Hematologic System,

Oncologic Disorders &

Anemias
Dr Ibrahreem Bashayreh, RN, PhD

5/12/2010 1
 Hematology
 Study of blood and blood forming tissues
 Key components of hematologic system are:
 Blood
 Blood forming tissues
 Bone marrow
 Spleen

 Lymph system

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 What Does Blood Do?
 Transportation
 Oxygen
 Nutrients
 Hormones
 Waste Products
 Regulation
 Fluid, electrolyte
 Acid-Base balance
 Protection
 Coagulation
 Fight Infections
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 Components of Blood
 Plasma
 55%
 Blood Cells
 45%
 Three types
 Erythrocytes/RBCs
 Leukocytes/WBCs

 Thrombocytes/Platelets

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 Erythrocytes/Red Blood Cells
 Composed of hemoglobin
 Erythropoiesis
 = RBC production
 Stimulated by hypoxia
 Controlled by erythropoietin

 Hormone synthesized in kidney

 Hemolysis
 = destruction of RBCs
 Releases bilirubin into blood stream
 Normal lifespan of RBC = 120 days
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 Leukocytes/White Blood Cells
 5 types
 Basophils
 Eosinophils
 Neutrophils
 Monocytes
 Lymphocytes

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 Types and Functions of Leukocytes
TYPE CELL FUNCTION
Granulocytes
Neutrophil Phagocytosis, early phase of
inflammation
Eosinophil Phagocytosis, parasitic infections
Basophil Inflammatory response, allergic
response
Agranulocytes
Lymphocyte Cellular, humoral immune response
Monocyte Phagocytosis; cellular immune response

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 Thrombocytes/Platelets
 Must be present for clotting to occur
 Involved in hemostasis

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 Normal Clotting Mechanisms
 Hemostasis
 Goal: Minimizing blood loss when injured
1. Vascular Response
 vasoconstriction
2. Platelet response
 Activated during injury
 Form clumps (agglutination)
3. Plasma Clotting Factors
 Factors I – XIII
 Intrinsic pathway
 Extrinsic pathway

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 Anticoagulation
 Elements that interfere with blood clotting
 Countermechanism to blood clotting—keeps
blood liquid and able to flow

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 Structures of the Hematologic System

 Bone Marrow
 Liver
 Lymph System

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 Bone Marrow
 Bone Marrow
 Soft substance in core of bones
 Blood cell production (Hematopoiesis):The
production of all types of blood cells generated
by a remarkable self-regulated system that is
responsive to the demands put upon it.
 RBCs
 WBCs

 Platelets

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 Liver

Receives 24% of the cardiac output (1500

ml of blood each minute)
 Liver has many functions
 Hematologic functions:
 Liver synthesis plasma proteins
including clotting factors and albumin
 Liver clears damaged and non-
functioning RBCs/erythrocytes from
circulation

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 Spleen

 Located in upper L quadrant of

abdomen
 Functions
 Hematopoietic function
 Produces fetal RBCs

 Filter function
 Filter and reuse certain cells

 Immune function
 Lymphocytes, monocytes

 Storage function
 30% platelets stored in spleen

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 Effects of Aging on the Hematologic
System

 CBC Studies
  Hemoglobin (Hb or Hgb)
  response to infection (WBC)
 Platelets=no change
 Clotting Studies
  PTT

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 Assessment of the Hematologic System

 Subjective Data
 Important Health Information
 Past health history
 Medications

 Surgery or other treatments

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 Assessment of
the Hematologic System (cont.)
 Functional Health Patterns
 Health perception – health management

 Nutritional – metabolic

 Elimination

 Activity – exercise

 Sleep – rest

 Cognitive – perceptual

 Self-perception – self-concept

 Role – relationship

 Sexuality – reproductive

 Coping – stress tolerance

 Value – belief

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 Assessment of
the Hematologic System (cont.)

 Objective Data
 Physical Examination
 Skin
 Eyes
 Mouth
 Lymph Nodes
 Heart and Chest
 Abdomen
 Nervous System
 Musculoskeletal System

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 Diagnostic Studies of the Hematologic System:
Complete Blood Count (CBC)
 WBCs
 Normal 4,000 -11,000 µ/ℓ
 Associated with infection, inflammation, tissue injury or
death
 Leukopenia--  WBC
 Neutropenia --  neutrophil count
 RBC
 ♂ 4.5 – 5.5 x 106/ℓ
 ♀ 4.0 – 5.0 x 106/ℓ

 Hematocrit (Hct)
 The hematocrit is the percent of whole blood that is composed
of red blood cells. The hematocrit is a measure of both
the number of red blood cells and the size of red blood cells.

