*LIST OF DISEASES

1. Conjunctivitis
2. Common cold
3. Hepatitis
4. Meningitis
5. Scabies
6. T.B
7. Measles
8. Rabies
9. Gout
10. Congestive heart failure
11. Hypertension
12. Pneumonia
13. HIV/AIDS
14. Tetanus
15. Asthma
16. Pharyngitis
17. Tonsillitis
18. Fungal infections
19. Diabetes Mellitus
20. Anemia
* Nazia Tabassum (Assistant professor)
21. Diarrhea & Dysentery * Faculty Of Pharmacy, UCP, Lahore.
22. Ulcer
23. Typhoid fever
13-

HIV- (Human Immunodeficiency Virus )

RNA based virus, that compromises the body’s ability to
handle disease and cause AIDS.
AIDS-( Acquired Immune Deficiency Syndrome)
It is related to HIV, but they are not one in the same. A person
has aids only in the final stages of HIV, after the immune system
becomes unable to defend itself against foreign invaders like
bacteria, other viruses and allow the development of certain
cancers.
 *Stages of HIV Infection
*STAGE I - ACUTE HIV INFECTION
* Early stage of HIV infection
* Develop between 2 to 4 weeks after infection.
* Virus attacks and destroy CD4 cells of immune system
* Stage 1 ends with the production of high titers of anti-HIV anti-
bodies at 2-3 months and detectable by ELISA BY 3-4 weeks.
* Mononucleosis symptoms
* Headache, fever. malaise ,myalgia
* STAGE II- CHRONIC HIV INFECTION
* Called asymptomatic HIV infection or clinical latency)
* Last for 6 or more years
* Anti-HIV antibodies are produced in large amount
* Detectable in
-Blood
-Semen
-Cervical secretions
STAGE III- AIDS (FINAL STAGE OF HIV INFECTION)
* Immune system severely damaged
* Severity is directly related to the decline of CD4 T cells.
AIDS defining conditions.
* Recurrent bacterial pneumonia
* Fungal infections
* Tumors
* Kaposi sarcoma (skin lesions)
* Primary lymphoma
* Signs and Symptoms
* Fatigue
* Diarrhea
* Window Period
* Nausea * The time period between a person’s
exposure and actual infection with HIV and
* Vomiting until antibodies are detectable in the body.
* Fever * After three months there are usually enough
* Chills antibodies to show on an AIDs test.
* Night sweats * Nearly 99% people develop antibodies by
* Wasting syndrome at last stages three months.

* Transmission * Prevention
* Sexual contact * Safe sex
* Blood transfusion * Safe use of needles and more
* Transplanted tissue effective early screening.
* IV drug use with shared needles * Vaccines: no vaccine is currently
approved by FDA. clinical trials are
* Trans-placental or by perinatal infection of currently conducted with a number of
neonates(breast milk) different vaccines
 *Medication
Class Generic Brand name Dose ADR

Nucleoside/ Abacavir Ziagen 300 mg orally t.i.d • GI disturbances

nucleotide reverse or 600 once daily • Headache
transcriptase • Allergic
inhibitor (NRTI) reactions

Non-nucleoside Efavirenz Sustiva 600 mg • Mental health

reverse problem
transcriptase • Liver problem
inhibitor • Allergic
reactions

Protease inhibitors darunavir prezista 600mg tab • Liver problem

(PI) • Allergic
reactions

Entry inhibitor enfuvirtide Fuzeon 108mg/vial • Injection site

reactions
(redness,
swelling)

Integrase inhibitors dolutegravir tivicay 10mg • Liver problem

25mg • Allergic
50mg reactions
14-
* Tetanus is an acute , often fatal disease caused by an exotoxin produced
by the bacterium Clostridium tetani.
* It is characterized by onset of hypertonia, generalized rigidity and
convulsive spasms of skeletal muscles .
* The muscle stiffness usually involves the jaw (lockjaw) and neck and then
becomes generalized.

* Etiology…..Clostridium tetani (causative agent)

* Clostridium tetani is an obligate, anaerobic, motile, gram-positive

bacillus, proliferates in puncture wounds.
* Found in human and animal feces, cultivated soil and warm climate.
 *Pathogenesis
The spores of organism
is non-pathogenic in soil Transformation occurs When transformed it
or contaminated tissues in the presence of produces 2 types of
until the condition locally decrease Toxins:
become favorable for oxygen reduction 1. Tetanolysin
transmission into potential. 2. Tetanospasmin
vegetative form.

* Mechanism of Action of Tetanus Toxins

* Tetanolysin is a hemolytic toxin it potentiates the infection.

