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-Anemia is a blood disorder that occurs when there is not enough hemoglobin in a person's blood. Hemoglobin is a substance in the red blood cells that makes it possible for the blood to transport oxygen through the body . 9-11 g/dL Diagnosis: hemoglobin, hematocrit, reticulocyte count, RBC indices, particularly the mean corpuscular volume (MCV) and red cell distribution width (RDW) -iron studies: iron levels, total iron binding capacity , ferritin -liquid forms : taken with straw(it causes staining), rinse the mouth with water, good oral hygiene after taking medication -stool may be dark green or black -IM injection: may stain the skin so use the Z track method into the buttock. Avoid rubbing the injection site 2. Anemias in Renal Disease -patients do not become significantly anemic until the serum creatinine level exceeds 3 mg/100 ml -caused by mild shortening of erythrocyte lifespan and a deficiency of erythropoietin produced by the kidneys(for erythropoiesis) due to decrease in renal function -long term hemodialysis may cause iron deficiency since they lose blood in the dialyzer folic acid deficiency occurs since this passes into the dialyzer -recombinant erythropoietin epoetin alfa (Epogen, Procrit) HPN is the most serious SE 3. Anemia of chronic disease -RA, severe chronic infection, cancer: associated with normochromic, normocytic anemia meaning the erythrocytes are normal in color and size -treat underlying disorder 4. Aplastic anemia - decrease in or damage to marrow stem cells, damage to the microenvironment within the marrow, and replacement of the marrow with fat -unknown etiology: T cells mediate an inappropriate attack against the bone marrow bone marrow aplasia (markedly reduced hematopoiesis). Significant neutropenia and thrombocytopenia (platelet deficiency) occur -can be congenital or acquired, infections, and pregnancy, medications, chemicals, radiation damage, benzene and benzene derivatives, arsenic, pesticides Manifestations: insidious/dangerous/subtle -infection andy symptoms of anemia (fatigue, pallor, dyspnea) -purpura (bruising), retinal hemorrhages, >bone marrow biopsy*idiosyncratic reaction Management: *lymphocytes destroy the stem cells and impair production of erythrocytes, leukocytes, and platelets -bone marrow transplant (BMT) or peripheral blood stem cell transplant (PBSCT)

- marrow cannot produce adequate number of erythrocytes low reticulocyte count 1. Iron deficiency Anemia -iron is inadequate for hemoglobin synthesis -most common type of anemia in all age group and all over the world >Children, adolescents, pregnant: inadequate iron in the diet to keep up with growth >Adults: bleeding/blood loss >Men & post menopausal women: bleeding from ulcers, gastritis, IBD, gastric tumors >Premenopausal women: menorrhagia >chronic alcoholics: often have chronic blood losses from GIT iron loss anemia >iron malabsorption as seen in celiac disease or after gastrectomy Manifestations: -smooth, sore tongue, brittle and ridged nails, angular cheilosis: subside after iron replacement Diagnostics: -bone marrow aspiration: definitive method -ferritin and hemoglobin values: most reliable and most useful currently Management: ferrous sulfate/gluconate/fumarate- take iron for 612 months. Vitamin C facilitates absorption -IV or IM of dextran (test should be done parenterally first) Nursing interventions -preventive education since it is common iin menstruating and pregnant women -high iron foods: organ meats(beef or calfs liver, chicken liver, beans, leafy green vegetables, raisins, molasses + Vit. C -take supplement an hour before meal because it is best absorbed on an empty stomach (constipation, n/v, cramping) -antacids or dairy products diminish its absorption

