Quick Answer
Vitamins contribute 4–6 NEET PG questions per paper across Biochemistry, Medicine and PSM. The exam-ready framework:
- Fat-soluble (ADEK) — stored, toxicity possible, malabsorption causes deficiency.
- Water-soluble (B-complex + C) — daily intake needed, B12 is the exception (liver stores 3–5 years).
- Classic syndromes — scurvy (C), beriberi (B1), pellagra (B3), megaloblastic anaemia (B12, B9), rickets (D), night blindness (A).
- Biochemical tests — erythrocyte transketolase (B1), MMA + homocysteine (B12), 25-OH vitamin D (D), prothrombin time (K).
- Toxicity — hypervitaminosis A (pseudotumor cerebri), D (hypercalcaemia), and pyridoxine (sensory neuropathy).
Vitamins are organic micronutrients required in milligram or microgram quantities for enzyme cofactor function, gene regulation and antioxidant defence. NEET PG examiners love vitamins because the questions blend pure biochemistry (cofactor chemistry) with bedside medicine (deficiency syndromes) and public health (national fortification programmes). A disciplined approach — solubility class, cofactor role, deficiency picture, biochemical test, toxicity — wins the marks.
This NEETPGAI deep dive walks through every NEET-PG-relevant vitamin, the biochemical reactions they participate in, the classic deficiency vignettes, and the laboratory tests that pin them down. Pair this with the Biochemistry common mistakes guide and the anaemias classification primer for full coverage.
Fat-soluble vitamins (A, D, E, K)
Fat-soluble vitamins require bile salts and pancreatic lipase for absorption. They travel in chylomicrons through the lymphatic system and are stored in the liver and adipose tissue. Malabsorption syndromes (cystic fibrosis, coeliac disease, chronic pancreatitis, cholestasis, ileal resection) cause combined ADEK deficiency.
Vitamin A (retinol, retinal, retinoic acid)
- Function: retinal forms rhodopsin (rod photoreceptors); retinoic acid regulates gene transcription via RAR/RXR receptors; supports epithelial differentiation and immune function.
- Sources: liver, fish-liver oil, eggs, milk (preformed retinol); carrots, leafy greens, sweet potato (beta-carotene precursor).
- Deficiency: night blindness (earliest), Bitot's spots (foamy keratin patches on conjunctiva), xerophthalmia, keratomalacia, follicular hyperkeratosis, recurrent infections. Leading cause of preventable childhood blindness globally.
- Toxicity: acute — headache, vomiting, raised ICP. Chronic — alopecia, dry skin, hepatotoxicity, bone pain, hypercalcaemia. Teratogenic — isotretinoin causes craniofacial, cardiac and CNS malformations.
- NEET PG trap: beta-carotene excess causes carotenoderma (yellow skin, sparing sclera) — benign, NOT toxicity.
Vitamin D (cholecalciferol → 1,25-dihydroxyvitamin D)
- Synthesis: 7-dehydrocholesterol → cholecalciferol (skin, UVB) → 25-OH-D (liver) → 1,25-(OH)2-D (kidney, 1-alpha-hydroxylase).
- Function: raises serum calcium and phosphate via gut absorption, bone resorption and renal reabsorption.
- Deficiency: rickets (children) — bowing of legs, rachitic rosary, frontal bossing, delayed fontanelle closure, widened wrists; osteomalacia (adults) — bone pain, proximal myopathy, Looser's zones (pseudofractures).
- Lab: low 25-OH vitamin D (best test), low Ca, low PO4, raised ALP, raised PTH.
- Toxicity: hypercalcaemia, nephrocalcinosis, soft-tissue calcification. Rare with native vitamin D; common with calcitriol overdose.
Vitamin E (alpha-tocopherol)
- Function: lipid-soluble antioxidant; protects PUFAs in cell membranes from peroxidation.
- Deficiency: rare; haemolytic anaemia in newborns (especially preterm), peripheral neuropathy, spinocerebellar ataxia, pigmented retinopathy. Seen in abetalipoproteinaemia.
- Toxicity: raised bleeding risk (interferes with vitamin K-dependent clotting).
Vitamin K (phylloquinone K1, menaquinone K2)
- Function: cofactor for gamma-glutamyl carboxylase — gamma-carboxylates glutamate residues on factors II, VII, IX, X, protein C and protein S.
- Deficiency: bleeding diathesis, haemorrhagic disease of the newborn (low maternal stores + sterile gut + low breast milk content). Indian Academy of Pediatrics recommends 1 mg IM at birth.
- Antagonist: warfarin inhibits vitamin K epoxide reductase (VKORC1). Reverse with vitamin K (slow) or 4-factor PCC (fast).
- NEET PG trap: PT/INR is the most sensitive test (factor VII has the shortest half-life).
