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Flashcards in biochem: nutrition Deck (52):

fat soluble vitamins

ADEK. absorption depends on gut and pancreas. toxicity more common b/c they accumulate in fat. malabsorption w/steatorrhea e.g. CF, sprue, mineral oil intake


water soluble vitamins

all Bs, C. all wash out easily except B12 and folate, which are stored in liver. B-deficiencies -> dermatitis, glossitis, diarrhea


vitamin A

= retinol, like retin-A, used topically for wrinkles and acne. found in liver and leafy veggies


vit A fxn

antioxidant, part of visual pigments, essential for differentiation into specialized tissue, prevents squamous cell metaplasia, Tx for measles and AML subtype M3


vit A deficiency

night blindness, dry, scaly skin, corneal degeneration, bitot spots on conjunctiva, immunosuppression


vit A excess

acute tox: nausea, vomiting, vertigo, blurred vision. chronic tox: alopecia, dry skin, hepatic toxicity/enlargement, arthralgias, pseudotumor cerebri. teratogenic: cleft palate, cardiac abnormalities.


vit B1

= thiamine. mnemonic: ATP: Alpha-ketoflutarate dehydrogenase, Transketolase, and Pyruvate dehydrogenase.


vit B1 fxn

cofactor for dehydrogenase rxns as part of TPP (e.g. links glycolysis to TCA cycle, part of TCA cycle, HMP shunt, and branched-chain ketoacid dehydrogenase


vit B1 deficiency

impaired glucose breakdown -> ATP depletion worsened by glucose infusion; highly aerobic tissues affected 1st (brain, heart). Wernicke-korsakoff syndrome and beriberi. seen in malnutrition and alcoholism. Dx by inc. in RBC transketolase activity following B1 administration


wernicke-korsakoff syndrome

confusion, opthalmoplegia, atatxia (classic triad), + confabulation, personality change, memory loss. damage to medial dorsal nucleus of thalamus and mammillary bodies


dry beriberi

polyneuritis, symmetrical muscle wasting. Ber1Ber1


wet beriberi

high-output cardiac failure (dilated cardiomyopathy), edema. Ber1Ber1


vit B2

= riboflavin


vit B2 fxn

component of flavins FAD and FMN, used as cofactors in redox rxns (e.g. succinate dehydrogenase rxn in TCA cycle).


vit B2 deficiency

2Cs = Cheilosis (inflammation of lips, scaling and fissures at mouth corners), Corneal vascularization


vit B3

= niacin


vit B3 fxn

constituent of NAD+, NADP+. derived from tryptophan. synthesis requires B2 and B6. used to treat dyslipidemia; lowers VLDL and raises HDL. N(AD) derived from Niacin


vit B3 deficiency

3 Ds: Diarrhea, Dementia (+ hallucinations), and Dermatitis (C3/C4 dermatome: broad collar rash and hyperpigmentation of sun-exposed limbs. Also glossitis and severe -> pellagra. can be caused by hartnup dz (dec. tryptophan absorption), malignant carcinoid syndrome (inc. tryptophan metabolism) and isoniazid (dec. B6).


vit B3 excess

facial flushing (induced by prostaglandin, can avoid by taking aspirin with niacin), hyperglycemia, hyperuricemia


vit B5 fxn

= panto("pento")thenic acid = essential component of CoA, the cofactor for acyl transfers, and fatty acid synthase


vit B5 deficiency

dermatitis, enteritis, alopecia, adrenal insufficiency


vit B6 fxn

= pyridozine. converted to PLP, a cofactor in transamination (e.g. AST, ALT), decarboxylation rxns, glycogen phosphorylase. necessary for synthesis of cystathionine, heme, niacin, histamine, 5HT, epinephrine, NE, DA, and GABA


vit B6 deficiency

convulsions, hyperirritability, peripheral neuropathy (inducible by isoniazid and OCPs), sideroblastic anemia


vit B7 fxn

= biotin = cofactor for carboxylation enzymes (add 1 C group): pyruvate carboxylase (pyruvate -> oxaloacetate), acetyl-CoA carboxylase (acetyl-CoA -> malonyl Co-A), and propionyl-CoA carboxylase (propionyl-CoA -> methylmalonyl-CoA


vit B7 deficiency

= rare. dermatitis, alopecia, enteritis. caused by Abx use or excessive ingestion of raw egg whites


vit B9

= folate. found in leafy greens. absorbed in jejunum. small reserve stored in the liver.


vit B9 fxn

converted to THF, a coenzyme for 1-C transfer/methylation rxns. important for synthesis of bases in DNA and RNA.