-immunosuppressive therapy-prevent lymphocytes from destroying the stem cells. Corticosteroids are not useful- aplastic anemia patients are particularly susceptible to the development of bone complications from corticosteroids(aseptic necrosis of the head of the femur) -supportove therapy like BT of PRBCs and platelets as necessary *death is usually cause by hemorrhage or infection 5. Megaloblastic Anemia -deficiency of folic acid or vitamin B12, identical bone marrow and peripheral blood changes occur because both vitamins are essential for DNA synthesis - is an anemia (of macrocytic classification) that results from inhibition of DNA synthesis in red blood cell production -erythrocytes are abnormally large, other cells derived from the myeloid stem cells like leukocytes and platelets are also abnormal, and the precursor erythroid and myeloid cells are bizarre in appearance destroyed in the bone marrow mature cells are few in number pancytopenia -the cells released into the bloodstream are often abnormally shaped(poikilocytosis)abnormally shaped RBCs Pathophysiology Folic acid deficiency Folic acid stored as folates (small in amount-quickly depleted when folate intake is deficient, within 4 months) -deficiency occurs in people who rarely eat uncooked vegetables, with hemolytic anemias, pregnant, patients with malabsorptive disease of the small bowel such as sprue since they may not absorb folic acid normally. ROH increases folate requirement -found in green vegetables and liver Vitamin B12 deficiency Inadequate dietary intake especially in vegetarians who consume no meat or dietary products, faulty absorption of the GI tract (Crohns disease, after ileal resection or gastrectomy, absence of intrinsic factor (normally secreted by cells in the gastric mucosa binds with dietary vitamin B12 and travels with it to the ileum where it is absorbed). In elders, the wall of the stomach or gastric mucosa atrophies and fails to secrete intrinsic factor *the body has large stores of vitamin B12 so years may pass before the deficiency results in anemia. Because the body compensates so well, the anemia can be severe before the patients become symptomatic *patients with pernicious anemia have a higher incidence of gastric cancer than the general population have regular

endoscopies at regular interval for 1 to 2 years Manifestations: *neurologic manifestations of B12 deficiency do not occur with folic acid deficiency and they persist if vitamin B12 is not replaced. Typical manifestations of anemia may not be apparent instead hematologic effects on organs particularly the GI tract and the nervous system *pernicious: smooth sore red tongue, mild diarrhea, extremely pale particularly in the mucous membrane , confused, paresthesia in the extremities(numbness and tingling in the feet and lower legs) difficulty maintaining balance because of damage to the spinal cord, lose position sense or proprioception. Patients die die to heart failure secondary to anemia Assessment and diagnostics B12: Schillings test patient takes small oral dose of radioactive B12, followed in a few hours by a large non-radioactive parenteral dose of B12 ( this aids in the excretion of the radioactive dose). If the oral vitamin is absorbed, more than 8 % is excreted in the urine for 24 hours. If no radioactivity in the urine (B12 stays in the GI tract), the cause is GI malabsorption of B12 -If radioactivity is detected in the urine the cause is not ileal disease or pernicious anemia -Later the procedure is repeated. Intrinsic factor is added to the oral radioactive vitamin. If radioactivity is detected in the urine (B12 was absorbed from the GI tract in the presence of intrinsic factor), diagnosis of pernicious anemia can be made *urine collection must be complete -intinsic factor antibody test. Positive test indicates presence of antibodies that bind the vitamin B12-intirisci factor complex and prevent it from binding to the receptors in the ileum thus preventing its absorption Management: Folate: increase folic acid intake in the diet and administering 1 gram of folic acid per day. Folic acid is administered IM only to people with malabsorption problems. *alcoholic patients should continue to take folic acid vitamins as long as they continue to consume ROH B12: B12 replacement. Monthly injections of Vitamin B12- deficiency is due to defect in absorption or lack of intrinsic factor. This must be continued lifetime to prevent recurrence of pernicious anemia Biermer's anemia, Addison's anemiapernicious anemia

Nursing Management: inspect skin and mucous membranes. Check sclera under fluorescent light for jaundice. -vitiligo and premature graying of skin-perni -smooth, sore, red tongue -neurologic assessment like test of position -assess in gait and stability -eat small amounts of bland soft foods frequently due to sore tongue -explain to stop taking ROH -Health education about importance of monthly B12 injections and ongoing screening and checkups. If parenteral teach the patient how to do it 6. Myelodysplastic Syndrome (MDS) -a group of disorders of the myeloid stem cells that causes dysplasia (abnormal development) in one or more of the typical cell lines. Dysplasia of the erythrocytes: most common feature of MDS- manifested as macrocytic anemia *leukocytes (myeloid cells particularly neutrophils) can also be affected -bone marrow is hypercellular but may cells die before being released into the circulation low number of cells in the circulation & not as functional as normal (quantitative and qualitative defect) -neutrophils: diminished ability to destroy bacteria by phagocytosis -platelets: less able to aggregate & less adhesive *all these result to increased risk of infection and bleeding *some case may evolve into acute myeloid leukemia (AML) which tend to be non-responsive to therapy primary MDS- disease of the elderly secondary MDS- may occur at any age, results from prior toxic exposure to chemicals like chemotherapeutic medications (alkalyting agents). This have poorer prognosis than primary MDS CM: many are symptomatic with the disease discovered incidentally when CBC is performed -fatigue: often present -risk for infection: neutrophils dysfunction recurrent pneumonias are common -bleeding can occur platelet dysfunction *complications increase in severity of the disease Assessment and diagnostics: CBC- macrocytic anemia, leukocyte and platelet counts may be diminished Serum erythropoietin and reticulocyte count- may be low *as the disease evolves into AML, more immature blast cells are noted on CBC

