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| 2150852947 | Take Aways | 1. anemia or macrocytosis may be absent 2. neuropsychiatric perturbations irreversible if diagnosis delayed 3. treatment is easy and cheap | 0 | |
| 2150917876 | Vitamin B12 (Cobalamin) | 1. water soluble 2. higher mammals can't make B12 3. essential to DNA 4. recommended 2-3ug/day 5. found in animal proteins 6. 50% of B12 stores are in liver 7. it takes 2-3 years to become deficient starting from full stores | 1 | |
| 2150924538 | Folate | 1. naturally occurring molecule from plants: fruits, nuts, peas, dairy, some animals sources, and beer 2. folic acid is synthetically produced and acts like folate in the body 3. recommended: 400ug/day | 2 | |
| 2150982752 | B12 and folate relationship | 1. DHF is converted to THF and then to methylene-THF 2. methylene-THF can be used to synthesize nucleic acids 3. it can also be converted into methyl-THF (trapped here during B12 deficiency), and then to THF while vitamin B12 becomes methyl-B12 4. methyl B12 gives up methyl group to convert homocysteine to methionin | 3 | |
| 2150997385 | B12 facilitated reactions | 1. methylcobalamin converts homocysteine to methionine. homocysteine is toxic to endothelial cells 2. adenosylcobalamin converts methylmalonyl-CoA to succinyl-CoA. MMA is toxic to nerve cells | 4 | |
| 2151025192 | B12/Folate deficiency | can't make DNA -> stops cell division. 1. hematologic: megaloblastic anemia, low platelets, leukopenia 2. dermatologic: rashes, hyperpigmentation 3. neuropsychiatric: neural tube defects, ataxia/balance, paresthesias, megaloblastic madness, depression, blindness. Can also occur with only B12 deficiency and abundant folate 4. Oral/GI: diarrhea, malabsorption, chelitis, glossitis (beefy red tongue; papellae gone) | 5 | |
| 2151045431 | Effect of folate | 1. fortification of flour products with folic acid to reduce incidence of neural tube defects 2. pre-natal vitamins also contain large doses of folate 3. "Mask" hematologic presentation of B12 deficiency | 6 | |
| 2151069642 | Cobalamin-binding proteins | 1. intrinsic factor: -made by gastric parietal cells -promotes absorption of cobalamin in ileum 2. transcobalamin II -made by all cells -transporter of cobalamin to cells (replace intrinsic factor after absorption) 3. R proteins -from exocrine glands, phagocytes -protects B12 from degradation in stomach -replaced by tissue factor after leaving stomach *folate absorbed in jejunum | 7 | |
| 2151070172 | B12 deficiency test | 1. B12 level, decrease, less reliable 2. methylmalonic acid, increase, more reliable (points to B12 deficiency) 3. homocysteine, increase, more reliable Also: -low reticulocyte count -abnormal blood smear -test for TSH to rule out hypothyroidism, which can also cause macrocytic anemia | 8 | |
| 2151131905 | Schilling Test | 1. give parenteral IM injection of normal cobalamin 2. give oral radioactive cobalamin 3. if absorption is normal, the radioactive cobalamin should all be present in the urine | 9 | |
| 2151132171 | Schilling Test (2) | 1. If radioactive B12 present in urine, the patient's condition is due to insufficient ingestion of B12 2. If radioactive B12 is low in urine, it's not being absorbed. Try adding radioactive B12 with intrinsic factor 3. If that fixes it, the patient has pernicious anemia. If not, give antibiotics (to reduce overgrowth of bacteria in the gut from eating all the B12) 4. If that also doesn't work, give pancreatic enzymes along with all the earlier things. If it works, patient has defects in pancreatic deficiency *test is just helpful to understand process. We don't do this test anymore | 10 | |
| 2151167567 | Diagnosis of B12 deficiency | 1. low blood level of vitamin B12 2. functional B12 deficiency can occur at "normal" serum levels (inc Hcy, inc MMA) 3. delayed diagnosis common -interpretation of laboratory results -neuropsychiatric symptoms can precede anemia and/or macrocytosis | 11 | |
