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81 Cards in this Set
- Front
- Back
What are vitamins, and what is their physiologic function? (general answer)
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necessary for metabolic fxns but can't be synthesized (or at least not in sufficient amts)
not energy sources, not used for structural purposes |
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What are the 13 required vitamins?
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1) 4 fat soluble: ADEK
2) 8 B-complex 3) Vit C |
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DRI stands for:
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dietary reference intakes
EAR RDA AI UL |
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What is EAR?
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est avg req
meets req of HALF of healthy individ in a given age/gender grp used to plan & assess dietary adequacies |
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What is RDA?
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recc dietary allowance
meets nearly all (98%) requirements in a given age/gender group |
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AI
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adequate intake
recommended avg daily intake based on approximations of intake in apparently healthy people, = assumed to be adequate used when RDA can't be determined |
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UL
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tolerable upper intake level
highest dose likely to pose no risk of adverse effects for almost all in gen pop'n. |
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intensive abx tx can cause a deficiency in these vitamins
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1) K
2) biotin synth by intestinal bacteria |
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kidney dz can cause a deficiency in this vitamin, leading to "renal rickets"
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vitamin D
a critical enzymatic alteration to a vit D precursor occurs in the kidney |
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these vitamins have enterohepatic circulation; since they need to be absorbed > once, malabsorption rapidly leads to clinical deficiency
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folate
B12 A D |
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patients w/ roux-en-Y bariatric surgery need supplementation of these vitamins
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ALL!
most vitamin absoprtion occurs in the proximal intestine |
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newborns particularly need these vitamins
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K - neonatal GI tract is sterile
E (and K) - don't cross placental membrane efficiently D - if infant is breastfeeding |
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ADRs associated w/ vitamins
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anti-convulsants interact w/ K, D, folate, biotin, B6
INH binds pyridoxine |
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vitamin that mediates calcium homeostasis
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vit D
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in what situations might you see vit D deficiency?
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20 min of sun on hand is sufficient. poor exposure when:
1) winter in northern latitudes 2) elderly (esp institutionalized) 3) dark skin 4) sunscreen decreases 5) ↓ intake of fortified foods (milk, yogurt, cheeses; OJ) - esp in lactose intolerant Asians, AA |
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what toxicities are associated with excess vitamin D?
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↓ appetite, nausea, thirst, stupor
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what role does vit D play in the body?
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steroid hormone acting on
1) intestines (absorption of Ca, PO3) 2) bones (mobilize Ca via PTH) 3) kidneys (reabsorption of Ca in DT via PTH) |
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what is rickets?
what are sx of rickets? what vitamin deficiency is it associated with? |
1) SOFT BONES <-> improper mineralization of cartilage in children
2) lordosis of spine, leg bowing 3) vitamin D |
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what are 3 possible causes of vitamin D deficiency?
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1) inadequate synthesis (or inadquate UV exposure)
2) inadequate absorption 3) inadequate dietary supply |
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what is osteomalacia?
what are the sx? |
1) demineralization of EXISTING bone (adults)
2) fx, W/O gross changes in bone contour |
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what is osteoporosis?
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↑porosity b/c skeletal remodeling tips in favor of net loss of bone mass beginning in 40s.
menopause accelerates FX common in vertebrae, femoral neck, pelvis |
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which is the single mineral for which the avg US diet is most deficient?
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calcium
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should elderly or young people take Ca & Vit D supplements?
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mixed study results
ERT + Ca + vit D in post menopausaul women effective in ↓ osteoporosis |
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what are tx for osteoporosis?
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biphosphonates (Fossamax)
PTH subQ injxns (teriparatide, Forteo) - ↑ osteoblast activity & bone density |
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what is the difference between
1) retinol 2) retinyl esters 3) retinal 4) retinoic acid 5) B-carotene |
1) retinol: transport
2) retinyl esters: storage 3) retinal: vision 4) retinoic acid: epithelial differentiation & growth 5) B-carotene: dietary (in veggies) -> converted to retinol in intestinal mucosa |
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roles of vit A in the body?
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1) vision in reduced light
2) differentiation of epithelium (mucus secretion) 3) anti-oxidant (B-carotene) 4) bone remodeling 5) enhanced immunity 6) glycoprotein, MPS synth |
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foods that vit A can be obtained from?
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1) largest amts of retinyl esters from animal products (egg yolks, liver, fish oil, milk, butter)
2) B-carotene from green & orange veggies |
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sx of vit A deficiency
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1) vision problems: leading cause of blindness; night blindness; xeropthalmia
2) defects in epith tissue maintainence (acne, psoriasis) 3) ↑infxns (↓immunity) |
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sx of vit A toxicity?
how does it occur? |
1) bone pain, dermatities, hepatosplenomegaly, nausea, diarrhea, birth defects
2) only yellow skin w/ B-carotenes occurs w/ high doses over mo/yrs |
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what are indications for synthetic retinoids? how do they work?
