WATER SOLUBLE VITAMINS

Transcription

1 MEDCH 402 FALL 2007 PRBLEM SET #4 WATER SLUBLE VITAMIS I. MATCH THE VITAMI R MIERAL WITH THE CRRESPDIG AMUT AD UIT. Answer (DV) Amount Unit 1. Thiamin g,x a) 20 x) mg 2. Biotin b,x b) 0.3 y) µg 3. Folacin i,x c) 400 z) IU 4. iacin a,x d) Pantothenic Acid f,x e) Vitamin C e,x f) Vitamin B 6 j,x g) Vitamin B 12 d,y h) Riboflavin h,x i) 0.4 j) 2.0 II. WATER SLUBLE VITAMIS I MAY CASES CA BE TAKE I HIGH DSES WITHUT SIDE EFFECTS. A. Explain why. Water soluble vitamins are readily metabolized and/or excreted due to their hydrophilicity. B. Give two examples where toxicity has been observed and list the symptoms of toxicity. B 6 toxicity: >200 mg/day leads to decreased prolactin; >1-2 g/day leads to neuropathy. iacin toxicity- peripheral vasodilation, GI upset, ulcers, diarrhea, liver damage. 1 P a g e

2 III. FR THE FLLWIG CDITIS: Do the following: A. ame the vitamin that has been shown to be of some benefit. B. What enzyme/reaction is activated by high doses of the vitamin? 1. Homocystinuera: B 6 activates cystathionine synthase 2. Wernicke-Korsakoff syndrome: B 1 (thiamin) activates transketolase 3. Methylmalonic acidurea: B 12 activates isomerase (methylmalonyl CoA to succinyl CoA) IV. PRVIDE A METABLIC EXPLAATI FR THE FLLWIG (A SCHEME MAY BE ECESSARY FR A CGET ASWERS-STRUCTURES ARE T ECESSARY). A. A folate deficiency is observed during a B 12 deficiency. 5 -methyl THFA B 12 THFA B 12 is required to convert 5 -methyl THFA to THFA. If B 12 is deficient, this conversion may not occur, and a folate deficiency will occur. B. Homocysteine levels may be elevated if B 6 intake is inadequate. [B 12 ] [B 6 ] [B 6 ] Methionine Homocysteine Cystathionine α-ketobutyrate + cysteine 2 P a g e

3 B 6 is involved in the conversion of homocysteine to cystathionine, and then alphaketobutyrate and cysteine. When B 6 is inadequate, homocysteine levels will be increased. C. iacin may be deficient if B 6 intake is inadequate. Tryptophan tryptophan oxygenase -formylkynurenine 3-hydroxykynurenine B 6 kynureninase 3-hydroxy anthranilic acid quinolinic acid niacin If B 6 is inadequate, the conversion from tryptophan to niacin may be blocked, resulting in niacin deficiency. V. THE FLLWIG ARE SIGS F A VITAMI DEFICIECY. FR EACH, LIST THE MST APPRPRIATE SIGLE DEFICIET VITAMI. A. increased urinary xanthurenic acid B 6 B. increased plasma pyruvate B 1 C. increased plasma homocysteine B 6, folic acid, or B 12 D. decreased erythrocyte glutathione reductase activity B 2 VI. WHAT VITAMIS ARE ASSCIATED WITH THE FLLWIG FUCTIS? A. decarboxylation B 1 and B 6 B. transamination B 6 C. purine and pyrimidine synthesis folic acid D. electron transport B 2 and B 3 E. niacin synthesis B 6 F. collagen synthesis C 3 P a g e

4 VII. WHY IS IT IMPRTAT THAT A WMA WH IS PREGAT R IS PLAIG BECMIG PREGAT SHULD BE RECEIVIG A SUPPLEMETAL FLATE? Folic acid deficiency early in a pregnancy could lead to teratogenesis with neural tube defects. It is recommended that women who are pregnant or are thinking about becoming pregnant should be receiving the RDA value of 0.4 mg/day folic acid from fortified foods or from a supplement. This is in addition to that provided in the diet. VIII. FLIC ACID REQUIRES A PRESCRIPTI FR HIGH DSES, EVE THUGH IT IS ESSETIALLY -TXIC. WHY? Folic acid deficiency (anemia) can be caused by two conditions: 1) lack of folic acid or 2) lack of B 12 (involved in the recycling of folic acid). By giving a high folate dose, nucleic acids will be synthesized even though folic acid is not regenerated in the process. Therefore, pernicious anemia associated with B 12 deficiency will be masked and nerve damage will progress irreversibly if not treated. IX. THE FLLWIG ARE VITAMI ATAGISTS. A. Suggest the vitamin antagonized. B. Suggest one symptom that you might expect with chronic administration of the antagonist. H 2 + S A. B 1 B. Wernike-Korsakoff syndrome (confusion, memory loss, etc) 4 P a g e

5 H A. B 6 B. Peripheral neuritis H A. Folic acid B. Megaloblastic anemia 5 P a g e