Step by Step
ADEK
The four fat-soluble vitamins
Vitamins A, D, E, and K are fat-soluble — they dissolve in lipids, not water. They require dietary fat and bile salts for absorption from the intestine. They are stored in adipose tissue and the liver. Because they accumulate, toxicity (hypervitaminosis) is possible with excess intake — unlike water-soluble vitamins which are excreted in urine.
Memory trick: ADEK = 'A Dog Eats Kibble' — four fat-soluble vitamins.
A
Vitamin A — vision and epithelial integrity
Vitamin A (retinol, retinal, retinoic acid): Retinal → visual pigment (rhodopsin) in rods → night vision. Retinoic acid → gene regulation → epithelial cell differentiation. Deficiency: night blindness (first sign), xerophthalmia, keratomalacia. Toxicity: teratogenic (birth defects), liver damage, pseudotumor cerebri.
D
Vitamin D — calcium homeostasis
Vitamin D3 (cholecalciferol) from skin (UV) or diet → liver (25-hydroxylation) → kidney (1α-hydroxylation) → active 1,25-(OH)₂D₃ (calcitriol). Actions: increases Ca²⁺ absorption (intestine), Ca²⁺ reabsorption (kidney), bone resorption. Deficiency: rickets (children), osteomalacia (adults). Toxicity: hypercalcemia.
EK
Vitamin E and K
Vitamin E (tocopherol): fat-soluble antioxidant — protects membranes from lipid peroxidation. Deficiency: hemolytic anemia (RBCs), peripheral neuropathy. Vitamin K (phylloquinone/menaquinone): essential for carboxylation of clotting factors (II, VII, IX, X) and proteins C and S. Deficiency: bleeding (prolonged PT). Warfarin antagonizes vitamin K. Newborns given prophylactic vitamin K injection.
Applied Walkthrough
1
Fat-soluble vitamins are absorbed in chylomicrons alongside dietary fat — patients with fat malabsorption (Crohn's, celiac, cystic fibrosis) develop deficiencies of all four.
2
Vitamin A stored in liver stellate cells — chronic excess → liver toxicity. Pregnant women avoid high-dose vitamin A (isotretinoin is a vitamin A derivative — severely teratogenic).
3
Vitamin D synthesis: sun on skin → cholecalciferol → liver → 25-OH-D → kidney → 1,25-(OH)₂D (calcitriol). Kidney disease impairs the final step → secondary hyperparathyroidism.
4
Vitamin K deficiency: PT prolonged (extrinsic pathway factors VII, X, II affected). Newborns have sterile guts (no gut bacteria to make menaquinone) → hemorrhagic disease of the newborn → prophylactic vitamin K injection at birth.
Exam Application
Exams test which vitamins are fat-soluble (ADEK), their specific functions, deficiency diseases, and toxicity risks. Key: Vitamin A = night blindness + teratogenicity. Vitamin D activation pathway (liver → kidney). Vitamin K = clotting factors II, VII, IX, X + warfarin mechanism. Vitamin E = antioxidant + hemolytic anemia in deficiency.
⚠ Common Trap
Students forget that fat-soluble vitamins CAN be toxic — vitamin C (water-soluble) is mostly safe in excess, but vitamin A and D toxicity is clinically significant. Also: vitamin K deficiency causes bleeding but does NOT affect the aPTT (intrinsic pathway) as much as PT (extrinsic pathway) — factor VII has the shortest half-life and is affected first.
✓ Quick Self-Check
1. Name the four fat-soluble vitamins.
Vitamins A, D, E, and K — remembered as ADEK.
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2. Why can fat-soluble vitamins cause toxicity?
They are stored in fat tissue and liver rather than excreted, so excess accumulates and can reach toxic levels.
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3. What is the active form of vitamin D?
1,25-dihydroxycholecalciferol (calcitriol) — produced by sequential hydroxylation in the liver (25-OH) and kidney (1α-OH).
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4. What clotting factors require vitamin K?
Factors II (prothrombin), VII, IX, and X — plus proteins C and S. All require vitamin K-dependent γ-carboxylation to function.
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5. What is the first sign of vitamin A deficiency?
Night blindness — retinal is needed for rhodopsin synthesis in rod photoreceptors.
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