vitamins – Chemistry Flashcard

what is the study of nutrition?
the study of how food nourishes our bodies and influences our health
what is the definition of wellness?
absence of disease, (physical, emotional, spiritual health)
what are diseases where nutrition plays some role?
osteoporosis, osteoarthritis, some forms of CA
what are diseases with a strong nutritional component?
type 2 diabetes, heart disease, HTN, obesity
what are diseases caused by nutritional deficiencies or toxicities?
pellagra, scurvy, iron-deficiency anemia, other vitamin/mineral deficiencies, nutrient toxicities
what percentage of the US population is overweight? why is this a growing problem?
65% obese children are being diagnosed with type 2 diabetes
what are the “goals of healthy people 2010”
increase quality and years of healthy life
eliminate health disparities
what are nutrients?
the chemicals in foods that are critical to human growth and function:
carbs, fats,oils,proteins,vitamins,minerals,water
what are vitamins?
organic molecules that assist in regulating body processes, but do not supply energy. they can be fat or water soluble
what are the fat soluble vitamins?
K,A,D,E -> can be stored in the body, (deficiencies in these can be harder, but if gall bladder is removed – possible)
what are the 2 important D vitamins?
ergocalciferol, (D2) and cholecalciferol, (D3)
where is ergocalciferol, (D2) found? what can it be converted to?
ergocalciferol, (D2) is exclusively found in plant foods, it can be converted to calcidiol in the liver
where is cholecalciferol, (D3) found? what can it be converted to?
cholecalciferol, (D3) is exclusively found in plant foods, it can be converted to calcidiol in the liver
what is 7-dehydrocholesterol? what population is this becoming more of a
vitamin D3, a provitamin in the skin, which gets converted to cholecalciferol in the sunlight.
what population is 7-dehydrocholesterol deficiency becoming more of a problem with? what has it been linked with?
the elderly, it has been linked with obesity, depression and osteoporosis.
what can be a problem with sunblock?
sunblock is not particularly effective in preventing skin CA, and that it can cause vit D3, (7-dehydrocholesterol) deficiencies
what angle of UVb light is needed to break the bonds of 7-dehydocholesterol -> cholecalciferol? what time of day is the sun at this angle? what else is a consideration?
120, 11am-1pm. also depends on season, location, sunscreen, skin type
what is calcitriol? what is it converted from? where? what hormone is involved?
the active form of vitamin D, it is converted from calcidiol in the kidneys under the influence of parathyroid hormone
can calcitriol be prescribed as an rx? what is its function in the body?
yes. it regulates blood Ca++ levels, thought to inhibit cell proliferation, (anti-CA), and enhance cell differentiation
why is prescribing calcium to pts with osteoporosis on its own ineffective?
it needs regulation by vit D
where does calcitriol bind?
cell nucleus, increases cell transcription
what needs to be closely monitored in dialysis pts?
Ca levels
where is 95% of Ca stored?
bones, teeth
what happens when Ca levels drop?
the parathyroid glands releases PTH, which stimulates the activity of osteoclasts, releasing Ca into the blood. PTH also stimulates the kidneys to activate vit D and decrease Ca excretion
what does calcitriol do to PTH?
calcitriol enhances the activity of PTH on bone cells and stimulates intestinal cells to synthesize Ca transport proteins -> enhancing Ca absorption from food
what is one effect of being on corticosteroids for a prolonged amount of time? how?
osteoporosis, they counteract the activity of hormones that control osteoblasts -> loose Ca
what is the optimal vit D blood level?
mildly deficient?
severely deficient?
possible toxicity?
optimal = 32-100 ng/mL
mildly deficient = 15-31
severely deficient = <14
possible toxicity = >100
where is vit D stored?
liver, adipose
what is AI recommendation for vit D? what is assumed in this recommendation?
