Hematologic Disorders Module PDF

Laoag City, Ilocos Norte
HEMATOLOGIC DISORDERS MODULE
WILJOHN M. DE LA CRUZ, M.A.N.

THRICIA BLESS S. VENTURA,R.N.
Professor
Care of Clients with Problems in Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory and Immunologic
Response, Cellular Aberrations, acute and chronic and Peri-operative Nursing
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Objectives:
Review the anatomy, physiology, and functions of the hematologic system.
Define the different disorders.
Understand the causes and/or risk factors associated with the disorders.
Trace the pathophysiology of common disorders, relating their manifestations to the pathophysiologic
Identify indicated diagnostic procedures appropriate for the different disorders.
Discuss appropriate management for specific patient and family members with ethical considerations
Since you have a background of the anatomy and physiology of the hematologic s
Activity 1 Diagram (Hematologic Components)
Instruction: Please label the three components of the blood in the photo below.
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In this part want you to answer the following questions related to our next topic. Be at your FINEST an
Activity 1 Exploring your Understanding
1. Based on the above figure, when you cut yourself, which part of the blood helps
you to stop bleeding? Support your answer in not more than 100 words.
2. Take an educated guess at this one, what happens to the number of white blood
cells when germs are in the body? Support your answer in not more than 100 words.
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In this part of our lesson we will be discussing the overview of the anatomy, physiology and functions
STRUCTURES OF HEMATOLOGIC SYSTEM
1. BONE MARROW - the site of the blood cell formation (hematopoiesis)

One of the largest organs of the body, making up 4% to 5% of the total body
weight.
Consist of cellular components.
 RED MARROW - major blood producing organs and found in
spongy bones.
 YELLOW MARROW – found in central cavity of long bones;
composed mainly of fat cells and does not participate in
hematopoiesis.
 STEM CELLS – primitive cells present in bone marrow. They
differentiate into mature blood cells.
 Have the ability to self – replicate, thereby ensuring a
continuous supply of stem cells throughout the life cycle.
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2. BLOOD – red, fluid connective

tissue composed of plasma and
various cell fragments which is
pumped by the heart to the cells
through the blood vessels.
Characteristics of Blood
1. pH – slightly alkaline
(7.35 – 7.45)
2. Color – (bright red) if
oxygenated:
(Dark red) if
Unoxygenated
:
3. Amount – 5-6 liters
for male.; 4-5 liters
for female
4. Type of tissue – connective tissue
5. Viscosity – 3-4 times more viscous than water
-heavier, thicker & more viscous than water
6. Temperature – 38 C higher than normal body temperature
7. Specific gravity – 1.048-1.066
General Functions of Blood

1. Transportation – blood transfer oxygen from the lungs to the cells of the
carbon dioxide from the cells to the lungs
2. Regulation – blood helps regulate pH through buffers
3. Protection – clotting mechanism protects against blood loss
- Phagocytic WBC & plasma proteins (antibodies, interferon)
protect against foreign microbes & toxins.
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Formed Elements/Blood cells

Cell Type Major Function
WBC (Leukocyte) Fights infection
Normal: 4500 11,000/mm3
Granulocytes
Neutrophil Essential in Preventing or limiting bacterial infection via
phagocytosis.
Eosinophil Involved in allergic reactions (neutralizes histamine),

digests foreign proteins
Agranulocytes
Monocyte Enters tissue as macrophage; highly phagocytic, especially

against fungus; immune surveillance.
T lymphocyte Responsible for cell- mediated immunity

Plasma Cell Secretes immunoglobulin (Ig/ antibody)
Most mature form of B lymphocytes
RBC (Erythrocyte) Carries hemoglobin to provide oxygen to tissues; average
Hemoglobin lifespan is 120 days
Male:13-18 g/dL
Female: 12-16 g/dL
Hematocrit
Male: 42-52%
Female: 35-47%
Platelet (Thrombocyte) Fragment of megakaryocyte; provides basis for
Normal: 150,000 coagulation to occur; maintains hemostasis; average
450,000/ mm3 lifespan is 10 days.
Formation of Blood Cells

 Hematopoiesis/Hemopoiesis – process of blood cell production
 Erythropoiesis – formation of RBC
 Leukopoiesis – formation of WBC
Hemopoeitic Growth Factors

