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M6 13-005

Exam 14: Anemia

Anemia: Definition a disorder characterized by red blood cells, and hemoglobin and hematocrit levels below normal range. Insufficient amounts of oxygen are delivered to tissues and cells.
Anemia: Causes (Many Factors) (a) Loss of red blood cells in hemorrhage. (b) ↑ destruction of red blood cells (hemolysis). (c) Impaired production of red blood cells (i.e. bone marrow depression). (d) Nutritional deficiencies (long-term iron deficiency).
Anemia: Pathophysiolgy Fun Fact (e) Loss of oxygen carrying element in the blood results in supply/demand imbalance in vital organs. Peripheral circulation compensates by shunting blood to vital organs thus causing a hypoxia in other areas of the body.
Anemia: Clinical Manifestations Anorexia. Cardiac dilation. Disorientation. Dizziness. Dyspepsia Dyspnea (exertional or at rest) Headache. Fatigue. Insomnia. Pallor (mucus membranes and skin). Shortness of breath. Tachycardia. Systolic murmur Vertigo.
Anemia: CBC Results Decreased RBCs, Hemoglobin and Hematocrit.
Anemia: Serum Ion Decreased serum iron, total binding capacity, and serum ferritin levels.
Anemia: Reticulocyte Count Increased reticulocyte count due to immature RBCs.
Anemia: Bone Marrow Biopsy May show abnormailities
Anemia: Peripheral Blood Smears enable id of abnormalities of shape/color of cells.
Anemia: Vitamin B12 Levels Decreased.
Anemia: Blood Loss Blood transfusions are appropriate for blood loss as is replacement for iron and vitamin B12 deficiency if these are deficient.
Hypovolemic Anemia (Blood Loss Anemia): Definition RBC and other component deficiencies caused by abnormally low circulating blood volume resulting from hemorrhage.
Blood loss of 1000 ml or more in adult can be Severe
Blood loss <500ml can be tolerated
Hypovolemic Anemia (Blood Loss Anemia): Clinical Manifestations Restlessness. Subtle rise in RR. Shock d/t ↓ of O2, vasoconstriction. ↓ blood vlume leading to tachycardia & hypotension. Internal hemorrhage. ↓ RBC, H&H.
Hypovolemic Anemia (Blood Loss Anemia): Subjective data Thirst. Weakness, irritability & restlessness.
Hypovolemic Anemia (Blood Loss Anemia): Objective data Hypotension. Rapid, weak, thready pulse. ↑ RR. Cool clammy skin w/ pallor. Oliguria. Mental disorientation and physical collapse with prostration can occur.
Hypovolemic Anemia (Blood Loss Anemia): Dx Testing Loss of RBCs is not reflected in lab data, and values may seem normal or high for 2 to 3 days. Once plasma is replaced, RBC mass is less concentrated. RBC, Hemoglobin, and hematocrit levels are severely decreased, often to half the normal values.
Hypovolemic Anemia (Blood Loss Anemia): Medical Management Control Hemorrhage. Fluid Replacement. Provide O2.
Pernicious Anemia: Definition absence of a glycoprotein intrinsic factor secreted by the gastric mucosa. Autoimmune disease in which antibodies in the parietal walls of the stomach prevent the production of intrinsic factor.
Pernicious Anemia: Fun Fact Intrinsic factor is essential for absorption of Vitamin B12 (cyanocobalamin).
Vitamin B12 is needed for. Growth and maturation of all body cells, including RBCs in the marrow. Vitamin is related to nerve myelination; its absence leads to progressive demyelination and degeneration of nerves and white matter.
Pernicious Anemia: Clinical Manifestations Fever. Extreme weakness. Dyspnea. Hypoxia. As condition progresses, weight loss is apparent, as is slight icterus (jaundiced) with pallor due to increased destruction of RBCs. Edema of legs. Intermittent constipation and diarrhea.
Pernicious Anemia: Subjective Data Palpitations. Nausea, flatulence, and indigestion. Weakness and difficulty swallowing (dysphagia) may occur. Neurologic symptoms include tingling of hands and feet and loss of sense of body position (impaired proprioception).
Pernicious Anemia: Objective Data Observation of smooth and erythematous tongue. Cerebral signs include: mental disorientation, mental issues. Severe neurological impairments can result including partial or total paralysis due to destruction of the nerve fibers of the spinal cord.
Pernicious Anemia: Schilling Test shows malabsorption of B12.
Pernicious Anemia: Bone Marrow Aspiration abnormal RBC development
Pernicious Anemia: Gastric analysis determine cause of B12 deficiency
Pernicious Anemia: Peripheral Smear shows abnormally large erythrocytes (macrocytic) with an abnormal shape.
Pernicious Anemia: Medical Management Drug Therapy. Blood Transfusion (If anemia is severe). CBC Monitoring q 3-6 months to monitor Tx effectiveness.
