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*type of abnormal hemoglobin *Hgb binds to CO instead of O2, then it can't bind to O2 *blood is cherry red color *causes hypoxia (decreased O2 to tissues) *causes: contact with CO |
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most immature form of a cell |
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*type of abnormal hemoglobin *Hgb binds to Sulfur instead of O2, then it can't bind to O2 *blood is lavender color *IRREVERSIBLE *caused by chemicals, drugs, fungicides |
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*production of blood cells in bone marrow *occurs in long bones (femur, radius), flat bones (sternum, ribs, pelvis) |
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extramedullary hematopoiesis |
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*secondary source of production of blood cells *occurs in spleen and lymph nodes |
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process by which RBCs are produced |
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methemoglobin (hemiglobin) |
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*type of abnormal hemoglobin *Hgb is oxidized to Fe3+, then it can't bind to O2 *blood is chocolate brown color *deficient NADH methemoglobin reductase (enzyme complex that converts methemoglobin back to hemoglobin *Hgb M |
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*cell's cytoplasm and organelles grow at an equal rate *results in normally proportioned cell shape and size |
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*cell's cytoplasm and organelles grow at an unequal rate *results in abnormally proportioned cell shape and size |
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*most common form in adults *2 alpha chains & 2 beta chains *accelerated in electrophoresis |
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*not common in adults *2 alpha & 2 delta chains *doesn't move in electrophoresis |
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*fetal hemoglobin *2 alpha and 2 gamma chains *moves fast in electrophoresis |
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Hgb molecule that is bonded to O2 (carrying it to tissues) |
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Hgb molecule that is free of O2 and is carrying CO2 away from tissues |
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*growth factor that stimulates RBC production/formation *produced in kidney |
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burst forming unit --> colony forming unit --> erythropoiesis --> rubriblast
*cell needs nucleus *3-4 mitotic divisions *begins with pleuripotent stem cell |
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*earliest identifiable RBC stage *size: 18-25 microns *deep blue cytoplasm because of protein synthesis *hemoglobin synthesis BEGINS here because of presence of mitochondria and nucleus |
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*2nd stage, formed after 1st mitotic division *nucleoli gone *deep blue cytoplasm *smaller than rubriblast *chromatin begins to clump |
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*3rd stage, formed after 2nd mitotic division *last stage in which heme is formed (no more cell division) *grayish pink cytoplasm because of increased Hgb |
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*4th stage *no more cell division *nucleus leaves cell *closer in size to mature RBC |
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*light bluish /pink cytoplasm with darker blue granules *granules are fragments from RNA *can still synthesize Hgb because of remaining bits of RNA *polychromasia |
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used to describe color of RBC as a bluish hue because |
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*liquid portion of whole blood *does not include clotted cells *contains proteins and other clotting factors |
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*liquid portion of whole blood minus proteins and clotting factors |
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protein used for clotting |
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Hgb *3 = Hct in normal patients |
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*blue granules present in cells *represents RNA fragments in cell *seen in cases of lead poisoning *defective heme synthesis |
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*malarial parasite invades host cell *uses hemoglobin for nourishment *parasite grows and eventually ruptures cell, releasing toxic Hgb |
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*dark spot on mature RBC that is evidence of a nuclear remnant *seen in megaloblastic anemia and thalassemias |
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*abnormal RBC shape *more rounded shape, not biconcave disk *gives appearance of hyperchromic cell, but it is actually normochromic for that cell shape |
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*abnormal cell shape *oval shaped cell *often looks macrocytic *seen in megaloblastic anemia |
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*abnormal RBC shape *chemical changes in membrane give it more surface area *hypochromic *seen in thalassemia, liver disease |
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*abnormal RBC shape *crescent shape (fragment of hemolized RBC) *valine substitution on beta chain *cells are rigid and inflexible because Hgb crystallizes *seen in sickle cell anemia |
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*abnormal RBC shape *spiny projections on cell because of altered surface cell membrane *usually occur as isolated cells **different from crenated cells |
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*abnormal RBC shape *spiny projections *usually occurs in large groups of these cells *often caused by exposure to hypotonic solution (EDTA), causes shriveling |
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schistocyte (helmet cells) |
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*abnormal RBC shape *fragmented RBC where RBC tears but keeps in some Hgb *seen in hemolytic conditions and burns |
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*abnormal RBC shape *abnormal peptide chains like in sickle cells *different crystalline arrangement of Hgb so it takes on a different shape *often accompanied by target cells |
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*ex. hemorrhage *morphology: normochromic, normocytic *over time... reticulocytosis as compensation (macrocytic) |
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*ex. slow bleeding ulcer, excessive menstruation *morphology: hypochromic, microcytic *****IRON DEFICIENCY******* |
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*needed for DNA synthesis *if faulty DNA synthesis --> asynchrony *need to consume meat and dairy products to get it *need intrinsic factor to be absorbed properly |
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*needed for DNA synthesis *if faulty DNA synthesis --> asynchrony *need to consume green leafy vegetables to get it *doesn't need any outside help for absorption |
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*bone marrow is over actively producing cells *leads to hypercellularity |
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*more than the normal number of cells |
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*bone marrow is under actively producing cells *leads to hypocellularity |
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*less than normal number of cells |
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