2.  The blood and the blood forming sites, including the
bone marrow and the reticuloendothelial system
 Blood
› Plasma
› Blood cells
 Hematopoiesis

3. Blood
Adult:
•Female 4-5L
•Males 5-6L

4.  Transport of:
› Gases, nutrients, waste products
› Processed molecules
› Regulatory molecules
 Regulation of pH and osmosis
 Maintenance of body temperature
 Protection against foreign substances
 Clot formation

5. Antibodies & complements
–part of immune system
Clotting factor
Once activated, converted
to fibrin (threadlike protein
that forms blood clot

6.  Liquid part of blood
› Pale yellow made up of 91% water, 9% other
 Colloid: Liquid containing suspended substances
that don’t settle out
› Albumin: Important in regulation of water movement
between tissues and blood
› Globulins: Immune system or transport molecules
› Fibrinogen: Responsible for formation of blood clots

7.  Erythrocyte: RBC
 Leukocyte: WBC
› Neutrophil
› Monocyte
› Eosinophil
› Basophil
› Lymphocyte: T lymphocyte and B lymphocyte
 Thrombocyte: platelet

9.  Hematopoiesis or hemopoiesis:
› Process of blood cell production
› Fetus: liver, thymus, spleen, lymph nodes, red bone
marrow
› After birth: red bone marrow, for WBC in some
lymphatic tissues
 Stem cells (hemocytoblast): All formed elements
derived from single population
› Proerythroblasts: Develop into red blood cells
› Megakaryoblasts: Develop into platelets

10. 19-
10

11.  Structure
› Biconcave, anucleate
 Components
› Hemoglobin (makes it red
in color)
› Lipids, ATP, carbonic
anhydrase
 Function
› Transport oxygen from
lungs to tissues and
carbon dioxide from
tissues to lungs

12. Unable to divide, grow, or synthesize proteins
Wear out in 100 to 120 days
Removed by phagocytes in the spleen or liver
New RBCs made by stem cells in bone marrow
Production increases when oxygen level decrease or during
pregnancy
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

13.  Consists of:
› 4 globin molecules: Transport carbon dioxide (carbonic anhydrase
involved), nitric oxide
 2 alpha and 2 beta globin chains
› 4 heme molecules: Transport oxygen
 Each heme contains 1 iron
 Iron is required for oxygen transport
› Hemoglobin + oxygen = bright red
› Hemoglobin with no oxygen = darker red

14. Erythrocytes: Levels in Blood
Live only four (4) months or ~120 days
Average RBC count:
Males: 5.4 million/mm3
Females: 4.8 million/mm3
Outnumber white blood cells 1000:1
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

15.  Happens in red bone marrow
 Components required:
› Precursor cells: PROERYTHROBLAST
› Proper microenvironment
› Adequate supplies of iron, vitamin B12, folic acid, protein,
pyridoxine and traces of copper
 Erythropoietin:
› Hormone to stimulate RBC production

16.  During cell division, the process requires B
vitamins folate and B12, necessary for synthesis
of DNA.
 Iron is required for production of hemoglobin
 RBC production is triggered by low blood
oxygen levels

24.  Cytotoxic cells
 Helper cells
 Memory cells
 Suppressor cells

25.  IgG
› chronic infxn, transplacental;
 IgA
› external secretions; “mucosal paint”
› through breastfeeding
 IgM
› acute infxn; 1O response Ab, 1st produced by infants
 IgE
› parasitic / allergic reactions
 IgD
› no specific function; antigen-binding

28.  factor I (fibrinogen)
 factor II (prothrombin) – Vit K dependent
 factor III (tissue thromboplastin)
 factor IV (calcium)
 factor V (proaccelerin)
 factor VI (no longer considered active in hemostasis)
 factor VII (proconvertin) - Vit K dependent
 factor VIII (antihemophilic factor)
 factor IX (plasma thromboplastin component; Christmas factor) -
Vit K dependent
 factor X (stuart factor) - Vit K dependent
 factor XI (plasma thromboplastin antecedent)
 factor XII (hageman factor)
 factor XIII (fibrin stabilizing factor).

