Eye and Ear Disorders
Figure 37.2
Lens
Cornea
Anterior
chamber
Iris
Flow of aqueous
Trabecular humor
meshwork
Open anterior
Canal of chamber angle
Schlemm: Posterior
aqueous humor chamber
exits here
Ciliary Process:
aqueous humor
Normal eye anatomy is formed here
Open anterior Closed anterior

Congestion in chamber angle chamber angle
trabecular meshwork Trabecular
reduces flow through meshwork and canal
canal of Schlemm of Schlemm blocked,
preventing outflow of
aqueous humor
(a) Open-angle glaucoma: slowly rising intraocular pressure (b) Closed-angle glaucoma: rapidly rising intraocular pressure
Forms of primary adult glaucoma: (a) in chronic, open-angle glaucoma, the anterior chamber angle remains open, but
drainage of aqueous humor through the canal of Schlemm is impaired; (b) in acute, narrow closed-angle glaucoma, the
angle of the iris and anterior chamber is smaller, obstructing the outflow of aqueous humor.
Glaucoma
Glaucoma is one of the most dreaded eye disorders. In some cases, glaucoma is genetic; in other cases,
glaucoma may be caused by eye trauma or disease. Some medications may contribute to the develop-
ment of glaucoma, including long-term use of topical corticosteroids, some antihypertensives, antihista-
mines, and antidepressants. The major risk factors associated with glaucoma include high blood pressure,
migraine headaches, high levels of nearsightedness or farsightedness, and older age.
Fast Facts Glaucoma
■ Worldwide, more than five million people have lost their vision as a result of glaucoma. More than
50,000 are in the United States.
■ Individuals of African heritage are affected more by glaucoma than any other ethnic group.
■ Glaucoma is most common in patients older than 60 years of age.
■ Acute glaucoma is often caused by head trauma, cataracts, tumors, or hemorrhage.
■ Chronic simple glaucoma accounts for 90% of all glaucoma cases.
Glaucoma is one of the leading causes of blindness. Core Concept 37.2
The presence of glaucoma may be detected by tonometry, an ophthalmic technique for measuring tono 5 pressure
increased pressure inside the eye. Other routine refractory and visual field tests may uncover glaucoma metry 5 measurement
signs. One problem with diagnosis is that patients with glaucoma typically do not experience symptoms
and, therefore, do not seek medical attention. In some cases, glaucoma occurs so gradually that patients do
not experience symptoms until late in the disease process.
Glaucoma is characterized by increased pressure inside the eyeball, termed intraocular pressure intra 5 inside
(IOP). The reason why IOP develops is because the normal flow of aqueous humor in the eye becomes ocular 5 eye
blocked. Over time, pressure around the optic nerve can build, leading to blindness. In some cases, eye
injury from the elevated IOP may be sudden, but in most cases it is gradual.
As shown in Figure 37.2, the two principal types of glaucoma are closed-angle glaucoma and open-angle
glaucoma. Both disorders result from the same problem: Pressure inside the eyeball leads to progressive dam-
age of the optic nerve. The differences between these two disorders include how quickly the IOP develops.
Open-angle, or chronic simple glaucoma, is the most common type of glaucoma, accounting for more
than 90% of all cases. With this disorder, IOP develops more slowly. It is called “open angle” because the
iris does not cover the trabecular meshwork (Figure 37.2a). If discovered early, open-angle glaucoma can
be treated successfully with medications.
Closed-angle glaucoma, sometimes referred to as acute glaucoma, is usually caused by stress, impact
injury, or medications. Pressure inside the anterior chamber increases suddenly because the iris is pushed
over the area where the aqueous fluid normally drains (Figure 37.2b). Symptoms include intense head-
aches, difficulty concentrating, bloodshot eyes, and blurred vision. Closed-angle glaucoma requires imme-
diate intervention (usually surgical).
Glaucoma therapy focuses on adjusting the circulation of aqueous humor. Core Concept 37.3
There are several approaches to glaucoma therapy. In cases of acute glaucoma, conventional or laser sur-
gery might be performed to return the iris to its original position. Most therapies focus on reducing the
amount of aqueous humor formed or unblocking its drainage. Generally, drug therapy for glaucoma func-
tions by either increasing the outflow of aqueous humor (canal of Schlemm location) or by decreasing the
formation of aqueous humor (ciliary body location).
Concept Review 37.1

■ Which components of the eye are specifically affected by glaucoma? Why is glaucoma such a
dreaded eye disease? Drug therapy for glaucoma centers around which major approach?
Some antiglaucoma medications increase the outflow of aqueous humor. Core Concept 37.4
Drugs increasing the outflow of aqueous humor include miotics, sympathomimetics, and prostaglandins. miotic 5 constricting pupil
These drugs are summarized in Table 37.1 ◆.
Although antiglaucoma drugs are not designed to directly alter pupil diameter, they often produce this
effect because of their physiologic properties. Cholinergic direct- and indirect-acting drugs cause constric-
tion of pupils or miosis. Sympathomimetics are drugs that activate the sympathetic nervous system and
cause dilation of pupils or mydriasis (see Chapter 8). Prostaglandins do not affect pupil diameter, but
instead they directly dilate trabecular meshwork within the anterior chamber of the eye.
Drug Prototype: Latanoprost (Xalatan)

Therapeutic Class: Antiglaucoma drug Pharmacologic Class: Prostaglandin, reducer of IOP
Actions and Uses: Latanoprost is a prostaglandin analog burning, pain, irritation, itching, sensation of a foreign body in
believed to reduce IOP by increasing the outflow of aqueous the eye, photophobia, and visual disturbances. The eyelashes on
humor. The recommended dose is one drop in the affected the treated eye may grow, thicken, and darken. Changes may
eye(s) in the evening. It is metabolized to its active form in the occur in pigmentation of the iris of the treated eye and in the
cornea, reaching its peak effect in about 12 hours. It is used to periocular skin. The most common systemic adverse effect is a
treat open-angle glaucoma and elevated IOP. flu-like upper respiratory infection. Rash, asthenia, or headache
may occur.
Adverse Effects and Interactions: Adverse effects include Latanoprost interacts with thimerosal: If mixed with eye-
ocular symptoms such as conjunctival edema, tearing, dryness, drops containing thimerosal, precipitation may occur.
Table 37.1 Antiglaucoma Drugs That Increase the Outflow of Aqueous Humor
Direct- and INDIRECT-Acting CholinergicS (MIOTIC DRUGS)
carbachol (Miostat) One or two drops 0.75–3% solution in the Ophthalmic solution; cholinergic drug; less useful in glaucoma
lower conjunctival sac every 4 hours three than other drugs; causes stinging of the eyes
times a day
echothiophate (Phospholine One drop of 0.03–0.25% solution one to two Ophthalmic solution; irreversible acetylcholinesterase inhibitor;
Iodide) times per day should be used cautiously due to an intense and persistent mio-
Acute glaucoma: 1 drop of 1–2% solution sis and ciliary-muscle contraction that may occur
every 5–10 min for three to six doses
Chronic glaucoma: 1 drop of 0.5–4% solu-
tion every 4–12 hours
pilocarpine (Isopto Carpine, Acute glaucoma: one drop 1–2% solution Ophthalmic solution; cholinergic drug; may be prescribed as
Pilopine) every 5–10 minutes for 3–6 doses an ocular therapeutic system, a slow release delivery method
Chronic glaucoma: one drop 0.5–4% solu- (Ocusert Pilo-20)
tion every 4–12 hours
NONSELECTIVE Sympathomimetics (MYDRIATIC DRUGS)
dipivefrin HCl (Propine) One drop 0.1% solution bid Ophthalmic solution; converted to epinephrine in the eye
Prostaglandins
bimatoprost (Lumigan) One drop 0.03% solution daily in the evening Ophthalmic solution
latanoprost (Xalatan) One drop (1.5 mg) solution daily in the Ophthalmic solution
evening
tafluprost (Zioptan) One drop of 0.0015% solution in the evening Ophthalmic solution; for reducing elevated intraocular pressure
in patients with open-angle glaucoma or ocular hypertension
travoprost (Travatan) One drop 0.004% solution daily in the Ophthalmic solution; maximum effect after about 12 hours
evening
Prostaglandins
Prostaglandins are the preferred drugs for glaucoma therapy because they have long durations of action
and produce fewer side effects than drugs from other classes. In resistant cases, they may be combined
with drugs from other classes. Drugs in this class increase aqueous humor outflow by reducing congestion
in trabecular meshwork. Their main side effect is a change in pigmentation, usually a change to a brown
cyclop 5 round eye iris color in patients with lighter colored eyes. These medications cause cycloplegia (blurred vision), local
plegia 5 paralysis irritation, and stinging of the eyes. Because of these effects, prostaglandins are normally administered just
before the patient goes to bed. Although prostaglandins can be irritating to the eyes, they usually do not
prevent the patient from falling asleep.
Direct- and Indirect-Acting Cholinergics (Miotic Drugs)

Carbachol (Miostat), and pilocarpine (Isopto Carpine, Pilopine HS) are cholinergic drugs. These drugs
directly activate the cholinergic receptors, producing various responses in the eye, including dilation of
trabecular meshwork, so that the canal of Schlemm can absorb more aqueous humor. When more aque-
ous humor is absorbed, IOP is reduced. Thus, draining of the aqueous humor has an impact on eye pres-
sure. Adverse effects include temporary cycloplegia. Cholinergic drugs are generally used in patients with
open-angle glaucoma who have not responded to other medications. Echothiophate iodide (Phospholine
iodide) is an indirect-acting cholinergic drug. It produces the same effects as direct-acting drugs, except
that it blocks cholinesterase, the enzyme responsible for breaking down the natural neurotransmitter
acetylcholine.
Nonselective Sympathomimetics (Mydriatic Drugs)

Dipivefrin (Propine) is a sympathomimetic drug. Dipivefrin is converted to epinephrine; epinephrine pro-
duces mydriasis, increased outflow of aqueous humor, and the subsequent fall of IOP. As discussed in
Chapter 21, when epinephrine is released into the general circulation, it increases blood pressure and heart
rate. Because of the potential for systemic adverse effects, this drug is rarely prescribed for the treatment
of glaucoma.
Other antiglaucoma medications decrease the formation

of aqueous humor. Core Concept 37.5
Although prostaglandins are preferred drugs for glaucoma, other medications may be needed to bring IOP to
normal levels. Beta-adrenergic blockers, alpha2-adrenergic drugs, carbonic-anhydride inhibitors, and osmotic
diuretics are drug classes that decrease the formation of aqueous humor. These are summarized in Table 37.2 ◆.
Beta Adrenergic Blockers

Beta-blocking drugs include betaxolol (Betaoptic), carteolol (Ocupress), levobunolol (Betagan), metipran-
olol (OptiPranolol), and timolol (Betimol, Timoptic, others). The exact mechanism by which these drugs
produce their effects is not fully understood. However, they all reduce IOP effectively without the ocular
adverse effects of other autonomic drugs. Beta blockers do not alter pupil diameter or produce cycloplegic
effects. The doses of ophthalmic beta blockers are generally not high enough to enter the general circula-
tion. Systemic adverse effects, if they occur, include bronchoconstriction, bradycardia, and hypotension.
Alpha2-Adrenergic Drugs
Alpha2-adrenergic drugs are less frequently prescribed than the other antiglaucoma medications. These
medications include apraclonidine (Iopidine) and brimonidine (Alphagan). The most significant adverse
effects are headache, drowsiness, dry mucosal membranes, blurred vision, and irritated eyelids.
Carbonic Anhydrase Inhibitors

Carbonic anhydrase inhibitors may be administered topically or PO to reduce IOP. Usually these medi-
cations are used as a second choice if beta blockers are not effective. Examples include acetazolamide
(Diamox), brinzolamide (Azopt), dichlorphenamide (Daranide, Oratrol), dorzolamide (Trusopt), and meth-
azolamide (Neptazane). These medications are more effective in cases of open-angle glaucoma. Patients
must be cautioned when taking these medications because they are sulfonamides—drugs that may cause
an allergic reaction. All of these drugs are diuretics, which means they can reduce IOP rather quickly and
dramatically, altering serum electrolytes with continuous treatment.
Table 37.2 Antiglaucoma Drugs That Decrease the Formation of Aqueous Humor
betaxolol (Betaoptic) One drop 0.5% solution bid Ophthalmic solution; beta1-blocker; reduces blood pressure,
heart rate
carteolol (Ocupress) One drop 1% solution bid Ophthalmic solution; nonspecific beta blocker; causes
bronchoconstriction
levobunolol (Betagan) One or two drops 0.25–0.5% solution once Ophthalmic solution; nonspecific beta blocker
or twice daily
metipranolol (OptiPranolol) One drop 0.3% solution bid Ophthalmic solution; nonspecific beta blocker
timolol (Betimol, Timoptic, One or two drops of 0.25–0.5% solution Ophthalmic solution; nonspecific beta blocker
others) once or twice daily; gel (salve): apply daily
Alpha2-Adrenergic Drugs
apraclonidine (Iopidine) One drop 0.5% solution bid Ophthalmic solution
brimonidine tartrate One drop 0.2% solution tid Ophthalmic solution
(Alphagan)
Carbonic Anhydrase Inhibitors
acetazolamide (Diamox) PO; 250 mg one to four times per day Oral diuretic; sulfonamide; also for seizures, high altitude sick-
ness, and renal impairment
brinzolamide (Azopt) One drop 1% solution tid Ophthalmic solution; sulfonamide
dorzolamide (Trusopt) One drop 2% solution tid Ophthalmic solution; sulfonamide
methazolamide (Neptazane) PO; 50–100 mg bid or tid Oral sulfonamide; less diuretic activity than acetazolamide
Osmotic Diuretics
isosorbide (Ismotic) PO; 1–3 g/kg bid–qid Used before and after eye surgery
mannitol (Osmitrol) IV; 1.5–2 mg/kg as a 15–25% solution over Raises osmotic pressure, causing diuresis; IV medication
30–60 minutes
Drug Prototype: Timolol (Betimol, Timoptic, Others)

Therapeutic Class: Antiglaucoma drug Pharmacologic Class: Beta-adrenergic blocker,
reducer of IOP, ocular hypotensive drug
Actions and Uses: Timolol is a nonselective beta-adrenergic Adverse Effects and Interactions: The most common adverse
blocker available as a 0.25% or 0.5% ophthalmic solution. effects are local burning and stinging on instillation. In most
Timolol reduces elevated IOP in chronic open-angle glaucoma patients there is no significant systemic absorption to cause
by reducing the formation of aqueous humor. The usual dose is adverse effects as long as timolol is applied correctly. If signifi-
one drop in the affected eye(s) twice a day. Timoptic XE allows cant systemic absorption occurs, however, drug interactions
for once-a-day dosing. Treatment may require two to four could occur. Anticholinergics, nitrates, reserpine, methyldopa,
weeks for maximum therapeutic effect. It is also available in and/or verapamil use could lead to increased hypotension and
tablets, which are prescribed to treat mild hypertension. bradycardia. Indomethacin and thyroid hormone use could lead
Cosopt PF is a solution of timolol with dorzolamide, a to decreased antihypertensive effects of timolol. Epinephrine
carbonic-anhydrase inhibitor. Combigan combines timolol with use could lead to hypertension followed by severe bradycardia.
brimonidine, an alpha adrenergic agonist. Theophylline use could lead to decreased bronchodilation.
hypo 5 reduced Osmotic Diuretics

tensive 5 tension Osmotic diuretics are used in cases of eye surgery or acute closed-angle glaucoma. Examples include isosorbide
thrombo 5 clot (Ismotic) and mannitol (Osmitrol). Because they have an ability to reduce plasma volume very quickly (see
phleb 5 vein Chapter 18), they may produce unpleasant adverse effects, including headache, tremors, d izziness, dry mouth,
itis 5 inflammation fluid and electrolyte imbalance, and thrombophlebitis (venous clot formation) near the site of IV administration.
Concept Review 37.2

■ Describe two major approaches for controlling IOP in patients with glaucoma. What major
drug classes are used in each case?
Nursing Process Focus Patients Receiving Pharmacotherapy for Glaucoma

Prior to drug administration: ■ Disturbed Sensory Perception related to disease process
■ Obtain a complete health history, including cardiovascular, respiratory, ■ Risk for Injury related to visual acuity deficits or adverse drug effects
thyroid, and renal conditions; eye trauma or infection; allergies; drug ■ Self-Care Deficit related to impaired vision
history; and possible drug interactions. ■ Acute Pain related to disease process or adverse drug effects
■ Acquire the results of physical examination focusing on vital signs, ■ Deficient Knowledge related to a lack of information about drug
visual acuity, visual fields (peripheral and central), presence of halos, therapy
blurred vision, and ocular pain.

The patient will:
■ Experience therapeutic effects (normal eye pressure and no progression of visual impairment).
■ Verbalize understanding of the drug’s use, adverse effects, and required precautions.
Implementation

■ Administer ophthalmic solutions correctly and evaluate patient’s Instruct the patient in the proper administration of eye drops to:
knowledge of correct administration. (Using proper technique en- ■ Remove contact lenses prior to administering eye drops and wait
sures that medication stays within the eye and helps to prevent 15 minutes before reinsertion.
complications.). ■ Wash hands prior to eye drop administration.
■ Avoid touching the tip of the container to the eye, which may
contaminate the solution.
■ Administer the eye drop in the conjunctival sac.
■ Apply pressure over the lacrimal sac for 1 minute.
■ Wait five minutes before administering other ophthalmic solutions.
■ Schedule glaucoma medications around daily routines such as waking,
mealtimes, and bedtime to lessen the chance of missed doses.
■ Monitor visual acuity, blurred vision, papillary reactions, extraocular ■ Instruct the patient to report to the healthcare provider any changes
movements, and ocular pain. (Periodic monitoring helps to determine in vision, eye pain, light sensitivity, halos around lights, or headache.
the effectiveness of drug therapy.)
(continued )

■ Monitor the patient for specific contraindications for the prescribed ■ Instruct the patient to inform the healthcare provider of all health-
drug. (There are many physiologic conditions for which ophthalmic related problems and prescribed and OTC medications.
solutions may be contraindicated.)
■ Provide for eye comfort such as an adequately lighted room. (Ophthal- ■ Caution patient about driving or other activities in low-lighting
mic drugs such as beta blockers used in the treatment of glaucoma can conditions or at night until the effects of the drug are known.
cause miosis and difficulty seeing in low-level lighting.)
■ Monitor for ocular reaction to the drug such as conjunctivitis and lid ■ Review with the patient the correct medication administration
reactions. (These reactions may indicate adverse reactions or infection technique.
due to improper administration.) ■ Instruct the patient to report itching, drainage, edema, ocular pain,
sensation of a foreign body in the eye, photophobia, and visual
disturbances to the healthcare provider.
■ Monitor the color of the iris and periorbital tissue of the treated eye. Inform the patient that:
(Prostaglandins can change the color of the iris over time.) ■ More brown color may appear in the iris and in the periorbital tissue
of the treated eye only.
■ Any pigmentation changes develop over months to years.
■ Monitor vital signs periodically for systemic absorption of ophthalmic Instruct the patient to:
preparations. (Systemic ophthalmic drugs such as beta blockers and ■ Take and record vital signs weekly.
cholinergic drugs may cause serious cardiovascular complications such ■ Immediately report palpitations, chest pain, shortness of breath, and
as hypertension, or bradycardia.) irregularities in pulse and blood pressure to the healthcare provider.
■ Monitor and adjust environmental lighting to aid in patient’s comfort. Instruct the patient to:
(People who have glaucoma are sensitive to excessive light, especially ■ Adjust environmental lighting as needed to enhance vision or reduce
extreme sunlight.) ocular pain.
■ Wear darkened glasses as needed.
■ Encourage compliance with the treatment regimen. (Nonadherence Instruct the patient:
may result in total loss of vision.) ■ To adhere to medication schedule for eyedrop administration.
■ About the importance of regular follow-up care with the
ophthalmologist.
■ That IOP readings should be done prior to beginning treatment
and periodically during treatment.

and 37.2 for lists of drugs to which these nursing actions apply.
Eye Examinations and Minor

Eye Conditions
Drugs provide relief for minor eye conditions and are used for eye exams. Core Concept 37.6
Drugs for minor irritation and injury come from a broad range of classes, including antimicrobials, local
anesthetics, corticosteroids, and nonsteroidal anti-inflammatory drugs (NSAIDs). A range of drug prepara-
tions may be used, including drops, salves, optical inserts, and injectable formulations. Some drugs only
provide moisture to the eye’s surface. For example, approved in 2009, bepotastine (Bepreve) is an antihis-
tamine approved for twice daily dosing for itching associated with allergic conjunctivitis. Others penetrate
and affect a specific area of the eye.
Some drugs are specifically designed for ophthalmic examinations. These include cycloplegic drugs
to relax ciliary muscles and mydriatic drugs to dilate the pupils. Caution must be used when administer- mydriatic 5 dilating pupil
ing anticholinergic mydriatics because these drugs can increase IOP and worsen glaucoma. In addition,
anticholinergic drugs have the potential for producing adverse effects of the central nervous system such as
confusion, unsteadiness, or drowsiness in adults. Children generally become restless and spastic. Examples
of cycloplegic, mydriatic, lubricant, and corneal edema drugs are listed in Table 37.3 ◆.
Concept Review 37.3

■ List examples of commonly used drugs for minor eye irritation and injury. What are the
major actions of cycloplegic and mydriatic drugs?
Table 37.3 Drugs for Eye Examinations and for Moistening Eye Membranes
Mydriatics: Sympathomimetics
phenylephrine (Neo-Synephrine) One drop 2.5% or 10% solution Decongestant and vasoconstriction properties; smaller doses provide
(see page 98 for the Prototype before eye exam temporary relief of eye redness; also for pupil dilation in closed-angle
Drug Box) glaucoma
Cycloplegics: Anticholinergics
atropine (Atro-Pen) (see page 95 One drop 0.5% solution daily Also provided as ointment; should not be administered to patients
for the Prototype Drug Box) with glaucoma; effects may be prolonged
cyclopentolate (Cyclogyl, Pentalair) One drop 0.5–2% solution 40–50 Not for patients with glaucoma; causes burning and irritation;
minutes before procedure possible central adverse effects with higher doses
homatropine (Isopto Homatropine, One or two drops 2 % or 5% solu- Not for patients with glaucoma; effects may be prolonged after
others) tion before eye exam treatment
scopolamine hydrobromide (Isopto One or two drops 0.25% solution Not for patients with glaucoma; effects may be prolonged after
Hyoscine) 1 hour before eye exam treatment; possible central adverse effects with higher doses
tropicamide (Mydriacyl, Tropicacyl) One or two drops 0.5–1% solution Not for patients with glaucoma; central adverse effects with higher
before eye exam doses
Lubricants CAUSING Vasoconstriction
naphazoline (Albalon, Allerest, One to three drops 0.1% solution Over-the-counter (OTC) and prescription medications available
ClearEyes, others) every 3–4 hours prn
oxymetazoline (OcuClear, One or two drops 0.025% solu- OTC and prescription medications available
Visine LR) tion qid
tetrahydrozoline (Murine Plus, One or two drops 0.05% solution Primarily OTC medication
Visine, others) bid–tid
General Purpose Lubricants
lanolin alcohol (Lacri-lube) Apply a thin film to the inside of Mixed with mineral oil and petroleum jelly as a salve
the eyelid
polyvinyl alcohol (Liquifilm, others) One or two drops prn Artificial tear solution
Drugs for Corneal Edema and itching
sodium chloride hypertonicity oint- Apply a thin film to the inside of Ophthalmic ointment for corneal edema; mixed with lanolin, mineral
ment (Muro 128 5% Ointment) the eyelid; instill one drop into the oil, purified water, and white petrolatum as a salve; for itching associ-
affected eye(s) twice a day (bid) ated with allergic conjunctivitis
Ear Conditions
The ear has two major sensory functions: hearing and maintenance of equilibrium and balance.
Three important structural areas—the outer ear, middle ear, and inner ear—carry out these functions
(Figure 37.3 ■).
externa 5 outside Otitis. inflammation of the ear, most often occurs in the outer and middle ear compartments. External
ot 5 ear otitis or otitis externa, commonly referred to as swimmer’s ear, is inflammation of the outer ear; otitis
itis 5 inflammation media is inflammation of the middle ear. Outer ear infections most often occur with water exposure. Middle
media 5 middle
ear infections most often occur with upper respiratory infections, allergies, or auditory tube irritation. Of
interna 5 inside all ear infections, the most difficult ones to treat are infections of the inner ear (otitis interna). Mastoiditis,
or inflammation of the mastoid sinus, can be a serious problem because if left untreated, it can result in
hearing loss.
Figure 37.3
Structures of the ex-

External ear Middle ear Inner ear ternal ear, middle ear,
and inner ear.
Semicircular
Auricle canals
Vestibule
Malleus Cranial
nerve VIII
Incus
Cochlea
Round
window
External
auditory Stapes Eustachian
canal Tympanic in oval tube
membrane window
Otic preparations treat infections, inflammation, and earwax buildup. Core Concept 37.7
Combination drugs effectively treat many different types of ear conditions, including infections, earaches,
edema, and earwax.
The basic treatment for ear infection is essentially the same as in all places of the body: antibiotics.
Topical antibiotics in the form of eardrops may be administered for external ear infections. Ciprofloxacin
(Cipro HC otic, Cetraxal) is a very common topical antibiotic used for ear infections. Adverse reactions
can occur with this medication. These include rashes; white patches in the mouth; vaginal itching or dis-
charge; and itching, pain, or mild irritation within the ear.
Systemic antibiotics (see Chapter 26) may be needed in cases in which outer ear infections are exten-
sive or in cases of middle or inner ear infections. Medications for pain, edema, and itching may also be
necessary. Corticosteroids are often combined with antibiotics or with other drugs when inflammation is
present. Examples of these drugs are listed in Table 37.4 ◆.
Table 37.4 Otic Preparations

acetic acid and hydrocortisone Three to five drops in the affected ear every Combination of acetic acid and glucocorticoid; for general ear
(Vosol HC) 4–6 hours for 24 hours, then five drops infections and inflammation
tid–qid
benzocaine and antipyrine Fill the ear canal with solution tid for For acute otitis media and the removal of earwax; reduces
(Auralgan) 2–3 days earache associated with the infection
carbamide peroxide (Debrox) One to five drops 6.5% solution bid for To soften, loosen, and remove excessive earwax; OTC
4 days medication
ciprofloxacin and dexametha- Four drops of the suspension instilled into Combination of fluoroquinolone antibiotic and corticosteroid;
sone (CiproDex) the affected ear bid for 7 days for ear infections and inflammation
ciprofloxacin and hydrocorti- Three drops of the suspension instilled into Combination of fluoroquinolone antibiotic and corticosteroid;
sone (Cipro HC) the affected ear bid for 7 days for ear infections and inflammation
polymyxin B, neomycin, and Four drops in the ear tid–qid Combination of antibiotics and glucocorticoid; for general ear
hydrocortisone (Cortisporin) or mastoid infections and inflammation; some patients may
develop dermatitis as a result of sensitivity to neomycin
Mineral oil, earwax softeners, and commercial products are also used for proper ear health.
When earwax accumulates, it narrows the ear canal and may interfere with hearing. This is especially
true for older patients who are not able to properly groom themselves. Healthcare providers working
with younger and elderly patients are trained to take appropriate measures when removing impacted
earwax.
Concept Review 37.4

■ Identify the areas of the ear where microbial infections are most likely. What kind of otic
preparations treat infections, inflammation, and earwax buildup?
Cam Therapy
Aloe Vera for Improving Eye and Ear Health
For centuries, Aloe vera has been hailed as the “medicine plant” because of its ability to treat
burns, cuts, scrapes, rashes, and abrasions. It has a reputation for treating inflammation and
acid indigestion, and even lowering blood cholesterol. Aloe may be able to treat eye irrita-
tion and conjunctivitis in addition to many other disorders.
One does not have to put aloe directly into the eyes to obtain its therapeutic effect. The
benefit comes from treating areas around the eyes, including the bridge of the nose and
the outside of the eyelids and cheeks. The skin around the ears may also be treated. The
antiseptic properties of aloe probably come from the many components found within its
sap and leaves. Some components have a reputation for killing microorganisms, including
salicylic acid, urea nitrogen, cinnamonic acid, phenols, sulphur, and lupeol. Other components
including plant sterols, immune modulating peptides, anti-inflammatory fatty acids, and
viscous-like polysaccharides qualify as healing agents.

Patients taking medications for eye and ear disorders need to know the following:
Regarding Eye Medications

1. Have regular eye exams after the age of 40.
2. Do not strain or lift heavy objects if risk for glaucoma is present. Any effort that might
produce eyestrain should be avoided.
3. Make sure that all allergies or sensitivities, including those to sulfa drugs, are known to
the healthcare providers.
4. Do not take OTC medications that “get the red out” for longer than 24 hours. Use eye
lubricants instead. Persistent irritation should be reported immediately.
5. Keep eye solutions clear and sterile; do not actually touch the eye when instilling drops.
Regarding Ear Medications
6. Take precautions to keep the ear canal dry when in or around water for an extensive
time. Use appropriate earplugs or a bathing cap.
7. Apply 2% acetic acid to the ear canal after swimming. Acetic acid acts as a drying agent
and restores the ear canal to its normal acidic condition.
8. Antibiotics (with or without steroids) may be needed to treat swimmer’s ear. Consult a
healthcare practitioner.
9. Do not place objects like cotton swabs in the ear canal, use a bulb syringe approved for
removing debris and warm water. Use any cerumen dissolving agent responsibly.
Chapter Review 609
Chapter Review
37.1 Knowledge of basic eye anatomy is essential and prostamides. Prostaglandins are the preferred
for an understanding of eye disorders and drug class of drugs for glaucoma treatment.
therapy.
37.5 Other antiglaucoma medications decrease the
The anterior cavity of the eye is the place where aque-
formation of aqueous humor.
ous humor is circulated. Aqueous humor originates
from the ciliary body located in the posterior cham- Medications that decrease the formation of aqueous
ber and drains into the canal of Schlemm found in the humor include beta blockers, alpha2-adrenergic drugs,
anterior chamber. carbonic-anhydrase inhibitors, and osmotic diuretics.
37.2 Glaucoma is one of the leading causes of 37.6 Drugs provide relief for minor eye conditions and
blindness. are used for eye exams.
Glaucoma develops because the flow of aqueous Mydriatic or pupil-dilating drugs and cyclopegic or
humor in the anterior eye cavity becomes disrupted, ciliary-muscle relaxing drugs are routinely used for
leading to increasing intraocular pressure (IOP). Two eye examinations. Some drugs constrict local blood
principal types of glaucoma are closed-angle glau- vessels. Others lubricate the eyes.
coma and open-angle glaucoma.
37.7 Otic preparations treat infections, inflammation,
37.3 Glaucoma therapy focuses on adjusting the circu- and earwax buildup.
lation of aqueous humor. Combination drugs provide relief of conditions asso-
Glaucoma therapy generally works by increasing the ciated with the outer, middle, and inner ear. Drugs
outflow of aqueous humor or decreasing aqueous include antibiotics, corticosteroids, and earwax dis-
humor formation. solving drugs.
37.4 Some antiglaucoma medications increase the out-

flow of aqueous humor.
Drugs that increase the outflow of aqueous humor
include miotics, sympathomimetics, prostaglandins,
Review Questions
The following questions are written in NCLEX-PN® style. 3. The patient is informed that the medication used to re-
Answer these questions to assess your knowledge of the chap- lieve the pressure in her eye by decreasing production of aque-
ter material, and go back and review any material that is not ous humor is:
clear to you. 1. Timolol (Timoptic)
1. A patient is at the optometric office to have her eyes 2. Atropine sulfate
examined. She is told that the doctor will have to dilate her 3. Pilocarpine (Ocusert)
pupils with ____________ eye drops so he can see the back of 4. Ciprofloxacin (Cipro)
the eye. 4. The patient has been given a prescription for acetazol-
1. Miotic amide (Diamox) 250 mg PO three times a day. What is the
2. Mydriatic total amount of Diamox the patient will take in a 24-hour
3. Constricting period?
4. Corticosteroids 1. 250 mg
2. In a plan of care, a patient is to receive a drug that re- 2. 500 mg
lieves pressure in the eye by increasing the outflow of aqueous 3. 750 mg
humor. This drug would be: 4. 1,000 mg
1. Timolol (Timoptic)
2. Betaxolol (Betaoptic)
3. Pilocarpine (Ocusert)
4. Ciprofloxacin (Cipro)
5. A patient has an ear infection and is taking Cipro. If he 8. In the plan of care for patients with glaucoma, the ratio-
also had inflammation, which of the following class of drug nale for giving antiglaucoma medications would be to reduce
would be added? the pressure within the eye by:
1. Corticosteroids 1. Decreasing aqueous humor production and increasing out-
2. Aluminum sulfate and calcium acetate (Domeboro) flow of aqueous humor
3. Osmotic diuretics 2. Increasing aqueous humor production and decreasing out-
4. Carbonic-anhydrase inhibitors flow of aqueous humor
3. Decreasing aqueous humor production and decreasing out-
6. Prior to administering eardrops, the nurse should inform flow of aqueous humor
the patient that: 4. Increasing aqueous humor production and increasing out-
1. The solution should stay in the ear for one hour. flow of aqueous humor
2. The solution will be removed within one hour.
3. There may be a decrease in hearing for a few minutes. 9. The patient started on travoprost (Travatan) is instructed
4. The medication will take effect immediately. that:
1. This medication is administered in the morning only.
7. A patient has just been prescribed ciprofloxacin for an 2. Due to pupil constriction, visual acuity may be affected.
ear infection. He asks the nurse if there is anything he should 3. This medication may change the pigmentation of the iris.
know about. The nurse tells him that the drug can cause ad- 4. Due to dilation of the pupils, visual acuity may be affected.
verse reactions. The symptoms can include: (Select all that
apply.) 10. If the patient is allergic to sulfonamides, the nurse under-
1. Rash stands that he should not take:
2. White patches in the mouth 1. Methazolamide (Neptazane)
3. Pain within the ear 2. Betaxolol (Betaoptic)
4. Total loss of hearing 3. Carteolol (Ocupress)
4. Beta blockers
Remember Ms. Saunders, the patient 2. Ms. Saunders states she knows that she should be taking
introduced at the beginning of the her medications but has some concerns. She asks the nurse if
chapter? Now read the remainder of timolol can cause any problems. The nurse responds that the
the case study. Based on the informa- most common adverse effect of timolol (Timoptic) is:
tion you have learned in this chapter, 1. Burning and stinging
answer the questions that follow. 2. Sinus irritation
Ms. Mary Saunders is a 65-year-old African American female 3. Bronchoconstriction
presenting with severe pain in the right eye, headache, and 4. Edema around the eyes
blurred vision. She has a history of primary hypertension and
3. In addition to the discussion about adverse effects, the
glaucoma. Her blood pressure is 140/90 mmHg. No other nurse tells Ms. Saunders that it is not advisable to take the fol-
obvious signs are noted. In the course of the examination, she lowing drugs with timolol (Timoptic): (Select all that apply.)
mentions that she has recently relocated. It has been a particu-
larly stressful time because she has not had much help from 1. Epinephrine
her family. She has not been taking her antiglaucoma medica- 2. Ciprofloxacin
tion, the beta blocker, timolol (Timoptic). 3. Nitrates
4. Corticosteroids
1. The nurse and Ms. Saunders begin to discuss the impor-
tance of taking the glaucoma medication. The nurse explains 4. Ms. Saunders wants to know how long it would be before
that if left untreated pharmacologically, glaucoma could she could tell if the medication was working. The nurse tells
lead to: her it would take about:
1. Mydriasis 1. One week
2. Cycloplegia 2. Up to two weeks
3. Blindness 3. Two to four weeks
4. Vertigo 4. One to two months

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Appendix B: B rief Answers to Nclex-Pn® Review
and Case Study Questions
Chapter 1 4. 1, 3, and 4 3. 3 4. 3
5. 3 4. 3 5. 2
Answers to NCLEX-PN®
6. 3 5. 2 6. 2
Questions
7. 4 6. 4 7. 3
1. 4
8. 3 7. 1, 2, and 4 8. 1
2. 3
9. 2 8. 2 9. 1–3
3. 1
10. 2 9. 1 10. 3
4. 1, 2, and 4
10. 1 Answers to Case Study
5. 2 Chapter 6
6. 2 Answers to Case Study Questions
7. 2 Answers to NCLEX-PN® Questions 1. 2
8. 4 Questions 1. 4 2. 1 and 4
9. 4 1. 1–3 2. 4 3. 2
10. 1–3 2. 2 4. 3
3. 2
Chapter 2 4. 1 Chapter 10 Chapter 13
Answers to NCLEX-PN® 5. 3 Answers to NCLEX-PN® Answers to NCLEX-PN®
Questions 6. 2 Questions Questions
1. 1 7. 2 1. 4 1. 4
2. 2 8. 4 2. 3 2. 3
3. 4 9. 3 3. 4 3. 4
4. 4 10. 4 4. 1 4. 1
5. 4 5. 1 5. 2
Chapter 7 6. 2
6. 1, 3, and 4 6. 3
7. 2 Answers to NCLEX-PN® 7. 2 7. 1, 2, and 4
8. 2 Questions 8. 3 8. 4
9. 3 1. 3 9. 2 and 3 9. 3
10. 3 2. 2 10. 3 10. 1
Chapter 3 Answers to Case Study
4. 1 Questions Questions
Answers to NCLEX-PN® 5. 2 1. 4 1. 3
Questions 6. 2 2. 2 2. 3
1. 3 7. 3 3. 3 3. 3
2. 2 8. 1 4. 1 and 3 4. 4
3. 1 9. 3
4. 3 10. 2 Chapter 11
5. 1 Chapter 14
6. 1 Chapter 8 Answers to NCLEX-PN®
Questions
7. 1–4 Questions
Answers to NCLEX-PN® 1. 2
8. 4 1. 4
Questions 2. 1–4
9. 4 2. 1
1. 4 3. 3
10. 1 3. 1
2. 2 4. 3
4. 4
Chapter 4 3. 4 5. 4
5. 3
4. 3 6. 1
Answers to NCLEX-PN® 6. 2 and 4
5. 1 and 2 7. 2
Questions 7. 3
6. 2 8. 3
1. 3 8. 1
7. 3 9. 2
2. 2 9. 1, 2, and 4
8. 3 10. 3
3. 3 and 4 10. 4
9. 4
5. 2 Questions
Questions
6. 1–3 Answers to Case Study 1. 3
1. 1, 2, and 4
7. 2 Questions 2. 1–4
2. 1
8. 3 1. 3 3. 2
3. 1–3
9. 1, 2, and 4 2. 2–4 4. 3
4. 3
10. 3 3. 4
4. 1–3
Chapter 5
Chapter 9 Answers to NCLEX-PN® Answers to NCLEX-PN®
Answers to NCLEX-PN® Questions Questions
Questions
Questions 1. 4 1. 4
1. 1
1. 4 2. 2 and 3 2. 1, 2, and 4
2. 3
2. 2 3. 3 3. 2
3. 2
621
622 Appendix B: Brief Answers
4. 3 7. 2 8. 3 9. 1
5. 1 8. 3 9. 2 10. 4
6. 2 9. 4 10. 2 Answers to Case Study
7. 1 10. 2 Answers to Case Study Questions
8. 2 Answers to Case Study Questions 1. 2
9. 4 Questions 1. 4 2. 1
10. 3 1. 3 2. 1 3. 3
Answers to Case Study 2. 1 3. 4 4. 2
Questions 3. 1 4. 4
1. 2 4. 4 Chapter 25
3. 2
4. 4 Chapter 19 Answers to NCLEX-PN® Questions
Answers to NCLEX-PN® Questions 1. 1, 2, and 4
Questions 1. 3 2. 1 and 2
Chapter 16 2. 2 3. 4
1. 2
Answers to NCLEX-PN® 2. 4 3. 2 4. 1
Questions 3. 4 4. 3 5. 3
1. 3 4. 1 5. 1 6. 3
2. 3 5. 2 6. 2 7. 2
3. 2 6. 1, 2, and 4 7. 1–3 8. 4
4. 3 7. 1 8. 2 9. 4
5. 1 8. 1 9. 2 10. 2
6. 1 9. 1 10. 1 Answers to Case Study
7. 1, 2, and 4 10. 3 Questions
Answers to Case Study
8. 2 1. 4
Answers to Case Study Questions
9. 3 2. 1
Questions 1. 4
10. 1–3 3. 3
1. 2 2. 2
Answers to Case Study 2. 2 3. 3 4. 1, 3, and 4
Questions 3. 1 4. 1
1. 2 4. 3 Chapter 26
2. 1
4. 4 Chapter 20 Answers to NCLEX-PN® Questions
Questions 1. 4
Chapter 17 1. 4 2. 2
Questions
2. 2 3. 3
3. 3 4. 1
Questions 2. 1
4. 2 5. 2
1. 3 3. 2
5. 1–4 6. 1
2. 4 4. 2
6. 2 7. 4
3. 2 5. 3
7. 3 8. 1–4
4. 2 6. 1, 2, and 4
8. 1 9. 4
5. 3 7. 4
9. 4 10. 4
6. 2 8. 1
7. 2 9. 3
8. 2 and 3 10. 1–4 Answers to Case Study Questions
9. 4 Questions 1. 1
10. 2 1. 4 2. 2
Questions
2. 3 3. 3
Answers to Case Study 1. 2
3. 2 4. 1 and 3
Questions 2. 2
4. 1
1. 3 3. 1
2. 1 4. 1 Chapter 27
4. 3 Answers to NCLEX-PN® Questions
Chapter 21 1. 3
Questions
Chapter 18 Answers to NCLEX-PN® 2. 4
1. 3
Answers to NCLEX-PN® Questions 2. 3 3. 3
Questions 1. 2 3. 3 4. 1
1. 3 2. 4 4. 4 5. 1 and 3
2. 1 3. 2 5. 2 6. 4
3. 2 4. 1–3 6. 4 7. 2–4
4. 2 5. 1 7. 1, 2, and 4 8. 2
5. 4 6. 4 8. 4 9. 4
6. 3 7. 2 10. 1
Appendix B: Brief Answers 623
Answers to Case Study 3. 1 3. 3 7. 3

