Fat-soluble vitamins: ADEK — can accumulate and become toxic
Fat-Soluble Vitamins
Four vitamins stored in body fat — excess can reach toxic levels
A (retinol): vision and immune function. D (calciferol): calcium absorption, bone. E (tocopherol): antioxidant. K (phylloquinone): blood clotting. Stored in liver and adipose tissue.
A
Vision, immune function
D
Calcium absorption, bone health
E
Antioxidant
K
Blood clotting
Water-Soluble Vitamins
Water-soluble: B vitamins + C — excess is urinated out safely
Water-Soluble Vitamins
Eight B vitamins plus vitamin C — not stored, need regular intake
Without vitamin C, proline and lysine residues can't be hydroxylated → unstable collagen → bleeding gums, poor wound healing, bruising, joint pain. Killed sailors on long voyages before citrus was understood.
Vitamin D Deficiency
Vitamin D deficiency: rickets (children — bowed bones), osteomalacia (adults)
Vitamin D Deficiency
Vitamin D is needed for calcium absorption — deficiency weakens bones
Made in skin from UV-B sunlight. Deficiency: rickets in children (soft, bowing bones), osteomalacia in adults (soft bones, pain). Also linked to immune dysfunction and depression. Common in northern latitudes.
Folate and B12
Folate (B9): DNA synthesis and repair — deficiency causes neural tube defects and megaloblastic anemia
Folate and B12
Two B vitamins that work together — deficiency in either causes anemia
Folate: required for nucleotide synthesis (DNA building blocks). Deficiency in early pregnancy → neural tube defects. B12: required for myelin synthesis and folate metabolism. Deficiency: megaloblastic anemia, neurological damage.
Thiamine — Vitamin B1
B1 thiamine: energy metabolism cofactor. Deficiency = beriberi (peripheral neuropathy) or Wernicke's (alcoholics)
Thiamine — Vitamin B1
The vitamin that alcoholics most commonly lack
Thiamine pyrophosphate (TPP — the active coenzyme form of B1): cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, transketolase. Beriberi: dry (peripheral neuropathy, muscle weakness), wet (heart failure, edema). Wernicke-Korsakoff syndrome: alcoholics — Wernicke's (confusion, ataxia, eye movement issues) → Korsakoff's (irreversible memory loss).
Riboflavin — Vitamin B2
B2 riboflavin: component of FAD and FMN — electron carriers in ETC. Deficiency = ariboflavinosis (cracks at corners of mouth)
Riboflavin — Vitamin B2
The vitamin whose deficiency causes characteristic mouth sores
Riboflavin forms FAD (flavin adenine dinucleotide) and FMN (flavin mononucleotide) — electron carriers in the electron transport chain. Deficiency (ariboflavinosis): angular cheilitis (cracks at corners of mouth), glossitis (inflamed tongue), seborrheic dermatitis. Rare in isolation — usually with other B vitamin deficiencies.
Niacin — Vitamin B3
B3 niacin: component of NAD⁺ and NADP⁺. Deficiency = pellagra — 4 Ds: Diarrhea, Dermatitis, Dementia, Death
Niacin — Vitamin B3
The vitamin whose deficiency causes pellagra
Niacin forms NAD⁺ and NADP⁺ — critical electron carriers in metabolism. Pellagra: the 4 Ds — Diarrhea, Dermatitis (sun-sensitive rash on exposed skin), Dementia, Death. Historically common where corn was the dietary staple (niacin in corn is bound form). High-dose niacin: raises HDL (High Density Lipoprotein — good cholesterol), lowers triglycerides.
The vitamin that requires a specialized carrier for absorption
B12 requires intrinsic factor (from gastric parietal cells) for absorption in ileum. Pernicious anemia: autoimmune destruction of parietal cells → no intrinsic factor → B12 deficiency. Subacute combined degeneration of spinal cord: B12 deficiency damages posterior and lateral spinal columns. Vegans at risk — B12 only in animal products.
Vitamin A
Vitamin A (retinol): vision (rhodopsin), immune function, epithelial integrity. Deficiency = night blindness.
Vitamin A
Fat-soluble vitamin essential for vision and epithelial health
Retinal (from retinol): component of rhodopsin — visual pigment in rod cells. Retinoic acid: regulates gene expression, epithelial differentiation. Deficiency: night blindness (earliest sign), xerophthalmia (dry eyes), increased infection susceptibility. Toxicity: teratogenic in pregnancy (liver, isotretinoin).
Vitamin K
Vitamin K: essential for blood clotting factors II VII IX X. Warfarin works by blocking vitamin K recycling.
Vitamin K
The clotting vitamin — and the target of anticoagulant drugs
Vitamin K: cofactor for gamma-carboxylation of clotting factors II (prothrombin), VII, IX, X, and anticoagulant proteins C and S. K1 (phylloquinone): green leafy vegetables. K2 (menaquinone): bacteria, fermented foods. Warfarin: inhibits vitamin K epoxide reductase → can't recycle vitamin K → reduced clotting factor activity.