| 2151182376 | B12 for vegetarians and babies | 1. bacteria on vegetables can provide enough B12 2. babies feeding on mother's milk can become B12 deficient if mother is B12 deficient | 12 | |
| 2151209440 | Pernicious Anemia | 1. 0.1% of general population; 1.9% of those over 60 2. autoimmune destruction of gastric parietal cells (can't make IF) -lymphocytic/plasma cell invasion -anti-IF and anti-parietal cell abs 3. association with other autoimmune disease | 13 | |
| 2151222493 | Folate deficiency | 1. Nutritional: old age, poverty, premature infancy, goat's milk anemia 2. decreased absorption: celiac sprue, tropical sprue, intestinal dz 3. increased turnover: pregnancy, chronic hemolysis, exfoliative dermatitis 4. dugs: DHF reductase inhibitors, antimetabolites, dRibonuclease inhibors, antiepileptics | 14 | |
| 2151233284 | Congenital disorders | 1. deficiencies of cobalamin-associated proteins -cubilin (terminal ileal receptor of Cbl-IF; Imerslund-Grasbeck disease) -IF -Transcobalamin II 2. Deficiencies of folate-associated proteins -dihydrofolate reductase -N-methyl FH4: homocysteine methyl-transferase | 15 | |
| 2151254792 | megaloblastic anemia | 1. a morphologically distinctive macrocytic anemia 2. impaired DNA synthesis 3. interruption of cell cycle from G2 growth stage to M2 (mitosis) 4. nuclear and cytoplasmic dyssynchrony 5. large cells (megaloblasts), shortened cell survival (release of bili, LDH) | 16 | |
| 2151282584 | megaloblastic anemia | 1. RBCs in their production still have large nucleus when they already have a lot of hemoglobin 2. neutrophils have too many lobes - hypersegmentation. 1PMN with >6 lobs, or 20 with >5 lobes | 17 | |
| 2151301262 | Neuropsychiatric pathology | 1. In B12 deficiency can develop in isolation 2. often not reversible (especially if patient had deficiency for over 6 months) 3. brain and spinal cord affected | 18 | |
| 2151312724 | Effect on Myeylin | 1. impaird methylmalony CoA -> succinyl CoA conversion -elevated levels of MMA -prevent normal FA synthesis or incorporated into FA -myelin destabilization -> demyelination 2. methylation of the myelin sheath phospholipids possibly also affected | 19 | |
| 2151379397 | Subacute combined degeneration of spinal cord | 1. gradual onset; progressive 2. often irreversible if B12 deficiecy present for > 6months 3. Nitrous oxide -irreversible oxidation of normally reduced Co in B12 -N2O anesthesia: precipitates SCAD in people with subclinical vitamin B12 deficiency -N2O abuse -> B12 deficiency | 20 | |
| 2151391286 | Other Neuropsychiatric effects | 1. depression/megaloblastic maddness/somnolence 2. S-adenosyl-methionine (SAMe) required for synthesis of catecholamines which maintain mood 3. deterioration of brain tissue: decay of nervous fibers decay and accumulation in astrocytes 4. blindness: optic nerve atrophy (rare) | 21 | |
| 2151399022 | Treatment of B12 deficiency | 1. Parenteral B12 -1mg IM daily x 1 week, then -1mg IM weekly x 4 weeks, then -1mg IM monthly thereafter 2. pernicious anemia -oral B12 in high dose (1-2mg daily) following parenteral replacement -mass action | 22 | |
| 2151408740 | treatment for B12 deficiency | 1. transfusion usually not required (chronic anemia) 2. monitor for recovery: -marrow: begins within 8-12 hours -reticulocytosis: within 3-5 days -PMN hypersegmentation persists for 1-2 weeks 3. Neuropsychiatric effects often NOT completely reversible | 23 | |
| 2151413795 | treatment for folate deficiency | 1. oral folate for 400-1000ug daily 2. response seen even in cases of malabsorption | 24 | |
| 2151417880 | Take Aways | 1. anemia or macrocytosis may be absent 2. neuropsychiatric perturbations IRREVERSIBLE if diagnosis delayed 3. treatment is easy and cheap | 25 | |
| 2151369504 | Sagittal T2 weighted MRI | 1. low cervical/upper thoracic spinal cord 2. hyperintensity in pyrimidal tracts of lateral and posterior columns 3. indicates loss of myelin | 26 | |
| 2151320949 | Staining spinal cord | White areas: loss of staining for myelin | 27 |
