4. Nutrition Flashcards
name the water soluble vitamins.
Vitamin B1 (thiamine), Vitamin B2 (riboflacin), Vitamin B3 (niacin), Vitamin B5 (pantothenate), Vitamin B6 (pyridoxine), Vitamin B7 (Biotin), Vitamin B12 (cobalamin), folate, Vit. C
T/F Water soluble vitamins are more likely to result in toxicity
false- fat soluble because they accumulate in fat
Which water soluble vitamins get stored in the liver with the fat soluble vitamins? which has a greater pool of storage in the liver? where do all the other water soluble vitamins go?
B12 and folate; B12; washed out
what are the common symptoms of B vitamin deficiencies?
dermatitis, glossitis, diarrhea
What is the other name of Vitamin A? What is its source?
Retinol; Beta carotenes (dark and yellow vegetables)
What is the function of Vitamin A?
differentiation of cells, vision in reduced light (retinol makes up rhodopsin cells), antioxidant
what does a deficiency cause?
night blindness, dry skin
what causes fat soluble vitamin deficiencies?
malabsorption problems (CF and sprue) and mineral oil intake
what can cause an excees of vit A? what are the symptoms?
consumption of bear liver, and overtreatment isoretinoin; constitutional symptoms and alopecia and skin changes
T/F no vitamin can be too much in pregnancy!
False- Vit A is teratogenic- causes cardiac problems and cleft palate; Vit K in excess can cause jaundice in newborns
What is retinoic acid used for in treatments?
wrinkles, acne and psoriasis topically, promyelocytic anemia, measles
What is the source of Vitamin B1? what is its other name? what causes a deficiency in B1?
enriched whole grain cereals and other things; thiamine; malnutrition (nonenriched white processed bread and rice) and alcohol second to malnutrition
what is the function of Vitamin B1?
it is apart of thiamine pyrophosphate which is a cofactor enzymes involved in ATP production: pyruvate dehydrogenase (glycolysis), alpha ketoglutarate dehydrogenase (TCA cycle), transketolase (HMP shunt), branched chain AA dehydrogenase
What generally results after Vitamin B1 deficiency? T/F treat b1 def, with glucose.
ATP depletion and highly aerobic tissues (heart and brain) are affected first; false- glucose infusion worsens
what 4 diseases specifically results with B1 deficiency?
1) Dry beriberi: peripheral neuropathy demyelination (symmetricul muscle wasting) 2) Wernicke: ataxia, confusion, nystagmus, mammilary body and medial dorsal nuc of thalamus hemorrhage 3) Korsakoff: anterograde and retrograde amnesia, demyelination of limbic system (personality change) 4) Wet BeriBeri: high output cardiac failure with congestive cardiomyopathy and edema
What is the other name of Vitamine B2? In what foods can it be found?
Riboflavin; dairy and meat
What is the function of B2? what can cause deficiency?
Riboflavin makes up FAD and FMN both used in redox reactions; vegans
What are the symptoms of B2 deficiency?
cheilosis and corneal vascularization
What is the other name of B3? What is its function? Synthesis of B3 requires what other vitamin? what else?
Niacin/Nicotinic acid; NAD+ and NADH used in redox reactions, and catabolic and anabolic reactions; B6; tryptophan
What does severe deficiency of B3 lead to? what are the causes?
Pellagra (dermatitis, diarrhea, dementia); INH use, B6 deficiency, Hartnup disease, malignant carcinoid syndrome, and a corn based diet (lacks trp and niacin in corn cant be absorbed)
how do you treat niacin deficiency do to corn based diet?
lime and CaCO3 to displace the niacin
what causes an excess of B3? what are the symptoms?
niacin treatment for hyperlipidemia; facial flushing
What is the other name for Vitamin B5? what is its function?
pantothenate; essential comp of CoA (needed for acyl transfers) and fatty acid synthase
what is the other name of Vitamin B6? what is its function?
pyridoxine; converted to pyridoxal phsophate used in transamination reaction,decarboxylations, heme synthesis, niacin synthesis from trp, glycogen phosphorylase, cystathionine synthesis, NT synthesis
what does a pyridoxine deficiency look like? what causes it?
convulsions, hyperirritiability, peripheral neuropathy, sideroblastic anemias; alcoholics and INH and fortified goats milk consumption
What is the other name for VIt b12? what is its function?
