Hypoproliferative Anemias PDF

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clinical hematology...

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 Hypoproliferative Anemias= DECREASE PRODUCTION RBCS, NOT MAKE ENOUGH RBCS  Learning Outcomes o Design a chart which will be used in differentiating the following disorders. Include causes, clinical data and laboratory features:  Aplastic Anemia  Pure Red cell Aplasia  Anemia of chronic renal failure o ALL THREE ARE HYPO o Identify the following anemias based on etiology, clinical and laboratory features:  Aplastic Anemia  Pure red cell aplasia  Anemia of Chronic Renal Failure  HYPOPROLIFERATIVE ANEMIAS  A. DEFINITION: o Anemia related to a disturbance of stem cell proliferation or differentiation. (MAYEBE STEM CELL DAMAGE)  HYPOPROLIFERATIVE ANEMIAS  B. Aplastic Anemia: o Bone marrow is characterized by a reduction of hemopoietic activity, fatty replacement of the red marrow and pancytopenia (PAN- TOATL, LOW REC COUNT, WHITE COUNT AND PLACELET COUNT). o BONE MARROW EMPTY  Hypoproliferative Anemias  Etiology: o a. Acquired  1. RadiationWHITE OUT BONE MARROW  2. Chemicals (benzene, insecticides, arsenic)  3. Drugs (Chloroamphenicol, phyenylbutazone)  4. Infections (EBV, CMV, Hepatitis)  5. Idiopathic THEY ALL DAMAGE THE BONE MARROW  HYPOPROLIFERATIVE ANEMIAS o b. Congential (Fanconi’s Anemia).AKA THE INHRETIED FORM OF APHLASTIC ANEMIA  Patient’s have physical abnormalities such as:  1. Cutaneous hyperpigmentation- BRONZING OF SKIN  2. Skeletal disorders, poor growth  3. Renal anomalies, microcephaly, mental retardation, strabismus, dwarfism  HYPOPROLIFERATIVE ANEMIAS  2. Aplastic Anemia Clinical Features: o Weakness and Fatigue o Fever and infections o Bruising and /or bleeding

 Hypoproliferative Anemias  2. Aplastic Anemia Laboratory Features: o Peripheral Blood:  a. Pancytopenia  b. Normocytic, normochromic red cells MCV AND MCHC NORMAL  c. Decreased retic count (correct rectic count)  d. Abn. bleeding time and clot retraction. (aspirin may prevent the platelet work, bleeding time may elevated)  e. M:E ratio may be normal (both is low M, and E)

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o Aplastic Anemia Lab features cont.:  e. Relative lymphocytosis (absolute may below so not use)  f. Increased erythropoietin levels (no bone marrow but enzyme still put in o Bone Marrow:  a. Hypocellular  b. Increased iron : not make cell so iron not use  c. “Dry tap” aspiration: pull up sringe and no thing in bone marrow Hypoproliferative Anemias 3. Aplastic Anemia Therapy: o Remove cause if known o Supportive care  Transfusions with packed red cells  Steroids  Androgens- testosterone= increase rbcs production o Stem Cell Transplant : bone marrow (150cc of peripheral original, or use drug) Aplastic Anemia Prognosis: o Most patients will die if untreated (infection or bleeding out) o Transfusion therapy will give the patient a 20% chance of living two years. o 60-80% of patients who receive bone marrow transplants will have complete hematopoietic recovery. (identical twin 90% to preven Gvs H disease) o Some patients will recover spontaneously without treatment. o Intracranial hemorrhage with coma is common. (bleeding in brain – coma- death) HYPOPROLIFERATIVE ANEMIAS C. Pure Red Cell Aplasia: (ONLY RBCs) o Anemia predominantly involving erythropoiesis. WBCs and Plts are NOT involved. 1. Etiology: o a. Acquired  Drugs, Infections, Malnutrition, Thymoma o b. Congenital  Diamond-Blackfan Syndrome:  Hypoproliferative Anemias Pure Red Cell Aplasia Laboratory Features: o Dec. red count, hgb and hct

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o Dec. retic o Normocytic, normochromic red cells o Normal wbc and plt. count o Increased erythropoietin levels o Bone marrow is absent of erythroid precursors. o M:E ratio increased o Hypoproliferative Anemias o Wbcs and platelet are normal 3. Pure Red Cell Aplasia Therapy: o Acquired:  Discontinue causative agent  Treat symptoms o Congenital  Androgens- testosterone 4. Prognosis o Patient can live many years but therapy eventually kills them. HYPOPROLIFERATIVE ANEMIAS D. Anemia of Chronic Renal Disease: 1. Etiology: o Decreased lifespan of red cells due to uremic blood.(high DUN => more burr cell not live 120 days o Failure of renal endocrine function. o Blood loss during dialysis. 2. Anemia of CRD Lab Findings: o Dec. red count, hgb and hct o Dec. retic count o Normocytic, normochromic red cells o Abn. red cell morphology associated with uremia (burr cells, schistocytes). o Dec. erythropoietin levels 3. Therapy: o Vitamins o Transfusions o Splenectomy ( maybe) because the rbcs live longer o Synthetic erythropoietin- reduce rbcs o Renal transplant...