review

SAMPLE QUESTIONS

1. Left ventricular function measure could be measured by a pulmonary artery catheter (Swan Ganz). This is because
1. It provides information about pulmonary resistance
2. It controls the afterload
3. it gives accurate tissue perfussion monitoring
4. it fires impulse for the heart to contract

2. the priority management for MI is
1. morphine sulphate
2. Oxygen
3. Nitroglycerine
4. cardiac monitor

3. Which of the following is true?
1. Semi-lunar valves are close and atrio-ventricular valves are open during ventricular systole
2. The Frank-Starling Law dictates that the more afterload, the more the stroke volume
3. Oxygenated blood flows out the pulmonary arteries and aorta
4. The venous return to the heart may also be considered as the preload

4. Client post angina is about to be discharge. You know that the client needs more health teaching when he states that:
1. “ I know I should exercise more vigorously to avoid it from happening again.”
2. “ I should consult a doctor first before starting an exercise program.”
3. “ I would do less stressful activities so that I may not experience it again.”
4. “ I understand that stable angina is relieved by rest.”

5. Side effects nitroglycerine include all of the following except:
1. throbbing headache
2. bradycardia
3. hypotension
4. tachycardia

6. You take the ABG of the client 30 mins after insertion of ET to check for
1. Placement of the tube
2. Confirmation of obstruction
3. The weaning process
4. Effectiveness of ventilation

7. Lidocaine is ordered after attempting cardioversion because
1. Anesthetics sedates the client
2. Alteration of the nerve impulse
3. To minimize pain of cardioversion
4. Control the client’s restlessness during procedure

8. After giving Lidocaine the client became restless and unmanageable. This indicates
1. Severe hypoxia
2. Side effect of introducing electricity to the body
3. Recurrence of previous mental ilness
4. Lidocaine toxicity
9. you will not give atropine if
1. Increase salivation
2. Pupil > 4mm
3. HR >75bpm
4. Presence of borborygmus sounds

10. watch out for PVC because they may precede V. tach when
1. Occur for more than 4-6 times per minute
2. Occur before every after p wave
3. Shapes are identical but different to a normal QRS complex
4. Occurs without a p wave

11. pulmonary artery catheter is inflated to get
1. Pulmonary artery pressure
2. Central venous pressure
3. Cardiac output
4. Coronary angiography

12. You should prepare what at bedside after pulmonary artery catheter insertion
1. Oxygen
2. Defibrillator
3. Emergency IV line
4. Basin for emesis

13. What is the not a reliable cardiac enzyme
1. Troponin
2. myoglobin
3. lactic dehydrogenase
4. CK MB

14. V fib is managed primarily by
1. Cardiac drugs
2. Cardiopulmonary resuscitation
3. Defibrillation
4. Pacemaker

15. what would you see in ECG of client with pace maker
1. A spike is seen before the QRS complex
2. A spike is seen after the QRS complex
3. There should be no spikes on the ECG
4. The rhythm should go back to normal sinus

16. What statement made by a post pacemaker insertion client indicates need for further information
1. ‘I should notify the doctors and dentists about my pacemaker before undergoing medical procedures’
2. ‘ My batteries could last up to 10 years with change’
3. ‘ I can use televisions and microwaves without experiencing problems’
4. ‘ I should never come in contact with any electrical devices because they may conduct electricity’

17. compression-ventilation ratio of CPR
1. 15:2
2. 1:2
3. 30:2
4. 2:2

18. Right sided heart failure is marked by all except
1. Peripheral edema
2. Pulmonary edema
3. Weight gain
4. Anasarca

19. which is not part of mgt of CHF
1. Wt reduction
2. Alcohol restriction
3. Stop smoking
4. Increase fluid intake

20. IABP is indicated to clients with which of the following
1. Septic shock
2. Post MI
3. DIC
4. Endocarditis

21. before IABP insertion you should do the following except
1. Obtain baseline V/S
2. Attach client to ECG machine
3. Check for allergy to seafoods
4. Insert indwelling urinary catheter

22. after IABP insertion you do which of the following
1. Assessment of proper balloon location by auscultation
2. Obtain chest X-ray
3. Monitor radial pulse
4. Perform passive ROM to affected limb

23. post CABG client report the following conditions except
1. Temperature more than 101°F for 24 hours
2. Suture line is separating
3. Foul smelling drainage from the suture line
4. Pain in the suture line

