lecture 13 shen
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3 basic mechanisms causing anemia | 1) bleeding // 2) decreased RBC production (hypoproliferation of marrow) // 3)premature red cell destruction (hemolysis)
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sideroblast | nucleated RBC containing granules of Fe in its cytoplasm
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sx of anemia | pallor, fatigue/weakness, palpitations/CP, SOB/DOE, dizziness, H/A
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(ab)nl values of MCV | normocytic = 80-100 fL // macrocytic = > 100 fL // microcytic = < 80 fL
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With chronic blood loss, RBCs are produced normally until all iron stores have been depleted, after which they become progressively more microcytic and hypochromic, and the reticulocyte response abates. |
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schistocytes | RBC fragments, "tear drops," spur cells, etc
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Howell-Jolly bodies | nuclear fragments that weren't extruded and persist in RBCs peripherally
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Heinz bodies | oxidized Hgb that precipitates out in RBCs
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Pappenheimer bodies | iron granules within RBCs that imply the cells have taken up excess amts of Fe
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thalasssemias usually display very low MCVs as well as target cells |
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serum ferritin usually reflects what? | whole body iron stores with high fidelity, hardly ever falsely low EXCEPT in acute inflammation or in some malignant conditions or liver dz
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ferroportin | the only cellular Fe exporter in vertebrates; present in macrophages, duodenum, hepatocytes and placenta
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hepcidin | "master modulator of Fe metabolism" - modulates this by inactivating ferroportin and stopping Fe from exiting cells. levels will be LOW in Fe-deficiency anemia but HIGH in anemia of chronic dz
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what one expects to find on blood smear of pt with macrocytic anemia | macrocytic, possibly oval-shaped RBCs; hypersegmented PMNs ( > 5 lobes)
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EtOH can suppress bone marrow | as well as providing empty calories that might drive one into folate or B12 deficiency
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the commonest form of childhood leukemia and what it's characterized by on CBC with diff | ALL, acute lymphoblastic leukemia; characterized by many many blasts or immature lymphocytes with high N/C ratios, usually with suppression of other precursors like plts and RBCs
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G6PD deficiency | in 15% of AfA men, causes hemolytic anemia with characteristic bite and blister cells as well as Heinz bodies (precipitated Hgb) due to oxidative stress on cells
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substance that binds RBC breakdown products in the blood (would be low or non-existent level in pt with hemolytic anemia) | haptoglobin
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