Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
46 Cards in this Set
- Front
- Back
Vitamin B1
common name two things that it does requirement for thiamin concentrated locations |
thiamin pyrophosphate
cofactor in decarboxylation(TPP in PDH, KDH, IDH) coenzyme in carbohydrate metabolism thiamin requirements are influenced by carbs consumed location: muscles and CNS |
|
beri beri
|
thiamin deficiency
causes the disease beriberi, in which the patient presents with muscle weakness, ataxia, footdrop, ophthalmoplegia, Beriberi is regarded as a medical emergency because it can progress to cardiac failure. Two forms of beriberi are "wet" (edematous) or "dry" (nonedematous) |
|
what types of eating habits induces thiamin deficiency?
|
not eating pork legumes and yeast
milling grains eating some foods that may destroy dietary thiamin thiamin may be destroyed in processing ethanol favors thiamin def |
|
Niacin
how is it found in the body? what are some common foods rich in niacin? |
NAD and NADP
legumes cereals meat fish |
|
what are some important roles of pyridine nucleotides(NAD)
|
cosubstrates for dehydrogenase
substrates for ADP ribosylation precursors of cyclic ADP-ribose |
|
what is niacin made from?
|
tryptophan
synthesis of niacin from trp requires B6 |
|
what does niacin deficiency cause?
|
pellagra
|
|
excess niacin vs excess nicotinamide
|
niacin = excess of 1 g, acute flushing, biomedical abnoralities
nicotinamide = nothing |
|
Folic acid, main biochemical purpose
|
a 1 C donor
folate easily destroyed by cooking |
|
what is niacin clinically used for
|
reductions of elevated blood cholesterol
|
|
biochemical structural features of folic acid
|
chain of glutamate residues
|
|
absorption and transport of folate
|
transport system takes it up and its then reduced and some is methylated, it must be demethylated to serve any purpose
|
|
demethylation of folic acid
rxn |
homocysteine + 5-methylTHF -> met + THF
note: need B12 can be trapped in the methyl stage |
|
folate deficiency causes?
|
macrocytic anemia
|
|
How can a B12 deficiency be masked?
|
if you take a loot of folic acid, not all of it will get methylated, and so it will look like you have enough vit B12
|
|
Folate deficiency
|
COMMON
|
|
what clinical diseases can folate decrease the risk of
|
homocysteineanemia -
because folate metabolizes homocysteine NTD |
|
inadequate folate will show a decrease of [folate] where in the body: start from what gets decreased first
|
serum folate decreases
RBC folate decreases get hypersegmented neutrophils and mean corpuscular volume increases, Hb decreases |
|
what are the syptoms of pellagra
|
diarrhea dementia dermatitis
|
|
Wernicke-Korsakoff syndrome
|
similar to beri beri thiamin def in that TPP binding is weak and which becomes manifested if thiamin intake is compromised
|
|
where does the body usually get niacin?
|
NADH from legumes and cereals
|
|
muscle weakness, anorexia, and skin eruptions, cracked, pigmented, and scaly skin in areas exposed to sun (hands, forearms, neck, and legs); Casal's necklace
what is this disease and what is it due to |
pellagra niacin def
|
|
inhibits the synthesis of new cells, causing anemia, villous atrophy, and depapillation of the tongue. In addition to showing hypochromic, megaloblastic red cells on a blood smear, hyperhomocysteinemia
|
folate deficiency, could also be B12 def,
hyperhomocysteinemia because homocytseine is converted to met when demethylating THF |
|
what else does a B12 deficiency cause?
|
conversion of methylmalonic acid to succinyl CoA
numbness and tingling of the extremities, weakness, and other neurological changes. Long-term effects on the nervous system can be irreversible,methylmalonic acid accumulates |
|
what does absorption of B12 require?
|
gastric acid releases B12, R-proteins bind it and then binds Intrinsic Factor (IF) in the duodenum
|
|
some patients must receive B12 by injection,why?
|
Pernicious anemia is a pathological B12 deficiency arising from an inability to properly absorb dietary B12 (defective IF), in 3-6 months will show deficiency
|
|
where does B12 reabsorption occur
|
ileum, very efficient receptor mediated process
|
|
how long can B12 stores last in the body? why?
|
10-20 years b/c B12 is recaptured for re-use
|
|
what are dietary sources of B12
|
meat, fish, dairy products and eggs; plants are devoid of B12
Vitamin B12 has no toxicity (a TUL has not been determined), allowing megadoses to be used in some cases of deficiency. |
|
what is the precursor of PLP
|
vitamin B6, found in various chemical forms - pyridoxine, pyridoxal, pyridoxamine
|
|
how does B6 effect homocysteine?
|
reducing elevated homocysteine because it is a factor in the reaction by which homocysteine is converted to cysteine
|
|
B6 is toxic?
|
toxic at high doses
|
|
what is the schilling test?
|
assess whether a deficiency is due to malabsorption of B12:
radioactive cobalamin (a chemical form of B12) is given by mouth and B12 storage sites are saturated by injected cobalamin. In a normal individual the radiolabeled cobalamin will be efficiently absorbed but excreted in the urine (since storage sites are blocked). Low urinary excretion confirms poor absorption |
|
how do you distinguish iron deficiency anemias fromn folate/B12 anemias
|
blood smear and complete blood counts
see microcystic anemia(iron) vs macrocystic anemia(folate/B12) may need to test serum folate RBC folate and serum B12 |
|
B6
|
aa metabolism, glycogen breakdown, H action
|
|
B6 deficiency
|
rare, vitamin is widley distributed, LARGE doses however can cause irreversible peripheral neuropathy (over 500mg/day)
|
|
B2
aka |
riboflavin
|
|
riboflavin is found in what?
|
a component of the enzyme prosthetic groups FAD FMN (oxidation reduction rxns)
|
|
uncomplicated riboflavin deficiency vs riboflavin deficiency
|
uncomplicated is uncommon and milder
|
|
a prosthetic group in enzymes of carboxylation
|
biotin
|
|
is biotin free or bound
|
both
bound is bound to epsilon-amino group of lysine(as an amide) |
|
biotin deficiency
|
not really seen
|
|
describe the structure of pantothenic acid
|
beta-alanine in amide linkage with pantoic acid
|
|
what is pantothenic acids role in the body
|
effect acyl group transfer as part of Coenz A (add a mercaptoethylamine and adenine to pantothenic acid and viola)
|
|
pantothenic acid deficiency
|
rare
|
|
Wernicke-Korsakoff syndrome
|
Wernicke-Korsakoff syndrome:a genetic defect that prevents them from effectively utilizing dietary vitamin B1. TPP binding is weak, becomes manifested if thiamin intake is compromised (by alcoholism, poor diet, or malabsorption). This syndrome presents with many of the signs of beriberi, but also with memory problems, disorientation, and coma.
|