Biochemistry
MBBS Biochemistry question bank: biomolecules, enzymes, metabolism, molecular biology, vitamins, nutrition and clinical biochemistry.
12chapters144questions75High-Yield
Definition
Vitamin A (retinol) is a fat-soluble vitamin essential for vision, epithelial integrity and growth.
Forms & Sources
- Retinol, retinal, retinoic acid
- β-carotene (provitamin, from plants)
- Sources: liver, fish oil, carrots
Functions
- Vision — rhodopsin (retinal)
- Epithelial integrity
- Growth & reproduction
- Antioxidant
Deficiency
- Night blindness (earliest sign)
- Xerophthalmia, Bitot’s spots
- Keratomalacia → blindness
Vitamin A supports vision and epithelium; lack causes night blindness first. Function Detail Vision Rhodopsin Epithelium Integrity Deficiency Night blindness Applied
- Vitamin A prophylaxis (children)
- Toxicity (hypervitaminosis A)
🔑KEY POINTS TO REMEMBER- Vitamin A: vision (rhodopsin), epithelium, growth.
- β-carotene = plant provitamin.
- Deficiency → night blindness, xerophthalmia.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Vitamin D is a fat-soluble vitamin (and prohormone) essential for calcium homeostasis and bone mineralisation.
Synthesis & Activation
- Skin: 7-dehydrocholesterol → vitamin D3 (UV light)
- Liver: 25-hydroxylation
- Kidney: 1-hydroxylation → calcitriol (active)
Functions
- ↑ Intestinal Ca²⁺ and phosphate absorption
- Bone mineralisation
- With PTH → calcium homeostasis
Deficiency
- Rickets (children)
- Osteomalacia (adults)
Vitamin D is activated in two steps to calcitriol, which raises calcium. Site Step Skin D3 formation Liver 25-OH Kidney 1-OH (active) Applied
- Rickets, osteomalacia
- Sunlight exposure
🔑KEY POINTS TO REMEMBER- Vitamin D activated: skin → liver (25-OH) → kidney (1-OH, calcitriol).
- ↑ Ca²⁺ & phosphate absorption; bone mineralisation.
- Deficiency → rickets / osteomalacia.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Vitamin K is essential for blood clotting; vitamin E is a major fat-soluble antioxidant.
Vitamin K
- Cofactor for γ-carboxylation of clotting factors (II, VII, IX, X)
- Sources: green vegetables, gut bacteria
- Deficiency → bleeding
Vitamin E (tocopherol)
- Antioxidant (protects membranes)
- Prevents lipid peroxidation
- Deficiency → haemolysis, neuropathy
Vitamin K enables clotting; vitamin E protects membranes. Vitamin Role K Clotting (II, VII, IX, X) E Antioxidant Applied
- Warfarin blocks vitamin K
- Newborn vitamin K injection
🔑KEY POINTS TO REMEMBER- Vitamin K: γ-carboxylates factors II, VII, IX, X.
- Vitamin E: membrane antioxidant.
- Warfarin antagonises vitamin K.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The water-soluble B vitamins — thiamine, riboflavin, niacin, pyridoxine — act as coenzymes in metabolism.
Thiamine (B1)
- Coenzyme TPP (decarboxylation)
- Deficiency → beriberi, Wernicke-Korsakoff
Riboflavin (B2) & Niacin (B3)
- B2 → FAD, FMN (redox); deficiency → angular stomatitis, cheilosis
- B3 → NAD, NADP; deficiency → pellagra (3 D’s)
Pyridoxine (B6)
- Coenzyme PLP (transamination, decarboxylation)
- Deficiency → neuropathy, anaemia
Each B vitamin becomes a coenzyme central to metabolism. Vitamin Coenzyme Deficiency B1 TPP Beriberi B2 FAD Cheilosis B3 NAD Pellagra B6 PLP Neuropathy Applied
- Pellagra (maize diet)
- Isoniazid → B6 deficiency
🔑KEY POINTS TO REMEMBER- B1→TPP, B2→FAD, B3→NAD, B6→PLP.
- Deficiencies: beriberi, cheilosis, pellagra, neuropathy.
- Pellagra = 3 D’s (dermatitis, diarrhoea, dementia).
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Folic acid, vitamin B12 and biotin are B-complex vitamins essential for one-carbon metabolism, DNA synthesis and carboxylation.
