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
acutely inflamed joint
–Relaxation techniques
–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
–Allow patient to verbalize
her 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
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
 Theleukemias 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