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81 Cards in this Set

  • Front
  • Back
What are vitamins, and what is their physiologic function? (general answer)
necessary for metabolic fxns but can't be synthesized (or at least not in sufficient amts)

not energy sources, not used for structural purposes
What are the 13 required vitamins?
1) 4 fat soluble: ADEK
2) 8 B-complex
3) Vit C
DRI stands for:
dietary reference intakes

What is EAR?
est avg req

meets req of HALF of healthy individ in a given age/gender grp

used to plan & assess dietary adequacies
What is RDA?
recc dietary allowance

meets nearly all (98%) requirements in a given age/gender group
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
tolerable upper intake level

highest dose likely to pose no risk of adverse effects for almost all in gen pop'n.
intensive abx tx can cause a deficiency in these vitamins
1) K
2) biotin

synth by intestinal bacteria
kidney dz can cause a deficiency in this vitamin, leading to "renal rickets"
vitamin D

a critical enzymatic alteration to a vit D precursor occurs in the kidney
these vitamins have enterohepatic circulation; since they need to be absorbed > once, malabsorption rapidly leads to clinical deficiency
patients w/ roux-en-Y bariatric surgery need supplementation of these vitamins

most vitamin absoprtion occurs in the proximal intestine
newborns particularly need these vitamins
K - neonatal GI tract is sterile
E (and K) - don't cross placental membrane efficiently

D - if infant is breastfeeding
ADRs associated w/ vitamins
anti-convulsants interact w/ K, D, folate, biotin, B6

INH binds pyridoxine
vitamin that mediates calcium homeostasis
vit D
in what situations might you see vit D deficiency?
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
what toxicities are associated with excess vitamin D?
↓ appetite, nausea, thirst, stupor
what role does vit D play in the body?
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)
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
what are 3 possible causes of vitamin D deficiency?
1) inadequate synthesis (or inadquate UV exposure)

2) inadequate absorption

3) inadequate dietary supply
what is osteomalacia?

what are the sx?
1) demineralization of EXISTING bone (adults)

2) fx, W/O gross changes in bone contour
what is osteoporosis?
↑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
which is the single mineral for which the avg US diet is most deficient?
should elderly or young people take Ca & Vit D supplements?
mixed study results

ERT + Ca + vit D in post menopausaul women effective in ↓ osteoporosis
what are tx for osteoporosis?
biphosphonates (Fossamax)

PTH subQ injxns (teriparatide, Forteo) - ↑ osteoblast activity & bone density
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
roles of vit A in the body?
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
foods that vit A can be obtained from?
1) largest amts of retinyl esters from animal products (egg yolks, liver, fish oil, milk, butter)

2) B-carotene from green & orange veggies
sx of vit A deficiency
1) vision problems: leading cause of blindness; night blindness; xeropthalmia

2) defects in epith tissue maintainence (acne, psoriasis)

3) ↑infxns (↓immunity)
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
what are indications for synthetic retinoids? how do they work?
1) acne & psoriasis

2) synthetic b/c ↓ toxicity compared to vit A = ↑ doses ok

3) ↓ sebum production & assoc. inflammatory response
differences bewteen vit K types:
1) K1
2) K2
3) K3
1) veggies
2) intestinal bacteria
3) synthesized from synthetic precursor
principal role of vit K?

blood clotting

coenzyme for glutamic acid carboxylase -->
clotting factors need this to bind Ca -->
bind phospholipids on plts
how do coumarin and warfarin work?
vit K antagonists
how *might* vit K favor calcification of bone?
proteins like osteocalcin also undergo vit K mediated carboxylation of gla residues
how do humans meet the bulk of vit K requirement?
gut bacteria

K1 in plants but only a few (spinach) contain large amts

cow milk = v little;
human milk = 20% of daily req
sx of vit K deficiency
↑ PT
causes of vit K deficiency
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)
vit K toxicity: cause & sx
1) infants w/ prolonged administration of K3

2) hemolytic anemia & jaundice (toxic to RBCs)
how is vit E obtained?
vegetable oils (rich); liver, eggs (moderate) -->

