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Viva Questions: Vitamins and Minerals

Below are the most commonly asked viva questions, organized by topic, with concise exam-ready answers drawn from Robbins' Pathologic Basis of Disease, Harper's Illustrated Biochemistry, Lippincott Biochemistry, Guyton & Hall Physiology, and "Viva in Biochemistry" (Chatterjea).

PART A: FAT-SOLUBLE VITAMINS

Vitamin A (Retinol)

Q1. What are the fat-soluble vitamins? A, D, E, K. They require bile and pancreatic lipase for absorption.

Q2. What is the active form of Vitamin A?

11-cis-retinal (for vision)
Retinoic acid (for gene regulation and epithelial differentiation)
Retinol (transport form)

Q3. What are the functions of Vitamin A?

Maintenance of normal vision - forms rhodopsin (in rods) and iodopsin (in cones)
Maintenance of specialized epithelia (prevents squamous metaplasia)
Resistance to infection (especially measles)
Bone growth and reproduction

Q4. What is the visual cycle? / How does Vitamin A help in vision? Retinol is oxidized to all-trans-retinal, then isomerized to 11-cis-retinal, which combines with opsin to form rhodopsin. A photon causes isomerization back to all-trans-retinal, generating a nerve impulse. Night blindness occurs when retinol stores are depleted.

Q5. What are the deficiency features of Vitamin A?

Night blindness (earliest sign)
Xerophthalmia (dry eyes)
Bitot's spots (triangular foamy patches on conjunctiva)
Keratomalacia (corneal ulceration - can cause permanent blindness)
Squamous metaplasia of respiratory, urinary, and GI epithelia
Increased susceptibility to infections (especially measles)
Growth retardation in children

Q6. What is Xerophthalmia? Dryness of conjunctiva and cornea due to Vitamin A deficiency causing squamous metaplasia and loss of goblet cells in the conjunctival epithelium.

Q7. What is hypervitaminosis A? Toxicity from excess Vitamin A. Acute: headache, vomiting, diplopia, raised intracranial pressure. Chronic: alopecia, dry skin, bone pain, liver damage (perisinusoidal fibrosis - can lead to cirrhosis), teratogenicity in pregnancy.

Q8. What are the sources of Vitamin A?

Animal: cod liver oil, halibut oil, liver, butter, egg yolk
Plant (as beta-carotene): green leafy vegetables, yellow/red vegetables - carrots, papaya, sweet potato

Vitamin D (Cholecalciferol)

Q9. What is the active form of Vitamin D? 1,25-dihydroxycholecalciferol (calcitriol = 1,25-(OH)2-D3). It is formed by:

Skin: 7-dehydrocholesterol + UV light → Cholecalciferol (D3)
Liver: 25-hydroxylation → 25-OH-D3
Kidney: 1-hydroxylation → 1,25-(OH)2-D3 (calcitriol)

Q10. What are the functions of Vitamin D?

Increases intestinal absorption of calcium and phosphorus
Promotes bone mineralization
Increases renal tubular reabsorption of calcium
Regulates PTH secretion

Q11. What is Rickets? What are its features? Rickets = Vitamin D deficiency in children (before epiphyseal fusion). Features:

Bowing of legs (genu varum or genu valgum)
Rachitic rosary (beading of ribs at costochondral junction)
Harrison's sulcus (groove along diaphragm attachment)
Craniotabes (softening of skull)
Delayed dentition and fontanelle closure
Knock knees, pigeon chest

Q12. What is Osteomalacia? Vitamin D deficiency in adults (after epiphyseal fusion) - causes softening of bones with inadequate mineralization. Features: bone pain, proximal muscle weakness, pathological fractures, Looser's zones on X-ray.

Q13. What is the difference between Rickets and Osteomalacia? Rickets = occurs in growing children (affects both cartilage and bone). Osteomalacia = occurs in adults (affects only bone - no cartilage involvement since growth plates are closed).

Q14. What is hypervitaminosis D? Hypercalcemia, hypercalciuria, metastatic calcification (especially in blood vessels and kidneys), nephrolithiasis, weakness, nausea.

Vitamin E (Tocopherol)

Q15. What is the function of Vitamin E? Major lipid-soluble antioxidant - scavenges free radicals, especially in cell membranes. Protects polyunsaturated fatty acids (PUFAs) from oxidation. Works synergistically with selenium (glutathione peroxidase).

Q16. What are the deficiency features of Vitamin E?

Spinocerebellar degeneration (ataxia, loss of deep tendon reflexes)
Hemolytic anemia in premature neonates (due to fragility of RBC membranes)
Peripheral neuropathy

Q17. What are the sources of Vitamin E? Seed oils (sunflower, groundnut, corn, soybean), wheat germ oil, green leafy vegetables.

