Week 5 HEMATOLOGIC PROBLEMS.ppt.pdf

Normal Values (Ignatavicius 5th Edition) RBC count SI units Female: 4.2 – 5.4 million/uL 4.2-5.4 x 1012 cells/L Male: 4.7 – 6.1 million/uL 4.7-6.1 x 1012cells/L Hgb Female 12-16 g/dL 120-160 g/L Male 14-18 g/dL...

Normal Values (Ignatavicius 5th Edition) RBC count SI units Female: 4.2 – 5.4 million/uL 4.2-5.4 x 1012 cells/L Male: 4.7 – 6.1 million/uL 4.7-6.1 x 1012cells/L Hgb Female 12-16 g/dL 120-160 g/L Male 14-18 g/dL 140-180 g/L Hct Female 37 – 47% 0.37 – 0.47 fraction Male 42 – 52% 0.42 – 0.52 fraction WBC count 5,000-10,000/uL 5.0-10 x 109 cells/L Platelets 150,000-400,000mm3 150-400 x 109/L Anemia Deficiency of RBCs, Hgb, Hct Hct -percentage of PRBCs/ dl of blood Anemia results from: Blood loss Inadequate or abnormal RBC production Destruction of RBCs Iron Deficiency Anemia Microcytic, Hypochromic anemia caused by: Inadequate intake of iron Decreased absorption of iron in GIT Excessive loss of iron (excessive bleeding or blood loss) Iron Deficiency Anemia Assessment Findings: Reduced energy, Cold sensitivity, Fatigue, DOE ⭣HR even at rest decreased CBC, Hgb, Hct, serum Fe Blood smear reveals microcytic & hypochromic RBCs Medical Management: Treat & eliminate the cause Correction of faulty diet, oral supplement or parenteral administration of iron is prescribed Blood Transfusion in severe cases Iron Deficiency Anemia Nursing Management: Monitor for signs and symptoms of abnormal bleeding especially from the GIT Provide for adequate rest: plan activities so as not to overtire Provide a thorough explanation of all diagnostic tests used to determine sources of possible bleeding (helps allay anxiety and ensure cooperation) Iron Deficiency Anemia Nursing Management: Administer iron preparations as ordered. Oral iron supplements for mild iron losses (FeSO4) prophylactic use:300-325mg therapeutic use- 600-1200mg daily in divided dose Take iron with or immediately after a meal to avoid GI upset Take with orange juice or vitamin C source (⭣ absorption) Use straw (elixir preparations) to prevent staining of teeth Expect iron to color stool dark green or black Causes constipation Iron Deficiency Anemia Nursing Management: Parenteral: used in clients intolerant to oral preparations, who are noncompliant with therapy, or who have severe iron deficiency anemia Use one needle to withdraw and another to administer iron preparations as tissue staining and irritation are a problem Use the Z-track injection technique to prevent leakage into tissues Iron Deficiency Anemia Nursing Management: Iron Deficiency Anemia Nursing Management: cont… Parenteral: Do not massage injection site but encourage ambulation as this will enhance absorption; advise against vigorous exercise and constricting garments Iron Deficiency Anemia Nursing Management: Provide dietary teaching regarding foods high in iron Liver especially pork & lamb Red meat, Organ meats, Kidney beans Whole-wheat breads and cereals Leafy green vegetables Carrots, Egg yolk, Raisins Encourage ingestion of roughage and increase fluid intake to prevent constipation if oral iron preparations are being taken Pernicious Anemia Caused by a deficiency of intrinsic factor (substance normally secreted by the gastric mucosa) Intrinsic Factor is necessary for absorption of Vitamin B12 Vitamin B12 is needed for the maturation of erythrocytes without Vitamin B12 precursor cells undergo improper DNA synthesis (few are released from the bone marrow) increased in size: MEGALOBASTIC or MACROCYTIC cells Paresthesia: Vitamin B12 is needed for normal nerve function Pernicious Anemia Assessment Findings: Usually seen in elderly (production of IF decreases with age & gastric mucosal atrophy) & in clients w/ history of surgical removal of stomach, bowel resection (ileum) Stomatitis, glossitis (a smooth, beefy-red tongue) Pallor, fatigue, DOE Severe cases: jaundice, irritability, confusion, Numbness & tingling in the arms & legs & difficulty with gait or balance (neurologic involvement) Pernicious Anemia Diagnostic Findings: Client’s history, Symptoms, Blood & BM studies Microscopic exam: large & immature erythrocytes Schilling test measures absorption of radioactive Vitamin B before and after parenteral administration of intrinsic factor Definitive test for pernicious anemia used to detect lack of intrinsic factor The Schilling test is