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BI8.1-6 | Vitamins and Nutrition — Gate Quiz

Graded 10 questions · 20 min · 3 attempts

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Q1 BI8.1 1 pt

Which of the following vitamins is fat-soluble and can accumulate to toxic levels with excessive supplementation?

A Vitamin B12
B Vitamin C
C Vitamin A
D Folic acid

Correct! Vitamin A is fat-soluble and stored in the liver. Excess intake (hypervitaminosis A) causes hepatotoxicity, teratogenicity, raised intracranial pressure, and peeling skin.

Fat-soluble vitamins: A, D, E, K (ADEK). Water-soluble: B-complex and C. Vitamin D toxicity causes hypercalcaemia. Vitamin A toxicity: teratogenic (avoid in pregnancy), hepatic fibrosis, pseudotumour cerebri.

Incorrect. Vitamin A is fat-soluble and toxic in excess. Water-soluble vitamins (B-complex, C) are generally not toxic.

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Q2 BI8.2 1 pt

A 2-year-old child presents with bowing of legs, frontal bossing, and a rachitic rosary. Serum calcium is low with elevated alkaline phosphatase. The most likely diagnosis is:

A Scurvy
B Rickets due to Vitamin D deficiency
C Osteogenesis imperfecta
D Hypophosphataemia

Correct! Rickets (Vitamin D deficiency in children) presents with bowing of legs, frontal bossing, rachitic rosary, low calcium and elevated alkaline phosphatase.

Vitamin D metabolism: Skin (UV-B) produces cholecalciferol (D3). Liver hydroxylates to 25-OH-D3 (storage form). Kidney produces 1,25-(OH)2-D3 (calcitriol, active form). Calcitriol increases intestinal Ca2+ absorption and bone mineralisation. Deficiency: rickets (children), osteomalacia (adults).

Incorrect. The triad of bowing legs, frontal bossing, and rachitic rosary is classic rickets from Vitamin D deficiency.

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Q3 BI8.3 1 pt

Vitamin K is required for which post-translational modification of clotting factors II, VII, IX, and X?

A Hydroxylation of proline
B Gamma-carboxylation of glutamate
C Phosphorylation of serine
D Glycosylation of asparagine

Correct! Vitamin K is a cofactor for gamma-carboxylase, which adds a carboxyl group to glutamate residues. Gamma-carboxyglutamate (Gla) binds calcium, enabling clotting factor activity.

Vitamin K-dependent clotting factors: II (prothrombin), VII, IX, X and proteins C and S. Warfarin inhibits Vitamin K epoxide reductase. Deficiency: haemorrhagic disease of newborn.

Incorrect. Vitamin K enables gamma-carboxylation of glutamate residues in clotting factors.

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Q4 BI8.4 1 pt

A 65-year-old strict vegetarian presents with macrocytic anaemia, peripheral neuropathy, and subacute combined degeneration of the spinal cord. Serum B12 is very low. The neurological damage in B12 deficiency is primarily caused by:

A Accumulation of homocysteine
B Impaired myelin synthesis due to defective methylmalonyl-CoA mutase reaction
C Impaired thymidine synthesis due to folate trap
D Direct neuronal toxicity of methylmalonic acid

Correct! B12 is required for methylmalonyl-CoA mutase. Deficiency accumulates methylmalonyl-CoA, which impairs fatty acid synthesis for myelin, causing demyelination (SACD).

B12 deficiency: (1) Methionine synthase defect (with folate): megaloblastic anaemia. (2) Methylmalonyl-CoA mutase defect (B12 only): demyelination. This explains why folate treats anaemia but NOT neuropathy.

Incorrect. B12 deficiency impairs methylmalonyl-CoA mutase, leading to abnormal fatty acids in myelin.

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Q5 BI8.4 1 pt

Periconceptional folic acid supplementation reduces the risk of neural tube defects. THF (tetrahydrofolate) is essential for:

A Collagen synthesis
B Synthesis of purines and thymidine for DNA
C Myelin synthesis
D Glucose metabolism

Correct! THF carries one-carbon units essential for purine synthesis and thymidylate synthesis (dUMP to dTMP), required for rapid DNA replication during neural tube closure.

Neural tube closes in weeks 3-4 of gestation. Folate (400 mcg/day) recommended periconceptionally. Methotrexate (folate antagonist) and valproate can cause neural tube defects.