24. discharge teaching of post CABG client is
1. Use of laxative
2. Let their children sit on their lap
3. Lift anything more than 10lbs for the first 2-3 months
4. Daily walking as exercise gradually increasing with tolerance

25. priority nursing action of post DVT client with black stools
1. Obtain history
2. Assist patient to the comfort room
3. Give supplementary oxygen
4. Notify physician because of possible emergency thoracentesis

26. Major causes of emphysema includes
1. Deficiency in alpha1- antitripsin
2. Deficiency in surfactant
3. Exposure to pollution
4. History of recurrent infection

27. orthopnic position principle is
1. The tongue do not totally block the airway and aspiration of secretions is prevented
2. Compression of the diaphragm by the abdominal organs
3. Allows the expansion of the diaphragm by pulling the abdominal organs towards gravity
4. Allows drainage of secretions after postural drainage

28. while giving supplemental O2 to COPD clients you should
1. Notify physician that this is contraindicated to pt with pulmonary insufficiency
2. Monitor pt’s condition
3. Give oxygen without humidication because pure oxygen is required
4. Advise client to avoid eating while on oxygen therapy due to risk of aspiration

29. how would you instruct your client in collecting sputum
1. ‘collect sputum after eating breakfast to not loose your appetite’
2. ‘collect sputum before going to bed so that you could rest afterwards’
3. ‘ collect sputum and put it in this container and wait until I get from you’
4. ‘collect sputum after you toothbrush and spit it in the container. Do this right after waking up’

30. physiotherapy is done by
1. moderately slap the chest wall
2. performing CPT after waking up before breakfast
3. performing CPT at least two hours after meals
4. performing CPT before meal and after meal

31. which is not a pleural effusion
1. hydrothorax
2. hemothorax
3. pneumothorax
4. empyema

32. CTT is properly placed if there is
1. Fluctuation in the water seal chamber
2. Bubbling of water upon inspiration and expiration
3. No fluctuation noted
4. Tube is attached at the 6^th or 7^th intercostals space

33. CTT client suddenly had SOB and became cyanotic, you should initially
1. Notify physician immediately
2. Check the bottles for detachment of tubes
3. Monitor the client’s RR, depth and breath sounds
4. Check the patient condition and connections

34. Your client’s chest tube was detached from his chest. As his nurse in charge for his care, what would appropriate action would you first do
1. Prevent drying of the membrane by instilling 2-3 drops on saline to his chest then cover with gauze
2. Notify physician immediately
3. Cover the wound with petroleumized gauze
4. Clamp the tube, then notify physician

35. what instruction would you give your client pre thoracenthesis
1. Hold his breath upon insertion of the needle and until the withdrawal of the needle
2. Do not deep breath or cough throughout the procedure
3. Deep breath while inserting the needle to reduce pain
4. Continuously cough after only the needle was inserted to promote drainage of secretions

36. Few hours after thoracentesis, you observed your client has become cyanotic, dyspnic and restless. What would you do first
1. Notify physician
2. Monitor patient vital signs
3. Observe for bleeding
4. Give supplemental oxygen as prescribed

37. To relieve pain and prevent hemorrhage of post tonsillectomy client, he is advise to drink or eat
1. Ice cream
2. Slurpee
3. Toasted bread
4. Hot chocolate

38. epistaxis is manage by
1. Tilt the head up and pinch the cartilage in the bridge of the nose
2. Bow forward and pinch the cartilage in the bridge of the nose
3. Placed in semi fowlers and pinch the cartilage in the bridge of the nose
4. Placed in sims position and pinch the cartilage in the bridge of the nose

39. Treatment for clients with PTB includes the following medications
1. Ethambutol and digoxin
2. Penicillin and rifanpicin
3. erythromycin and isoniazid
4. streptomycin and isoniazid

40. include in health teaching that rifampicin causes
1. All secretions may secrete rifampicin
2. Urine may turn orange
3. Breast milk may secrete the drug thus breastfeeding is contraindicated
4. Sweat may be orange tinge

41. . You know that PTB client did not understood his regimen if he stated that
1. ‘ I will no longer be contagious few days after starting my medications’
2. ‘After three months of clear cough and sputum, I can already stop taking my medications’
3. ‘I will need to take these medications everyday for half a year’
4. ‘ it is necessary not to miss my daily medication’

42. These are types of asthma except
1. status asthmaticus
2. allergic
3. intrinsic
4. mixed

43. Status asthmaticus is suspected to a pt if he is
1. Experiencing the attack for more than an hour
2. Having recurrent attack
3. Having an attack after a strong emotion
4. No longer responding to conventional therapy

44. Client with Fe supplements should say the ff except
1. ‘I should take the supplements with food’
2. ‘I should take the supplements on empty stomach’
3. ‘It is better if I take the supplements with citrus juices’
4. ‘It is normal to have black stools while on supplements’

45. how to do Homan’s sign
1. Elevate the leg, apply tourniquet then instruct client to stand before releasing the tourniquet
2. Have the client lie down then flex the neck
3. Have the client lie down then dorsiflex the foot
4. Have client lie down. Place your fingertips over area of umbilicus. Feel the pulsation.

