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23 Cards in this Set
- Front
- Back
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Fat soluble vitamins
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ADEK
-Toxicity more common (accumulate in fat) -Malabsorption syndromes (cystic fibrosis, sprue, mineral oil intake which result in steatorrhea can cause malabsorption) |
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Associated metabolite for the following water soluble vitamins
(a) B1 (b) B2 (c) b3 (d) B5 (e) B6 (f) B12 |
Associated metabolite for the following water soluble vitamins
(a) B1 (thiamine: TPP) (b) B2 (riboflavin: FAD, FMN) (c) b3 (Niacine: NAD+) (d) B5 (pantothenic acid: CoA) (e) B6 (pyridoxine: PLP) (f) B12 (cobalamin) Note biotin and folate are also water soluble and that all water soluble vitamins are easily washed out from body except folate and B12 which are stored in liver. |
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VitA (retinol)
(a) aka (b) Fct/Source (c)Deficiency (d) excess |
(a) retinol
(b) Antioxidant; constituent of retinal visual pigments; found in liver and leafy vegetables (c) night blindness, dry skin (d) excess gives you arthralgias, HA, skin changes, sore throat, alopecia, teratogenic (cleft palate, cardiac abnormalities) |
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VitB1
(a) aka (b) Fct/Source (c)Deficiency |
(a)thiamine
(b) thiamine pyrophosphate is a cofactor for several enzymes: -pyruvate dehydrogenase (glycolysis) -alpha ketoglutarate (TCA) -transketolase (HMP shunt) -branched chain AA dehydrogenase (c)Wernicke Korsakoff syndrome and berber. Seen in malnutrition and alcoholism. |
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Wenicke Korsakoff
(a) cause (b) clinical presentation |
(a) B1 deficiency
(b) confusion, ataxia+memory loss, confabulation, personality change. |
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Beriberi
(a) cause (b) clinical presentation |
(a) B1 deficiency
(b) Dry beriberi-polyneuritis, symmetrical muscle wasting Wet beriberi-high output cardiac failure (dilated cardiomyopathy), edema. |
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VitB2
(a)aka (b) Fct (c)Deficiency |
(a) riboflavin
(b) cofactor in oxidation and reduction (FAD and FMN derived from B2; B2=2ATP) (c) Cheilosis (inflammation of lips, scaling, fissures at corner of mouth), corneal vascularization |
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VitB3
(a) AkA (b) Fct (c)Deficiency/Causes (d) excess |
(a) niacin
(b) Constituent of NAD+, and NADP+ (used in redox rxn). Derived from tryptophan (b3=3NAD+) (c) Glossitis. Severe deficiency leads to pellagra (diarrhea, dermatitis, dementia); may be caused by Hartnup disease (decr. Tryptophan absorption), malignant carcinoid syndrome (incr tryptophan metabolism), and INH (decr vitB6-need to turn tryp into B3). (d) Excess causes flushing |
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VitB5
(a) aka (b) Fct (c)deficiency |
(a) pantothenate
(b) essential component of CoA (a cofactor for acyl transfers) and FA synthesis (c) dermatitis, enteritis, alopecia, adrenal insufficiency |
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VitB6
(a) AKA (b) Fct (c)Deficiency |
(a) pyridoxine
(b) Converted to pyridoxal phosphate, a cofactor used for transamination, decarboxylation, glycogen phosphrylase, and heme synthesis. Required for synthesis of niacin from tryptophan. (c) Convulsions, hyperirritability, peripheral neuropathy (deficiency inducible by INH and contraceptives). |
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vitB12
(a) AKA (b) Fct (c)Deficiency (d) causes of deficiency |
(a) cobalamin
(b) Cofactor for homocysteine methyltransferase and methylmalonyl CoA mutase (c) Macrocytic megaloblastic anemia; neuro symptoms (parasethsia, subacute combined degeneration) due to abnormal myelin. Prolonged deficiency leads to irreversible damage. (d) Large reserve pool mainly in liver; cause usually malabsorption (sprue, diphyllobothrium latum), lack of IF (PA, gastric bypass surgery), or absence of terminal ileum. |
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Folic acid
(a) function/source (b) deficiency (c) causes of deficiency |
(a) Converted to THF used for 1 carbon transfer rxns/found in green leaves and small reserve in liver
(b) macrocytic, megaloblastic anemia; most common vit def in US. (c) seen in alcoholism and pregnancy (supplementation reduces neural tube defects); can be caused by several drugs (MTX, phenytoin, sulfonamides) |
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S-adenosyl-methionine
(a) fct (b) causes of deficiency |
(a) ATP+methionine =SAM which transfers methyl units.