Questions 4. 2 4. 4 8. 3
1. 3 5. 1 9. 1 and 4
2. 3 6. 2 10. 4
Chapter 33
3. 2 7. 2 Answers to Case Study
4. 1, 3, and 4 8. 1 Answers to NCLEX-PN®
Questions
9. 1 and 2 Questions
1. 4
Chapter 28 10. 1 1. 1–3
2. 1–4
2. 3
Answers to NCLEX-PN® Answers to Case Study 3. 3
3. 2
Questions Questions 4. 4
4. 4
1. 3 1. 1 5. 3
2. 2 2. 2 and 3 6. 1 Chapter 36
3. 1 and 4 3. 1 and 2 7. 2
4. 2 4. 1 Answers to NCLEX-PN®
8. 1–3
5. 2 Questions
9. 4
6. 4 Chapter 31 1. 2
10. 4
7. 2 and 4 2. 4
8. 2 Answers to Case Study 3. 4
Questions
9. 3 Questions 4. 1
1. 3
10. 2 1. 1 and 2 5. 2
2. 4 2. 1, 2, and 4 6. 1, 2, and 4
Answers to Case Study 3. 1 3. 2–4 7. 2
Questions 4. 2 4. 1 8. 2
1. 3 5. 3
2. 2 6. 4 9. 1
Chapter 34 10. 3
3. 2 7. 2
4. 1 8. 1–4 Answers to NCLEX-PN® Answers to Case Study
9. 3 Questions Questions
Chapter 29 10. 3 1. 2 1. 2
2. 1 2. 4
Answers to NCLEX-PN® Answers to Case Study 3. 3 3. 2
Questions Questions 4. 2 4. 2–4
1. 1 1. 2 5. 1–3
2. 2 2. 4 6. 2
3. 1–3 3. 1–4 7. 3 Chapter 37
4. 2 4. 3 8. 4 Answers to NCLEX-PN®
5. 2
9. 4 Questions
6. 2
Chapter 32 10. 4 1. 2
7. 1
8. 3 Answers to NCLEX-PN® Answers to Case Study 2. 3
9. 2 Questions Questions 3. 1
10. 1 1. 1 1. 3 4. 3
2. 4 2. 4 5. 1
3. 3 3. 1 and 3 6. 3
Questions
4. 2 4. 2 and 4 7. 1–3
1. 4
5. 2 8. 1
2. 3
3. 1
6. 1 and 2 Chapter 35 9. 3
7. 3 Answers to NCLEX-PN® 10. 1
4. 3
8. 4 Questions
Chapter 30 1. 2
10. 2 and 3 2. 4 Questions
Answers to Case Study 3. 1
Questions 2. 1
Questions 4. 3
1. 3 3. 1 and 3
1. 3 and 4 5. 3
2. 1 and 4 4. 3
2. 3 6. 1
NOTE: The complete rationales and answers are located on the textbook’s website.
Appendix C: Calculating Dosages
I. Calculating Dosage Using Ratios II. Calculating Dosage by Weight

and Proportions
Doses for pediatric patients are often calculated by using
A. A ratio is used to express a relationship between two body weight. The nurse must use caution to convert be-
or more quantities. Ratios may be written using the tween pounds and kilograms, as necessary (see Table 3.2
following notations. in Chapter 3, page 25). Use the formula:
1:10 means 1 part of drug A to 10 parts of Body weight (kg) * amount mg/kg = X mg of drug
solution/solvent. Example 3: The healthcare provider orders 10 mg/kg
In drug calculations, ratios are usually expressed as a of methsuximide for a client who weighs 90 kg. How
fraction: much should be administered?
1 part drug A 1 The patient should receive 900 mg of methsuximide.
=
10 parts solution 10 Example 4: The healthcare provider orders 5 mg/kg/
A proportion shows the relationship between two ra- day of amiodarone. The patient weighs 110 pounds.
tios. It is a simple and effective means for calculating How much of the drug should be administered daily?
certain types of doses. Step 1: Convert pounds to kilograms.
Dose on hand Desired dose
= 110 lb * 1 kg/2.2 lb = 50 kg
Quantity on hand Quantity desired (X)
Step 2: Perform the drug calculation.
Using cross-multiplication, we can write the same
formula as follows: 50 kg (body weight) * 5 mg/ kg = 250 mg
Desired dose * Quantity on hand The patient should receive 250 mg of amiodarone per
Quantity desired (X) =
Dose on hand day.
Example 1: The healthcare provider orders erythro-
mycin 500 mg. It is supplied in a liquid form contain-
ing 250 mg in 5 mL. How much drug should the nurse
III. Calculating Dosage by Body
administer? Surface Area
To calculate the dosage, use the formula: Many antineoplastic drugs and most pediatric doses are
Dose on hand (250 mg) Desired dose (500 mg) calculated using body surface area (BSA).
= The formula for BSA in metric units is:
Quantity on hand (5 mL) Quantity desired (X)
Then, cross-multiply: BSA = weight (kg) * height (cm)
7 3600
250 mg * X = 5 mL * 500 mg
The formula for BSA in household units is
Therefore, the dose to be administered is 10 mL.
BSA = weight (lb) * height (inches)
B. The same proportion method can be used to solve solid 7
dosage calculations. 3131
Example 2: The healthcare provider orders metho Example 5: The healthcare provider orders 10 mg/
trexate 20 mg/day. The methotrexate is available in m2 of an antibiotic for a child who is 2 feet tall and
2.5-mg tablets. How many tablets should the nurse ad- weighs 30 lb. How many milligrams should be
minister each day? administered?
Dose on hand (2.5 mg) Desired dose (20 mg) Step 1: Calculate the BSA of the child.
=
1 tablet Quantity desired (X tablets) 30 * 24
BSA =
7 3131
Cross-multiplication gives:
BSA = 720
2.5 mg X = 20 mg * 1 tablet 7 3131
Therefore, the nurse should administer 8 tablets daily. BSA = 2 0.230 = 0.48 m 2
624
Appendix C: Calculating Dosages 625
Step 2: Calculate the drug amount. Other IV conversion formulas you may use include
2 2 the following:
10 mg/m * 0.48 m
mcg/kg/h S mL/h
The nurse should administer 4.8 mg of the antibiotic
to the child. mcg / kg mg mL mL
kg * * * =
h 1,000 mcg mg h
IV. Calculating IV Infusion Rates
mcg/m 2 /h S mL/h
Intravenous fluids are administered over time in units of mcg / m 2 mg mL mL
mL/min or gtt/min (gtt = drops). The basic equation for m2 * * * =
IV drug calculations is as follows: h 1,000 mcg mg h
mL of solution * gtt/mL gtt mcg/kg/min S gtt/min
=
h of administration * 60 min/h min
mcg / kg mg mL 10 gtt gtt
Example 6: The healthcare provider orders 1,000 mL kg * * * * =
of 5% normal saline to infuse over 6 hours. What is min 1,000 mcg mg mL min
the flow rate?
1,000 mL * 10 gtt/ mL 28 gtt
=
6 h * 60 min/ h min
Index
Indexing style: Prototype drugs appear in bold face. Information in tables is denoted with a “t” after the page number. Information in figures is denoted with
an “f” after the page number.
5-FU. See fluorouracil acrivastine, 460t adjuvant chemotherapy, 433

5-HT (serotonin), 128 acromegaly, 516. See also growth hormone ado-trastuzumab, 445t
5-hydroxytryptamine (5-HT), 211 (GH) adrenal atrophy, 521
6-MP. See mercaptopurine Actemra. See tocilizumab adrenal disorders, 520–522
ACTH (adrenocorticotropic hormone), 513f, adrenal gland(s), 271f
A 520, 521, 521f, 522 Adrenalin. See epinephrine
Acticin. See permethrin adrenergic, 90, 97
abacavir, 419t
Actifed Cold and Allergy, 461t adrenergic blockers (sympatholytics), 91
abatacept, 576t
action potential, 189, 333 actions, 99, 291f
abciximab, 350f, 355t
Actiq. See fentanyl adverse effects, 282
Abilify. See aripiprazole
Activase. See alteplase clinical uses, 99
abiraterone, 444t
activated partial thromboplastin time hypertension, 281–282, 281t
absence seizures, 183. See also petit mal
(aPTT), 352 drugs classified as, 91, 281t
seizures; seizure(s)
active immunity, 377, 378f Nursing Process Focus, 101t
succinimides treating, 191, 192t
Activella. See ethinyl estradiol with norethin- Patients Need to Know, 102t
absorption, 42f, 43
drone acetate prototypes of, 99
Abstral. See fentanyl
Actonel. See risedronate adrenergic drugs, 91, 97, 97t
acamprosate calcium, 76
Actos. See pioglitazone fight-or-flight symptoms of, 91
acarbose, 535t
Actron. See ketoprofen adrenocortical insufficiency, 521–522
Accupril. See quinapril
Acuprin. See aspirin adrenocorticotropic hormone (ACTH), 513f,
Accutane. See isotretinoin
acute dystonias, 148 520, 521, 521f, 522
ACE (angiotensin-converting enzyme), 274
acute glaucoma, 600f, 601. See also glaucoma adult-onset diabetes. See type 2 diabetes
ACE inhibitors. See angiotensin-converting
acute gouty arthritis, 577 mellitus
enzyme (ACE) inhibitors
acute promyelocytic leukemia (APL), 591t Advicor, 242, 244
acebutolol, 100t
acyclovir, 17t Advil. See ibuprofen
clinical uses, 100
Drug Prototype, 425t AEB (as evidenced by), 54
angina, 306t
route and adult dose, 424t aerosol, 456
dysrhythmias, 339t
Adalat. See nifedipine African Americans, antihypertension therapy
hypertension, 281t
Adalat CC. See nifedipine in, 273
route and adult dose, 281t, 306t
adalimumab, 576t Afrin. See oxymetazoline
Aceon. See perindopril
adapalene, 590t afterload, 289, 304
acetaminophen
adaptive body defenses, 375 Aggrastat. See tirofiban
actions, 369t
ADD (attention deficit disorder), 78, 137 agonist(s), 47
adverse effects, 369t
addiction, 16, 71. See also substance abuse agoraphobia, 107t
black box warning, 369t
agent or drug factors, 71 Agrylin. See anagrelide
clinical uses, 369t
drug, 80–81 akathisia, 147t, 148
fever, 209t, 210
environmental factors, 71 Akineton. See biperiden
Drug Prototype, 369t
to opioids, 75 Albalon. See naphazoline
interactions, 369t
user factors, 71 albendazole, 426t, 427
route and adult dose, 209t
Addison’s disease, 521 albuterol, 97t
acetazolamide, 256, 257t, 603t
adefovir, 425 clinical uses, 97
acetic acid and hydrocortisone, 607t
Adenocard. See adenosine for asthma, 468t
acetylcholine (Ach), 88, 160, 164
adenohypophysis. See anterior pituitary shock, 328
acetylcholinesterase (AchE), 165
adenoma(s), 432 Alcaine. See proparacaine
acetylcholinesterase inhibitors
Adenoscan. See adenosine alclometasone dipropionate, 592t
adverse effects, 165
adenosine, 341t, 342 alcohol
for Alzheimer’s disease, 164, 165t
adenosine diphosphate (ADP) receptor chronic consumption of, 75
drugs classified as, 165t
blockers, 354, 355t as CNS depressant, 75
acetylcysteine, 465
Aδ fibers, 199. See also sensory neurons cross-tolerance, 73
Acetylsalicylic acid. See aspirin
ADH (antidiuretic hormone; vasopressin), 270, metabolism, 75
acid-base imbalances, 260, 260f, 260t
514–515, 514t, 515t overdose of, 75
acidosis, 260, 260f, 260t
ADHD (attention deficit hyperactivity dis- physical dependence and, 72
Aclovate. See alclometasone dipropionate
order). See attention deficit hyperactivity physiological and psychological effects
acne, 589–590, 590t
disorder (ADHD) of, 73t
Acova. See argatroban
adjuvant analgesics, 201 withdrawal syndrome, 75
acquired resistance, 392, 392f
626
Index 627
alcohol abuse, 499 causes, 164 with furosemide, 254t

Alcoholics Anonymous, 72, 75 characteristics, 164 with hydrochlorothiazide, 255t
“alcoholic” smell, 75 drugs used for, 165t with prednisone, 369t
alcohol intoxication, 75 ginkgo biloba use in, 167t route and adult dose, 415t
alcoholism, 75 pharmacotherapy, 92, 165 ampicillin, 393, 394t
alcohol sensitivity, 75 symptoms, 164 Amrix. See cyclobenzaprine
alcohol withdrawal syndrome, 75 Amanita muscaria, 90 amyloid plaques, 164
Aldactone. See spironolactone amantadine amyotrophic lateral sclerosis (ALS), 158t
aldesleukin, 379, 379t clinical uses Amytal. See amobarbital
Aldomet. See methyldopa influenza, 424 Anacin. See aspirin
aldosterone, 274, 520 parkinsonism, 161t Anadrol. See oxymetholone
alemtuzumab, 445t multiple sclerosis, 168t, 169 Anadrol-50. See oxymetholone
alendronate route and adult dose, 424t Anafranil. See clomipramine
Drug Prototype, 572t Amaryl. See glimepiride anagrelide, 355t
for osteoporosis, 571t ambenonium, 92t anakinra, 381t, 576t
Aler-Dryl. See diphenhydramine Ambien. See zolpidem analgesics, 201
Aleve. See naproxen sodium amcinonide, 592t adjuvant, 201
Alfenta. See alfentanil amebiasis, 426 categories of, 201
alfentanil, 204, 226t, 228t amenorrhea, 550 anaphylaxis/anaphylactic shock
alfuzosin, 100t, 558t Amerge. See naratriptan diagnosis, 320
alimentary canal, 478 Americaine. See benzocaine pathophysiology, 320t, 364
alkaloids. See ergot alkaloids; vinca alkaloids American Pharmaceutical Association pharmacotherapy, 326–328
alkalosis, 260, 260f, 260t (APhA), 5, 6f symptoms, 327f
alkylating agents, 437, 437t, 438f American Psychiatric Association, 123 Anaprox. See naproxen sodium
alkylation, 435 Amicar. See aminocaproic acid anastrozole, 444t
Allerest. See naphazoline Amidate. See etomidate Anbesol. See benzocaine
Allergia-C. See diphenhydramine amides, 220–221, 221t, 222 Andro 100. See testosterone
allergic reaction, 22 amikacin, 399t Androderm. See testosterone
anaphylaxis and, 22 amiloride, 256t, 274t Androgel. See testosterone
signs of, 22 aminocaproic acid androgens, 554, 555t
allergic rhinitis, 458, 459f actions, 358t Android. See methyltestosterone
H1-receptor antagonists for. See adverse effects, 358t Anectine. See succinylcholine
H1-receptor antagonists clinical uses, 357t, 358t anemia, 436t, 446
intranasal corticosteroids for, 462, 463t Drug Prototype, 358t iron-deficiency, 501, 501t
allergy(ies), 459t interactions, 358t megaloblastic (pernicious), 499
allopurinol route and adult dose, 357t Anestacon. See lidocaine
Drug Prototype, 578t aminoglycosides, 399–400, 399t anesthesia, 218. See also general anesthesia;
for gout and gouty arthritis, 577, 577t aminopenicillins, 393 local anesthesia
almotriptan, 212t aminophylline, 468t angina pectoris, 302–303, 303t, 347t
aloe, 341t amiodarone Nursing Process Focus, 308t
aloe vera, 608t actions, 341t Patients Need to Know, 315t
for skin conditions, 592t adverse effects, 341t pharmacotherapy, 304–305
alopecia, 436 black box warning, 341t beta blockers, 307
Alora. See estradiol clinical uses, 341t mechanisms of action, 305f
alpha2-adrenergic drugs, for glaucoma, 603, Drug Prototype, 341t organic nitrates, 305–306, 306t
603t interactions, 341t ranolazine, 305
alpha-adrenergic blockers. See alpha blockers route and adult dose, 340t angioedema, 409t
alpha (α) blockers, 99, 281t. See also amitriptyline, 112t, 126t, 201 Angiomax. See bivalirudin
adrenergic blockers clinical uses angiotensin-converting enzyme (ACE), 274
Alphagan. See brimonidine tartrate depression, 112, 126t angiotensin-converting enzyme (ACE)
alpha (α) receptors, 90, 91t migraine prophylaxis, 213, 213t inhibitors
alprazolam, 70, 74, 114t amitryptiline, 17t actions, 272f, 291f, 294
Altace. See ramipril amlodipine, 278t, 306t clinical uses
alteplase amobarbital, 116t heart failure, 292, 293t
actions, 357t for sedation and insomnia, 116t hypertension, 275t
adverse effects, 357t Amoeba, 389f myocardial infarction, 313
clinical uses, 357t amoxapine, 126t drugs classified as, 275t
Drug Prototype, 357t amoxicillin, 17t, 393, 394t Nursing Process Focus, 276–277t
interactions, 357t Amoxil. See amoxicillin Patients Need to Know, 297t
route and adult dose, 312t amphetamines, 70, 78, 202 angiotensin II, 274, 520
alternate healthcare systems, 60t high doses of, 78 angiotensin-receptor blockers (ARB)
Altoprev. See lovastatin physiological and psychological effects actions, 272f, 294
altretamine, 445t of, 73t clinical uses, 275t
aluminum hydroxide, 482t withdrawal syndrome for, 78 drugs classified as, 275t
alveoli, 455 amphotericin B, 414 anidulafungin, 414, 415t
Alzheimer’s disease, 164 Drug Prototype, 416t anorexia, 480
brain changes in, 164 interactions anorexiants, 491
628 Index
Ansaid. See flurbiprofen actions, 335–336, 336f drugs classified as, 355t
Antabuse. See disulfiram adverse effects, 336 interactions
antacids, 485 classes with alteplase, 357t
drugs classified as, 482t adenosine, 341t, 342 with clopidogrel, 356t
interactions beta-adrenergic blockers, 339, 339t antiprotozoans, 426t, 427t
with aspirin, 208t calcium channel blockers, 341–342, antipsychotics
with ciprofloxacin, 401t 341t atypical (second generation), 146,
with haloperidol, 149t digoxin, 341t, 342 151–153, 151t
with isoniazid, 406t potassium channel blockers, 340, 340t conventional (first-generation), 146–151,
with levodopa, 163t classification, 336 146t, 148t
antagonism, 393 Nursing Process Focus, 336–337t dopamine system stabilizers (DSSs) or
antagonists (blockers), 47 sodium channel blockers, 338, 338t third generation antipsychotics, 146, 154
Antara. See fenofibrate antiemetics, 489, 490t, 492t Patients Need to Know, 153t
anterior pituitary, 511. See also pituitary gland antiepileptic drugs (AED). See antiseizure drugs antipyretics, 369–370
anthralin, 593t, 594 antifibrinolytics. See hemostatics goal of, 370
anthrax, 401 antiflatulent, 485 marketing of, 370
antibiotic, 390. See also anti-infectives antifungal drugs Patients Need to Know, 370t
antibody(ies), 375 Nursing Process Focus, 417t antiretrovirals, 420
anticholinergics (cholinergic blockers), 91, Patients Need to Know, 427t for HIV-AIDS, 418–422, 419t
94–95, 95t, 227 systematic, 414–416, 415t Nursing Process Focus, 422–423t
adverse effects, 92, 163 topical and oral, 416–417, 417t antiseizure drugs, 182, 185t
clinical uses, 95t, 228t antigen(s), 326, 374 actions, 186
asthma, 468–469, 468t antihelminthics, 426, 426t adjunctive therapy and, 185
parkinsonism, 163, 163t antihistamines, 95t clinical uses
drugs classified as, 91, 163t, 228t, 468t interactions bipolar disorder, 135, 135t
interactions with atropine, 95t seizures, 181–196
with procainamide, 339t anti-infectives, 390 disadvantages of, 185
with TCAs, 125 actions, 390–391, 391f discontinuation, 184
Nursing Process Focus, 96t allergic reactions, 409t drugs classified as
Patients Need to Know, 102t bacterial resistance to, 391–392, 392f barbiturates, 187t
anticipatory anxiety, 111 classifications, 390–391 benzodiazepines, 187t
anticoagulants, 350 aminoglycosides, 399–400, 399t GABA-related drugs, 186, 187t, 189
actions, 350, 350f cephalosporins, 395–397, 396t hydantoins and related drugs, 189–190t
adverse effects, 350 fluoroquinolones, 400–401, 400t succinimides, 184t
clinical uses, 312–313, 347t, 351t macrolides, 398–399, 398t FDA warnings, 184
drugs classified as, 351t miscellaneous antibacterial, interactions
interactions 403–404, 404t with chlorpromazine, 147t
with alteplase, 357t tetracyclines, 397–398, 397t with levodopa, 163t
with aspirin, 208t Nursing Process Focus, 404t–405t with oral contraceptives, 182, 185,
with clopidogrel, 356t Patients Need to Know, 409t 188t, 190t, 190t
with gemfibrozil, 244t prophylactic, 392 Nursing Process Focus, 192–193t
with hydrochlorothiazide, 255t selection of, 393 in pregnancy, 185
with methylphenidate, 137t Antilirium. See physostigmine pregnancy category, 182
with tamoxifen, 444t antimalarials, 426t antiseptics, urinary, 403
Nursing Process Focus, 353–354t antimetabolites, 439–440, 439t, 440f antispasmodic drugs
oral, 352 antineoplastic drugs centrally acting. See skeletal muscle
parenteral, 350–352 adverse effects, 435–436, 436t relaxants
reversal, 350 cell cycle and, 435–436, 435f direct-acting, 174t
anticonvulsants, 182. See also antiseizure classifications antithrombin, recombinant, 351t
drugs alkylating agents, 437, 437t, 438f antithymocyte globulin, 381t
antidepressants, 110, 125, 126–127t antimetabolites, 439–440, 439t, 440f antitubercular drugs
atypical antidepressants, 126–127t, 129 antitumor antibiotics, 440–441, 441t dosing regimens and schedules, 406–407t
clinical uses hormones and hormone antagonists, drugs classified as, 407t
anxiety and insomnia, 111, 112t 443, 443t–444t Nursing Process Focus, 407–408t
depression, 126–127t, 126t–127t plant extracts, 442–443, 442t for prophylaxis, 408
monoamine oxidase inhibitors (MAOIs), taxanes, 442, 442t antitumor antibiotics, 440–441, 441t
127t, 132 topoisomerase inhibitors, 442, 442t antitussives, 457f, 465
Nursing Process Focus, 130–131t dosing schedules and regimens, 435–436 antiviral drugs
Patients Need to Know, 139t Nursing Process Focus, 447t–448t clinical uses
primary classes of, 125, 126t Patients Need to Know, 449t herpesvirus infections, 423–424, 424t
selective serotonin reuptake inhibitors antiobesity drugs, 491 HIV-AIDS, 418–422, 419t
(SSRIs), 126t, 128–129 antiplatelet drugs influenza, 424, 424t
tricyclic antidepressants (TCAs), 125, 126t actions, 350, 354 Patients Need to Know, 427t
antidiarrheals, 489t classes, 354 strategies for use of, 418
antidiuretic hormone (ADH; vasopressin), 270, clinical uses Anturane. See sulfinpyrazone
514–515, 514t, 515t coagulation disorders, 354–356, 355t anxiety, 106
antidysrhythmics myocardial infarction, 312–313 in Alzheimer’s disease, 164, 166
Index 629
anticipatory, 111 Drug Prototype, 208t Patients Need to Know, 139t

areas of brain responsible for, 108t vs. ibuprofen, 47 pharmacotherapy
insomnia and, 109–110 interactions, 208t CNS stimulants, 78, 137, 138t
management, 108–109 with alteplase, 357t non-CNS stimulants, 137, 138t
antidepressants for, 111–113, 112t with clopidogrel, 356t symptoms, 136
benzodiazepines for, 113–114, 114t with methotrexate, 440t atypical antidepressants
nonbenzodiazepine, nonbarbiturate with spironolactone, 256t adverse effects, 113
agents for, 117–119, 117t with valproic acid, 191t clinical uses
nonpharmacologic strategies for, routes and adult dose, 209t, 355t, 365t anxiety, 111, 112t
108–109 assessment phase of nursing process, depression, 126–127t
pharmacologic strategies for, 108–109 52–53, 52f drugs classified as, 129
Nursing Process Focus, 115t asthma, 465 atypical antipsychotics
panic disorder, 106 characteristics, 465–466, 467f adverse effects, 152
Patients Need to Know, 119t Nursing Process Focus, 469–470t in Alzheimer’s disease, 166
performance, 106 pharmacotherapy, 467f discovery of, 146
phobias, 106 anti-inflammatory drugs, 470t, 471 Nursing Process Focus, 153t
situational, 106 bronchodilators, 467–469, 468t aura
treatment of, 110–111 symptoms, 466 migraine, 211
anxiolytics, 109. See also anxiety, management triggers, 466t seizure, 183
Apidra. See insulin glulisine Astramorph PF. See morphine Auralgan. See benzocaine and antipyrine
apixaban, 351t, 352 astringent effect, 31 autoantibodies, 575
APL (acute promyelocytic leukemia), 591t Atacand. See candesartan automaticity, 333
apomorphine, 161, 161t atazanavir, 419t autonomic nervous system, 87
apothecary system, 25 atenolol drugs affecting functions of, 86–104
apraclonidine, 603t actions, 272f, 282, 309t parasympathetic nervous system, 87
Apresazide, 255 adverse effects, 309t sympathetic nervous system, 87
Apresoline. See hydralazine black box warning, 309t two primary neurotransmitters of, 88–91
aPTT (activated partial thromboplastin cardioselective effects of, 99 Avage. See tazarotene
time), 352 clinical uses, 100t, 212t, 281t, 306t, 309t avanafil, 556t
Aquatensen. See methyclothiazide anxiety, 111, 117, 117t Avandia. See rosiglitazone
aqueous humor, 599 Drug Prototype, 309t Avapro. See irbesartan
Arava. See leflunomide interactions, 309t AV (atrioventricular) bundle, 333
ARB (angiotensin-receptor blockers), 272f, route and adult dose, 212t, 281t, 306t Aventyl. See nortriptyline
275t, 294 atherosclerosis, 235, 302–303, 303f Avita. See tretinoin
Arduan. See pipecuronium Ativan. See lorazepam AV (atrioventricular) node, 333, 334f
Aredia. See pamidronate atomoxetine, 137, 138t Avodart. See dutasteride
arformoterol, 468t atonic seizures, 183. See also drop attacks; Avonex. See interferon beta-1a
argatroban, 351, 351t seizure(s) Axert. See almotriptan
Aricept. See donepezil atopic dermatitis, 591 axitinib, 445t
aripiprazole, 146, 151t, 154 atorvastatin Azasan. See azathioprine
Aristocort. See triamcinolone acetonide actions, 240t azathioprine, 381t, 576t
Aristospan. See triamcinolone adverse effects, 240t azelaic acid, 590t
Arixtra. See fondaparinux clinical uses, 240t azelastine, 459t, 460
Armour Thyroid. See thyroid dessicated Drug Prototype, 240t Azelex. See azelaic acid
arsenic trioxide, 445t interactions, 240t azilsartan, 275t
Artane. See trihexyphenidyl route and adult dose, 239t azithromycin, 398t
artemether/lumefantrine, 426t atovaquone/proguanil, 426t Azopt. See brinzolamide
arthritis atracurium, 176t aztreonam, 404t
description, 574 atrial flutter, 333t Azulfidine. See sulfasalazine
gouty, 577, 577t atrial tachycardia, 333t
osteoarthritis, 574, 575 atrioventricular bundle, 333
rheumatoid, 575, 576t atrioventricular (AV) node, 333, 334f B
articaine, 221t Atromid-S. See clofibrate bacille calmette-guérin (BCG) vaccine,
ASA. See aspirin Atro-Pen. See atropine 379, 379t
ASAP order, 24t atropine, 95t, 227, 228t, 606t Bacillus anthracis, 390t, 401
Ascaris, 427 actions, 95t, 163 baclofen, 170, 171t, 173
asenapine, 135t, 151t adverse effects, 95t, 163 bacteria
Asendin. See amoxapine clinical uses of, 95t acquired resistance to anti-infectives,
Aspergillus, 389f, 414t Drug Prototype, 95t 391–392, 392f
Aspergum. See aspirin interactions, 95t characteristics, 389f
aspirin, 15, 15t Atrovent. See ipratropium classifications, 391–392, 392f
actions, 208t, 350f, 355, 365t ATryn. See antithrombin, recombinant common disease-causing, 390t
adverse effects, 208t, 366 attention deficit disorder (ADD), 78, 137 descriptive methods, 390t
clinical uses, 208t attention deficit hyperactivity disorder infections caused by, 390t
as antiplatelet agent, 355, 355t (ADHD), 78, 136 bacteriocidal, 391
fever, 370t causes, 136 bacteriostatic, 391
myocardial infarction, 312 Fast Facts, 136t balanced anesthesia, 224
630 Index
Balnetar. See coal tar clinical uses, 95t, 148, 164t Patients Need to Know, 245t
Banflex. See orphenadrine Drug Prototype, 164t bile acids, 241
barbiturates, 74, 116–117 interactions, 164t bimatoprost, 602
clinical uses, 186 with MAOIs, 164t binding, 43
sedation and insomnia, 116–117, 117t with phenothiazines, 164t bioavailability, 15–16, 43
seizures, 186 with procainamide, 164t bioequivalence, 16
drugs classified as, 187t with quinidine, 164t biologic response modifiers, 375, 379, 379t
interactions with tricyclic antidepressants, 164t biologics, 4
with clopidogrel, 356t route and adult dose, 163t characteristics of, 4t
with lidocaine, 222t bepotastine, 605 stages of approval for, 7–9
with prednisone, 369t Bepreve. See bepotastine Biologics Control Act, 5, 6f
physiological and psychological effects bepridil, 306t biologic therapies, 60t
of, 73t beta-adrenergic agonists, 467, 468t bioterrorism, 9
tolerance, 114 beta (β) blockers, 99. See also adrenergic anthrax, 401
withdrawal syndrome, 78, 116 blockers Bioterrorism Act, 6f
baroreceptors, 270, 271f actions, 272f, 306t biotin (vitamin B7), 498t
baseline data, 52 adverse effects, 307 biotransformation, 43
basiliximab, 381t clinical uses biperiden, 163t
Bayer. See aspirin angina and myocardial infarction, 305, biphasic OC, 546, 546t
B cell, 375 306t, 307, 312 bipolar disorder, 133
BCG (bacille calmette-guérin) vaccine, 379 anxiety, 111, 117, 117t characteristics of, 134
beclomethasone dysrhythmias, 339, 339t lithium for treating, 134–135
inhaled, 470t glaucoma, 603, 603t pharmacotherapy, 135t
intranasal, 463t heart failure, 295t, 296 symptoms of, 134
behavioral insomnia, 110. See also short-term hypertension, 281t bisacodyl, 487t
insomnia migraine prophylaxis, 212t bismuth salts, 489t
Benadryl. See diphenhydramine drugs classified as, 99, 281t, 295t, 339t bisoprolol, 281t
Benadryl Allergy/Cold, 461t interactions, 149t bisphosphonates
benazepril, 275t with amiodarone, 341t for osteoporosis, 571t, 572
bendamustine, 437t with digoxin, 295t for Paget’s disease, 574
bendroflumethiazide and nadolol, 254t with dopamine, 326t bivalirudin, 351t
Benemid. See probenecid with epinephrine, 327t black box warning, 6, 111, 113, 129, 133, 137,
Benicar. See olmesartan with haloperidol, 149t 203t, 205t, 228t, 277t, 292t, 309t, 326t, 339t,
Benicar HCT, 255 with norepinephrine, 326t 340t, 341t, 352t, 353t, 356t, 366t, 369t, 537t,
benign prostatic hyperplasia (BPH), 556, 557, with propranolol, 340t 547t, 551t, 552t, 553t, 554t, 571t, 591t
557f, 558t Patients Need to Know, 343t blackheads, 589
benign tumors, 432 Betagan. See levobunolol Blastomyces dermatitidis, 414t
Bentyl. See dicyclomine beta-lactamase, 393 bleomycin, 441t
benzocaine beta-lactam ring, 393 Blocadren. See timolol
Drug Prototype, 589t betamethasone, 368t, 522t, 592t blockers (antagonists), 47. See also adrenergic
as local anesthetic, 221t, 222 betamethasone benzoate, 592t blockers
for sunburn and minor skin irritation, 589 betamethasone valerate, 592t alpha, 99
benzocaine and antipyrine, 607t Betaoptic. See betaxolol beta. See beta (β) blockers
benzodiazepines, 113–114 Betapace. See sotalol blood-brain barrier, 43
abuse of, 74–75 Betapace AF. See sotalol blood glucose level, 529, 530f
actions, 113–114 beta (β) receptors, 90, 91t blood-placental barrier, 43
adverse effects, 1113–114 Betaseron. See interferon beta-1b blood pressure. See also hypertension
clinical uses betaxolol, 281t, 603t control of, 269–271f, 270f
as adjunct to anesthetics, 228t bethanechol, 228t, 229 diastolic, 267
anxiety and insomnia, 113–114, 114t actions, 93t factors affecting, 269, 269f
bipolar disorder, 135 adverse effects, 93t physiology, 267, 268f
intravenous anesthetic, 226t clinical uses, 92t systolic, 267, 268f
muscle relaxation, 170 Drug Prototype, 93t blood products, 322, 323t
seizures, 186 interactions, 93t blood-testicular barrier, 43
drugs classified as, 110, 187t, 226t, 228t with ambenonium, 93t blood thinners. See anticoagulants;
interactions with epinephrine, 93t antiplatelet drugs
with propofol, 227t with neostigmine, 93t blood volume, 269
introduction of, 113 with quinidine, 93t bone deposition, 565
parenteral administration, 114 Betimol. See timolol; timolol maleate bone resorption, 565
Patients Need to Know, 119t bevacizumab, 445t Boniva. See ibandronate
physiological and psychological effects Bextra. See valdecoxib boosters, 376
of, 73t bicalutamide, 444t Borrelia burgdorferi, 390t
benzonatate, 465 BiDil, 273, 283t, 295t Botox. See onabotulinumtoxin A
benzoyl peroxide, 590, 590t bile acid-binding agents botulinum toxin, 173, 174f
benztropine actions, 243f Bowman’s capsule, 250
actions, 164t adverse effects, 242 BPH (benign prostatic hyperplasia), 556, 557,
adverse effects, 164t drugs classified as, 239t 557f, 558t
Index 631
bradycardia, 282 calcifediol, 565 cannabinoids, 76