vit B9 deficiency

macrocytic, megaloblastic anemia, hypersegmented PMNs, glossitis, NO neuro symptoms. labs: inc. homocysteine, normal methylmalonic acid. most common deficiency in US. seen in EtOHics and pregnancy. also caused by phenytoin, sulfas, methotrexate. take folate to reduce risk of neural tube defects


vit B12

= cobalamin. found in animal products. synthesized only by microorganisms. large reserve pool (several years) stored in liver. absorbed w/intrinsic factor in terminal ileum


vit B12 fxn

cofactor for homocysteine methyltransferase and methylmalonyl-CoA mutase


vit B12 deficiency

macrocytic, megaloblastic anemia, hypersegmented PMNs, paresthesias, subacute combined degeneration (abnormal myelin). inc. serum homocysteine and methylmalonic acid levels. prolonged deficiency -> irreversible nerve damage. caused by veganism, malabsorption, lack of intrinsic factor, or lack of terminal ileum


pernicious anemia

anti-intrinsic factor Abs


vit C fxn

= ascorbic acid. antioxidant. facilitates Fe absorption by reducing it to Fe2+ state. necessary for hydroxylation of proline and lysine in collagen synthesis. necessary for DA conversion to NE via beta-hydroxylase. Tx for methemoglobinemia b/c it reduces Fe.


vit C deficiency

sCurvy due to Collagen synthesis defect. swollen gums, bruising, petechiae, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, "corkscrew" hair. weakened immune response


vit C excess

nausea, vomiting, diarrhea, fatigue, Ca oxalate nephrolithiasis. can inc. risk of Fe toxicity (e.g. people w/chronic blood Tx)


vit D

D2 = ergocalciferol, found in plants. D3 = cholecalciferol, consumed in milk, formed in sun-exposed skin (stratum basale). 25-OH D3 = storage form. 1,25-(OH)2D3 = cacitriol = active form.


vit D fxn

inc. intestinal absorption of Ca and phosphate, inc. bone mineralization.


vit D deficiency

rickets (bone pain and deformity) in children, osteomalacia (bone pain and muscle weakness) in adults. hypocalcemic tetany. deficiency exacerbated by no sun, skin pigment, and prematurity.


vit D excess

hypercalcemia, hypercalciuria, dec. appetite, stupor. seen in granulomatous dz (inc. activation of vit D by epithelioid macrophages)


vit E fxn

= tocopherol/tocotrienol. antioxidant, protecting RBCs and membranes from free radical damage. can enhance anticoagulant effects of warfarin


vit E deficiency

hemolytic anemia, acanthocytosis, muscle weakness, posterior column and spinocerebellar demyelination.looks like B12 deficiency but w/o megaloblastic anemia, hypersegmented PMNs, or inc. serum methylmalonic acid.


vit K fxn

= phytomenadione, phylloquinone, phytonadione. cofactor for gamma-carboxylation of glutamic acid residues on various clotting factors - II, VII, IX, X, proteins C and S. made by intestinal flora. K = Koagulation. warfarin = vit K antagonist


vit K deficiency

neonatal hemorrhage with inc. PT and aPTT but normal bleeding time. neonates have sterile intestines. can also be caused by prolonged use of broad spectrum Abx. not in breast milk so neonates are given an injection at birth


zinc fxn

essential for 100+ enzymes. zinc fingers = transcription factor motif


zinc deficiency

delayed wound healing, hypogonadism, dec. adult hair, dysgeusia, anosmia, acrodermatitis enteropathica. may predispose to alcoholic cirrhosis



from a protein-deficient MEAL: Malnutrition Edema Anemia, Liver (fatty). = protein malnutrition -> skin lesions, edema (dec. oncotic pressure), liver malfunction (fatty change from dec. apolipoprotein synthesis). small child w/swollen abd.



Marasmus -> Muscle wasting. = total calorie malnutrition -> tissue and muscle wasting, loss of subQ fat, and variable edema



inhibits EtOH dehydrogenase and is antidote for methanol or ethylene glycol poisoning



inhibits acetaldehyde dehydrogenase -> accumulation of acetaldehyde -> hangover Sx



= limiting reagent in EtOH metabolism


EtOH dehydrogenase...

operates via zero-order kinetics (enzyme = saturated, rate is not proportional to reagent [ ] )


EtOH metabolism -> inc. NADH/NAD+ ratio in liver causing:

pyruvate -> lactate (lactic acidosis
oxaloacetate -> malate (prevents gluconeogenesis -> fasting hypoglycemia)
dihydroxyacetone phosphate -> glycerol-3-phosphate (combines w/fatty acids to make triglycerides -> hepatosteatosis)
--> clinical picture of chronic alcoholism.
also disfavors TCA production of NADH -> ketoacidosis and lipogenesis (-> hepatosteatosis)