30. Spleen
› Left upper quadrant of the abdomen behind abdomen
› Produces RBC during fetal development
› Filter function – remove old defective cells from circulation and
breaks down RBC and recycles the iron to bone marrow
Liver
› Receives blood from the spleen through portal circulation
› Produce procoagulants necessary for hemostasis and blood
coagulation
› Storage of iron and B12
› Detoxify drugs
› Kupffer cells carry out phagocytosis
› Bile production from erythrocyte destruction

31. Lymphatics
 Lymph capillaries
› Carries lymph to the subclavian vein in the
chest
 Lymph nodes
› Small rounded structures that filter bacteria
and foreign particles

33.  Reduction below normal in the # of RBC,
the quantity of hemoglobin and volume of
RBC (hematocrit)
 Result from:
› ↓RBC production
› ↑RBC destruction
› Acute or chronic blood loss

34.  Three broad categories
1. Loss of RBC- occurs with bleeding
2. Decreased RBC production
› IDA
› FADA
› Thalassemia
3. Increased RBC destruction

35.  Normocytic
› Normal RBC size
› IDA
 Macrocytic
› Large RBC due to impaired division of RBC precursor cells
› Cobalamin and folate deficiency
 Microcytic
› Small RBC
 Normochromic
› Normal hemoglobin concentration
 Hypochromic
› Decrease hemoglobin concentration
 Hyperchromic
› Increased hemoglobin concentration

37.  Iron Deficiency Anemia
› dietary intake of iron is inadequate to produce
hemoglobin
› Most common type of anemia
› May occur with removal of the duodenum
› Associated with chronic blood loss.

38.  Iron Deficiency Anemia
Etiologic Factors
1. Bleeding- the most common cause
2. Mal-absorption
3. Malnutrition
4. Alcoholism

39.  Iron Deficiency Anemia
Pathophysiology
› The body storage of iron decrease, leading
to depletion of hemoglobin synthesis
› The oxygen carrying capacity of
hemoglobin is reduced tissue hypoxia

40.  Iron Deficiency Anemia
Assessment Findings
1. Pallor of the skin and mucous membrane
2. Weakness and fatigue
3. General malaise
4. Pica

41. Assessment Findings
5. Brittle nails
6. Smooth and sore tongue
7. Angular cheilosis

42.  Iron Deficiency Anemia
Laboratory findings
1. CBC
› Low levels of Hct, Hgb and RBC count
2. Low serum iron, low ferritin
3. Bone marrow aspiration- MOST definitive

43.  Iron Deficiency Anemia
Medical management
 1. Iron replacement
 2. Blood transfusion

44. Nursing Management
1. Provide iron rich-foods
› Organ meats (liver)
› Beans
› Leafy green vegetables
› Raisins and molasses
2. Administer iron
› Oral preparations tablets- Fe fumarate, sulfate and
gluconate
› Advise to take iron ONE hour before meals
› Take it with vitamin C
› Monitor for adverse reaction like pyrosis (heartburn),
constipation, diarrhea, dark stool
› Continue taking it for several months even with normal iron
level

45. Nursing Management
2. Administer iron
› Oral preparations- liquid
 It stains teeth
 Drink it with a straw
› Stool may turn blackish- dark in color
› Advise to eat high-fiber diet and to ↑fluid
intake to counteract constipation

46. Nursing Management
2. Administer iron
› IM preparation
 Administer DEEP IM
 Include 0.5ml air in syringe to clear iron from the needle
 Use the Z-track method
› Avoid vigorous rubbing
› Can cause local pain and staining
 Note:
› Iron should be taken for 2-3 mos after Hb level returns to
normal