46. Thromboangitis obliterans is also called
1. Kawasaki’s Disease
2. Buerger’s Diseases
3. Giant Cell Arteritis
4. Raynaud’s Disease

47. which is not included in health teaching with HPN clients
1. Never adjust or discontinue dosage without advice
2. Never skip dosage
3. Always report untoward effects
4. Double dose if symptoms persists

48. Nsg Mgt for anti thrombolytics stocking
1. It should be removed at least every 8 hours for 20-30 mins
2. It should never be removed until the end of therapy
3. It should be changed every 3 days
4. It should only be worn for 20 mins every 8 hours

49. care for buerger’s is all but what
1. foot care
2. elevate head of the bed 3-6 inches
3. elevate foot to prevent venous pooling
4. do not elevate affected limb

50. teach client with VV all of the ff except
1. do not cross legs while sitting
2. do not stand for a long period of time
3. elevate legs
4. massage painful legs

51. pulmonary embolism is caused by all except
1. Femur fracture
2. Pregnancy
3. Use of oral contraceptives
4. Congestive heart failure

cardiomyopathy

Cardiomyopathy

- diseases of the cardiac muscles with an idiopathic cause

Causes

- idiopathic, or primary, disease, but some are secondary to identifiable causes. Hypertrophic cardiomyopathy is almost always inherited as a non–sex-linked autosomal dominant trait.

Pathophysiology

Dilated cardiomyopathy results from extensively damaged myocardial muscle fibers. Consequently, there is reduced contractility in the left ventricle. As systolic function declines, stroke volume, ejection fraction, and cardiac output fall. As end-diastolic volumes rise, pulmonary congestion may occur. The elevated end-diastolic volume is a compensatory response to preserve stroke volume despite a reduced ejection fraction. The sympathetic nervous system is also stimulated to increase heart rate and contractility. The kidneys are stimulated to retain sodium and water to maintain cardiac output, and vasoconstriction also occurs as the renin-angiotensin system is stimulated. When these compensatory mechanisms can no longer maintain cardiac output, the heart begins to fail. Left ventricular dilation occurs as venous return and systemic vascular resistance rise. Eventually, the atria also dilate as more work is required to pump blood into the full ventricles. Cardiomegaly occurs as a consequence of dilation of the atria and ventricles. Blood pooling in the ventricles increases the risk of emboli.

Unlike dilated cardiomyopathy, which affects systolic function, hypertrophic cardiomyopathy primarily affects diastolic function. The features of hypertrophic cardiomyopathy include asymmetrical left ventricular hypertrophy; hypertrophy of the intraventricular septum; rapid, forceful contractions of the left ventricle; impaired relaxation; and obstruction to left ventricular outflow. The hypertrophied ventricle becomes stiff, noncompliant, and unable to relax during ventricular filling. Consequently, ventricular filling is reduced and left ventricular filling pressure rises, causing a rise in left atrial and pulmonary venous pressures and leading to venous congestion and dyspnea. Ventricular filling time is further reduced as a compensatory response to tachycardia. Reduced ventricular filling during diastole and obstruction to ventricular outflow lead to low cardiac output. If papillary muscles become hypertrophied and do not close completely during contraction, mitral regurgitation occurs. Moreover, intramural coronary arteries are abnormally small and may not be sufficient to supply the hypertrophied muscle with enough blood and oxygen to meet the increased needs of the hyperdynamic muscle.

Restrictive cardiomyopathy is characterized by stiffness of the ventricle caused by left ventricular hypertrophy and endocardial fibrosis and thickening, thus reducing the ability of the ventricle to relax and fill during diastole. Moreover, the rigid myocardium fails to contract completely during systole. As a result, cardiac output falls.