Pernicious Anemia: Drug Therapy Vitamin B12 replacement therapy or individual will die in 1 to 3 yrs Injections B12 are given daily for two weeks, weekly until hematocrit is normal and then monthly for life. Folic acid and iron supplements Cyanocobalamin injections.
Apalasia failure of the normal process of cell generation and development.
Aplastic Anemia: Classifications Congenital Origin. Acquired aplastic anemia. Mostly Idopathic.
Aplastic Anemia: Congenital caused by chromosomal alterations. 30% of cases that appear in childhood are inherited
Aplastic Anemia: Acquired directly related to exposure to viral invasion, medications, chemicals, radiation, or chemotherapy in which the hematopoietic tissue is replaced by fatty marrow causing a defect in RBC production.
Depression of erythrocyte production results in: low hemoglobin and RBCs. Leukopenia and thrombocytopenia may develop.
pancytopenic low RBCs, platelets and WBCs
Aplastic Anemia: Clinical manifestation Repeated infection with high fever. Weakness, fatigue, general malaise. Dyspnea, palpitations. High mortality rate from complications of infections and hemorrhage. Bleeding tendencies (petechiae, ecchymoses, GI/GU bleeding).
Aplastic Anemia: Subjective Data 1) History of exposure to chemicals. 2) Level of fatigue experienced while completing ADLs.
Aplastic Anemia: Objective Data 1) Pallor. 2) Signs of infection. 3) Bleeding tendencies. 4) Dyspnea. 5) Tachycardia.
Aplastic Anemia: Dx Tests Bone marrow biopsy. Peripheral blood smears.
Aplastic Anemia: Bone Marrow Bx 1) Shows hypoplastic or aplastic fatty deposits. 2) Decrease in cellular elements with increased yellow marrow (fat content). 3) Depressed hematopoietic activity.
Aplastic Anemia: Peripheral blood smears show that blood cells may be normocytic and normochromic.
Aplastic Anemia: Medical Management Identify cause and remove. Blood transfusions are avoided, if possible. Splenectomy may be required if that is the cause of thrombocytopenia. Drug therapy. Bone marrow transplant.
Aplastic Anemia: Blood transfusions are avoided, if possible because 1) Prevention of iron overloading. 2) Prevention of antibody development to tissue antigens. Necessary for the potential bone marrow transplant candidate. 3) Platelet transfusions for the thrombocytopenic patient should be HLA typed.
Aplastic Anemia: Drug therapy (Steroids) Steroids and androgens to stimulate bone marrow.
Aplastic Anemia: Drug therapy (Immunosupressive Therapy) antithymocyte globulin and cyclosporine has become important for patient who are not candidates for bone marrow transplant or hematopoietic stem cell transplant.
Aplastic Anemia: Granulocytic-macrophage colony-stimulating factor (GM-CSF) Used to control the cause of aplastic anemia.
Iron Deficiency Anemia RBCs contain decreased levels of hemoglobin.
Iron Deficiency Anemia: Causes Excessive Iron loss. Chronic intestinal or uterine bleeding bu can be caused by other things. Blood loss related to menstration or pregnancy. Body's iron demand exceeds absorption. Malabsorption d/t celiac disease & sprue. Subtotal gastrectomy. Poor
Chronic intestinal or uterine bleeding but can also be caused from: a) Gastric or duodenal ulcers. b) Esophageal varices, hiatal hernia. c) Colonic diverticula. d) Tumors
Iron Deficiency Anemia: Clinical Manifestations (a) Pallor - most common finding. (b) Glossitis (inflammation and soreness of the tongue). (c) Fatigue, weakness, shortness of breath. (d) Signs and symptoms typical of angina and heart failure may also occur.
Iron Deficiency Anemia: Subjective data 1) GI symptoms: Glossitis (inflammation of the tongue) and pagophagia (desire to eat ice, clays, or starches). 2) Headache, paresthesias, burning sensation of tongue (all due to iron depletion in tissues).
Iron Deficiency Anemia: Objective Data 1) Pallor. 2) Tachycardia. 3) Finger nails may be fragile and shaped like the head of a spoon with a central depression and raised borders. 4) Stomatitis (inflamed mucous membranes of the mouth). 5) Lips are erythemic with cracking at the angl
Iron Deficiency Anemia: CBC results decreased RBC, hemoglobin and hematocrit.
Iron Deficiency Anemia: Serum Iron Levels Decreased
Iron Deficiency Anemia: Medical Management Drug Therapy. Diet.
Iron Deficiency Anemia: Ferrous Sulfate a) Administered orally or by injection. b) If patient unable to tolerate oral iron, parenteral iron can be given using z-tract method for IM injections.
Food sources rich in iron fish, meat, poultry, eggs, green leafy vegetable, whole grains and dry beans.
Sickle Cell Anemia: severe, chronic and incurable condition that occurs in people homozygous (having two identical genes inherited from each parent for a given hereditary characteristic) for Hg-S.
sickle cell abnormal, crescent-shape RBC containing hemoglobin S (Hg-S) - a defective hemoglobin molecule. Normal hemoglobin is hemoglobin A (Hg-A).