Medical management: Allogeneic bone marrow transplant (BMT), chemo has been used but with disappointing effects *5-azacytadine, lenolidomide, decifibinedecreased transfusion requirements, decreased evolution towards AML and improved quality of life -transfusion of red cells: SE- iron overloadtreat with chelation therapy (iron is bound to the chelating agent and excreted in the urine, effective as a SQ infusion administered over 8 to 12 hours, most patients prefer to do this at night), platelet transfusion to prevent bleeding. *overtime, patients develop into iso-sensitization to donor platelets suboptimal increases in the platelet counts after platelet transfusion. Infections need to be managed asap -erythropoietin and granulocyte-colony stimulating factor (G- CSF) or both: growth factors- successful in increasing neutrophils and diminishing anemia in certain patients. However these are expensive and effect is lost of the medication is stopped Nursing Management: -extensive instruction about infection risk, measures to avoid it, signs and symptoms of developing infection, appropriate actions to take should symptom occur. -instruction regarding with instruction of bleeding -neutropenic precautions for hospitalized patients -chelation therapy-removes only small amount of iron motivate patients and instruct about SQ infusion technique, infusion pump maintenance, and side effect management. Local erythema at site of injection-common -they should have baseline and annual auditory and eye examinations: hearing loss and visual changes can occur with chelation treatment

-erythrocytes have shortened lifespan number in circulation is reduced decreased available oxygen hypoxia stimulates erythropoietin release from kidney bone marrow is stimulated to compensate produces new erythrocytes releases them into the circulation somewhat prematurely as reticulocytes -if red cell destruction persists, hemoglobin is broken down excessively; about 80% of heme is converted to bilirubin, conjugated in the liver, and excreted in the bile *reticulocyte count is elevated, the fraction of indirect (unconjugated) bilirubin is increased, supply of haptoglobin (a binding protein for free hemoglobin) is depleted as more hemoglobin is released. plasma

haptoglobin is low if marrow cannot compensate to replace erythrocytes (indicated by decreased reticulocyte count), anemia will progress 1. Sickle Cell Anemia -severe hemolytic anemia, results from inheritance of the sickle hemoglobin (HbS)it causes the hgb molecule to be defective. The HbS acquires a crystal like shape when exposed to low oxygen tension Its round, pliable, biconcave disk shape becomes deformed, rigid, and sickle shaped,long and rigid adhere to the endothelium of small vessels decreased blood flow ischemia *sickling crises are intermittent- RBCs can go back to normal shape with enough oxygen. Oxygen delivery is impaired by cold temperature, increased blood viscosity. *HbS gene- inherited in people of African descent *sickle cell anemia- most severe form of sickle cell disease CM: symptoms and complications result from chronic hemolysis or thrombosis. Hgb7-10 g/dL, jaundice obvious in the sclera. The bone marrow expands in childhood in a compensatory effort to offset anemia, sometimes leading to enlargement of the bones of the face and skull. Chronic anemiatachycardia, cardiac murmurs, enlarged heart (cardiomegaly), dysrhytmias and heart failure may occur *spleen, lungs, and CNS- Primary sites for thrombosis due to slower circulation. Tissues are prone to ischemic or hypoxic necrosis/tissue damage, susceptible to infection, stroke , renal failure, impotence, heart failure, pulmo hpn Sickle cell crisis: types: 1. Sickle crisis-painful, results from tissue hypoxia and necrosis due to inadequate blood flow to a specific region of tissue or organ 2. Aplastic crisis- results from infection with the human parvovirus, hgb levels fall rapidly and the marrow cannot compensate manifested by absence of reticulocytes(o g/ml) 3. Sequestration crisis- results when other organs pool the sickled cells. *spleen0 most common organ responsible for sequestration in children, most sickle cell anemia have had a plenic infarction by 10 years of age, and the spleen is then no longer functional (autosplenectomy)- primary site of sickling In adults, the common sites for sequestration are the liver, and mire seriously the lungs (2-3 g/100ml)