Signs and symptoms

Clinical manifestations of dilated cardiomyopathy may include:

Ø shortness of breath, orthopnea, dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, and a dry cough at night due to left-sided heart failure

Ø peripheral edema, hepatomegaly, jugular venous distention, and weight gain caused by right-sided heart failure

Ø peripheral cyanosis associated with a low cardiac output

Ø tachycardia as a compensatory response to low cardiac output

Ø pansystolic murmur associated with mitral and tricuspid insufficiency secondary to cardiomegaly and weak papillary muscles

Ø S3 and S4 gallop rhythms associated with heart failure

Ø irregular pulse if atrial fibrillation exists.

Clinical manifestations of hypertrophic cardiomyopathy may include:

Ø angina caused by the inability of the intramural coronary arteries to supply enough blood to meet the increased oxygen demands of the hypertrophied heart

Ø syncope resulting from arrhythmias or reduced ventricular filling leading to a reduced cardiac output

Ø dyspnea due to elevated left ventricular filling pressure

Ø fatigue associated with a reduced cardiac output

Ø systolic ejection murmur along the left sternal border and at the apex caused by mitral regurgitation

Ø peripheral pulse with a characteristic double impulse (pulsus biferiens) caused by powerful left ventricular contractions and rapid ejection of blood during systole

Ø abrupt arterial pulse secondary to vigorous left ventricular contractions

Ø irregular pulse if an enlarged atrium causes atrial fibrillation.

Clinical manifestations of restrictive cardiomyopathy may include:

Ø fatigue, dyspnea, orthopnea, chest pain, edema, liver engorgement, peripheral cyanosis, pallor, and S3 or S4 gallop rhythms due to heart failure

Ø systolic murmurs caused by mitral and tricuspid insufficiency.

Complications

Ø Possible complications of cardiomyopathy include:

Ø heart failure

Ø arrhythmias

Ø systemic or pulmonary embolization

Ø sudden death.

Diagnosis

Ø The following tests help diagnose cardiomyopathy:

Ø Echocardiography confirms dilated cardiomyopathy.

Ø Chest X-ray may reveal cardiomegaly associated with any of the cardiomyopathies.

Ø Cardiac catheterization with possible heart biopsy can be definitive with hypertrophic cardiomyopathy.

Ø Diagnosis requires elimination of other possible causes of heart failure and arrhythmias.

Treatment

Correction of dilated cardiomyopathy may involve:

Ø treatment of the underlying cause, if identifiable

Ø angiotensin-converting enzyme (ACE) inhibitors, as first-line therapy, to reduce afterload through vasodilation

Ø diuretics, taken with ACE inhibitors, to reduce fluid retention

Ø digoxin, for patients not responding to ACE inhibitor and diuretic therapy, to improve myocardial contractility

Ø hydralazine and isosorbide dinitrate, in combination, to produce vasodilation

Ø beta-adrenergic blockers for patients with New York Heart Association class II or III heart failure

Ø antiarrythmics such as amiodarone, used cautiously, to control arrhythmias

Ø cardioversion to convert atrial fibrillation to sinus rhythm

Ø pacemaker insertion to correct arrhythmias

Ø anticoagulants (controversial) to reduce the risk of emboli

Ø revascularization, such as coronary artery bypass graft surgery, if dilated cardiomyopathy is due to ischemia

Ø valvular repair or replacement, if dilated cardiomyopathy is due to valve dysfunction

Ø heart transplantation in patients refractory to medical therapy

Ø lifestyle modifications, such as smoking cessation; low-fat, low-sodium diet; physical activity; and abstinence from alcohol.

Correction of hypertrophic cardiomyopathy may involve:

Ø beta-adrenergic blockers to slow the heart rate, reduce myocardial oxygen demands, and increase ventricular filling by relaxing the obstructing muscle, thereby increasing cardiac output

Ø antiarrhythmic drugs, such as amiodarone, to reduce arrhythmias

Ø cardioversion to treat atrial fibrillation

Ø anticoagulation to reduce risk of systemic embolism with atrial fibrillation

Ø verapamil and diltiazem to reduce ventricular stiffness and elevated diastolic pressures

Ø ablation of the atrioventricular node and implantation of a dual-chamber pacemaker (controversial), in patients with obstructive hypertrophic cardiomyopathy and ventricular tachycardias, to reduce the outflow gradient by altering the pattern of ventricular contraction

Ø implantable cardioverter-defibrillator to treat ventricular arrhythmias

Ø ventricular myotomy or myectomy (resection of the hypertrophied septum) to ease outflow tract obstruction and relieve symptoms

Ø mitral valve replacement to treat mitral regurgitation

Ø cardiac transplantation for intractable symptoms.