47. 3. Administer packed red blood cell
transfusion if patient is symptomatic

49.  Normally hemoglobin contain 4 globin chains
 Decreased production of hemoglobin due to abnormal hemoglobin synthesis
 Reduced production or no production of 1 of the globin chains that make up
hemoglobin
 Microcytic and hypochromic
 Autosomal recessive genetic disorder common among Mediterranean people.
 Chronic bone marrow hyperplasia
 Altered globin synthesis of hemoglobin
 Treatment causes chronic iron toxicity

50.  Thalassemia minor
› Has 1 thalassemic and 1 normal gene with
mild clinical manifestations
› Requires no tx
 Thalassemia major
› Has 2 thalassemic genes causing severe
conditions

52. Assessment:
1. Skin: pale/jaundiced
2. Splenomegaly and hepatomegaly
3. Thickened cranium and maxillary sinus space from
bone marrow hyperplasia

53. Diagnostics:
1. CBC
1. Anemia lower Mean corpuscular volume
2. Hemoglobin electrophoresis

54. Nursing Management
1. Administer BT and chelation therapy (remove heavy
metals) to reduce iron overload
2. Monitor for transfusion reactions or diseases
acquired through transfusions
3. Instruct about tx, medications and physical energy
conservation techniques
4. Strengthen client support and family systems.

56.  Life-threatening stem cell disorder with many possible
etiological mechanisms
 Decreased number of RBC as well as WBC and
platelets
 Characterized as:
› hypoplastic( incomplete development of a tissue or
organ)
› Fatty bone marrow
› Pancytopenia (reduction in # of RBC, WBC and platelets)

57. CAUSATIVE FACTORS
1. Environmental toxins- pesticides, benzene
2. Certain drugs
› Chemotherapeutic agents
› Chloramphenicol
› Phenothiazines
› Sulfonamides
3. Heavy metals
4. Radiation

58. Pathophysiology
Toxins cause a direct bone marrow
depression
↓
acellular bone marrow
↓
decreased production of blood elements

60.  ASSESSMENT FINDINGS
1. fatigue
2. pallor
3. dyspnea
4. bruising
5. splenomegaly
6. retinal hemorrhages

61.  LABORATORY FINDINGS
1. CBC
› decreased blood cell numbers
2. Bone marrow aspiration confirms the
anemia- hypoplastic or acellular marrow
replaced by fats

62.  Medical Management
1. Bone marrow transplantation
2. Immunosupressant drugs
3. Rarely, steroids
4. Blood transfusion

63.  Nursing management
1. Assess for signs of bleeding and infection
2. Pancytopenia plan of care to prevent
complications like infection and bleeding.
1. Private room
2. Strict hand washing
3. Minimizing invasive procedures
3. Provide client and family with support for
lengthy hospitalization and tx

65.  abnormally large RBC secondary to
impaired DNA synthesis
 due to deficiency of Folic acid and/or
vitamin B12

66. 1. Folic Acid deficiency
› Folate is required for DNA synthesis in erythrocyte formation
› Without neurologic involvement
Causative factors
1. Alcoholism
2. Mal-absorption
3. Diet deficient in uncooked vegetables
4. Use of oral contraceptives

67. Pathophysiology of Folic acid deficiency
Decreased folic acid
↓
impaired DNA synthesis in the bone marrow
↓
impaired RBC development
impaired nuclear maturation but Cytoplasmic maturation continues
↓
large size

68. Assessment (Folate Deficiency)
1. Poor nutrition
2. Alcohol abuse
3. Anorexia
4. Impaired absorption in the small intestine
5. Undergoing hemodialysis (folate is dialyzable)
6. Certain drugs can block folate absorption
1. Oral contraceptives
2. Antiseizure drugs (phenytoin)
3. Antibiotics

69. Diagnosis (Folate deficiency)
1. CBC
1. ↓ RBC, hgb & hct and ↑ MCV
2. Serum folate levels are low
3. Serum cobalamin is normal

70. Nursing Management
1. Promote compliance with replacement therapy
(1-5 mg oral folate/day)
2. Administer prenatal vitamins in pregnancy
3. Instruct on food high in folate such as leafy
greens, liver, citrus fruits, nuts and grains