Acute chest syndrome- manifested by rapidly decreasing hgb level, tachycardia, fever, bilateral infiltrates seen on CXR. -common cause is infarction within pulmonary vasculature, pulmonary fat embolism- fatty acids can cause increased permeability of the pulmonary endothelium and leakage of pulmonary capillaries Pulmonary hypertension- common sequela of sickle cell. Difficult to diagnose because clinical symptoms rarely occur until damage is irreversible, changes not evident on CXR, CT demonstrates microvascular occlusion and diminished perfusion to the lungs Assessment and diagnostics: a patient with sickle cell trait usually has normal hgb level, normal hematocrit, and normal blood smear -sickle cell anemia- low hct and sickled cells on the smear. Diagnosis is confirmed by electrophoresis

-inability of the blood to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients -also referred as CHF in the past due to pulmonary peripheral congestion -myocardial disease in which there is a problem with contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) that may or may not cause pulmonary or systemic congestion 1. Dyspnea-shortness of breath (DOE) 2. Orthopnea- DOB when lying flat 3. PND- paroxysmal nocturnal dyspnea *Fluid that accumulated in the dependent extremities during the day begins to be reabsorbed into the circulating blood volume when the patient lies down. The impaired left ventricle cannot eject the increased circulating blood volume pressure in the pulmonary circulation increases fluid shift into the alveoli inability to exchange oxygen and carbon dioxide due to fluid filled alveoli insufficient O2 dyspnea 4. Cough initially dry and nonproductive and may become moist overtime (blood-tinged) 5. Adventitious breath soundcrackles(bibasilar) 6. Low oxygen saturation levels 7. S3 or ventricular gallop- large volume of fluid entering the ventricle at the beginning of diastole *inadequate tissue perfusiondominant feature of HF >oliguria- decreased urine output >nocturia- renal perfusion pressure falls release of renin aldosterone secretion increased intravascular volume. However, at sleep, the cardiac workload is decreased, improving renal perfusion, which may then lead to nocturia >altered digestion >dizziness, light headedness, confusion, restlessness, anxiety >pale/ashen, cold and clammy skinperipheral constriction of blood vessels (SNS stimulation) >tachycardia/palpitation-decrease in ejected ventricular volume causing the SNS to increase heart rate >weak and thready pulse >easy fatigability/decreased activity tolerance- may also result from increased energy expended in breathing and insomnia that result from respiratory distress, coughing, and nocturia Right sided heart failure- peripheral tissue congestion. The right side of the heart cannot eject blood and cannot accommodate all the blood that normally returns to it from the venous circulation. Increased venous pressure JVD and increased hydrostatic pressure throughout the venous system 1. Edema of the lower extremities(dependent)- worsens when the patient stands or dangles the legs

Two types of HF
-identified by assessment of left ventricular functioning usually by echocardiogram A. Systolic heart failure -more common, alteration in ventricular contraction -weakened heart muscle, severely reduced EF B. Diastolic heart failure -less common, normal EF -stiff and non compliant heart muscles making it difficult for the ventricle to fill *ejection fraction-percentage of blood volume in the ventricles at the end of diastole that is ejected during systole, a measurement of contractility, subtract the amount of blood at the end of systole from the amount at the end of diastole and calculating the percentage of blood that is ejected Normal: 55-65%

>CAD-primary cause of HF > ischemic heart disease-hypoxia & acidosis from lactic acid >cardiomyopathy- disease of the myocardium Dilated- most common, causes diffuse cellular necrosis and fibrosis decreased contractility Hypertrophic- decreased distensibility and ventricular filling (diastolic failure) Restrictive- same as hypertrophic >hypertension-increased heart workload >valvular diseases- blood has difficulty moving forward, increasing pressure within the heart and increasing cardiac workload HF >iron overload (from hemochromatosis), hypoxia, and severe anemia-require increase in CO

