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HEMATOLOGY

Blood disorders
Anemia
Nutritional anemia
Hemolytic anemia
Aplastic anemia
Sickle cell anemia
ANEMIA

Acondition in
which the
hemoglobin
concentration is
lower than normal
ANEMIA
 Three broad categories
 1. Loss of RBC- occurs with
bleeding
 2. Decreased RBC
production
 3. Increased RBC
destruction
Hypoproliferative Anemia
Iron Deficiency Anemia
–Results when the dietary
intake of iron is
inadequate to produce
hemoglobin
Hypoproliferative Anemia
Iron Deficiency Anemia
– Etiologic Factors
– 1. Bleeding- the most
common cause
– 2. Mal-absorption
– 3. Malnutrition
– 4. Alcoholism
Hypoproliferative Anemia
IronDeficiency Anemia
Pathophysiology
–The body stores of iron
decrease, leading to
depletion of hemoglobin
synthesis
Hypoproliferative Anemia
IronDeficiency Anemia
Pathophysiology
–The oxygen carrying capacity
of hemoglobin is reduced
tissue hypoxia
Hypoproliferative Anemia
 Iron Deficiency Anemia
 Assessment Findings
 1. Pallor of the skin and
mucous membrane
 2. Weakness and fatigue
 3. General malaise
 4. Pica
Hypoproliferative Anemia
Iron Deficiency Anemia
Assessment Findings
5. Brittle nails
6. Smooth and sore
tongue
7. Angular cheilosis
Hypoproliferative Anemia
 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
Hypoproliferative Anemia
Iron Deficiency Anemia
Medical management
1. Hematinics
2. Blood transfusion
Hypoproliferative Anemia
Iron Deficiency Anemia
Nursing Management
 1. Provide iron rich-foods
– Organ meats (liver)
– Beans
– Leafy green vegetables
– Raisins and molasses
Hypoproliferative Anemia

Nursing Management
2. Administer iron
 Oral preparations tablets- Fe
fumarate, sulfate and gluconate
 Advise to take iron ONE hour
before meals
 Take it with vitamin C
 Continue taking it for several
months
Hypoproliferative Anemia
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 to
counteract constipation
Hypoproliferative Anemia
Nursing Management
2. Administer iron
 IM preparation
 Administer DEEP IM using the
Z-track method
 Avoid vigorous rubbing
 Can cause local pain and
staining
APLASTIC ANEMIA

