hematology/anemias/RBC
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| Hematocrit lab value - normal | 40-50 percent
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| hemoglobin normal lab value | 13.5 - 18.0
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| RBC count normal | 4.2 - 6.0 times 10 to the 6th/mcL
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| WBC count normal | 5.0 - 10.0 times 10 to the 3rd/mcL
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| if WBC count < 1000 | indicates risk of infection
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| if WBC count < 500 | indicates risk of life-threatening infection
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| normal platelet count | 140,000 - 340,000 per mm cubed
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| platelet count < 100,000 | indicates thrombocytopenia
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| platelet count <50,000 | indicates risk of increased beeding from minor trauma
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| platelet count > 400,000 | indicates thrombocytosis
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| platelet count > 1 million | indicates thrombosis
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| What is the most abundant granulocyte | neutrophils
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| normal neutrophil lab value | 2,500 - 7,500
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| neutrophil shift to left | immature neutrophils being released by bone marrow - demand exceeds supply
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| neutrophil shift to right | indicates inflammation or infection has subsided and supply now meeting lowered demands
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| neutrophils <100 indicates | serious condition such as granulocytopenia, agranulocytosis or can be found in some chemo therapy
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| main causes of anemia | impaired RBC production, bone loss, increased RBC destruction, any combination thereofe
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| In general, how will body compensate for anemia | these sysetmes compensate: CV, resp, hematological
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| what happens with fluid compartments in anemia | fluid moves from interstitum to vascular space --> diluted blood moves faster, more turbulently
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| if blood is 'thinned' by anemia (fluid into intravasculature), what manifestions might we see? | ventricular dysfunction, cardiac dilation, valve insufficiency
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| what is the impact of anemia with respect to hypoxia manifestations | hypoxia --> increased respirations/increased CO, may lead to RAA activation, may lead to CHF as heart over worked to meet oxygen demands
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| if anemia is due to Vit B12 deficiency, what other types of manifestions might we see | neurological symptoms
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| name two types of macrocytic normochromic anemias | pernicious anemia, folate-deficient anemia
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| what causes pernicious anemia | defective intrinsic factor-->cant absorb Vit B12, which is needed for nuclear maturity/DNA synth --> delayed divsion/large cells
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| what causes the defective intrinsic factor in macrocytic normochromic pernicious anemia | congenital IF defect, adult onset gastric mucousal atrophy, H. pylori, gastritis, gastrectomies
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| how do we treat pernicious anemia | tx with Vit B12
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| what is MOA of folate-deficiency macrocytic normochromic anemia | insufficient folate --> impaired RNA synth-->decreased RBC production, maturation
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| what causes the folate deficiency state in this anemia | improper diet - alcoholics, malnourished
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| how do we treat folate-deficient anemia | admin folate replacements
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| name 3 microcytic hypochromic anemias | iron-deficiency, sideroblastic, thalassemia
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| Class of iron-deficiency anemia | microcytic hypochromic
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| class of sideroblastic anemia | microcytic hypochromic
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| class of thalassemia | microcytic hypochromic
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| iron-deficiency anemia causes | men: GI bleed women: profuse menstruation both: meds --> insufficient Fe absorbtion, pica
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| tx of iron-deficient anemia | eliminate blood loss, iron replacement
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| causes of sideroblastic anemia | mitochondrial congenital Fe metabolism, drug/toxin effects
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| tx of sideroblastic anemia | admin Vit B6
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| cause of thalassemia anemia | congenital defect in globin synthesis
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| name 5 types of normocytic-normochromic anemias | aplastic, post-hemorrhagic, hemolytic, sickle cell, anemia of chronic inflammation
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| what class is anemia of chronic inflammation | normocytic-normochromic
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| what class is sickle cell anemia | normoctyic-normochromic
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| what class is hemolytic anemia | normoctyic-normochromic
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| what class is post-hemorrhagic anemai | normoctyic-normochromic
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| what class is aplastic anemia | normoctyic-normochromic
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| what are 2 types of polycythemia | absolute (overproduction of RBCs) or relative (decrease of plasma volume)
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| what is primary polycythemia | due to factors intrinsic to red cell precursors
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| name a type of primary polycythemia | polycythemia vera, a myeloproliferative disease
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| what is MOA of polycythemia vera | it is a myeloproliferative disease where the pluripotent stem cell overproduces RBCs. may also overproduce WBCs and platelets
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| what is the definition of a secondary polycythemia | caused by either natural or artificial increased production of EPA
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| what is MOA of secondary polycythemia | physiological response to hypoxic conditions, such as high altitude, CHF, COPD where body compensates by increasing EPO
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| how does secondary polycythemia manifest clinically | redness, enlarged spleen/liver, angina, thrombotic dx, cerebral insufficiency
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| what is a complication of secondary polycythemia | bleeding may develop because clotting factors have been consumed
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| what are the symptoms of secondary polycythemia | HA, visual disturbances, Dizz/weak, HTN, weakness
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| how do we tx secondary polycythemia | phlebotomy, stop smoking, tx CHF/COPD
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