Sickle Trait heterozygous (having two different genes) form of sickle cell anemia whereby the individual has both Hg-S and Hg-A. Those with the trait do not have signs or symptoms, but risk passing the disorder on to their children.
Sickle Cell crisis An episode of acute "sickling" of erythrocytes which causes occlusion and ischemia in distal blood vessels. Sickling leads to clumping, or aggregation of these misshapen RBCs, which lodge in small vessels. Causes tissue hypoxia and ischemia.
Sickle Cell Anemia: Precipitated by 1) Dehydration. 2) Infection. 3) Overexertion. 4) Weather changes (cold). 5) Ingestion of alcohol. 6) Smoking. 7) Emotional stress.
Sickle Cell Anemia: Clinical Manifestations Anemic Pt asymptomatic except during painful episodes.Infections are a major complication resulting in loss of appetite and irritability. (g) Multisystem failure, infarctions, hemorrhage and retinal damage causing blindness.
Sickle Cell Anemia: Subjective data 1) Assess patient’s knowledge and feelings about disease process. 2) Known precipitating factors. 3) Fatigue when anemia is severe. 4) Pain description; location, intensity, character, duration.
Sickle Cell Anemia: Objective Data Abdominal enlargement and jaundice. 2) Edema of extremities. 3) Signs of hemorrhage. 4) Accelerated RBCs breakdown with jaundice and elevated serum bilirubin levels.
Sickle Cell Anemia: Hemoglobin electrophoresis Shows more than 80% of hemoglobin is Hg-S.
Sickle Cell Anemia: Stained blood smear shows only anemia.
Sickle Cell Anemia: CBC decreased hematocrit and hemoglobin.
Sickle Cell Anemia: WBCs increased with infection
Sickle Cell Anemia: Medical Management No specific treatment. Supportive Care. O2. Fluids. Analgesics. Daily folic Acid. Hydroxyurea therapy. Rest. Blood Transfusions. Vaccination (regular).
Hydroxyurea therapy significantly boosts the production of Hg-F, reduces hemolysis, increases hemoglobin concentrations and decreases sickled cells.
Hematopoietic stem cell transplantation (HSCT) is the only therapy that can cure selected patients with sickle cell anemia. Use is limited because of scarcity of appropriate donors, selection of appropriate recipients, and the risks as well as cost effectiveness.
Sickle Cell Anemia; Nursing interventions Pain control... Stomp Stomp Stomp!!!
Polycythemia Vera (Primary) Myeloproliferative disorder with hyperplasia of bone marrow causing increased circulating erythrocytes, granulocytes and platelets. 3) Associated elevated WBC with basophilia (increased concentration of basophils).
Secondary polycythemia Caused by hypoxia rather than a defect in the evolution of the RBC. Hypoxia stimulates erythropoietin in the kidneys which stimulates erythrocyte production. May result from high altitude, pulmonary disease, cardiovascular disease, or tissue hypoxia.
Polycythemia vera: Clinical manifestations ↑ blood volume and viscosity, which can result in HTN, angina pectoris, heart failure and thrombophlebitis. Venous distention and platelet dysfunction cause esophageal varices, epistaxis, GI bleeding, and petechiae.
Polycythemia vera: Subjective Data Sensitivity to hot and cold. Pruritus. Headaches, vertigo, tinnitus and blurred vision. Painful burning of the hands and feet.
Polycythemia vera: Objective data Eczema and dermatological changes, including erythema. Hypertension with left ventricular hypertrophy and angina (due to hypervolemia and hyperviscosity).
Polycythemia vera: Plasma & RBC Volume is increased.
Polycythemia vera: Elevations are seen hematocrit and hemoglobin levels, reticulocytes and erythrocyte counts, platelets and WBCs with basophilia.
Polycythemia vera: ____ alkaline phosphatase, uric acid, and histamine levels are noted Elevated.
Polycythemia vera: Bone Marrow Examination shows hypercellularity of RBCs, WBCs, and platelets.
Polycythemia vera: (e) BMR (Basic Metabolic Rate) increased without thyroid function alteration.
Polycythemia vera: Fun Fact (f) Splenomegaly is found in 90% of patients with primary polycythemia but does not accompany secondary polycythemia.
Polycythemia vera: Medical Management Directed at decreasing blood volume and viscosity and bone marrow activity. -Repeated phlebotomy to maintain Hct between 45 & 48%. -Drugs
Polycythemia vera: Drugs Myelosuppressive agents: busulfan, hydroxyurea, melphalan. Radioactive phosphorous.
Nursing Interventions (Secondary Polycythemia) 1) Maintain adequate oxygenation to prevent secondary polycythemia. 2) Control pulmonary disease and avoid high altitudes.
Nursing Interventions (Polycythemia Vera) Monitor Fluid balance.
Jehovah's Witnesses opposed to homologous blood transfusions (blood obtained through a blood bank via donations).
Created by: jtzuetrong