72. Normal Condition:
Parietal cells of stomach secreted intrinsic
factor to absorb ingested cobalamin
(vit.b12)

73. Vitamin B12 deficiency
(Pernicious Anemia)
› Lack of intrinsic factor (needed for B12 absorption)
› Common among Northern European ancestry over age of 40 and young African
American
Causative factors
1. Strict vegetarian diet
2. Gastrointestinal malabsorption
3. Crohn's disease
4. Yrs of Gastritis
5. Gastrectomy

74.  Vitamin B12 deficiency
Pernicious Anemia
 Due to the absence of intrinsic factor secreted by
the parietal cells
 Intrinsic factor binds with Vit. B12 to promote
absorption

75. Assessment findings
1. Weakness
2. Fatigue
3. Neurologic manifestations are present only in
Vit. B12 deficiency
1. Weakness, paresthesia of feet and hands, impaired
thought processes
4. Coagulation deficiencies

76.  Assessment findings
Pernicious Anemia
› Beefy, red, swollen tongue
› Mild diarrhea
› Extreme pallor
› Paresthesias in the extremities

77.  Laboratory findings
1. Peripheral blood smear- shows giant RBCs, WBCs with giant
hypersegmented nuclei
2. Very high MCV
3. Schilling’s test
› Radioactive vit B12 malabsorption is measured by small amount of
secreted in urine
› When vit B12 us administered with gastric IF parenterally, its absence in
urine will diagnose pernicious anemia
4. Intrinsic factor antibody test

78.  Medical Management
1. Vitamin supplementation
Folic acid 1 mg daily
2. Diet supplementation
Vegetarians should have vitamin intake
3. Lifetime monthly injection of IM Vit B12
› w/o cobalamin replacement, patient can die in 1-3yrs.

79.  Since Pernicious anemia results from an
inability to absorb cobalamin, dietary
intake of the vitamin is not a treatment
option, nor is bone marrow transplant

80.  Nursing Management
1. Monitor patient
2. Provide assistance in ambulation
3. Oral care for tongue sore
4. Explain the need for lifetime IM injection of vit B12

82.  Decrease in erythrocyte precursor
production that occurs in some chronic
conditions
 End-stage renal failure
 Chronic liver disease
 Alcohol abuse
 hypothyroidism

83. Clinical Manifestations
ALL ASSESSMENT FINDINGS FOR ANEMIA
APPLY

84. Diagnosis:
1. CBC
2. FERRITIN
1. Iron stores may be high in contrast to IDA

85.  Nursing Management
1. Facilitate diagnosis and tx if underlying, contributory
condition
2. Inform that this type of anemia does not respond to
folic acid, iron or vitamin B12
3. Erythropoietin therapy is administered to a client
with anemia related to renal failure

87. 2 SITES OF HEMOLYSIS
1. INTRAVASCULAR DESTRUCTION
› Occurs within the circulation
2. EXTRAVASCULAR DESTRUCTION
› Occurs in liver, spleen, or bone marrow

88. CLASSIFICATION OF HEMOLYTIC ANEMIAS
1. INTRINSIC HEMOLYTIC ANEMIAS
› Usually hereditary
› Defects in RBC themselves
1. Abnormal hgb = sickle cell anemia
2. Enzyme deficiencies = G6PD
3. Cell membrane abnormalities

89. CLASSIFICATION OF HEMOLYTIC ANEMIAS
2. EXTRINSIC HEMOLYTIC ANEMIAS
› Normal RBCs are damaged by external factors
› Cause:
 antibodies, toxins,
 mechanical injury (prosthetic heart valves)
 dialysis,
 transfusion reaction
 trapping of cells within the liver and spleen

92.  A severe chronic incurable hemolytic anemia that results from
heritance of the sickle hemoglobin gene.
 Produces specific mutant form of beta-globin
 Hypoxia-induced change in RBCs
 Associated with vascular occlusion and tissue infarction
 Anemia is caused by accelerated breakdown of abnormal RBC