* Tetanospasmin binds to neuromuscular junction at the site of injury and reaches
presynaptic nerve terminal where it prevents the inhibitory neurotransmitters
Glycine and GABA.
* In normal state these neurotransmitter prevents the release of Ach from excitatory
neurons thus prevent muscle contraction.
In the presence of toxins these inhibitory
impulses (Glycine) are prevented leading to
uncontrolled contraction of muscle.
 Practical Prescribing for Tetanus (lock jaw)
Therapeutic Pharmacological Generic Brand Age Dose
class class
Board Beta-lactam Penicillin-G Pfizerpen Adult 10- 20 M U d aily,
spectrum antibiotics (Pfizer) 300 mg (0ral), q.i.d
Antibacterial
Anti infective Nitroimidazole Metronidazole Flagyl Adult 500 mg, oral, t.i.d
agent (Sanofi
aventis) Child 200mg/5ml, (sus),
t.i.d
Board Tetracycline Doxycycline Doxyn Adult 100mg, oral, b.i.d
spectrum
Antibacterial (Acto) Child 1mg/Ib, (IV) b.i.d

Muscle Benzodiazepine Diazepam Valium Adult 5mg, I.V, q.i.d

relaxant (Roche)
Child 0.04-0.3 mg/kg/dose
every 2-4 hour
Muscle GABA agonist Baclofen Lioresal Adult 5 mg, oral t.i.d
relaxant (Novartis)
Child 2.5 mg, oral q.i.d
TT: Tetanus Toxoid >7 Y 0.5 ml I.M
Tetanus immunoglobulin (TIG) >7y, 750U (I.M) ,<7y, 250U
(I.M)
DTP: Diphtheria-Tetanus-Pertussis Infanix 0.5 ml I.M
Trivac
15- *ASTHMA
Asthma is a chronic inflammatory disorder of the airways
that causes recurrent episodes of wheezing,
breathlessness, chest tightness, and cough associated with
bronchoconstriction and airflow limitation.

The hallmarks of the disease are: increased airway

responsiveness to a variety of stimuli, resulting in episodic
bronchoconstriction; inflammation of the bronchial walls;
and increased mucus secretion.
 TYPES OF ASTHMA:
Atopic asthma (evidence of allergen sensitization)

Non atopic asthma (Viral infection, cold air, exercise, irritant)

Drug induced asthma (Aspirin-sensitive asthma)

Occupational asthma (fumes, gases, chemical dust)

* Etiology

Inflammatory factors
Respiratory infection, Environmental factors, work

Irritants
Exercise, strong odors, temperature change, cold air, stress and emotion

Others
Tabaco, gastric reflux, pollutant, food additives, medication
 * Pathophysiology:
Major
characteristic
Air way features: Bronchial hyper
obstruction sensitization Type-
1 to stimuli.

Stimulates
Mucus Secretion Bronchoconstriction,
from bronchial sub degrees of vasodilation
mucosal glands with increased vascular
Permeability

Epithelial damage, Inflammatory

Leukocyte recruitment is changes in the
stimulated by chemokines airway;
produced by mast cells

Important mediators: histamine,

LTC4, LTD4, TH2 etc.
Clinical manifestation
(Sequence of events))

Chest tightness

Dyspnea

Wheezing

Coughing

Increase respiration rate

 Practical Prescribing for Asthma
Therapeutic Pharmacological Generic Brand Age Dose
class class

Bronchodilator Selective β2 Salbutamol Ventolin Adult 1-2 puff as required.

agonist Inhalar & Per dose (100 mcg;
(GSK) Child 200 dose units)

Anti- Corticosteroid Beclomethasone Clenil Adult 2 (100 mcg) to 5

inflammatory (inhaled) Inhalar (250 mcg)
(Chiesi) inhalations (puffs)
b.i.d
Child 1 (50 mcg)
inhalation (puff)
b.i.d
Bronchodilator Methylxanthines Theophylline Quibron Adult 175-350 mg oral,
SR b.i.d
(GSK) Child 60-12 mg, oral,
b.i.d
Anti-allergic Mast cell Nedocromil Telide Adult 1-2 puffs as
stabilizers Inhalar & required
(Sanofi) Child 2 mg per actuation

Anti- Leukotriene Montelukast Montika Adult 5-10 mg, oral, b.i.d

inflammatory antagonist (Sami)
Child Not recommended
in children
Step-wise approach to the treatment of asthma according to recent WHO
guidelines.

NOTE: ONION IS A SUPER FOOD FOR ASTHMA

 16- *Pharyngitis
*Overview
*Pharyngitis is inflammation of the pharynx, which is in the
back of the throat. It’s most often referred to simply as
“sore throat.”
*Pharyngitis can also cause scratchiness in the throat and
difficulty swallowing.
* More cases of pharyngitis occur during the colder months
of the year.
*In order to properly treat a sore throat, it’s important to
identify its cause.
*Pharyngitis may be caused by bacterial or viral infections.
 *Etiology
* NORMAL PHARYNX V/
* Pharyngitis is caused by swelling in the back of the throat between
the tonsils and the larynx.
* Most sore throats are occur during colder months and are caused by
viral infections such as the common cold, flu, mono, measles,
chickenpox, and croup.
* However, bacteria such as Group A Strep, whooping cough (caused
by the bacteria Bordetella pertussis), and diphtheria can sometimes
cause pharyngitis.
* Other causes of a sore throat may include allergies, dryness,
irritants, straining your throat muscles, gastroesophageal reflux
disease (GERD), HIV infection, or tumors of the throat, tongue, or
larynx (voice box).
 * Pathophysiology
* With infectious pharyngitis, bacteria or viruses may directly invade
the pharyngeal mucosa, causing a local inflammatory response.
* Other viruses, such as rhinovirus and coronavirus, can cause
irritation of pharyngeal mucosa secondary to nasal secretions.
* Streptococcal infections are characterized by local invasion and
release of extracellular toxins and proteases.