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1) acne & psoriasis
2) synthetic b/c ↓ toxicity compared to vit A = ↑ doses ok 3) ↓ sebum production & assoc. inflammatory response |
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differences bewteen vit K types:
1) K1 2) K2 3) K3 |
1) veggies
2) intestinal bacteria 3) synthesized from synthetic precursor |
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principal role of vit K?
mechanism? |
blood clotting
coenzyme for glutamic acid carboxylase --> clotting factors need this to bind Ca --> bind phospholipids on plts |
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how do coumarin and warfarin work?
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vit K antagonists
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how *might* vit K favor calcification of bone?
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proteins like osteocalcin also undergo vit K mediated carboxylation of gla residues
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how do humans meet the bulk of vit K requirement?
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gut bacteria
K1 in plants but only a few (spinach) contain large amts cow milk = v little; human milk = 20% of daily req |
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sx of vit K deficiency
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↑ PT
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causes of vit K deficiency
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unusual, b/c synth in gut, except in
1) newborns (poor transference across placenta, sterile GI tract) - receive injxn @ birth to prevent bleeding 2) broad spectrum abx 3) ↓ fat absorption (eg CF) |
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vit K toxicity: cause & sx
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1) infants w/ prolonged administration of K3
2) hemolytic anemia & jaundice (toxic to RBCs) |
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how is vit E obtained?
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vegetable oils (rich); liver, eggs (moderate) -->
GI lymphatics --> a-tocopherol incorporated into VLDL in liver --> blood |
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role of vit E?
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anti-oxidant: protect membranes from free radicals & lipid peroxidation
most effective of the lipid soluble |
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vit E toxicity
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unlikely- least toxic of the fat soluble vits (no toxicity at 300mg/day)
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vit E deficiency
-populations affected |
1) mostly premature infants
in children or adults, assoc w/ ↓fat absoprtion 2) CF 3) chronic cholestasis ie ↓bile in duodenum 4) abetalipoproteinemia 5) transport defect (eg in a-tocopheral transport protein) |
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vit E deficiency
-sx |
neuro:
1) spinocerebellar degeneration, ataxia, areflexia 2) mild-mod sensory neuropathy (in adults, may develop 10-20yrs post-malabsorption) |
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what are the major ROS?
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1) superoxide (O2-): moderately reactive; forms H2O2 via superoxide dismutase
2) h peroxide (H202): not a free radical itself, but can give rise to to OH- 3) hydroxyl radical (OH-): usu reacts w/ 1st molecule it encounters (ie, rate is diffusion controlled). Most often formed by H2O2 + Fe++ (Fenton rxn) |
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how do ROS cause damage?
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1) protein oxid'n -> degradation by proteases, catalytically less or inactive, more thermo-labile
2) lipid peroxid'n: loss of membrane integrity =↓ cell fxn 3) DNA oxid'n: strand breaks, base modific'n |
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types of antioxidants?
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1) enzymes:
superoxide dismutase, glut peroxidase, catalase 2) endogenous chemicals: glutathione, ubiquinol 3) exogenous chemicals: vit E, C, B-carotenes, phenolics, lycopenes (tomatoes) |
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what are lycopenes?
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almost exclusively from tomatoes
50% of caretonids in human serum single highest ROS quenching capacity of all dietary carotenoids |
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what are potential benefits of vit E supplementation?
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1) ↓ risk of MI (obs study) b/c of ↓ LDL oxid'n
2) delay onset of cataracts (WITH vit C & B carotene; no evidence w/ pure vit E in RCT so far) |
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water-soluble vitamins
1) excretion method? 2) storage amts? 3) biological fxn? |
1) urine
2) stores generally not significant 3) coenzymes (most are non-covalently bound & regenerated at end of rxn, so v. small amts required in diet) |
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what are the H2O-soluble vitamins?
what are their coenzyme forms? |
Thiamine (B1) / TPP
Riboflavin (B2) / FMN, FAD Niacin (B3) / NAD pantothenic acid (B5) / CoA Pyridoxine (B6) / pyridoxal phosphate Biotin (B7) / pyruvate carboxylases (& other carboxylases) Cobalamine (B12) / Cobalamine Ascorbic acid (C) / prolyl OHase (& others) Folic Acid / THF |
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what is TPP?
what are its physiological fxns? |
thiamine pyrophosphate
cofactor used by many enzymes: 1) energy metabolism of most tissues (pyruvate decarboxylase, a-ketoglutarate dehydrogenase) 2) transketolase in pentose-P path 3) synthesis of ACh |
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1) what are the sources of thiamine?