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 Diagnostic Studies of the Hematologic System:
Complete Blood Count (CBC) Cont’d

 Platelet count
 Normal 150,000- 400,000
 Thrombocytopenia- platelet count
 Spontaneous hemorrhage likely when count is
below 20,000

 Pancytopenia
 Decrease in number of RBCs, WBCs, and platelets

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 Diagnostic Studies
of the Hematologic System

 Radiologic Studies
 CT/MRI of lymph tissues
 Biopsies
 Bone Marrow examination
 Lymph node biopsies

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Common Laboratory Tests for Hematologic and Lymphatic Disorders
Common Laboratory Tests for Hematologic and Lymphatic Disorders
 Anemia

 Anemia is a reduction in the number of

RBCs, the quantity of hemoglobin, or the
volume of RBCs
 Because the main function of RBCs is
oxygenation, anemia results in varying
degrees of hypoxia

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 Anemia
 Prevalent conditions
 Blood loss
 Decreased production of erythrocytes
 Increased destruction of erythrocytes

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 Anemia (cont’d)
 Clinical Manifestations:
1. Pallor.
2. Fatigue, weakness.
3. Dyspnea.
4. Palpitations, tachycardia.
5. Headache, dizziness, and restlessness.
6. Slowing of thought.
7. Paresthesia.

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 Anemia (cont’d)

 Nursing Management:
1. Direct general management toward addressing the cause of
anemia and replacing blood loss as needed to sustain
adequate oxygenation.
2. Promote optimal activity and protect from injury.
3. Reduce activities and stimuli that cause tachycardia and
increase cardiac output.
4. Provide nutritional needs.
5. Administer any prescribed nutritional supplements.
6. Patient and family education

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 Nursing Actions for a Patient who is
Anemic or Suffered Blood Loss

 Administer oxygen as prescribed

 Administer blood products as prescribed
 Administer erythropoietin as prescribed
 Allow for rest between periods of activity
 Elevate the pt’s head on pillows during
episodes of shortness of breath
 Provide extra blankets if the pt feels cool
 Teach the pt/family about underlying
pathophysiology and how to manage the
symptoms of anemia
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 Anemia Caused by Decreased Erythrocyte
Production

 Iron Deficiency Anemia

 Thalassemia
 Megablastic Anemia

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 Iron-Deficiency Anemia
Etiology
1. Inadequate dietary intake
 Found in 30% of the
world’s population
2. Malabsorption
 Absorbed in duodenum
 GI surgery
3. Blood loss
 2 mls blood contain 1mg iron
 GI, GU losses
4. Hemolysis
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 Iron-Deficiency Anemia
 Clinical Manifestations
 Most common: pallor
 Second most common: inflammation of the tongue
(glossistis)
 Cheilitis=inflammation/fissures of lips
 Sensitivity to cold
 Weakness and fatigue
 Diagnostic Studies
 CBC
 Iron studies Diagnostics:
 Iron levels: Total iron-binding capacity (TIBC), Serum
Ferritin.
 Endoscopy/Colonscopy
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 Iron-Deficiency Anemia
 Collaborative Care
 Treatment of underlying disease/problem
 Replacing iron
 Diet
 Drug Therapy
 Iron replacement
 Oral iron
 Feosol, DexFerrum, etc

 Absorbed best in acidic environemtn

 GI effects

 Parenteral iron
 IM or IV

 Less desirable than PO

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 Iron-Deficiency Anemia
Nursing Management

 Assess cardiovascular & respiratory status

 Monitor vital signs
 Recognizing s/s bleeding
 Monitor stool, urine and emesis for occult blood
 Diet teaching—foods rich in iron
 Provide periods of rest
 Supplemental iron
 Discuss diagnostic studies
 Emphasize compliance
 Iron therapy for 2-3 months after the hemoglobin
levels return to normal
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 Thalassemia
 Etiology
 Autosomal recessive genetic disorder of inadequate
production of normal hemoglobin
 Found in Mediterranean ethnic groups
 Clinical Manifestations
 Asymptomatic  major retardation  life
threatening
 Splenomegaly, hepatomegaly

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 Thalassemia
Collaborative Care

 No specific drug or diet are effective in

treating thalassemia
 Thalassemia minor
 Body adapts to ↓ Hgb
 Thalassemia major
 Blood transfusions with IV deferoxamine

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 Megaloblastic Anemias
 Characterized by large
RBCs which are fragile
and easily destroyed
 Common forms of
megaloblastic anemia
1. Cobalamin deficiency
This picture shows large, dense,
2. Folic acid deficiency oversized, red blood cells (RBCs)
that are seen in megaloblastic
anemia.

