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