* CLINICAL FEATURES
* A Sore, Dry, Or Scratchy Throat
* Sneezing
* Runny Nose
* Headache
* Cough
* Fatigue
* Body Aches
* Chills
* Fever (A Low-grade Fever With A Cold And Higher-grade Fever With The
* NORMAL PHARYNX V/S PHARYNGITIS
 * MEDICATION
Class of Generic Brand name age Adult Adverse effects Contraindications interactio pregn
drugs name Dose ns ancy

Antiinfla Ibuprofen Brufen Over age of 6 10 mg GIT issues, Heart patient, Aspirin No
m- Wilfen months dose is per Kg vertigo ulcer, kidney Methotrex
matory calculated headaches, problems, ate
bleeding disorder

Acetaminop Panadol Adults and 1g to Nausea,vomitin Cirrhosis, a history Alcohol,A Safe

hen Tylenol children 4g/day g,hepatoxicity of alcoholism nticonvuls
-ants

Antibioti Cephalexin Keflex Over 1 year of 250- Abd pain, Hepatic and renal Furosemid Categ
cs Ceporax age 750mg fatigue, gast impairment e,aspirin, ory B
ritis, atorvastat
dyspepsia, in
headache,conf.

Ceftriaxone Cephtron Both children 1 to 2g Jaundice,eryth hypersensitivity Aspirin,au No

Cephtrix and adult per ema,leucopeni gmentin
day a,eosinophilia

Corticost Prednisone Cortan Both children 5 to electrolyte Systemic fungal Phenobarb Not
eroids Deltasone and adult 60mg/ disturbance, infections, ital, safe
day myopathy hypersensitivity phenytoin
 17- TONSILITIS
* Introduction
* Tonsils are the two lymph nodes located on each side of the back of your throat.
They function as a defence mechanism. They help prevent your body from
infection. When the tonsils become infected, the condition is called tonsillitis.
Tonsillitis can occur at any age and is a common childhood infection.
* There are two types of tonsillitis:
* Recurrent tonsillitis: multiple episodes of acute tonsillitis a year
* Chronic tonsillitis: episodes last longer than acute tonsillitis in addition to other
symptoms that include:
* Chronic sore throat
* Bad breath, or halitosis
* Tender lymph nodes in the neck
 * Etiology

* Most cases of tonsillitis are caused by a viral infection, such as the

viruses that cause the common cold or flu virus (influenza).
* Some cases can also be caused by a bacterial infection, typically a strain
of bacteria called group A streptococcus bacteria.
* These types of infections spread easily, so it's important to try to avoid
passing the infection on to others by:
* staying away from public places, such as work, school or nursery, until
your GP says it's safe to return (usually after the symptoms have passed)
* coughing and sneezing into a tissue and disposing of the tissue
* washing hands before eating, after going to the toilet and, if possible,
after coughing and sneezing.
*Pathophisology
*Clinical features
* A very sore throat
* Difficulty swallowing or painful swallowing
* A scratchy-sounding voice
* Bad breath
* Fever
* Chills
* Earaches
* Stomachaches
* Headaches
* A stiff neck
* Jaw and neck tenderness due to swollen lymph nodes
* Tonsils that appear red and swollen
* Tonsils that have white or yellow spots
* MEDICATION
Sr. Generic Brand Age Dose ADRs Interaction
no
1. Amoxicillin Amoxil Children 80-90mg/ Anaphylaxis cause false
5-10 yr. kg/day Anemia positive
15-25 (max 3g AST/ALT results with
adult daily) elevation certain
Diarrhea diabetic urine
Rash,Serum testing.
sickness-like
reactions

2. Ceftriazone DICEPHIN Children 50mg/kg/ headaches, interfere with

IV 5-10 yr. day dizziness,ab certain lab
15-25 (max 1g dominal tests (such as
adult daily) pains, certain urine
reduction of glucose tests)
the renal causing false
functions, test results.
vaginitis, etc
 18- * FUNGAL INFECTIONS
(MYCOSES)
*Etiology
* Infectious diseases caused by fungi are called
mycoses and they are often chronic in nature.
* We all have regular contact with fungi. They are so
widely distributed in our environment that thousands of
fungal spores are inhaled or ingested every day. Other
species are so well adapted to humans that they are
common members of the normal flora.
* Unlike bacteria, fungi are eukaryotic. They have rigid
cell walls composed of largely of chitin rather than
peptidoglycan.