Water-soluble vitamins — B-complex
Vitamin B1 (thiamine)
- Cofactor (TPP) for: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, branched-chain alpha-keto acid dehydrogenase, transketolase (HMP shunt).
- Deficiency:
- Wet beriberi — high-output cardiac failure, peripheral oedema.
- Dry beriberi — symmetrical peripheral neuropathy, muscle wasting.
- Wernicke encephalopathy — confusion + ophthalmoplegia + ataxia (CAN — Confusion, Ataxia, Nystagmus). Mammillary body involvement on MRI.
- Korsakoff psychosis — anterograde amnesia + confabulation (irreversible).
- Lab: raised erythrocyte transketolase activity after TPP loading.
- Treatment: IV thiamine BEFORE glucose in suspected Wernicke (glucose precipitates Wernicke in deficient patients).
Vitamin B2 (riboflavin)
- Cofactor: FMN, FAD — electron carriers in the ETC and many oxidoreductase reactions.
- Deficiency: angular stomatitis, cheilosis, magenta tongue (glossitis), seborrheic dermatitis, normocytic anaemia, photophobia.
Vitamin B3 (niacin)
- Cofactor: NAD+, NADP+ (synthesised endogenously from tryptophan via 60:1 conversion).
- Deficiency — pellagra (3 D's): Dermatitis (photosensitive Casal's necklace), Diarrhoea, Dementia, Death.
- Causes: maize-dependent diet (niacin in maize is bound), Hartnup disease (defective tryptophan absorption), carcinoid syndrome (tryptophan diverted to serotonin), prolonged isoniazid therapy.
- Pharmacology: niacin (1.5–2 g/day) raises HDL but causes flushing (prostaglandin-mediated, reduced by aspirin pre-treatment).
Vitamin B5 (pantothenic acid)
- Cofactor: coenzyme A (acyl carrier in fatty acid synthesis, TCA cycle); ACP of fatty acid synthase.
- Deficiency: rare — burning feet syndrome, dermatitis.
Vitamin B6 (pyridoxine → pyridoxal phosphate)
- Cofactor: transaminations (AST, ALT), decarboxylations (heme synthesis — ALA synthase, neurotransmitter synthesis — GABA, dopamine, serotonin, histamine), glycogen phosphorylase.
- Deficiency: sideroblastic anaemia (microcytic with ringed sideroblasts), peripheral neuropathy, seizures (especially neonatal, INH-induced), cheilosis.
- Drug interaction: isoniazid binds pyridoxine → deficiency neuropathy. Always co-prescribe pyridoxine 10–40 mg/day.
- Toxicity: sensory neuropathy with chronic high-dose (>200 mg/day).
Vitamin B7 (biotin)
- Cofactor: carboxylase enzymes — pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase, methylcrotonyl-CoA carboxylase.
- Deficiency: dermatitis, alopecia, lactic acidosis. Seen with raw egg-white ingestion (avidin binds biotin) and prolonged TPN.
Vitamin B9 (folate)
- Function: one-carbon transfers — purine and pyrimidine synthesis (dTMP from dUMP via thymidylate synthase), methionine regeneration.
- Sources: leafy greens, legumes, fortified cereals; destroyed by prolonged cooking.
- Deficiency: macrocytic megaloblastic anaemia, hypersegmented neutrophils (>5 lobes), glossitis, raised homocysteine, neural tube defects in fetus.
- Drugs causing deficiency: methotrexate (DHFR inhibitor), trimethoprim, phenytoin, sulfasalazine, oral contraceptives.
- NEET PG trap: giving folate alone in B12 deficiency reverses anaemia but worsens neuropathy — always confirm B12 first.
Vitamin B12 (cobalamin)
- Cofactor: methylmalonyl-CoA mutase (propionate to succinate); methionine synthase (homocysteine + methyl-tetrahydrofolate to methionine + THF).
- Absorption: dietary B12 → bound to R-protein in stomach → released by pancreatic proteases in duodenum → binds intrinsic factor (parietal cells) → absorbed in terminal ileum via cubilin receptor.
- Sources: animal products only (meat, fish, eggs, dairy). Strict vegans need supplements.
- Deficiency: macrocytic megaloblastic anaemia + subacute combined degeneration (dorsal column ataxia, corticospinal weakness, glove-and-stocking neuropathy).
- Causes: pernicious anaemia (autoimmune anti-intrinsic factor, anti-parietal cell antibodies), gastrectomy, terminal ileal disease (Crohn, resection), tropical sprue, fish tapeworm (Diphyllobothrium latum).
- Lab: low serum B12, raised methylmalonic acid, raised homocysteine, Schilling test (historical).
Vitamin C (ascorbic acid)
- Function: cofactor for prolyl and lysyl hydroxylase (collagen synthesis), dopamine beta-hydroxylase (noradrenaline synthesis), iron absorption (reduces Fe3+ to Fe2+), antioxidant.