bradykinesia, 148, 159 Calciferol. See ergocalciferol Cannabis sativa, 76
bradykinin, 208 Calcijex. See calcitriol capecitabine, 439t
brainstem, 107, 108t calcipotriene, 593t, 594 Capoten. See captopril
brand name, 14, 15–16 Calcite-500. See calcium carbonate capsaicin, 173t
breakthrough bleeding, 550 calcitonin capsid, 417
breastfeeding, medication use during, 44 in calcium homeostasis, 565, 566f capsules, 26t, 27
Brethine. See terbutaline for osteoporosis, 570 guidelines for administering, 26t
Brevibloc. See esmolol for Paget’s disease, 574 sustained-release, 27
Brilinta. See ticagrelor calcitonin nasal spray, 574 captopril, 275t, 293t, 313
brimonidine tartrate, 603t calcitonin–salmon, 571t carbachol, 602t
brinzolamide, 603t calcitriol, 565 carbamazepine, 185t, 190t, 201
broad-spectrum antibiotic, 393 Drug Prototype, 569 adverse effects, 189
broad-spectrum penicillins, 393 route and adult dose, 568t for mood disorders, 135, 135t
bromocriptine, 161, 161t, 515t, 536t in vitamin D activation, 565, 567f for seizures, 185t, 189
brompheniramine, 459t calcium, 501t, 565, 566f. See also for trigeminal neuralgia, 189
bronchi, 455 hypocalcemia carbamide peroxide, 607t
bronchioles, 455 calcium acetate, 502t, 568t carbapenems, 404
bronchoconstriction/bronchospasm, 466 calcium carbonate, 482t, 502t, 568t carbenicillin, 393
bronchodilation, 467 calcium carbonate with magnesium carbidopa, 160
bronchodilators hydroxide, 482t actions and uses, 163t
for asthma, 467–469, 468t calcium channel blockers (CCB), 132 adverse effects, 163t
drugs classified as, 468t actions, 272f, 307, 309, 341–342, 341t Drug Prototype, 163t
Nursing Process Focus, 469–470t adverse effects, 309, 342 interactions, 163t
Patients Need to Know, 472 clinical uses Carbocaine. See mepivacaine
buccal route, 26t, 27 angina and myocardial infarction, 305, carbonic anhydrase, 256
budesonide, 463t, 470t 306t, 307, 309 carbonic anhydrase inhibitors
Bufferin. See aspirin dysrhythmias, 341, 341t actions, 253f
bumetanide, 252, 253t, 274t, 293t hypertension, 278, 278t for glaucoma, 603, 603t
Bumex. See bumetanide migraine prophylaxis, 212t carboplatin, 437t
bundle branches, 333, 334f drugs classified as, 278t carboprost, 553t
bupivacaine, 221t interactions carcinogens, 432
bupivicaine, 221t with dantrolene sodium, 175t Cardene. See nicardipine
Buprenex. See buprenorphine Nursing Process Focus, 279–280t cardiac conduction pathway, 333–335, 334f
buprenorphine, 204t, 206 Patients Need to Know, 343t cardiac glycosides
bupropion, 112t calcium chloride, 568t actions, 291f, 294
for bipolar disorder, 135 calcium citrate, 502t, 568t for heart failure, 294, 295t
for depression, 126t calcium gluconate, 502t, 568t interactions
for nicotine withdrawal, 72 calcium ion channels, 335, 336f with succinylcholine, 228t
smoking cessation and, 129 calcium lactate, 502t, 568t Patients Need to Know, 297t
burns, 583–584. See also skin disorders calcium metabolism, 497 cardiac output, 269
BuSpar. See buspirone calcium phosphate tribasic, 568t cardiogenic shock, 320, 320t. See also shock
buspirone, 117–118, 117t calcium polycarbophil, 487t cardiotonic drugs. See inotropic drugs
busulfan, 437t calcium salts Cardizem. See diltiazem
butabarbital, 116t Drug Prototype, 569t Cardura. See doxazosin
butamben, 222 for osteomalacia and hypocalcemia, 566, Cardura XL. See doxazosin XL
butenafine, 415t 567–568, 568t carisoprodol, 171t
Butisol. See butabarbital calcium supplements carmustine, 437t
butoconazole, 415t interactions with phenytoin, 190t carnitine, 293t
butorphanol, 204t Cal-Lac. See calcium lactate carteolol, 100t, 603t
Butrans. See buprenorphine Cambia. See diclofenac Cartia XT. See diltiazem
Byetta. See exenatide camphorated opium tincture, 489t Cartrol. See carteolol
Campral. See acamprosate calcium carvedilol
CAM Therapy, 60–61, 60t actions, 291f, 296t
C See also Guide to Special Features adverse effects, 296t
cabazitaxel, 442t canagliflozin, 535 clinical uses, 100t
CABG (coronary artery bypass graft) cancer, 431 heart failure, 296, 296t
surgery, 304 causes, 432 hypertension, 281t
Caduet, 244 characteristics, 431–432 Drug Prototype, 296t
Cafergot. See ergotamine with caffeine chemotherapy, 433–434, 434f. See also interactions, 296t
caffeine, 78–79, 79t antineoplastic drugs route and adult dose, 281t, 295t
as CNS stimulant, 79 incidence, 431 caspofungin acetate, 414, 415t
content of common drugs, foods, and metastases, 432f castor oil, 487t
beverages, 79t risk reduction methods, 433 Cataflam. See diclofenac
diuretic effect of, 79 candesartan, 275t, 293t, 294 Catapres. See clonidine
physical effects of, 79 Candida, 389f catecholamine O-methyl transferase
Calan. See verapamil Candida albicans, 414t (COMT), 128
632 Index
catechol-O-methyl transferase (COMT) cetirizine, 460t cholinergic, 90, 92

inhibitors, 162 cetuximab, 445t cholinergic drugs, 175
cathartic, 486 cevimeline HCl, 92t chondroitin sulfate, 578t
catheter ablation, 336 C fibers, 199 Chronic alcohol consumption, 75
cayenne (Capsicum annum), 173t CFSAN (Center for Food Safety and Applied chronic bronchitis, 471–472
CBER (Center for Biologics Evaluation and Nutrition), 7 chronic obstructive pulmonary disease
Research), 5 chemical group name, 13, 14 (COPD), 471–472
CDC (Centers for Disease Control and chemical name, 14 chronic simple glaucoma, 600f, 601. See also
Prevention), 9 chemoprophylaxis glaucoma
CDER (Center for Drug Evaluation and for cancer, 434 Cialis. See tadalafil
Research), 5 for infections, 392 ciclesonide, 463t, 470t
cefaclor, 396t chemotherapy, cancer, 433–434, 434f. See also ciclopirox, 415t
cefadroxil, 396t Antineoplastic Drugs cidofovir, 424t
cefazolin, 396t chest pain, 302–303, 303t ciliary body, 599
cefdinir, 396t Childhood Vaccine Act, 6f, 7t cilostazol, 355t
cefditoren, 396t children cimetidine, 482t
cefepime, 396t AED use and development of, 184 Cimzia. See certolizumab pegol
cefixime, 396t dorsogluteal site for, 36 cinacalcet, 571t
cefotaxime epilepsy in, 182 CiproDex. See ciprofloxacin and
Drug Prototype, 396t febrile seizures and, 182 dexamethasone
route and adult dose, 396t vastus lateralis site for, 36 ciprofloxacin
cefotetan, 396t Chlamydia trachomatis, 390t for anthrax exposure, 401
cefprozil, 396t chlorambucil, 437t Drug Prototype, 401t
ceftriaxone, 396t chloramphenicol, 404t for ear infections, 607, 607t
cefuroxime, 396t chlordiazepoxide, 113, 114t route and adult dose, 400t
Celebrex. See celecoxib chloride, 501t ciprofloxacin and dexamethasone, 607t
celecoxib, 8, 208, 209t, 365t, 366 chloroethane, 221t ciprofloxacin and hydrocortisone, 607t
Celestone. See betamethasone Chloromag. See magnesium chloride Cipro HC. See ciprofloxacin and hydrocortisone
Celexa. See citalopram chloroprocaine, 221t cirrhosis, 75
cell kill, 434, 434f chloroquine, 426, 426t cisatracurium, 176t
cell-mediated immunity, 375–376, 375f chlorothiazide, 254t, 274t cisplatin, 437t
Cenestin. See estrogen, conjugated chlorpheniramine, 459t citalopram, 112t, 126t
Center for Biologics Evaluation and Research chlorpromazine Citracal. See calcium citrate
(CBER), 5 actions and uses, 147t cladribine, 439t
Center for Drug Evaluation and Research adverse effects, 147t clarithromycin, 398t, 485
(CDER), 5 Drug Prototype, 147t Clearasil. See benzoyl peroxide
Center for Food Safety and Applied Nutrition interactions, 147t ClearEyes. See naphazoline
(CFSAN), 7 with kava, 147t clemastine, 459t
Centers for Disease Control and Prevention with phenobarbital, 147t Climara. See estradiol
(CDC), 9 with St. John’s wort, 147t clindamycin, 403, 404t
central nervous system (CNS), 87, 88f, 199, with tricyclic antidepressants, 147t clinical depression, 111. See also major
200, 432 interaction with valproic acid, 191t depressive disorder
cholinergic drugs and, 92 introduction of, 143 clinical pharmacology, 7
central nervous system (CNS) depressants route and adult dose, 146t clinical phase trials, 7–8
abuse of, 74–76 chlorpropamide, 536t Clinoril. See sulindac
alcohol, 75–76 chlorthalidone, 254, 254t, 274t clobetasol, 592t
for anxiety and sleep disorders, 110–111 Chlor-Trimeton Allergy/Decongestant, 461t clocortolone, 592t
barbiturates, 74 chlorzoxazone, 171t Cloderm. See clocortolone
benzodiazepines, 74–75 cholecalciferol, 565 clofarabine, 439t
categorization of, 111 cholesterol clofibrate, 243
opioids, 75 bad, 236 clomipramine, 112t, 125, 126t
Patients Need to Know, 119t biosynthesis and excretion, 238, 239t clonazepam, 74, 114t
sedatives and sedative-hypnotics, 74 dietary, 235 for anxiety, 114t
withdrawal syndrome, 111 functions, 235 for muscle spasms, 170, 171t
central nervous system (CNS) stimulants good, 236 for seizures, 187t
abuse of, 78–79 laboratory values, 238t clonic phase, tonic-clonic seizure, 183
for ADHD, 137, 138t levels, 235t clonic spasm, 169. See also muscle spasms
drugs classified as, 137, 138t red yeast rice and, 238t clonidine, 138t
cephalexin, 396t total, 238t actions, 282
cephalosporins, 395–397, 396t cholestyramine clinical uses, 97t
cerebral cortex, 107 actions, 240t attention deficit-hyperactivity
cerebrovascular accident (stroke), adverse effects, 240t disorder, 138t
314–315, 347t clinical uses, 240t hypertension, 281t
Cerebyx. See fosphenytoin Drug Prototype, 240t clopidogrel
certolizumab pegol, 576t interactions, 240t actions, 350f, 355t, 356t
Cervidil. See dinoprostone Patients Need to Know, 245t adverse effects, 356t
Cetamide. See sulfacetamide sodium route and adult dose, 239t black box warning, 356t
Index 633
clinical uses, 356t compliance, 22 Corvert. See ibutilide

myocardial infarction, 312 Compoz Nighttime Sleep Aid. See Corzide. See bendroflumethiazide and nadolol
stroke, 314 diphenhydramine Coumadin. See warfarin
Drug Prototype, 356t Comprehensive Drug Abuse Prevention and Cozaar. See losartan
interactions, 356t Control Act, 16 cranberry, 251t, 353t
route and adult dose, 355t COMT (catecholamine O-methyl Crestor. See rosuvastatin
clorazepate, 114t, 187t, 188 transferase), 128 cretinism, 516
closed-angle glaucoma, 600f, 601. See also Comtan. See entacapone Crinone. See progesterone
glaucoma Comvax, 377t Critical Path Initiative (FDA), 6f
closed comedones, 589 Concerta. See methylphenidate Crohn’s disease, 480
Clostridium botulinum, 173 congestive heart failure, 289. See also heart cromolyn, 471
clotrimazole, 415t failure (HF) route and adult dose, 470t
clotting factors, 347 conjugated estrogens with medroxyprogester- cross-tolerance, 73
cloves, for dental pain, 223t one, 551t crotamiton, 587
cloxacillin, 393 constipation, 486–487, 487t crushing, tablets or capsules, 27
clozapine, 151t, 152 contact dermatitis, 591 Cryptococcus neoformans, 414t
interactions with risperidone, 152t contractility, 289, 304 crystalloids, 323, 323t
Clozaril. See clozapine controlled substance, 16 crystamine. See cyanocobalamin
CMV (cytomegalovirus), 423 Controlled Substances Act of 1970, 16 culture, 7
CNS (central nervous system). See central conventional antipsychotics culture and sensitivity (C&S) testing, 393
nervous system (CNS) adverse effects, 147t Cushing’s syndrome, 514t, 522
coagulation, 347 nonphenothiazines, 148t Cutar. See coal tar
coagulation cascade, 347, 348f Nursing Process Focus, 149–151t Cutivate. See fluticasone propionate
coagulation disorders, 347t phenothiazines and phenothiazine-like Cuvposa. See glycopyrrolate
incidence, 349t drugs, 146t cyanocobalamin
Patients Need to Know, 358t convulsions, 181. See also seizure(s) Drug Prototype, 499t
coal tar, 593t, 594 Copaxone. See glatiramer cyclic lipopeptides, 403–404
co-analgesics. See adjuvant analgesics COPD (chronic obstructive pulmonary cyclizine, 490t
cocaine, 70, 78 disease), 471–472 cyclobenzaprine
Andean cultures and use of, 78 Cordarone. See amiodarone actions and uses, 171t
history of uses, 78 Cordran. See flurandrenolide adverse effects, 171t
as local anesthetic, 222 Coreg. See carvedilol Drug Prototype, 171t
overdose of, 78 Corgard. See nadolol interactions, 171t
physiological and psychological effects coronary arteries, 302 route and adult dose, 171t
of, 73t coronary artery bypass graft (CABG) Cyclocort. See amcinonide
as Schedule II drug, 78 surgery, 304 Cyclogyl. See cyclopentolate
withdrawal syndrome for, 78 coronary heart disease, 302–303, 303f, 303t cyclooxygenase, 208, 366
Coccidioides immitis, 414t corpora cavernosa, 555 cyclooxygenase type 1 (COX-1), 208
codeine, 204t, 465 corpus luteum, 544 cyclooxygenase type 2 (COX-2), 208
coenzyme Q10, 242t corpus striatum, 160, 162f cyclopentolate, 95t, 606t
Cogentin. See benztropine Cortef. See hydrocortisone cyclophosphamide
Cognex. See tacrine corticosteroids Drug Prototype, 438t
cognitive-behavioral therapy, 125 for chemotherapy, 443 route and adult dose, 437t
Colace. See glycerin clinical uses cycloplegia, 602
colchicine, 577, 577t adrenocortical insufficiency, 521, 522t cycloplegic drugs, 605, 606t
Colcrys. See colchicine allergic rhinitis, 31, 461 Cycloset. See bromocriptine
colesevelam, 239t, 242 anaphylaxis, 328 cyclosporine
Colestid. See colestipol asthma, 470–471, 470t Drug Prototype, 382t
colestipol, 239t dermatitis, 591, 592t interactions, 398t
colloids, 323, 323t inflammation, 201, 365, 368, for psoriasis, 593t, 594
combination drugs, 15 368t, 381 route and adult dose, 381t
common cold inflammatory pain, 201 Cymbalta. See duloxetine
antitussives for, 465 control of, 520 cytarabine, 439t
decongestants for, 463–464, 464t defined, 520 cytokines, 375
expectorants for, 465 drugs classified as cytomegalovirus (CMV), 423
common collecting ducts, 250 inhaled, 470–471, 470t Cytomel. See liothyronine
Compazine. See prochlorperazine intranasal, 462, 463t cytotoxic T cells, 375–376
competitive antagonists, 205 oral, 471
complement, 364t systemic, 522, 523–524t D
complementary and alternative medicine topical, 28, 591, 592t, 594
dabigatran, 351, 351t
(CAM), 60–61. See also herbal products; inflammatory and immune responses,
dacarbazine, 437t
specialty supplements suppression, 522
dactinomycin, 441t
common characteristics of, 60 corticotropin-releasing factor (CRF), 520
Dalmane. See flurazepam
complementary and alternative medicine cortisone, 368t
dalteparin, 351t
(CAM) therapy, 4, 57t Cortisporin. See polymyxin B, neomycin, and
danazol, 555t
complex partial seizures, 183. See also hydrocortisone
d- and l-amphetamine racemic mixture, 137
seizure(s) Cortizone. See hydrocortisone
634 Index
Danocrine. See danazol Nursing Process Focus, 130–131t dicloxacillin, 394t

dantrolene postpartum, 124 dicyclomine, 95t
actions, 175t psychotic, 124 didanosine, 419t
adverse effects, 175t seasonal affective disorder (SAD), 124 Didronel. See etidronate
clinical uses, 175t situational, 124 diencephalon, 107, 108t
Drug Prototype, 175t situational and biological causes of, 123t dietary fiber, 486
interactions, 175t symptoms of, 123 Dietary Reference Index (DRI), 498
with alcohol, 175t dermatitis, 591, 592t Dietary Supplement and Nonprescription Drug
with antihistamines, 175t Dermatop. See prednicarbate Consumer Protection Act, 67
with verapamil, 175t dermis, 583 Dietary Supplement Health and Education Act
route and adult dose, 174t DES (diethylstilbestrol), 443t (DSHEA) of 1994, 6f, 7, 66
daptomycin, 403, 404t desflurane, 225t significant weaknesses of, 66
darunavir, 419t designer drugs, 70 dietary supplements, 66. See also herbal
“date rape” drug. See ketamine desipramine, 112t, 126t products; specialty supplements
daunorubicin, 441t desirudin, 351, 351t defined, 66
daunorubicin liposomal, 441t desloratadine, 460t Dietary Supplement and Nonprescription
Daypro. See oxaprozin desmopressin Drug Consumer Protection Act and, 67
Daytrana. See methylphenidate for diabetes insipidus (DI), 515 DSHEA and, 66
DDAVP. See desmopressin Drug Prototype, 514t nonherbal. See specialty supplements
DEA (Drug Enforcement Administration), 16 Desonate. See desonide regulation of, 66–67
Debrox. See carbamide peroxide desonide, 592t sales of, 60
Decaspray. See dexamethasone DesOwen. See desonide diethylstilbestrol (DES), 443t
decongestants, 463–464, 464t desoximetasone, 592t difenoxin with atropine, 489t
in combination products, 461t Detrol. See tolterodine Differin. See adapalene
Patients Need to Know, 472 dexamethasone, 522t, 592t diflorasone, 592t
deep vein thrombosis (DVT), 347t, 349 as antiemetic, 490t diflunisal, 209t, 365t
defecation, 486 as antineoplastic agent, 443t digestion, 478
deficient knowledge (drug teaching), 53 route and adult dose, 368t digestive system, 478, 478f. See also
degarelix, 444t dexchlorpheniramine, 459t gastrointestinal disorders
dehydration, 273 Dexedrine. See dextroamphetamine digoxin
Delatestryl. See testosterone enanthate Dexferrum. See iron dextran actions, 291f, 294, 295t
delavirdine, 419t dexmethylphenidate, 138t adverse effects, 294, 295t
Delestrogen. See estradiol valerate dextroamphetamine, 78, 137, 138t clinical uses, 295t
deltoid site, intramuscular injection, 36 dextromethorphan, 465 dysrhythmias, 341t
delusions, 143 D.H.E. 45. See dihydroergotamine mesylate Drug Prototype, 295t
Demadex. See torsemide DiaBeta. See glyburide interactions, 295t
demeclocycline, 397t diabetes insipidus (DI), 514–515 with amiodarone, 341t
dementia, 164. See also Alzheimer’s disease diabetes mellitus (DM) with atorvastatin, 240t
characteristics, 164 causes, 529 with carvedilol, 296t
gingko biloba use in, 167t description, 529 with cyclophosphamide, 438t
Patients Need to Know, 176t Patients Need to Know, 539t with diltiazem, 309t
Demerol. See meperidine type 1. See type 1 diabetes mellitus with diuretics, 252
demyelination, 167–168 type 2. See type 2 diabetes mellitus with furosemide, 254t
denosumab, 571t diabetic ketoacidosis (DKA), 530 with heparin, 352t
dental pain, cloves for, 223t Diabinese. See chlorpropamide with hydrochlorothiazide, 255t
Depakene. See valproic acid diagnosis, medical, 53 with psyllium, 487t
Depakote. See valproic acid diagnosis, nursing, 52f, 53, 54t with spironolactone, 256t
dependence, 16 Diagnostic and Statistical Manual of Mental with vincristine, 443t
drugs causing, 16 Disorders, 5th edition (DSM-5), 123 route and adult dose, 295t, 325t, 341t
physical, 16, 17t Diamox. See acetazolamide digoxin immune fab, 294
psychological, 16, 17t diarrhea, 488–489, 489t dihydroergotamine, 211
depolarization (blockers), 175, 335 diastolic pressure, 267, 268f dihydroergotamine mesylate, 212t
depolarizing blockers, 175, 176t, 229. See also diazepam, 72, 74, 185t Dilacor XR. See diltiazem
neuromuscular blocking drugs actions and uses, 188t Dilantin. See phenytoin
Depo-Medrol. See methylprednisolone adverse effects, 113–114, 188t Dilaudid. See hydromorphone
Depo-Provera. See medroxyprogesterone clinical uses, 185t Dilocaine. See lidocaine
Depo-SubQ-Provera. See alcohol withdrawal, 72 diltiazem
medroxyprogesterone anxiety, 114t actions, 309t
Depo-Testosterone. See testosterone cypionate intravenous anesthetic, 226t adverse effects, 309t
depression, 123 muscle spasms, 170, 171, 173 clinical uses
in Alzheimer’s disease, 164, 166 seizures, 185t, 187t, 187t angina, 306t
biological, 123 Drug Prototype, 188t dysrhythmias, 341t
bipolar disorder and, 134 interaction with omeprazole, 483t Drug Prototype, 309t
clinical, 123 introduction of, 113 interactions, 309t
management route and adult dose, 187t route and adult dose, 278t, 306t, 309t, 341t
short-term psychotherapies, 124–125 dibucaine, 221t dimenhydrinate, 459t, 489, 490t
St. John’s wort, 134t diclofenac, 209t, 365t Dimetapp Children’s Cold and Allergy, 461t
Index 635
dinoprostone, 553t DOM (2,5 dimethoxy-4-methylamphetamine, onset of, 45

Diovan. See valsartan “STP”) drug, 77 termination of, 46
Diovan HCT, 273 donepezil drug administration
Diphedryl. See diphenhydramine actions, 167t common abbreviations used to give
Diphenadryl. See diphenhydramine adverse effects, 167t directions about, 24t
diphenhydramine, 15, 15t clinical uses, 92t, 167t compliance with, 22–23
for allergic reactions, 119 Drug Prototype, 167t enteral, 26t, 27–28
clinical uses interactions, 167t health support staff responsibilities, 21
as antiemetic, 490t with dexamethasone, 167t nurse’s responsibilities, 21–22
extrapyramidal symptoms, 160 with phenobarbital, 167t parenteral, 32–39, 34–35t
insomnia, 111, 117t with rifampin, 167t protocols and techniques, 25–26
parkinsonism, 163t route and adult dose, 165t six rights, 22
shock, 328 dong quai, for premenstrual syndrome, 549t three checks, 22
Drug Prototype, 460t dopamine topical, 28–32, 30–31t
route and adult dose, 459t actions, 326t drug–drug interactions, 42, 46f
diphenoxylate with atropine adverse effects, 326t Drug Enforcement Administration (DEA), 16
Drug Prototype, 488t black box warning, 326t drug forms, administration guidelines for, 26t,
route and adult dose, 489t clinical uses, 97t 30–31t, 34–35t
diphtheria, tetanus, and pertussis vaccine, 377t shock, 325, 325t, 326t drug interaction, 42
Dipivefrin HCl, 602, 602t Drug Prototype, 326t drug–drug interactions, 42, 46f
Diprivan. See propofol interactions, 326t food–drug interactions, 42, 46f
Diprolene. See betamethasone with isoflurane, 225t drug prototype. See Guide to Special
dipyridamole, 355t in neurodegenerative disorders, 160, Features
dirithromycin, 398t 161, 162f drug(s)
Disalcid. See salsalate route and adult dose, 325t antibiotics, 13
disease-modifying antirheumatic drugs in schizophrenia, 145f anti-inflammatory, 13
(DMARDs), 575, 576t dopamine blocker, 228t approval process, U.S., 7–9, 8f
disopyramide, 338t dopamine partial agonists. See dopamine bioavailability of, 15
disorganized behavior, 143 system stabilizers (DSS) brand name, 15–16
distal tubule, 250, 250f dopaminergic drugs, 160, 161t chemical group name of, 14
distribution, 42f, 43 dopamine system stabilizers (DSS), 146, 154 chemical name of, 14
disulfiram, 75–76, 129t Dopastat. See dopamine classification, 4
diuretics, 252 Doral. See quazepam combination, 15
actions, 252, 269, 272f, 291f, 294 doripenem, 404t controlled substance, 16
adverse effects, 252, 273, 294 dorsogluteal site, intramuscular injection, 36 diuretic, 13
classifications dorzolamide, 603t efficacy of, 47, 48f
carbonic anhydrase inhibitors, dose-response curve, 47 FDA-unapproved uses of, 9
256–257, 257t Dovonex. See calcipotriene generic name of, 14
loop diuretics, 252–253, 253f doxazosin, 558t grapefruit juice and, 23
potassium-sparing diuretics. See actions, 282t half-life (t1/2) of, 45
potassium-sparing diuretics adverse effects, 282t labels, 7f
clinical uses, 252 clinical uses, 99, 100t, 282t names, 14–15
heart failure, 293t, 294 hypertension, 281t off-label use of, 9
hypertension, 273–274, 274t Drug Prototype, 282t pharmacologic classification, 13–14, 14t
drugs classified as, 253t interactions, 282t plasma half-life of, 45
interactions route and adult dose, 281t potency of, 47, 48f
with prazosin, 100t doxazosin XL, 558t pregnancy categories, 17
interventions doxepin, 112t, 126t prodrugs, 43
with digoxin, 295t doxercalciferol, 568t prototype, 13
with prednisone, 369t doxorubicin reactions to, 23
with warfarin, 353t Drug Prototype, 441t regulation of, 5
osmotic, 257 interaction with vincristine, 443t schedules, 16
Patients Need to Know, 257–258t, 262t, 297t route and adult dose, 441t therapeutic classification, 13–14, 13t
Diuril. See chlorothiazide doxorubicin liposomal, 441t therapeutic range of, 45
Divigel. See estradiol doxycycline, 590, 590t trade name of, 14
DKA (diabetic ketoacidosis), 530 actions, 397t drug therapy
DMARDs (disease-modifying antirheumatic clinical uses, 426t factors influencing effectiveness of, 46t
drugs), 575, 576t route and adult dose, 397t metabolism and, 43
dobutamine, 97, 97t, 325, 325t doxylamine, 111, 117t DSS (dopamine system stabilizers),
Dobutrex. See dobutamine DPI (dry powder inhaler), 456 146, 154
docetaxel, 442t DRI. See Dietary Reference Index (DRI) duloxetine, 112t, 126t
docosanol, 424t Drisdo. See ergocalciferol for anxiety disorders, 112t
docusate, 487t dronedarone, 340t for depression, 126t
dofetilide, 340t drop attacks, 183. See also atonic seizures for generalized anxiety disorder, 129
dolasetron, 490t droperidol, 225t, 227, 228t for neuropathic pain, 129
Dolgesic. See ibuprofen drug action Durabolin. See nandrolone
Dolophine. See methadone duration of, 46 Duragesic. See fentanyl
636 Index
Duramorph. See morphine electrocardiogram (ECG), 333, 334f classification of, 183–184
duration of drug action, 46 electroconvulsive therapy (ECT), 125 Fast Facts, 182t
dutasteride, 558t electroencephalogram (EEG), 181, 181f idiopathic, 182
DVT (deep vein thrombosis), 347t, 349 electrolyte(s) ketogenic diet for, 188t
dwarfism, 515 defined, 258, 273 Lennox-Gastaut syndrome (LGS), 191
Dyclone. See dyclonine imbalances, 258–259, 259t onset of, 183t
dyclonine, 221t Elestrin. See estradiol symptoms of, 181
DynaCirc. See isradipine eletriptan, 212t epileptic seizures, 183
Dyrenium. See triamterene elimination, 45. See also excretion generalized, 183
dysentery, 426 Elimite. See permethrin partial, 183
dysfunctional uterine bleeding, 549–550 Eliquis. See apixaban special epileptic syndromes, 184
dyslipidemia, 235 Elitek. See rasburicase epinephrine, 90
dysphoric symptoms, 134 Ella. See ulipristal actions, 98t, 327t
dyspnea, 466 Elocon, ses mometasone furoate adverse effects, 282, 327t
Dysport. See onabotulinumtoxin A embolus, 349 clinical uses, 97t, 98t
dysrhythmias, 332 emergency contraception (EC), 547 in local anesthetics, 220
classification, 332–333 emesis, 489 shock, 325, 325t, 327t
diseases associated with, 333 emetics, 490 Drug Prototype, 327t
incidence, 332t emphysema, 472 interactions, 327t
nonpharmacologic therapy, 336 Empirin. See aspirin with isoflurane, 225t
Nursing Process Focus, 336–337t Empirin with Codeine No. 2, 205 route and adult dose, 325, 325t
pathophysiology, 333–335 Emsam. See selegiline epirubicin, 441t
Patients Need to Know, 343t emtricitabine, 419t eplerenone, 256t, 274t, 293t
pharmacotherapy enalapril epoetin alfa
adenosine, 341t, 342 actions, 277t in cancer chemotherapy, 252, 446
beta-blockers, 339, 339t. See also beta adverse effects, 277t Drug Prototype, 446t
(β) blockers black box warning, 277t eprosartan, 275t
calcium channel blockers, 341–342, clinical uses, 277t EPS (extrapyramidal symptoms), 148, 160,
341t. See also calcium channel heart failure, 293t 166
blockers (CCB) hypertension, 275t Epsom salt. See magnesium sulfate
digoxin, 341t, 342 Drug Prototype, 277t Epstein-Barr virus, 424
potassium channel blockers, 340, 340t. interactions, 277t eptifibatide, 355t
See also potassium channel blockers route and adult dose, 275t, 293t Ercaf. See ergotamine with caffeine
sodium channel blockers, 338, 338t. Enbrel. See etanercept erectile dysfunction, 555–556, 556t
See also sodium channel blockers endocrine system, 511, 512f ergocalciferol, 568t
symptoms, 332 endogenous opioids, 199–200 Ergostat. See ergotamine tartrate
dysrhythmic drugs, 201 endometrial carcinoma, 550 ergot alkaloids, 211
dysthymic disorder, 124. See also depression Endometrin. See progesterone ergotamine tartrate, 211, 212t
dystonias, 148, 172. See also spasticity endometriosis, 550 ergotamine with caffeine, 212t
with conventional antipsychotics, 148 end-stage renal disease (ESRD), 251 eribulin, 442t
Enduron. See methyclothiazide erlotinib, 445t
enflurane, 225t ER (extended-release) medications, 27
E enfuvirtide, 419t, 420 ertapenem, 404, 404t
ear, 606, 607f Enjuvia. See estrogen, conjugated erythema, 584
ear disorders, 606–608, 607t enoxaparin, 351t erythromycin
EC (emergency contraception), 547 entacapone, 161, 161t, 162 Drug Prototypes, 398t
ECG (electrocardiogram), 333, 334f actions and uses, 163t interactions
echinacea, 376 adverse effects, 163t with atorvastatin, 240t
interactions, 341, 440t Drug Prototype, 163t with valproic acid, 191t
echothiophate iodide, 602, 602t interactions, 163t route and adult dose, 398t
eclampsia, 183 route and adult dose, 161t erythropoietin, 252
econazole, 415t enteral nutrition, 504–505, 504f Erythroxylon coca, 222
Ecotrin. See aspirin enteral route, 27 Escherichia coli, 390t
Ecstasy (MDMA), 77 buccal, 27, 28f escitalopram
ECT (electroconvulsive therapy), 125 nasogastric and gastrostomy tubes, 27t, 28 actions, 113t
ectopic foci/pacemakers, 335 sublingual, 27, 28f adverse effects, 113t
eczema, 591, 592t tablets and capsules, 27 clinical uses, 113t
Edarbi. See azilsartan enteric-coated tablets, 27 for anxiety disorders, 112t
Edecrin. See ethacrynic acid Enterobius, 427 Drug Prototype, 113t
edrophonium, 92t Enterococci, 390t escitalopram oxalate, 126t
Edular. See zolpidem enterohepatic recirculation, 44, 45f Eskalith. See lithium
EEG (electroencephalogram), 181, 181f enzalutamide, 444t esmolol, 100t, 339t
efavirenz, 419t ephedra, 66, 133t esomeprazole, 482t
Effexor. See venlafaxine epidermis, 583 estazolam, 114t
efficacy, of drugs, 5, 47, 48f Epidermophyton floccosum, 414t esters, 220–222, 221t. See also local
Elavil. See amitriptyline; amitryptiline epidural anesthesia, 219f, 219t anesthetics
Eldepryl. See selegiline epilepsy, 181. See also seizure(s) Estrace. See estradiol
Index 637
Estraderm. See estradiol eye disorders first-dose phenomenon, 100t

estradiol, 550t glaucoma. See glaucoma first-pass effect (first-pass metabolism), 29, 31,
estradiol valerate, 550t minor conditions, 605, 606t 32, 33, 37, 43, 44f
estradiol with norethindrone Patients Need to Know, 608t fish oil, 244
Drug Prototype, 547t eye examination, 605, 606t flecainide, 201, 338t
estradiol with norgestimate, 551t ezetimibe, 239t, 243f, 244 Fleet Mineral Oil. See mineral oil
estramustine, 437t ezogabine, 187t Flexeril. See cyclobenzaprine
estrogen, conjugated Flomax. See tamsulosin
Drug Prototype, 551t Florinef. See fludrocortisone
route and adult dose, 550t F floxuridine, 439t
estrogen-progestin oral contraceptives, 546t false neurotransmitter, 282 fluconazole, 414, 415t
adverse effects, 546 famciclovir, 424t flucytosine, 415t
description, 546 famotidine, 482t fludarabine, 439t
types, 546 Fanapt. See iloperidone fludrocortisone, 522t
estrogens fasciculations, 175 fluid replacement drugs, 322–323, 323t
interaction with phenytoin, 190t Fast Facts. See Guide to Special Features blood products, 322, 323t
sex hormone, 544 fat-soluble vitamin, 497–498. See also colloids, 323, 323t
estropipate, 550t vitamin(s) crystalloids, 323, 323t
eszopiclone, 111, 117t, 119 FDA (Food and Drug Administration). See Nursing Process Focus, 324t
etanercept, 576t Food and Drug Administration (FDA) flunisolide, 463t, 470t
ethacrynic acid, 253t FDA Amendments Act, 6f flunitrazepam, 74
ethambutol, 407t FDA Drug Modernization Act, 6f, 9 fluocinolone acetonide, 592t
ethinyl estradiol, 546, 590t. See also estrogen- FDA Food Safety Modernization Act, 6f fluocinonide, 592t
progestin oral contraceptives febrile seizures, 182, 184 fluoroquinolones, 400–401, 400t
clinical uses, 443t febuxostat, 577, 577t fluorouracil, 439t
ethinyl estradiol with norethindrone acetate, Federal Bureau of Chemistry, 6f fluoxetine, 17t
551t felbamate, 190t, 191 anxiety, 112t
ethosuximide Felbatol. See felbamate clinical uses, 126t
actions, 192t Feldene. See piroxicam depression, 126t
adverse effects, 192t felodipine, 278t fluoxymesterone, 443t, 555t
clinical uses, 185t, 192t fenofibrate, 239t, 243 fluphenazine, 146t
Drug Prototype, 192t fenoprofen, 209t, 365t flurandrenolide, 592t
interactions, 192t fentanyl, 75 flurazepam, 114t
with valproic acid, 192t as adjuncts to anesthesia, 228t flurbiprofen, 209t, 365t
route and adult dose, 192t adverse reactions, 204 flutamide, 444t
ethotoin, 189t clinical uses, 203, 204t fluticasone
Ethrane. See enflurane as intravenous anesthetic, 226t Drug Prototype, 463t
ethyl alcohol. See alcohol Fentora. See fentanyl inhaled, 470t
ethyl chloride, 221t Feosol. See ferrous sulfate route and adult dose, 463t
etidronate, 571t Feostat. See ferrous fumarate fluticasone propionate, 592t
etiologies, 53 Fergon. See ferrous gluconate fluvastatin, 239t
etodolac, 209t, 365t Ferranol. See ferrous fumarate fluvoxamine, 112t, 126t
etomidate, 226t ferrous fumarate, 17t, 502t Focalin. See dexmethylphenidate
etoposide, 442, 442t ferrous gluconate, 502t Focalin-XR. See dexmethylphenidate
etravirine, 419t ferrous sulfate folic acid antagonists, 439t
euphoria, 75, 76, 78 Drug Prototype, 501t folic acid/folate, 498t, 499
Eurax. See crotamiton route and adult dose, 502t folic acid/folate (vitamin B9):
evaluation criteria, 54 fesoterodine, 95t chemical structure, 440f
evaluation phase, of nursing process, 52f, feverfew, 208t, 352t, 353t, 357t, 366t functions, 440t
56–57 fexofenadine, 460t follicle-stimulating hormone (FSH), 543
evening primrose oil for pain, 211t fibric acid drugs, 239t, 243, 243f follicular cells, 516
Evista. See raloxifene Fibricor. See fenofibrate fondaparinux, 351t
Evithrom. See thrombin fibrillation, 332 Food, Drug, and Cosmetic Act, 5, 6f, 7, 66
Evoxac. See cevimeline HCl fibrin, 347 Food and Drug Administration (FDA), 5, 6f, 7,
Exalgo. See hydromorphone fibrinogen, 347 8–9, 201, 238t
excretion, 42f, 44. See also elimination fibrinolysis, 349, 349t antiseizure drug therapy related warnings
Exelon. See rivastigmine field block (infiltration) anesthesia, 219f, 219t issued by, 184
exemestane, 444t fight-or-flight response, 87 black box warnings
exenatide, 535t, 537 filgrastim, 436, 446 for antidepressants, 111, 113
exercise-induced asthma, 466 filtrate, 250 dietary supplement regulations, 66–67
expectorants, 457f, 465 Finacea. See azelaic acid herbal products and dietary supplements,
Extavia. See interferon beta-1b finasteride administration of, by, 7
extended-release (ER) medications, 27 for benign prostatic hyperplasia, 558t new drug approval process, 8–9
extended-spectrum penicillins, 393 Drug Prototype, 558t restructuring of, 9
external otitis, 606 Fioricet with Codeine, 205 Food and Nutrition Board of the National
extrapyramidal symptoms (EPS), 148, Fiorinal, 205 Academy of Sciences, 498
160, 166 first-degree burns, 583 food–drug interactions, 42, 46f
638 Index
Foradil. See formoterol clinical uses, 243, 244t clinical uses