2) where is deficiency found? |
1) synthesized by plants or microorganisms - whole wheat, peas, beans
2) wherever polished rice is a major component of the diet |
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thiamine (B1) deficieny - sx
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beriberi (wet & dry)
wernicke korsakoff |
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what is wet beriberi?
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thiamine deficiency
impacts CV fxn swelling of legs, fluid in lungs, tachycardia |
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what is dry beriberi?
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thiamine deficiency
affects nerves & muscles memory loss & confusion pain- hands & feet trouble standing/moving involuntary eye movements |
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what is wernicke-korsakoff?
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thiamine deficiency
chronic alcoholics: dietary insuffiency or impaired absorption confusion, ataxia |
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what is the physiologic role of riboflavin (B2)?
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synthesis of FMN, FAD =
used in NADH dehydrogenase, succinate dehyrog, methylene THF reducatse |
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riboflavin deficiency - sx?
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not associated w/ major human dz, but accompanies other deficiencies (causing dermatitis, chelosis, glossitis)
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physiologic role of niacin (B3)
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NAD, NADP - coenzymes in redox rxns - esp FA, cholesterol, steroid synth
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what is pellagra?
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niacin deficiency
4D's: dermatitis, diarrhea, dementia, death (if un-tx'd) |
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what is a pharmacologic use of niacin?
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to tx hyperlipidemia, along w/ statins
(↓ lipolysis in adipose, VLDL, LDL) |
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where can niacin be obtained?
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esp rich in MEAT
Trp can be converted, but usu not enough for human bodies common (along w/ other defiicencies) in roux-en-Y bypass pts |
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physiologic role of pyridoxine (B6)
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many - PLP coenzyme used in:
1) AA metabolism (sythesis, catabolism, energy prodxn from AA) 2) heme catabolism 3) synth of 5HT & NE 4) synth of sphingolipids for myelinization 5) NAD synthesis 6) homocysteine metabolism |
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which drug can cause B6 (pyridoxine) deficiency?
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INH
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B6 (pyridoxine) deficiency sx
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MANY - b/c involved in so many diff rxns
include 1) behavioral changes (b/c of role in NTM & myelin synth) 2) anemia |
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what is the main source of biotin (B7)?
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intestinal bacterial synthesis
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physiologic fxns of biotin?
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coenzyme in carboxylase rxns:
pyruvate carboxylase (gluconeogen) acetyl-CoA carboxylase mt propionyl-CoA carboxylase |
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biotin deficiency is caused by?
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1) long abx therapies
2) excessive consumption of raw eggs (avidin in egg whites have high affinity for biotin, preventing absorption) |
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panthothenic acid (B5) fxns?
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1) coenz in CoA (fat, CHO, protein metabolism<-- transfer of acyl groups)
2) phosphopantetheine in FA synth |
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B5 sources & deficiences?
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pantothenic acid deficiency rare b/c of ess nature of CoA.
eggs, liver, yeast (but widely distributed) |
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cobalamin (B12) fxns?
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1) homocys Me-transferase (HCys + 5Me-THF --> Met + THF)
2) Methylmalonyl CoA mutase: isomerizes (odd # C FAs) & (methylmal CoA) |
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B12 sources
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animal meat, not plants
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causes of B12 deficiency
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liver can store up to 6 years' worth- deficiencies usually result from inadequate absorption rather tahn supples (eg anti-IF)
also vegans (abstain from all animal products) body has low requirement (small stores but small losses) |
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sx of B12 deficiency
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megaloblastic anemia / pernicious
(rapidly dividing cells THF for nucleotide synthesis for DNA replication) progressive demyelination of nerve cells (accumulation of abnormal FA & incorporation into cell membranes) |
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folic acid fxn
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1 carbon metabolism
(folate conjugated to PABA --> pteroic acid) |
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folic acid sources
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yeasts, leafy vegetables, liver
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describe folic acid storage & metabolism
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also reduced to THF via DHFR
<-- stored in liver in poly-glu form --> intestinal mucosal cells remove glu --> pass into bloodstream --> |
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folate deficiency - sx
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1) megaloblastic anemia
2) NTD in fetus |
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vitamin C (ascorbic acid) - fxns
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1) collagen stability (Lys, Pro -OHase
2) catabolism of Tyr 3) bile acid synth 3) absorption of Fe (reducing agent: ferric --> ferrous) 4) biosynth of cortisol, aldosterone, cholesterol --> bile acids 5) antioxidant |
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what is scurvy?
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vit C deficiency
↓ collagen stability = easily bruised skin soft swollen gums ↓ wound healing, ↑ hemorrhaging osteoporosis anemia vit C = well absorbed, so primary cause of deficiency is poor diet |
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how should vitamin C supplements be stored?
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avoid long-term storage
avoid exposure to alkali most unstable of all the vitamins |