Moulds are clinically responsible for Asthma allergy

* Compared with bacterial,
viral, and parasitic disease,
less is known about the
*Classification
pathogenic mechanisms and
Superficial Mycoses
virulence factors involved in
fungal infections
* Most fungi are opportunistic, Subcutaneous Mycoses

producing
serious disease only Systemic Mycoses
in individuals
with
impaired host defense
systems.
* Only a few fungi are able to
cause
disease in previously
healthy persons.
 * SUPERFICIAL MYCOSES
Infections limited to the outermost layers of the skin and
hair. These Infections extend deeper into the
epidermis, as well as hair and nail and are caused by
dermatophytes( a group of fungi that invade and grow in
dead keratin)
Most common infections are :
1. Candidiasis
2. Tinea capitis
3. Tinea Pedis
Disease Etiology Clinical Diagnosis Treatment
features

Candidiasis Caused by Sore throat, Microscopy-swab Topical Fungicides-

candida albicans. Vaginal of the affected Nystatin and
Drugs such as discharge, area is taken and Amphotericin.
corticosteroids, swelling or cultured then Systemic Fungicides-
oral bolstering of the culture is Fluconazole and
contraceptive, nail folds. analyze Itraconazole,
antibiotics Ketoconazole.
*Major problem
in patients with
AIDS
Tinea capitis Microsporum Area of scaling Wood’s light Griseofulvin upto 3
canis, which is on the scalp and Produces a months or
transmitted from hair loss. greenish Turbinafine
coats of dogs and Scarring Alopecia fluorescence of 250mg/day for 4-8
cats the scalp weeks

Tinea Pedis Trichophyton Inflammatory Potassium

rubrum and dry scaly permanganate
eruptions. 0.001% solution may
discharge infection
by preventing
maceration.
 * SUBCUTANEOUS MYCOSES

* These involve the deeper layers of the skin (the dermis,

subcutaneous tissue, muscle & fascia and even bone).
* The causative organisms normally live in the soil living on
rotting vegetation. They can get pricked into the skin as a
result of an injury but usually stay localized at the site of
implantation.
* Deeper skin infections include:
1. Mycetoma
2. Chromoblastomycosis
3. Sporotrichosis
 * SYSTEMIC MYCOSES
* May result from breathing in the spores of fungi, which normally live in the soil

A. Inhaled fungal infection (By True pathogens)

* Although uncommon, some may infect healthy individuals. Ocasionally these
infections are more serious and chronic (especially in the immune suppressed). The
organisms causing systemic fungal infections include:
1. Histoplasmosis
2. Coccidioidomycosis

B. Opportunistic infections
* Other systemic mycoses only infect those who are already sick or with an
immunodeficiency disorder i.e. they are ‘opportunists’. Repeated infection may
occur.
* Opportunistic fungal infections include:
1. Aspergillosis (found everywhere)
2. Zygomycosis
3. Cryptococcosis (where there are pigeon droppings)
Disease Etiological Pathophysiology Clinical Diagnosis
agent Features

Aspergillosis Aspergillus – It occurs in patients fever, cough, Certain antibodies

A Fungus who are dyspnea, level can be found
immunosuppressed chest pain, elevated upon
due to any underlying and rapidly hematology
lung disease, progress to
continued necrosis of
immunosuppressive lungs
drug therapy, or
immunodeficiency in
body
 *Herbal treatment
*Apple cidar vinegar douche
*Organic garlic
*Tea tree oil
*Cranberries
*Plain yogurt

*Management
* Keep affected skin clean and dry. Take care to dry between the toes and
skin folds.
* Hot wash socks, towels, bathmats at a temperature of at least 60 degrees.
* Regularly ash floors where you walk barefoot.
* To reduce reinfection, do not share towel, sheets or other personal
clothing.
* Wear open toed sandals, avoid wearing occlusive clothing and footwear
for a long period of time.
19- * DIABETES MELLITUS
DIABETES describes a group of metabolic diseases in which the person has high blood
glucose (blood sugar), either because insulin production is inadequate, or because the
body's cells do not respond properly to insulin, or both.

* Glucometer
A glucometer is a medical
device for determining
the approximate
concentration of glucose
in the blood.
BLOOD SUGAR LEVEL
Fasting state Fed state
NORMAL 70-100 mg/dL 70-140 mg/dL
DIABETIC 125 mg/dL plus 200 mg/dL plus
 * CLINICAL
MANIFESTATION

* COMPLICATIONS
* PATHOPHYSIOLOGY
Diabetes mellitus is a serious chronic disease that affects people of
all ages.
Type 1 Diabetes is an autoimmune disorder characterized
by the destruction of the insulin-secreting beta cells in the
pancreas, leading to absolute insulin deficiency.
Type 2 Diabetes is the result of insulin resistance by the
tissues and usually a decrease in insulin production.
Gestational Diabetes mellitus(GDM) occurs when a woman’s
pancreatic function is not sufficient to overcome the insulin
resistance created by the anti-insulin hormones secreted by the
placenta.

Obesity
Hypertension
* RISK FACTORS Lack of exercise
High cholesterol
Family history of diabetes
 * TYPES OF DIABETES MELLITUS
* 1.Type 1 Diabetes
Known as Insulin-Dependent Diabetes Mellitus (IDDM)
Destruction of beta cells. Hence, little or no insulin production.
Require daily insulin administration.
It may occur at any age but usually diagnosed in children below age 15.
It is affected by hereditary.

* 2.Type 2 diabetes
Most common type and is known as ‘non-insulin dependent’
Usually occurs in adulthood but diagnosis is increasing in the younger
generation
Body is incapable of responding to insulin.
Rates rising due to increased obesity and failure to exercise and eat healthy
* 3.Gestational Diabetes
This type affects females during pregnancy.
The majority of gestational diabetes patients can control their
diabetes with exercise and diet.
Undiagnosed or uncontrolled gestational diabetes can raise the risk
of complications during childbirth.
The baby may be bigger than he/she should be.