Forane. See isoflurane Drug Prototype, 244t allergic rhinitis, 462, 463t
formoterol, 97t, 468t interactions, 244t asthma, 470, 470t
formularies, 5 route and adult dose, 239t drugs classified as, 368t
Fortamet. See metformin gemifloxacin, 400t inhaled, 470t
Forteo. See teriparatide gemtuzumab, 445t intranasal, 463t
Fortesta. See testosterone general anesthesia, 218, 224. See also general interactions
Fortical. See calcitonin–salmon anesthetics with aspirin, 208t
Fosamax. See alendronate stages of, 224t with corticosteroids, 254t
fosamprenavir, 419t general anesthetics with cyclophosphamide, 438t
foscarnet, 424t adjuncts, 227 with phenytoin, 190t
fosfomycin, 402t administration routes, 224 with warfarin, 353t
fosinopril, 275t, 293t inhaled Glucophage. See metformin
fosphenytoin, 189t gas. See nitrous oxide Glucophage XR. See metformin
fosphenytoin sodium, 189, 189t volatile liquid, 225t, 226 glucosamine sulfate, 578t
fospropofol, 226t intravenous, 226–227, 226t glucose, 529, 530f
Fostex. See benzoyl peroxide benzodiazepines, 226t Glucotrol. See glipizide
Fragmin. See dalteparin etomidate, 226t Glumetza. See metformin
Frova. See frovatriptan fospropofol, 226t glutamate, 165, 186, 189
frovatriptan, 212t ketamine, 77, 226t glyburide, 536t
fungal infections, 413–414, 414t opioids, 226t glyburide micronized, 536t
fungi, 389f, 413, 414t propofol, 226t glycerin, 257t
furosemide, 17t generalized anxiety disorder (GAD), 106 glycoprotein IIb/IIIa, 356
actions, 252, 253f, 254t, 291f generalized seizures, 183. See also seizure(s) glycoprotein IIb/IIIa blockers, 355t, 356
adverse effects, 254t absence seizures, 183 glycopyrrolate, 95t
clinical uses, 254t atonic seizures, 183 Glynase. See glyburide micronized
heart failure, 293t tonic-clonic seizures, 183 Glyset. See miglitol
hypertension, 274t generic drugs, 15–16 goal (outcome), 54
Drug Prototype, 254t generic name, 14 goldenseal, 395t
interactions, 254t Genotropin. See somatropin golimumab, 576t
route and adult dose, 253t, 274t, 293t Genpril. See ibuprofen gonadocorticoids, 521
gentamicin gonadotropin-releasing hormone
Drug Prototypes, 400t (GnRH), 543
G route and adult dose, 399t goserelin, 444t
GABA (gamma-aminobutyric acid), 114 Geodon. See ziprasidone gout
gabapentin, 185t, 187t, 201 GERD (gastroesophageal reflux acute gouty arthritis, 577
for multiple sclerosis, 168t, 169 disease), 480 classification, 576
for seizures, 185t, 187t ginger description, 576
Gabitril. See tiagabine interactions, 352t, 353t, 357t pharmacotherapy, 577, 577t
GAD (generalized anxiety disorder), 106 ginkgo biloba gouty arthritis, 577
galantamine, 92, 92t, 165t in dementia, 167t grand mal epilepsy, 183
gamma-aminobutyric acid (GABA), 114 interactions, 352t, 353t, 357t grand mal seizures, 183
gamma-aminobutyric acid (GABA) receptor, ginseng granisetron, 490t
116, 118, 186, 186t for cardiovascular disease, 314t grapefruit juice, drug interactions with,
antiseizure drugs activating, 187t GI (gastrointestinal) tract, 457 23, 240t
ganciclovir, 424t glatiramer, 168–169, 168t grape seed extract, 280t
ganglia, 90 glaucoma, 600 Graves’ disease, 516
ganglionic blocking drugs, 175 forms, 600f, 601 green tea, 352t, 353t, 357t
garlic, 353t, 355t, 357t Nursing Process Focus, 604–605t griseofulvin, 415t
gastroesophageal reflux disease (GERD), 480 pharmacotherapy growth hormone (GH), 515–516
gastrointestinal disorders, 477t alpha2-adrenergic drugs, 603, 603t guaifenesin, 465
constipation, 486–487, 487t beta-blocking drugs, 603, 603t
diarrhea, 488–489, 489t carbonic-anhydrase inhibitors,
nausea and vomiting, 489–490, 490t 603, 603t H
Nursing Process Focus, 487–488t miotics, 602, 602t H+, K+-ATPase, 482
pancreatic insufficiency, 492 osmotic diuretics, 603t, 604 H1-receptor antagonists (antihistamines), 458,
Patients Need to Know, 492t prostaglandins, 601, 602, 602t 460–461
peptic ulcer disease. See peptic ulcer sympathomimetics, 602, 602t in combination products, 461t
disease glimepiride, 536t drugs classified as, 459–460t
gastrointestinal (GI) tract, 457 glioma(s), 432 for insomnia, 117t
gastrostomy tubes, 27t, 28 glipizide, 536t interactions
gatifloxacin, 400t GLP-1 receptor, activation, 537 with dantrolene, 175t
gefitinib, 445t glucagon, 529 with heparin, 352t
gemcitabine, 439t hyperglycemic effect, 529 Nursing Process Focus, 461–462t
gemfibrozil glucocorticoids, 520. See corticosteroids onset and duration, 117t
actions, 244t actions, 365, 368, 462 Patients Need to Know, 472
adverse effects, 244t adverse effects, 368 prophylactic use, 460
Index 639
H2-receptor blockers: cardiac glycosides, 294 herb(s), 61

actions, 483 diuretics, 293t, 294 heroin, 72, 73, 75, 78, 202, 205
adverse effects, 483 mechanisms of action, 291f herpes simplex viruses (HSVs), 423
clinical uses, 483 phosphodiesterase inhibitors, herpesviruses, 423–424, 424t
drugs classified as, 482t 295t, 297 high-density lipoprotein (HDL), 236,
HAART (highly active antiretroviral vasodilators, 295t, 296 237f, 238t
therapy), 420 signs and symptoms, 289, 290f highly active antiretroviral therapy
Haemophilus, 390t Hectorol. See doxercalciferol (HAART), 420
Haemophilus influenza type B conjugate Helicobacter pylori, 479, 485 histamine, 363–364, 364t
vaccine, 377t helminths, 427, 427t Histoplasma capsulatum, 414t
halcinonide, 592t helper T cells, 375–376 histrelin, 444t
Halcion. See triazolam Hemabate. See carboprost HIV (human immunodeficiency virus), 9, 418,
Haldol. See haloperidol hemoglobin, 501t 421f. See also HIV-AIDS
half-life (t1/2), 45 hemorrhagic stroke, 314 HIV-AIDS, 418–422, 419t
hallucinations, 143, 144, 147 hemostasis, 347–348f hives, 583
hallucinogens, 76–77, 202. See also psychedelics hemostatics, 350, 357, 357t HMG-CoA reductase, 238
physiological and psychological effects heparin HMG-CoA reductase inhibitors (statins)
of, 73t actions, 350f, 352t actions, 238, 243f
halobetasol, 592t administration, 33, 34t, 36 adverse effects, 240
Halog. See halcinonide adverse effects, 352t drugs classified as, 239t
haloperidol black box warning, 352t interactions
actions and uses, 149t clinical uses, 352t with gemfibrozil, 244t
adverse effects, 149t Drug Prototype, 352t Nursing Process Focus, 241t
Drug Prototype, 149t interactions, 352t Patients Need to Know, 245t
interactions, 149t LMWH, 351, 351t homatropine, 606t
with benztropine, 164t low molecular weight heparin, 36, hormone antagonists: as antineoplastic agents,
with beta blockers, 149t 351, 351t 443, 443t–444t
with levodopa, 149t, 163t route and adult dose, 351t hormone replacement therapy (HRT), 549,
with lithium, 149t Safety Alert, 358t 550–551t
with phenobarbital, 149t hepatic portal circulation, 43 hormones. See also androgens; estrogens;
with phenytoin, 149t hepatitis A, 425 specific hormone
with rifampin, 149t vaccine, 377t clinical uses
route and adult dose, 148t hepatitis B, 425 as antineoplastic drugs, 443,
Halotestin. See fluoxymesterone hepatitis B vaccine 443t–444t
halothane, interactions with dopamine, 326t Drug Prototypes, 378t pituitary, 543
Haltran. See ibuprofen schedule, 377t host flora, 393, 418
hBNP (natriuretic peptide), 297 hepatitis C, 425 household system of measurement, 25, 25t
HDL (high-density lipoprotein), 236, 237f, herbal products, 61–65, 62t. See also CAM HSVs (herpes simplex viruses), 423
238t Therapy huffing, 70
headache allergic reactions and use of, 64 Humalog. See insulin lispro
incidence, 199t basic formulations of, 62 human immunodeficiency virus (HIV), 9, 418,
tension, 211 history of use, 61 421f. See also HIV-AIDS
types, 211 interactions with drugs, 63–64 human papillomavirus vaccine, 377t
healthcare practitioners, 3 acetaminophen, 369t Humatrope. See somatropin
health care providers, 3 alteplase, 357t Humira. See adalimumab
biological and chemical attack, threat of, with amiodarone, 341t humoral immunity, 375, 375f
and, 9–10 aspirin, 208t Humulin N. See insulin isophane
CAM Therapy and, 4 chlorpromazine, 147t Humulin R. See insulin; insulin regular
Health Care Reform law, 6f diazepam, 188t Huntington’s chorea, 158t
hearbal products haloperidol, 149t Hybolin. See nandrolone
interactions with drugs heparin, 352t Hycodan. See hydrocodone
aspirin, 208t imipramine, 129t Hycort. See hydrocortisone
heart levodopa, 163t hydantoins and related drugs. See also
electrical conduction pathway, 333–335, lorazepam, 116t antiseizure drugs
334f morphine, 203t drugs classified as, 189–190t
function, 289, 290f, 291 phenelzine, 133t Patients Need to Know, 194t
heart block, 333t phenytoin, 190t route and adult dose, 189–190t
heart failure (HF), 288 risperidone, 152t for seizures, 189–190t
causes, 289 warfarin, 353t hydralazine
disorders associated with, 288t zidovudine, 421t actions, 283t, 296
incidence, 288t popular, 62t adverse effects, 283t
nonpharmacologic therapy, 291–292 pregnant or lactating women and, 63–64 in African Americans, 273
pathophysiology, 289, 290f, 291 regulation of, 65–67 clinical uses, 283t
Patients Need to Know, 297t standardization, 62, 63t Drug Prototype, 283t
pharmacotherapy herb–drug interactions, 64t interactions, 283t
ACE inhibitors, 292, 293t, 294 herb extracts, standardization of route and adult dose, 283t
beta blockers, 295t, 296 selected, 63t Hydramine. See diphenhydramine
640 Index
hydrochlorothiazide, 17t hypertriglyceridemia, 235 impotence, 555. See also erectile dysfunction
actions, 253f, 255t hyperuricemia, 577 IM (intramuscular) route, 34t, 36
adverse effects, 255t hypervitaminosis, 499 Imuran. See azathioprine
clinical uses, 255t hypnotics, 111 inamrinone, 295t
heart failure, 293t, 296 hypocalcemia, 259t, 565–566, 568t Inapsine. See droperidol
hypertension, 274t hypochloremia, 259t incobotulinumtoxin A, 173, 174t
in combination of drugs, 255, 273 hypodermis, 583 Increlex. See mecasermin
Drug Prototype, 255t hypoglycemia, insulin and, 532 incretin enhancers, 535t, 537
interactions, 255t hypogonadism, 554 incretin–glucose control mechanism, 537
route and adult dose, 254t, 274t, 293t hypokalemia, 259t, 260, 274 incretins, 537
hydrocodone, 204t, 465 with diuretic therapy, 252 indapamide, 254, 254t, 274t
hydrocortisone hypomagnesemia, 259t Inderal. See propranolol
Drug Prototype, 522t hyponatremia, 259, 259t Indocin. See indomethacin
route and adult dose, 368t hypophosphatemia, 259t indomethacin, 209t
routes and adult dose, 522t hypothalamus, 271f, 511, 513f infantile spasms, 184
topical, 592t hypothyroidism, 516 infiltration (field block) anesthesia, 219t
hydrocortisone valerate, 592t hypovolemic shock, 320, 320t. See also shock inflammation, 363, 584
Hydrocortone. See hydrocortisone Hytrin. See terazosin clinical mediators of, 363–364, 364t
hydromorphone, 75, 204t pharmacotherapy
HydroURIL. See hydrochlorothiazide goals, 365
hydroxychloroquine I principles, 364–365
Drug Prototype, 575 I-131. See radioactive iodide steps in, 364f
for helminth and protozoan infections, 426t ibandronate, 571t inflammatory bowel disease (IBD), 480
for rheumatoid arthritis, 576t IBD (inflammatory bowel disease), 480 infliximab, 576t
hydroxyprogesterone, 553t IB Pro. See ibuprofen influenza
hydroxyzine, 490t ibuprofen, 15, 15t antiviral drugs for, 424, 424t
Hygroton. See chlorthalidone adverse effects, 366 vaccine, 377t
hypercalcemia, 259t, 565 vs. aspirin, 47 inhalants
hyperchloremia, 259t clinical uses, 209t, 365t, 370t abuse of, 70
hypercholesterolemia, 235, 235t route and adult dose, 209t, 365t volatile, 70
hyperkalemia, 256, 259, 259t, 274 ibutilide, 340t withdrawal from, 72
hyperlipidemia, 235 ICDs (implantable cardioverter inhalation route, of drug administration,
laboratory values, 238t defibrillators), 336 456–457, 457f, 472t
lifestyle changes for, 236–237 icosapent, 239t, 244 innate body defenses, 374
pharmacotherapy idarubicin, 441t Innohep. See tinzaparin
bile-acid binding agents, 239t, 241–242 idinavir, 419t InnoPran XL. See propranolol
combinations of drugs, 244 ID (intradermal) route, 33, 34t Inocor. See inamrinone
diuretics, 273–274, 274t IFNs (interferons), 379 inotropic drugs, 325, 325t
fibric acid agents, 239t, 242 ifosfamide, 437t inotropic effect, 289
HMG-CoA reductase inhibitors, Ig (immunoglobulin), 375 INR (international normalized ratio), 352
238–240, 239t illusions, 143 insomnia, 109, 110
mechanisms of action, 274f iloperidone, 151t anxiety and, 109–110
niacin, 239t, 242 imatinib, 445t barbiturates for, 116–117, 116t
hypermagnesemia, 259t Imdur. See isosorbide mononitrate benzodiazepines for, 113–114, 114t
hypernatremia, 259, 259t imipenem, 404 Fast Facts, 110t
hyperphosphatemia, 259t imipenem-cilastatin, 404t long-term, 110
hypersecretion of thyroid hormone, 516 imipramine, 201 nonbenzodiazepine, nonbarbiturate agents
hypertension, 266 actions, 129t for, 117–118, 117t
classification, 266t adverse effects, 129t nonpharmacologic means of relieving, 110
consequences of, 267, 267t anxiety, 112t in older adults, 110t
grape seed extract for, 280t clinical uses, 129t rebound, 110
incidence, 267t depression, 126t short-term or behavioral, 110
nonpharmacologic therapy, 271–272 migraine prophylaxis, 213t inspiration, 455
pharmacotherapy Drug Prototype, 129t Inspra. See eplerenone
adrenergic blockers, 281–282, 281t route and adult dose, 213t insulin, 529, 530f
in African Americans, 273 Imitrex. See sumatriptan adverse effects, 531, 532
angiotensin-converting enzyme inhibi- immune response, 375 hypoglycemia and, 532
tors, 274–275, 275t immunization (vaccination), 376 Nursing Process Focus, 533–534t
angiotensin-receptor blockers, 275t immunoglobulin (Ig), 375 types of, actions and administration,
calcium channel blockers, 278, 278t immunomodulator, 374 531, 531t
initial, 266t immunostimulants, 168, 376 insulin analogs, 531
Patients Need to Know, 284t immunosuppressants, 380, 381t insulin aspart, 531t
selection of drugs, 272–273 Imodium. See loperamide insulin-dependent diabetes mellitus. See type 1
vasodilators, 282–283, 283t implantable cardioverter defibrillators diabetes mellitus
primary, 267 (ICDs), 336 insulin detemir, 531t
secondary, 267 implementation phase, of nursing process, 52f, insulin glargine, 531t
hypertensive emergency, 283 55–56 insulin glulisine, 531t
Index 641
insulin isophane, 531t interactions Kineret. See anakinra

insulin lispro, 531t with amino-glycosides, 225t Klaron. See sulfacetamide sodium
insulin pump, 531, 532f with dopamine, 225t Klebsiella pneumoniae, 390t
insulin regular with epinephrine, 225t Klonopin. See clonazepam
actions and administration, 531t with levodopa, 225t K-Phos MF. See potassium/sodium phosphates
Drug Prototype, 532t with nitrous oxide, 225t K-Phos neutral. See potassium/sodium
insulin resistance, 534, 535 with phenothiazine, 225t phosphates
insulin(s) with systemic polymyxin, 225t K-Phos original. See potassium/sodium
interactions isoniazid phosphates
with aspirin, 208t Drug Prototype, 406t Krystexxa. See pegloticase
with carvedilol, 296t route and adult dose, 407t Kwell. See lindane
with furosemide, 254t isoproterenol, 97, 97t Kynamro. See mipomersan
with hydrochlorothiazide, 255t Isoptin. See verapamil
long-acting, administration, 33–34 Isopto Atropine. See atropine L
Integrilin. See eptifibatide Isopto Carpine. See pilocarpine labor, 552
interferon(s) (IFNs), 379, 380t Isopto Homatropine. See homatropine Lacri-lube. See lanolin alcohol
interferon alfa, 425 Isopto Hyoscine. See scopolamine LA (long-acting) medications, 27
interferon alfa-2b, 379t hydrobromide Lamictal. See lamotrigine
Drug Prototype, 446t isosorbide, 603t lamivudine, 419t, 425
route and adult dose, 445t isosorbide dinitrate lamotrigine, 135t, 185t, 190t
interferon alfacon-1, 379t actions, 291f, 296, 306 for bipolar disorder, 135, 135t
interferon alfa-n3, 379t in African Americans, 273 for seizures, 185t, 190t, 191
interferon beta-1a, 168, 168t, 379t clinical uses lanolin alcohol, 606t
interferon beta-1b, 168, 168t, 379t angina, 306t Lanoxicaps. See digoxin
interleukin(s), 379 heart failure, 295t, 296 Lanoxin. See digoxin
intermittent infusion, 37 route and adult dose, 306t lanreotide, 515t
International Classification of Epileptic isosorbide mononitrate, 306t lansoprazole, 482t
Seizures, 183 isotretinoin, 590t Lantus. See insulin glargine
International Diabetes Federation, 529 isradipine, 278t large-volume infusion, 37
international normalized ratio (INR), 352 Isuprel. See isoproterenol Lasix. See furosemide
International Union of Pure and Applied itraconazole, 414, 415t
latanoprost
Chemistry (IUPAC), 14 IUPAC (International Union of Pure and
interpersonal therapy, 124–125 Applied Chemistry), 14
intervention(s), 53 ivermectin, 426t, 587
laughing gas. See nitrous oxide
intracellular parasites, 418 IV (intravenous) route, 35t, 37
laxatives, 486–487, 487t, 492t
intractable pain, 201 Lazanda. See fentanyl
intradermal (ID) route, 33, 34t J L-carnitine, 66f
intramuscular (IM) route, 34t, 36
Januvia. See sitagliptin LDL (low-density lipoprotein), 236, 237f, 238t
intranasal corticosteroids, 462, 463t
juvenile-onset diabetes. See type 1 diabetes leflunomide, 576t
intraocular pressure (IOP), 601
mellitus lepirudin, 350f, 351, 351t
intravenous bolus (push) administration, 35t, 37
Juxtapid. See lomitapide leprosy, 406
intravenous (IV) route, 35t, 37 Lescol. See fluvastatin
intrinsic factor, 499t
Intropin. See dopamine
K letrozole, 444t
leukemia, 432
Invega. See paliperidone Kabikinase. See streptokinase
leukopenia, 436t
Inversine. See mecamylamine Kalcinate. See calcium gluconate
leukotriene modifiers, 470t
Invokana. See canagliflozin kanamycin, 399t
leukotriene(s), 364t
iodine, 516 Kaon Tablets. See potassium gluconate
leuprolide, 444t
IOP (intraocular pressure), 601 kappa receptors, 202, 202f, 202t
levalbuterol, 468t
Iopidine. See apraclonidine Kapvay. See clonidine
levamisole, 445t
ipratropium, 95t Kayexalate. See sodium polystyrene sulfate
Levemir. See insulin detemir
for asthma, 95t, 468t KCl. See potassium chloride
levetiracetam, 185t, 190t, 191
for nasal congestion, 464, 464t Kenalog. See triamcinolone; triamcinolone
Levitra. See vardenafil
Iprivask. See desirudin acetonide
levobunolol, 603t
irbesartan, 275t Keppra. See levetiracetam
levocetirizine, 460t
irinotecan, 442, 442t keratinization, 589
keratolytic agents, 590 levodopa
iron dextran, 502t
Kerlone. See betaxolol actions and uses, 163t
iron supplements, 501, 501t, 503t
Ketalar. See ketamine adverse effects, 163t
islets of Langerhans, 529, 529f
ketamine, 77, 226t, 227 Drug Prototype, 163t
Ismo. See isosorbide mononitrate
ketoacids, 530 interactions, 163t
Ismotic. See isosorbide
ketoconazole, 414, 415t with atropine, 95t
Isocaine. See mepivacaine
ketoprofen, 209t, 365t with diazepam, 188t
isocarboxazid, 127t
ketorolac, 209t with haloperidol, 149t
isoflurane, 225t
kidney(s) with isoflurane, 225t
anatomy, 249–250, 249f for parkinsonism, 160, 161t
clinical uses, 225t
functions, 249–250, 249f, 250f route and adult dose, 161t
642 Index
levodopa–carbidopa, 161t, 162, 176t monitoring, 134 lubricants, eye, 606t

Levo-Dromoran. See levorphanol as mood stabilizer, 134–135, 135t Ludiomil. See maprotiline
levofloxacin, 400t toxicity, 134–135 Lugol’s solution. See potassium iodide and
levonorgestrel, 547 U.S. approval for, 134 iodine
Levophed. See norepinephrine lithium toxicity, 134–135 lumefantrine/artemether, 426t
levorphanol, 204t Livalo. See pitavastatin lumen, 269
Levothroid. See levothyroxine liver fluke, 389f Lumigan. See bimatoprost
levothyroxine, 17t LMWHs (low molecular weight heparins), Luminal. See phenobarbital
levothyroxine 351, 351t. See also heparin Lusedra. See fospropofol
Drug Prototype, 518t local anesthesia, 218. See also local anesthetics luteinizing hormone (LH), 543
route and adult dose, 518t Nursing Process Focus, 223t Luvox. See fluvoxamine
Lexicaps. See escitalopram Patients Need to Know, 229t lymphocyte immune globulin, 381t
Lexapro. See escitalopram routes and methods, 218–219, 219f, 219t lymphocytes, 375
libido, 554 local anesthetics lymphoma(s), 432
Librium. See chlordiazepoxide actions, 220, 220f Lyrica. See pregabalin
lice, pharmacotherapy, 587 adverse effects, 222, 222t lysergic acid diethylamide (LSD), 70,
Lidex. See fluocinonide drugs classified as, 221t 76–77, 77f
lidocaine Lodosyn. See carbidopa effects of, 77
actions, 222t Lofibra. See fenofibrate street names of, 76
adverse effects, 222t lomitapide, 239t Lysteda. See tranexamic acid
clinical uses, 221t, 222, 222t lomustine, 437t
dysrhythmias, 338t long-acting (LA) medications, 27
Drug Prototype, 222t long-term insomnia, 110 M
epinephrine with, 220 Loniten. See minoxidil MAB (Monoclonal antibodies), 445
route and adult dose, 338t loop (high ceiling) diuretics, 252–253, MAC (Mycobacterium avium complex), 406
Life Span Facts, See Guide to Special Features 253f, 253t macrolides, 398–399, 398t
limbic system, 107 loop of Henle, 250, 250f magaldrate, 482t
linagliptin, 535t, 537 loperamide, 17t, 488t, 489 Magnaprin. See aspirin
lincomycin, 404t Lopid. See gemfibrozil magnesium, 501t
lindane, 587 lopinavir/ritonavir, 419t magnesium chloride, 502t
linezolid, 403, 404t Lopressor. See metoprolol magnesium hydroxide, 482t, 487t, 502t
liothyronine, 518t Lopressor HCT, 255 magnesium hydroxide and aluminum
liotrix, 518t Lopurin. See allopurinol hydroxide with simethicone, 482t
lipids, 235 loratadine, 460t magnesium oxide, 502t
elevated levels, preventing, 236–237 lorazepam magnesium sulfate, 502t, 553t
lipoproteins and, 236 actions, 116t Mag-Ox. See magnesium oxide
profile, 238t adverse effects, 116t major depressive disorder, 123. See also
role of, in diet, 235 clinical uses, 116t depression
types of, 235 as antiemetic, 490t criteria for diagnosis of, 124
Lipitor. See atorvastatin anxiety, 114t symptoms of, 124
lipoma(s), 432 intravenous anesthetic, 226t TCAs for, 125
lipoproteins, 236 muscle spasms, 170, 171t major minerals (macrominerals), 499, 501t
high-density, 236, 237f digoxin toxicity and, 116t Makena. See hydroxyprogesterone
low-density, 236, 237f Drug Prototype, 116t malaria, 426
very low-density, 236, 237f seizures, 185t, 187t, 188 malathion, 587
liposomes, 441t losartan, 275t malignant, 432
liquid medications, 26t Lotensin. See benazepril manic depression. See bipolar disorder
Liquifilm. See polyvinyl alcohol Lotrel, 273 mannitol, 257, 257t, 603t
liraglutide, 535t, 537 Lovasa. See omega-3-acid ethyl esters manual healing, 60t
lisinopril lovastatin, 239t MAO (monoamine oxidase), 128
actions, 291f, 292t “love drug.” See MDA (3,4-methylenedioxy- MAOI (monoamine oxidase inhibitor),
adverse effects, 292t amphetamine) 98t, 132
black box warning, 292t Lovenox. See enoxaparin Maox. See magnesium oxide
clinical uses low-density lipoprotein (LDL), 236, 237f, 238t maprotiline, 126t
heart failure, 292t, 293t lower respiratory tract (LRT), 455 MAR (medication administration record), 22,
hypertension, 275t low molecular weight heparin, 36 24, 25–26, 29, 37
myocardial infarction, 313 low molecular weight heparins (LMWHs), maraviroc, 419t
Drug Prototype, 292t 351, 351t. See also heparin Marcaine. See bupivicaine
interactions, 292t loxapine, 148t margin of safety, 4
route and adult dose, 275t, 293t Loxitane. See loxapine marijuana, 76, 202
lithium, 135t Lozol. See indapamide physical dependence or tolerance, 76
interactions LRT (lower respiratory tract), 455 physiological and psychological effects
with enalapril, 277t LSD (lysergic acid diethylamide), 70, of, 73t
with furosemide, 254t 76–77, 77f street names of, 76
with haloperidol, 149t effects of, 77 symptom of use of, 76
with hydrochlorothiazide, 255t street names of, 76 masculinization, 554
with sodium bicarbonate, 261t lubiprostone, 487t mast cell(s), 363
Index 643
mast cell stabilizer, 457f, 470t, 471 metered-dose inhalers (MDIs), 456 Mexitil. See mexiletine
mastoiditis, 606 metformin Miacalcin. See calcitonin–salmon
maturity-onset diabetes. See type 2 diabetes Drug Prototype, 537t micafungin, 415t
mellitus for type 2 diabetes, 535t Micardis. See telmisartan
Mavik. See trandolapril methadone, 75, 204t miconazole, 415t
Maxalt. See rizatriptan as maintenance treatment, 75, 206 Micronase. See glyburide
Maxiflor. See diflorasone for opioid withdrawal, 72, 206 Micronor. See norethindrone
MDA (3,4-methylenedioxyamphetamine), 77 withdrawal from, 75 Microsporum, 414t
MDIs (metered-dose inhalers), 456 methamphetamine, 70, 74, 78, 137, 138t microvilli, 478
MDMA (3,4-methylenedioxymethamphet- methazolamide, 257t, 603t Microzide. See hydrochlorothiazide
amine), 77 methcathinone, 78 Midamor. See amiloride
measles, mumps, and rubella (MMR) vaccine, methenamine, 402t midazolam, 74, 113
376, 377t Methergine. See methylergonovine midazolam hydrochloride, 226t, 228t
measurement systems, 24–25 methicillin-resistant Staphylococcus aureus midodrine, 97t
apothecary system, 25, 25t (MRSA), 392 Midol. See ibuprofen
household system, 25, 25t methimazole, 518t miglitol, 535t
metric system, 24–25, 25t methocarbamol, 171t migraine, 211
Mebaral. See mephobarbital methotrexate incidence, 199t
mebendazole, 426t, 427 clinical uses, 381t pharmacotherapy
mecamylamine, 175 psoriasis, 593t, 594 approach, 211
mecasermin, 515t rheumatoid arthritis, 576t prophylaxis, 211
mechanism of action, 13. See also pharmaco- Drug Prototype, 440t antiseizure drugs for, 212t
logic classification interactions beta-blockers for, 212t
mechlorethamine, 437t with aspirin, 208t calcium channel blockers for, 212t
meclizine, 490, 490t with vincristine, 443t methysergide for, 213t
medical diagnosis, 53 route and adult dose, 381t, 439t riboflavin for, 213t
medication administration record (MAR), 22, methscopolamine, 95t tricyclic antidepressants for, 213t
24, 25–26, 29, 37 methsuximide, 192t Migranal. See dihydroergotamine; dihydroer-
medication errors methyclothiazide, 254t gotamine mesylate
consequences of, 21 methylcellulose, 487t milk–alkali syndrome, 261t
Medrol. See methylprednisolone methyldopa, 97t Milk of Magnesia. See magnesium hydroxide
medroxyprogesterone actions, 281t milrinone
clinical uses for hypertension, 97t, 281t actions, 291f, 297t
as antineoplastic agent, 444t methylergonovine, 553t adverse effects, 297t
with conjugated estrogens, 551t Methylin. See methylphenidate clinical uses, 297t
Drug Prototype, 552t methylparaben, 222 Drug Prototype, 297t
route and adult dose, 551t methylphenidate interactions, 297t
mefenamic acid, 209t abuse of, 78 route and adult dose, 295t
megaloblastic (pernicious) anemia, 499 actions, 137t mind–body interventions, 60t
megestrol, 444t adverse effects, 137t mineralocorticoids, 520
melanocytes, 583 clinical uses, 78, 137t mineral oil, 17t, 487t
melatonin receptor drugs, 117t ADHD, 138t minerals, 500–501, 501t
Mellaril. See thioridazine Drug Prototype, 137t for pharmacotherapy, 502t
meloxicam, 209t, 365t methylprednisolone, 522t minimum effective concentration, 45
melphalan, 437t as antiemetic, 490t minipills. See progestin-only OC
memantine, 165, 165t for multiple sclerosis, 168t, 169 Minipress. See prazosin
memory B cells, 375 route and adult dose, 368t Miniprin. See aspirin
menopause, 124, 549 methyltestosterone, 555t Minocin. See minocycline
menorrhagia, 550 methysergide, 213t minocycline, 397t, 590t
menstrual cycle, 124 metipranolol, 603t minoxidil, 283t
meperidine, 204t metoclopramide, 486, 490t miosis, 601
mephobarbital, 116t, 186, 187t metolazone, 254, 254t Miostat. See carbachol
mepivacaine, 221t metoprolol, 281t, 295t, 306t miotics, 602, 602t
mercaptopurine, 439t actions, 282 mipomersan, 239t
meropenem, 404, 404t clinical uses, 100t mirabegron, 97t
mescaline, 77, 77f migraine prophylaxis, 212t Mirapex. See pramipexole
Mestinon. See pyridostigmine interaction with diazepam, 188t mirtazapine, 112t, 127t, 129
metabolic acidosis, 261t route and adult dose, 212t misoprostol, 485
metabolic alkalosis, 261t metric system of measurement, 24–25, 25t mitomycin, 441t
metabolism, 42f, 43 MetroCream. See metronidazole mitotane, 445t
biotransformation reactions and, 43 Metrogel. See metronidazole mitotic inhibitors, 442
drug therapy and, 43 metronidazole, 590t mitoxantrone
prodrugs and, 43 Drug Prototype, 427t for acute nonlymphocytic leukemia, 441t
Metadate. See methylphenidate for peptic ulcer disease, 485 for multiple sclerosis, 168t, 169
metaproterenol, 97t route and adult dose, 404t, 426t mitral stenosis, 303t
metastasis, 432 Mevacor. See lovastatin Mivacron. See mivacurium
metaxalone, 171t mexiletine, 201, 338t mivacurium, 176t, 228t, 229
644 Index
MMR (measles, mumps, and rubella) mu receptors, 202, 202f, 202t naltrexone, 204t
vaccine, 376 Murine Plus. See tetrahydrozoline Namenda. See memantine
Mobic. See meloxicam Muro 128 5% ointment. See sodium chloride NANDA (North American Nursing Diagnosis
modafinil, 168t, 169 hypertonicity ointment Association), 53
moexipril, 275t muromonab-CD3, 381t nandrolone, 555t
mometasone, 463t, 470t muscarinic blockers, 94 naphazoline, 464t, 606t
mometasone furoate, 592t muscarinic receptors, 90, 90f, 91t Naprelan. See naproxen
Monascus purpureus, 238t muscle rigidity, 159 Naprosyn. See naproxen
monoamine oxidase (MAO), 128 muscle spasms, 169 naproxen, 209t
monoamine oxidase inhibitors (MAOIs), causes, 169 actions, 366t
98t, 132 clonic spasms, 169 adverse effects, 366t
adverse effects, 113, 132 etiology of, 169–170 black box warning, 366t
clinical uses Fast Facts, 170t clinical uses, 365t, 366t
anxiety, 112t nonpharmacologic treatment, 169–170 Drug Prototype, 366t
depression, 127t Nursing Process Focus, 172–173t interactions, 366t
drugs classified as, 110, 125 Patients Need to Know, 176t route and adult dose, 365t
interactions, 113 pharmacotherapy, 170 naproxen sodium, 209t
with benztropine, 164t tonic spasm, 169 actions, 366t
with carvedilol, 296t treatment of, 169–170 adverse effects, 366t
with diphenhydramine, 460t mutations, 391 black box warning, 366t
with diphenoxylate with atropine, 488t myasthenia gravis, 92t clinical dose, 209t, 365t, 366t
with dopamine, 326t prednisone interactions in, 369t Drug Prototype, 366t
with epinephrine, 327t Mycobacterium avium complex (MAC), 406 interactions, 366t
with methylphenidate, 137t Mycobacterium bovis, 379 route and adult dose, 209t, 365t
with morphine, 203t Mycobacterium leprae, 390t, 406 naratriptan, 212t
with phenylephrine, 98t Mycobacterium tuberculosis, 390t, 406 Narcan. See naloxone
with propranolol, 340t mycophenolate, 381t narcolepsy, 78
with sertraline, 133t mycoses, 413, 414t narcotics, 201–202
with sumatriptan, 213t Mydfrin. See phenylephrine Nardil. See phenelzine
Patients Need to Know, 139t Mydriacyl. See tropicamide Naropin. See ropivacaine
serotonin syndrome and, 113 mydriasis, 601 narrow-spectrum antibiotic, 393
Monoclonal antibodies (MAB), 445 mydriatic drugs, 605, 606t nasal administration, 30t, 31. See also transmu-
Monoket. See isosorbide mononitrate Myobloc. See rimabotulinumtoxin B cosal administration
monophasic OC, 546, 546t myocardial infarction (MI), 303t, 310, 347t nasogastric tubes, 26t, 28
Monopril. See fosinopril pathophysiology, 310, 311f Natazia. See quadriphasic OC
montelukast, 470t pharmacotherapy nateglinide, 536t
mood disorders, 123, 124, 125, 137. See also goals, 310 National Center for Complementary and
bipolar disorder; depression thrombolytics, 310, 312t. See also Alternative Medicine (NCCAM), 7, 61
electroconvulsive therapy (ECT) and, 125 thrombolytics National Cholesterol Education Program
perinatal, 124 of symptoms and complications, 312–313 (NCEP), 236, 237
mood stabilizers, 134, 135t. See also lithium myocardial ischemia, 302 National Formulary (NF), 5, 6f
morphine myoclonic seizures, 184 National Institutes of Health, 236
actions, 203t Myolin. See orphenadrine Natrecor. See nesiritide
adverse effects, 203t Myrbetriq. See mirabegron natriuretic peptide (hBNP), 297
black box warning, 203t Mysoline. See primidone Natural Alternatives, 4
clinical uses, 203t, 204t Mytelase. See ambenonium natural alternative therapies, 4
Drug Prototype, 203t myxedema, 516 characteristics of, 4t
interactions nausea and vomiting, 489–490, 490t
with monoamine oxidase inhibitors N Navane. See thiothixene
(MAOIs), 203t NCCAM (National Center for Complementary
Na+ (sodium ions), 220, 220f
with tricyclic antidepressants and Alternative Medicine), 7, 61
nabumetone, 209t, 365t
(TCAs), 203t NCEP (National Cholesterol Education
nadolol, 100t, 281t, 306t
route and adult dose, 204t Program), 236
nafcillin, 394t
motion sickness, 461, 489 NDA (new drug application), 6f, 7–8, 9
naftifine, 415t
Motrin. See ibuprofen nebulizers, 456
NaHCO3. See sodium bicarbonate
Mountain Dew, 79t nedocromil sodium, 470t, 471
nalbuphine, 204t
moxifloxacin, 400t nefazodone, 127t, 129
Nalfon. See fenoprofen
MRSA (methicillin-resistant Staphylococcus negative formulary, 16
nalidixic acid, 400t, 402t
aureus), 392 negative symptoms, of schizophrenia, 144
naloxone
mucolytics, 457f, 465 Neisseria gonorrhoeae, 390t
actions, 202, 205t
Multaq. See dronedarone Neisseria meningitidis, 390t
multicellular parasites, 389f nelarabine, 439t
black box warning, 205t
multiple sclerosis, 158t, 167 nelfinavir, 419t
clinical uses, 204t, 205t
drugs for treating, 168t Nembutal. See pentobarbital
etiology of, 167–168 neomycin, 399t
interactions, 205t
relapsing-remitting MS (RRMS), 168 neoplasm, 432
symptoms of, 167–168 neostigmine, 92, 92t
Index 645
interactions cardiovascular effects of, 80 nondepolarizing blockers, 175, 176t, 229. See
with bethanechol, 93t dependence, 80 also neuromuscular blocking drugs
Neo-Synephrine. See phenylephrine effects, 80 nonnucleoside reverse transcriptase inhibitors
nephron(s), 249–250, 250f nicotine replacement therapy (NRT) and, (NNRTIs), 419t, 420
nephrotoxicity, 400 72 nonopioid analgesics
Neptazane. See methazolamide Patients Need to Know, 80t acetaminophen. See acetaminophen
nerve agents, 92 physiological and psychological effects centrally acting, 210
nervous system, 87, 88f of, 73t nonsteroidal anti-inflammatory drugs. See
autonomic, 87 symptoms of withdrawal of, 72 nonsteroidal anti-inflammatory drugs
basic functions of, 87 withdrawal syndrome, 72 (NSAIDs)
central. See central nervous system (CNS) nicotinic blocking drugs, 175 nonphenothiazines
peripheral. See peripheral nervous system nicotinic receptors, 90, 90f adverse effects, 148
(PNS) nifedipine, 553t drugs classified as, 146, 146t
somatic, 87 actions, 279t Nursing Process Focus, 149–151t
Nesacaine. See chloroprocaine adverse effects, 279t route and adult dose, 148t
nesiritide, 295t, 297 clinical uses, 279t nonsteroidal anti-inflammatory drugs
neuroamidase inhibitors, 424 angina, 306t (NSAIDs), 8
neurodegenerative diseases, 158t migraine prophylaxis, 212t actions, 208
Alzheimer’s disease. See Alzheimer’s Drug Prototype, 279t adverse effects, 208
disease interactions, 279t clinical uses, 208
amyotrophic lateral sclerosis (ALS). See route and adult dose, 212t, 278t, 306t drugs classified as
amyotrophic lateral sclerosis (ALS) nilutamide, 444t aspirin and salicylates, 209t, 365t, 366
Fast Facts, 159t Nimbex. See cisatracurium ibuprofen and ibuprofen-like drugs,
Huntington’s chorea. See Huntington’s nimodipine, 212t 209t, 365t, 366
chorea Nimotop. See nimodipine selective COX-2 inhibitors, 209t, 210f,
multiple sclerosis. See multiple sclerosis Nisocor. See nisoldipine 365t, 366
Parkinson’s disease. See Parkinson’s nisoldipine, 278t interactions
disease Nitro-Bid. See nitroglycerin with alteplase, 357t
neurofibrillary tangles, 164 Nitro-Dur. See nitroglycerin with aspirin, 208t
neurogenic shock, 320, 320t. See also shock nitrofurantoin, 402t, 487t with cefotaxime, 396t
neurohypophysis. See posterior pituitary nitrogen mustards, 435 with clopidogrel, 356t
neuroleptanalgesia, 227 nitroglycerin with enalapril, 277t
neuroleptic malignant syndrome, 147t actions, 307t with lisinopril, 292t
neuroleptic(s), 146. See also antipsychotics adverse effects, 307t with methotrexate, 440t
neuromuscular blocking drugs, 175, 176t clinical uses, 307t with warfarin, 353t
actions, 175 angina, 306t and nociceptors, 200
classification, 175 Drug Prototype, 307t Nursing Process Focus, 367t
clinical uses, 175, 176t interactions, 307t Patients Need to Know, 383t
as adjunct to anesthetics, 227, 228t Nursing Process Focus, 308t Patients Need to Know, 370t
depolarizing blockers, 175, 176t Patients Need to Know, 315t usage statistics, 363t
drugs classified as, 176t, 228t route and adult dose, 306t Norcuron. See vecuronium
nondepolarizing blockers, 175, 176t Nitropress. See nitroprusside Norditropin. See somatropin
Patients Need to Know, 176t nitroprusside, 283, 283t norepinephrine, 88, 90f, 91t
neuron, 88 Nitrostat. See nitroglycerin actions, 98t, 326t
postsynaptic, 88 nitrous oxide adverse effects, 326t
presynaptic, 88 actions, 225t black box warning, 326t
Neurontin. See gabapentin adverse effects, 225t clinical uses, 98t
neuropathic pain, 198 clinical uses, 225t shock, 325, 326t
types of, 199t Drug Prototype, 225t Drug Prototype, 326t
neurotransmitter(s), 88, 91t interactions interactions, 326t
acetylcholine (Ach), 88, 91t with isoflurane, 225t route and adult dose, 325t
false, 282 nits, 587 norethindrone, 546, 551t. See also estrogen-
norepinephrine (NE), 88, 91t Nix. See permethrin progestin oral contraceptives
in pain transmission, 199–200, 200f nizatidine, 482t Norflex. See orphenadrine
Neutra-Phos-K. See potassium/sodium phos- NMDA (N-methyl-D-aspartate) receptors, 165 norfloxacin, 400t
phates N-methyl-D-aspartate (NMDA) receptors, 165 Norlutin. See norethindrone
Neutrogena. See salicylic acid NNRTIs (nonnucleoside reverse transcriptase normal serum albumin
nevirapine, 419t inhibitors), 419t, 420 actions, 323t
new drug application (NDA), 6f, 7–8, 9 nociceptor pain, 198, 210f adverse effects, 323t
NF (National Formulary), 5, 6f nodules, 589 clinical uses, 323t
niacin (vitamin B3), 498t Nolvadex. See tamoxifen Drug Prototype, 323t
as lipid-lowering agent, 239t, 242, 245t nonbenzodiazepine, nonbarbiturate CNS interactions, 323t
Niacor. See niacin (vitamin B3) agents Norpace. See disopyramide
Niaspan. See niacin (vitamin B3) for anxiety and insomnia, 117–118, 117t Norpramin. See desipramine
nicardipine, 278t, 306t drugs classified as, 110 Nor-Q.D. See norethindrone
nicotinamide, 242 noncompliance, 22–23, 53 North American Nursing Diagnosis
nicotine, 90 Association (NANDA), 53
646 Index
nortriptyline, 112t, 126t, 201 oligomenorrhea, 550 interactions