Correction of restrictive cardiomyopathy may involve:

Ø treatment of the underlying cause, such as administering deferoxamine to bind iron in restrictive cardiomyopathy due to hemochromatosis

Ø although no therapy exists for restricted ventricular filling, digoxin, diuretics, and a restricted sodium diet may ease the symptoms of heart failure

Ø oral vasodilators may control intractable heart failure.

Nursing Intervention

Ø administer medication as ordered to promote sufficient heart function

Ø assess hemodynamic status at least every 2 hours

Ø Monitor I/O

Ø Continous cardiac monitoring

Ø Assess for side effects of medication

Ø Auscultate heart and breath sounds. HR>100, RR>20, SBP<90>

Ø Give supplemental O2

Ø Assess LOC

Ø Promote periods of rests

Ø Prepare pt if invasive procedure should be done

Sources: Brunner and Suddarth's textbook of Medical-Surgical Nursing, Frizzell- handbook of pathophysiology, Saunder's Manual of Nursing Care, Lippincott's Critical Care Challenges

Megaloblastic Anemia

Megaloblastic anemia

Causes :

•Vit B12 (cobalamine) def. including Pernicious anemia

Vit B12 def : (2-3mg/day)

Ø ↓ intake, vegetarianism

Ø ↓ absorption – IF def, gastrectomy, malabs, fish tape worm infestation

Ø ↑ requirement – pregnancy, cancer

•

•Folate (folic Acid) deficiency

Ø

Ø Folate def : (50-200mg/day)

Ø Alcohol, malabsorption, pregnancy, cancer, folate antagonists(anticonvulsants, oral contraceptives)

Unresponsive to B12 & folate therapy – methotrexate,

Pernicious Anemia

Pernicious anemia, the most common type of megaloblastic anemia, is caused by malabsorption of vitamin B12. AGE ALERT Onset typically occurs between the ages of 50 and 60 years, and incidence increases with age. It's rare in children. If not treated, pernicious anemia is fatal. Its manifestations subside with treatment, but some neurologic deficits may be permanent.

Pathophysiology

Pernicious anemia is characterized by decreased production of hydrochloric acid in the stomach, and a deficiency of intrinsic factor, which is normally secreted by the parietal cells of the gastric mucosa and is essential for vitamin B12 absorption in the ileum. The resulting vitamin B12 deficiency inhibits cell growth, particularly of RBCs, leading to production of few, deformed RBCs with poor oxygen-carrying capacity. It also causes neurologic damage by impairing myelin formation.

Causes

Possible causes of pernicious anemia include:

Ø genetic predisposition (suggested by familial incidence)

Ø immunologically related diseases, such as thyroiditis, myxedema, and Graves' disease (significantly higher incidence in these patients)

Ø partial gastrectomy (iatrogenic induction)

Ø older age (progressive loss of vitamin B12 absorption).The elderly often have a dietary deficiency of B12 in addition to or instead of poor absorption.

Sign and Symptoms

Characteristically, pernicious anemia has an insidious onset but eventually causes an unmistakable triad of symptoms:

Ø weakness due to tissue hypoxia

Ø sore tongue due to atrophy of the papillae

Ø numbness and tingling in the extremities as a result of interference with impulse transmission from demyelination.

Other common manifestations include:

Ø pale appearance of lips and gums

Ø faintly jaundiced sclera and pale to bright yellow skin due to hemolysis-induced hyperbilirubinemia

Ø high susceptibility to infection, especially of the genitourinary tract.

Ø Pernicious anemia may also have gastrointestinal, neurologic, and cardiovascular effects.

Gastrointestinal symptoms include:

Ø nausea, vomiting, anorexia, weight loss, flatulence, diarrhea, and constipation from disturbed digestion due to gastric mucosal atrophy and decreased hydrochloric acid production

Ø gingival bleeding and tongue inflammation (may hinder eating and intensify anorexia).

Neurologic symptoms include:

Ø neuritis; weakness in extremities

Ø peripheral numbness and paresthesia

Ø disturbed position sense

Ø lack of coordination; ataxia; impaired fine finger movement

Ø positive Babinski and Romberg signs

Ø light-headedness

Ø altered vision (diplopia, blurred vision), taste, and hearing (tinnitus); optic muscle atrophy

Ø loss of bowel and bladder control; and, in males, impotence, due to demyelination (initially affects peripheral nerves but gradually extends to the spinal cord) caused by vitamin B12 deficiency

Ø irritability, poor memory, headache, depression, and delirium (some symptoms are temporary, but irreversible central nervous system [CNS] changes may have occurred before treatment).