Clinical manifestations
Left sided heart failure -pulmonary congestion

*pitting edema- evident after retention of at least 4.5 kg/10 lb/ 4.5 L of fluid 2. Hepatomegaly (enlargement of the liver) + tenderness in the RUQvenous engorgement of the liver. May also cause pressure on the diaphragm respiratory distress 3. Ascites- may be due to progress of hepatic dysfunction increased pressure within the portal vessels force fluid into the peritoneum. -may increase pressure on the stomach and intestines GI distress 4. Anorexia- loss of appetite, nausea, abdominal pain- venous engorgement and venous stasis within the abdominal organ 5. Weakness-reduced CO, impaired circulation, inadequate removal of catabolic waste products from tissues 6. Weight gain due to fluid retention Diagnostic findings >echocardiogram- underlying cause, for EF >radionuclide ventriculography >CXR, EKG >BUN, creatinine, TSH, CBC, urinalysis > BNP (B-type natriuretic peptide)- key diagnostic indicator for HF for cardiac filling pressure >exercise test/stress test Medical management Goal: relieve symptoms, improve functional status and quality of life, extend survival by reducing etiologic factors especially those that may be reversible, reduce workload of the heart, optimize therapeutic regimen,, prevent exacerbations of HF, Medications 1. ACE inhibitors- promote vasodilation and dieresis by decreasing afterload and preload -decrease secretion of aldosterone -stimulate kidney to excrete sodium and fluid while retaining potassium -started at low dose that is increased every 2 weeks until hemodynamically stable *Monitor for hypotension, hypovolemia, hyperkalemia (discontinue if K levels remains greater than 5 mEq/L or if serum creatinine is 3 mg/dL or more), and alteration in renal function especially if receiving diuretics, dry, persistent coughmay indicate worsening of ventricular function and failure >captopril(capoten), enalapril(Vasotec) II. Angiotensin II receptor blockersblock the effect of Angiotensin 11 at the

Angiotensin 11 receptor decreased BP, decreased systemic vascular resistance, and improved CO -usually prescribed as alternative to ACE due to cough III. Hydralazine and Isosorbide dinitrate- Apresoline + Dilatrate SR, Isordil, Sorbitrate Nitrates- venous dilation reduced blood return to the heart lowers preload Hydralazine- lowers systemic vascular resistance and left ventricular afterload IV. Beta-Blockers- carvedilol( Coreg) and metoprolol (Lopressor, Toprol) reduces the adverse effects due to constant stimulation of the SNS SE: dizziness, hypotension, bradycardia, bronchiole constriction- beta-1-selective betablocker (blocks the beta adrenergic receptors in the heart)such as metoprolol is recommended. *any type of beta-blocker is contraindicated in patients with severe or uncontrolled asthma V. DiureticsA. Thiazide- inhibits sodium and chloride reabsorption in the early distal tubule, also increase K and bicarbonate excretion (Zaroxolyn) B. Loop- inhibit sodium and chloride reabsorption mainly in the ascending loop of Henle (Lasix) furosemide -both may be used in patients who are unresponsive to single diuretic with severe HF C. Potassium-sparing- inhibits sodium reabsorption in the late distal tubule and collecting duct. Monitor serum crea and potassium (Aldactone)spironolactone SE: electrolyte imbalances, hypotension, hyperuricemia (causing gout), ototoxicity VI. Digitalis-digoxin (Lanoxin)- increases the force of myocardial action and slows conduction through the AV node. It improves contractility increased LV output increased diuresis *hypokalemia increases the action of digoxin and predisposes patients to digoxin toxicity and dysrhthmia Therapeutic level: 0.5 to 2.0 ng/mL Toxicity S/S: anorexia, n/v, fatigue, depression, malaise, ECG indicatinv AV block, new onset of irregular rhythm VII. Ca Channel blocker- used in patients with diastolic dysfunction. Verapamil(Calan, Isoptil), nifedipine(Adalat, Procardia), diltiazem(Cardizem ,Tiazac), amlodipine (Norvasc)- causes vasodilation, may be used to improve symptoms expecially in patients with nonischemic cardiomyopathy VIII. IV infusions Milrinone (Primacor)- phosphodiesterase inhibitor-delays the release of calcium from

intracellular reservoirs and prevents the uptake of extracellular calcium by the cells vasodilation Dobutamine (dobutrex)- catecholamine, stimulates the beta-1-adrenergic receptors, increases cardiac contractility Nutritional therapy-low sodium (2 to 3 g per day) die, avoid excessive fluid, tell patients to check for sodium levels, avoid processed food, use alternative additives or flavorings such as lemon juice, vinegar, herbs(specify sources of sodium and quantify) * Supplemental oxygen Nursing management -administer medications & assessing response to medications -assess fluid balance, I & O -weigh patient daily at the same time on the same scale usually in the morning after urination; monitoring for a 2-3 lb gain in a day or 5-lb gain in a week -ausculate lung sounds-determine improvement or not -determine degree of JVD -identify and evaluate severity of edema -monitor PR, BP, check for postural hypotension -assess symptoms of fluid overload -promote activity tolerance- 10-15 minutes warm up plus 30 minutes exercise: increases functional capacity, decreases dyspnea. Begin with warm up. Perform in room temperature. Wait 2 hours after meal before performing activity. Stop if SOB, pain, or dizziness develops. End with cool-down activities -manage fluid volume: diuretics should be given in the morning to avoid dieresis in the evening -control anxiety through relaxation techniques