Erstellt von Lesley Howard
vor mehr als 8 Jahre
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Frage | Antworten |
Macrocytic anemia | Characterized by larger than normal RBCs MCV > 100 Can be megaloblastic or not |
Macrocytic anemia labs | MCHC WNL MCH elevated due to large cytosol HBC decreased due to less RBCs |
Non-megaloblastic anemia | Milder form No DNA synthesis impairment MCV up to 110 fL |
Megaloblastic anemia | MCV = 110 - 160 fL DNA synthesis impaired B12 or folate deficiency Large cytoplasm / normal protein synthesis Megaloblast cells in bone marrow Hypersegmented neutrophils |
Folate deficiency | Usually dietary Body doesn't store much folate |
Methotrexate | Used to treat cancer Structural analog of folate Inhibits DHFR Strongly affects rapidly dividing cells Side effect of MB anemia |
Dihydrofolate reductase | Repeat reactions with folate produces tetrahydrofolate NADPH dependent Uses folate as a substrate |
Tetrahydrofolate | Carbon carrier for metabolic reactions Supplies carbon for nucleotide synthesis Cannot be synthesized without folate |
Homocystiene methyltransferase | Transfers the methyl group from N5 methyl THF to methionine Requires B12 as cofactor B12 deficiency means THF is not recycled and SAMe is not created |
Pernicious anemia | Autoimmune mediated by T cells Destruction of parietal cells reduces IF secretion and stomach acidity Inhibits ability of body to absorb B12 |
MB anemia blood smear | Low RBC Oval macrocytes Anisocytosis Poikilocytosis Large hypersegmented neutrophils Low/normal reticulocytes Thrombocytopenia Leukocytopenia |
MB anemia bone marrow | Megaloblastic changes in all stages of development due to impairment of DNA synthesis Increased destruction of platelet precursors Increased destruction of granulocytes |
Methylation | Stabilizes myelin Without B12 there is no SAMe Without SAMe there is no methylation Without methylation myelin is destabilized Neuropathy results in B12 deficiency |
Folate trap | Result of B12 deficiency Homocystiene methyltransferase inactive N5 methyl THF cannot be recycled back to THF and is trapped Becomes a functional folate deficiency |
Methylmalonyl CoA mutase | Requires B12 as a cofactor Used to determine whether MB anemia is from folate or B12 If B12, will result in a buildup of substrate If folate, will be ineffective |
R Binder | Secreted in mouth Binds to B12 released from protein in the stomach Facilitated by pepsin and low pH from parietal cells Degraded in duodenum at neutral pH |
Intrinsic factor | Secreted in stomach by parietal cells Binds B12 in duodenum Binds with B12 to IF receptors in the ileum |
Intrinsic factor receptors | Present on the apical membrane of ileal cells Binds to IF2/B12 complex and promotes endocytosis and absorption Once inside IF will release B12 |
Transcobalamin II | Binds B12 within ileal cells and transports it to tissues B12/TCII complex exits the basal side of the ileal cell and goes into portal circulation |
Folate deficiency symptoms | MB anemia Glossitis |
B12 deficiency symptoms | MB anemia Glossitis Peripheral neuropathy |
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