performed by administering 58Co-labeled cobalamin and collecting urine for 24 h and is dependent upon normal renal and bladder function. As a consequence, cobalamin absorption may be abnormal in Pernicious anemia The Schilling test is performed to evaluate vitamin B12 absorption. B12 helps in the formation of red blood cells, the maintenance of the central nervous system, and is important for metabolism. Normally, ingested vitamin B12 combines with intrinsic factor, which is produced by cells in the stomach. Intrinsic factor is necessary for vitamin B12 to be absorbed in the small intestine. Certain diseases, such as pernicious anemia, can result when absorption of vitamin B12 is inadequate. Pernicious Anemia Medical Management: Administration of Vitamin B12 (IM) weekly & monthly for maintenance Nursing Management: Provide a Vitamin B12-rich diet Liver, Organ meats, Dried beans, Nuts, Green leafy vegetables, Citrus fruit, Brewer’s yeast Avoid highly seasoned, coarse, or very hot foods if client has stomatitis & glossitis Provide mouth care before & after meals using a soft toothbrush and nonirritating rinses Bed rest may be necessary if anemia is severe Pernicious Anemia cont… Nursing Management: Provide safety when ambulating (especially if carrying hot items, etc.) Provide client teaching and discharge planning concerning Dietary instruction Importance of lifelong Vitamin B12 therapy Rehabilitation and physical therapy for neurologic deficits, as well as instruction regarding safety Folic Acid Deficiency Anemia Folic acid Proper DNA Proper cell synthesis division Vitamin B12 helps Folic Acid to move Mature RBCs into the cell Folic acid deficiency can also cause megaloblastic anemia Manifestations are similar to those of Vitamin B12 deficiency except for the nervous system involvement (folic acid does not affect nerve function) Absence of neurologic problems in FADA Folic Acid Deficiency Anemia 3 main causes of FADA: Poor nutrition Beef liver, organ meats, eggs, green leafy vegetables, cabbage, broccoli, yeast, citrus fruits, peanut butter, oatmeal, asparagus Malabsorption Crohn’s disease Chronic alcohol abuse (malnutrition) Drugs Anticonvulsants, oral contraceptives prevent absorption & conversion of folic acid to its active form leading to folic acid deficiency & anemia Folic Acid Deficiency Anemia Assessment Findings: Severe fatigue, sore & beefy red tongue Dyspnea, nausea, anorexia, headaches, weakness, lightheadedness ⭣Hgb/Hct, ⭣serum folate Schilling test – differentiates pernicious anemia & FADA Medical management: Oral or parenteral folic acid supplements Well-balanced diet Nursing Management: Encourage to eat soft, bland & high in folic acid foods Good oral hygiene, adequate rest periods (fatigue)  Aplastic Anemia Deficiency of circulating RBCs usually accompanied by leukopenia & thrombocytopenia There is PANCYTOPENIA in aplastic anemia Causes: Failure of he BM to produce cells (pluripotent stem cell injury) Long-term exposure to toxic agents (drugs, chemical) ionizing radiation viral infection autoimmune 50% of cases UNKNOWN???  Aplastic Anemia Assessment Findings: Weakness & fatigue (typical for any type of anemia) Frequent opportunistic infections Coagulation abnormalities (unusual bleeding, petechiae & ecchymoses “bruises”) Splenomegaly accumulation of client’s blood cells destroyed by lymphocytes that failed to recognize them as normal cells CBC – macrocytic anemia, leukopenia, thrombocytopenia BM aspiration/ biopsy Aplastic Anemia Medical Management: Blood Transfusion: MAINSTAY of treatment Discontinued if client’s own marrow begins to produce blood cells Antibiotic for infection Corticosteroids (if autoimmune) Bone marrow transplantation Identification and withdrawal of offending agent or drug Aplastic Anemia Nursing Management: Administer blood transfusions as ordered Provide nursing care for client with BM transplantation Administer medications as ordered Monitor for signs of infection and provide care to minimize risk Implement special isolation procedures Encourage high-protein, high-Vitamin diet to help reduce incidence of infection Provide mouth care before and after meals. Aplastic Anemia cont… Nursing Management: Monitor for signs of bleeding and provide measures to minimize risk Use a soft toothbrush and electric razor Avoid IM injection Check for occult blood