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 Cobalamin (Vitamin B12) Deficiency
 Cobalamin Deficiency--formerly known as
pernicious anemia
 Vitamin B12 (cobalamin) is an important water-
soluble vitamin.
 Intrinsic factor (IF) is required for cobalamin
absorption
 Causes of cobalamin deficiency
 Gastric mucosa not secreting IF
 GI surgery loss of IF-secreting gastric mucosal cells
 Long-term use of H2-histamine receptor blockers
 Nutritional deficiency
 Hereditary defects of cobalamine utilization
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 Cobalamin (Vitamin B12) Deficiency
 Clinical manifestations
 General symptoms of anemia
 Sore tongue
 Anorexia
 Weakness
 Parathesias of the feet and hands
 Altered thought processes
 Confusion  dementia

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 Cobalamin Deficiency
Diagnostic Studies

 RBCs appear large

 Abnormal shapes
 Structure contributes to erythrocyte destruction
 Schilling Test: a medical investigation used for
patients with vitamin B12 deficiency. The
purpose of the test is to determine if the patient
has pernicious anemia.

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 Cobalamin Deficiency

 Collaborative Care
 Parenteral administration of cobalamin
 ↑ Dietary cobalamin does not correct the anemia
 Still important to emphasize adequate dietary intake
 Intranasal form of cyanocobalamin (Nascobal) is
available
 High dose oral cobalamin and SL cobalamin can use
be used

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 Cobalamin Deficiency
 Nursing Management
 Familial disposition
 Early detection and treatment can lead to reversal of
symptoms
 Potential for Injury r/t patient’s diminished sensations
to heat and pain
 Compliance with medication regime
 Ongoing evaluation of GI and neuro status
 Evaluate patient for gastric carcinoma frequently

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 Folic Acid Deficiency
 Folic Acid Deficiency also causes megablastic
anemia (RBCs that are large and fewer in
number)
 Folic Acid required for RBC formation and
maturation
 Causes
 Poor dietary intake
 Malabsorption syndromes
 Drugs that inhibit absorption
 Alcohol abuse
 Hemodialysis
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 Folic Acid Deficiency
 Clinical manifestations are similar to those of cobalamin
deficiency
 Insidious onset: progress slowly
 Absence of neurologic problems
 Treated by folate replacement therapy
 Encourage patient to eat foods with large amounts of folic
acid
 Leafy green vegetables
 Liver

 Mushrooms

 Oatmeal (‫مجروش‬TT‫شوفان لا‬TT‫) لا‬

 Peanut butter

 Red beans

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 Anemia of Chronic Disease
 Underproduction of RBCs, shortening of RBC
survival
 2nd most common cause of anemia (after iron
deficiency anemia
 Generally develops after 1-2 months of sustained
disease
 Causes
 Impaired renal function
 Chronic, inflammatory, infectious or malignant disease
 Chronic liver disease
 Folic acid deficiencies
 Splenomegaly
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 Hepatitis 47
 Aplastic Anemia
 Characterized by Pancytopenia
 ↓ of all blood cell types
 RBCs
 White blood cells (WBCs)

 Platelets

 Hypocellular bone marrow

 Etiology
 Congenital
 Chromosomal alterations

 Acquired
 Results from exposure to ionizing radiation, chemical agents,

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viral and bacterial infections 48
 Aplastic Anemia
 Etiology
 Low incidence
 Affecting 4 of every 1 million persons

 Manageable with erythropoietin or blood transfusion

 Can be a critical condition
 Hemorrhage

 Sepsis

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 Aplastic Anemia
 Clinical Manifestations
 Gradual development
 Symptoms caused by suppression of any or all bone
marrow elements
 General manifestations of anemia
 Fatigue

 Dyspnea

 Pale skin

 Frequent or prolonged infections

 Unexplained or easy bruising

 Nosebleed and bleeding gums

 Prolonged bleeding from cuts

 Dizziness

 headache
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 Aplastic Anemia
 Diagnosis
 Blood tests
 CBC
 Bone marrow biopsy

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 Aplastic Anemia
 Treatment
 Identifying cause
 Blood transfusions
 Antibiotics
 Immunosuppressants (neoral, sandimmune)
 Corticosteroids (Medrol, solu-medrol)
 Bone marrow stimulants
 Filgrastim (Neupogen)
 Epoetin alfa (Epogen, Procrit)

