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20 Cards in this Set
- Front
- Back
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sites of hematopoiesis
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fetal sites are yolk sac, liver, and spleen. childhood sites are skull, long bones and axial skeleton. adults is primarily in the axial skeleton. note some have extramedullary sites including spleen, liver, and nodes. this usually happens in ppl.
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important cytokines and steps
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from stem cell to erythroid stem cell (BFU-E or burst forming unit - erythroid) via IL-6 and 3, and GM-CSF. from BFU-E to mature blood cell via EPO.
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steps in erythropoiesis
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quiescent stem cell, activated stem cell, BFU-E, CFU-E, RBC
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explain the oxygen sensor model of erythropoiesis
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O2 and Fe are needed for hydroxylation of HIFa which will then be degraded by proteosomes. HIFa is needed for txn of EPO, thus more O2 means leass HIFa and less EPO, but if O2 levels decrease, hydroxylation decreases, HIFa rises and EPO expression increases
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two classes of anemia?
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decreased production of RBCs or increased destruction/loss of RBCs
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4 causes of decreased RBC production?
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nutritional deficiencies, metabolic issues, marrow replacement (due to cancer cells taking over the marrow and inability to make new RBCs), and aplasia (damage to marrow or loss of cellular activity)
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describe marrow seen with B12 deficiency.
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megaloblastic anemia. large precursors with open chromatin. pink cytoplasm. defect is in nuclear maturation not cytoplasm, thus plenty of Hb but no division
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describe the bone marrow of anemia of chronic disease.
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hypoplastic (hypocellular)
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causes of anemia characterized by increased RBC destruction.
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immune hemolysis, hostile environment via DIC (firbrin clots cause destruction), membrane protein abnormalities (spherocytosis), hemoglobinopathies, RBC enzyme defects
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describe the CBC
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RBC #, Hb, Hct, RBC indicies (MCV, MCH, MCHC), WBC count w/ differential, platelet count, blood cell morphology, reticulocyte count.
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ok random fact, acording to dr glass, polychromatophilic RBCs are shift cells are reticulocytes and stain blue bc of rna...
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dunno man
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tests to evaluate anemias aside from CBCs.
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bone marrow exam: aspiration for morphology and biopsy for architecture. serum measurements: LDH (lactic dehydrogenase from inside RBC will go up in hemolytic states), bilirubin levels, coombs test (direct to see Abs on RBC surface and indirect to see Abs in serum), iron studies, B12 and folate levels
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how do you tell if the RBC's are hypochromic?
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the central pallor of them is about 1/3 the diameter of the RBC
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what kinds of anemia show nuclear/cytoplasmic asynchrony?
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B12 deficiencies
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corrected reticulocyte count?
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reticulocyte percentage X pt Hct/45
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normal myeloid precursor to erythroid precursor (ME) ratio?
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3:1
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clues to increased RBC destruction?
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decreased Hct, morphological changes, reticulocytosis, increased unconjugated bilirubin, increased LDH
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if we see increased reticulocytes, what questions should you figure out for differentials?
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first is it due to hemolysis or blood loss. if it is hemolysis then is it extracorpuscular (due to the environment of the RBC), intracorpuscular (due to something acquired within the RBC) or due to membrane defects
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what are the differentials for decreased RBC production?
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hypoproliferative states: aplastic anemia, red cell aplasia, renal failure, drugs, radiation. marrow failure associated with nutrient deficiencies: iron issues like impaired Hb synth (hypochromic, microcytic anemias), B12 and folate (macrocytic anemias). myelophthisic disorders: metastasis, granulomatous disease (TB or histo), hematopoietic malignancies, myelofibrosis, storage diseases (gaucher's disease)... myelophthisic refers to something in the bone marrow that is replacing the RBCs
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physical exam signs of anemia?
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petechiae and pale mucous membranes, adenopathy, check CV, hepatosplenomegaly, neuropathy (if B12 deficient), stool for occult blood loss.
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