GI lymphatics -->
a-tocopherol incorporated

into VLDL in liver -->

role of vit E?
anti-oxidant: protect membranes from free radicals & lipid peroxidation

most effective of the lipid soluble
vit E toxicity
unlikely- least toxic of the fat soluble vits (no toxicity at 300mg/day)
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)
vit E deficiency
1) spinocerebellar degeneration, ataxia, areflexia
2) mild-mod sensory neuropathy

(in adults, may develop 10-20yrs post-malabsorption)
what are the major ROS?
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)
how do ROS cause damage?
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
types of antioxidants?
1) enzymes:
superoxide dismutase, glut peroxidase, catalase

2) endogenous chemicals:
glutathione, ubiquinol

3) exogenous chemicals:
vit E, C, B-carotenes, phenolics, lycopenes (tomatoes)
what are lycopenes?
almost exclusively from tomatoes
50% of caretonids in human serum
single highest ROS quenching capacity of all dietary carotenoids
what are potential benefits of vit E supplementation?
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)
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)
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
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
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
thiamine (B1) deficieny - sx
beriberi (wet & dry)
wernicke korsakoff
what is wet beriberi?
thiamine deficiency

impacts CV fxn

swelling of legs, fluid in lungs, tachycardia
what is dry beriberi?
thiamine deficiency

affects nerves & muscles

memory loss & confusion
pain- hands & feet
trouble standing/moving
involuntary eye movements
what is wernicke-korsakoff?
thiamine deficiency

chronic alcoholics: dietary insuffiency or impaired absorption

confusion, ataxia
what is the physiologic role of riboflavin (B2)?
synthesis of FMN, FAD =
used in NADH dehydrogenase, succinate dehyrog, methylene THF reducatse
riboflavin deficiency - sx?
not associated w/ major human dz, but accompanies other deficiencies (causing dermatitis, chelosis, glossitis)
physiologic role of niacin (B3)
NAD, NADP - coenzymes in redox rxns - esp FA, cholesterol, steroid synth
what is pellagra?
niacin deficiency

4D's: dermatitis, diarrhea, dementia, death (if un-tx'd)
what is a pharmacologic use of niacin?
to tx hyperlipidemia, along w/ statins

(↓ lipolysis in adipose, VLDL, LDL)
where can niacin be obtained?
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
physiologic role of pyridoxine (B6)
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
which drug can cause B6 (pyridoxine) deficiency?
B6 (pyridoxine) deficiency sx
MANY - b/c involved in so many diff rxns

1) behavioral changes (b/c of role in NTM & myelin synth)
2) anemia
what is the main source of biotin (B7)?
intestinal bacterial synthesis
physiologic fxns of biotin?
coenzyme in carboxylase rxns:
pyruvate carboxylase (gluconeogen)
acetyl-CoA carboxylase
mt propionyl-CoA carboxylase
biotin deficiency is caused by?
1) long abx therapies
2) excessive consumption of raw eggs (avidin in egg whites have high affinity for biotin, preventing absorption)
panthothenic acid (B5) fxns?
1) coenz in CoA (fat, CHO, protein metabolism<-- transfer of acyl groups)

2) phosphopantetheine in FA synth
B5 sources & deficiences?
pantothenic acid deficiency rare b/c of ess nature of CoA.

eggs, liver, yeast (but widely distributed)
cobalamin (B12) fxns?
1) homocys Me-transferase (HCys + 5Me-THF --> Met + THF)

2) Methylmalonyl CoA mutase: isomerizes (odd # C FAs) & (methylmal CoA)
B12 sources
animal meat, not plants
causes of B12 deficiency
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)
sx of B12 deficiency
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)
folic acid fxn
1 carbon metabolism
(folate conjugated to PABA --> pteroic acid)
folic acid sources
yeasts, leafy vegetables, liver
describe folic acid storage & metabolism
also reduced to THF via DHFR
<-- stored in liver in poly-glu form -->
intestinal mucosal cells remove glu -->
pass into bloodstream -->
folate deficiency - sx
1) megaloblastic anemia
2) NTD in fetus
vitamin C (ascorbic acid) - fxns
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
what is scurvy?
vit C deficiency

↓ collagen stability =

easily bruised skin
soft swollen gums
↓ wound healing, ↑ hemorrhaging

vit C = well absorbed, so primary cause of deficiency is poor diet
how should vitamin C supplements be stored?
avoid long-term storage
avoid exposure to alkali

most unstable of all the vitamins