93.  Causative factor
› Genetic inheritance of the sickle
gene- Hbs gene

94. Pathophysiology
 Decreased O2, Cold, Vasoconstriction can
precipitate sickling process

95. Pathophysiology
Factors
↓
cause defective hemoglobin to acquire a rigid, crystal-like C-
shaped configuration
↓
Sickled RBCs will adhere to endothelium
↓
pile up and plug the vessels
↓
ischemia results
↓
pain, swelling and fever

97.  Assessment Findings
1. jaundice
2. enlarged skull and facial bones
3. tachycardia, murmurs and cardiomegaly

98. Assessment Findings
 Primary sites of thrombotic occlusion: spleen,
lungs and CNS
 Chest pain, dyspnea

99.  Assessment Findings
1. Sickle cell crises
› Results from tissue hypoxia and necrosis
2. Acute chest syndrome
› Manifested by a rapidly falling hemoglobin
level, tachycardia, fever and chest infiltrates in
the CXR

100. During the sickling crisis,
the sickling cells clog small capillaries and the resulting hemotasis
promotes a self-prepetuating cycle of local hypoxia,
deoxygenation of more erythrocytes and more sickling.
MEDICAL MGT:
Administration of large doses of narcotic analgesics
Since pain last 4-6 days

101. Medical Management
1. Bone marrow transplant
2. Hydroxyurea
3. Long term RBC transfusion

102. Nursing Management
1. manage the pain
› Support and elevate acutely inflamed joint
› Relaxation techniques to reduce metabolic
needs
› analgesics

103. Nursing Management
2. Prevent and manage infection
› Monitor status of patient
› Initiate prompt antibiotic therapy

104. Nursing Management
3. Promote coping skills
› Provide accurate information
› Allow patient to verbalize her concerns about
medication, prognosis and future pregnancy

105. Nursing Management
4. Monitor and prevent potential
complications
› Provide always adequate hydration
› Avoid cold, temperature that may cause
vasoconstriction

106. Nursing Management
4. Monitor and prevent potential
complications
› Leg ulcer
Aseptic technique

107. Nursing Management
4. Monitor and prevent potential complications
Priapism
 Sudden painful erection
 Instruct patient to empty bladder, then take a warm
bath
5. Maintain F & E balance to reduce blood
viscosity

109.  Glucose-6-phosphate dehydrogenase
 Results from lack of an RBC enzyme that
leads to RBC damage when metabolic
needs of RBCs are increased.

110.  A group of X-linked familial hemolytic mutations of the
gene
 Deficiency predisposes to oxidative denaturation of
hemoglobin, with resultant red cell injury and lysis.
 Hemolysis occurs as the result of oxidative stress generated
by either an infection or exposure to certain drugs.
 More common among males of Mediterranean or African
descent

111. •Jaundice
•Headache
Assessment
•Dizziness
•Easy fatigabilty

112. Diagnostic:
Use of G6PD assay or screening test
Quantification of G6PD levels during
nonhemolytic phase

113. Nursing Management
1. Provide periods of rest
2. Provide adequate hydration
3. Administer antibiotics and other tx as
ordered to minimize complications.

115.  Refers to an INCREASE volume of RBCs
 The hematocrit is ELEVATED to more than
55%

116.  POLYCYTHEMIA VERA
› Primary Polycythemia
 A proliferative disorder in which the
myeloid stem cells become uncontrolled
 Neoplastic disorder where there is an
increased in 3 types of blood cells

117.  POLYCYTHEMIA VERA
Causative factor
› unknown

118.  POLYCYTHEMIA VERA
 Pathophysiology
› The stem cells grow uncontrollably
› The bone marrow becomes HYPERcellular and all the
blood cells are increased in number

119.  POLYCYTHEMIA VERA
Pathophysiology
› The spleen resumes its function of hematopoiesis and
enlarges
› Blood becomes thick and viscous causing sluggish
circulation
› Overtime, the bone marrow becomes fibrotic