- Deficiency — scurvy: swollen bleeding gums, perifollicular haemorrhage, corkscrew hairs, poor wound healing, subperiosteal haemorrhage, anaemia (mixed iron/folate). High-yield in NEET PG.
- Sources: citrus fruits, amla (Indian gooseberry — highest natural source), guava, capsicum.
- Toxicity: rare — oxalate kidney stones with chronic mega-dose.
Biochemical tests at a glance
| Vitamin | Best test |
|---|
| A | Serum retinol; dark adaptometry |
| D | 25-OH vitamin D (storage form) |
| E | Serum alpha-tocopherol |
| K | PT/INR |
| B1 | Erythrocyte transketolase activity (with TPP loading) |
| B6 | Plasma PLP |
| B9 | RBC folate (more reliable than serum) |
| B12 | Serum B12 + methylmalonic acid + homocysteine |
| C | Plasma or leucocyte ascorbic acid |
NEET PG MCQ traps (high-yield list)
- Wernicke before glucose — IV thiamine first in suspected Wernicke; glucose precipitates encephalopathy.
- Folate masks B12 — folate corrects anaemia but not neuropathy; always check B12.
- Methylmalonic acid is specific for B12 — homocysteine rises in both B12 and folate deficiency.
- Niacin from tryptophan — Hartnup, carcinoid, INH all impair this conversion.
- Vitamin K in newborns — IM injection prevents haemorrhagic disease; oral preparation has higher failure rate.
- Isoniazid + pyridoxine — always combined to prevent peripheral neuropathy.
- Beta-carotene yellow skin — sclera spared; harmless. Jaundice — sclera yellow.
- Scurvy bone changes — subperiosteal haemorrhage, scorbutic rosary (sharp angle, vs rachitic which is rounded).
- Vitamin A teratogenicity — isotretinoin contraindicated in pregnancy; pregnancy test before prescription.
- Pellagra in carcinoid — tryptophan diverted to serotonin; treat with niacinamide.
- Pernicious anaemia — autoimmune destruction of parietal cells; raised gastrin, achlorhydria, increased gastric cancer risk.
- Folic acid 4 mg/day — for women with previous NTD pregnancy; 400 mcg standard.
Recent updates (2025–2026)
- WHO 2024: vitamin A supplementation continues for children 6–59 months in high-mortality countries (200,000 IU 6-monthly); India runs the National Vitamin A Prophylaxis Programme.
- IAP 2025: vitamin D 400 IU/day for all infants 0–12 months; 600 IU/day from 1 year.
- NMC 2024 syllabus lists vitamin biochemistry under both Phase 1 (Biochemistry) and Phase 3 (Medicine), reinforcing high MCQ frequency.
- Anaemia Mukt Bharat (India): integrated iron-folic acid supplementation for adolescents and pregnant women — a high-yield PSM crossover topic.
Frequently Asked Questions
Which vitamins are fat-soluble and which are water-soluble?
Fat-soluble vitamins are A, D, E and K — they require bile and dietary fat for absorption and are stored in liver and adipose tissue. All other vitamins (B-complex group: B1, B2, B3, B5, B6, B7, B9, B12 and vitamin C) are water-soluble. Water-soluble vitamins are not stored in significant amounts (except B12) and require regular dietary intake.
What is the classic triad of pellagra?
Pellagra is caused by niacin (vitamin B3) deficiency and presents with the classic 3 D's — Dermatitis (sun-exposed areas with photosensitive Casal's necklace), Diarrhoea, and Dementia. A fourth D, Death, occurs if untreated. It is seen in maize-dependent populations, carcinoid syndrome, Hartnup disease and isoniazid therapy.
How does vitamin B12 deficiency differ from folate deficiency?
Both cause megaloblastic anaemia with macrocytic red cells and hypersegmented neutrophils. Only B12 deficiency causes neurological features — subacute combined degeneration of the spinal cord (dorsal column and corticospinal tract). Methylmalonic acid is raised in B12 deficiency only; homocysteine is raised in both. Always treat B12 first to prevent worsening of neuropathy.
What causes hypervitaminosis A and how does it present?
Hypervitaminosis A is caused by chronic excess vitamin A (retinol >25,000 IU/day for months) or acute ingestion (>100,000 IU). Features include pseudotumor cerebri (raised ICP, papilledema, headache), hepatotoxicity, alopecia, dry skin, bone pain and teratogenicity. Isotretinoin is contraindicated in pregnancy because of severe craniofacial and cardiac malformations.
Which vitamin prevents neural tube defects and what is the recommended dose?
Folate (vitamin B9) deficiency in early pregnancy causes neural tube defects (spina bifida, anencephaly, encephalocele). All women planning pregnancy should take 400 micrograms folic acid daily, starting at least 1 month before conception and continuing through the first trimester. Women with a previous NTD pregnancy need 4 mg/day.
This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: May 2026