Norvasc. See amlodipine olmesartan, 275t with antiseizure drugs, 182, 185
nosocomial infections, 392 olopatadine, 460, 460t with diazepam, 188t
Novantrone. See mitoxantrone omega-3-acid ethyl esters, 239t, 244 with imipramine, 129t
Novastan. See argatroban omega-3 fatty acids, 235, 237, 244, 534 with phenytoin, 190t
Novocain. See procaine omeprazole with tetracycline, 397t
Novolin N. See insulin isophane Drug Prototype, 483t Nursing Process Focus, 548–549t
Novolin R. See insulin regular route and adult dose, 482t Oralet. See fentanyl
NovoLog. See insulin aspart onabotulinumtoxin A, 173, 174t, 213, 213t oral hypoglycemics
NPH. See insulin isophane ondansetron, 229, 490t interactions
NRTIs (nucleotide reverse transcriptase actions, 490t with aspirin, 208t
inhibitors), 419t adverse effects, 490t with carvedilol, 296t
Nubain. See nalbuphine Drug Prototype, 490t Orap. See pimozide
nucleoside reverse transcriptase inhibitors interactions, 490t Orazinc. See zinc sulfate
(NRTIs), 419t Onglyza. See saxagliptin Orencia. See abatacept
Nupercainal. See dibucaine onset of drug action, 45 organic nitrates
Nuprin. See ibuprofen Onsolis. See fentanyl adverse effects, 307
nurse(s) Opana. See oxymorphone for angina, 305–306, 306t
diagnosis by, 53 open-angle glaucoma, 600f, 601. See also drugs classified as, 306t
licensed practical nurse (LPN), 51 glaucoma Patients Need to Know, 315t
licensed vocational nurse (LVN), 51 open comedones, 589 organophosphate insecticides, 92
registered nurse (RN), 51 ophthalmic administration, 29, 29f, 30t organ transplants, 380
substance abuse in, 81 Ophthetic. See proparacaine Orinase. See tolbutamide
nursing diagnosis, 52f, 53, 54t opiates, 201. See also opioid (narcotic) anal- orlistat, 491
nursing process, 51–58 gesics orphenadrine, 171t
assessment phase, 52–53, 52f interactions with phenelzine, 133t orthostatic hypotension, 125, 132, 282
diagnosis, 52f, 53, 54t opioid agonists, 203 Orudis. See ketoprofen
evaluation phase, 52f, 56–57 with high effectiveness, 204t Os-Cal. See calcium carbonate
implementation phase, 52f, 55–56 mixed agonist-antagonist, 204t oseltamivir, 424, 424t
patient teaching in, 54, 55–56, 55t with moderate effectiveness, 204t Osmitrol. See mannitol
planning phase, 52f, 53–55 opioid (narcotic) analgesics. See also narcotics Osmoglyn. See glycerin
Nursing Process Focus. See Guide to Special abuse of, 70, 71, 73 osmotic diuretics, 257
Features actions, 203 clinical uses, 257
Nutropin. See somatropin clinical uses drugs classified as, 257, 257t
nystatin adjuncts to anesthesia, 228t for glaucoma, 603t, 604
Drug Prototype, 416t drugs classified as osteitis deformans. See Paget’s disease
route and adult dose, 415t agonists with high effectiveness, 204t osteoarthritis (OA), 574, 575
Nytol. See diphenhydramine agonists with moderate effectiveness, osteoclasts, 565
204t osteomalacia
combination drugs, 205 cause of, 566
O intravenous anesthetics, 226t description, 566
obesity, 529 mixed agonist-antagonist, 204t pharmacotherapy
objective data, 52 Nursing Process Focus, 206–207t calcium salts, 567–568, 568t
obsessive-compulsive disorder (OCD), 106 Patients Need to Know, 214t vitamin D supplements, 567, 568, 568t
OC (oral contraceptives). See oral opioid antagonists, 205 signs and symptoms of, 567
contraceptives (OC) opioid(s), 72, 75, 201. See also opioid osteoporosis, 501
octreotide, 489t, 514t, 515t, 516 (narcotic) analgesics calcium metabolism in, 570f
OcuClear. See oxymetazoline acute intoxication, 205 description, 569
Ocufen. See flurbiprofen addiction to, 75 Nursing Process Focus, 572–573t
Ocupress. See carteolol adverse effects, 203 pharmacotherapy
Ocusert. See pilocarpine effects of oral, 75 bisphosphonates, 571t, 572
odansetron, 436 endogenous, 199–200 calcitonin, 570
ofatumumab, 445t physiological and psychological effects selective estrogen-receptor modulators
off-label medications, 201 of, 73t (SERMs), 570, 571t
off-label use, of drugs, 9 receptors, 202, 202f, 202t risk factors for, 569, 570
ofloxacin, 400t withdrawal from, 75 OTC (over-the-counter) drugs, 4–5, 7
Ogen. See estropipate withdrawal syndrome, 72 otic administration, 30t, 31
olanzapine, 151t, 154, 166 oprelvekin, 379, 446 otic preparations, 607t
older adults OptiPranolol. See metipranolol otitis externa, 606
bleeding complications in, 352t oral anticoagulants, 352. See also anticoagu- otitis interna, 606
blood pressure control in, 271t lants; warfarin otitis media, 606
constipation in, 486t oral contraceptives (OC), 546–547 ototoxicity, 400
epilepsy in, 183t adverse effects, 546 outcome (goal), 54
laxative misuse in, 486t alternative formulations, 547 overproductive oil glands, 589
medication-related sleep problems in, 110t emergency contraception, 547 over-the-counter (OTC) drugs, 4–5, 7
tricyclic antidepressant use in, 125t estrogen–progestin, 546, 546t Ovide. See malathion
Oleptro. See trazodone formulation types, 546, 546t ovulation, 543
Index 647
oxacillin, 393, 394t parasympathomimetics (cholinergic drugs), 91 PediaCare Children’s Allergy. See
oxaliplatin, 437t actions, 92 diphenhydramine
Oxandrin. See oxandrolone clinical uses pediculicides, 587
oxandrolone, 555t as adjunct to anesthetics, 228t Pediculus, 587
oxaprozin, 209t, 365t drugs classified as, 163, 163t, 228t Peganone. See ethotoin
oxazepam, 114, 114t Nursing Process Focus, 96t pegaspargase, 445t
oxazolidinones, 403 Patients Need to Know, 102t peginterferon, 425
oxcarbazepine, 185t, 189, 190t parathyroid hormone (PTH), 565–566, 566f peginterferon alfa-2a, 379t
Oxecta. See oxycodone Parcopa. See levodopa–carbidopa PEG-L-asparaginase, 445t
oxiconazole, 415t Pardryl. See diphenhydramine pegloticase, 577, 577t
oxybutynin, 95t parenteral anticoagulants, 350–352 pegvisomant, 515t
oxycodone, 75, 215t parenteral route, 32–39 pemetrexed, 439t
oxycodone terephthalate, 204t intradermal, 33, 34t penciclovir, 424t
OxyContin. See oxycodone intramuscular, 34t, 36 penicillinase, 393
oxymetazoline, 606t intravenous, 35t, 37, 38f action of, 394f
clinical uses, 97t subcutaneous, 33–34, 34t penicillinase-resistant penicillins, 393
Drug Prototype, 464t paricalcitol, 568t penicillin G benzathine, 394t
route and adult dose, 464t parkinsonism, 147t, 148, 159. See also Parkin- penicillin G procaine, 394t
oxymetholone, 17t, 555t son’s disease penicillin G sodium/potassium
oxymorphone, 204t Parkinson’s disease, 158t, 159 Drug Prototype, 395t
oxytocics, 552 characteristics, 160 route and adult dose, 394t
oxytocin extrapyramidal symptoms (EPS) in, 160 penicillin(s), 17t
Drug Prototype, 553t incidence, 159 actions, 393, 394f
for labor, 552 Patients Need to Know, 176t adverse effects, 395
route and adult dose, 553t pharmacotherapy, 163 drugs classified as, 394t
anticholinergics, 163, 163t. See also fixed-dose combinations, 395
anticholinergics interactions
P dopaminergic agents, 160–162, 161t with aspirin, 208t
Pacerone. See amiodarone symptoms, 159–160 with cholestyramine, 240t
paclitaxel, 442, 442t affective flattening, 160 Patients Need to Know, 409t
Paget’s disease, 573–574 bradykinesia, 159 penicillin V, 394t
pain, 198 muscle rigidity, 159 Pentalair. See cyclopentolate
assessment, 198 postural instability, 160 pentamidine, 426t
CAM Therapy, 211t tremors, 159 pentazocine, 202, 204t
classification, 198 Parlodel. See bromocriptine pentobarbital, 116t
incidence, 199t Parnate. See tranylcypromine pentostatin, 439t
mechanisms, 210f paromomycin, 399t, 426t pentoxifylline, 350f, 351t, 352
nonpharmacologic management, 200–201 paroxetine, 112t peptic ulcer disease, 479
Patients Need to Know, 214t for anxiety disorders, 112t causes, 479, 479f
transmission, 199–200, 200f for depression, 126t natural defenses against, 479–480, 480f
pain-reducing drugs, 70 partial (focal) seizures, 183. See also nonpharmacologic therapy, 481
paliperidone, 151t seizure(s) Nursing Process Focus, 484t
palliation, 433 complex partial seizures, 183 Patients Need to Know, 492f
Pamelor. See nortriptyline simple partial seizures, 183 pharmacotherapy, 481f, 485–486
pamidronate, 571t passive immunity, 376, 378f antacids, 482t, 485
Pamine. See methscopolamine pathogen(s), 389, 389f antibiotics, 485
pancreas bacterial, 390t H2-receptor blockers, 482t, 483
endocrine function, 529, 529f fungal, 414t proton-pump inhibitors, 482, 482t
exocrine function, 529 protozoan, 425 risk factors, 479
pancreatic enzymes, 492 viruses, 417–418 symptoms, 479–480
pancreatic insufficiency, 492 pathogenicity, 389 Percocet, 205
pancrelipase, 492 pathophysiology, 3 Percocet-5. See oxycodone terephthalate
panic disorder, 106 patient adherence. See compliance Percodan, 205
benzodiazepines for, 113 patient-controlled analgesia (PCA), 216 percutaneous transluminal coronary angio-
characteristics of, 106 Patients Need to Know. See Guide to Special plasty (PTCA), 304
pantoprazole, 482t Features performance anxiety, 106
pantothenic acid (vitamin B5), 498t patient teaching perfusion, 455
papules, 589 adult and, 55t perindopril, 275t
Paraflex. See chlorzoxazone children and, 55t peripheral edema, 289
parafollicular cells, 516 implementation, 55–56 peripheral nervous system (PNS), 87, 88f
Parafon Forte. See chlorzoxazone in nursing process, 54, 55–56, 55t basic divisions of, 88f
paranoia, 143 older adults and, 55t cholinergic drugs and, 92
parasympathetic nervous system, 87 planning, 54 peripheral resistance, 269
activation of, 91 Paxil. See paroxetine peristalsis, 478
effects of, 89f pazopanib, 445t permethrin, 587
inhibition of, 91 PCP (phencyclidine), 70, 77 Drug Prototype, 587t
rest-and-digest response and, 87 peak plasma level, 46, 46f pernicious (megaloblastic) anemia, 499
648 Index
perphenazine, 146t, 490t decongestant, 464t Plan B One Step. See levonorgestrel
Persantine. See dipyridamole shock, 325, 325t planning phase, of nursing process, 52f, 53–55
pertuzumab, 445t Drug Prototype, 98t plant extracts, 442–443, 442t
petit mal epilepsy, 183 route and adult dose, 325t plaque, 235
petit mal seizures, 183. See also absence Phenytek. See phenytoin arterial, 302, 303f
seizures phenytoin, 185t Plaquenil. See hydroxychloroquine
pH, 260 actions, 190t plaques
pharmaceutics, 5 adverse effects, 190t in psoriasis, 593
pharmacists, 5 approved as a drug, 189t plasma cells, 375
pharmacodynamics, 46 clinical uses, 190t plasma half-life, 45
pharmacokinetics, 42, 42f dysrhythmias, 338t plasmids, 392
pharmacologic classification, 13–14, 14t. seizures, 185t plasmin, 349
See also mechanism of action Drug Prototype, 190t plasminogen, 349
pharmacology, 3 hematologic toxicities and, 189 Plasmodium, 426
pharmacopoeia, 5 interactions, 190t Plavix. See clopidogrel
pharmacotherapeutics, 3 with aspirin, 208t Plendil. See felodipine
pharmacotherapy with calcium supplements, 190t Pletal. See cilostazol
common nursing diagnoses in, 54t with cyclophosphamide, 438t PMS (premenstrual syndrome), 550
diagnosis phase of the nursing process with diazepam, 188t pneumococcal 7-valent vaccine, 377t
and, 53 with digoxin, 190t pneumococcal polyvalent vaccine, 377t
pharmacy, 5 with donepezil, 167t Pneumococcus, 390t
phencyclidine (PCP), 70, 77 with dopamine, 326t Pneumocystis jiroveci, 414t
phenelzine with doxorubicin, 441t polarized, 335
actions, 133t with doxycycline, 190t poliovirus vaccine, 377t
adverse effects, 133t with estrogens, 190t Polocaine. See mepivacaine
anxiety disorders, 112t with ethosuximide, 192t polymyxin B, neomycin, and hydrocortisone,
clinical uses, 133t with folic acid, 190t 607t
depression, 127t with furosemide, 190t polyvinyl alcohol, 606t
Drug Prototype, 133t with glucocorticoids, 190t Ponstel. See mefenamic acid
interactions with H2 antagonists, 190t Pontocaine. See tetracaine
with herbal supplements, 133t with haloperidol, 149t posaconazole, 415t
with meperidine, 133t with omeprazole, 483t positive feedback, 552
phenobarbital, 185t with oral anticoagulants, 190t positive symptoms, of schizophrenia, 144
actions, 188t with oral contraceptives, 190t posterior pituitary, 511, 514, 515t. See also
adverse effects, 188t with oral theophylline, 190t pituitary gland
antiseizure properties of, 186 with prednisone, 369t postmarketing studies. See postmarketing
clinical uses, 188t with valproic acid, 191t surveillance
route and adult dose, 187t with vitamin D, 190t postmarketing surveillance, 8–9, 8f
sedation and insomnia, 116t route and adult dose, 189t, 338t postmenopausal bleeding, 550
seizures, 185t phobias, 106 postpartum depression, 124
Drug Prototype, 188t PhosLo. See calcium acetate postsynaptic neuron, 88
interactions, 188t phosphodiesterase, 297 post-traumatic stress disorder (PTSD), 106,
with aspirin, 208t phosphodiesterase-5 (PDE-5) inhibitors, 556 111
with chlorpromazine, 147t phosphodiesterase inhibitors postural instability, 160
with cyclophosphamide, 438t actions, 297 Posture. See calcium phosphate tribasic
with donepezil, 167t drugs classified as, 295t potassium, 501t
with doxorubicin, 441t for heart failure, 295t, 297 potassium channel blockers, 340, 340t
with haloperidol, 149t Phospholine iodide. See echothiophate iodide potassium chloride, 17t, 502t
with valproic acid, 191t phosphorus, 501t actions, 260t
phenothiazines and phenothiazine-like drugs photosensitivity, 398 adverse effects, 260t
adverse effects, 147t physical dependence, 16, 17t, 72 clinical uses, 260t
clinical uses physostigmine, 92, 92t Drug Prototype, 260t
as adjuncts to anesthesia, 228t pill-rolling behavior, 159 interactions, 260t
drugs classified as, 146t pilocarpine, 92t, 602t potassium gluconate, 17t
interactions Pilopine. See pilocarpine potassium imbalances. See hyperkalemia;
with atropine, 95t pimozide, 148t hypokalemia
with benztropine, 164t pindolol, 281t potassium iodide and iodine, 518t
with cyclobenzaprine, 171t pioglitazone, 536t potassium ion channels, 335, 336f
with isoflurane, 225t pipecuronium, 176t potassium/sodium phosphates, 502t
with succinylcholine, 228t piperacillin, 393, 394t potassium-sparing diuretics, 255–256
long-term use of, 148 piperacillin/tazobactam, 394t actions, 253f
Nursing Process Focus, 149–151t pirbuterol, 468t defined, 274
phentolamine, 100t piroxicam, 209t, 365t drugs classified as, 256t
phenylephrine, 97, 97t, 606t pitavastatin, 239t interactions
actions, 98t Pitocin. See oxytocin with enalapril, 277t
adverse effects of, 98t pituitary gland, 511, 513f potency, of drugs, 47, 48f
clinical uses, 98t Plan B. See levonorgestrel Potiga. See ezogabine
Index 649
PPIs (proton-pump inhibitors), 481f, 482, 482t prn order, 23 propylthiouracil, 513
Pradaxa. See dabigatran ProAmatine. See midodrine as an antihormone, 513
pralatrexate, 439t Probalan. See probenecid Drug Prototype, 519t
pramipexole, 161–162, 161t Pro-Banthine. See propantheline route and adult dose, 518t
pramoxine, 221t probenecid, 577t Proquad, 377t
Prandin. See repaglinide procainamide Proscar. See finasteride
prasugrel, 355t, 356 actions, 339t prostaglandins, 208, 552
Pravachol. See pravastatin adverse effects, 339t for glaucoma, 601, 602, 602t
pravastatin, 239t black box warning, 339t in pain and inflammation, 210f, 364t
praziquantel, 426t clinical uses, 339 Prostigmin. See neostigmine
prazosin, 100t dysrhythmias, 338t Prostin E2. See dinoprostone
actions, 100t, 282 Drug Prototype, 339t protamine sulfate, 350
adverse effects of, 100t interactions, 339t protease inhibitors, 419t, 420
clinical uses, 100t with atropine, 95t Proteus mirabilis, 390t
hypertension, 281t with benztropine, 164t prothrombin, 347
Drug Prototype, 100t with bethanechol, 93t prothrombin activator, 347
interactions route and adult dose, 338t prothrombinase. See prothrombin activator
with antihypertensives, 100t procaine, 221t, 222 prothrombin time (PT), 352
with diuretics, 100t procarbazine, 445t proton-pump inhibitors (PPIs), 481f,
route and adult dose, 281t Procardia. See nifedipine 482, 482t
preclinical investigation, 7, 8f Procardia XL. See nifedipine prototype drug, 13
Precose. See acarbose Prochieve. See progesterone See also Drug Prototypes in Guide to Special
prednicarbate, 592t prochlorperazine, 146t Features
prednisolone, 368t, 522t as antiemetic, 436, 490t protozoan(s), 389f, 425, 427t
prednisone as antipsychotic, 146t protriptyline, 126t, 213t
actions, 369t route and adult dose, 146t, 490t Proventil. See albuterol
adverse effects, 369t prodrugs, 43 Provera. See medroxyprogesterone
as antineoplastic agent, 444t product name, 14 Provigil. See modafinil
clinical uses, 369t progesterone, 544, 551t provitamins, 497
Drug Prototype, 369t progestin-only OC, 546t, 547. See also proximal tubule, 250, 251, 253f
interactions, 369t estrogen-progestin oral contraceptives Prozac. See fluoxetine
with vincristine, 443t proguanil/atovaquone, 426t pseudoephedrine, 97, 97t, 460t, 463, 464t
route and adult dose, 368t, 522t prolactin, 552 Pseudomonas aeruginosa, 390t
pre-eclampsia, 183 Prolia. See denosumab psilocybin, 76, 77f
Prefest. See estradiol with norgestimate Proloid. See thyroglobulin psoralens, 594
pregabalin, 185t, 187t, 189, 201 promethazine psoriasis, 593–594, 593t
pregnancy as antiemetic, 490t psychedelics, 76. See also hallucinogens
drug safety categories, 17 as antihistamine, 459t psychodynamic therapies, 125
herbal products and, 63–64 Prometrium. See progesterone psychological dependence, 16, 17t, 72
preload, 289, 304 propafenone, 338t psychologically dependent individual, 16
Prelone. See prednisolone propantheline, 95t psychomotor seizures, 183. See also complex
Premarin. See estrogen, conjugated proparacaine, 221t, 222 partial seizures; seizure(s)
premature atrial contractions, 333t Propine. See Dipivefrin HCl psychosis
premature ventricular contractions (PVCs), Propionibacterium acnes, 589 acute, 143
333t propofol, 226t chronic, 143
premenstrual dysphoric disorder, 133t adverse effects, 227t Fast Facts, 144t
premenstrual syndrome (PMS), 550 clinical uses, 227t incidence, 143
premenstrual syndrome, dong quai for, 549t Drug Prototype, 227t pharmacotherapy, 146. See also antipsy-
Premphase. See conjugated estrogens with interactions chotics
medroxyprogesterone with benzodiazepines, 227t signs and symptoms, 143
Prempro. See conjugated estrogens with me- with opioids, 227t psychotic depression, 124
droxyprogesterone propranolol psyllium mucilloid
Prepidil. See dinoprostone actions, 340t Drug Prototype, 487t
prescription drugs, 4, 5 adverse effects, 340t route and adult dose, 487t
Prescription Drug User Fee Act, 6f, 9 black box warning, 340t PT (prothrombin time), 352
presynaptic neuron, 88 clinical uses, 100t, 340t PTCA (percutaneous transluminal coronary
preterm labor, 552 angina, 306t angioplasty), 304
Prialt. See ziconotide anxiety, 111, 117t PTH (parathyroid hormone), 565–566, 566f
prilocaine, 221t dysrhythmias, 339t PTSD (post-traumatic stress disorder), 106,
primaquine, 426 hypertension, 281t 111
primary adrenocortical insufficiency, 521 migraine prophylaxis, 212t PTU. See propylthiouracil
primary gout, 576. See also gout Drug Prototype, 340t Public Health Service Act, 6f
primary hypertension, 267 interactions, 340t pulmonary embolus, 347t
primary hypogonadism, 554 Patients Need to Know, 343t Pure Food and Drug Act of 1906, 5, 6f
primidone, 185t, 186, 187t route and adult dose, 212t, 281t, purine(s), 439
Prinivil. See lisinopril 306t, 339t purine analogs, 439t
Prinzmetal’s (vasospastic) angina, 303, 309 proprietary name, 14 Purkinje fibers, 333, 334f
650 Index
pustules, 589 red-man syndrome, 403 Riomet. See metformin

PUVA (psoralen plus ultraviolet light) therapy, reflex tachycardia, 270, 283, 326 risedronate, 571t
594 Refludan. See lepirudin Risperdal. See risperidone
PVCs (premature ventricular contractions), regional anesthesia, 218–219, 219f, 219t risperidone
333t Regonol. See pyridostigmine actions, 152t
P wave, 334f Relafen. See nabumetone adverse effects, 152t
pyrantel, 426t, 427 relapsing-remitting multiple sclerosis (RRMS), clinical uses, 152t, 166
pyrazinamide, 407t 168. See also multiple sclerosis Drug Prototype, 152t
pyrethrin, 587 releasing hormones, 511 interactions, 152t
pyridostigmine, 92, 92t ReliOn N. See insulin isophane with chamomile, 152t
pyridoxine (vitamin B6), 498t Relpax. See eletriptan with valerian, 152t
pyrimethamine, 426t Remeron. See mirtazapine route and adult dose, 151t
pyrimidine(s), 439 Remicade. See infliximab Ritalin. See methylphenidate
pyrimidine analogs, 439t remifentanil, 204, 226t, 228t ritonavir/lopinavir, 419t
Reminyl. See galantamine Rituxan. See rituximab
Q renal failure, 250t, 251–252 rituximab, 445t, 576t
renin-angiotensin-aldosterone system (RAAS), rivaroxaban, 351t, 352
QRS complex, 334f
274–275 rivastigmine, 92, 92t, 165, 165t
quadriphasic OC, 546
ReoPro. See abciximab rizatriptan, 212t
quazepam, 114t
repaglinide, 536t Robaxin. See methocarbamol
Questran. See cholestyramine
repetitive transcranial magnetic stimulation Robinul. See glycopyrrolate
quetiapine, 135t, 151t
(rTMS), 125 Rocaltrol. See calcitriol
Quillivant XR. See methylphenidate
Requip. See ropinirole rocuronium, 176t
Quinamm. See quinine sulfate
respiration, 455 rofecoxib, 8, 366
quinapril, 275t, 293t
respiratory acidosis, 261t Rohypnol. See flunitrazepam
Quinidex. See quinidine sulfate
respiratory alkalosis, 261t Rolaids. See calcium carbonate
quinidine sulfate, 338, 338t
respiratory disorders ropinirole, 161–162, 161t
quinine sulfate, 175
allergic rhinitis. See allergic rhinitis ropivacaine, 221t
quinupristin/dalfopristin, 403, 404t
chronic obstructive pulmonary disease, rosacea, 589, 590, 590t
Quiphile. See quinine sulfate
471–472 rosiglitazone, 536t
common cold. See common cold rosuvastatin, 239t, 240
R respiratory system, 455–456, 456f, 457f rotavirus vaccine, 377t
rabeprazole, 482t rest-and-digest response, 87 roundworm, 389f, 427
rabeprazole sodium, 482t Restoril. See temazepam routine orders, 24
radioactive iodide, 518t restricted drugs, 16 Roxicet. See oxycodone terephthalate
raloxifene Retavase. See reteplase rTMS (repetitive transcranial magnetic
as antineoplastic agent, 444t reteplase stimulation), 125
Drug Prototype, 571 actions, 312t Rufen. See ibuprofen
for osteoporosis, 571t adverse effects, 312t Rythmol. See propafenone
raltegravir, 419t, 420 clinical uses, 312t
ramelteon, 111, 117t, 119 Drug Prototype, 312t S
ramipril, 275t, 293t interactions, 312t Sabril. See vigabatrin
Ranexa. See ranolazine route and adult dose, 312t SAD (seasonal affective disorder), 124
ranitidine, 17t reticular activating system (RAS), 107 Safety Alerts. See Guide to
Drug Prototype, 483t reticular formation, 78, 107 Special Features
route and adult dose, 482t reticular activating system (RAS) and, 107 Saizen. See somatropin
ranolazine, 305, 306t stimulation of, 107 Salagen. See pilocarpine
Rapaflo. See silodosin Retin-A. See tretinoin Salax. See salicylic acid
RAS (reticular activating system), 107 retinoids, 590 salicylates, 209t
rasburicase, 577, 577t reverse transcriptase, 420 salicylic acid, 593t
rate of elimination, 45–46 ReVia. See naltrexone salicylism, 366
drug responsiveness and, 45–46 rhabdomyolysis, 240 salmeterol, 468t
Razadyne. See galantamine rheumatoid arthritis (RA), 575, 576t for asthma, 97t
RDA (recommended dietary allowances), rheumatoid factors, 575 Salmonella enteritidis, 390t
498–499, 498t Rheumatrex. See methotrexate salsalate, 209t
reabsorption, 250 riboflavin, 213t Sandostatin. See octreotide
Rebif. See interferon beta-1a riboflavin (vitamin B2), 498t SA (sinoatrial) node, 333, 334f
rebound congestion, 463 rickets. See osteomalacia Sansert. See methysergide
rebound insomnia, 110 Rickettsia rickettsii, 390t Saphris. See asenapine
receptor(s), 47 RID. See pyrethrin saquinavir, 419t
cellular, 47f Ridiprin. See aspirin Sarcoptes scabiei, 586
receptor theory, 47 rifabutin, 407t sargramostim, 379, 436
Reclast. See zoledronate rifampin, 407t sarin, 92
recommended dietary allowances (RDA), rifapentine, 407t saxagliptin, 535t, 537
498–499, 498t rilpivirine, 419t scabicides, 587
Recothrom. See thrombin rimabotulinumtoxin B, 173, 174t scabies, 586
rectal administration, 31t, 32 rimantadine, 424, 424t scheduled drugs, 16, 17t
Index 651
Schedule I drugs, 16, 17t selective estrogen-receptor modulators inotropic drugs, 325, 325t
Schedule II drugs, 16, 17t (SERM), 570, 571t vasoconstrictors, 324–325, 325t
Schedule V drugs, 16, 17t selective serotonin reuptake inhibitors (SSRIs), symptoms, 320, 321f
Schedule I drugs, 16, 17t, 76. See also hal- 126t, 128–129 short stature, 515. See also growth hormone
lucinogens advantages of, 128 (GH)
Schedule II drugs, 16, 17t, 78 adverse effects, 113, 128–129 short-term insomnia, 110. See also behavioral
Schedule V drugs, 16, 17t clinical uses insomnia
schizoaffective disorder, 144 anxiety disorders, 112t short-term psychotherapies
schizophrenia, 143 depression, 126t cognitive-behavioral therapy, 125
causes of, 145 drugs classified as, 110, 125 interpersonal therapy, 124–125
negative symptoms, 144 interactions sibutramine, 491
pharmacotherapy for patients with, 146 with phenelzine, 133t sildenafil
positive symptoms, 144 with risperidone, 152t administration, 24
scinitinib, 445t with sumatriptan, 213t Drug Prototype, 556t
scopolamine, 95t, 489, 490t with warfarin, 353t for erectile dysfunction, 556, 556t
scopolamine hydrobromide, 606t Patients Need to Know, 139t interaction with nitroglycerin, 307t
seasonal affective disorder (SAD), 124 serotonin syndrome (SES) and, 129 Silenor. See doxepin
sea vegetables, 504t selegiline, 127t, 161, 161t silodosin, 100t, 558t
seborrhea, 589 selenium, 435t silver sulfadiazine, 402t
seborrheic dermatitis, 591 senna, 487t Simcor, 242
secobarbital, 116t Senokot. See senna simethicone, 482t, 485
Seconal. See secobarbital Sensipar. See cinacalcet simple partial seizures, 183. See also seizure(s)
secondary adrenocortical insufficiency, 521 Sensorcaaine. See bupivicaine Simponi. See golimumab
secondary gout, 576, 577. See also gout sensory neurons, 199 simvastatin, 239t
secondary hypertension, 267 September 11, 2001, terrorist attacks, 9 Sinequan. See doxepin
secondary hypogonadism, 554 septic shock, 320, 320t. See also shock single order, 23
second-degree burns, 583–584 Septocaine. See articaine sinoatrial (SA) node, 333, 334f
secretion, tubular, 250f, 251 Serevent. See salmeterol sinus bradycardia, 333t
Sectral. See acebutolol SERM (selective estrogen-receptor modula- sinus rhythm, 333
sedative-hypnotics, 74, 111 tors), 570, 571t sirolimus, 381t
sedative(s), 74, 111. See also tranquilizers Seroquel. See quetiapine sitagliptin, 535t, 537
clinical uses Serostim. See somatropin situational anxiety, 106
for anxiety and insomnia, 117t serotonin (5-HT), 128 situational depression, 124
seizure(s), 181 serotonin-norepinephrine reuptake inhibitors six rights of drug administration, 22
causes, 181, 182–183 (SNRIs), 129 Skelaxin. See metaxalone
chronic depression and, 183 actions, 129t skeletal muscle relaxants, 171t
classification, 183–184 adverse effects, 113, 129t Skelid. See tiludronate
convulsions and, 181 black box warning, 129t skin disorders
febrile, 182 clinical uses acne, 589–590, 590t
generalized seizures, 183 anxiety, 112t parasites, 586–587
absence seizures, 183 depression, 129 Patients Need to Know, 594t
atonic seizures, 183 drugs classified as, 110 psoriasis, 593–594, 593t
tonic-clonic seizures, 183 generalized anxiety disorder and, 129 rosacea, 589, 590, 590t
impact on quality of life, 183 serotonin syndrome (SES), 129 sunburn and minor irritation, 588–589
infectious diseases and, 182 sertaconazole, 415t Sklice. See ivermectin
ketogenic diet for, 188t sertraline, 112t Sloprin. See aspirin
metabolic disorders and, 182 actions, 133t Slow-Mag. See magnesium chloride
neoplastic disease and, 182 adverse effects, 133t slow-release (SR) medications, 27
partial (focal) seizures, 183 clinical uses SL (sublingual) route, 26t, 27, 28f
complex partial seizures, 183 depression, 126t smoking, 555
simple partial seizures, 183 Drug Prototype, 132t SNRIs (serotonin-norepinephrine reuptake
pediatric disorders and, 182 interactions inhibitors). See serotonin-norepinephrine
pharmacotherapy. See also antiseizure with digoxin, 133t reuptake inhibitors (SNRIs)
drugs with warfarin, 133t social anxiety disorder, 106
goals, 186 sevoflurane, 225t social phobia. See social anxiety disorder
initiation of, 184 sex hormones, 544. See also estrogen; proges- sodium, 501t
selection of, 184 terone; testosterone sodium bicarbonate, 502t
in pregnancy, 182–183 Sherley Amendment, 5, 6f actions, 261t
special epileptic syndromes, 184 shock, 320 adverse effects, 261t
febrile seizures, 184 classification, 320, 320t clinical uses, 261t, 482t
myoclonic seizures, 184 Fast Facts, 321 Drug Prototype, 261t
trauma and, 182 initial treatment, 320–322, 322f interactions, 261t
vascular diseases and, 182 Patients Need to Know, 328 in local anesthetics, 220
selective cox-2 inhibitors. See also nonsteroi- pharmacotherapy sodium channel blockers, 220, 338, 338t
dal anti-inflammatory drugs (NSAIDs) fluid replacement drugs, 322–323, interactions with lidocaine, 222t
actions, 210f 323t sodium chloride, interaction with lithium, 134
drugs classified as, 209t, 365t, 366 Nursing Process Focus, 324t sodium chloride hypertonicity ointment, 606t
652 Index
sodium hydroxide, 220 statins. See HMG-CoA reductase inhibitors route and adult dose, 176t
sodium imbalances. See hypernatremia; (statins) sucralfate, 485
hyponatremia STAT order, 23–24 Sudafed PE Nighttime Cold, 461t
sodium ion channels, 335, 336f status asthmaticus, 467 Sudafed PE Sinus and Allergy, 461t
sodium ions (Na+), 220, 220f status epilepticus, 184 Sufenta. See sufentanil
sodium oxybate, 74 stavudine, 419t sufentanil, 204, 226t, 228t
sodium polystyrene sulfate, 259 steatorrhea, 492 sulconazole, 415t
Solorcaine. See benzocaine Stendra. See avanafil sulfacetamide sodium, 590t
Solu-Cortef. See hydrocortisone steroid(s), 236 sulfadiazine, 402t, 403
Solu-Medrol. See methylprednisolone St. John’s wort sulfadoxine–pyrimethamine, 402t, 403
Soma. See carisoprodol interactions sulfasalazine, 43, 402t, 576t
somatic nervous system, 87, 88f with anesthetics, 218t sulfinpyrazone, 577t
somatic pain, 198 with chlorpromazine, 147t sulfisoxazole, 402t
somatotropin. See growth hormone (GH) with cyclophosphamide, 438t sulfites, 222
somatropin, 515t with imipramine, 129t sulfonamides
Somatuline Depot. See lanreotide with isoflurane, 225t actions, 401–402
Somavert. See pegvisomant with sertraline, 133t adverse effects, 403
Sominex. See diphenhydramine with zidovudine, 421t drugs classified as, 402t
Sonata. See zaleplon Strattera. See atomoxetine interactions
Sorine. See sotalol stratum germinativum, 583 with aspirin, 208t
sotalol, 100t, 340t Streptococci, 390t with furosemide, 254t
spasticity, 171 streptogramins, 403 Patients Need to Know, 409t
causes, 172 streptokinase, 312t resistance to, 402
characteristics, 172 streptomycin, 399t uses, 403
nonpharmacologic therapy, 169 streptozocin, 437t sulfur, 501t
Nursing Process Focus, 172–173t Striant. See testosterone sulindac, 209t
Patients Need to Know, 176t Stroke, 314–315, 347t sumatriptan, 211
pharmacotherapy subcutaneous layer, 583 actions, 213t
direct-acting antispasmodics, 174f subcutaneous (SC or SQ) route, 33–34, 34t adverse effects, 213t
signs and symptoms, 171 subjective data, 52 clinical uses, 212t, 213t
treatment for, 172, 173 Sublimaze. See fentanyl Drug Prototype, 213t
special epileptic syndromes, 184 sublingual (SL) route, 26t, 27, 28f interactions, 213t
febrile seizures, 184 Suboxone. See buprenorphine route and adult dose, 212t
myoclonic seizures, 184 substance abuse, 69–83 Sumycin. See tetracycline
specialty supplements, 65, 65t. See also Cam chronic, 72 sunburn, 588–589
Therapy classification, 70–71 sunitinib, 445t
popular, 65t commonly abused substances, 71t superficial mycoses, 413
regulation of, 65–67 in health care providers, 80–81 superinfections, 393
spectinomycin, 404t opioids, 205 Suprane. See desflurane
"speedball.” See heroin in the U.S., 70 supraventricular, 332
spinal anesthesia, 219f, 219t substance P, 199 surface anesthesia. See regional anesthesia
spiritual healing, 60t substantia nigra, 160 surgical anesthesia, 224
Spiriva. See tiotropium succinimides. See also antiseizure drugs Surmontil. See trimipramine
spironolactone for absence seizures, 191–192 sustained-release capsules, 27
actions, 253f, 256, 256t drugs classified as, 185t sustained-release tablets, 27
adverse effects, 256t Patients Need to Know, 194t sympathetic nervous system, 87
clinical uses, 256t route and adult dose, 192t activation of, 91
heart failure, 293t succinylcholine effects of, 89f
hypertension, 274t adverse effects, 176, 228t fight-or-flight response and, 87
Drug Prototype, 256t black box warning, 228t inhibition of, 91
interactions, 256t clinical uses, 176, 228t norepinephrine (NE) and, 88
with aspirin, 208t as adjuncts to anesthesia, 228t sympathomimetics (adrenergic drugs),
route and adult dose, 293t Drug Prototype, 228t 91, 97t
routes and adult dose, 256t, 274t interactions actions, 97
Sporothrix schenckii, 414t with aminoglycosides, 228t clinical uses, 97t
SR (slow-release) medications, 27 with cardiac glycosides, 228t for asthma, 467
SSRIs (selective serotonin reuptake inhibitors). with clindamycin, 228t glaucoma, 602, 602t
See selective serotonin reuptake inhibitors with diazepam, 228t drugs classified as, 91t, 468t
(SSRIs) with furosemide, 228t effects of, 97
stable angina, 303 with lidocaine, 228t Nursing Process Focus, 98–99t
Stadol. See butorphanol with lithium, 228t Patients Need to Know, 102t
Stalevo. See entacapone with narcotics, 228t Synalar. See fluocinolone acetonide
standing order, 24 with phenothiazines oxytocin, 228t synapses, 88
Staphylococcus aureus, 390t with promazine, 228t synaptic cleft, 88
methicillin-resistant, 392 with quinidine, 228t Synthroid. See levothyroxine
Starlix. See nateglinide with tacrine, 228t systemic mycoses, 413
stasis dermatitis, 591 with thiazide diuretics, 228t systolic pressure, 267, 268f
Index 653
T tetracaine, 221t thyroid-releasing hormone (TRH), 516