Cardiovascular symptoms include:

Ø low hemoglobin levels due to widespread destruction of RBCs caused by increasingly fragile cell membranes

Ø palpitations, wide pulse pressure, dyspnea, orthopnea, tachycardia, premature beats, and, eventually, heart failure due to compensatory increased cardiac output.

Complications

Possible complications include:

Ø hypokalemia (first week of treatment)

Ø permanent CNS symptoms (if the patient is not treated within 6 months of appearance of symptoms)

Ø gastric polyps

Ø stomach cancer.

Diagnosis

Laboratory screening must rule out other anemias with similar symptoms but different treatments, such as:

Ø folic acid deficiency anemia

Ø vitamin B12 deficiency resulting from malabsorption due to GI disorders, gastric surgery, radiation, or drug therapy.

Ø Decreased hemoglobin levels by 1 to 2 g/dl in elderly men and slightly decreased hematocrit in both men and women reflect decreased bone marrow and hematopoiesis and, in men, decreased androgen levels; they aren't an indicator of pernicious anemia.

Diagnosis of pernicious anemia is established by:

Ø positive family history

Ø hemoglobin 4 to 5 g/dl

Ø low RBC count

Ø mean corpuscular volume greater than 120 µl due to increased amounts of hemoglobin in larger-than-normal RBCs

Ø serum vitamin B12 less than than 0.1 µg/ml

Ø bone marrow aspiration showing erythroid hyperplasia (crowded red bone marrow), with increased numbers of megaloblasts but few normally developing RBCs

Ø gastric analysis showing absence of free hydrochloric acid after histamine or pentagastrin injection

Ø Schilling test for excretion of radiolabeled vitamin B12 (definitive test for pernicious anemia)

Stage I

—Oral dose – radiolabelled, 1ug

—Parenteral dose – 4mg

—24 hr urine – N >7%, ↓ PA

Stage II : repeat with IF supplements

Stage III : if I & II abnormal, repeat after course of antibiotics / antimicrobial

o Used to detect lack of intrinsic factor

o Fast client for 6-12hrs

o A radioactive Vit B12 is given by mouth and nonradioactive B12 IM to saturate tissue binding site and permit excretion of radioactive via urine

o 24-48 hr urine collection-encourage fluid intake

o If indicated, repeat after 1 week w/ intrinsic factors

Ø serologic findings including intrinsic factor antibodies and antiparietal cell antibodies.

Treatment

Treatment for pernicious anemia is:

Ø early parenteral vitamin B12 replacement (can reverse pernicious anemia, minimize complications, and possibly prevent permanent neurologic damage)

Ø concomitant iron and folic acid replacement to prevent iron deficiency anemia (rapid cell regeneration increases the patient's iron and folate requirements)

Ø after initial response, decrease vitamin B12 dosage to monthly self-administered maintenance dose (treatment must be given for life)

Ø bed rest for extreme fatigue until hemoglobin rises

Ø blood transfusions for dangerously low hemoglobin

Ø digoxin (Lanoxin), diuretic, low-sodium diet (if patient is in heart failure)

Ø antibiotics to combat infections.

Assessment for Folic Acid Deficiency:

Folic acid deficiency:

Ø Serum folic acid ↓

Ø —FIGLU in urine

Ø ↑ (intermediate product in conversion of histidine to glutamate)

Bone Marrow assessment for megaloblastic anemia :

Ø hypercellular, may completely replace the fatty marrow

Ø Megaloblasts – larger in size, open seive-like chromatin and well hemoglobinized cytoplasm

Ø Giant metamyelocytes and band forms

Ø Megakaryocytes – large and bizarre multilobate nuclei

Treatment for megaloblastic anemia

Ø Drug therapy

Ø Vit B12 injections for monthly maintenance

Ø Folic acid supplements

Ø Transfusion therapy

Nursing Intervention For Megaloblastic Anemia

Ø Provide diet high in protein, iron and vitamins

Ø Avoid seasoned or hot foods if client has mouth sores

Ø Provide mouth care w/ soft toothbrush and non irritating rinses

Ø Safety precautions

Ø Bed rest

Sources: Brunner and Suddarth's textbook of Medical-Surgical Nursing, Frizzell- handbook of pathophysiology, Saunder's Manual of Nursing Care, Lippincott's Critical Care Challenges