* Management
Eat healthy.
Exercise for at least 30 minutes per day.
Check HbA1c level every 3 months if your levels are greater than 7.
Check feet daily for sores.
Avoid smoking.
Take your medication instructed by your doctor.
* TREATMENT

*Type 1 diabetes medication

Insulin is used for type 1
regularly, and sometimes for
Type 2 diabetes if the patient is
experiencing stress on body
like surgery or illness.
 Type 2 Diabetes Medication
DRUG CLASS DRUG NAME BRAND NAME Adult DOSE ADR

Bigunaides Glucophage 500mg, 750mg Difficult

Metformin (Merk) urinatin, fever
chills

Sulfonylureas 5mg,10mg Affect liver

(2nd Glipzide Glucotrol and kidney
Generation) (Pfizer)

Meglitinides Starlix 60mg, 120mg Kidney

Nateglinide (Novartis) impairement

Thiazolidinedi Avandia 4mg Fatigue and

ones (TZDs) Rosiglitazone (GSK) chest pain

Alpha- Glyset 100mg Stomach pain

Glucosidase Miglitol (Pfizer) and Diarrhea
Inhibitors
20- *ANEMIA
*DEFINITION
Anemia (An-without,emia-blood)is a decrease in the RBC count,
hemoglobin and/or Hematocrit values resulting in a lower ability for the
blood to carry oxygen to body tissues .
 * ETIOLOGY:
 The RBC mass represents the balance between production and destruction or loss of RBCs. Thus,
anemia can result from one or more of 3 basic mechanisms.

 Blood loss:
during mensturation in females,pregnancy, trauma & injury .
 Deficient erythropoiesis:
Complete cessation of erythropoiesis results in a decline in RBCs of about 7 to 10%/wk (1%/day).

 Excessive hemolysis
can be caused by intrinsic abnormalities of RBCs or by extrinsic factors, such as the presence
of antibodies or complement on their surface, that lead to their early destruction.
*
*PATHOPHYSIOLOGY
 *CLASSIFICATION
Based on clinical picture-
 Iron deficiency anemia.
 Iron deficiency anemia
 Megaloblastic anemia.  excessive loss of iron .
 Pernicious anemia. Women are at risk. ---- For menstrual blood and
growing fetus.
 Hemorrhagic anemia.
 Hemolytic anemia.
 Megaloblastic anemia
 Less intake of vitamin B 12 and folic acid.
-Thalassemia anemia  Red bone marrow produces abnormal RBC.
-Sickle cell anemia  Pernicious anemia
 Aplastic anemia  Inability of stomach to absorb vitamin B 12 in
small intestine.
 Hemorrhagic anemia
 Excessive loss of RBC through bleeding,stomach
ulcers,menstruation
Hemolytic anemia
 RBC plasma membrane ruptures.
may be due to
parasites,toxins,antibodies.
i. Thalassemia
 Less synthesis of hemoglobin .Found in
population of Mediterranean sea.
ii. Sickle cell anemia
Hereditary blood disorder,
characterized by red blood cells that
assume an abnormal, rigid, sickle shape.

Aplastic anemia
 destruction of red bone marrow .
 caused by toxins,gamma radiation
* Non Pharmacological treatment
 Tea and coffee inhibit iron absorption when consumed with a meal or shortly after a meal.
 Vitamin C (ascorbic acid) is also a powerful enhancer of iron absorption from nonmeat foods
when consumed with a meal.
 Use of beet root,spinach,soybean,red meat,whole grain bread,egg and oat meal improve the
absorption of iron.

MEDICATIONS
DISEASE DRUGS TRADE NAME / DOSE ADR’s
BRAND NAME
(oral) ACEFER-F One tablet Urticaria
Iron supplements (100mg) 2 times a day Malaise
Saffron pharma
IRON DEFICIENCY (IM) COSMOFER on alternate days hypotension
ANEMIA Iron dextran Inj (100 mg ) for 2 weeks
PHARMACOSMOS
cyanocobalamin CYANOCOBALAMIN Once weekly or Pulmonary edema
Inj (1000mcg As recommended
MEGALOBLASTIC /10ml)
ANEMIA EMPOWER Pharma

Folic acid FEFOL VIT (5mg) One tablet per Neuropathy

GSK day Bronchospasm
SICKLE CELL ANEMIA hydroxyurea HYDRA One tablet two hyperurecemia
(500mg) times a day
21-*DIARRHEA
* Definition
* “A condition in which faeces are discharged from the bowel
frequently and in a liquid form”.
* It often lasts for a few days and can result in dehydration due to fluid
loss.
* Diarrhea is usually a symptom of infection in the intestinal tract,
which can be caused by a variety of bacterial , viral and parasitic
organisms.
* People of all ages can get diarrhea, but it is more common in children
below 5 years of age.
* Diarrhea in children are mainly caused by rotavirus which spreads by
a fecal matter.
 *Types
* There are 3 clinical types of diarrhea
Acute watery diarrhea:
Lasts several hours or days and includes cholera
Acute bloody diarrhea:
Also called dysentery
Persistent diarrhea:
Lasts for 14 days or longer

