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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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