Vitamin K

Q18. What is the function of Vitamin K? Cofactor for hepatic gamma-carboxylation of glutamate residues on coagulation factors. Activates clotting factors II (prothrombin), VII, IX, X, protein C, and protein S.

Q19. What are the deficiency features of Vitamin K? Abnormal bleeding (prolonged PT and PTT). Hemorrhagic disease of newborn (HDN) - because placenta does not transfer Vitamin K well and newborn gut flora is absent.

Q20. Why are newborns given Vitamin K at birth? Newborns have sterile guts (no intestinal bacteria to synthesize Vitamin K), low levels of Vitamin K at birth, and low breast milk Vitamin K content - making them susceptible to HDN.

Q21. Name the Vitamin K-dependent clotting factors. II, VII, IX, X + Protein C and Protein S.

PART B: WATER-SOLUBLE VITAMINS (B-COMPLEX)

Q22. Classify water-soluble vitamins.

B-Complex: B1 (Thiamine), B2 (Riboflavin), B3 (Niacin), B5 (Pantothenic acid), B6 (Pyridoxine), B7 (Biotin), B9 (Folic acid), B12 (Cobalamin)
Vitamin C (Ascorbic acid)

Q23. Name sulphur-containing vitamins. Thiamine (B1), Biotin (B7), Lipoic acid (thioctic acid). Coenzyme A (contains -SH group) can also be included.

Vitamin B1 (Thiamine)

Q24. What is the active/coenzyme form of Thiamine? Thiamine pyrophosphate (TPP) - also called thiamine diphosphate (TDP).

Q25. What reactions require TPP?

Pyruvate dehydrogenase (pyruvate → Acetyl-CoA)
Alpha-ketoglutarate dehydrogenase (TCA cycle)
Branched-chain alpha-keto acid dehydrogenase
Transketolase (pentose phosphate pathway)

Q26. What is Beriberi? Classify it. Thiamine (B1) deficiency. Two types:

Dry Beriberi: peripheral neuropathy (symmetrical, ascending) - burning feet, wrist drop, foot drop
Wet Beriberi: cardiomegaly, cardiac failure, peripheral edema due to high-output heart failure
Wernicke-Korsakoff syndrome: seen in alcoholics - Wernicke's encephalopathy (confusion, ataxia, ophthalmoplegia) + Korsakoff's psychosis (anterograde amnesia, confabulation)

Q27. Why is Thiamine deficiency common in polished rice diets? Thiamine is concentrated in the outer bran layer of rice, which is removed during milling/polishing.

Vitamin B2 (Riboflavin)

Q28. What are the coenzyme forms of Riboflavin? FMN (Flavin Mononucleotide) and FAD (Flavin Adenine Dinucleotide).

Q29. What is Ariboflavinosis? Deficiency of Riboflavin. Features: cheilosis (cracking at corners of mouth), angular stomatitis, glossitis (magenta tongue), seborrheic dermatitis, corneal vascularization.

Vitamin B3 (Niacin)

Q30. What are the coenzyme forms of Niacin? NAD+ (Nicotinamide Adenine Dinucleotide) and NADP+ (NAD Phosphate) - essential for redox reactions.

Q31. What is Pellagra? What are the "4 Ds"? Niacin deficiency. The "3 Ds" (or 4 Ds):

Dermatitis (photosensitive skin rash - Casal's necklace)
Diarrhea
Dementia
Death (if untreated)

Q32. Why does Pellagra occur in maize (corn) diet populations? Maize is deficient in niacin AND tryptophan (from which niacin can be synthesized endogenously - 60 mg tryptophan = 1 mg niacin). Also, niacin in corn is in bound form (niacytin) and not bioavailable.

Q33. In which disease does Pellagra occur secondary to tryptophan malabsorption? Hartnup disease (autosomal recessive disorder of tryptophan absorption).

Vitamin B6 (Pyridoxine)

Q34. What is the active form of Vitamin B6? Pyridoxal phosphate (PLP).

Q35. What are the important reactions requiring PLP?

Transamination reactions (ALT, AST)
Decarboxylation (synthesis of serotonin, dopamine, GABA, histamine)
Glycogen phosphorylase
Synthesis of delta-ALA (heme synthesis)

Q36. What are the deficiency features of B6? Cheilosis, glossitis, dermatitis, peripheral neuropathy, microcytic anemia (since heme synthesis is impaired), convulsions in infants.

Q37. Isoniazid (INH) causes deficiency of which vitamin? Vitamin B6 - INH forms a hydrazone complex with pyridoxal and inhibits PLP formation. That is why Pyridoxine is given with INH.

Vitamin B12 (Cobalamin)

Q38. Which vitamin contains cobalt? Vitamin B12 (Cyanocobalamin/Cobalamin).