120.  POLYCYTHEMIA VERA
Assessment findings
1. Skin is ruddy, pruritic due to histamine release
2. Splenomegaly in primary PV only
3. headache, tinnitus
4. dizziness, blurred vision
5. Angina, intermittent claudication, dyspnea and
thrombophlebitis

121.  POLYCYTHEMIA VERA
 Laboratory findings
1. CBC- shows elevated RBC mass
2. Normal oxygen saturation
3. Elevated WBC and Platelets

122.  POLYCYTHEMIA VERA
Complications
1. Increased risk for:
1. Thrombophlebitis
 Due to hypervolemia & hyperrviscosity,
 Tx: active/passive leg exercise and ambulation
2. CVA
3. MI
2. Bleeding due to dysfunctional blood cells

123. POLYCYTHEMIA VERA
Medical Management
1. To reduce the high blood cell mass- PHLEBOTOMY
2. Allopurinol
3. Dipyridamole
4. Chemotherapy to suppress bone marrow

124.  Nursing Management
1. Primary role of the nurse is EDUCATOR
2. Regularly asses for the development of complications
3. Assist in weekly phlebotomy
4. Advise to avoid alcohol and aspirin
5. Advise tepid sponge bath or cool water to manage pruritus

126.  Malignant disorders of blood forming cells
 characterized by UNCONTROLLED proliferation of
WBC in the bone marrow- replacing marrow
elements .
 The WBC can also proliferate in the liver, spleen
and lymph nodes.

127.  named after the specific lines of blood
cells afffected primarily
› Myeloid
› Lymphoid
› Monocytic

128.  The leukemias are named also according
to the maturation of cells
 ACUTE
› The cells are primarily immature
 CHRONIC
› The cells are primarily mature or diferentiated

129.  ACUTE myelocytic leukemia
 ACUTE lymphocytic leukemia
 CHRONIC myelocytic leukemia
 CHRONIC lymphocytic leukemia

130.  ETIOLOGIC FACTORS
› UNKNOWM
› Probably exposure to radiation
› Chemical agents
› Infectious agents
› Genetic

131. PATHOPHYSIOLOGY of ACUTE Leukemia
Uncontrolled proliferation of immature cells
↓
suppresses bone marrow function
↓
severe anemia, thrombocytopenia and
granulocytopenia

132. PATHOPHYSIOLOGY of CHRONIC Leukemia
Uncontrolled proliferation of DIFFERENTIATED cells
↓
slow suppression of bone marrow function
↓
milder symptoms

133.  ASSESSMENT FINDINGS
 ACUTE LEUKEMIA
› Pallor
› Fatigue
› Dyspnea
› Hemorrhages
› Organomegaly
› Headache
› vomiting

134.  ASSESSMENT FINDINGS
 CHRONIC LEUKEMIA
› Less severe symptoms
› organomegaly

135. LABORATORY FINDINGS
 Peripheral WBC count varies widely
 Bone marrow aspiration biopsy reveals a large
percentage of immature cells- BLASTS
 Erythrocytes and platelets are decreased

136. Medical Management
1. Chemotherapy
2. Bone marrow transplantation

137. Nursing Management
 1. Manage AND prevent infection
› Monitor temperature
› Assess for signs of infection
› Be alert if the neutrophil count drops
below 1,000 cells/mm3

138. Nursing Management
2. Maintain skin integrity
3. Provide pain relief
4. Provide information as to therapy- chemo
and bone marrow transplantation

140. Read on the following remaining topics:
1. Thrombocytopenia
2. Disseminated Intravascular Coagulation
3. Hemophilia
4. Von Willebrand’s disease
5. Neutropenia

141. On September 12, 2011, we will have
our
UNIT EXAM
on the following topics:
Fluids and Electrolytes
And
Hematologic Disorders

142. NEXT TOPIC TO BE DISCUSSED WOULD BE:
CARDIOVASCULAR DISORDERS
AND
PERIPHERAL DISORDERS BY S’ CLAY
ENDOCRINE DISORDERS BY M’ LUDY