tetracycline, 397–398, 397t, 409t thyroid-stimulating hormone (TSH), 511, 513f
t1/2 (half-life), 45
clinical uses Thyroid USP. See thyroid dessicated
tablets, 27
acne, 590, 590t Thyrolar. See liotrix
enteric-coated, 27
peptic ulcer disease, 485 thyroxine, 516
guidelines for administering, 26t
Drug Prototype, 397t tiagabine, 185t, 187t
orally disintegrating tablets (ODTs), 27
interactions ticagrelor, 355t, 356
sustained-release, 27
with heparin, 352t ticarcillin, 394t
Tab-Profen. See ibuprofen
with sodium bicarbonate, 261t Ticlid. See ticlopidine
tacrine, 92, 92t, 165, 165t
pregnancy category, 397, 397t ticlopidine, 355, 355t
tacrolimus, 381t
route and adult dose, 397t tigecycline, 397t
tadalafil, 556, 556t
tetrahydrocannabinol (THC), 76 Tikosyn. See dofetilide
tafluprost, 602t
tetrahydrozoline, 464t, 606t tiludronate, 571t
Talwin. See pentazocine
Teveten. See eprosartan timolol
Tambocor. See flecainide
Thalitone. See chlorthalidone clinical uses, 100t, 212t
tamoxifen, 443, 513
THC (tetrahydrocannabinol), 76 glaucoma, 603t
theophylline, for asthma, 468t, 469 hypertension, 281t
therapeutic classification, 13–14, 13t. See also Drug Prototype, 604t
tamsulosin, 100t, 558t
therapeutic usefulness route and adult dose, 212t, 281t
Tapazole. See methimazole
therapeutic lifestyle changes timolol maleate, 306t
tapeworm, 389f
for angina, 304 Timoptic. See timolol
tardive dyskinesia, 147t, 148
for hyperlipidemia, 236–237 tinidazole, 426t
Tasmar. See tolcapone
for hypertension, 271–272 tinzaparin, 351t
Tavist Allergy, 461t
therapeutic range of drug, 45 tioconazole, 415t
taxanes, 442, 442t
therapeutics, 3 tiotropium, 95t
tazarotene, 590t, 593t, 594
therapeutic usefulness, 13. See also therapeutic tipranavir, 419t
Tazorac. See tazarotene
classification tirofiban, 355t
T cells, 375
thiamine (vitamin B1), 498t tissue plasminogen activator (tPA), 349
Tegretol. See carbamazepine
thiazide and thiazide-like diuretics titer, 376
telavancin, 404t
actions, 253f tizanidine, 170, 171t
telithromycin, 404t
adverse effects, 254 TNF (tumor necrosis factor), 375
telmisartan, 275t
drugs classified as, 254t TNKase. See tenecteplase
temazepam, 74, 114t
interactions tobramycin, 399t
Temovate. See clobetasol
with cholestyramine, 240t tocilizumab, 576t
temozolomide, 437t
with enalapril, 277t tocolytics, 552
temporal lobe seizures, 183. See also complex
thioguanine, 439t Tofranil. See imipramine
partial seizures; seizure(s)
thioridazine, 146t tolazamide, 536t
TEN (toxic epidermal necrolysis), 583
thiotepa, 437t tolbutamide, 536t
tenecteplase, 312t
thiothixene, 148t tolcapone, 161–162, 161t
teniposide, 442, 442t
third-degree burns, 584 Tolectin. See tolmetin
tenofovir, 419t
three checks of drug administration, 22 tolerance, 73
Tenormin. See atenolol
thrombin, 347, 357, 357t immunity and, 73
Tensilon. See edrophonium
Thrombinar. See thrombin marijuana and, 76
tension headache, 211
thrombocytopenia, 436t resistance and, 73
teratogen, 17
thromboembolic disorder, 349 Tolinase. See tolazamide
terazosin, 100t, 281t, 558t
thrombolytics, 350 tolmetin, 209t, 365t
terbinafine, 415t
adverse effects, 310 tolnaftate, 415t
terbutaline, 97t, 553t
clinical uses, 356–357 tolterodine, 95t
terconazole, 415t
myocardial infarction, 310 tonic-clonic seizures, 183. See also grand mal
teriparatide, 571t
stroke, 314 seizures; seizure(s)
termination of drug action, 46
interactions clonic phase, 183
Testim. See testosterone
with clopidogrel, 356t hydantoin and related drugs for treating,
testolactone, 444t
Nursing Process Focus, 313t 189–190t
Testopel. See testosterone
thrombophlebitis, 604 status epilepticus and, 184
testosterone
thrombotic stroke, 314 tonic phase, 183
androgen base, 544, 554
thrombus, 349 tonic phase, tonic-clonic seizure, 183
buccal system, 554, 555t
Thyrar. See thyroid dessicated tonic spasm, 169. See also muscle spasms
Thyro-block. See potassium iodide tonometry, 601
for hypogonadism, 554, 555t
and iodine Topamax. See topiramate
implantable pellets, 554, 555t
thyroglobulin, 17t topical anesthesia, 219f, 219t
intramuscular, 554
thyroid dessicated, 518t topical route, 28–29
thyroid disorders, 514t, 516–519, 518t nasal, 30t, 31
transdermal gel, 554, 555t
thyroid gland ophthalmic, 29, 29f, 30t
transdermal patch, 554, 555t
anatomy, 512f otic, 30t, 31
testosterone cypionate, 555t
feedback mechanisms, 517f rectal suppositories, 31t, 32
testosterone enanthate, 555t
function, 516 transdermal, 29, 30t
Testred. See methyltestosterone
pituitary gland and, 513f vaginal, 30t, 31–32
654 Index
Topicort. See desoximetasone chronic pain impluses, 201 Nursing Proces Focus, 538–539t
topiramate, 185t, 187t, 189, 191, 212t depression, 126t pharmacotherapy, 535–536t, 535–537
topoisomerase inhibitors, 442, 442t migraine prophylaxis, 213t alpha-glucosidase inhibitors,
topotecan, 442, 442t neuropathic pain impluses, 201 535t, 536
Toprol. See metoprolol contraindications, 113 biguanide, 535t, 536
Toradol. See ketorolac drugs classified as, 110, 125 incretin enhancers, 535t, 537
toremifene, 444t half-life of, 125 meglitinides, 536, 536t
torsemide, 252, 253t, 274t, 293t imipramine, 201 sulfonylureas, 536, 536t
total parenteral nutrition (TPN), 505 interactions, 133t thiazolidinediones, 536, 536t
Toviaz. See fesoterodine with atropine, 95t tyramine, 132
toxic concentration, 45 with benztropine, 164t
toxic epidermal necrolysis (TEN), 583 with chlorpromazine, 147t
toxins, 389 with epinephrine, 327t U
toxoid vaccines, 376 with levodopa, 163t ulcerative colitis, 480
tPA (tissue plasminogen activator), 349 with morphine, 203t ulipristal, 547
TPN (total parenteral nutrition), 505 with norepinephrine, 326t Uloric. See febuxostat
trabecular meshwork, 599 with phenelzine, 133t Ultane. See sevoflurane
trace minerals, 499, 501t with phenylephrine, 98t Ultiva. See remifentanil
trade name, 14 nortriptyline, 201 Ultram. See tramadol
traditional therapeutic drugs, 4 Patients Need to Know, 139t Ultraprin. See ibuprofen
characteristics of, 4t pregnancy category, 113 Ultravate. See halobetasol
stages of approval for, 7–9, 8f trifluoperazine, 146t ultraviolet A (UVA) phototherapy, 594
Tradjenta. See linagliptin trifluridine, 424t ultraviolet B (UVB) phototherapy, 594
tramadol, 209t, 210 triglycerides, 235, 236, 238t undecylenic acid, 415t
trandolapril, 275t trihexyphenidyl, 95, 95t, 163t undernutrition, 504
tranexamic acid, 357, 357t triiodothyronine, 516 Uni-Buff. See aspirin
tranquilizer, 111 trimethoprim-sulfamethoxazole Unisom. See diphenhydramine
tranquilizers, 74. See also sedative(s) Drug Prototype, 402t Uni-Tren. See aspirin
transdermal administration, 29, 30t route and adult dose, 402t Univasc. See moexipril
transdermal testosterone gel, 554, 555t trimipramine, 112t, 126t unstable angina, 303
transdermal testosterone patch, 554, 555t Triostat. See liothyronine upper respiratory tract (URT), 455
transmucosal administration, 31. See also nasal triphasic OC, 546, 546t urea, 257t
administration triple therapy, 481 Ureaphil. See urea
transplant rejection, 380 Triplix. See fenofibrate Urecholine. See bethanechol
Tranxene. See clorazepate triptans, 211 uric acid inhibitors, 577, 577t
tranylcypromine, 112t, 127t triptorelin, 444t uricosurics, 577, 577t
trastuzumab, 445t Tronothane. See pramoxine urinary antiseptics, 403
Travatan. See travoprost Tropicacyl. See tropicamide urinary system, 249–251, 249f, 250f
travoprost, 602t tropicamide, 606t urinary tract infections (UTIs)
trazodone, 112t, 127t, 129 Trusopt. See dorzolamide hospital-acquired, 390t
tremors, 159, 162f Trypanosoma, 389f urine, 250
Trental. See pentoxifylline tube feeding, 504, 504f. See also enteral nutrition Uro-KP neutral. See potassium/sodium
tretinoin tubercles, 406 phosphates
clinical uses, 590t tuberculin syringes (TB), 34 UroXatral. See alfuzosin
Drug Prototype, 591t tuberculosis Uroxatral. See alfuzosin
Trexall. See methotrexate Nursing Process Focus, 407–408t URT (upper respiratory tract), 455
Trexan. See naltrexone pathophysiology, 406 urticaria, 583
TRH (thyroid-releasing hormone), 516 pharmacotherapy, 406, 407t U.S. Department of Defense, 9
triamcinolone, 522t tubocurarine, 175, 176t, 228t U.S. Department of Health and Human
inhaled, 470t tubular secretion, 250f, 251 Services, 5, 6f
intranasal, 463t tumor, 432 U.S. Department of Homeland Security, 9
for severe inflammation, 368t tumor necrosis factor (TNF), 375 U.S. Pharmacopoeia (USP), 5, 6f
triamcinolone acetonide, 592t tumor suppressor genes, 432 U.S. Pharmacopoeia-National Formulary
Triaminic Cold/Allergy, 461t Tums. See calcium carbonate (USP-NF), 5, 6f
triamterene, 253f, 256t, 274t T wave, 334f uterine stimulants and relaxants, 552, 553t
triazolam, 74, 114t Twinrix, 377t Uticort. See betamethasone benzoate
Trichophyton, 414t Tylenol. See acetaminophen
Tricor. See fenofibrate Tylenol Allergy Multisystem, 461t
tricyclic antidepressants (TCAS), 125, 126t Tylenol PM, 461t V
actions, 125 Tylenol with Codeine, 205 vaccination (immunization), 376
adverse effects, 113, 125 type 1 diabetes mellitus vaccine(s), 374, 376–378, 377t, 378t, 383t
amitriptyline, 201 description, 530 toxoid, 376
chemical structure, 125 pharmacotherapy. See insulin vaginal administration, 30t, 31–32
childhood enuresis (bed-wetting), treatment signs and symptoms, 530 valacyclovir, 424t
of, 125 type 2 diabetes mellitus valdecoxib, 8, 366
clinical uses description, 534 valerian, for anxiety and insomnia, 118t
anxiety disorders, 112t insulin resistance, 534, 535 Valisone. See betamethasone valerate
Index 655
Valium. See diazepam with dantrolene, 175t drugs classified as, 568t
valproic acid, 201 with doxorubicin, 441t for osteomalacia, 567, 568
actions, 191t route and adult dose, 212t, 278t, 306t, 341t vitamin E, 498t
adverse effects, 191t Verdeso. See desonide vitamin K
clinical uses, 191t Versed. See midazolam; midazolam deficiency, 498t
anxiety, 117t, 118 hydrochloride functions, 498t
bipolar disorder, 135t vertigo, 461 interactions with cholestyramine, 240t
migraine prophylaxis, 212t very low-density lipoprotein (VLDL), recommended dietary allowance, 498t
seizures, 185t, 189, 190t 236, 237f for warfarin reversal, 350
Drug Prototype, 191t Viagra. See sildenafil Vivactil. See protriptyline
interactions, 191t Vibramycin. See doxycycline Vivatrol. See naltrexone
with aspirin, 191t Vicodin, 205 VLDL (very low-density lipoprotein),
with chlorpromazine, 191t Victoza. See liraglutide 236, 237f
with cimetidine, 191t vigabatrin, 187t volatile inhalants, abuse of, 70
with clonazepam, 191t Viibryd. See vilazodone volatile liquid anesthetics. See general
with diazepam, 188t vilazodone, 126t anesthetics, inhaled
with erythromycin, 191t villi, 478 Voltaren. See diclofenac
with ethosuximide, 192t vinblastine, 442, 442t vomiting, 489–490, 490t
with felbamate, 191t vinca alkaloids, 442, 442t voriconazole, 415t
with lamotrigine, 191t vincristine, 442 Vosol HC. See acetic acid and hydrocortisone
with phenytoin, 191t Drug Prototype, 443t VoSpire. See albuterol
with rifampin, 191t route and adult dose, 442t VRE (vancomycin-resistant enterococci), 392
route and adult dose, 190t, 212t vincristine liposome, 442t Vytorin, 244
valsartan, 275t, 293t, 294 vinorelbine, 442t
valvular heart disease, 347t Vioxx. See rofecoxib W
vancomycin virilization, 554
clinical uses, 403, 404t Virilon. See methyltestosterone warfarin
Drug Prototype, 403t virulence, 389 actions, 350f, 353t
route and adult dose, 404t virus(es), 389f, 417 adverse effects, 353t
vancomycin-resistant enterococci (VRE), 392 visceral pain, 198 black box warning, 353t
vardenafil, 556, 556t Visine. See tetrahydrozoline clinical uses, 313, 352, 353t
varicella vaccine, 377t Visine LR. See oxymetazoline Drug Prototype, 353t
varicella-zoster virus, 424 Visken. See pindolol interactions, 353t
Vascepa. See icosapent vismodegib, 445t with acetaminophen, 369t
Vascor. See bepridil vitamin(s) with aspirin, 208t
vasoconstrictors, 324–325, 325t accidental overdose of, 505t with ciprofloxacin, 401t
vasodilators characteristics, 497 with erythromycin, 398t
actions, 282–283, 295t, 296 classification, 497–498 with omeprazole, 483t
adverse effects, 296 deficiency, 499 with psyllium, 487t
clinical uses description, 497 with sertraline, 133t
heart failure, 295t, 296 fat-soluble, 497–498 with valproic acid, 191t
hypertension, 283, 283t recommended dietary allowances (RDA), route and adult dose, 351t
drugs classified as, 283t, 295t 498–499, 498t water-soluble vitamin, 497. See also
vasomotor center, 270, 271f water-soluble, 497 vitamin(s)
vasopressin (antidiuretic hormone), 270, vitamin A, 498t weight loss, 491
514–515, 514t, 515t vitamin B1 (thiamine), 498t Welchol. See colesevelam
vasospastic (Prinzmetal’s) angina, 303, 309 vitamin B2. See riboflavin Wellbutrin. See bupropion
Vasotec. See enalapril vitamin B2 (riboflavin), 498t Westcort. See hydrocortisone valerate
vastus lateralis site, intramuscular injection, 36 vitamin B3 (niacin), 498t whiteheads, 589
vecuronium, 176t vitamin B5 (pantothenic acid), 498t withdrawal, 16
venlafaxine, 112t, 127t, 129 vitamin B6 (pyridoxine), 498t withdrawal syndromes, 72
ventilation, 455–456 vitamin B7 (biotin), 498t
Ventolin. See albuterol vitamin B9. See folic acid/folate X
ventricular flutter/fibrillation, 333t vitamin B12 Xalatan. See latanoprost
ventricular tachycardia, 333t deficiency, 498t, 499 Xanax. See alprazolam
ventrogluteal site, intramuscular injection, metabolism of, 500f xanthines, 468t, 469
34t, 36 recommended dietary allowance, 498t Xarelto. See rivaroxaban
verapamil vitamin C, 498t Xeomin. See incobotulinumtoxin A
actions, 342t vitamin D Xgen. See denosumab
adverse effects, 342t deficiency, 498t, 499 XTC (MDMA), 77
clinical uses, 342t functon, 498t Xylocaine. See lidocaine
angina, 306t interaction xylometazoline, 464t
dysrhythmias, 341t with phenobarbital, 188t Xyrem. See sodium oxybate
migraine prophylaxis, 212t with phenytoin, 190t
Drug Prototype, 342t pathway for activation and action, 567f
recommended dietary allowance, 498t
Y
interactions, 342t
with clopidogrel, 356t supplements yeasts, 413
656 Index
Z interactions Zoloft. See sertraline

with acyclovir, 425t zolpidem
zafirlukast, 470t
with interferon alfa-2b, 446t actions, 118t
zaleplon, 111, 117t, 119
route and adult dose, 419t adverse effects, 118t
Zanaflex. See tizanidine
zileuton, 470t clinical uses, 117t
zanamivir, 424, 424t
Zincate. See zinc sulfate Drug Prototype, 118t
Zantac. See penicillins; ranitidine
zinc gluconate, 502t Zometa. See zoledronate
Zaroxolyn. See metolazone
zinc sulfate, 502t Zomig. See zolmitriptan
Zebeta. See bisoprolol
Zioptan. See tafluprost Zonegran. See zonisamide
Zelapar. See selegiline
ziprasidone, 135t, 151t zonisamide, 185t, 185t, 190t, 191
Zemplar. See paricalcitol
Zipsor. See diclofenac Zorbtive. See somatropin
Zemuron. See rocuronium
Zocor. See simvastatin Zorcaine. See articaine
Zestoretic, 255, 273
Zofran. See ondansetron Zorprin. See aspirin
Zestril. See lisinopril
zoledronate, 571t Zovirax. See acyclovir
Zetia. See ezetimibe
zoledronic acid, 571t Zuplenz. See ondansetron
ziconotide, 209t, 210
zoledronic acid (zoledronate sodium), 445t Zyban. See bupropion
zidovudine
Zollinger-Ellison syndrome, 482, 483t Zyloprim. See allopurinol
zolmitriptan, 212t Zyprexa. See olanzapine
Guide to Special Features
calcitriol, p. 569, Ch. 35
calcium salts, p. 569, Ch. 35
CAM Therapy
carbidopa, p. 163, Ch. 12
Aloe Vera for Improving Eye and Ear Health, p. 608, Ch. 37 carvedilol, p. 296, Ch. 19
Aloe Vera for Skin Conditions, p. 592, Ch. 36 cefotaxime, p. 396, Ch. 26
Carnitine and Heart Disease, p. 293, Ch. 19 chlorpromazine, p. 147, Ch. 11
Cayenne for Muscular Tension, p. 173, Ch. 12 cholestyramine, p. 240, Ch. 16
Coenzyme Q10 for Heart Disease, p. 242, Ch. 16 ciprofloxacin, p. 401, Ch. 26
Cranberry for Urinary System Health, p. 251, Ch. 17 clopidogrel, p. 356, Ch. 23
Dong Quai for Premenstrual Syndrome, p. 549, Ch. 34 cromolyn, p. 471, Ch. 29
Echinacea for Boosting the Immune System, p. 376, Ch. 25 cyanocobalamin, p. 499, Ch. 31
Evening Primrose Oil for Pain and Eczema, p. 211, Ch. 14 cyclobenzaprine, p. 171, Ch. 12
Garlic for Cardiovascular Health, p. 355, Ch. 23 cyclophosphamide, p. 438, Ch. 28
Ginger for Nausea, p. 491, Ch. 30 cyclosporine, p. 382, Ch. 25
Ginkgo biloba for Dementia, p. 167, Ch. 12 dantrolene, p. 175, Ch. 12
Ginseng and Cardiovascular Disease, p. 314, Ch. 20 desmopressin, p. 514, Ch. 32
Glucosamine and Chondroitin for Osteoarthritis, p. 578, Ch. 35 diazepam, p. 188, Ch. 13
Grape Seed Extract for Hypertension, p. 280, Ch. 18 digoxin, p. 295, Ch. 19
Medication Errors and Dietary Supplements, p. 57, Ch. 5 diltiazem, p. 309, Ch. 20
Milk Thistle for Liver Damage, p. 74, Ch. 7 diphenhydramine, p. 460, Ch. 29
Oil of Cloves for Dental Pain, p. 223, Ch. 15 diphenoxylate with atropine, p. 488, Ch. 30
Omega-3 Fatty Acids and Diabetes, p. 534, Ch. 33 donepezil, p. 167, Ch. 12
Red Yeast Rice and Cholesterol, p. 238, Ch. 16 dopamine, p. 326, Ch. 21
Sea Vegetables, p. 504, Ch. 31 doxazosin, p. 282, Ch. 18
Selenium’s Role in Cancer Prevention, p. 435, Ch. 28 doxorubicin, p. 441, Ch. 28
St. John’s Wort for Depression, p. 134, Ch. 10 enalapril, p. 277, Ch. 18
The Antibacterial Properties of Goldenseal, p. 395, Ch. 26 entacapone, p. 163, Ch. 12
The Ketogenic Diet for Epilepsy, p. 188, Ch. 13 epinephrine, p. 327, Ch. 21
Valerian for Anxiety and Insomnia, p. 118, Ch. 9 epoetin alfa, p. 446, Ch. 28
erythromycin, p. 398, Ch. 26
escitalopram, p. 113, Ch. 9
Drug Prototype estradiol with norethindrone, p. 547, Ch. 34
estrogen, conjugated, p. 551, Ch. 34
acetaminophen, p. 369, Ch. 24
ethosuximide, p. 192, Ch. 13
acyclovir, p. 425, Ch. 27
ferrous sulfate, p. 501, Ch. 31
alendronate, p. 572, Ch. 35
finasteride, p. 558, Ch. 34
allopurinol, p. 578, Ch. 35
fluticasone, p. 463, Ch. 29
alteplase, p. 357, Ch. 23
furosemide, p. 254, Ch. 17
aminocaproic acid, p. 358, Ch. 23
gemfibrozil, p. 244, Ch. 16
amiodarone, p. 341, Ch. 22
gentamicin, p. 400, Ch. 26
amphotericin B, p. 416, Ch. 27
haloperidol, p. 149, Ch. 11
aspirin, p. 208, Ch. 14
heparin, p. 352, Ch. 23
atenolol, p. 309, Ch. 20
hepatitis B vaccine, p. 378, Ch. 25
atorvastatin, p. 240, Ch. 16
hydralazine, p. 283, Ch. 18
atropine, p. 95, Ch. 8
hydrochlorothiazide, p. 255, Ch. 17
benzocaine, p. 589, Ch. 36
hydrocortisone, p. 522, Ch. 32
benztropine, p. 164, Ch. 12
hydroxychloroquine, p. 575, Ch. 35
bethanechol, p. 93, Ch. 8
657
658 Guide to Special Features
imipramine, p. 129, Ch. 10 succinylcholine, p. 228, Ch. 15

insulin regular, p. 532, Ch. 33 sumatriptan, p. 213, Ch. 14
interferon alfa-2b (intron-A), p. 380, Ch. 25 tamoxifen, p. 444, Ch. 28
interferon alfa-2b, p. 446, Ch. 28 testosterone, p. 554, Ch. 34
isoflurane, p. 225, Ch. 15 tetracycline, p. 397, Ch. 26
isoniazid, p. 406, Ch. 26 timolol, p. 604, Ch. 37
latanoprost, p. 601, Ch. 37 tretinoin, p. 591, Ch. 36
levodopa, p. 163, Ch. 12 trimethoprim-sulfamethoxazole, p. 402, Ch. 26
levothyroxine, p. 518, Ch. 32 valproic acid, p. 191, Ch.13
lidocaine, p. 222, Ch. 15 vancomycin, p. 403, Ch. 26
lisinopril, p. 292, Ch. 19 verapamil, p. 342, Ch. 22
lorazepam, p. 116, Ch. 9 vincristine, p. 443, Ch. 28
medroxyprogesterone, p. 552, Ch. 34 warfarin, p. 353, Ch. 23
metformin, p. 537, Ch. 33 zidovudine, p. 421, Ch. 27
methotrexate, p. 440, Ch. 28 zolpidem, p. 118, Ch. 9
methylphenidate, p. 137, Ch. 10
metronidazole, p. 427, Ch. 27
milrinone, p. 297, Ch. 19 Fast Facts
morphine, p. 203, Ch. 14 ADHD, p. 136, Ch. 10
naloxone, p. 205, Ch. 14 Allergies, p. 458, Ch. 29
naproxen, p. 366, Ch. 24 Alternative Therapies in America, p. 61, Ch. 6
naproxen sodium, p. 366, Ch. 24 Anesthesia and Anesthetics, p. 218, Ch. 15
nifedipine, p. 279, Ch. 18 Angina Pectoris and Coronary Heart Disease, p. 304, Ch. 20
nitroglycerin, p. 307, Ch. 20 Anxiety Disorders, p. 107, Ch. 9
nitrous oxide, p. 225, Ch. 15 Arthritis and Joint Disorders, p. 575, Ch. 35
norepinephrine, p. 326, Ch. 21 Asthma, p. 467, Ch. 29
normal serum albumin, p. 323, Ch. 21 Bacterial Infections, p. 388, Ch. 26
nystatin, p. 416, Ch. 27 Cancer, p. 431, Ch. 28
omeprazole, p. 483, Ch. 30 Clotting Disorders, p. 349, Ch. 23
ondansetron, p. 490, Ch. 30 Diabetes Mellitus, p. 530, Ch. 33
oxymetazoline, p. 464, Ch. 29 Dysrhythmias, p. 332, Ch. 22
oxytocin, p. 553, Ch. 34 Epilepsy, p. 182, Ch. 13
penicillin G, p. 395, Ch. 26 Fungal, Viral, and Parasitic Diseases, p. 413, Ch. 27
permethrin, p. 587, Ch. 36 Gastrointestinal Tract Disorders, p. 477, Ch. 30
phenelzine, p. 133, Ch. 10 Glaucoma, p. 600, Ch. 37
phenobarbital, p. 188, Ch. 13 Grapefruit Juice and Drug Interactions, p. 23, Ch. 3
phenylephrine, p. 98, Ch. 8 Heart Failure, p. 288, Ch. 19
phenytoin, p. 190, Ch. 13 High Blood Cholesterol, p. 235, Ch. 16
potassium chloride, p. 260, Ch. 17 Hypertension, p. 267, Ch. 18
prazosin, p. 100, Ch. 8 Inflammatory Disorders, p. 363, Ch. 24
prednisone, p. 369, Ch. 24 Insomnia, p. 110, Ch. 9
procainamide, p. 339, Ch. 22 Muscle Spasms, p. 170, Ch. 12
propranolol, p. 340, Ch. 22 Myocardial Infarction, p. 310, Ch. 20
propylthiouracil, p. 519, Ch. 32 Neurodegenerative Diseases, p. 159, Ch. 12
psyllium mucilloid, p. 487, Ch. 30 Pain, p. 199, Ch. 14
raloxifene, p. 571, Ch. 35 Potentially Fatal Drug Reactions, p. 23, Ch. 3
ranitidine, p. 483, Ch. 30 Psychosis, p. 144, Ch. 11
reteplase, p. 312, Ch. 20 Renal Disorders, p. 250, Ch. 17
risperidone, p. 152, Ch. 11 Shock, p. 321, Ch. 21
sertraline, p. 133, Ch. 10 Skin Disorders, p. 587, Ch. 36
sildenafil, p. 556, Ch. 34 Stroke, p. 315, Ch. 20
sodium bicarbonate, p. 261, Ch. 17 Substance Abuse in the United States, p. 70, Ch. 7
spironolactone, p. 256, Ch. 17 Thyroid Disorders, p. 517, Ch. 32
Guide to Special Features 659
Vaccines and Immune Disorders, p. 374, Ch. 25 Patients Receiving Antidepressant Therapy, p. 130, Ch. 10
Vitamins, Minerals, and Dietary Supplements, Patients Receiving Antidysrhythmic Drugs, p. 336, Ch. 22
p. 497, Ch. 31 Patients Receiving Antihistamine Therapy, p. 461, Ch. 29
Patients Receiving Antineoplastic Therapy, p. 447, Ch. 28
Patients Receiving Antiseizure Drug Therapy, p. 192, Ch. 13
Life Span Fact
▼
Patients Receiving Antitubercular Drugs, p. 407, Ch. 26

Absorption of Food Diminishes with Age, p. 499, Ch. 31 Patients Receiving Atypical Antipsychotic Therapy, p. 153,
ADHD in Children, p. 137, Ch. 10 Ch. 11
Administering Ophthalmic Drugs to Children, p. 29, Ch. 3 Patients Receiving Bronchodilators, p. 469, Ch. 29
Administering Otic Drugs to Children, p. 31, Ch. 3 Patients Receiving Calcium Channel Blocker Therapy,
Anticholinergic Side Effects in Older Adults, p. 339, Ch. 22 p. 279, Ch. 18
Bleeding Complications in Elderly Patients, p. 352, Ch. 23 Patients Receiving Cholinergic Blocker (Anticholinergic)
Chewing and Swallowing Difficulties in Older Adults, Therapy, p. 96, Ch. 8
p. 504, Ch. 31 Patients Receiving Direct- and Indirect-Acting Cholinergic
Childhood Vaccine Act, p. 7, Ch. 3 Drug Therapy, p. 93, Ch. 8
Constipation in Older Adults, p. 486, Ch. 30 Patients Receiving Diuretic Therapy, p. 257, Ch.17
Crushing Medications for Children and Elderly Patients, Patients Receiving Drugs for Muscle Spasms or Spasticity,
p. 27, Ch. 3 p. 172, Ch. 12
Decrease in Bone Mass with Aging, p. 500, Ch. 31 Patients Receiving Drug Therapy for Peptic Ulcer Disease,
Depression in Elderly Patients, p. 124, Ch. 10 p. 484, Ch. 30
Drug Compliance Among Elderly Patients, p. 23, Ch. 3 Patients Receiving Drug Therapy with HMG-CoA Reductase
Drug Therapy in Older Adults, p. 57, Ch. 5 Inhibitors (Statins), p. 241, Ch. 16
Effects of BPH, p. 556, Ch. 34 Patients Receiving Immunosuppressants, p. 382, Ch. 25
Elderly Patients May Need Vitamin D Supplements, p. 499, Patients Receiving Insulin Therapy, p. 533, Ch. 33
Ch. 31 Patients Receiving Intravenous Fluid Therapy, p. 324,
Epilepsy in Youth and Elderly, p. 183, Ch. 13 Ch. 21
Herbs and Dietary Supplements for Children, p. 62, Ch. 6 Patients Receiving Iron Supplements, p. 503, Ch. 31
High Fever in Children, p. 183, Ch. 13 Patients Receiving Laxative Therapy, p. 487, Ch. 30
Laxative Misuse in Older Adults, p. 486, Ch. 30 Patients Receiving Local Anesthesia, p. 223, Ch. 15
Medication-Related Sleeping Problems in Elderly Patients, Patients Receiving NSAID Therapy, p. 367, Ch. 24
p. 110, Ch. 9 Patients Receiving Opioids, p. 206, Ch. 14
Older Adults at Particular Risk for Dehydration, p. 274, Ch. 18 Patients Receiving Oral Contraceptive Therapy, p. 548, Ch. 34
Potassium Channel Blocker Side Effects in Older Adults, Patients Receiving Organic Nitrate Therapy, p. 308, Ch. 20
p. 342, Ch. 22 Patients Receiving Pharmacotheraphy for HIV-AIDS,
Potential Vitamin Deficiency in Infancy and Childhood, p. 422, Ch. 27
p. 499, Ch. 31 Patients Receiving Pharmacotherapy for Glaucoma, p. 604,
Reduced Metabolic Enzyme Activity in Very Young and Ch. 37
Elderly Patients, p. 44, Ch. 4 Patients Receiving Pharmacotherapy for Lice or Mite
TCA Use in Elderly Patients, p. 125, Ch. 10 Infestation, p. 588, Ch. 36
Ventrogluteal Site for IM Injections in Children, p. 36, Ch. 3 Patients Receiving Pharmacotherapy for Osteoporosis,
Vitamin D Deficiency in Breastfed Infants, p. 499, Ch. 31 p. 572, Ch. 35
Patients Receiving Pharmacotherapy for Type 2 Diabetes,
p. 538, Ch. 33
Patients Receiving Phenothiazines and Nonphenothiazine
Therapy, p. 149, Ch. 11
Patients Receiving ACE Inhibitor Therapy, p. 276, Ch. 18 Patients Receiving Superficial Antifungal Therapy, p. 417,
Patients Receiving Adrenergic Blocker Therapy, p. 101, Ch. 8 Ch. 27
Patients Receiving Adrenergic Drug Therapy, p. 98, Ch. 8 Patients Receiving Systemic Corticosteroid Therapy, p. 523,
Patients Receiving Antianxiety Therapy, p. 115, Ch. 9 Ch. 32
Patients Receiving Antibacterial Therapy, p. 404, Ch. 26 Patients Receiving Thrombolytic Therapy, p. 313, Ch. 20
Patients Receiving Anticoagulant and Antiplatelet Therapy, Patients Receiving Thyroid Hormone Replacement, p. 519,
p. 353, Ch. 23 Ch. 32
660 Guide to Special Features
Neuromuscular System Disorders, p. 176, Ch. 12