Cobalamin; cofactor for homocysteine methyltransferase (transfers SAM to THF to give to dUMP) and for methylmalonyl coA mutaseto make succinyl coA
what dose a deficiency in Vit B12 cause? what causes it?
macrocytic megaloblastic anemia, hypersegmented PMNs, subacute combined degeneration myelopathy which results in degeneration of the dorsal and lateral columns (loss of position and vibration sense, spastic paresis and ataxia) due to abnormal myelin (methyl malonyl coA incorporated into myelin!); malabsorption, lack of IF (PA or bypass surgery) or absence of terminal ileum
how do you detect the different reasons that cause cobalamin def?
Schilling test
what is folic acid? what is its function?
water soluble vitamin stored in liver; converted to THF by dihydrofolate reductase and is a coenzyme in 1 methyl transfers- impt for DNA synth
what does a def in folic acid cause? is it more or less common than cobalamin def? how do you differentiate it with cobalamin def?
macrocytic megaloblastic anemia; it is the most common vit def in the US; no neuro symptoms and no methylmalonyl coA in the urine
what are the causes of folate def?
cancers (rapidly synthesizing); MTX (blocks dihyrdofolate reductase); phenytoin (prevent conjugase from breaking down polyglutamate form to monoglutamate form; reabsorption in jejunum is blocked by alcohol and OCPs; also blocked by sulfonamides
What is the importance of folic acid?
prevents neural tube defects in 1st trimester
what is SAM?
s- adenosyl methionine
what is the job of S adenosyl methionine? what is it made of ? give an example of a reaction it participates in.
to transfer methyls; a methionine and an ATP; norepinephrine plus a methyl makes epinephrine
What happens to S adenosyl methionine after it donates a methyl? What enzyme regenerates methionine? what two factors are necessary to do this? who gives the methyl?
S adenosyl homocysteine; homocysteine transferase; B12 and THF; M-THF
what reactions occur in the mitochondrial matrix? mit inner membrane?
TCA cycle, FA oxidation, acetyl coA production; ox phos
what are the symptoms of infantile beriberi and when do they present?
cardiomegaly, cyanosis, tachycardia, dyspnea, vomitting; 2-3 months
what is the difference between wet and dry beriberi?
dry is just the symmetrical neuropathy with both motor and sensory symptoms; wet includes both the neuropathy and cardiac involvement of high output failure with peripheral edema, tachycardia, cardiomegaly
what is the major cause of B12 def? what is the clinical picture of this?
pernicious anemia; older, mentally slow european woman who is anemic and icteric with a smooth shiny tongue and has broad based shuffling gait
what is vitamin B7? what is its main job? in what reactions?
Biotin; cofactor for carboxylation; pyruvate carboxylase (turning pyruvate to oxaloacetate), acetyl coA carboxylase (acetyl coA to malonyl Co A), and proprionyl coA caroboxylase for (propionyl CoA to methylmalonyl coA)
what is the source of Biotin?
bacterial synthesis in the intestine
what can cause Biotin deficiency? what are the symptoms?
avidin in raw egg whites prevents their reabsorption; also antibiotic use; dermatitis, alopecia, glossitis, lactic acidosis, enteritis
what is ascorbic acid? what is its 5 main function?
vitamin C; facilitates iron absorption by making sure its in its reduced state (Fe2+), hydroxylation for lysine and proline which is necessary for crosslinking; necessary for dopamine Beta hydroxylase for conversion of dopamine to NE; keeps FH4 in its reduced form; ANTIOXIDANT!
which form of iron is most absorbable? what form is non heme ingested iron in (vegetables for ex)?
Fe2+; Fe3+
what cofactor is necessary for conversion of dopamine to NE? NE to epinephrine?
SAM; Vit C
which vitamin keeps Fh4 in its reduced form?
