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lecture 13 shen

3 basic mechanisms causing anemia 1) bleeding // 2) decreased RBC production (hypoproliferation of marrow) // 3)premature red cell destruction (hemolysis)
sideroblast nucleated RBC containing granules of Fe in its cytoplasm
sx of anemia pallor, fatigue/weakness, palpitations/CP, SOB/DOE, dizziness, H/A
(ab)nl values of MCV normocytic = 80-100 fL // macrocytic = > 100 fL // microcytic = < 80 fL
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.
schistocytes RBC fragments, "tear drops," spur cells, etc
Howell-Jolly bodies nuclear fragments that weren't extruded and persist in RBCs peripherally
Heinz bodies oxidized Hgb that precipitates out in RBCs
Pappenheimer bodies iron granules within RBCs that imply the cells have taken up excess amts of Fe
thalasssemias usually display very low MCVs as well as target cells
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
ferroportin the only cellular Fe exporter in vertebrates; present in macrophages, duodenum, hepatocytes and placenta
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
what one expects to find on blood smear of pt with macrocytic anemia macrocytic, possibly oval-shaped RBCs; hypersegmented PMNs ( > 5 lobes)
EtOH can suppress bone marrow as well as providing empty calories that might drive one into folate or B12 deficiency
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
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
substance that binds RBC breakdown products in the blood (would be low or non-existent level in pt with hemolytic anemia) haptoglobin
Created by: sirprakes