 Bone marrow transplantation

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 Aplastic Anemia
 Nursing Management
 Preventing complications from infection and
hemorrhage
 Prognosis is poor if untreated
 75% fatal

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 Anemia Caused By Blood Loss
 Acute Blood Loss
 Chronic Blood Loss

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 Acute Blood Loss
 Result of sudden hemorrhage
 Trauma, surgery, vascular disruption
 Collaborative Care
1. Replacing blood volume
2. Identifying source of hemorrhage
3. Stopping blood loss

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 Chronic Blood Loss
 Sources/Symptoms
 Similar to iron deficiency anemia
 GI bleeding, hemorrhoids, menstrual blood loss
 Diagnostic Studies
 Identifying source
 Stopping bleeding
 Collaborative Care
 Supplemental iron administration

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 Anemia caused by Increased Erythrocyte
Destruction

 Hemolytic Anemia
 Sickle Cell disease (peds)
 Acquired Hemolytic Anemia
 Hemochromatosis
 Polycythemia

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 Hemolytic Anemia
 Destruction or hemolysis of RBCs at a rate that exceeds
production
 Third major cause of anemia
 Intrinsic hemolytic anemia
 Abnormal hemoglobin
 Enzyme deficiencies
 RBC membrane abnormalities
 Extrinsic hemolytic anemia
 Normal RBCs
 Damaged by external factors
 Liver

 Spleen

 Toxins

 Mechanical injury (heart valves)

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 Sequence of Events in Hemolysis

Fig. 30-1
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 Acquired Hemolytic Anemia
 Causes
 Medications
 Infections
 Manifestations
 S/S of anemia
 Complications
 Accumulation of hemoglobin molecules can
obstruct renal tubules  Tubular necrosis
 Treatment
 Eliminating the causative agent
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 Potential Nursing Dx for Patients with
Anemia
 Activity Intolerance r/t weakness, malaise m/b
difficulty tolerating ↑’d activity
 Imbalance nutrition: less than body requirements
r/t poor intake, anorexia, etc. m/b wt loss,  serum
albumin,  iron levels, vitamin deficiencies, below
ideal body wt.
 Ineffective therapeutic regimen management r/t
lack of knowledge about nutrition/medications etc.
m/b ineffective lifestyle/diet/medication adjustments
 Collaborative Problem: Hypoxemia r/t
hemoglobin

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 Hemochromatosis
 Iron overload disease
 Over absorption and
storage of iron causing
damage especially to
liver, heart and pancreas

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 Polycythemia
 Polycythemia is a condition in which there is
a net increase in the total number of red
blood cells
 Overproduction of red blood cells may be
due to
 a primary process in the bone marrow (a so-called
myeloproliferative syndrome)
 or it may be a reaction to chronically low oxygen
levels or
 malignancy

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 Polycythemia
 Complications
 ↑d viscosity of blood
  hemorrhage and thrombosis
 Treatment
 Phlebotomy
 Myelosupressive agents: A number of new
therapeutic agents such as, interferon alfa-2b (Intron A)
therapy, agents that target platelet number (e.g., anagrelide
[Agrylin]), and platelet function (e.g., aspirin).

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 Thrombocytopenia
 Disorder of decreased platelets
 platelet count below 150,000
 Causes
 Low production of platelets
 Increased breakdown of platelets

 Symptoms
 Bruising
 Nosebleeds
 Petechiae (pinpoint microhemorrhages)

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 Thrombocytopenia
 Types of Thrombocytopenia
 Immune Thrombocytopenic Purpura
 Abnormal destruction of circulating platelets

 Autoimmune disorder

 Destroyed in hosts’ spleen by macrophages

 Thrombotic Thrombocytopenic Purpura

 d agglutination of platelets that from microthrombi

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 Heparin-Induced Thrombocytopenia (HIT)
 HIT
 Associated with administration of heparin
 Develops when the body develops an antibody, or allergy to
heparin
 Heparin (paradoxically) causes thrombosis
 Immune mediated response that casues intense platelet activation
and relaese of procoaggulation particles.
 Clinical features
 Thrombocytopenia

 Possible thrombosis after heparin therapy

 Can be triggered by any type, route or amount of heparin

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 Thrombocytopenia
Diagnostic Studies
 Platelet count
 Prothrombin Time (PT)
 Activated Partial Thromboplastin Time (aPTT)
 Hgb/Hct
 Treatment
 Based on cause
 Corticosteroids
 Plasmaphoresis
 Splenectomy
 Platelet transfusion

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