in urine and stool (Hematest) Observe for oozing from gums, petechiae, or ecchymoses. Hemolytic Anemia Anemia cause by increase destruction of RBCs Acquired Cardiopulmonary bypass surgery, arsenic or lead poisoning, malarial infection, toxins & hazardous chemicals, transfusion reactions Hereditary Hereditary spherocytosis, G6PD deficiency, sickle cell anemia, thalassemia Hemolytic Anemia Assessment Findings: Clinical manifestations vary depending on severity of anemia and the rate of onset (acute vs chronic) Dyspnea, Pallor, Fatigue, Jaundice (chronic) Chills, Fever, Irritability, Precordial pain Abdominal pain, N&V, diarrhea, melena, hematuria Splenomegaly, hepatomegaly & symptoms of cholelithiasis Hemolytic Anemia cont… Assessment Findings: Laboratory tests ⭣ Hgb/Hct ⭣ Retic count Coombs’ test (direct): positive if autoimmune features present Bilirubin (indirect): elevated unconjugated fraction Hemolytic Anemia Medical Management: Identify & eliminate the cause (if possible) Administration of corticosteroids (autoimmune) Blood transfusion Splenectomy (fails to respond to medical treatment) Nursing Management: Monitor for signs and symptoms of hypoxia including confusion, cyanosis, shortness of breath, tachycardia, and palpitations presence of jaundice may make assessment of skin color in hypoxia unreliable Hemolytic Anemia cont… Nursing Management: If jaundice and associated pruritus are present, avoid soap during bathing and use cool or tepid water Frequent turning and meticulous skin care are important as skin friability is increased Hemostasis/ Blood Clotting Blood clotting mechanism involves 3 sequential process: Platelet aggregation with formation of a platelet plug Blood clotting cascade Formation of a complete fibrin clot Calcium, Collagen  Plateletplug formation triggers the blood clotting cascade mechanism Intrinsic pathway Intrinsic factors are problems or substances directly in the blood itself that first make platelets clump & then activate the blood-clotting cascade Example: Ag-Ab reaction, circulating debris, prolonged venous stasis, bacterial toxins Extrinsic pathway Outside the blood: TRAUMA Idiopathic Thrombocytopenic Purpura/ Autoimmune Thrombocytopenic Purpura Destruction of platelets causing a slow blood clotting process Cause: autoimmune Autoantibodies directed towards own platelets Assessment Findings: Ecchymoses (Bruises), petechial rashes on the arms, legs, upper chest & neck Mucosal bleeding occurs easily Significant blood loss ⭣ anemia Intracranial bleed-induced stroke (very rare) Assess for neurologic function & mental status Idiopathic Thrombocytopenic Purpura/ Autoimmune Thrombocytopenic Purpura Diagnostic Findings: Decrease platelet count Large amount of megakaryocytes in the bone marrow Presence of antiplatelet antibodies Decrease Hgb/Hct (due to bleeding) Idiopathic Thrombocytopenic Purpura Medical Management: Treatment of underlying condition & protection from trauma-induced bleeding episodes Corticosteroids & Azathioprine (Imuran) Suppresses immune function Platelet transfusion (not performed routinely because they will be destroyed also) Maintain a safe environment & protect the client from conditions that can lead to bleeding Idiopathic Thrombocytopenic Purpura Nursing interventions Control bleeding Administer platelet transfusions as ordered. Apply pressure to bleeding sites as needed. Position bleeding part above heart level if possible. Prevent bruising. Provide support to client and be sensitive to change in body image. Idiopathic Thrombocytopenic Purpura cont… Nursing interventions Measure normal circumference of extremities for baseline. Administer medications orally, rectally, or IV, rather than IM; if administering immunizations, give subcutaneously (SC) and hold pressure on site for 5 minutes. Administer analgesics (acetaminophen) as ordered; avoid aspirin. Disseminated Intravascular Coagulation Diffuse fibrin deposition within arterioles and capillaries with widespread coagulation all over the body and subsequent depletion of clotting factors Hemorrhage (kidneys, brain, adrenals, heart, and other organs) Cause: UNKNOWN Clients are usually critically ill with an obstetric, surgical, hemolytic, or neoplastic disease May be linked with entry of thromboplastic substances into the blood Mortality rate is high, usually because underlying disease