 Erythropoeitin – produced by kidneys; a red blood cell precursor.
 Throbopoeitin/TPO – produced by the liver for the formation of platelets.
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Pathological conditions of the Blood Cells

a.Erythrocytosis – increase amount of RBC in the blood
b.Polycythemia – excess in number of RBC in the blood.
c.Erythrocytopenia – decrease amount of RBC in the blood.
d.Aplastic Anemia – decrease RBC due to damage in the bone
marrow.
e. Pernicious Anemia – reduction in the formation of RBC due to deficiency in Vit.B12.
f. Hemolytic Anemia – reduced life span of RBC
g. Sickle cell Anemia – abnormality in the protein portion of
hemoglobin. h.Thalassemia – disorder in hemoglobin synthesis.
i. Iron Deficiency Anemia – number of RBC is normal but smaller & paler.
j. Leukocytosis – increase circulating in WBC
k.Leukopenia – decrease circulating in WBC.
l. Thrombocytosis – increase platelets
m. Thrombocytopenia – decrease platelets.
n. Hemophilia – deficiency of blood clotting factors leading to bleeding
Blood Clotting Factors

Factor I Fibrinogen Forms fibrin
Factor II Prothrombin Forms thrombin which converts fibrinogen to fibrin
Factor III Thromboplastin Converts prothrombin to thrombin
Factor IV Calcium Serves as catalyst in converting prothrombin to
thrombin
Factor V Labile Formation of active thromboplastin
Factor VI Proconvertin Accelerates the action of tissue thromboplastin
Factor VII Anti-hemophilic Promotes the breakdown of thrombocytes & the
formation of active platelet thromboplastin.
Factor Christmas Similar to antihemophilic
VIII
Factor IX Stuart Promotes the action of thromboplastin
Factor X Plasma Promotes the clumping & breakdown of
thromboplastin thrombocytes & release of thromboplastin
factor
Factor XI Hageman Factor Similar to factor IX
Factor XII Fibrin stabilizing Converts the loose fibrin mesh to dense tight mesh.
Factor
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BLOOD GROUPS
 Antigen – substance in the body that stimulates the formation of antibody.
 Antibody – protein produced in response to antigen.
 Type AB – Universal Recipient
 Type O – Universal Donor
A B AB O
Antigen on RBC A B A,B NONE
Antibody on plasma ANTI – B ANTI – A NONE ANTI – A, ANTI - B
Compatible A, O B,O A,B,AB O
Incompatible B,AB A,AB A,B,AB
You have already finished the overview of the anatomy, physiology and functions of the hematologic syste
Care of Clients with Hematologic Disorders

1. ANEMIA
- An abnormally low
number of circulating
RBCs, low hemoglobin
concentration, or both.
- The primary problem
in anemia is decreased
availability of oxygen.
CAUSES
a. Acute or chronic blood loss
b. Inadequate dietary intake of vitamins and minerals needed for RBC
production
c. Decrease red blood cell production by the bone marrow
d. Increased destruction of red blood cell.
e. Increased demands of vitamins and minerals needed for RBC production.
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COMMON MANIFESTATIONS
a. Pallor
b. Easy fatigability
c. Weakness
d. Anorexia
e. Weight loss
f. Shortness of breath
g. Headache/Dizziness
h. Tachycardia/Palpitations
i. Syncope
j. Brittle hair and nails
k. Parethesia
l. Cold sensitivity and
Amenorrhea
LABORATORY/DIAGNOSTIC TESTS
a. CBC- done to determine

blood cell counts,
hemoglobin, hematocrit and
RBC indices.
b.Iron levels and total iron-
binding capacity- detects
IDA
c.Serum ferritin- low due to
depletion of the total iron
reserves available for
hemoglobin synthesis.
d.Sickle cell test- screening
test to evaluate hemolytic
anemia.
e.Hemoglobin electrophoresis- separates normal hemoglobin from abnormal
forms.
f. Schilling Test- measures vitamin B12 absorption before and after intrinsic
factor administration to differentiate between pernicious anemia and intestinal
malabsorption of the vitamin.
g.Bone marrow examination- done to diagnose aplastic anemia.
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TYPES OF ANEMIA
A. ANEMIA CAUSED BY BLOOD LOSS/HEMORRRHAGIC ANEMIA
1. Acute Blood Loss – associated with the decrease in circulating

