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UCI SOM Dai

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Question
Answer
Can vitamins be synthesized in the human body   no  
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Two classes of vitamins   water-soluble and fat-soluble  
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Fat soluble vitamins   A,D,K,E  
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Water soluble vitamin classes   b vitamins, folic acid and ascorbic acid (C)  
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B vitamins   thiamine (B1), Riboflavin (B2), Niacin (B3), Pantothenic Acid (B5), Pyridoxine (B6; pyridoxal; pyridoxamine), biotin (B7), B12 (cobalamine)  
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Sources of vitamins   food intake and synthesis by intestinal microorganisms  
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6 ways to have vitamin deficiency   inadequate dietary intake, inadequate absorption, inadequate use (inadequate conversion), increased requirements, increased excretion, drug-associated deficiency  
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thiamine cofactor/s, reaction/s, and disease/s   thiamine pyrophosphate; pyruvate DH, alpha ketoglutarate DH, branched chain alpha keto acid DH; Beriberi  
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riboflavin cofactor/s, reaction/s, and disease/s   FAD, FMN;oxidation-reduction;no disease  
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Niacin cofactor/s, reaction/s, and disease’s   NAD, NADP; oxidation-reduction; pellagra  
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Pantothenic acid cofactor/s, reaction/s, and disease/s   Coenzyme A; acyl transfer, pyruvate DH, alpha keto glutarate DH; no disease  
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What B vitamin can be made in small amounts in the body   niacin (made from tryptophan)  
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Pyridoxine cofactor/s, reaction/s, and disease/s   pyridoxal phosphate; transamination, decarboxylation, dehydration; seizure in infants  
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Cobalamin cofactor/s, reaction/s, and disease/s   5’-deoxyadenosylcobalamin, methylcobolamin; methylmalonyl-CoA mutase, 5’methylTHF homocys transferase; pernicious anemia and others  
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Folate cofactor/s, reaction/s, and disease/s   tetrahydrofolate; 1 C transfer, dTMP biosynthesis, purine synthesis; megaloblastic anemia and others  
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Biotin cofactor/s, reaction/s, and disease/s   no cofactors; carboxylation; no disease  
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Ascorbic acid cofactor/s, reaction/s, and disease/s   ascorbid acid; hydroxylation (collagen); scurvy  
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Beriberi   thiamine deficiency; mostly in areas that used polished rice; lethargy, weight loss, irregular heart rate, convulsions, death  
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Pellagra   niacin deficiency; dermatitis, diarrhea, dementia, death  
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Most common vitamin deficiency   folic acid  
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Normal folic acid requirement   100-200 mg/day/adult (more for pregnant women)  
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Causes of folic acid deficiency   inadequate intake, impaired absorption (intestinal diseases), impaired metabolism, increased demand  
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Diagnosis of folic acid deficiency   ingest test dose of Histidine and test forminimoglutamate level in urine; if there is forminimoglutamate in urine, folic acid deficiency is present  
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Consequences of folic acid deficiency   7 weeks-nothing; 13 wks-formiminoglutamate in urine, altered read blood cells; 4 months-irritability, forgetfulness, anemia; upon addition of folic acid, everything normalized  
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Biochemical consequences of folic acid deficiency   defective glycine cleavage (neurological problems), defective homocys (met conversion->neurological defects); defective purine/pyrimidine synthesis (DNA and hematopoietic defects)  
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B12 deficiency comes from   impaired absorption  
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B12 storage   up to 6 years in liver  
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B12 absorption   parietal cell in stomach makes instrinsic factor (IF) which binds B12 and transports it to the ileum; transported in blood by TC (transcobalomine) which takes it to the liver  
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Pernicious anemia   IF (intrinsic factor) deficiency through impaired absorption of B12  
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Affects of pernicious anemia   impaired: regeneration of tetrahydrofolate pool, impaired purine/dTMP biosynthesis, hematopoietic defects, neurological defects  
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Neurological defects of pernicious anemia   accumulation of methylmalonyl CoA intereferes with myelination of nervous tissue b/c methylmalonyl CoA is a competitor of malonyl CoA in FA synthesis  
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Treatment for pernicious anemia   intramuscular B12 injection and folate supplement  
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N metabolism consequences of THF deficiency due to B12 deficiency   defective: purine/pyrimidine synthesis, glycine cleavage  
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N metabolism consequences from direct B12 difficency   defective: homocys->Met conversion, methylmalonyl CoA->succinyl CoA conversion  
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B12 and THF correlation   B12 is necessary in THF regeneration  
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5 groupings of biosynthesis of non-essential AA   1)Ala, Asp, Glu, Gln, Asn 2)Arg, Pro 3)Ser, Gly 4)Tyr 5)Cys  
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alanine synthesis   pyruvate transamination  
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aspartate synthesis   oxaloacetate transamination  
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glutamate synthesis   alpha ketoglutarate transamination  
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glutamine synthesis   add ATP and NH3 to glutamate  
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asparagines synthetase   add ATP and N to aspartate  
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Arginine and proline synthesis   glutamate->glutamate semialdehyde->proline and arginine  
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Tyrosine synthesis   phenylalanine hydroxylase; 3/4 of Phe in diet goest to Tyr  
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Cystein synthesis   comes from cystathionine which comes from serine and homocysteine which comes from methionine; cystathionine goes to cysteine and alpha ketobutyrate  
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Serine synthesis   3-phosphoglycerate (phosphogylcerate) 3-phosphopyruvate (aminotransferase) 3-phosphoserine (phosphatase) serine  
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Glycine synthesis   serine (serine hydroxymethyl transferase) glycine; the rxn uses N5N10methylene THF which becomes THF; THF returns to N5N10 through a rxn with another glycine  
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Almost all non-essential AA’s can be synthesized from   glycolysis products  
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