Vit C
what causes scurvy? what are the symptoms of scurvy?
vit C deficiency; glossitis, anemia, weakened vessels, hemorrahges, hemarthroses, swollen gums, bruises,
other than scurvy what else does vit C def cause? also, what kind of anemias and why?
decreased would healing; microcytic anemia (d/t decreased iron [not absorbable]; macrocytic anemia (d/t Fh4 not reduced)
what does vit C excess cause?
renal calculi of uric acid (replaces uric acid in excretion)
where is vit C found?
fruits and vegetables
what can cause a vit C deficiency?
smoking (FR takes up all the antioxidants); diets lacking fruit
what type of vitamin is Vit D? where do we get it? in what form?
fat soluble; either endogenous production or exogenous; D2 ergocalciferol is ingested from plants and D3 cholecalciferol is formed in sun exposed skin (and can be consumed in fortified milk)
what form of Vitamin D is in plants? milk fortified with vit D? formed in sun exposed skin?
D2 (ergocalciferol), D3 (cholecalciferol), D3 (cholecalciferol)
what is the precursor in the skin that the sun turns to D3?
7 dehydrocholesterol
what is the storage form of vit D? active form?
25 OH D3; 1,25 (OH)2 D3 (Calcitriol)
what is calcitriol?
the active form of Vit D (1,25 (OH)2 D3)
what is the function of Vit D?
to increase serum Ca and Phosphate for ultimate bone deposition by: increase intestinal absorption of calcium and phosphate (also renal); and increase resorption of bone by stimulating macrophages (osteoclasts)
where are receptors for Vit D? (think how does it increase serum Ca and Phosphate)
intestine, renal, bone
T/F with hypervitaminosis D you will see increased alk phos
true! vit D causes bone turnover, and stimulates osteoblasts also
in what organ is D3 converted from 25 OH D3? with what enzymes?
liver; P450 hydroxylation
in what organ is the storage form of D3 converted to its active form? what enzyme? what hormone stimulates this action?
kidney; 1 alpha hydroxylase; Parathyroid hormone
other than increase Parathyroid hormone what else increases 1 alpha hydroxylase activity in the kidney?
decreased serum phosphate
other than bone resorption to release Ca and phosphate, what is the ultimate point of increasing the serum Ca2+ and phosphate?
to increase serum Ca and phosphate for bone deposition
what does Vit D stimulation of osteoblasts do?
release alk phos
from where is alk phos release in the bone? what enzyme does it act on? what is the result?
osteoblasts; de phosphorylates pyrophosphate which inhibits bone mineralization; bone mineralization
what is rickets? what is it caused by?
bendy bones seen in children due to decreased Vit D; craniotabes, skeletal deformities, growth retardation, rosary
what is the difference between rickets and osteomalacia?
osteomalacia is vit D def seen in adults and causes bowed legs and results in increased fractures
what is scurvy caused by? rickets?
def in Vit C; def in Vit D
T/F Breast milk has a lot of Vit D and K
False- has little of both!
what can cause hypervitaminosis D?
iatrogenic, granulomatous disease (sarcoidosis d/t epitheloid macrophage release of calcitriol); hypercalcemia, hypercalciuria (renal calculi!), loss of appetite, stupor
what can cause a def in vit D?
renal failure, decreased sun, fat malabsorption, chronic liver disease, p450 induction, hypoparathyroidism (activates 1 alpha hyrdoxylase)
T/F p450 induction increases Vit D levels.
false! actually decreases by increased metabolism
what are the two main function of Vit E?
helps make Vit K and antioxidant
which cells have the most FA and thus are the most susceptible to FR injury?
neurons and RBCs
where is antioxidant activity of Vit E most important?
neurons and RBCs
which oxidant is most attributable to damage of RBCs?
LDL; LDL oxidize atherosclerosis
what is the effect of defiiency of VIt E?
hemolytic anemia (fragility of RBCs), muscle weakness and posterior column and spinocerebellar tract demyelination (neuron damage) resulting in decreased proprioception and vibration sensation, and peripheral neuropathy, and retinal degeneration
what is def of Vit E caused by?
fat malabsorption (CF) and abetalipoproteinemia (damage takes up all antioxidants)
which antioxidant does cigarette smoke injury eat up? which antioxidant does LDL injury eat up?