Patients Need To Know Pain Medications, p. 214, Ch. 14
Psychoses and Degenerative Diseases of the Nervous
Antidepressants, p. 139, Ch. 10 System, p. 154, Ch. 11
Antiseizure Medications, p. 194, Ch. 13 Pulmonary Disorders, p. 472, Ch. 29
Anxiolytics and CNS Depressants, p. 119, Ch. 9 Reproductive Disorders, p. 558, Ch. 34
Autonomic Medications, p. 102, Ch. 8 Shock, p. 328, Ch. 21
Bacterial Infections, p. 409, Ch. 26 Skin Disorders, p. 594, Ch. 36
Bone or Joint Disorders, p. 578, Ch. 35 Taking Medications, p. 39, Ch. 3
Cancer, p. 449, Ch. 28 Treatment for Diabetes Mellitus, p. 539, Ch. 33
Coagulation Disorders, p. 358, Ch. 23 Vitamins, Minerals, or Nutritional Supplements, p. 505,
Digestive Disorders, p. 492, Ch. 30 Ch. 31
Drugs for Fluid, Acid–Base, and Electrolyte Disorders,
p. 262, Ch. 17
Drugs for Pain, p. 315, Ch. 20 SAFETY Alert
Dysrhythmias, p.343, Ch. 22
Endocrine Disorders, p. 524, Ch. 32 Accidental Overdose of Vitamins and Other Medications,
Eye and Ear Disorders, p. 608, Ch. 37 p. 505, Ch. 31
Fungal, Viral, or Parasitic Infections, p. 427, Ch. 27 Allergic Reactions and Antibiotics, p. 409. Ch. 26
Heart Failure, p. 297, Ch. 19 Drug-to-Food Interactions, p. 284, Ch. 18
Hypertension, p. 284, Ch. 18 Expiration Dates on Multidose Vials, p. 539, Ch. 33
Immune Disorders, p. 383, Ch. 25 Interpreting Physician Orders, p. 119. Ch. 9
Inflammatory Disorders, p. 370, Ch. 24 Medication Administration Error–Mistaken Patient Identity,
Lipid Disorders, p. 245, Ch. 16 p. 37, Ch. 3
Local Anesthetic Medications, p. 229, Ch. 15 Medication Label Confusion: Heparin, p. 358. Ch. 23
Medications with Abuse Potential, p. 80, Ch. 7 Soundalike Drug Names, p. 579, Ch. 35
Glossary
A fibers nerves that transmit sensations of sharp pain adrenergic blocker a drug that blocks the actions of the
(14) / page 199 sympathetic nervous system as in marijuana (8) / page 91
absorption (ab-SORP-shun) the process of moving a adrenergic drugs autonomic drugs that work by activating
drug across body membranes (4) / page 43 the sympathetic nervous system (8) / page 91
acetylcholine (Ach) (ah-SEET-ul-KOH-leen) primary neu- adrenocorticotropic hormone (ACTH) (uh-dreen-oh-
rotransmitter of the parasympathetic nervous system; also kor-tik-o-TRO-pik) hormone secreted by the pituitary
present at somatic neuromuscular junctions and at parasym- that stimulates the release of glucocorticoids by the adrenal
pathetic and sympathetic preganglionic nerves (8) / page 88 cortex (32) / page 520
acetylcholinesterase (AchE) (AS-ee-til-KOH-lin-ES-ter-ays) adverse drug events negative health effects caused by a
an enzyme that degrades acetylcholine within the syn- drug (3) / page 21
apse, enhancing the effects of the neurotransmitter (12) / adverse effects unwanted nontherapeutic effects (3) /
page 165 page 21
acidosis (ah-sid-OH-sis) condition of having too much aerosol (AIR-oh-sol) suspension of small liquid droplets
acid; plasma pH below 7.35 (17) / page 260 of drug, usually to cause bronchodilation (29) / page 456
acquired resistance when a microbe is no longer affected afterload pressure that must be overcome for the ventri-
by a drug following treatment with anti-infectives (26) / cles to eject blood from the heart (19) / page 289
page 392 agonists (AG-on-ists) drugs that are capable of binding
action potential (poh-TEN-shial) an electrical signal of with receptors in order to cause a cellular response (4) /
a single cell (muscle or nerve) generated by the opening page 47
and closing of special ion channels located on the cell’s akathisia (ACK-ah-THEE-shea) uncontrolled limb and
membrane (13) / page 189 body movements (11) / page 148
activated partial thromboplastin time (aPTT) (throm- alcohol intoxication (AL-ku-hol in-tak-su-KA-shun) a
bow-PLAS-tin) blood test used to determine how long it takes condition of altered mental and physical function result-
clots to form to regulate heparin dosage (23) / page 352 ing from drinking more alcoholic beverages within a time
active immunity stimulating the body to produce antibod- frame than the body can tolerate (7) / page 75
ies through the administration of a vaccine (25) / page 376 aldosterone (al-DOH-stair-own) hormone secreted by
acute gouty arthritis (ah-CUTE GOW-ty are-THRYE-tis) the adrenal cortex that increases sodium reabsorption in the
condition where uric acid crystals quickly accumulate in distal tubule of the kidney (17, 18) / pages 256, 274
the joints of the big toes, heels, ankles, wrists, fingers, alimentary canal (AL-uh-MEN-tare-ee) the hollow tube
knees, or elbows, resulting in red, swollen, or inflamed in the digestive system that starts in the mouth and includes
tissue (35) / page 577 the esophagus, stomach, small intestine, and large intestine
adaptive body defenses a second line of immune defense (30) / page 478
which are specific to particular threats (25) / page 375 alkalosis (al-kah-LOH-sis) condition of having too much
addiction (ah-DIK-shun) the continued use of a substance base; plasma pH above 7.45 (17) / page 260
despite its negative health and social consequences (7) / alkylation (AL-kill-AYE-shun) process by which cer-
page 71 tain chemicals attach to DNA and change its structure and
Addison’s disease (ADD-iss-uns) hyposecretion of glu- function (28) / page 437
cocorticoids and aldosterone by the adrenal cortex (32) / allergic reaction a hyper-response of body tissues to a
page 521 foreign substance (allergen), in which patients experience
adenoma (AH-den-OH-mah) benign tumor of glandular uncomfortable and potentially serious symptoms, includ-
tissue (28) / page 432 ing difficulty breathing, pain, swelling, skin rash, and other
adjuvant analgesics (ADD-jeh-vent an-ul-JEE-ziks) ad- unfavorable signs (3) / page 22
ditional pain killers provided when another is not provid- allergic rhinitis (rye-NYE-tis) syndrome of sneezing,
ing sufficient relief (14) / page 201 itchy throat, watery eyes, and nasal congestion resulting
adjuvant chemotherapy (AD-ju-vent) technique in which from exposure to antigens; also known as hay fever (29) /
antineoplastics are administered after surgery or radiation to page 458
effect a cure (28) / page 433 alopecia (AL-oh-PEESH-ee-uh) hair loss (28) / page 436
adrenal atrophy (AT-troh-fee) shrinkage of the adrenal alpha receptor type of subreceptor found in the sympa-
glands (38) / page 521 thetic nervous system (8) / page 90
adrenergic (add-rah-NUR-jik) a term relating to nerves alternate-day therapy taking a drug every other day in
that release norepinephrine or epinephrine (8) / page 90 order to minimize adverse effects (24) / page 368
G-1
G-2 Glossary
alveoli (al-VEE-oh-lie) dilated sacs at the end of the bron- anticholinergics drugs that inhibit the action of acetylcho-
chial tree where gas exchange occurs (29) / page 455 line at its receptor (8) / page 91
Alzheimer’s disease (AD) (ALLZ-heye-mers) most com- anticoagulant (ANT-eye-co-AG-you-lent) an agent that
mon dementia, characterized by loss of memory, confu- inhibits the formation of blood clots (23) / page 350
sion, disorientation, and loss of judgment; hallucinations antidepressants (AN-tee-dee-PRESS-ahnts) drugs used
and delusions may also occur (12) / page 164 for the treatment of depression and a range of anxiety
amenorrhea (ah-men-oh-REE-ah) lack of normal men- disorders, including panic, obsessive-compulsive, social
strual periods (34) / page 550 phobia, and post-traumatic stress disorders (9, 10) / pages
amides (AM-ides) type of chemical linkage found in some 110, 125
local anesthetics involving carbon, nitrogen, and oxygen antidiuretic hormone (ADH) (ANT-eye-deye-your-ET-ik)
(—NH—CO—) (15) / page 220 hormone produced by the hypothalamus that stimulates the
analgesic (an-ul-JEE-zik) drug used to reduce or elimi- kidneys to conserve water (18, 32) / pages 270, 514
nate pain (7, 14) / pages 70, 201 antiemetic (AN-tie-ee-MET-ik) drug that prevents vomit-
anaphylactic (ann-ah-fuh-LAK-tick) shock acute, life- ing (30) / page 489
threatening type of shock characterized by a history of al- antiflatulent (an-tie-FLAT-u-lent) drug that reduces gas
lergy with a sudden onset of symptoms following food or formation in the GI tract (30) / page 485
drug intake (21) / page 320 antigen (ANN-tih-jenz) a foreign organism or substance
anaphylaxis (ANN-a-fah-LAX-iss) an acute allergic re- that induces the formation of antibodies (21, 25) / pages
sponse to an antigen that results in severe hypotension and 326, 374
may cause death if untreated (3, 24) / pages 22, 364 anti-infective (ann-tie-in-FEK-tive) general term for any
androgens (AN-droh-jens) steroid sex hormones that medication effective against pathogens (26) / page 390
promote the appearance of masculine characteristics (34) / antiplatelet drugs (ant-eye-PLAY-tuh-let) medications
page 554 that decrease the coagulation function of platelets (23) /
anemia (ah-NEE-mee-ah) shortage of functional red page 350
blood cells or decreased oxygen-carrying ability of the antipsychotic drugs class of drugs used to treat psychosis
blood (28) / page 446 and other mental and emotional conditions (10) / page 135
anesthesia (ANN-ess-THEE-zee-uh) medical procedure antiretroviral (an-tie-RET-roh-veye-ral) type of drug
involving drugs that block the transmission of nerve im- effective against retroviruses (27) / page 420
pulses and cause loss of sensation and/or consciousness antitussive (anti-TUSS-ive) drug used to suppress cough
(15) / page 218 (29) / page 465
angina pectoris (an-JEYE-nuh PEK-tore-us) acute pain anxiety state of apprehension or dread due to a perceive
in the chest on physical or emotional exertion due to inad- threat or danger (9) / page 106
equate oxygen supply to the myocardium (20) / page 302
anxiolytics (ANG-zee-oh-LIT-iks) drugs that relieve anx-
angiotensin II (AN-geo-TEN-sin) chemical released in iety agents for mood stabilization (9) / page 109
response to falling blood pressure that causes vasoconstric-
apothecary system (ah-POTH-eh-kare-ee) former sys-
tion and release of aldosterone (18) / page 274
tem of weights and measures used by healthcare provid-
angiotensin-converting enzyme (ACE) (angeo-TEN-sin) ers and pharmacists; replaced by the metric system (3) /
enzyme responsible for converting angiotensin I to angio- page 25
tensin II (18) / page 274
assessment phase appraisal of a patient’s condition that
anorexia (AN-oh-REX-ee-uh) loss of appetite (30) / page 480 involves gathering and interpreting data (5) / page 52
anorexiant (AN-oh-REX-ee-ant) drug used to suppress asthma (AZ-muh) chronic inflammatory disease of the
appetite (30) / page 491 airways (29) / page 465
antacid (an-TASS-id) drug that neutralizes stomach acid astringent effect (ah-STRIN-jent) the shrinkage of swollen
(30) / page 485 membranes or binding together of body surface material (3) /
antagonism type of drug interaction in which one drug in- page 31
hibits the effectiveness of another (26) / page 393 atherosclerosis (ath-ur-oh-skler-OH-sis) a buildup of
antagonists (an-TAG-oh-nists) drugs that block the re- fatty substances and loss of elasticity of the arterial walls
sponse of another drug (4) / page 47 (16, 20) / pages 235, 302
anterior pituitary an area of the pituitary gland also atrioventricular (AV) node (ay-tree-oh-ven-TRIK-you-
known as adenohypophysis (32) / page 511 lur noad) mass of cardiac tissue that receives electrical
antibiotic (ann-tie-bye-OT-ik) substance produced by a impulses from the SA node and conveys them to the ven-
microorganism that inhibits or kills other microorganisms tricles (22) / page 333
(26) / page 390 atrioventricular bundle (ay-tree-oh-ven-TRIK-you-lur
antibodies (ANN-tee-BOD-eez) protein produced by the BUN-dul) specialized cardiac tissue that receives electrical
body in response to an antigen; used interchangeably with impulses from the AV node and sends them to the bundle
the term immunoglobulin (25) / page 375 branches also known as the bundle of His (22) / page 333
Glossary G - 3
attention deficit disorder (ADD) consistent difficulty in biotransformation (BEYE-oh-trans-for-MAY-shun) the

focusing attention on a task for a sufficient length of time chemical conversion of drugs from one form to another that
(7, 10) / pages 78, 137 may result in increased or decreased activity (4) / page 43
attention deficit–hyperactivity disorder (ADHD) a dis- bipolar disorder (bi-PO-ler) a disorder characterized by
order typically diagnosed in childhood and adolescence extreme and opposite feelings, such as euphoria and de-
characterized by hyperactivity as well as attention, organi- pression or calmness and rage; also called manic depres-
zation, and behavior control issues (7, 10) / pages 78, 136 sion (10) / page 133
aura (AUR-uh) sensory cue such as bright lights, smells, bisphosphonates (bis-FOSS-foh-nayts) family of drugs
or tastes that precede a migraine (14) / page 211 that block bone resorption by inhibiting osteoclast activity
autoantibodies (AW-tow-ANN-tee-BAH-dees) proteins (35) / page 572
called rheumatoid factors released by B lymphocytes; black box warning warning label surrounded by a black
these tear down the body’s own tissue (35) / page 575 border and issued by the FDA to emphasize the important
automaticity (aw-toh-muh-TISS-uh-tee) ability of cer- and serious life-threatening risks associated with use of the
tain myocardial cells to spontaneously generate an action drug (1, 9) / pages 6, 111
potential (22) / page 333 bone deposition the opposite of bone resorption; the pro-
B cell type of lymphocyte that is essential for the humoral cess of depositing mineral components into bone (35) /
immune response (25) / page 375 page 565
bacteriocidal (bak-teer-ee-oh-SY-dall) substance that bone resorption (ree-SORP-shun) process of bone de-
has ability to kill bacteria (26) / page 391 mineralization or the breaking down of bone into mineral
bacteriostatic (bak-teer-ee-oh-STAT-ik) substance that components (35) / page 565
can inhibit the growth of bacteria (26) / page 391 boosters an additional dose of a vaccine given months or
barbiturates (bar-bi-CHUR-ates) class of drugs de- years after the initial dose to increase the effectiveness of
rived from barbituric acid; they act as CNS depressants the vaccine (25) / page 376
and are used for their sedative and antiseizure effects (9) / bradycardia (bray-dee-KAR-DEE-ah) a condition of
page 116 slow heartbeat (18) / page 282
baroreceptors (BARE-oh-ree-sep-tours) nerves located bradykinin (bray-dee-KYE-nin) chemical mediator of
in the walls of the atria, aortic arch, vena cava, and carotid pain released following tissue damage (14) / page 208
sinus that sense changes in blood pressure (18) / page 270 breakthrough bleeding bleeding at abnormal times dur-
benign (bee-NINE) neither life threatening nor fatal (28) / ing the menstrual cycle (34) / page 550
page 432 broad-spectrum antibiotic anti-infective that is effective
benign prostatic hypertrophy (BPH) (bee-NINE pros- against many different gram-positive and gram-negative
TAT-ik hy-PURR-tro-fee) nonmalignant enlargement of organisms (26) / page 393
the prostate gland (34) / page 557 bronchi (BRON-ky) primary passageway of the bronchial
benzodiazepines (ben-zo-di-AZ-eh-peenz) class of drugs tree that contains smooth muscle (29) / page 455
used to treat anxiety and insomnia (9) / page 113 bronchioles (BRON-key-oles) very small bronchi (29) /
beta-lactam ring (bay-tuh LAK-tam) chemical structure page 455
found in most penicillins and some cephalosporins (26) / bronchoconstriction (BRON-koh-kun-STRIK-shun)
page 393 decrease in diameter of the airway due to contraction of
beta-lactamase/penicillinase (bay-tuh-LAK-tam-ace/ bronchial smooth muscle (29) / page 466
pen-uh-SILL-in-ace) enzyme present in certain bacteria bronchodilation (BRON-koh-dye-LAY-shun) increase
that is able to inactivate many penicillins and some cepha- in diameter of the airway due to relaxation of bronchial
losporins (26) / page 393 smooth muscle (29) / page 467
beta-receptor type of subreceptor found in the sympathet- bronchospasm (bron-koh-SPAZ-um) rapid constriction
ic nervous system (8) / page 90 of the airways (29) / page 466
bile acid (BEYE-ul) chemicals secreted in bile that aid in buccal route (BUCK-ahl) the administration of medica-
the digestion of fats (16) / page 241 tions by the cheek or mouth (3) / page 27
bioavailability (BEYE-oh-ah-VALE-ah-BILL-ih-TEE) bundle branches (BUN-dul BRAN-chez) electrical con-
the ability of a drug to reach its target cells and produce its duction pathway in the heart leading from the AV bundle
effect (2) / page 15 and through the wall between the ventricles (22) / page 333
biologic response modifiers natural substances that are C fibers nerves that transmit dull, poorly localized pain
able to enhance or stimulate the immune system (25) / (14) / page 199
page 379 calcifediol (kal-SIF-eh-DYE-ol) intermediate form of vi-
biologics (beye-oh-LOJ-iks) chemical agents that produce tamin D (35) / page 565
biological responses within the body; they are synthesized by calcitonin (kal-sih-TOH-nin) treatment typically adminis-
cells of the human body, animal cells, or microorganisms (1) / tered to women who cannot take estrogen or bisphosphonate
page 4 therapy or for clients with Paget’s disease (35) / page 565
G-4 Glossary
calcitriol (kal-si-TRY-ol) substance that is transformed in club drugs substances taken at dance clubs, all-night par-
the kidneys during the second step of the conversion of ties, and raves (7) / page 70
vitamin D to its active form (35) / page 565 CNS depressants (dee-PRESS-ahnts) drugs that lower
calcium channel blockers (CCBs) drugs that block the neuronal activity within the CNS (9) / page 110
flow of calcium ions into myocardial cells (18) / page 278 coagulation (co-ag-you-LAY-shun) the process of blood
calcium ion channel (KAL-see-um) pathway in a plasma clotting (23) / page 347
membrane which allows calcium ions to enter the cell dur- coagulation cascade (cass-KADE) a complex series of
ing an action potential (22) / page 335 steps by which blood flow stops (23) / page 347
cancer (KAN-sir) malignant disease characterized by rap- colloids (KO-loyds) type of IV fluid replacement solution
idly growing, invasive cells that spread to other regions of consisting of large protein molecules that are unable to
the body and eventually kill the host (28) / page 431 cross membranes (21) / page 323
capsid (CAP-sid) protein coat that surrounds a virus (27) / combination drugs drug product with more than one ac-
page 417 tive generic ingredient (2) / page 15
carbonic anhydrase (kar-BON-ik an-HY-drase) enzyme complementary and alternative medicine (CAM) thera-
that forms carbonic acid by combining carbon dioxide and pies an extremely diverse set of therapies and healing sys-
water (17) / page 256 tems that are considered to be outside of mainstream health
carcinogen (kar-SIN-oh-jen) any physical, chemical, or bi- care (1, 6) / pages 4, 60
ological factor that causes or promotes cancer (28) / page 432 compliance (kom-PLY-ans) taking a medication in the
cardiac output amount of blood pumped by each ventricle way it was prescribed by the practitioner; in the case of
in 1 minute (18) / page 269 OTC drugs, following the instructions found on the label
cardiogenic shock (kar-dee-oh-JEN-ik) type of shock (3) / page 22
caused when the heart is diseased such that it cannot main- constipation (kon-stah-PAY-shun) infrequent passage of
tain circulation to the tissues (21) / page 320 abnormally hard and dry stools (30) / page 486
cathartic (kah-THAR-tik) drug that causes complete contractility (kon-trak-TILL-eh-tee) the strength by
evacuation of the bowel (30) / page 486 which the myocardial fibers contract (19) / page 289
chemical name strict chemical nomenclature used for contraindications (CON-trah-EN-deh-KAY-shuns)
naming drugs established by the International Union of situations under which drugs should not be used (3) /
Pure and Applied Chemistry (IUPAC) (2) / page 14 page 21
chemoprophylaxis (kee-moh-pro-fill-AX-is) use of a controlled substance in the United States, a drug restricted
drug to prevent an infection (26) / page 392 by the Comprehensive Drug Abuse Prevention and Control
chemotherapy drug treatment of cancer (28) / page 433 Act (2) / page 16
cholecalciferol (KOH-lee-kal-SIF-er-ol) inactive form of convulsions (kon-VULL-shuns) uncontrolled muscle
vitamin D (35) / page 565 contractions or spasms that occur in the face, torso, arms,
cholinergic (kol-in-UR-jik) a term relating to nerves that or legs (13) / page 181
release acetylcholine (8) / page 90 coronary artery bypass graft (CABG) surgery surgical
cholinergic blocker a drug that blocks the actions of the procedure performed to restore blood flow to the myocar-
parasympathetic nervous system (8) / page 91 dium by using a section of the saphenous vein or internal
cholinergic drugs another name for parasympathomimetic mammary artery to go around the obstructed coronary ar-
drugs (8) / page 91 tery (20) / page 304
chronic bronchitis (KRON-ik bron-KEYE-tis) chronic coronary arteries (KOR-un-air-ee AR-tur-ees) vessels
disease of the lungs characterized by excess mucus produc- that bring oxygen and nutrients to the myocardium (20) /
tion and inflammation (29) / page 472 page 302
clinical depression a major depressive disorder comprising corpora cavernosa (KORP-us kav-ver-NOH-sum) tis-
a depressed affect plus at least five of the common symp- sues in the penis that fill with blood during an erection (34) /
toms lasting for a minimum of two weeks (10) / page 123 page 555
clinical pharmacology an area of medicine devoted to the corpus luteum (KORP-us LUTE-ee-uhm) temporary
evaluation of drugs used for human therapeutic benefit (1) / hormone-secreting gland in women which is formed when
page 7 a follicle releases its oocyte (34) / page 544
closed comedones (KOME-eh-dones) commonly called corticosteroid (KORT-ik-ko-STARE-oyd) class of hor-
whiteheads, this type of acne develops just beneath the sur- mones secreted by the outer cortex of the adrenal glands
face of the skin (36) / page 589 (32) / page 520
closed-angle glaucoma (glaw-KOH-mah) called acute cretinism (KREE-ten-izm) dwarfism and mental retarda-
glaucoma, this type of glaucoma is caused by the iris tion caused by lack of thyroid hormone during infancy (32) /
blocking trabecular meshwork, hindering outflow of aque- page 516
ous fluid (37) / page 601 Crohn’s disease (KROHNS) chronic inflammatory bowel
clotting factors substances contributing to the process of disease affecting the ileum and sometimes the colon (30) /
blood clotting (23) / page 347 page 480
Glossary G - 5
cross-tolerance (krause TOL-er-ans) the process of diastolic pressure (DEYE-ah-stall-ik) blood pressure
adapting to a new drug as a result of having already been during the relaxation phase of heart activity (18) / page 267
exposed to a related drug (7) / page 73 dietary fiber substance neither digested nor absorbed that
crystalloids (KRIS-tuh-loyds) type of IV fluid replace- contributes to the fecal mass (30) / page 486
ment solution that resembles blood plasma and is capable Dietary Supplement and Nonprescription Drug
of crossing membranes (21) / page 323 Consumer Protection Act law that requires companies
culture and sensitivity (C&S) testing laboratory test used that market herbal and dietary supplements to include their
to identify bacteria and to determine which antibiotic is address and phone number on the product labels so con-
most effective (26) / page 393 sumers can report adverse events (6) / page 67
Cushing’s syndrome (KUSH-ings) condition caused by Dietary Supplement Health and Education Act (DSHEA)
excessive corticosteroid secretion by the adrenal glands or of 1994 primary law in the United States regulating herb
by overdosage with corticosteroid medication (24, 32) / and dietary supplements (6) / page 66
pages 368, 522 dietary supplements a nondrug substance regulated by the
cyclooxygenase (COX) (sye-klo-OK-sah-jen-ays) key DSHEA (6) / page 66
enzyme in the prostaglandin metabolic pathway that is digestion (dye-JES-chun) process by which the body
blocked by aspirin and other NSAIDs (14, 24) / pages breaks down ingested food into small molecules that can
208, 366 be absorbed (30) / page 478
cycloplegia (sy-kloh-PLEE-jee-ah) blurred vision (37) / directly observed therapy (DOT) treatment protocol by
page 602 which a healthcare worker or other trained individual admin-
cycloplegic drug (sy-kloh-PLEE-jik) drugs that relax or ister the medications and watch the patient swallow the dose
temporarily paralyze ciliary muscles (37) / page 605 to ensure that the medication is taken exactly as prescribed
cytokines (SYE-toh-kines) chemicals produced by white to decrease the risk for relapse, the spread of the infection in
blood cells, such as interleukins, leukotrienes, interferon, the community, and the development of drug resistance that
and tumor necrosis factor, that guide the immune response could result from erratic or partial treatment (26) / page 408
(25) / page 375 disease-modifying antirheumatic (ANTY-roo-MATIK)
cytotoxic T cell type of lymphocyte that directly attacks drugs (DMARDs) drugs that reduce destruction of the joints
and destroys antigens (25) / page 375 and progression of rheumatoid arthritis (35) / page 575
deep venous thrombosis (DVT) a condition in which distribution (dis-tree-BU-shun) the process of transport-
thrombi in the venous system form in the veins of the legs ing drugs through the body (4) / page 43
due to sluggish blood flow (23) / page 349 diuretic (deye-your-ET-ik) drug that increases urine flow
defecation (def-ah-KAY-shun) evacuation of the colon; (17, 18) / pages 252, 269
bowel movement (30) / page 486 dry powder inhaler (DPI) device used to convert a solid drug
dementia (dee-MEN-she-ah) degenerative disorder char- to a fine powder for the purpose of inhalation (29) / page 456
acterized by progressive memory loss, confusion, and duration of drug action the amount of time it takes for a
the inability to think or communicate effectively (12) / drug to maintain its desired effect (4) / page 46
page 158 dwarfism below normal height caused by a deficiency in
depolarization (dee-po-lur-eye-ZAY-shun) condition in thyroid hormone or growth hormone (32) / page 514
which the plasma membrane charge is changed such that dysentery (DISS-en-tare-ee) severe diarrhea that may in-
the inside is made less negative (22) / page 335 clude bleeding (27) / page 426
depression (dee-PRESS-shun) an emotional disorder dysfunctional uterine bleeding hemorrhage that occurs at
characterized by many symptoms, some of which are de- abnormal times or in abnormal quantities during the men-
pressed mood, lack of energy, sleep disturbances, abnor- strual cycle (34) / page 549
mal eating patterns, and feelings of despair, guilt, and mis- dyslipidemia (dys-lip-i-DEEM-ee-uh) an abnormal amount
ery (10) / page 123 of lipid in the blood (16) / page 235
dermatitis (dur-mah-TIE-tiss) inflammatory condition of dysrhythmias (diss-RITH-mee-uhz) abnormalities in
the skin characterized by itching and scaling (36) / page 591 cardiac rhythm (22) / page 332
designer drugs (de-ZEYE-ner drugs) drugs that are pro- dysthymic disorder (dis-THEYE-mick) less severe type
duced in a laboratory and are intended to mimic the effects of mood disorder that may prevent a person from feeling
of other psychoactive controlled substances (7) / page 70 well or functioning normally (10) / page 124
diabetes insipidus (die-uh-BEE-tees in-SIP-uh-dus) ex- dystonia (diss-TONE-ee-ah) muscle spasm characterized
cessive urination due to lack of secretion of antidiuretic by rigidity and abnormal, occasionally painful, movements
hormone (32) / page 514 or postures (12) / page 172
diabetic ketoacidosis (DKA) potentially life-threatening eclampsia (ee-KLAMP-see-uh) condition in which seizures
condition of patients with diabetes mellitus caused by aci- and/or a coma develop in a patient with pre-eclampsia (13) /
dosis and the uncontrolled accumulation of ketones bodies page 183
(33) / page 530 ectopic foci/pacemakers (ek-TOP-ik FO-si) cardiac tis-
diarrhea abnormal frequency and liquidity of bowel sue outside the normal cardiac conduction pathway that
movements (30) / page 488 generates action potentials (22) / page 335
G-6 Glossary
eczema (ECK-zih-mah) also called atopic dermatitis, a etiologies (e-tee-OL-o-gees) causes of the patient’s dis-
skin disorder with unexplained symptoms of inflammation, ease or condition (5) / page 53
itching, and scaling (36) / page 591 evaluation criteria objective assessment of the effective-
efficacy (EFF-ik-ah-see) the effectiveness of a drug in ness and impact of interventions (5) / page 54
producing a more intense response as its concentration is evaluation phase part of the nursing process that provides
increased (4) / page 47 an objective assessment of the effectiveness of the inter-
electrocardiogram (ECG) (e-lek-tro-KAR-dee-oh-gram) ventions (5) / page 56
device that records the electrical activity of the heart (22) / excretion (eks-KREE-shun) the process of removing sub-
page 333 stances from the body (4) / page 44
electrolytes (ee-LEK-troh-lites) charged substances in expectorant (eks-PEK-tor-ent) drug used to increase
the blood, such as sodium, potassium, calcium, chloride, bronchial secretions (29) / page 465
and phosphate (17, 18) / pages 258, 273 external otitis (oh-TYE-tiss) commonly called swim-
embolus (EM-boh-luss) a blood clot carried in the blood- mer’s ear, this is inflammation of the outer ear (37) /
stream (23) / page 349 page 606
emesis (EM-eh-sis) vomiting (30) / page 489 extrapyramidal symptoms (EPS) (peh-RAM-ed-el)
emetic (ee-MET-ik) drug used to induce vomiting (30) / symptoms where muscles become very rigid because of
page 490 overmedication with antipsychotics or by lack of dopamine
emphysema (em-fuss-EE-muh) terminal lung disease function in the corpus striatum (11) / page 148
characterized by dilation of the alveoli (29) / page 472 false neurotransmitter (NYUR-oh-TRANS-mitt-ur)
endogenous opioids (en-DAHJ-en-nuss O-pee-oyds) chemical that simulates a natural neurotransmitter but does
chemicals produced naturally within the body that de- not produce the same physiologic effect (18) / page 282
crease or eliminate pain; they closely resemble the actions of febrile seizures abnormal state of neuronal discharge re-
morphine (14) / page 200 sulting from high fever (13) / page 182
endometrial carcinoma (en-doh-MEE-tree-ahl CAR-sin- fibrillation (fi-bruh-LAY-shun) type of dysrhythmia in
OH-mah) cancer of the endometrium (34) / page 550 which the chambers beat in a highly disorganized manner
endometriosis (en-doh-MEE-tree-oh-sis) abnormal loca- (22) / page 332
tion of endometrial tissues (34) / page 550 fibrin (FEYE-brin) an insoluble protein formed from fi-
end-stage renal disease (ESRD) when the kidneys are brinogen by the action of thrombin in the blood-clotting
no longer able to function at a level necessary for day-to- process (23) / page 347
day living, and dialysis and kidney transplantation become fibrinogen (feye-BRIN-oh-jen) blood protein converted
treatment alternatives (17) / page 251 to fibrin by the action of thrombin in the blood-clotting
enteral nutrition treatment of undernutrition by the oral process (23) / page 347
route or through a feeding tube (31) / page 504 fibrinolysis (feye-brin-OL-oh-sis) removal of a blood
enteral route (EN-tur-ul) the major route by which clot (23) / page 349
drugs enter the body through the digestive tract (3) / filtrate (FIL-trate) fluid in the nephron that is filtered at
page 27 Bowman’s capsule (17) / page 250
enteric-coated (in-TARE-ik) hard, waxy coating that en- first-pass effect a mechanism whereby drugs are ab-
ables drugs to resist the acidity of the stomach; enables sorbed across the intestinal wall and enter into blood ves-
drugs to dissolve in the small intestine (3) / page 27 sels, known as the hepatic portal circulation, which carries
enterohepatic recirculation (EN-ter-oh-HEE-pah-tik) blood directly to the liver (4) / page 43
recycling of drugs and other substances by the circulation folic acid (foh-lik) B vitamin that is a coenzyme in pro-
of bile through the intestine and liver (4) / page 44 tein and nucleic acid metabolism; also known as folate (28) /
epilepsy (EPP-ih-lepp-see) disorder of the CNS charac- page 440
terized by seizures and/or convulsions (13) / page 181 follicle-stimulating hormone (FSH) hormone secreted by
epinephrine (EH-pin-NEF-rin) neurotransmitter or medi- the pituitary gland that regulates sperm or egg production
cation that activates the sympathetic nervous system (8) / (34) / page 543
page 90 follicular cells (fo-LIK-yu-lur) cells in the thyroid gland
erythema (ear-ih-THEE-mah) redness associated with that secrete thyroid hormone (32) / page 516
skin irritation (36) / page 584 formularies (FOR-mew-LEH-reez) lists of drugs and
erythropoietin (ee-rith-ro-po-EE-tin) hormone secreted drug recipes commonly used by pharmacists (1) / page 5
by the kidney that stimulates red blood cell production (17) / fungi (FUN-jeye) kingdom of organisms that includes
page 252 mushrooms, yeasts, and molds (27) / page 413
esters (ES-turs) type of chemical linkage found in some local ganglia (GANG-lee-ah) collections of neuron cell bodies
anesthetics involving carbon and oxygen (—CO—O—) (15) / located outside the CNS (8) / page 90
page 220 gastroesophageal reflux disease (GERD) (GAS-troh-
estrogen (ES-troh-jen) class of steroid sex hormones pro- ee-SOF-ah-JEEL REE-flux) the regurgitation of stomach
duced by the ovary (34) / page 544 contents into the esophagus (30) / page 480
Glossary G - 7
general anesthesia medical procedure that produces loss hemostasis (hee-moh-STAY-sis) the slowing or stopping
of sensation throughout the entire body and unconscious- of blood flow (23) / page 347
ness (15) / page 218 hemostatics (hee-moh-STAT-iks) drugs used to prevent
generalized anxiety disorder (GAD) difficult-to-control, and treat excessive bleeding from surgical sites (23) /
excessive anxiety that lasts 6 months or more (9) / page 106 page 350
generalized seizures seizures that travel throughout the herb a plant with a soft stem that is used in healing or as a
entire brain on both sides (13) / page 183 seasoning (6) / page 61
generic name (je-NARE-ik) nonproprietary name of a high-density lipoprotein (HDL) lipid-carrying particle in
drug assigned by the government (2) / page 14 the blood that contains high amounts of protein and lower
gliomas (glee-OH-muhz) malignant tumors of the brain amounts of cholesterol; considered to be “good” choles-
(28) / page 432 terol (16) / page 236
glucagon (GLUE-kah-gon) pancreatic hormone that in- highly active antiretroviral therapy (HAART) type of
creases blood sugar (33) / page 529 drug therapy for HIV infection that includes high doses of
glucocorticoids (glu-ko-KORT-ik-oydz) type of hor- multiple medications that are given together (27) / page 420
mone secreted by the outer portion of the adrenal gland histamine (HISS-tuh-meen) chemical released by mast
that includes cortisol (32) / page 520 cells in response to an antigen; causes dilation of blood
glycoprotein IIb/IIIa (GLEYE-koh-proh-teen) enzyme vessels, smooth muscle constriction, tissue swelling, and
responsible for platelet aggregation (23) / page 356 itching (24) / page 363
goal an objective that the patient or nurse seeks to attain or HMG-CoA reductase (ree-DUCK-tase) primary enzyme
achieve (5) / page 54 in the biochemical pathway for the synthesis of cholesterol
(16) / page 238
gonadocorticoids (go-NAD-oh-KORT-ikoyds) hormones
secreted by the adrenal cortex; they are mostly androgens hormone replacement therapy (HRT) treatment for
(male sex hormones), though small amounts of estrogens menopausal symptoms and to prevent long-term conse-
(female sex hormones) are produced (32) / page 521 quences of estrogen loss that provides doses of estrogen,
sometimes combined with a progestin (34) / page 549
gonadotropin releasing hormone (GnRH) (go-NAD-
oh-TROPE-en) hormone secreted by the hypothalamus hormones chemicals secreted by endocrine glands that
which travels to the pituitary gland to stimulate the secre- act as chemical messengers to affect homeostasis (32) /
tion of follicle-stimulating hormone (34) / page 543 page 511
gout (GOWT) metabolic disorder characterized by the ac- host an organism that is being infected by a microbe (27) /
cumulation of uric acid in the bloodstream or joint cavities page 418
(35) / page 576 host flora (host FLOR-uh) normal microorganisms found
Graves’ disease syndrome caused by hypersecretion of in or on a patient (26) / page 393
thyroid hormone (32) / page 516 household system older system of measurement involv-
H+, K+-ATPase enzyme responsible for pumping acid ing teaspoons, tablespoons, cups, drops, pounds, etc. (3) /
onto the mucosal surface of the stomach (30) / page 482 page 25
H1-receptor blocker drug that blocks the effects of hista- humoral immunity (HYOU-mor-ul eh-MEWN-uh-tee)
mine in smooth muscle in the bronchial tree (29) / page 456 a specific body defense mechanism involving the produc-
tion and release of antibodies (25) / page 375
H2-receptor blocker drug that inhibits the effects of hista-
mine at its receptors in the GI tract (30) / page 483 hypercholesterolemia (HEYE-purr-koh-LESS-tur-ol-
EEM-ee-uh) high levels of cholesterol in the blood (16) /
half-life (t1/2) the length of time required for a drug to de- page 235
crease its concentration in the plasma by one-half of the
original amount (4) / page 45 hyperglycemic effect (hi-pur-gli-SEEM-ik) describes
the action of lowering blood sugar (33) / page 529
heart failure (HF) disease in which the heart muscle can-
not contract with sufficient force to meet the body’s meta- hyperkalemia (heye-purr-kah-LEE-mee-ah) high potas-
bolic needs (19) / page 288 sium levels in the blood (17, 18) / pages 256, 274
Helicobacter pylori (hee-lick-oh-BAK-tur py-LOR-eye) hyperlipidemia (HEYE-purr-LIP-id-EEM-ee-uh) ex-
bacterium associated with a large percentage of peptic ulcer cess amounts of lipids in the blood (16) / page 235
disease (30) / page 479 hypernatremia high sodium level in the blood (17) /
helminth (HELL-minth) type of flat, round, or segmented page 259
worm (27) / page 427 hypertension (HTN) (heye-purr-TEN-shun) high blood
helper T cell type of lymphocyte that coordinates both pressure (18) / page 266
the humoral and cell-mediated immune responses and that hypertriglyceridemia (HEYE-purr-tri-gliss-ur-i-DEEM-
is the target of the human immunodeficiency virus (25) / ee-uh) elevated triglycerides (16) / page 235
page 375 hypervitaminosis excess intake of vitamins (31) /
hemorrhagic stroke (hee-moh-RAJ-ik) type of stroke page 499
caused by bleeding from a blood vessel in the brain (20) / hypoglycemic effect (hi-po-gli-SEEM-ik) describes the
page 314 action of increasing blood sugar (33) / page 529
G-8 Glossary
hypogonadism (hi-poh-GO-nad-izm) below normal se- insulin analogs (ANNAH-logs) recombinant human DNA
cretion of the steroid sex hormones (34) / page 554 insulins that have been modified to have rapid or prolonged
hypokalemia (hi-poh-kah-LEE-mee-ah) low potassium durations (33) / page 531
levels in the blood (17, 18) / pages 252, 274 insulin resistance phenomena in which target tissues have
hyponatremia (hi-po-nay-TREE-mee-uh) low levels of become unresponsive to insulin (33) / page 534
sodium in the blood (17) / page 259 international normalized ratio (INR) laboratory value
hypothalamus (hi-po-THAL-ih-mus) region of the brain used to monitor the degree of blood anticoagulation during
that affects emotions and drives and that secretes releasing warfarin therapy (23) / page 352
factors that affect the pituitary gland (32) / page 511 interventions actions that produce an effect or that is in-
hypovolemic shock (hi-poh-voh-LEEM-ik) type of tended to alter the course of a disease or condition (5) /
shock caused by loss of fluids such as that which occurs page 53
during hemorrhaging, extensive burns, or severe vomiting intracellular parasite an infectious microbe that lives in-
or diarrhea (21) / page 320 side host cells (27) / page 418
immune response adaptive response to defend the body intradermal (ID) route (IN-trah-DERM-ul) method of
against a particular threat (25) / page 375 parenteral drug delivery in which drugs are injected into
immunoglobulin (Ig) (ih-MEW-noh-GLOB-you-lin) the dermis of the skin (3) / page 33
protein produced by the body in response to an antigen; used intramuscular (IM) route (IN-trah-musk-u-lar) method
interchangeably with the term antibody (25) / page 375 of parenteral drug delivery in which drugs are injected into
immunomodulator (ih-mew-no-MOF-you-layter) a layers of muscle beneath the skin (3) / page 36
general term referring to any drug that affects body de- intravenous (IV) route (IN-trah-VEE-nus) method of
fenses (25) / page 374 parenteral drug delivery in which drugs are injected into
immunosuppressant (ih-MEW-noh-suh-PRESS-ent) the venous circulation (3) / page 37
any drug, chemical, or physical agent that lowers the natural intrinsic factor chemical secreted by the stomach that is
immune defense mechanisms of the body (25) / page 380 required for absorption of vitamin B12 (31) / page 499
implementation phase part of the nursing process during islets of Langerhans (EYE-lits of LANG-gur-hans) clus-
which the nurse carries out activities that assist in accom- ters of cells in the pancreas responsible for the secretion of
plishing established goals (5) / page 55 insulin and glucagon; also called the pancreatic islets (33) /
impotence (IM-poh-tense) inability to obtain or sustain page 529
an erection; also called erectile dysfunction (34) / page 555 keratinization (keh-RAT-en-eye-zay-shun) development
incretin–glucose control mechanism in response to a of the stratum corneum or horny layer of epithelial tissue (36) /
meal, the mechanism by which incretins (intestinal hor- page 589
mones) signal the pancreas to increase insulin secretion keratolytic agents (keh-RAT-oh-lih-tik) drugs used to
and the liver to stop producing glucagon, thereby lowering promote shedding of old skin (36) / page 590
blood glucose levels (33) / page 537 ketoacids (KEY-to-ass-ids) waste products of fat metabo-
incretins (EN-kreh-tenz) hormones secreted by the intes- lism that lower the pH of the blood (33) / page 530
tines in response to a meal when blood glucose is elevated leukemia (lew-KEE-mee-ah) cancer of the blood character-
(33) / page 537 ized by overproduction of white blood cells (28) / page 432
inflammation (IN-flah-MAY-shun) nonspecific body de- libido (lih-BEE-do) interest in sexual activity (34) / page 554
fense that occurs in response to an injury or antigen (24) / limbic system (LIM-bik) area in the brain responsible for
page 363 emotion, learning, memory, motivation, and mood (9) /
inflammatory bowel disease (IBD) diseases with ulcer- page 107
ation of the intestine, including Crohn’s disease and ulcer- lipoma (lip-OH-mah) benign tumor of fat tissue (28) /
ative colitis, characterized by abdominal cramping, diar- page 432
rhea, and weight loss (30) / page 480 lipoproteins (LIP-oh-PROH-teenz) substance carrying
influenza (in-flew-EN-zah) common viral infection of the lipids in the bloodstream (16) / page 236
respiratory system; often called flu (27) / page 424 liposomes (LIP-oh-sohms) small sacs of lipids designed
innate body defenses first line of protection from patho- to carry drugs inside them (28) / page 441
gens which serve as general barriers to microbes or envi- local anesthesia loss of sensation to a relatively small part
ronmental hazards (25) / page 374 of the body without loss of consciousness (15) / page 218
inotropic drug (eye-noh-TROW-pik) medication that low-density lipoprotein (LDL) lipid-carrying particle
changes the force of contraction of the heart (21) / page 325 that contains lower amounts of protein and high amounts
inotropic effect (in-oh-TRO-pik) change in the strength of cholesterol; considered to be “bad” cholesterol (16) /
or contractility of the heart (19) / page 289 page 236
insomnia (in-SOM-nee-uh) the inability to fall asleep or low molecular weight heparins (LMWHs) heparin-like
stay asleep (9) / page 109 drugs that inhibit blood clotting (23) / page 351
insulin (IN-sule-in) pancreatic hormone that decreases lumen (LOO-men) the cavity or channel of a hollow tube
blood sugar levels (33) / page 529 such as a blood vessel (18) / page 269
Glossary G - 9
luteinizing hormone (LH) (LEW-ten-iz-ing) hormone muscarinic (MUS-kah-RIN-ik) type of cholinergic re-
secreted by the pituitary gland that triggers ovulation in the ceptor found in smooth muscle, cardiac muscle, and glands
female and stimulates sperm production in the male (34) / (8) / page 90
page 543 mutations (myou-TAY-shuns) permanent, inheritable
lymphomas (lim-FOH-mahz) cancer of lymphatic tissue changes to DNA (26) / page 391
(28) / page 432 mycoses (my-KOH-sees) diseases caused by fungi (27) /
major depressive disorder a disorder characterized by at page 413
least five symptoms of depression (10) / page 123 mydriasis (mih-DRY-uh-siss) dilation of the pupil (37) /
major mineral (macromineral) inorganic compound page 601
needed by the body in amounts of 100 mg or more daily mydriatic drugs (mih-DRY-atik) drugs that dilate the
(31) / page 500 pupils (37) / page 605
malaria (mah-LARE-ee-ah) tropical disease character- myocardial infarction (MI) (meye-oh-KAR-dee-ul in-
ized by severe fever and chills; caused by the protozoan FARK-shun) medical emergency in which a blood clot
Plasmodium (27) / page 426 blocks a portion of a coronary artery (20) / page 310
malignant (mah-LIG-nent) life threatening or fatal (28) / myocardial ischemia (meye-oh-KAR-dee-ul ik-SKEE-
page 432 mee-uh) condition in which there is a lack of blood supply
mast cell connective tissue cell located in tissue spaces to the myocardium due to a constriction or obstruction of a
that releases histamine following injury (24) / page 363 blood vessel (20) / page 302
mastoiditis (mass-toy-DYE-tuss) inflammation of the myxedema (mix-uh-DEEM-uh) condition caused by in-
mastoid sinus (37) / page 606 sufficient secretion of thyroid hormone (32) / page 516
mechanism of action how a drug exerts its effects (2) / narcolepsy (NAR-koh-lep-see) condition characterized
page 13 by uncontrolled daytime sleepiness (7) / page 78
menopause (MEN-oh-paws) time when females stop se- narcotic (nar-KOT-ik) natural or synthetic drug related
creting estrogen and menstrual cycles cease (34) / page 549 to morphine; may be used as a broader legal term referring
menorrhagia (men-oh-RAGE-ee-uh) prolonged or ex- to hallucinogens (LSD), CNS stimulants, marijuana, and
cessive menstruation (34) / page 550 other illegal drugs (14) / page 202
metabolism (meh-TAHB-oh-liz-ehm) the sum total of all narrow-spectrum antibiotic anti-infective that is effec-
chemical reactions in the body or an organ (e.g., the liver) tive against only one or a small number of organisms (26) /
(4) / page 43 page 393
metastasis (mah-TAS-tah-sis) travel of cancer cells from natriuretic peptide (hBNP) (na-tree-ur-ET-ik) hormone
their original site to a distant tissue (28) / page 432 that increases the urinary excretion of sodium and dilates
metered-dose inhaler (MDIs) device used to deliver a blood vessels (19) / page 297
precise amount of drug to the respiratory system (29) / natural alternative therapies herbs, natural extracts, vita-
page 456 mins, minerals, or dietary supplements (1) / page 4
metric system the most common system of measurement; nebulizer (NEB-you-lyes-ur) device used to convert liq-
involves kilograms (kg), grams (g), milligrams (mg), mi- uid drugs into a fine mist for the purpose of inhalation (29) /
crograms (mcg), and so on (3) / page 24 page 456
migraine (MYE-grayne) severe headache preceded by au- negative symptoms symptoms that subtract from normal
ras that may include nausea and vomiting (14) / page 211 behavior; signs that are used to assist with the diagnosis of
mineralocorticoid (min-ur-al-oh-KORT-ik-oyd) hor- schizophrenia (11) / page 144
mone involved in the regulation of fluid and electrolytes neoplasm (NEE-oh-PLAZ-um) same as tumor; an abnor-
by its effects in the kidney (32) / page 520 mal swelling or mass (28) / page 432
minimum effective concentration the amount of drug re- nephrons (NEF-ronz) functional units of the kidney (17)
quired to produce a therapeutic effect (4) / page 45 / page 249
miosis (my-OH-sis) constriction of the pupil (37) / page 601 nephrotoxicity (NEF-row-toks-ISS-ih-tee) an adverse
monoamine oxidase inhibitors (MAOIs) (mon-oh-AHM- effect on the kidneys (26) / page 400
een OK-se-daze) drugs inhibiting monoamine oxidase, neurogenic shock (nyoor-oh-JEN-ik) type of shock re-
an enzyme that terminates the actions of neurotransmitters sulting from brain or spinal cord injury (21) / page 320
such as dopamine, norepinephrine, epinephrine, and sero- neuroleptic malignant syndrome (NMS) (noo-roh-LEP-
tonin (10) / page 132 tik) a potentially fatal condition caused by some antipsy-
mood stabilizers drugs that level mood to treat bipolar dis- chotic medications; symptoms include an extremely high
order and mania (10) / page 134 body temperature, drowsiness, changing blood pressure,
mucolytic drug used to loosen thick mucus (29) / page 465 irregular heartbeat, and muscle rigidity (11) / page 147
multiple sclerosis (MS) (skle-ROH-sis) autoimmune dis- neuroleptics (noo-roh-LEP-ticks) drugs used to treat “ner-
order of the central nervous system; a condition in which vous-type” conditions such as psychoses (11) / page 146
antibodies slowly destroy tissues in the brain and spinal neuromuscular blockers anesthetics that cause paralysis
cord (12) / page 167 without loss of consciousness (15) / page 227
G-10 Glossary
neuromuscular blocking drugs (NEWR-oh-musc-you- osteoporosis (OSS-tee-oh-poh-ROH-sis) condition in

