MEGALOBLASTIC ANEMIA

What is Megaloblastic Anemia ?

•In addition to the cells being large ,the inner contents of each cell are not
completely developed.

•This malformation cause the bone marrow to produce fewer cell ,and
sometimes the cells die than the 120 day life expentancy.

•Instead of being round or disc-shaped ,the red blood cells can be oval.

•Megaloblastic anemia also that a results from inhibition of DNA synthesis in

red blood cell production.

•This is often due to deficiency of vitamin B12 and folic acid.

•Megaloblastic anemia not due to hypovitamosis may be caused by

antimetabolites that poison DNA production ,such as alcohol and some
chemotherapeutic or antimicrobial drugs.

•Megaloblastic anemia is a type of anemia characterized by very large red

blood cells.
 Pathophysiology

•Megaloblastic states result from defective DNA synthesis.

•RNA synthesis continues ,resulting in a large cell with a large nucleus.

•All cell lines have dyspoiesis ,in which cytoplasmic maturity is greater
than nuclear maturity.

•This dyspoiesis produces megaloblasts in the marrow before they appear

in the peripheral blood.

•Dyspoiesis results in intramedullary cell death ,making erythropoiesis

innefecctive and causing indirect hyperbilirubinemia and hyperuricemia.

•Because dyspoiesis affects all cell lines ,retilocytopenia and during later
stages leukopenia and thrombocytopenia develop.

•Large or oval RBCs (macro-ovalocytes) enter the circulation.

 Etiology
1. Megaloblastic anemia is an anemia (of macrocytic classification) that result from
inhibition of DNA synthesis in RBC productions. This is often due to deficiency of
vitamin B12 and folic acid. Vitamin B12 deficiency will not cause the syndrome in
the presence of sufficient folate for the mechanism is loss of B12 ,dependent the
folate recycling ,followed by folate deficiency loss of nucleic acid synthesis
leading to the defect in DNA synthesis.

2. Other causes are:

• Alcohol abuse.

• Chemotherapy drugs.
•Inherited disorder.
•Myelodysplastic syndrome.
 Sign and Symptom

1) Change in skin colour. 4) Numbness

•One of the most noticeable is a gradual •Another progressive symptom of the
change in skin color. The skin will start disease is a tingling sensation in the
to become pale all over the body. hand and the feet. If the condition goes

2) Loss of appetite untreated this tingling may return to

numbness.
•Will cause a loss of appetite which
lead to weight loss. If the condition
5) Nausea

continuous ,the weight loss could After a while ,the condition will begin to
become significant. affect the digestive system and this will

3) Mouth and tongue create a persistent felling of nausea

that may be a accompanied by
•The mouth and tongue become sore.
vomiting.
The tongue also may start to smooth
and change color to bright red.
 MOUTH AND
LOSS OF APPETITE
TONGUE SORE

NUMBNESS
 Diagnostic Test
A. Complete blood count (FBC ,CBC).

B. Serum B12 level .

C. Serum folate level.

D. Serum methylmalonic acid .

E. Schilling test.
• Injection or tablet of nonradioactive vitamin B12 .
• Then urine sample are collected.

F. Bone marrow examination.

 Treatment
Specific treatment for Megaloblastic (pernicious) anemia will be
determined by your physician based on :
 Based on client age ,overall health condition and medical history extend
of the disease.
 Your tolerance for specific medication ,procedure or therapies.

 Expectation for the course of the disease.

 Your opinion or preference.

Treatment may include :

• Vitamin B12 oral supplement (for replacement and severe anemia).

• Intramuscular injection (for malabsorbtion disorder or lack of intrinsic factor).

 Nursing Care Plan
Problem Expected Planning Implementation with Evaluation
identified outcome rationale
Δnutrition •pt regain •Assess pt condition •Assess the daily weight at •Pt able to
imbalance less good appetite the same time, same scale tolerate with
than body within 24 and same pt. R :to detect any food.
requirement due hour. changes of body weight.
to loss appetite
r/t disease • diet and nutrition •Encourage pt to take small
process control. amount of food but frequent
R :to maintain metabolic rate.

•Serve food rich in folic acid

and vitamins B12 eg: eggs
,meat ,milk and poultry as a
supplement .

•Encourage home food. •To promote pt appetite.

•Monitoring i/o chart. •To evaluate intake amount of
food.

•Medication. •Administer medication

follow doctor order eg:
vitamin B complex R: to
regain pt appetite
 Nursing Care Plan
Problem Expected Planning Implementation with Evaluation
identified outcome rationale
Δdiarrhea r/t •pt stop •assess pt condition. •Assess by taking vital sign eg: •No complaint
dysfunction of diarrhea temperature and pulse. R: to of diarrhea
bowel absorption. within 4 hour. obtain baseline data so that after 4 hour.
nurses can plan further
treatment.

•Monitoring bowel •To evaluate the severity of

sound by palpate and diarrhea.
auscultate.

•Diet and nutrition •Give IV therapy to pt by

control. doctor prescription. R: to rest
the bowel and prevent
dehydration.

•Do the observation. •Observe the characteristic of

stool including the color
,odor, volume and amount. R:
to detect bacteria that causes
the disease.

•Medication. •Give antidiarrhea drug follow

doctor order eg: loperamide
@ imodium R: to treated the
diarrhea by decreasing
digestion tract peristalsis.
 Nursing Care Plan
Problem Expected Planning Implementation with Evaluation
identified outcome rationale
Δnausea r/t •Stomach •Assess pt condition. •Assess the symptom of •No complaint
stomach disturbance vomiting to. R: obtain of nausea
disturbance reduce within baseline data so that nurses after
2 hour. can plan further treatment. treatment.

•Monitoring i/o chart. •Monitor every 2 hour. R: to

evaluate output and detect
loss of fluid if pt vomit.

•Positioning. •Prop up pt to avoid choking.

•Do the observation. •Inform the physician if

nausea or vomiting persist to
treat the disease
immediately.

•Encourage CRIB • promote fully rest to reduce

weakness.
GROUP MEMBERS :

HAMAS
JULIANA
LYSA
MELISA
TINEY