* Transmission Factors
* Infection factors
* Food factors
* Malabsorption factors
* Psychological factors
 *Aetiology
1. Organisms involved 2. Sources of infection 3. Non infectious
Viral infections Poor personal hygiene * Malabsorption
Rota virus Cystic fibrosis
Norovirus (adults)
Improper sanitation * Food intolerance or allergy
Adenovirus types 40 and 41 Water and food Lactose intolerance
Astroviruses Systemic infections Cow’s milk protein
Parasitic infections
* Urinary tract infection allergy
Giardia and entamoeba Drug induced
histolytica * Pneumonia antibiotics
Bacterial infections * Otitis media * Inflammation
E. coli
Salmonellae
* Meningitis Ulcerative colitis
* Surgical conditions
Shigellae * Septicemia
Campylobacter
Appendicitis
Vibrio cholera Partial bowel
obstruction
*Pathophysiology
* Infection factors
* Food factors
* Malabsorption factors
* Psychological factors
* Contaminate food & H20 by infected faeces.
* Bacteria Shigella enter to the gut.
* Growth in the small intestine.
* Spread to the colon, inflame the epithelium mucosa cell and
produce or secrete toxin.
* Break through the colon wall & necrosis the epithelium cell cause
haemorrhage, more mucus, purulent at the epithelium surface.
* At the end, ulcer colon occurs.
*Clinical features

* Signs and symptoms associated with diarrhea may

include:

* Loose, watery stools

* Abdominal cramps
* Abdominal pain
* Fever
* Blood in the stool
* Nausea
 *Pharmacological Treatment
* Antidiarrheal medicines include:
o Loperamide
(for example, Imodium) is an anti motility
drug that reduces stool passage.
oDose: The dose is two tablets (4 mg) initially, then 1 tablet
(2 mg) after each unformed stool. No more than 16 mg is
recommended per day.
oBismuth subsalicylate.
(for example, Pepto-Bismol) reduces
diarrheal stool output in adults and children and it is not as
effective as loperamide.
o Dose : The dose of bismuth subsalicylate is 30 mL or two
tablets every 30 minutes for up to eight doses.
*Non pharmacological treatment
* For all cases of diarrhea, the first important step in treatment is to
rehydrate:

* Fluids can be replaced by simply drinking more fluids, or they can be

received intravenously in severe cases.

* Oral rehydration solution/salts (ORS) - this is water that contains salt

and glucose. It is absorbed by the small intestine to replace the water
and electrolytes lost in the stool.

* Oral rehydration products are available commercially - for example

Oralyte and Rehydralyte. Zinc supplementation may reduce the
severity and duration of diarrhea in children.
 * Difference Between Diarrhea And Dysentery
* Diarrhea is a condition that involves the frequent passing of loose or
watery stools while
* Dysentery is an intestinal inflammation, especially in the colon, that can
lead to severe diarrhea with mucus or blood in the feces.
Sr no. Diarrhea Dysentery

1 Diarrhea is presented as watery stool with Dysentery is presented as a mucoid stool that
no blood and mucus. may be accompanied by blood.

2 The patient may or may not be The patient usually complains of cramps and
accompanied by cramps or a pain. pain in the lower abdominal area.

3 Fever is less common in diarrhea. Fever is more common in dysentery.

4 Diarrhea is a disease that affects the small Dysentery is a disease that affects the colon.
bowel.
5 Diarrheal infection is located and targets Dysentery not only upper epithelial cells are
only intestinal lumen and upper epithelial targeted but colon ulceration also results.
cells.
Sr no. Diarrhea Dysentery

6 There is no cell death in diarrhea When a person gets dysentery, the upper
and the infection is only caused epithelial cells are attacked and destroyed
because of the release of some by the pathogen or disease causing agent.
toxins by the infecting agent.

7 The antimicrobial that are used to Treatment for dysentery can eradicate the
treat diarrhea do not eradicate the pathogen that is causing the infection and
toxin left behind. stop the inflammation.

8 The effects of diarrhea are not that Dysentery can cause a lot of complications,
serious, apart from a risk of if left untreated.
dehydration.
9 Diarrhea is mostly viral. E. coli Dysentery is mostly bacterial. E coli,
can also cause watery diarrhea. Shigella, and Salmonella are the most
common causative organisms.

10 Diarrhea does not need antibiotics. Dysentery almost always requires

Oral rehydration solutions or antibiotic treatment. Intravenous antibiotics
intravenous fluid therapy may be may be needed in severely ill children.
used.
 22- *Ulcer
* Ulcer is the inflammation and necrosis of the mucosal tissue of an organ.
* It occurs in following regions of the body:
• Stomach
• Rectum
• Mouth

* The ulcer of stomach or peptic ulcer is most common.