cannot be corrected Disseminated Intravascular Coagulation Disseminated Intravascular Coagulation Assessment Findings: Petechiae and ecchymoses on the skin, mucous membranes, heart, lungs, and other organs Prolonged bleeding from breaks in the skin (e.g., IV or venipuncture sites) Severe and uncontrollable hemorrhage during childbirth or surgical procedures Oliguria and acute renal failure Convulsions,coma, death Disseminated Intravascular Coagulation Laboratory findings: PT/ PTT/ Thrombin prolonged Fibrinogen level & Platelet count usually depressed Factor assays (II, V, VII) depressed Disseminated Intravascular Coagulation Medical Management: Identification and control of underlying disease is key Blood transfusions: WB, PRBC, platelets, plasma, cryoprecipitates, & volume expanders Heparin administration Somewhat CONTROVERSIAL!!! Inhibits thrombin thus preventing further clot formation, allowing coagulation factors to accumulate Disseminated Intravascular Coagulation Nursing Interventions: Monitor blood loss and attempt to quantify Observe for signs of additional bleeding or thrombus formation Monitor appropriate laboratory data Prevent further injury Avoid IM injections Apply pressure to bleeding sites Gently turn & position client frequently Provide frequent nontraumatic mouth care (soft toothbrush or gauze sponge) Provide emotional support to client and significant others Administer blood transfusions and medications as ordered.  Arteriosclerosis – Thickening or hardening of the arterial wall Atherosclerosis – A type of arteriosclerosis that involves the formation of plaque within the arterial wall Hypertension New classification(2003) “Normal adult BP”: 100mmHg Hypertension Etiology:  Hypertension Assessment: History (review client’s risk factors for hypertension) Physical assessment most clients have no symptoms; however, they may experience headaches, dizziness, fainting Check for Orthostatic hypotension (decrease in BP of 20mmHg systolic &/or 10mmHg diastolic when the client changes position from lying to sitting in 2 minutes interval) tachycardia, sweating & pallor suggest a pheochromocytoma or adrenal medulla tumor Psychosocial assessment assess for psychosocial stressors (job-related, economic & other life stressors) Hypertension Assessment: Diagnostic assessment No laboratory tests are diagnostic of essential hypertension but several laboratory tests can assess possible causes of secondary hypertension presence of CHONs, RBCs, pus, ↑BUN & CREA indicate renal disease CXR reveals cardiomegaly, ECG determines the degree of cardiac involvement Hypertension Interventions: Lifestyle modifications Sodium restriction – ↓ sodium intake from the average of 150mEq/L to 1 ounce of ethanol (2 ounces of liquor, 8 ounces of wine or 24 ounces of beer daily). Excessive alcohol intake elevates BP & can add “empty” calories Exercise – start an exercise program slowly & gradually work up to more rigorous activities Tobacco & caffeine avoidance Hypertension Interventions: Drug therapy Diuretics – DOC for hypertensive clients who have asthma, chronic airway limitation (CAL) & chronic renal disease Mc SE: hypokalemia (monitor K+ level, assess for irregular pulse & muscle weakness) Thiazide (low-ceiling) diuretics – prevent Na+ & water reabsorption in the distal tubules while promoting K+ excretion Loop (high-ceiling) diuretics – depress Na+ reabsorption in the ascending loop of henle & promote K+ excretion (ex; Lasix) K+-sparing diuretics – inhibits reabsorption of Na+ in DCT in exchange for K+, thereby retaining K+ [Spironolactone (aldactone)] Hypertension Interventions: Drug therapy Calcium channel blocking agents Lower Bp by interfering with transmembrane flux of Ca++ ion resulting to vasodilation & subsequent ↓ in BP (Verapamil, Amlodipine, Diltiazem) ACE inhibitors – inhibits conversion of angiotensin I to II, one of the most powerful vasoconstrictors in the body (Captopril, Enalapril, Lisinopril) Angiotensin II receptor blockers (Candesartan, Losartan, Telmisartan) Aldosterone receptor antagonist Beta blockers – DOC for hypertensive clients with ischemic heart disease because the heart is the most common target of end-organ damage w/ hypertension  Aneurysm A permanent localized dilation of an artery, which enlarges the artery to at least 2 times its normal diameter Types: Fusiform – diffuse