Q39. What is the active form of Vitamin B12? Methylcobalamin and Adenosylcobalamin (deoxyadenosylcobalamin).

Q40. What are the functions of Vitamin B12?

Methylcobalamin: required for methionine synthesis (methyl transfer from methyltetrahydrofolate to homocysteine)
Adenosylcobalamin: cofactor for methylmalonyl-CoA mutase (converts methylmalonyl-CoA to succinyl-CoA)

Q41. What is the "methyl trap hypothesis"? When B12 is deficient, folate gets trapped as methyltetrahydrofolate (cannot be converted to THF). This leads to folate deficiency within cells and impaired DNA synthesis, even when dietary folate is adequate.

Q42. What is Pernicious Anemia? Megaloblastic anemia caused by B12 deficiency due to lack of intrinsic factor (IF). IF is produced by gastric parietal cells and is essential for B12 absorption in the terminal ileum. Autoimmune destruction of parietal cells → no IF → no B12 absorption.

Q43. What is the unique neurological feature of B12 deficiency? Subacute combined degeneration (SACD) of spinal cord - demyelination of posterior (dorsal columns) and lateral (corticospinal) tracts. Presents with ataxia, loss of vibration/position sense, upper motor neuron signs, and peripheral neuropathy. This does NOT occur in isolated folate deficiency.

Q44. Where is Vitamin B12 found? Exclusively in animal sources (meat, fish, eggs, dairy). No plant sources. This is why strict vegans are at risk.

Q45. What are the differences between B12 and Folate deficiency?

Feature	B12 Deficiency	Folate Deficiency
Megaloblastic anemia	Yes	Yes
SACD of spinal cord	Yes	No
Neural tube defects	No	Yes
Serum methylmalonic acid	Elevated	Normal
Serum homocysteine	Elevated	Elevated
Source	Animal only	Green leafy veg

Folic Acid

Q46. What is the active form of Folic acid? Tetrahydrofolate (THF) - formed by dihydrofolate reductase (DHFR).

Q47. What are the functions of Folic acid? Transfer and use of single-carbon units (one-carbon metabolism) essential for:

Purine synthesis
Thymidylate (dTMP) synthesis - needed for DNA
Methylation of homocysteine → methionine

Q48. What are the deficiency features? Megaloblastic anemia, neural tube defects (anencephaly, spina bifida) in the fetus if mother is deficient periconceptionally.

Q49. Which drugs cause folate deficiency? Methotrexate, trimethoprim, pyrimethamine - all inhibit dihydrofolate reductase (DHFR). Phenytoin reduces folate absorption.

Biotin

Q50. What is the role of Biotin? Cofactor for carboxylase enzymes:

Pyruvate carboxylase (pyruvate → OAA)
Acetyl-CoA carboxylase (acetyl-CoA → malonyl-CoA - fatty acid synthesis)
Propionyl-CoA carboxylase

Q51. Eating raw egg white causes deficiency of which vitamin? Biotin - raw egg white contains avidin, a glycoprotein that binds biotin tightly and prevents its absorption. Cooking denatures avidin.

Vitamin C (Ascorbic Acid)

Q52. What are the functions of Vitamin C?

Hydroxylation of proline and lysine during collagen synthesis (cofactor for prolyl and lysyl hydroxylase)
Antioxidant - regenerates Vitamin E
Enhances iron absorption (reduces Fe3+ to Fe2+ in the intestine)
Synthesis of carnitine, norepinephrine, bile acids

Q53. What is Scurvy? Vitamin C deficiency. Features due to defective collagen synthesis:

Perifollicular petechiae and hemorrhages
Coiled (corkscrew) hairs
Inflamed and bleeding gums (gingival hemorrhage)
Poor wound healing
Hemarthrosis (bleeding into joints)
Subperiosteal hemorrhage in children
Scorbutic rosary (epiphyseal enlargement)

Q54. Which test can diagnose Scurvy? Capillary fragility test (Hess test / Rumpel-Leede test). Also: decreased serum ascorbic acid levels.

Q55. Why does Vitamin C enhance iron absorption? It reduces ferric iron (Fe3+) to ferrous iron (Fe2+), which is more readily absorbed in the duodenum.

PART C: MINERALS

Q56. Name the macro-minerals (major minerals). Calcium, Phosphorus, Magnesium, Sodium, Potassium, Chloride, Sulfur.

Q57. Name the trace elements. Iron, Zinc, Copper, Iodine, Selenium, Fluoride, Chromium, Manganese, Cobalt, Molybdenum.

Iron

Q58. What are the different forms of iron in the body?