*Causes: NSAIDS
Heredity
Helicobacter Pylori
Smoking
Steroids
*Pathophysiology:
* The first line of defense is mucus and bicarbonate secretion. It
stabilizes the pH between the lumen and epithelial cells surface.
Mucus gel in Patient with H.Pylori infection was found to be
structurally weak.
* Duodenal mucus as well as bicarbonate secretion is reduced in
patient who smoke.
* The second line of defense is the intrinsic epithelial cell
defense.the mucosal surface is a barrier to acid back diffusion
thus maintain normal intracellular pH.

* Extension phase
* The third line of defense is the rich mucosal blood flow. The
blood provides a buffer for acid neutralization as well as
adequate nutrition for the metabolic demand to maintain
mucosal integrity.
* Gastric mucosa has ability to repair minor injury and therefore
prevent progression to deep ulcer.
*Signs and symptoms:
Abdominal Pain
Indigestion
Headache/Dizziness
Fatigue/Weakness
Pale Skin
Vomit of Blood
 *Treatment
Category Generic Brand name Age Dose ADRS
name
Antacid  Aluminiu  Almagel(Zafa Adul  300-  Hyperacidity
m ), t 600m  Constipation
hydroxide Fercid(werri g/tid  Osteomalaci
, ck) a
magnesiu  Milk of
m magnesia(GS
hydroxide K)

Histamin  Ranitidin  Anzol(Indus); Adul  300  Hypotension

e e Stomacid(we t mg/O  Dizziness
antagonis rrick) D
ts  Cimetidin  Tagamet(GSK  300m
e ) g/qid
Endonil(Werr
ick)
Proton  Omepraz  Sante(Macter Adul  20mg  Rash
pump ole ) t /OD  Itching
inhibitor  Omega(Feroz  Headache
Sons)
 *Traditional treatment:
•
•
soybeans
legumes *prevention
• red grapes
• kale
• broccoli  One should limit alcohol.
• apples  Do not smoke or chew tobacco.
• berries  Avoid rational use of ibuprofen and
• teas, especially green aspirin.
tea  Avoid too much spicy food.
• honey
 *Chances of Recurrence
* If the Helicobacter Pylori infection is successfully
treated, the chances of recurrence of peptic ulcer are
little. Where this is not achieved, or the ulcer is not
caused by infection than patient should take acid
reducing tablets to avoid it.
 23- *Typhoid Fever
* Introduction
It a prolonged , systemic illness marked by an initiating bacteraemia and fever
followed by spread of organisms in reticuloendothelial system through out the
body.
It is also called “Enteric fever”
Enteric fever caused by serotype Typhil is called typhoid fever.

* Aetiology:
It is caused by salmonella typhli, if caused by any other serotype ; it is
referred to as paratyphoid fever.
Infection is usually spread by sewage contamination water.
Man is the only host for the organism, so personal hygiene is very
important.
The bacilli may live in the gallbladder of carriers for months to years and
pass intermittently in the stool.
The incubation period of typhoid fever is about 10-14 days
 * Pathophysiology :
After incubation period, the Salmonella bacteria Invade
Ingestion of contaminated
bacilli penetrate the small food or water
small intestine and enter
bowel mucosa and rapidly enters the bloodstream
the lymphatic system and hence
the blood stream.
They picked up by macrophages
and monocytic cell throughout
the reticuloendothelial system. Carried by white blood
Multiply and reenter the
Replication within and bloodstream
cells in the liver, spleen,
destruction of macrophages and bone marrow
leads to reemergence of
organisms and induction of
recurrent waves of bacteremia.
The organisms then localize in Bacteria invade the Then pass into the intestinal
peyer’s patches in terminal gallbladder, biliary system, tract and can be identified for
ileum, spleen, bone marrow and and the lymphatic tissue of diagnosis in cultures from
mesenteric lymph nodes. These the bowel and multiply in the stool tested in the
high numbers laboratory
swell at first, then ulcerate and
ultimately heal, but during this
sequence they may perforate or
bleed.
 * Clinical features
* During first week usually fever 40oc(104°F),headache, myalgia,
relative bradycardia, constipation, diarrhoea and vomiting in
children.
* At the end of first week rose spots on trunk, splenomegaly,
cough, abdominal distention, diarrhea.
* At the end of second week delirium, complication, then coma
and death(if untreated).
* MEDICATION :
*Other treatments
* Other treatments include:
* Drinking fluids. This helps prevent the dehydration that results from a prolonged fever
and diarrhea. If you're severely dehydrated, you may need to receive fluids through a
vein (intravenously).
* Surgery. If your intestines become perforated, you'll need surgery to repair the hole.

* Prevention
Vaccines
* A vaccine is recommended if you're traveling to areas where the risk of getting
Typhoid Fever is high.
* Two vaccines are available.
* One is injected in a single dose at least one week before travel.
* One is given orally in four capsules, with one capsule to be taken every other day.
* Drinking fluids. This helps prevent the dehydration that results from a prolonged fever and
diarrhea.