Acondition
characterized by
decreased number
of RBC as well as
WBC and platelets
APLASTIC ANEMIA
CAUSATIVE FACTORS
 1. Environmental toxins-
pesticides, benzene
 2. Certain drugs-
Chemotherapeutic agents,
chloramphenicol,
phenothiazines, Sulfonamides
 3. Heavy metals
 4. Radiation
APLASTIC ANEMIA
Pathophysiology
Toxins cause a direct bone
marrow depression
acellualr bone marrow
decreased production of
blood elements
APLASTIC ANEMIA
 ASSESSMENT FINDINGS
 1. fatigue
 2. pallor
 3. dyspnea
 4. bruising
 5. splenomegaly
 6. retinal hemorrhages
APLASTIC ANEMIA
LABORATORY FINDINGS
1. CBC- decreased blood
cell numbers
2. Bone marrow aspiration
confirms the anemia-
hypoplastic or acellular
marrow replaced by fats
APLASTIC ANEMIA
Medical Management
1. Bone marrow
transplantation
2. Immunosupressant
drugs
3. Rarely, steroids
4. Blood transfusion
APLASTIC ANEMIA
Nursing management
1. Assess for signs of
bleeding and
infection
2. Instruct to avoid
exposure to offending
agents
Megaloblastic Anemias
Anemias characterized by
abnormally large RBC
secondary to impaired
DNA synthesis due to
deficiency of Folic acid
and/or vitamin B12
Megaloblastic Anemias
Folic Acid deficiency
Causative factors
1. Alcoholism
2. Mal-absorption
3. Diet deficient in
uncooked vegetables
Megaloblastic Anemias
 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
Megaloblastic Anemias
 Vitamin B12 deficiency
 Causative factors
 1. Strict vegetarian diet
 2. Gastrointestinal
malabsorption
 3. Crohn's disease
 4. gastrectomy
Megaloblastic Anemias
 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
Megaloblastic Anemias
 Assessment findings
 1. weakness
 2. fatigue
 3. listless
 4. neurologic manifestations
are present only in Vit. B12
deficiency
Megaloblastic Anemias
 Assessment findings
 Pernicious Anemia
– Beefy, red, swollen tongue
– Mild diarrhea
– Extreme pallor
– Paresthesias in the extremities
Megaloblastic Anemias
 Laboratory findings
 1. Peripheral blood smear- shows
giant RBCs, WBCs with giant
hypersegmented nuclei
 2. Very high MCV
 3. Schilling’s test
 4. Intrinsic factor antibody test
Megaloblastic Anemias
 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
Megaloblastic Anemias
 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
Hemolytic Anemia: Sickle
Cell
Asevere chronic
incurable hemolytic
anemia that results
from heritance of the
sickle hemoglobin
gene.
Hemolytic Anemia: Sickle
Cell
Causative factor
–Genetic inheritance
of the sickle gene-
HbS gene
Hemolytic Anemia: Sickle
Cell
Pathophysiology
Decreased O2, Cold,
Vasoconstriction can
precipitate sickling
process
Hemolytic Anemia: Sickle
Cell
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
Hemolytic Anemia: Sickle
Cell
Assessment Findings
1. jaundice
2. enlarged skull and
facial bones
3. tachycardia,
murmurs and
cardiomegaly
Hemolytic Anemia: Sickle
Cell
Assessment Findings
Primary sites of
thrombotic occlusion:
spleen, lungs and
CNS
Chest pain, dyspnea
Hemolytic Anemia: Sickle
Cell
 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
Hemolytic Anemia: Sickle
Cell
Medical Management
1. Bone marrow
transplant
2. Hydroxyurea
–Increases the HbF
3. Long term RBC
trnasfusion
Hemolytic Anemia: Sickle
Cell
Nursing Management
1. manage the pain
Support and elevate
–Support
acutely inflamed joint
Relaxation techniques
–Relaxation
analgesics
–analgesics
Hemolytic Anemia: Sickle
Cell
Nursing Management
2. Prevent and manage
infection
–Monitor status of patient
–Initiate prompt antibiotic therapy
Hemolytic Anemia: Sickle
Cell
Nursing Management
3. Promote coping skills
Provide accurate information
–Provide
Allow patient to verbalize her
–Allow
concerns about medication,
prognosis and future
pregnancy
Hemolytic Anemia: Sickle
Cell
Nursing Management
4. Monitor and prevent
potential complications
– Provide always adequate
hydration
– Avoid cold, temperature that
may cause vasoconstriction
Hemolytic Anemia: Sickle
Cell
Nursing Management
4. Monitor and
prevent potential
complications
–Leg ulcer
Aseptic technique
Hemolytic Anemia: Sickle
Cell
Nursing Management
4. Monitor and prevent
potential complications
Priapism
–Priapism
Sudden painful erection
Instruct patient to empty
bladder, then take a warm bath
Polycythemia
Refers to an INCREASE
volume of RBCs
The hematocrit is
ELEVATED to more than
55%
Clasified as Primary or
Secondary
Polycythemia
POLYCYTHEMIA VERA
– Primary Polycythemia
– A proliferative disorder
in which the myeloid
stem cells become
uncontrolled
Polycythemia
POLYCYTHEMIA VERA
Causative factor
– unknown
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
– The stem cells grow uncontrollably
– The bone marrow becomes
HYPERcellular and all the blood
cells are increased in number
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
– The spleen resumes its function of
hematopoiesis and enlarges
– Blood becomes thick and viscous
causing sluggish circulation
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
– Overtime, the bone
marrow becomes fibrotic
Polycythemia
POLYCYTHEMIA VERA
Assessment findings
– 1. Skin is ruddy
– 2. Splenomegaly
– 3. headache
– 4. dizziness, blurred vision
– 5. Angina, dyspnea and thrombophlebitis
Polycythemia
POLYCYTHEMIA VERA
Laboratory findings
– 1. CBC- shows elevated RBC mass
– 2. Normal oxygen saturation
– 3 Elevated WBC and Platelets
Polycythemia
POLYCYTHEMIA VERA
Complications
– 1. Increased risk for
thrombophlebitis, CVA and
MI
– 2. Bleeding due to
dysfunctional blood cells
Polycythemia
POLYCYTHEMIA VERA
Medical Management
– 1. To reduce the high blood cell
mass- PHLEBOTOMY
– 2. Allopurinol
– 3. Dipyridamole
– 4. Chemotherapy to suppress bone
marrow
Polycythemia
 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
Leukemia
 Malignant disorders of blood forming
cells characterized by UNCONTROLLED
proliferation of WHITE BLOOD CELLS in
the bone marrow- replacing marrow
elements . The WBC can also proliferate
in the liver, spleen and lymph nodes.
Leukemia
 The leukemias are named after
the specific lines of blood cells
afffected primarily
– Myeloid
– Lymphoid
– Monocytic
Leukemia
 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
Leukemia
 ACUTE myelocytic leukemia
 ACUTE lymphocytic leukemia

 CHRONIC myelocytic leukemia


 CHRONIC lymphocytic leukemia
Leukemia
 ETIOLOGIC FACTORS
– UNKNOWN
– Probably exposure to radiation
– Chemical agents
– Infectious agents
– Genetic
Leukemia
– PATHOPHYSIOLOGY of
ACUTE Leukemia
Uncontrolled proliferation of
immature cells suppresses
bone marrow function
severe anemia,
thrombocytopenia and
granulocytopenia
Leukemia
– PATHOPHYSIOLOGY of
CHRONIC Leukemia
Uncontrolled proliferation of
DIFFERENTIATED cells
slow suppression of bone
marrow function milder
symptoms
Leukemia
 ASSESSMENT FINDINGS
 ACUTE LEUKEMIA
– Pallor
– Fatigue
– Dyspnea
– Hemorrhages
– Organomegaly
– Headache
– vomiting
Leukemia
 ASSESSMENT FINDINGS
 CHRONIC LEUKEMIA
– Less severe symptoms
– organomegaly
Leukemia
LABORATORY FINDINGS
 Peripheral WBC count varies widely
 Bone marrow aspiration biopsy
reveals a large percentage of
immature cells- BLASTS
 Erythrocytes and platelets are
decreased
Leukemia
Medical Management
1. Chemotherapy
2. Bone marrow transplantation
Leukemia
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
Leukemia
Nursing Management
 2. Maintain skin integrity

 3. Provide pain relief

 4. Provide information as to therapy-


chemo and bone marrow transplantation