RBC’s Normal Volume- 6,000 ml
Bleeding – decreased volume of blood for about 500cc
Hemorrhage – decreased volume of blood more than 500cc
Shock – 1/3 of the total volume of blood
500ml ml loss – no lasting/serious effects
1,000 ml loss – serious, acute consequences may result
Causes
 Trauma resulting to severe blood loss
 Hemorrhage disorder circumcision, dental extraction
 Spontaneous rupture of aneurysm
Early manifestations
 Weakness
 Cool moist skin
 Tachycardia
 Hypotension
 Stupor
 Irritability
Late manifestations
Decreased Hgb & Hct few hours after blood loss has occurred
Paleness
Disorientation/coma
2. Chronic Blood Loss – develops gradually, continuous loss of small amount of
blood over a long period of time.
a. Results to continuous loss of small number of erythrocyte
b. Results to continuous loss of Fe resulting to total depletion of Fe stores
Causes:
GIT or other
malignancy Bleeding
ulcers Bleeding
hemorrhoids
Menorrhagia
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Manifestations
 Decreased RBCs
 Decreased Hgb
 Decreased MCV (mean corpuscular volume)
 Fatigue
Medical Management
1. Immediate identification of the source of the loss & institute
appropriate treatment.
2. Blood transfusion as needed or as ordered by the physician.
3. Iron supplement
Nursing Intervention
1. Immediate identification of the source of the loss & institute
appropriate treatment.
2. Administer blood transfusion as ordered by the physician.
Responsibilities in Administering Blood Transfusion

a. Check that the blood has been typed and cross matched.
b. Explain the procedure/rationale for giving blood transfusion to
reassure patient and significant others and secure consent. Get
patient histories regarding previous transfusion
c. Blood must never be administered straight from the refrigerator.
d. A baseline vital signs must be determined prior to transfusion.
e. Before starting the infusion, it is advised that two nurses verify the
blood type, RH factors, patients name, blood numbers & expiration
date.
f. Do hand hygiene before and after the procedure
g. Prepare equipment needed for BT (IV injection tray, compatible
BT set, IV catheter/ needle G 19/19, plaster, torniquet, blood,
blood components to be transfused, Plain NSS 500cc, IV set,
needle gauge 18 (only if needed), IV hook, gloves, sterile 2×2
gauze.
h. If main IVF is with dextrose 5% initiate an IV line with
appropriate IV catheter with Plain NSS on another site, anchor
catheter properly and regulate IV drops.
i. Open compatible blood set aseptically and close the roller clamp.
Spike blood bag carefully; fill the drip chamber at least half full;
prime tubing and remove air bubbles (if any). Use needle g.18 or
19 for side drip (for adults) or g.22 for pedia (if blood is given to
the Y-injection port, the gauge of the needle is disregarded).
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j. Disinfect the Y-injection port of IV tubing (Plain NSS) and insert

the needle, from BT administration set and secure with adhesive
tape.
k. Close the roller clamp of IV fluid of Plain NSS and regulate to
KVO while transfusion is going on.
l. Transfuse the blood via the injection port and regulate at 10-
15gtts/min initially for the first 15 minutes of transfusion and refer
immediately to the physician for any adverse reaction.
m. Observe for signs of hemolytic reaction which usually occur the
early transfusion.
n. Observe for signs of febrile reaction.
o. Observe for allergic reaction.
 If any reaction occur:
 Stop infusion immediately.
 Notify the physician
 Maintain in patency of intravenous with normal saline.
 Send the blood to the laboratory.
 Monitor vital signs and intake and output.
p. When blood is consumed, close the roller clamp, of BT, and
disconnect from IV lines then regulate the IVF of plain NSS as
prescribed.
q. Continue to observe and monitor patient post transfusion, for
delayed reaction could still occur.
r. Re-check Hgb and Hct, bleeding time, serial platelet count within
specified hours as prescribed and/or per institution’s policy.
s. Evaluate the patient responses to the procedure.
3. Encourage to eat foods rich in iron or take iron supplements as