dilation affecting the entire circumference of the artery Saccular – an outpouching affecting only a distinct portion of the artery Aneurysm Aneurysm tends to occur at specific anatomic sites but most commonly in the abdominal aorta Aneurysm Aneurysm Aneurysm forms when the middle layer (T. media) of the artery is weakened, producing a stretching effect in the inner layer (T. intima) and outer layers (T. adventitia) of the artery As the aneurysm grows, the risk of arterial rupture increases Aneurysm Etiology Atherosclerosis is the most common cause of all aneurysm with hypertension & cigarette smoking being contributing factors Aneurysm Assessment Findings: Most are asymptomatic until discovered by routine examination or during radiographic study performed for another reason Steady with a gnawing quality abdominal, flank, or back PAIN especially if its AAA With a rupturing AAA, signs include hypotension, diaphoresis, mental obtundation, oliguria & dysrhytmias (S/S of hypovolemic shock) Aneurysm Diagnostic Assessment X-ray reveals “eggshell” appearance in cases of AAA Aneurysm Diagnostic Assessment Standard tool: CT scan (determines the size and location)  Aneurysm Diagnostic Assessment Ultrasonography; noninvasive technique that provides accurate diagnosis, as well as information about the size & location of AAA  Aneurysm Interventions Nonsurgical management: goal is to monitor the growth of the aneurysm (frequent CT scanning) and maintenance of BP at a normal level to ↓ risk of rupture w/ hypertension; treated with anti-hypertensive agents Surgical Management Abdominal Aortic Aneurysm Resection – excision of aneurysm from the abdominal aorta to prevent or repair the rupture Goal: to secure a stable aortic integrity & tissue perfusion throughout the body Peripheral Vascular Disease Disorders that alter the natural flow of blood through the arteries & veins of the peripheral circulation most frequently affected are the lower extremities Peripheral Arterial Disease : chronic partial or total arterial occlusion resulting from systemic atherosclerosis leading to deprivation of O2 & nutrients PAD of lower extremities is also called “Lower Extremity Arterial Disease” (LEAD)  Peripheral Arterial Disease Peripheral Arterial Disease Classification: Inflow obstruction – involves the distal end of the aorta & the common, internal, external iliac arteries (located above the inguinal ligament) Outflow obstruction – involves femoral, popliteal & tibial arteries (below the superficial femoral artery) Peripheral Arterial Disease Etiology & risk factors: Atherosclerosis – most common cause Risk factor includes hypertension, hyperlipedimia, DM, CIGARETTE SMOKING, obesity & familial predisposition  Peripheral Arterial Disease Assessment: Clients initially seek treatment for a characteristic leg pain known as intermittent claudication (usually they can walk only a certain distance before a cramping, burning muscle discomfort or pain forces them to stop) presence of Rest Pain – numbness or burning sensation often describe as a feeling like a toothache, that is severe enough to awaken clients at night located in the distal portion of the extremities (heal, toes) Inflow disease – discomfort in the lower back, buttocks or thighs Outflow disease – burning or cramping in the calves, ankles, feet & toes  Peripheral Arterial Disease Assessment: Loss of hair on the lower calf, ankle & foot; dry, scaly, dusky, pale or mottled skin; thickened toenails Cold extremity & cyanotic; pallor occurs when the extremity is elevated Palpate all pulses in both legs – most sensitive & specific indicator of arterial function is the quality of the posterior tibial pulse (not palpable) Note for early signs of ulcer formation  Peripheral Arterial Disease Assessment:  Peripheral Arterial Disease Radiographic assessment: Arteriography – not commonly performed today because this procedure involves injecting contrast medium into the arterial system and can have risks which include hemorrhage, thrombosis, embolus & death Segmental Systolic BP measurements Inexpensive, noninvasive method of assessing PAD using a Doppler probe. Normally, BP readings in the thigh and calf are higher than those in the upper extremities; with the presence of arterial disease, these pressures are lower than the brachial pressure Ankle-Brachial Index – an ABI of