Essential Mineral Cofactors
Mineral cofactors: zinc (wound healing, immune, taste), iron (hemoglobin, ETC), iodine (thyroid hormones), calcium (bones, signaling)
Essential Mineral Cofactors
Four essential minerals and their key biochemical roles
Zinc: 300+ enzymes, wound healing, immune function, taste and smell, DNA synthesis. Deficiency: growth retardation, impaired immunity, hypogeusia. Iron: hemoglobin (O₂ transport), myoglobin, cytochromes. Iodine: thyroid hormones T3 (triiodothyronine) and T4 (thyroxine) — deficiency causes goiter, hypothyroidism, cretinism. Calcium: bones/teeth, muscle contraction, nerve signaling, second messenger.
Zinc
300+ enzymes, immunity, wound healing
Iron
Hemoglobin, ETC
Iodine
Thyroid hormones T3/T4
Calcium
Bones, muscle, nerve signaling
Mnemonic
What it means
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🎓 Common Exam Questions
Q: Distinguish fat-soluble from water-soluble vitamins — absorption, storage, and toxicity.
A: Fat-soluble vitamins (ADEK): absorbed with dietary fat via chylomicrons in the lymphatic system; stored in liver and adipose tissue; can accumulate to toxic levels with excess intake (hypervitaminosis A and D are clinically significant). Deficiency develops slowly due to stores. Water-soluble vitamins (B vitamins + C): absorbed directly into the bloodstream; not stored significantly; excess is excreted in urine (hence safer in supplementation). Deficiency develops relatively quickly. Exception: B12 is stored in the liver for 3-5 years. Clinical implication: fat malabsorption (celiac disease, Crohn's, pancreatic insufficiency) causes fat-soluble vitamin deficiencies even with adequate dietary intake.
Q: Explain the role of B vitamins as enzyme cofactors in metabolism.
A: B vitamins are precursors to coenzymes essential for energy metabolism. B1 (thiamine) → TPP: cofactor for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase (key Krebs enzymes). B2 (riboflavin) → FAD and FMN: electron carriers in ETC and beta-oxidation. B3 (niacin) → NAD+ and NADP+: the most important electron carriers in metabolism — accept hydride ions in glycolysis, Krebs, and beta-oxidation; NADP+ is used in biosynthetic reactions. B5 (pantothenate) → CoA: carrier of acyl groups in fatty acid synthesis and oxidation. B6 (pyridoxine) → PLP: cofactor for amino acid metabolism, transamination. B7 (biotin): cofactor for carboxylation reactions (pyruvate carboxylase, acetyl-CoA carboxylase).
Q: What is pernicious anemia and how does it relate to B12 deficiency?
A: Vitamin B12 (cobalamin) requires intrinsic factor (IF) — a glycoprotein produced by gastric parietal cells — for absorption in the terminal ileum. Pernicious anemia is an autoimmune condition where parietal cells are destroyed, eliminating IF production → B12 malabsorption even with adequate dietary intake. Consequences: megaloblastic anemia (impaired DNA synthesis → large, immature RBCs); subacute combined degeneration of the spinal cord (demyelination affecting posterior and lateral columns → sensory and motor deficits). Trap: B12 deficiency and folate deficiency both cause megaloblastic anemia, but only B12 deficiency causes neurological damage. Giving folate to a B12-deficient patient corrects the anemia but allows neurological damage to progress — dangerous.
Q: How does warfarin work and what is its relationship to vitamin K?
A: Vitamin K is a cofactor for gamma-carboxylation of glutamate residues in clotting factors II (prothrombin), VII, IX, and X, as well as proteins C and S. This carboxylation enables the clotting factors to bind calcium and activate. Vitamin K epoxide reductase recycles vitamin K from its oxidized (epoxide) form back to the active reduced form. Warfarin (Coumadin) inhibits vitamin K epoxide reductase — blocking vitamin K recycling → depleting active vitamin K → reduced carboxylation of clotting factors → anticoagulation. Reversal: vitamin K administration (restores active vitamin K). Antidote for overdose: fresh frozen plasma (provides active clotting factors immediately) plus vitamin K. Drug interactions: antibiotics killing gut bacteria (a source of vitamin K2) potentiate warfarin.
Q: What are the consequences of pellagra and what causes it?
A: Pellagra is niacin (B3) deficiency — historically common in populations subsisting on corn (maize) without lime treatment (nixtamalization releases bound niacin). Classic presentation: the 4 Ds — Diarrhea, Dermatitis (sun-exposed skin rash — casal collar), Dementia (encephalopathy), Death if untreated. Niacin is the precursor to NAD+ and NADP+ — without it, energy metabolism collapses. Special case: Hartnup disease (tryptophan transport defect) causes pellagra despite adequate niacin intake, because tryptophan is a precursor for niacin synthesis. Carcinoid syndrome also depletes tryptophan (diverted to serotonin synthesis) → secondary pellagra. Treatment: niacin supplementation. High-dose niacin also used pharmacologically to raise HDL cholesterol.