prescribed.
4. Promote rest
5. Prevent shock
6. Provide warmth
B. ANEMIA CAUSED BY IMPAIRED PRODUCTION OF RBC
1. APLASTIC ANEMIA
 This type of anemia is the result of depressed BM or destruction of BM
 Maybe an actual reduction in the amount of blood forming marrow or
the marrow may have functional defect
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 Typically, the marrow is replaced by fatty tissues, fibrous tissue or tumor

cells
 Usually results in a deficiency of RBC, WBC, platelets
 Maybe congenital/acquired or idiopathic
Cause of Aplastic Anemia:

a. Causes of Bone Marrow depression or destruction
1. Toxins
2. Drugs/medications
3. Industrial chemicals
4. Insecticides
5. Presence of tumor
b. Idiopathic cause – without apparent cause it accounts most with

aplastic anemia
c. Congenital – congiometic effect in Bone Marrow
Manifestations
 General symptoms of anemia (fatigue, pallor, dyspnea due to decrease
Hgb/Hct)
 Prone to infection (sore throat) associated with neutropenia; fever
headache; malaise.
 Spontaneous bleeding due to decrease platelet, may lead to hemorrhage
Laboratory and Diagnostic tests

1. Bone Marrow Examination (BM aspiration) – 1-2ml adult (posterior
iliac crest, prone position); child (tibia)
2. Blood counts
Treatment: removal of the cause

 Frequent Blood transfusion of whole blood or as prescribed.
 Antibiotics to prevent infection.
 Corticoid preparation (e.g. prednisone and androgen)
 Marrow transplant (treatment of choice) from the donor of identical
HLA (human leukocyte antigen)
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Nursing Care – Supportive care

1. Instruct patient to have frequent rest period to reduce O2 demand of tissues.
2. Patient is advised to use stool softener & increase fiber diet,
constipation thereby preventing rectal bleeding.
3. Close observation for infection, hemorrhage & correct hypoxia.
4. Precautions to prevent infection, frequent hand washing.
5. Reverse isolation technique (single room, linens/equipment are sterile,
personal mask & gown, limited visitors, plastic tent or “life island”).
6. To minimize risk of infection:
 Implement reverse/ protective isolation- provide private room,
practice strict handwashing.
 Encourage good personal hygiene.
 Monitor vital signs including temperature frequently.
 Avoid eating raw foods, do not permit fresh fruits or fresh flowers
in the client’s unit.
 Limit visitors, do not allow people with s/sy of infection to visit
the client.
 Avoid crowds.
 Minimize invasive procedures or possible trauma to skin or
mucous membranes.
7. To minimize risk of bleeding:
 Use of soft toothbrush for mouth care; electric razor for
shaving, keep nails short by filing.
 Avoid IM injections and other invasive procedures.
 Prevent constipation by use of stool softener as prescribed.
 Restrict activity based on platelet count and active bleeding.
 Monitor pad count for menstruating patient.
 Control bleeding by applying pressure to the site, using ice
packs and prescribed topical hemostatic agents.
 Advice the client to use water-soluble lubricants as needed
during sexual intercourse.
C. NUTRITIONAL DEFICIENCY ANEMIA

- Essential nutrients for RBC production may be lacking in the diet or there may
defective absorption of essential factor such as Iron, Folic acid, Vitamin B12 and
Vitamin C.
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1. IRON DEFICIENCY ANEMIA

 Caused by a deficiency in Fe, inadequate absorption or excessive loss of Fe.
 Characterized by small RBC (microcytic) and low Hgb level/content
(hypochromic)
 Slight reduction in the number of Hgb content of RBC
 Most common form of anemia.
Causes
a. Insufficient dietary intake needed for RBC production seen on
vegetarian people.
b. Chronic or acute blood loss (bleeding, blood donation, prolonged
menses).
c. Impaired intestinal absorption of iron in cases of gastrectomy
d. An increased requirement (Pregnancy, lactating, puberty, maturity)
High Risk Groups

a. Children 6-24 months
b. Premature infants
c. Adolescent girls
d. Pregnant/lactating women
Manifestations (general s/s of anemia (severe)

a. Fatigue, SOB on exertion, anorexia
b. Paleness
c. Headache, dizziness, tingling or pins & needles like feeling in the
extremities
d. Increase in PR & RR as a compensatory mechanism
Specific for Fe Deficiency Anemia

a. Soreness inflammation of the mouth & tongue
b. Plummer – Vinson Syndrome
c. Triad symptoms in severe cases of IDA (dysphagia, stomatitis,
atropic glossitis)
d. Brittle & concave fingernails (spoon shaped) – koilonychias
e. cheilosis (cracks at the side of lips)
f. tinnitus