5 mcg/day. the assumption is no vit D is produced in the skin
what foods have vit D?
fortified foods, fish (oil), sometimes egg yolk
how does vit D deficiency manifest itself?
rickets in children, osteomalacia in adults, (dialysis, CA, glandular disease pts)
what is osteomalacia?
osteomalacia is the softening of the bones due to defective bone mineralization
is osteoporosis associated with Vit D deficiency? can supplementation increase bone density of people without of deficiency?
yes and yes
can toxicity from Vit D occur from sun exposure?
what does toxicity from Vit D cause?
hypercalcemia, overly high levels of intestinal Ca transporter expression, bone loss from too much osteoclast expression
what group of compounds is vit K associated with? what sources do they come from? which is most active?
quinones, phylloquinones are the most active, they come from plant sources, menaquinones are from animal sources and human intestinal synthesis, (accomplished by e coli)
what is the function of vit K? are there drugs that inhibit it?
is is necessary for 7 of the proteins necessary for clotting. coumadin and warfarin both inhibit it, (plavix doesn’t)
how does vit K affect bone formation?
vitamin K facilitates carboxylation of osteocalcin, a bone protein necessary for mineralization/maturation, this carboxylation enhances its Ca binding properties
how can a vitamin K deficiency cause Ca stones? does decreasing dairy help with Ca stones?
lack of Vit D decreases osteocalcin’s Ca binding properties, and it’s “sticky state” causes Ca buildup to form stones. decreasing dairy doesn’t help with Ca stones, in fact it makes the situation worse, b/c Ca deficiency is the cause of the stones
what are sources of vit K?
intestinal bacteria, green leafy vegetables
what is the RDA for males, women?
80 mcg males, 65 mcg females, (lower b/c they rely on endogenous source)
what does vit K do for cosmetic concerns?
it can decrease melasma
what happens with vit K deficiency? what can cause it?
it is rare
usually associated with prolonged use of antibiotics or people with their gall bladder removed, (food isn’t properly broken down, essential nutrients are not absorbed), megadosing of other fat-soluble vitamins like A and E, (all use the same transport).
what type of vitamin is easier to have a deficiency in? why?
water soluble vitamins are eliminated by the kidneys and cannot be stored in our bodies
what are the water soluble vitamins?
C and B
what is vitamin B1?
what what is the structure of thiamin, (vit B1) like?
thio- means sulfur. it has a sulfur containing ring attached to the central carbon atom, and heat easily breaks this attachment
most of the B vitamins are heat labile, what does this mean?
heat easily destroys them
what is the function of vitamin B1, thiamin?
it is part of thiamin pyrophosphate, (TPP), which is a cofactor in the decarboxylation of pyruvate in the pyruvate->acetyl-CoA rxn as well as a cofactor in the very similar alphaketoglutarate dehydrogenase rxn of the TCA cycle, as well as the non-oxidative portion of the PPP, (ribose, NADPH produced). IMPORTANT FOR BETA OXIDATION, NERVOUS SYSTEM CONSTRUCTION
what are good sources of vitamin B1? what are RDAs for males/females?
pork, and wheat germ, (little in most animal foods). RDA for males: 1.2 mg/day, females:1.1
what is vitamin B1 deficiency called?
beriberi: muscle weakness, appetite loss, nerve degeneration, (myelin sheath is mostly omega 3 FAs). shortness of breath, heart failure, (prefer FAs as fuel to glucose)
what does beta oxidation require?
vitamin B1
what is “wet beriberi”?
edema, fluid retention, enhanced protein excretion, due to albumin loss -> decreased contractility of the heart, fluids stay in tissues
what is “dry beriberi”?
muscle weakness, not enough ATP supplied, (speech difficulties, vomiting, strange eye movements)
how does beriberi affect the brain?
the brain and nervous system rely on TPP for glucose metabolism which makes up its primary energy source.
why is beriberi associated with alcoholism?