(b) regeneration of methionine from homocysteine (and thus SAM) depends on vitB12 and folate. |
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Biotin
(a) fct (b) deficiency (c) causes of deficiency |
(a) Cofactor for carboxylation enzymes:
Pyruvate carboxylase: pyruvate-->oxaloacetate Acetyl coA carboxylase: avetyl CoA-->malonyl-CoA Propionyl CoA carboxylase: propionyl CoA-->methylmalonyl CoA (b) Rare. Dermatitis, alopecia, enteritis. (c) Antibiotic use or excessive ingestion of raw eggs (as avidin in egg whites binds biotin) |
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VitC
(a) AKA (b) Fct (c)Deficiency |
(a) ascorbic acid
(b) Antioxidant. Also: 1-facilitates iron absorption by keeping it in reduced state (more abs) 2-Necessary for hydroxylation of proline and lysin in collagen synth 3-Necessary for dopamine beta hydroxylase, which converts dopamine to NE (c) deficiency leads to scurvy (swollen gums, bruising, anemia, poor sound healing). |
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VitD
(a) different forms/sources (b) fct (c) deficiency (d) excess/cause |
(a) D2=ergocalciferol-ingested from plants and used as a pharm agent
D3=cholecalciferol-consumed in milk, formed in sun exposed skin 25-OH D3=storage form 1,25 (OH)2D3=calcitriol=active form (b) incr intestinal absorption of Ca2+ and phosphate, incr bone resorption (c) Rickets in children (bending bones) and osteomalacia in adults (soft bones), hypocalcemic tetany (d) Excess leads to hypercalcemia, hypercalcuria, loss of appetite, stupor. Seen in sarcoidosis (incr activation of vitD by epithelioid macs) |
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VitE
(a) fct (b) Deficiency |
(a) Antioxidant (protects erythrocytes and membranes from free radical damage)
(b) increased RBC fragility (hemolytic anemia), muscle weakness, motor dysfct |
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VitK
(a) fct (b) deficiency (c) causes |
(a) Catalyzes gamma carboxylation of glutamic acid on coag factors in the liver (II, VII, IX, X, protein C and S)
(b) Neonatal hemorrhage with incr PT and PTT but normal bleeding time (neonates have sterile intestines). (c) being a neonate (thus given an injection at birth); prolonged use of antibiotics |
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Zinc
(a) fct (b) deficiency |
(a) Essential for the activity of many anzymes. Important in formation of zinc fingers.
(b) delayed wound healing, hypogonadism, decr adult hair (axillary, facial, pubic). May predispose to alcoholic cirrhosis. |
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MOA of fomepizole and disulfiram
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EtOH-->acetaldehyde-->acetate (NAD+-->NADH at both steps)
Fomepizole inhibits alcohol dehydrogenase. Disulfiram (antabuse) inhibits acetaldehyde dehydrogenase (which incr acetaldehyde which contributes to hangover sx) |
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Mechanism of ethanol hypoglycemia
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EtOH increased NADH/NAD+ratio in liver, which diverts pyruvate to lactate and OAA to malate inhibiting gluconeogenesis and stimulationg FA synth. Leads to hypoglycemia and hepatic fatty change seen in chronic alcoholics.
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Describe kwashiorkor
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Protein malnutrition causing skin lesions, edema, liver malfunction (fatty change). Clinically see child with swollen belly.
MEAL (malnutrition, edema, anemia, liver is fatty) |
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Describe marasmus
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Energy malnutrition results in tissue and muscle wasting, loss of subq fat and variable edema.
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