1. Complete Blood Count ( hgb)
2. Serum iron concentration & iron binding capacity.
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Medical management
1. blood transfusion
2. iron supplement
3. oxygen therapy
Nursing Considerations
1. Promote rest to reduce oxygen demands of tissues. Best priority.
2. Take oral meds with meals to prevent GI upset (1-2 hours after meal/pc)
- It should be taken with Vitamin C because it increases iron absorption.
- Do not administer with milk or antacid because it will inhibit the
absorption.
3. Assess elimination pattern to detect changes
4. For constipation, increase fluid intake (3-4L), increase fiber, laxative as
ordered
5. For IM, do not massage the site of injection to prevent leakage of
medication into subcutaneous layer.
6. Increase intake of Vitamin C to enhance Fe absorption.
7. Inform the patient about the possible changes in the color of the stool
8. Give good oral care to prevent stomatitis.
9. Provide good skin care to prevent pressure sore, especially among
bedridden clients.
2. MEGALOBLASTIC ANEMIA
 Characterized by production and peripheral proliferation of large immature
and dysfunctional RBC.
A. Pernicious Anemia
 Also called macrocytic, hyperchromic anemia
 Vitamin B12 deficiency anemia.
 There is lack of intrinsic factor production by the parietal cells in the
stomach and this prevents the absorption of vitamin B 12 in the lower part
of the ileum, producing defective DNA synthesis and abnormal RBC
maturation.
 Decreased Vitamin B12 absorption results to the following:
 Decreased RBC production.
 Decreased DNA synthesis in maturing RBC’s; the RBCs do not
divide normally so, they grow big resulting to megaloblastic
anemia.
 Impaired integrity of cells in the GI (mouth, stomach, and anus),
vagina, and axon of neurons.
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Causes
 Dietary deficiency
 Surgical removal of the stomach
 Extensive resection of the small intestines due to intestinal disease
 Autoimmune gastric mucosal atrophy. Antibodies are produced that
can block the production of intrinsic factor. Tendency to run in the
families
Manifestations
 General signs and symptoms of anemia
 Neurological signs and symptoms due to destruction of axons of neurons.
- Tingling pins & needles
- Coldness
- Numbness (brought abt. By the disturbances of the NS functioning
- GIT changes/disturbances
- Stomatitis/beefy tongue – red inflamed tongue (characteristic
manifestation of vitamin B12 deficiency anemia)
- Anorexia
 If the deficiency is not corrected – motor disturbances
- Muscle weakness
- Ataxia (loss of coordination/balance)
- Staggering
- Paralysis
 Positive Babinski reflex – if present in adults-indicates
neurologic prob.
 Jaundice – due to faulty erythropoiesis.

1. CBC
2. Peripheral smear – RBC are oval, macrocytic & hyperchromic:
decreased hgb & hct
3. Gastric analysis – to check for the presence of hydrochloric acid;
findings will be low volume of gastric secretion, high pH & free Hcl
4. BM aspiration/analysis
5. Schilling test – to determine the absorption of B12 in the GIT, detects
the lack of intrinsic factor. The most definitive diagnostic test for
pernicious anemia.
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Preparation
- 12 hour NPO prior to the test
- Radioactive B12 is given per orem
- 24 hour urine collection
- (+) result above shows that less than the N amount of B12’s is
absorbed
- N- 10- 20% of the oral dose is excreted
Management (depends on the cause)