alcohol displaces other foods and interferes with the adsorption of thiamin, (inhibits anti-diuretic hormone, urinating a lot, water soluble vitamins included)
what is riboflavin? what reducing equivalent is it associated with? what action does it perform?
vitamin B2, (vitamin G). flavin adenine dinucleotide = FAD, which acts as a hydrogen & electron acceptor. FADH2 delievers electrons to the electron transport chain -> ATP production
what are B vitamins involved with?
fat, carb, and protein metabolism, (essentially all vital functions of body)
what is riboflavin involved with?
deamination of some amino acids, TCA cycle, beta oxidation
what environmental condition causes riboflavin requirements to be higher?
colder weather
what physiologic situation would lead to a higher need for riboflavin, (vit B2)? why?
overweight pt dieting, due to a higher rate of beta oxidation
what are symptoms of riboflavin deficiency?
angular stomatitis, (irritation/cracking at corners of the mouth), glossitis, (irritation of the tongue)
why is (unfortified) milk in a clear container not a good source of riboflavin?
UV light degrades vit B2
what is niacin? what can it be used for?
vitamin B3, (nicotinic acid/nicotinamide), it can help lower bad cholesterol, (LDL, VLDL), and increase levels of HDL. it can be more effective than some more expen$ive rxs, (those that block HMG CoA inhibitors or are statins)
can niacin be endogenously produced? what do compounds containing it do?
vit B3, niacin, can be endogenously produced. NAD accepts H+ and electrons to form NADH which alternately carries electrons to the electron transport chain or powers the pyruvate -> lactate conversion.
what are good sources of niacin? what amino acid can it be derived from?
meat, poultry, fish grains. 60 mg tryptophan = 1 mg niacin/NE
what is the niacin/vit B3/NE RDA for males? females?
males: 16 mg NE
females: 14 mg NE
what are the 3 “Ds” of niacin deficiency?
dementia, diarrhea, dermatitis
what is pellegra?
rough/red skin at areas of sun exposure related to niacin deficiency
what 3 cofactors are needed for the conversion of tryptophan to niacin?
riboflavin, (vit B2), B6, and iron
what is the recommended dose for medicinal niacin? what is the one common adverse effect?
3000mg/day. hot flashes
what is pantothenic acid? what compound is it associated with?
vitamin B5. it is a component of CoA, (acyl carrier)
what processes is pantothenic acid involved with?
both energy yielding, (catabolic), and biosynthetic – component of elongase, (increases FA chain length), (anabolic), pathways
are vitamin B5 deficiencies common? where is it abundant in the body?
no. it is abundant in the liver
what is biotin? can it be endogenously produced?
vit B7, sulfur containing, (biocytin amount in food has not been accurately evaluated – B7 food form). there is some synthesis of biotion by bacteria in the large intestine, therefore it can be affected by antibiotics
what does biotin do?
biotin, (vit B7), catalyzes carboxylation rxns:
pyruvate->oxaloacetate, (via pyruvate carboxylase)
3C FAs -> TCA ,(propionyl CoA -> succinyl-CoA via propionyl-CoA carboxylase)
elongation of FA chains in FA synthesis
if infants have a build up of LCFAs, is this evidence of a biotin deficiency?
no, biotin deficiencies have not been adequately studied. this would be due to a lack of propionyl-CoA carboxylase
how is biotin deficiency related to diabetes?
pts are creating propionyl-CoA, but instead of it being made in to succinyl-CoA and used in the TCA or elongated,(both via biotin), it gets made into glucose in the liver
what symptoms have been noted among test volunteers who went off biotin?
nausea, loss of appetite, numbness, muscle pains, rashes, depression, anemia and high cholesterol
is biotin deficiency related to hair loss?
yes, including male baldness
can a rare form of infant SK respond to biotin treatment?
yes, but the reason is unknown
how can biotin deficiency occur in the elderly? how is this treated?
the enzymes in the intestine that extract biotin get “worn out” and unable to process the nutrient. larger doses of vit B7 can bypass this and go -> bloodstream
what are food sources of biotin? what is its AI?
cauliflower, peanuts, liver. egg yolks do but egg whites have a protien that binds biotin, therefore biotin deficiencies can occur from over consumption of raw eggs. AI is 30 mg/day
what are pyridoxal, pyridoxine, and pyridoxamine?