Incorrect. THF is essential for purine and thymidylate synthesis, required for cell division in neural tube formation.

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Q6 BI8.5 1 pt

A patient from a region where maize is the primary dietary staple presents with dermatitis, diarrhoea, and dementia (the 3 Ds). The diagnosis is pellagra, caused by deficiency of:

A Vitamin B1 (thiamine)
B Vitamin B2 (riboflavin)
C Vitamin B3 (niacin)
D Vitamin B6 (pyridoxine)

Correct! Pellagra is caused by niacin (Vitamin B3) deficiency. Maize contains bound niacin (niacytin) that is not bioavailable, and maize is low in tryptophan (niacin precursor).

Niacin: component of NAD+ and NADP+. Pellagra endemic in corn-eating populations. Isoniazid (anti-TB) and Hartnup disease also cause pellagra by reducing tryptophan-to-niacin conversion.

Incorrect. Pellagra (3 Ds: Dermatitis, Diarrhoea, Dementia) is caused by niacin (B3) deficiency.

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Q7 BI8.5 1 pt

Biotin (Vitamin B7) is a coenzyme for which class of enzymes that add CO2 to organic substrates?

A Decarboxylases
B Transaminases
C Carboxylases
D Dehydrogenases

Correct! Biotin is the coenzyme for carboxylases: Pyruvate carboxylase (gluconeogenesis), Acetyl-CoA carboxylase (fatty acid synthesis), Propionyl-CoA carboxylase, and 3-methylcrotonyl-CoA carboxylase.

Biotin deficiency causes dermatitis and alopecia. Avidin in raw egg white binds biotin (cooking denatures avidin). Biotinidase deficiency causes multiple carboxylase deficiency.

Incorrect. Biotin is the coenzyme for all carboxylase enzymes (CO2 addition).

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Q8 BI8.6 1 pt

A 3-year-old malnourished child has severe oedema, fatty liver, flaky paint dermatosis, and depigmented hair with markedly low serum albumin. The diagnosis is:

A Marasmus
B Kwashiorkor
C Iron deficiency anaemia
D Vitamin A deficiency

Correct! Kwashiorkor is protein deficiency with adequate caloric intake. Features: pitting oedema (low albumin), fatty liver (impaired VLDL secretion), skin lesions, and hair depigmentation.

Marasmus = caloric deficiency (wasting, no oedema, no fatty liver). Kwashiorkor = protein deficiency (oedema, fatty liver, apathetic, moon face). Kwashiorkor fatty liver: low protein impairs ApoB synthesis, preventing VLDL formation and fat export from liver.

Incorrect. Kwashiorkor = protein deficiency with caloric adequacy; oedema + fatty liver + skin changes are hallmarks.

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Q9 BI8.3 1 pt

Vitamin E (alpha-tocopherol) is the primary lipid-soluble antioxidant in biological membranes. It protects against:

A Protein oxidation in cytoplasm
B Lipid peroxidation of polyunsaturated fatty acids in membranes
C DNA oxidation in nucleus
D Oxidation of haemoglobin iron

Correct! Vitamin E is a lipid-soluble antioxidant embedded in cell membranes. It donates hydrogen to lipid peroxyl radicals, breaking the chain reaction of lipid peroxidation of PUFAs.

Antioxidant network: Vitamin E (lipid-soluble, membranes), Vitamin C (water-soluble, cytoplasm), Glutathione/NADPH (intracellular). Vitamin C regenerates oxidized Vitamin E. Selenium is required for glutathione peroxidase (synergistic with Vitamin E).

Incorrect. Vitamin E is lipid-soluble and specifically protects against lipid peroxidation of membrane PUFAs.

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Q10 BI8.6 1 pt

The basal metabolic rate (BMR) is measured under which specific conditions?

A After a full meal, at room temperature, lying down
B After 12 hours of fasting, at thermoneutral temperature, at complete physical rest
C During light exercise, after fasting
D At any time, corrected for body weight

Correct! BMR conditions: post-absorptive (12 hours fasting), thermoneutral temperature, complete rest (lying awake), morning.

BMR factors: higher in males, young adults, hyperthyroidism, fever; lower in females, elderly, hypothyroidism, malnutrition. Total energy expenditure = BMR + physical activity + thermic effect of food.

Incorrect. BMR requires 12-hour fast, thermoneutral environment, and complete physical rest.

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