1. Monthly vitamin B12 injection (IM) for life. Oral Vitamin B12 cannot
be absorbed because of inadequate intrinsic factor.
2. Diet – light, easily digested food, rich in CHON, Fe and vitamins
3. BT – PRBC as needed
4. Oral care – done to reduce further stomatitis
5. Bed rest.
6. Physical Examination every 6 months for hematologic studies and GI
evaluation. The client may develop hematologic or neurologic relapse if
therapy is inadequate.
NOTE: patients with pernicious anemia have higher incidence of

gastric cancer and thyroid dysfunction; periodic stool examinations for
occult blood, gastric cytology and thyroid function test are done.
B. FOLIC ACID AND VIT. C DEFICIENCY ANEMIA

 Folic acid is another vitamin necessary for normal RBC production and
Vitamin C enhances the catalytic reaction of folic acid which promotes
erythropoiesis.
Cell characteristic
- megaloblastic cells (large and immature)
- macrolytic and normochromic
- Not stored in the body in large amounts, therefore a constant supply
is needed.
Causes
a. Malnutrition/poor diet-lack of green leafy vegetable liver.
b. Chronic alcoholism – incomplete OH partially blocks the response of
the BM and folic acid interfering erythropoiesis.
c. Impaired/inadequate absorption (disturbance in the GIT, chronic
diarrhea, parasitism).
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d. Pregnancy – most common in 3rd tri; needs 6x the N amount of folic

acid because of incomplete demand of the developing fetus.
 Folic acid deficiency among pregnant clients may cause
congenitally acquired neural tube defects (spina bifida)
e. Prolonged drug therapy (e.g Anticonvulsants; antineoplastic agents;
oral contraceptive)
Manifestations
 General symptoms of anemia
 Smooth sore tongue, cracked lips
 Diarrhea, impaired coordination, confusion
 Decreased RBC, hemoglobin, hematocrit.

a. BM exam – aspiration of BM
b. Blood serum\exam
Management
1. Well balanced Diet (lemon, melon, green leafy veg., fish, legumes,
mushroom, beans, milk, soya beans)
- Vitamin intake – vitamin C promotes erythropoiesis
2. Folic acid prep – oral or IM
3. With mal absorption syndrome – pt. needs parenteral folic acid
followed by maintenance therapy with oral doses.
D. Increased Destruction of RBC (HEMOLYTIC ANEMIA)

 Anemia caused by the premature destruction (shortened lifespan of RBC
thereby reducing number of RBC)
 There is a distortion in the shape of erythrocytes.
 RBC plasma membrane ruptures prematurely (hemolysis) there is
breakdown of RBC & releases of Hgb.
1. THALASSEMIA ANEMIA
 An inherited disorder affecting primarily Italians, Greeks, Chinese,
Southeast Asians and Black Persons.
 There is defective Hgb chain synthesis.
 It is characterized by a decreased synthesis of one of the globin chains of
Hgb (the B chain is most often affected (B-thalassemia), as a result, there
is a decreased synthesis of Hgb and an accumulation of alpha globin chain
in
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the erythrocytes. These alterations result in decreased RBC production and

chromic hemolytic anemia.
2 Types of Thalassemia
a. Thalassemia A / Thalassemia minor – is associated with a mild anemia
that is usually asymptomatic, no therapy is required.
b. Thalassemia B / Thalassemia major – is characterized by a severe
anemia. The RBCs are characteristically hypochromic (low MCH) and
macrolytic (low MCV). Therapy is Blood transfusion.
Manifestations
- Resembles with hemolytic anemia
- Jaundice, leg ulcers, splenomegaly
- Characterized by bone hypersensitivity that causes thickening of
cranium and a mongoloid appearance as a result of the expansion of BM
as a compensatory mechanism or effort to offset the anemia
- Hemosiderosis

a. Hgb electrophoresis - growth failure begins about ages 10-12 years.
Eventually cardiac failure develops and death usually occurs between ages
17-30
Collaborative Management
1. Frequent Transfusion - to alleviate severe symptoms or to maintain the Hgb
at a near N level continually to allow for a more normal lifestyle.
- Disadvantage – approach may produce Fe overload but can be
ameliorated by the use of Fe-chelating agent such as deferoxamine,
(overload-excessive amount of Fe obtained through the RBC
transfusion.
2. Iron chelation therapy with Desferal (deferoxamine).
3. Splenectomy
4. Monitor cardiovascular status.
5. Relieve bone pain.
6. Avoid contact sports to reduce risk of fracture.
7. Encourage prompt medical attention for fever or signs of infection.
8. Familiarization with transfusion therapy.
9. Sensitivity to the emotional needs of patients receiving frequent transfusion.
10. Genetic counseling is necessary before getting married.
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2. POLYCYTHEMIA/ ERYTHROCYTOSIS
- is an increase in number and
concentration of RBCs, above normal
level
TYPES: primary and secondary polycythemia