PL, PN, PM are all forms of vit B6, and the phosphorylated forms, PLP,PNP,and PMP also exist in fat and protein metabolism. (however, if in food, the Pi is removed in digestion)
what is the function of vit B6 related to proteins?
pyridoxal, pyridoxine, and pyridoxamine are all involved in transamination of the 11 non-essential AAs, (however w/out B6, all AAs are “essential”)
non-essential AAs are often used for ________and essential AAs are often used for _________
non-essential AAs are often used for catabolic processes and essential AAs are often used for anabolic processes
which vitamins are necessary for RBC and WBC formation?
vit B6 + vit B12 (important for anemia tx)
other than synthesis, how can vit B6 be related to anemia?
inadequate B6 disturbs the binding process of O2 to Hb, resulting in microcytic hypochromic anemia, (smaller cells w/less Hb)
what vitamins influence, (reduce), homocysteine levels? why is this important?
vit B6,9, 12. homocysteine is a substrate in the SAM cycle to produce methionine, cysteine, (+ precursor molecules for DNA synth), and if it builds up in the arteries it stimulates the immune system which attacks it, causing inflammation/plaque build-up
what are sources of vit B6, (pyridoxal, pyridoxine, and pyridoxamine)?
fortified cereals, bananas, fish, meat, poultry.
how does alcohol affect levels of vit B6? what consideration does a high protein diet require in terms of vit B6?
alchol decreases absorption, along with synthesis of PLP. high protein diets require more vit B6, (pyridoxal, pyridoxine, and pyridoxamine)
what is folate?
vit B9. it has 3 parts:
para-aminobenzoic acid (PABA)
when one glutamate is removed in small intestine = folic acid
what happens with a PABA deficiency?
fast-proliferating hair and skin cells degenerate. seen in anti-CA rxs, which stop folic acid from being converted to its active form.
what is the function of folate, vit B9?
it is converted in the body to tetrahydrofolic acid, (THFA), which has 5 forms that accept/donate 1 C units during DNA syth, AA metabolism, cell division, and RBC maturation, (esp important in fast proliferating cells, hair, skin RBC). also works with vit B6,12 to reduce homocystiene
where is folate found? is it heat/light labile?
yes it is heat/light labile. fortified cereals, dark leafy vegetables. prescence of food decreases absorption, so DRI is expressed as DFE, which is 400 mcg per day, (male, but x2 for pregnant women)
what are deficien
what are causes of vit 9/folate deficiency?
inadequate consumption of right foods
inadequate absorption due to GI tract problems
increased requirement, (pregnancy, can cause spina bifida)
impaired B9 utilization paired with B6 deficiency
altered fotate metabolism due to alcohol/drug abuse
excessive excretion due to diarrhea
how can deficiency in either vit B9 or B12 affect RBCs?
lack of either can impair DNA synth, creating large, misshapen cells called megaloblasts. megaloblasts mature into macrocytes, which have shorter life spans and their presence will decrease normal RBC levels -> lowering total O2 carrying capacity
how does folate, B9 depend on B12? what other disease can this appear as?
folate needs b12 to convert to THFA to its (active) methylene form. therefore, B12 deficiency can cause a B9 deficiency. deficiency of both can appear as bell’s palsy
how does vit B12 affect the SAM cycle?
it converts homocysteine to methionine, reducing homocysteine levels
what does vit B12 do in terms of FAs?
it maintains the mylein sheath as well as prepares FAs to enter the TCA. remember for pts on diuretics, vegetarian diet.
what rxs can cause deficiencies in vit B9+12?
anti-seizure drugs

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