Hemoglobin iron (major)
Myoglobin iron
Transport iron (transferrin-bound)
Storage iron (ferritin, hemosiderin)
Enzyme iron (cytochromes, iron-sulfur proteins)

Q59. What are the stages of iron deficiency?

Depletion of stores (low ferritin, serum iron normal)
Iron-deficient erythropoiesis (low serum iron, high TIBC, low transferrin saturation)
Iron deficiency anemia (microcytic, hypochromic anemia)

Q60. What factors increase and decrease iron absorption?

Increase: Vitamin C, acidic pH, ferrous form (Fe2+), increased erythropoiesis
Decrease: Phytates, oxalates, tannins (tea), antacids, high phosphate, ferric form (Fe3+)

Zinc

Q61. What are the functions of Zinc? Component of many metalloenzymes (oxidases, carbonic anhydrase, alkaline phosphatase, DNA/RNA polymerase). Essential for growth, wound healing, immune function, taste and smell, and reproductive function.

Q62. What is Acrodermatitis Enteropathica? An inborn error of zinc metabolism (autosomal recessive, mutation in ZIP4 transporter) causing severe zinc deficiency. Features: rash around eyes, mouth, nose, and anus (acral and periorificial dermatitis), alopecia, diarrhea, growth retardation, impaired wound healing, impaired night vision.

Iodine

Q63. What is the role of Iodine? Essential component of thyroid hormones (T3 and T4). Deficiency causes goiter and hypothyroidism. Severe deficiency in pregnancy causes cretinism (irreversible intellectual disability in the child).

Copper

Q64. What are the functions of Copper? Component of:

Cytochrome c oxidase (oxidative phosphorylation)
Dopamine beta-hydroxylase (catecholamine synthesis)
Tyrosinase (melanin synthesis)
Lysyl oxidase (collagen cross-linking)
Ceruloplasmin (ferroxidase - iron metabolism)
Superoxide dismutase

Q65. What conditions are associated with copper metabolism disorders?

Wilson's disease: copper accumulation (hepatolenticular degeneration) - Kayser-Fleischer rings
Menkes syndrome: copper deficiency due to defective transport - kinky hair, hypopigmentation, neurodegeneration

Selenium

Q66. What is the function of Selenium? Component of glutathione peroxidase - acts as an antioxidant (works synergistically with Vitamin E to protect against oxidative damage).

Q67. What is Keshan disease? Cardiomyopathy caused by Selenium deficiency - first described in Keshan county, China.

Calcium and Phosphorus

Q68. What are the factors affecting Calcium absorption?

Increase: Vitamin D (calcitriol), PTH, acidic pH, high protein diet, optimal Ca:P ratio (1:1)
Decrease: Phytates, oxalates, fatty acids, excess phosphate, excess dietary fiber, neomycin

Q69. What hormones regulate blood calcium?

PTH (parathyroid hormone): increases blood calcium by acting on bone, kidney, and stimulating calcitriol production
Calcitriol (active Vitamin D): increases intestinal absorption
Calcitonin: decreases blood calcium by inhibiting osteoclasts

Chromium

Q70. What is the role of Chromium? Trivalent chromium (Cr3+) is a component of Glucose Tolerance Factor (GTF) - potentiates the action of insulin in carbohydrate metabolism. Sources: brewer's yeast, cereals.

Q71. What is the occupational hazard of Chromium? Hexavalent chromium (Cr6+) is toxic. Chronic occupational exposure to chromates is associated with increased risk of lung cancer.

HIGH-YIELD QUICK VIVA POINTS

Vitamin	Coenzyme form	Deficiency disease
B1 (Thiamine)	TPP	Beriberi, Wernicke-Korsakoff
B2 (Riboflavin)	FMN, FAD	Ariboflavinosis, cheilosis
B3 (Niacin)	NAD+, NADP+	Pellagra (3 Ds)
B5 (Pantothenic acid)	Coenzyme A	No clinical syndrome
B6 (Pyridoxine)	PLP	Peripheral neuropathy, sideroblastic anemia
B7 (Biotin)	-	Dermatitis, alopecia (raw egg white)
B9 (Folate)	THF	Megaloblastic anemia, NTDs
B12 (Cobalamin)	Methylcobalamin, Adenosylcobalamin	Pernicious anemia, SACD
A	Retinal, Retinoic acid	Night blindness, Xerophthalmia
D	Calcitriol	Rickets / Osteomalacia
E	-	Hemolytic anemia, ataxia
K	-	Bleeding, HDN
C	-	Scurvy

Sources: Robbins & Cotran Pathologic Basis of Disease 10th Ed; Harper's Illustrated Biochemistry 32nd Ed; Lippincott's Biochemistry 8th Ed; Guyton & Hall Medical Physiology; Viva in Biochemistry - Chatterjea (Koracademy)

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