* Wash your hands. Frequent hand-washing in hot, soapy water is the best way to
control infection.
* Avoid drinking untreated water
* Avoid raw fruits and vegetables
24- MALARIA
* Overview
Malaria is a vector borne infectious disease caused by Protozoans Parasites and
typically transmitted through the bite of an infected Anopheles mosquito.
A serious, sometimes fatal, disease that is caused by a parasitic infection of the red
blood cells.
The World Health Organization (WHO) estimates that each year, more than 200 million
people are infected with malaria worldwide.
Malaria is a common problem in areas of Asia, Africa and Central and South America.
Unless precautions are taken, anyone living in or travelling to a country where malaria is
present can contract the disease

In early stages only red blood cells

get affected.
* Organs Affected by Later, Malaria mostly affects liver and spleen
malaria causing hepato and spleenomegaly. In
advanced cases brain also gets affected causing
cerebral malaria.
 * Aetiology
 Malaria is transmitted by the bite of an infected ANOPHELES mosquito
that introduces sporozoites(tissue parasite) of the plasmodia
(P.falciparum , P.vivax, P.malariae and P.ovale) into the blood stream.
 STAGES:
1.Asexual reproduction stage develops in humans
Exoerythrocytic shizogony (pre-erythrocytic)
Erythrocytic shizogony
2.Sexual stage occurs in mosquito
* pathophysiology
 *Pathophysiology

The SPOROZOITES invade parenchymal hepatocytes, multiply in stages

referred to as exoerythrocytic stages, and become hepatic vegetative forms
or schizonts.

SHIZONTS rupture to release daughter cells< or merozoites that then

infect erythrocytes.

The MEROZOITES that invade the erythrocytes develop sequentially

into ring forms, trophozoites, schizonts, and finally merozoites, which
can be invade other erythrocytes or can develop into gametocytes,
which undergo the sexual stage in the Anopheles vector.
 *Cont….

Because erythrocytic forms never

reinvade the liver without developing
into sporozoites in the vector, malaria
infections from transfusion never results
in the exorythrocytic or “liver” form

P.Falciparum can result in high

levels of parasitemia because of its
ability to invade erythrocytes of all
ages, unlike P.vivax and P.ovale,
which only invade young cells.
Plasmodium is living organism. It is required food and nutrition for their growth and
development. They obtain food by break down of RBCs. The RBCs are contained
Hb(Heme) and Globin (Protein). When Plasmodium attack on RBCs, they break RBCs
into Hb and Globin. Globins are further break down into polypeptides, dipeptides,
monopeptides and then Amino acid respectively. Amino acids are utilized as food of
plasmodium. The remaining part of RBCs is Hb (Heme) is undergoes the process of
polymerization in the presence of polymerase enzyme which is produced by
plasmodium. The results polymerization Hb is converted into Hemozoin which is toxic
metabolites and cause the symptoms of malaria.
 * Clinical features

INITIAL PRESENTATION:
• Non-specific fever, rigors, diaphoresis, malaise
• Orthostatic hypotension
• Electrolyte abnormalities
ERYTHROCYTIC PHASE:
• PRODROME:
Headache, anorexia, malaise, fatigue,
myalgia
• NON-SPECIFIC COMPLAINTS:
Abdominal pain, diarrhea, chest pain,
arthralgia
• PAROXYSM:
High fever, chills, rigor
• COLD PHASE: P.falciparum
Severe pallor, cyanosis of lips and cutis infections:
anserina (goose flesh) Hypoglycemia
• HOT PHASE: Acute renal failure
Fever between 40.5oC (104.9oF) and 41oC Pulmonary edema
(105.8oF) Severe anemia
• SWEATING PHASE: Follows hot phase by 2-6 Thrombocytopenia
hours
High output heart failure
Fever resolves
Cerebral congestion
Marked fatigue and drowsiness, warm, dry
skin, tachycardia, cough, severe headache, nausea,
Seizures and coma
vomiting, abdominal pain, diarrhea and delirium Adult respiratory syndrome
Anemia
Splenomegaly
 * Pharmacological therapy
• Falciparum malaria:
Quinine+Fansidar+Doxycycline
• Benign malaria:
Plasmodium vivax, P.ovale and P.malariea
Chloroquine
• Radial cure of malaria due to P.vivax and P.ovale:
Course of Primaquine

drugs brands dose adrs

Pyrimethamine25/ Fensidar 3 tabs for 5 days Stevens-Johnson
sulfadoxin500mg syndrome and toxic
epidermal necrolysis

Artemether:80mg, Arceva 2 Cap (40mg) for 4 days

Lumefantrine:480mg 2 Injection 80mg at start
& 1 inj for 4 days

Mefloquin Lariam 1.25g/24 hrs Anxiety, chills,

Confusion
Chloroquine phosphate Chloroquin 40mg tab. Appetite loss;
4 tab in start then 2 tab clumsiness; diarrhea; d
after 6hrs interval, izziness;
1 tab b.i.d. for next 2
days
* Prevention

1. Avoiding mosquito bites; use long sleeves, repellent creams, sprays, coils and
mosquito nets
2. Travelling in endemic areas; use mefloquine for prophylaxis
3. Chemoprophylaxis: In chloroquine resistant areas mefloquine or doxycycline or
proguanil+ atovaquuone are drug of choice. In chloroquine resistance absent
areas chloroquine or proguanil is drug of choice
4. Malaria control in endemic areas:
 Roll back malaria programme
 New combination drugs such as artemether-lumefantrine and pyronaridine are
being assessed in trials.
 Trial vaccines are being evaluated.