a. Primary Polycythemia or Polycythemia
Vera is a neoplasm (cancer) caused by a
genetic mutation in which bone marrow
makes too many RBCs. Also, blood
viscosity increases, affecting oxygen
transport to tissues.
Manifestations
 Ruddy complexion
 Splenomegaly
 Headache and dizziness
 Tinnitus, fatigue and paresthesia
 Blurred vison
 Increased blood viscosity: angina,
claudication, dyspnea and
thrombophlebitis
 Elevated blood pressure
 Uric acid maybe elevated resulting in
gout and renal stone formation
 Generalized pruritus
 Erythromyalgia (burning sensation in
fingers and toes)
Diagnostic Procedures
1. CBC
2. Serum erythropoietin – low level
3. Bone Marrow Aspiration - hyperplasia of all hematopoietic elements
Complications
a. Cerebrovascular Accident
b. Myocardial Infarction
c. Bleeding due to dysfunctional large amount of platelet
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Management
1. Phlebotomy – removing enough blood (initially 500 mL once or twice weekly)
to reduce blood viscosity and to deplete the patient’s iron stores.
2. Chemotherapeutic agents (eg, hydroxyurea) can be used to suppress marrow
function.
3. Anagrelide (Agrylin) – inhibits platelet aggregation.
4. Interferon alfa-2b (Intron-A) – for management of pruritus (WOF: flulike
syndrome and depression)
5. Radiation therapy
6. Antihistamine
7. Allopurinol
Nursing Management
1. Increase fluid intake to reduce blood viscosity
2. Instruct the patient to avoid sedentary behaviors, crossing of legs, wearing tight
or restrictive clothing.
3. Avoid aspirin and aspirin-containing medications.
4. Minimize alcohol intake.
5. Instruct the patient to avoid iron supplements.
6. For pruritus:
- Bathing in tepid or cool water.
- Avoiding vigorous toweling off after bathing.
- Use of cocoa butter or oat meal-based lotions and bath products.
- Dissolved baking soda in bath water
b. Secondary Polycythemia is usually associated with increased erythropoietin

production in response to low blood oxygen level.
- This is the most common form of polycythemia
MANIFESTATIONS: same as primary polycythemia EXCEPT SPLENOMEGALY
LABORATORY/DIAGNOSTIC TEST/S
a. Serum erythropoietin - high level
b. Bone marrow studies - shows only red stem cell hyperplasia
MANAGEMENT: Requires treatment of the underlying cause
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3. Hemophilia
 Inherited bleeding disorder
 Hemophilia A – caused by genetic disease that results in deficient or defective factor
VIII.
 Hemophilia B (Christmas disease) – genetic defect that causes deficient or
defective factor IX.
 Both types of hemophilia are inherited as X-linked traits, so almost all affected
people are males; females can be carriers.
 Recognized in early childhood, usually in the toddler age group.
Manifestations
a. Hemorrhages into various parts of the body
b. Hemarthroses and hematomas
c. 75% of all bleeding occurs into joints
d. Chronic pain or ankylosis (fixation) of the joint occurs
e. Spontaneous hematuria and GI bleeding
f. Intracranial or extracranial bleeding – most dangerous
Management
a. Administration of factor VIII and factor IX concentrates.
b. Infusion of fresh frozen plasma.
c. Plasmapheresis or concurrent immunosuppressive therapy.
d. Aminocaproic acid inhibits fibrinolysis and therefore stabilizes the clot.
e. Desmopressin (DDAVP) – induces a significant but transient rise in factor VII
levels.
Nursing Management
1. Assist the child in coping with the condition.
2. Encouraged to be self-sufficient and to maintain independence by preventing
unnecessary trauma that can cause acute bleeding episodes.
3. Instruct the patient to avoid OTC medications such as aspirin, NSAIDs, herbs,
nutritional supplements and alcohol.
4. Nasal packing should be avoided, because bleeding frequently resumes when
the packing is removed.
5. All injections should be avoided.
6. Splints and other orthopedic devices may be useful in patients with joint or
muscle hemorrhages.
7. Warm baths promote relaxation, improve mobility, episodes.
8. Provide genetic testing and counselling to female carriers.
Page 23 of
Laoag City, Ilocos
In this portion you will answering case study related to our previous discussion. Ans
Activity 1 Case Study