Vit C; Vit E
What is the function of Vit K?
catalyze gamma carboxylation of glutamic acid residues on coag factors so they can bind to Ca complex
how is Vit K activated? what drug blocks this? what is the source of Vit K?
by epoxide reductase in the liver; coumadin; intestinal flora and leafy vegetables
what vit def occur from antibiotic use?
biotin (vit B7) and Vit K
what factors is Vit K responsible for the synthesis? and what else?
10, 9, 7, 2; protein C and S
what vitamin is given at birth to prevent hemorrhage? why?
vit K; neonates have sterile intestine and can not synthesize vit K
what does deficiency of Vit K cause?
hemorrhage with increased PT and PTT time but normal bleeding time
what can cause deficiency in Vit K?
prolonged Ab use
what does excess Vit K cause?
hemolytic anemia; jaundice in newborn if mom gets too much vit K
what are the functions of zinc?
(cofactor for 100+ enzymes!) needed for zinc fingers transcription motif, collagen synthesis, alcohol metabolism
what does a def in zinc result in?
delayed wound healing, hypogonadism, decreased adult hair, dysgeusia, anosmia, and alcoholic cirrhosis, perioral rash
what is dysgeusia?
inability to taste
what are causes of zinc deficiencies?
alcoholism, RA, inflammatory disease, chronic diarrhea
what is the first enzyme and step in ethanol metabolism? second step? what is a cofactor in both of these steps? what vitamin does this come from?
alcohol dehyrogenase (alcohol to acetaldehyde); acetaldehyde dehydrogenase (acetaldehyde to acetate); NAD+; B3 (niacin)
which is the rate limiting enzyme in ethanol metabolism? where is this enzyme located? where is the other enzyme located? what is the limiting reagent?
alcohol dehydrogenase; cytosol; mitochondria; NAD+
what kind of kinetics does alcohol dehydrogenase work under? what are the implications of this?
zero order; increased production of NADH no matter the amount of end products produced
what drug blocks alcohol dehydrogenase? what is it used for?
fomepizole; antidote for methanol or ethylene glycol poisoning
what drug blocks acetaldehyde dehyrogenase? what are its side effects?
disulfiram (antabuse); acetaldehyde accumulate contributing to hangover
what are the three results that come from increased NADH in alcohol metabolism?
pyruvate to lactate (results in lactic acidosis and decreased pyruvate for oxaloacetate for gluconeogenesis), increased production of glycerol 3 phosphate from DHAP for TG synthesis; and increased betahydroxybutyrate ketoacid production from increased acetate
what contributes to the acidosis in alcoholism?
lactic acidosis and ketoacidosis
what three things contribute to fatty change in the liver in alcoholism?
increased G3P for TG synthesis, increased acetyl CoA (Fatty acid synthesis for TG synthesis), and decreased oxidation of FA in the mitochondria due to alcohols toxicity on the mit
what causes hypoglycemia in alcoholism?
decreased substrate for gluconeogenesis (pyruvate to lactate and not oxaloacetate); and pyruvate doing only lactic acidosis and not glycolysis
what causes gout in alcoholism?
increased acid production competes with uric acid for excretion
what else decreases production of oxaloacetate in alcoholism other than decreased pyruvate?
oxaloacetate gets shifted to malate d/t excess NADH
what is hepatocellular steatosis?
hepatic fatty change
what liver enzymes are increased in alcoholism? why?
AST (mit damage), and GGT (d/t SER hyperplasia d/t induction of p450 generation)
what does alcohol do to the P450 system?
induction in chronic alcoholism (increases tolerance); inhibition in acute alcoholism
why is there decreased immunity in kwashiokor and marasmus?
no protein!
what explains the fatty change in kwashiokor?
abetalipoproteinemia and increased G3P production from all the carbs!
what is the swollen belly from in a child with kwashiokor?
ascites from liver damage
how does a kwashiokor patient present?
malnutrition, edema (hypoalbuminemia), anemia liver (fatty change), diarrhea d/t no brush border enzymes (no protein!)
what results in marasmus? what kind of muscle wasting? what kind of muscle wasting do you see in kwashiokor?
loss of subcutaneous fat, tissue and muscle wasting (somatic muscle); visceral, not somatic
T/F kwashiokor patients are calorie deficient
false!
what causes liver damage in kwashiokor?
increased TG synthesis from increased Glycerol 3 P and abetalipoproteinemia
