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What are the 4 fat-soluble vitamins?
A, D, E, K
What are the 9 water-soluble vitamins?
B1, B2, B3, B5, B6, B7, B9, B12, C
Why are fat-soluble vitamins more likely to cause toxicity?
They are stored in liver/adipose tissue, allowing them to accumulate.
How are dietary fat-soluble vitamins transported after intestinal absorption?
In chylomicrons.
What are the major functions of vitamin A?
Vision, gene transcription, growth, and differentiation.
What vitamin A derivative is required for vision?
Retinal; retinal + opsin forms rhodopsin.
What vitamin A derivative regulates gene transcription?
Retinoic acid, through nuclear RAR receptors.
What are the major findings of vitamin A deficiency?
Night blindness → xerophthalmia → Bitot spots → keratomalacia.~s
What are major toxicities of vitamin A excess?
Teratogenicity, increased intracranial pressure, dry skin/alopecia, bone abnormalities.
What are the 3 important retinoid drugs and their uses?
Tretinoin: acne; isotretinoin: severe acne; ATRA: acute promyelocytic leukemia.
How is vitamin D activated?
Skin: D3 → liver: 25-OH-D → kidney: 1,25-(OH)₂-D (calcitriol).
What is the active form of vitamin D and how does it work?
Calcitriol; binds VDR, a nuclear receptor, to alter gene transcription.
What is the main function of vitamin D?
Increase Ca²⁺ and phosphate availability, especially by increasing intestinal absorption.
What are the bone diseases caused by vitamin D deficiency?
Rickets in children; osteomalacia in adults.
What is the major toxicity of excess vitamin D?
Hypercalcemia.
What is the major function of vitamin E?
Antioxidant protection of membrane lipids.
What are classic findings of vitamin E deficiency?
Hemolytic anemia, ataxia, peripheral neuropathy, muscle weakness.
What is vitamin K required for?
γ-carboxylation of glutamate residues, allowing Ca²⁺ binding by clotting proteins.
Which clotting factors require vitamin K?
II, VII, IX, X, C, S.
How does warfarin work?
Inhibits vitamin K epoxide reductase → decreases regeneration of active vitamin K → decreases γ-carboxylation → anticoagulation.
What is the active form of vitamin B1?
TPP (thiamine pyrophosphate).
What enzymes require B1/TPP?
Pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, BCKDH, transketolase.
What are the major clinical manifestations of B1 deficiency?
Wernicke encephalopathy, Korsakoff syndrome, and beriberi.
What are the 3 classic features of Wernicke encephalopathy?
Confusion/encephalopathy, oculomotor dysfunction, ataxia.
What are dry vs wet beriberi?
Dry: peripheral neuropathy. Wet: high-output heart failure + edema.
What are the active forms of B2 and their main function?
FMN and FAD; electron transfer/redox reactions.
What are classic findings of B2 deficiency?
Dermatitis, cheilosis/angular stomatitis, glossitis, corneal vascularization.
What are the active forms of B3 and their functions?
NAD⁺/NADH: redox/electron transfer. NADP⁺/NADPH: reductive biosynthesis and antioxidant reactions.
What is pellagra and what causes it?
Niacin deficiency; classically diarrhea, dermatitis, dementia, death.
How can Hartnup disease cause pellagra?
↓ tryptophan absorption → ↓ niacin synthesis → pellagra.
What is B5's major function?
Forms CoA, which transfers acyl groups; also part of ACP.
What is the active form of B6 and its major function?
PLP; amino acid metabolism, especially transamination and decarboxylation.
What are important functions of B6 besides amino acid metabolism?
Heme synthesis, neurotransmitter synthesis, glycogen phosphorylase, cystathionine synthesis, niacin synthesis.
What does B6 deficiency cause, and what drug commonly causes it?
Peripheral neuropathy + sideroblastic anemia; isoniazid can cause B6 deficiency.
What is the major function of biotin (B7)?
Carries CO₂ for carboxylation reactions.
What are the 3 major biotin-dependent carboxylases?
Pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase.
How can raw egg whites cause biotin deficiency?
Avidin binds biotin and decreases its intestinal absorption.
What is the major function of folate (B9)?
THF carries one-carbon units required for purine and dTMP synthesis.
What does folate deficiency cause?
Megaloblastic anemia and increased risk of neural tube defects.
What are the 2 major B12-dependent reactions?
Methionine synthase: homocysteine → methionine. Methylmalonyl-CoA mutase: methylmalonyl-CoA → succinyl-CoA.
What is the folate trap?
B12 deficiency prevents methionine synthase from converting 5-methyl-THF → THF, trapping folate as 5-methyl-THF and causing a functional folate deficiency.
How do B12 and folate deficiency differ in labs?
Both: ↑ homocysteine. B12: ↑ methylmalonic acid. Folate: normal methylmalonic acid.
What uniquely distinguishes B12 deficiency from folate deficiency clinically?
Neurologic dysfunction occurs with B12 deficiency.
What causes pernicious anemia?
Autoimmune destruction of parietal cells → ↓ intrinsic factor → ↓ B12 absorption in terminal ileum.
What are the major functions and deficiency findings of vitamin C?
Collagen hydroxylation, antioxidant activity, ↑ iron absorption. Deficiency → scurvy: bleeding/fragile vessels, gum disease, poor wound healing, anemia.