lahr) drugs that bind to acetylcholine receptors, preventing which bones become brittle and susceptible to fracture (35) /
contraction of skeletal muscle (12) / page 175 page 569
nicotinic (NIK-oh-TIN-ik) type of cholinergic receptor otitis media (oh-TYE-tuss MEE-dee-ah) inflammation
found in ganglia of both the sympathetic and parasympa- of the middle ear (37) / page 606
thetic nervous systems (8) / page 90 ototoxicity (OH-toh-toks-ISS-ih-tee) an adverse effect on
nitrogen mustards class of chemicals that are alkylating hearing (26) / page 400
agents (28) / page 437 outcome objective measures of goals (5) / page 54
nociceptor (no-si-SEPP-ter) receptor connected with ovulation (ov-you-LAY-shun) release of an egg by the
nerves that receive and transmit pain signals to the spinal ovary (34) / page 543
cord and brain (14) / page 198
oxytocics (ox-ee-TOH-sicz) drugs that stimulate uter-
norepinephrine (nor-EH-pin-NEF-rin) primary neurotrans- ine contractions to promote the induction of labor (34) /
mitter in the sympathetic nervous system (8) / page 88 page 552
nosocomial infections (noh-soh-KOH-mee-ul) infections oxytocin (ox-ee-TOH-sin) hormone secreted by the pitu-
acquired in a healthcare setting such as a hospital, physi- itary gland that stimulates uterine contractions and milk
cian’s office, or nursing home (26) / page 392 ejection (34) / page 552
nursing diagnosis clinically based judgment about the Paget’s disease (PAH-jets) disorder characterized by
patient and his or her response to health and illness (5) / weak, enlarged, and abnormal bones (35) / page 573
page 53
palliation (PAL-ee-AYE-shun) form of chemotherapy in-
nursing process five-part decision-making system that in-
tended to alleviate symptoms rather than cure the disease
cludes assessment, nursing diagnosis, planning, implemen-
(28) / page 433
tation, and evaluation (5) / page 51
pancreatic insufficiency condition in which the pancreas
obsessive-compulsive disorder (OCD) anxiety character-
is not secreting sufficient amounts of digestive enzymes,
ized by recurrent, intrusive thoughts or repetitive behaviors
resulting in malabsorption syndromes (30) / page 492
that interfere with normal activities or relationships (9) /
page 106 panic disorder anxiety characterized by intense feelings
of immediate apprehension, fearfulness, terror, or impend-
off-label use when a drug is being prescribed for a condi-
ing doom (9) / page 106
tion for which it is not FDA-approved (1) / page 9
oligomenorrhea (ol-ego-men-oh-REE-uh) infrequent papules (PAP-yools) inflammatory bumps without pus
menstruation (34) / page 550 that swell, thicken, and become painful (36) / page 589
onset of drug action the amount of time it takes to produce parafollicular cells (par-uh-fo-LIK-u-lur) cells in the
a therapeutic effect after drug administration (4) / page 45 thyroid gland that secrete calcitonin (32) / page 516
open comedones type of acne in which sebum has parasympathetic nervous system (PAIR-ah-SIM-pah-
plugged the oil gland; commonly called blackheads (36) / THET-ik) portion of the autonomic system that is ac-
page 589 tive during periods of rest and digestion (8) / page 87
open-angle glaucoma (glaw-KOH-mah) also called parasympathomimetics (PAIR-ah-SIM-path-oh-mah-
chronic simple glaucoma, this type of glaucoma is caused MET-iks) drugs that mimic the actions of the parasympa-
by congestion in trabecular meshwork, hindering outflow thetic nervous system (8) / page 91
of aqueous fluid (37) / page 601 parenteral route (pah-REN-tur-ul) the major route by
opiate (OH-pee-aht) natural substance extracted from the which drugs enter the body other than the enteral or topical
poppy plant (14) / page 201 route (3) / page 32
opioids (OH-pee-oydz) natural or synthetic morphine- parkinsonism degenerative disorder of the nervous sys-
like substance obtained from the unripe seeds of the poppy tem caused by a deficiency of the brain neurotransmitter
plant (7, 14) / pages 72, 201 dopamine; this deficiency results in disturbances of muscle
orally disintegrating tablets (ODTs) drug formulation movement (11, 12) / pages 148, 159
that allows for quick dissolving and absorption of medica- partial (focal) seizures seizures that start on one side of
tions (3) / page 27 the brain and travel a short distance before stopping (13)
orthostatic hypotension (or-tho-STAT-ik) fall in blood / page 183
pressure that occurs when someone changes position from passive immunity administration of antibodies; provides
recumbent to upright (18) / page 282 short-term immunity (25) / page 376
osteoarthritis (OA) (OSS-tee-oh-are-THRYE-tis) dis- pathogen (PATH-oh-jen) organism that is capable of
order characterized by degeneration of joints such as the causing disease (26) / page 389
fingers, spine, hips, and knees (35) / page 574 pathogenicity (path-oh-jen-ISS-ih-tee) ability of an or-
osteomalacia (OSS-tee-oh-muh-LAY-shee-uh) rick- ganism to cause disease in humans (26) / page 389
ets in children; disease characterized by softening of the pathophysiology (PATH-oh-fiz-ee-OL-oh-jee) the study of
bones without alteration of basic bone structure (35) / diseases and the functional changes occurring in the body as a
page 566 result of diseases (1) / page 3
Glossary G - 11
patient-controlled analgesia (PCA) (patient-controlled phosphodiesterase (fos-fo-die-ES-tur-ase) enzyme in

an-ul-JEE-ziah) use of an infusion pump to deliver a pre- muscle cells that cleaves phosphodiester bonds; its inhibi-
scribed amount of pain relief medication over a designated tion increases myocardial contractility (19) / page 297
time (14) / page 203 photosensitivity condition that occurs when the skin is
peak plasma level when the medication has reached its very sensitive to sunlight (26) / page 398
highest concentration in the bloodstream (4) / page 46 physical dependence (FI-zi-kul dee-PEN-dens) the con-
pediculicides (puh-DIK-you-lih-sides) medications that dition of experiencing unpleasant withdrawal symptoms
kill lice (36) / page 587 when a substance is discontinued (7) / page 72
peptic ulcer erosion of the mucosa in the alimentary ca- pituitary gland (pit-TOO-it-air-ee) endocrine gland in
nal, most commonly in the stomach and duodenum (30) / the brain responsible for controlling many other endocrine
page 479 glands (32) / page 511
percutaneous transluminal coronary angioplasty (PTCA) planning phase stage of the nursing process that links
(per-cue-TAIN-ee-us trans-LOO-min-ul KOR-un-air- strategies or interventions to established goals and out-
ee ANN-gee-oh-plas-tee) procedure by which a balloon- comes (5) / page 53
shaped catheter is used to compress fatty plaque against an plaque (PLAK) fatty material that builds up in the lin-
arterial wall for the purpose of restoring normal blood flow ing of blood vessels and may lead to hypertension, stroke,
(20) / page 304 myocardial infarction, or angina (16, 20) / pages 235, 302
perfusion (purr-FEW-shun) blood flow through a tissue plasma cell type of cell derived from B cells that produces
or organ (29) / page 455 antibodies (25) / page 375
peripheral edema (purr-IF-ur-ul eh-DEE-mah) swell- plasmids (PLAZ-midz) small piece of circular DNA
ing in the limbs, particularly the feet and ankles, due to an found in some bacteria that is able to transfer resistance
accumulation of interstitial fluid (19) / page 289 from one bacterium to another (26) / page 392
peripheral resistance (per-IF-ur-ul) the amount of fric- plasmin (PLAZ-min) enzyme formed from plasminogen
tion encountered by blood as it travels through the vessels that dissolves blood clots (23) / page 349
(18) / page 269 plasminogen (plaz-MIN-oh-jen) protein that prevents fi-
peristalsis (pair-ih-STAL-sis) involuntary wavelike brin clot formation (23) / page 349
contraction that occurs in the alimentary canal (30) / polarized (POLE-uh-rized) condition in which the inside
page 478 of a cell is more negatively charged than the outside of the
pernicious (megaloblastic) anemia (pur-NISH-us ah- cell (22) / page 335
NEE-mee-ah) type of anemia usually caused by lack of positive symptoms symptoms that add on to normal be-
secretion of intrinsic factor (31) / page 499 havior; signs that are used to assist with the diagnosis of
pH a measure of the acidity or alkalinity of a solution (17) / schizophrenia (11) / page 144
page 260 posterior pituitary area of the pituitary gland, also known
pharmaceutics (far-mah-SOO-tiks) the science of pre- as neurohypophysis (32) / page 511
paring and dispensing drugs (1) / page 5 postmenopausal bleeding (POST-men-oh-pause-ahl)
hemorrhage following menopause (34) / page 550
pharmacodynamics (FAR-mah-koh-deye-NAM-iks)
the study of how the body responds to drugs and natural postpartum depression depression experienced by a
substances (4) / page 46 woman during the first several weeks after the birth of her
baby (10) / page 124
pharmacokinetics (FAR-mah-koh-kee-NET) the study
of what the body does to drugs (4) / page 42 post-traumatic stress disorder (PTSD) anxiety charac-
terized by a sense of helplessness and the reexperiencing
pharmacologic classification (FAR-mah-koh-LOJ-ik) of a traumatic event, for example, war, physical or sexual
method for organizing drugs on the basis of their mecha- abuse, natural disasters, or murder (9) / page 106
nism of action (how they work pharmacologically) (2) /
page 13 potassium ion channel (po-TASS-ee-um) pathway in a
plasma membrane which allows potassium to leave the cell
pharmacology (far-mah-KOL-oh-jee) the study of medi- during an action potential (22) / page 335
cines; the discipline pertaining to how drugs improve the
potency (POH-ten-see) the power or strength of a drug at
health of the human body (1) / page 3
a specified concentration or dose (4) / page 47
pharmacopoeia (far-mah-KOH-pee-ah) medical refer- pre-eclampsia (pree-ee-KLAMP-see-uh) condition in
ence summary indicating standards of drug purity, strength, which hypertension develops because of pregnancy or re-
and directions for synthesis (1) / page 5 cent pregnancy. Hypertension is accompanied by protein-
pharmacotherapeutics (far-mah-koh-THER-ah-PEW-tiks) uria and/or edema (13) / page 183
treatment of diseases by the use of drugs (1) / page 3 preload degree of stretch of the cardiac muscle fibers just
pharmacy the preparation and dispensing of drugs (1) / before they contract (19) / page 289
page 5 premenstrual syndrome (PMS) (PREE-men-stroo-ahl)
phobias (FO-bee-ahs) fearful feelings attached to situa- symptoms develop during the luteal phase of the menstrual
tions or objects (9) / page 106 cycle (34) / page 550
G-12 Glossary
prn order Latin pro re nata; physician’s order; means rebound insomnia increased sleeplessness that occurs
“to administer as required by the patient’s condition” (3) / when long-term antianxiety or hypnotic medication is dis-
page 23 continued (9) / page 110
prodrugs drugs that become more active after they are me- receptor (ree-SEP-tor) the structural component of a cell
tabolized (4) / page 43 to which a drug binds in a dose-related manner to produce
progesterone (pro-JESS-ter-own) hormone responsible a response (4) / page 47
for building up the uterine lining in the second half of the receptor theory a cellular mechanism by which most
menstrual cycle and during pregnancy (34) / page 544 drugs produce their effects (4) / page 47
prolactin (pro-LAK-tin) hormone secreted by the pitu- recommended dietary allowance (RDA) amount of vi-
itary gland that stimulates milk production in the mam- tamin or mineral needed daily to avoid a deficiency in a
mary glands (34) / page 552 healthy adult (31) / page 498
prostaglandins (pros-tah-GLAN-dins) chemicals re- red-man syndrome rash on the upper body caused by cer-
leased after tissue damage, leading to pain, inflammation, tain anti-infectives (26) / page 403
and other body reactions (14, 34) / pages 208, 552 reflex tachycardia (ta-kee-CAR-dee-ah) temporary
prothrombin (PRO-throm-bin) blood protein converted speeding up of heart rate that occurs when blood pressure
to thrombin in the blood-clotting process (23) / page 347 falls (18) / page 270
prothrombin time (PT) blood test used to determine the refractory period (ree-FRAK-tor-ee) time during which
time needed for plasma to clot, used to regulate warfarin the myocardial cells rest and are not able to contract (22) /
dosage (23) / page 352 page 335
proton-pump inhibitor (PPI) drug that inhibits the en- releasing hormones hormones secreted by the hypothala-
zyme H+, K+-ATPase (30) / page 482 mus that travel via blood vessels a short distance to tell the
prototype drug (PRO-toh-type) an original, well-understood pituitary which hormone to release (32) / page 511
drug model from which other drugs in a pharmacologic class renal failure decrease in the kidneys’ ability to maintain
have been developed (2) / page 13 electrolyte and fluid balance and excrete waste products
protozoan (PRO-toh-ZOH-en) single-celled microorgan- (17) / page 251
ism (27) / page 425 renin-angiotensin-aldosterone system (RAAS) (REN-
provitamin an inactive chemical that is converted to a vi- in–an-geo-TEN-sin-al-DOS-ter-own) series of enzy-
tamin in the body (31) / page 497 matic steps by which the body raises blood pressure (18) /
pruritus (proo-RYE-tus) itching associated with dry, page 274
scaly skin (36) / page 583 respiration (res-purr-AY-shun) exchange of oxygen and
psoralen (SOR-uh-len) drug used along with phototherapy carbon dioxide (29) / page 455
for the treatment of psoriasis and other severe skin disorders reticular activating system (RAS) the brain structure that
(36) / page 593 projects from the brainstem and thalamus to the cerebral
psychedelics (seye-keh-DEL-iks) substances that alter cortex; responsible for sleeping and wakefulness and per-
perception and reality (7) / page 76 forms an alerting function (9) / page 107
psychological dependence (seye-koh-LOJ-i-kul dee- reticular formation (re-TIK-u-lurr) a network of neu-
PEN-dens) an unpleasant, intense craving for a drug after rons found along the entire length of the brainstem con-
it has been withdrawn (7) / page 72 nected with the reticular activating system (9) / page 107
psychotic depression condition characterized by the ex- retinoids (RETT-ih-noydz) vitamin A-like compounds
pression of mood shifts and unusual behaviors. Intense used in the treatment of severe acne and psoriasis (36) /
behaviors include hallucinations, combativeness, and dis- page 590
organized speech patterns (10) / page 124 retinol (RETT-in-nall) chemical name for vitamin A (36) /
purines (PYUR-eenz) building blocks of DNA and RNA, page 591
either adenine or guanine (28) / page 439 reverse transcriptase (ree-VERS trans-CRIP-tace) viral
Purkinje fibers (purr-KEN-gee FI-burrs) electrical con- enzyme that converts RNA to DNA (27) / page 420
duction pathway leading from the bundle branches to all rheumatoid arthritis (RA) (ROO-mah-toyd are-THRYE-
portions of the ventricles (22) / page 333 tis) systemic autoimmune disorder characterized by inflam-
pustules (PUSS-chools) inflammatory bumps with pus mation of multiple joints (35) / page 575
(36) / page 589 rosacea (roh-ZAY-shee-uh) skin disorder characterized
pyrimidine (peer-IM-uh-deen) building block of DNA by clusters of papules (36) / page 589
and RNA, either thymine or cytosine in DNA, and cytosine routine orders standard order usually carried out within
and uracil in RNA (28) / page 439 two hours of the time it was written by the physician (3)
reabsorption movement of substances from the kidney tu- / page 24
bule back into the blood (17) / page 250 salicylism (sal-IH-sill-izm) poisoning due to aspirin and
rebound congestion a condition of hypersecretion of mu- aspirin-like drugs (24) / page 366
cus following use of intranasal sympathomimetics (29) / scabicides (SKAY-bih-sides) drugs that kill scabies and
page 463 mites (36) / page 587
Glossary G - 13
scabies (SKAY-beez) skin disorder caused by the female mite six rights of drug administration practical guidelines for
burrowing into the skin and laying eggs (36) / page 586 nurses to use during drug preparation, delivery, and admin-
scheduled drugs in the United States, a term describing a istration of drugs (3) / page 22
drug placed into one of five categories (I through V) based social anxiety disorder social phobia, a kind of anxiety
on its potential for misuse or abuse (2) / page 16 disorder characterized by excessive and unreasonable fear
schizoaffective disorder (SKIT-soh-ah-FEK-tiv) disor- of social situations (9) / page 106
der with symptoms similar to schizophrenia and mood dis- sodium ion channels (SO-dee-um) pathways in the plas-
orders (11) / page 144 ma membrane that allow sodium ions to enter the cell dur-
schizophrenia (SKIT-soh-FREN-ee-uh) type of psy- ing an action potential (22) / page 335
chosis characterized by abnormal thoughts and thought somatotropin (so-mat-oh-TROH-pin) another name for
processes, withdrawal from other people and the outside growth hormone (32) / page 514
environment, and apparent preoccupation with one’s own spasticity (spas-TISS-ih-tee) condition in which certain
mental state (11) / page 143 muscle groups remain in a continuous contracted state (12) /
seasonal affective disorder (SAD) depression experi- page 172
enced during the winter months; associated with a re- specialty supplement a nonherbal dietary supplement
duced release of the brain neurohormone melatonin (10) / used to enhance body functions (6) / page 65
page 124 stable angina type of angina that occurs in a predictable
seborrhea (seb-oh-REE-ah) condition characterized by pattern, usually relieved by rest (20) / page 303
overactivity of oil glands (36) / page 589 standing order a physician’s order written in advance of a
secretion movement of substances from the blood into the situation, which is to be carried out under specific circum-
kidney tubule after filtration has occurred (17) / page 251 stances (3) / page 24
sedative-hypnotic (SED-ah-tiv hip-NOT-ik) drug that STAT order comes from statim, the Latin word meaning
produces a calming effect when given in lower doses, and “immediately”; the time frame between writing the STAT
produces sleep when given in higher doses (9) / page 111 order and administering the drug may be five minutes or
sedatives (SED-ah-tivs) drugs that relax or calm the pa- less, depending on facility rules (3) / page 23
tient (9) / page 111 status asthmaticus (STAT-us az-MAT-ik-us) acute form
seizure (SEE-zhurr) symptom of epilepsy characterized of asthma requiring immediate medical attention (29) /
by abnormal neuronal discharges within the brain (13) / page 467
page 181 status epilepticus (ep-ih-LEP-tih-kus) condition charac-
selective estrogen-receptor modulators (SERMs) drugs terized by repeated seizures (13) / page 184
that directly produce an action similar to estrogen in body stroke a major cause of permanent disability caused by
tissues; used for the treatment of osteoporosis in postmeno- blockage of blood to the brain or rupture of a blood vessel
pausal women (35) / page 570 in the brain (20) / page 314
selective serotonin-reuptake inhibitors (SSRIs) (sir-eh- subcutaneous (SC or SQ) route (sub-kew-TAY-nee-us)
TO-nin) drugs that selectively inhibit the reuptake of sero- method of parenteral drug delivery in which drugs are in-
tonin into nerve terminals (10) / page 128 jected into the hypodermis of the skin (3) / page 33
septic shock (SEP-tik) type of shock caused by severe in- sublingual (SL) route (sub-LIN-gwal) method of enteral
fection in the bloodstream (21) / page 320 drug delivery in which drugs are placed under the tongue
serotonin-norepinephrine reuptake inhibitors (SNRIs) (3) / page 27
drugs that block the recycling of two neurotransmitters, se- substance abuse the self-administration of a drug in a way
rotonin and norepinephrine (10) / page 129 that one’s culture or society views as abnormal and not ac-
serotonin syndrome (SES) a set of signs and symptoms ceptable (7) / page 70
associated with overmedication with antidepressants (10) / substance dependence when a person has an overwhelm-
page 129 ing desire to take a drug and cannot stop (7) / page 72
shock condition in which there is inadequate blood flow to substance P neurotransmitter within the spinal cord in-
meet the body’s needs (21) / page 320 volved in the neural transmission of pain (14) / page 199
single order a physician’s order for a drug that is to be superficial mycoses fungal diseases of the hair, skin, nails,
given only once and at a specific time; an example is a and mucous membranes (27) / page 413
preoperative order (3) / page 23 superinfection condition caused when a microorganism
sinoatrial (SA) node (si-no-AYE-tree-ul noad) center of grows rapidly as a result of having less competition in its
autorhythmicity, the ability of excitable cells to rhythmi- environment (26) / page 393
cally generate their own action potentials in the heart (22) / sustained-release tablets or capsules that are designed to
page 333 dissolve very slowly (3) / page 27
sinus rhythm (SI-nuss) number of beats per minute nor- sympathetic nervous system (SIM-pah-THET-ik) por-
mally generated by the SA node (22) / page 333 tion of the autonomic system that is active during periods
situational depression short-term depression resulting of stress and which produces the fight-or-flight response
from circumstances in a person’s life (10) / page 124 (8) / page 87
G-14 Glossary
sympatholytic (SIM-path-oh-LIT-ik) a drug that blocks thrombus (THROM-bus) blood clot (23) / page 349
the actions of the sympathetic nervous system (8) / page 91 tissue plasminogen activator (tPA) natural enzyme and a
sympathomimetic (sim-path-oh-mih-MET-ik) a drug drug that dissolves blood clots (23) / page 349
that mimics the actions of the sympathetic nervous system titer (TIE-ter) measurement of the amount of a substance
(8) / page 91 in the blood (25) / page 376
systemic mycoses fungal diseases affecting internal or- tocolytic (toh-koh-LIT-ik) drug used to inhibit uterine
gans (27) / page 414 contractions (34) / page 552
systolic pressure (SIS-tol-ik) blood pressure during the tolerance (TOL-er-ans) the process of adapting to a drug
contraction phase of heart activity (18) / page 267 over time and requiring higher doses to achieve the same
T cell type of lymphocyte that is essential for the cell-me- effect (7) / page 73
diated immune response (25) / page 375 tonometry (toh-NAHM-uh-tree) technique for measur-
tardive dyskinesia (TAR-div dis-ki-NEE-zee-uh) invol- ing eye tension and pressure (37) / page 601
untary movements of facial muscles and the tongue that oc- topical route (TOP-ik-ul) the route by which drugs are
cur due to long-term antipsychotic therapy (11) / page 148 placed directly onto the skin and associated membranes (3) /
targeted therapy antineoplastic drugs that target specific page 28
aspects of cancer cell physiology (28) / page 445 topoisomerase (TOH-poh-eye-SOM-er-ase) enzyme that
taxanes (TAKS-anez) natural antineoplastics isolated assists in the repair of DNA damage (28) / page 442
from the Pacific yew (28) / page 442 total parenteral nutrition (TPN) treatment of undernutri-
tension headache common type of head pain caused by tion through the parenteral infusion of dextrose, amino ac-
stress and relieved by nonnarcotic analgesics (14) / page 211 ids, emulsified fats, vitamins, and minerals (31) / page 505
teratogen any substance that will harm a developing fetus toxic concentration the level of drug that will result in
or embryo (2) / page 17 serious adverse effects (4) / page 45
termination of drug action when the drug effect stops (4) toxins (TOX-inz) chemical produced by a microorganism
/ page 46 that is able to cause injury to its host (26) / page 389
testosterone (test-AHST-erh-own) the primary male sex toxoid vaccine (TOX-oid vaks-EEN) vaccine containing
hormone responsible for male secondary sex characteris- bacterial toxins that have been chemically modified to be
tics (34) / page 544 incapable of causing disease (25) / page 376
tetrahydrocannabinol (THC) (TEH-trah-HEYE-droh- trace mineral inorganic compound needed by the body in
cah-NAB-in-ol) the active chemical in marijuana (7) / amounts of 20 mg or less daily (31) / page 500
page 76 trade name proprietary name of a drug assigned by the
therapeutic (THARE-ah-PEW-tick) range the plasma manufacturer; also called the brand name or product name
drug concentration between the minimum effective con- (2) / page 14
centration and the toxic concentration (4) / page 45 transdermal (trans-DER-mul) method of drug delivery,
therapeutic classification (ther-ah-PEW-tik) method for usually by a patch, in which drugs are absorbed across the
organizing drugs on the basis of their therapeutic useful- layers of the skin for the purpose of entering the blood-
ness (2) / page 13 stream (3) / page 29
therapeutic lifestyle changes nondrug changes which, transmucosal (trans-mew-KOH-sul) method of topical
when implemented, can reduce blood cholesterol levels drug delivery in which drugs are applied directly to mu-
(16) / page 236 cosal membranes, including the nasal and respiratory path-
therapeutics (ther-ah-PEW-tiks) the branch of medicine ways and vagina (3) / page 31
concerned with the treatment of disease and suffering (1) / transplant rejection when the immune system recognizes
page 3 a transplanted tissue as being foreign and attacks it (25) /
three checks of drug administration checks used by page 380
nurses together with the six rights to help ensure patient tricyclic antidepressants (TCAs) (treye-SICK-lick)
safety and drug effectiveness (3) / page 22 drugs with a three-ring chemical structure that inhibit the
thrombin (THROM-bin) enzyme formed in coagulating reuptake of norepinephrine and serotonin into nerve termi-
blood from prothrombin; it converts fibrinogen to fibrin, nals (10) / page 125
which forms the basis of a blood clot (23) / page 347 triglyceride (tri-GLISS-ur-ide) type of lipid that contains
thromboembolic disorder (THROM-bow-EM-bow-lik) three fatty acids and a chemical backbone of glycerol (16)
disease associated with the formation of blood clots (23) / / page 235
page 349 triple therapy common therapy for the management of
thrombolytics (throm-bow-LIT-iks) drugs used to dis- PUD consisting of a combination of a proton pump inhibi-
solve existing blood clots (23) / page 350 tor plus two antibiotics (30) / page 481
thrombotic stroke (throm-BOT-ik) type of stroke caused tubercles (TOO-burr-kyouls) cavity-like lesions in the
by a blood clot blocking an artery in the brain (20) / lung characteristic of infection by Mycobacterium tuber-
page 314 culosis (26) / page 406
Glossary G - 15
tumor (TOO-more) abnormal swelling or mass (28) / immune system with the intention of preventing disease
page 432 (25) / page 374
tumor suppressor genes genes that inhibit the transforma- vasomotor center (VAZO-mo-tor) area of the medulla
tion of normal cells into cancer cells (28) / page 432 that controls baseline blood pressure (18) / page 270
type 1 diabetes mellitus (die-uh-BEE-tees MEL-uh-tiss) vasopressin (vaz-oh-PRESS-in) another name for antidi-
disease characterized by lack of secretion of insulin by uretic hormone (32) / page 514
the pancreas that usually begins in the early teens (33) / vasospastic (Prinzmetal’s) angina type of angina in
page 530 which decreased myocardial blood flow is caused by
type 2 diabetes mellitus disease characterized by insuffi- spasms of the coronary arteries (20) / page 303
cient secretion of insulin by the pancreas or by lack of sen- ventilation (ven-tah-LAY-shun) process by which air is
sitivity of insulin receptors that usually begins in middle moved into and out of the lungs (29) / page 455
age, though increasingly diagnosed in younger people (33) /
page 534 very low-density lipoprotein (VLDL) lipid-carrying par-
ticle that is converted to LDL in the liver (16) / page 236
ulcerative colitis (UL-sir-ah-tiv koh-LIE-tuss) inflam-
matory bowel disease of the colon (30) / page 480 vinca alkaloids (VIN-ka AL-kah-loids) chemicals ob-
tained from the periwinkle plant (28) / page 442
undernutrition taking in or absorbing fewer nutrients than
required for normal body growth and maintenance (31) / virulence (VEER-you-lens) the severity of disease that an
page 504 organism is able to cause (26) / page 389
unstable angina type of angina that occurs frequently with virulization (veer-you-lih-ZAY-shun) appearance of mascu-
severe symptoms and which is not relieved by rest (20) / line secondary sex characteristics (34) / page 554
page 303 viruses nonliving particles containing RNA or DNA that
uricosurics (YOUR-ik-cose-youriks) drugs that increase are able to cause disease (27) / page 417
the excretion of uric acid by blocking its reabsorption in vitamins organic compounds required by the body in small
the kidney (35) / page 577 amounts (31) / page 497
urinary antiseptics drugs given by the PO route for their withdrawal syndrome (with-DRAW-ul SIN-drom)
antibacterial action in the urinary tract (26) / page 403 unpleasant symptoms experienced when a physically de-
urticaria (EHR-tik-air-ee-ah) raised, red, itchy bumps, pendent client discontinues the use of an abused drug (7) /
commonly referred to as hives (36) / page 583 page 72
vaccination (immunization) (VAK-sin-AYE-shun/IH- yeast (YEEST) type of fungus that is unicellular and di-
mewn-ize-AYE-shun) receiving a vaccine or toxoid to vides by budding (27) / page 413
prevent disease (25) / page 376 Zollinger–Ellison syndrome (ZOLL-in-jer ELL-ih-sun)
vaccine (vaks-EEN) preparation of microorganism disorder of having excess acid secretion in the stomach
particles that are injected into a patient to stimulate the (30) / page 483

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Brief Contents

Chapter 17 Diuretics and Drugs for Electrolyte

Chapter 18 Drugs for Hypertension 265 Appendix B Brief Answers to NCLEX-PN®

Enhance your SUCCESS with the additional resources below.

Holland_0133449815_frontmatter_ad.indd 1 11/20/13 2:07 PM

Unit I Chapter 21 Drugs for Shock and Anaphylaxis 319

Basic Concepts in Pharmacology 1 Chapter 22 Drugs for Dysrhythmias 331

Chapter 11 Drugs for Psychoses 142

Appendix A References 611 INDEX 626

*Appendix D (Complete Answers and Rationales for

Leland Norman Holland, Jr., PhD

Michael Patrick Adams, PhD, RT(R)

Jeanine Lynn Brice, RN, MSN

Holland, Leland Norman.

Publisher: Julie Levin Alexander

Pearson® is a registered trademark of Pearson plc.

Design and Features

Focus on Core Information

and provide an overview of the chapter.

Special Epileptic Syndromes DRUg SNaPShOT

or toxicity is observed, stopping the heparin infusion will result

Drug Prototype: Ethosuximide (Zarontin)

Highlights key Information for safe, Effective Nursing Care

NURSING PROCESS FOCUS patients receiving atypical antipsychotic therapy

Nursing Process Focus charts provide a succinct,

PlaNNINg: PaTIENT gOalS aND EXPECTED OUTCOmES

seizures within 72 hours postpartum.

identified using theolder adult considerations

Fast Facts epilepsy

12.1 medications are unable to cure most degenerative

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Chapter 1 Introduction to Pharmacology: Drug Regulation

Chapter 2 Drug Classes, Schedules, and Categories 12

Chapter 3 Methods of Drug Administration 20

Chapter 4 What Happens After a Drug Has Been Administered 41

Chapter 5 the nursing process IN PHARMACOLOGY 51

Chapter 6 The Role of Complementary and Alternative Therapies

Chapter 7 Substance Abuse 69

Chapter 8 Drugs Affecting Functions of the Autonomic

Chapter 9 Drugs for Anxiety and Insomnia 105

Chapter 10 Drugs for Emotional, Mood, and Behavioral

Chapter 11 Drugs for Psychoses 142

Nonphenothiazine Drugs 148

Chapter 12 Drugs for Degenerative Diseases and Muscles 157

Chapter 13 Drugs for Seizures 180

Chapter 14 Drugs for Pain Management 197

Opioid Antagonists 205

Chapter 15 Drugs for Anesthesia 217

Chapter 16 Drugs for Lipid Disorders 234

Chapter 17 Diuretics and Drugs for Electrolyte and Acid–Base

Nursing Process FOCUS Patients Receiving Diuretic Therapy 257

Chapter 18 Drugs for Hypertension 265

Chapter 19 Drugs for Heart Failure 287

Chapter 20 Drugs for Angina Pectoris, ­Myocardial Infarction,

Chapter 21 Drugs for Shock and Anaphylaxis 319

Chapter 22 Drugs for Dysrhythmias 331

Chapter 20 Drugs for Angina Pectoris, Myocardial Infarction,

Table 1.1 Characteristics of Traditional Therapeutic Drugs, Biologics, and Natural