SITUATION: Jerry has been admitted to the hospital with a diagnosis of pernicious anemia
and has a hemoglobin of 8 g/dL. He has been type and cross matched for two units of packed
RBCs and is to receive his first unit.
1. The nurse is performing a pre transfusion history. What information should be

obtained prior to the transfusion? Support your answer in not more than 100 words.
2. The nurse begins the transfusion of packed cells after obtaining vital signs. Fifteen
minutes after the infusion begins, Jerry informs the nurse that he is itching all over. How
does the nurse respond? Support your answer in not more than 100 words.
Page 24 of
Laoag City, Ilocos
This part can be in the form of a QUIZ/ EXAMS or a

Thank You!
Congratulations for completing this module. I hope you study a lot and help you in achieving your d
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Laoag City, Ilocos Norte

HEMATOLOGIC DISORDERS MODULE

WILJOHN M. DE LA CRUZ, M.A.N.

Activity 1 Diagram (Hematologic Components)

Activity 1 Exploring your Understanding

STRUCTURES OF HEMATOLOGIC SYSTEM

1. BONE MARROW - the site of the blood cell formation (hematopoiesis)

2. BLOOD – red, fluid connective

General Functions of Blood

Formed Elements/Blood cells

Eosinophil Involved in allergic reactions (neutralizes histamine),

Monocyte Enters tissue as macrophage; highly phagocytic, especially

T lymphocyte Responsible for cell- mediated immunity

Formation of Blood Cells

Hemopoeitic Growth Factors

Pathological conditions of the Blood Cells

Blood Clotting Factors

Care of Clients with Hematologic Disorders

a. CBC- done to determine

A. ANEMIA CAUSED BY BLOOD LOSS/HEMORRRHAGIC ANEMIA

1. Acute Blood Loss – associated with the decrease in circulating

Responsibilities in Administering Blood Transfusion

j. Disinfect the Y-injection port of IV tubing (Plain NSS) and insert

3. Encourage to eat foods rich in iron or take iron supplements as

B. ANEMIA CAUSED BY IMPAIRED PRODUCTION OF RBC

 Typically, the marrow is replaced by fatty tissues, fibrous tissue or tumor

Cause of Aplastic Anemia:

b. Idiopathic cause – without apparent cause it accounts most with

Laboratory and Diagnostic tests

Treatment: removal of the cause

Nursing Care – Supportive care

C. NUTRITIONAL DEFICIENCY ANEMIA

1. IRON DEFICIENCY ANEMIA

High Risk Groups

Manifestations (general s/s of anemia (severe)

Specific for Fe Deficiency Anemia

Laboratory and Diagnostic tests

Laboratory and Diagnostic tests

Management (depends on the cause)

NOTE: patients with pernicious anemia have higher incidence of

B. FOLIC ACID AND VIT. C DEFICIENCY ANEMIA

d. Pregnancy – most common in 3rd tri; needs 6x the N amount of folic

Laboratory and Diagnostic tests

D. Increased Destruction of RBC (HEMOLYTIC ANEMIA)

the erythrocytes. These alterations result in decreased RBC production and

Laboratory and Diagnostic tests

TYPES: primary and secondary polycythemia

b. Secondary Polycythemia is usually associated with increased erythropoietin

MANIFESTATIONS: same as primary polycythemia EXCEPT SPLENOMEGALY

MANAGEMENT: Requires treatment of the underlying cause

Activity 1 Case Study

1. The nurse is performing a pre transfusion history. What information should be

This part can be in the form of a QUIZ/ EXAMS or a

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