Folic Acid
- Coenzyme THF (one-carbon transfer)
- DNA / nucleotide synthesis
- Deficiency → megaloblastic anaemia, neural tube defects
Vitamin B12 (cobalamin)
- Needs intrinsic factor for absorption
- Coenzyme (methylmalonyl-CoA, homocysteine)
- Deficiency → megaloblastic anaemia + neuropathy
Biotin
- Coenzyme for carboxylation
- Deficiency rare (raw egg white — avidin)
Folate and B12 power DNA synthesis; biotin drives carboxylations. Vitamin Role Deficiency Folate DNA synthesis Megaloblastic anaemia B12 + neuro Anaemia + neuropathy Biotin Carboxylation Rare Applied
- Folic acid in pregnancy (NTDs)
- Pernicious anaemia (B12)
🔑KEY POINTS TO REMEMBER- Folate & B12: one-carbon metabolism, DNA synthesis.
- B12 needs intrinsic factor; deficiency adds neuropathy.
- Biotin = carboxylation coenzyme.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Vitamin C (ascorbic acid) is a water-soluble vitamin essential for collagen synthesis and antioxidant defence.
Functions
- Collagen synthesis (hydroxylation of proline/lysine)
- Antioxidant
- ↑ Iron absorption
- Wound healing
Deficiency
- Scurvy — bleeding gums, poor wound healing
- Corkscrew hair, perifollicular haemorrhages
Vitamin C is essential for collagen; deficiency causes scurvy. Function Detail Collagen Hydroxylation Deficiency Scurvy Applied
- Scurvy
- Citrus fruits
🔑KEY POINTS TO REMEMBER- Vitamin C: collagen synthesis (hydroxylation), antioxidant.
- ↑ iron absorption; wound healing.
- Deficiency → scurvy.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Pantothenic acid (vitamin B5) is a component of coenzyme A, essential for acyl-group transfer in metabolism.
Functions
- Part of coenzyme A (CoA)
- Forms acetyl-CoA (TCA, fatty-acid metabolism)
- Part of fatty acid synthase (ACP)
Pantothenic acid forms coenzyme A, the universal acyl carrier. Feature Detail Coenzyme Coenzyme A Role Acyl transfer Applied
- Deficiency rare (burning-feet syndrome)
🔑KEY POINTS TO REMEMBER- Pantothenic acid = part of coenzyme A.
- Central to acetyl-CoA and fatty-acid metabolism.
- Deficiency rare.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Many coenzymes are derived from B-complex vitamins and are essential for enzyme activity.
Vitamin → Coenzyme
- B1 (thiamine) → TPP
- B2 (riboflavin) → FAD, FMN
- B3 (niacin) → NAD, NADP
- B6 (pyridoxine) → PLP
- B5 → coenzyme A; folate → THF
B vitamins are converted to the coenzymes that many enzymes require. Vitamin Coenzyme Function B1 TPP Decarboxylation B2 FAD Redox B3 NAD Redox B6 PLP Transamination Applied
- Vitamin deficiency → ↓ enzyme activity
🔑KEY POINTS TO REMEMBER- B1→TPP, B2→FAD, B3→NAD, B6→PLP, B5→CoA, folate→THF.
- Coenzymes bind apoenzymes for activity.
- Deficiency impairs enzymes.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Wernicke–Korsakoff syndrome is a neurological disorder due to thiamine (B1) deficiency, often in alcoholics.
Wernicke Encephalopathy (acute)
- Confusion
- Ophthalmoplegia (eye-movement palsy)
- Ataxia (classic triad)
Korsakoff Psychosis (chronic)
- Memory loss (amnesia)
- Confabulation
Thiamine lack impairs brain glucose use, causing this two-stage syndrome. Phase Features Wernicke Confusion, ophthalmoplegia, ataxia Korsakoff Amnesia, confabulation Applied
- Give thiamine before glucose (in alcoholics)
- Reversible if treated early
🔑KEY POINTS TO REMEMBER- Wernicke-Korsakoff = thiamine (B1) deficiency.
- Wernicke triad: confusion, ophthalmoplegia, ataxia.
- Korsakoff: amnesia, confabulation.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Pernicious anaemia is a megaloblastic anaemia caused by vitamin B12 deficiency due to lack of intrinsic factor.
Mechanism
- Autoimmune destruction of gastric parietal cells
- ↓ Intrinsic factor → ↓ B12 absorption
- ↓ B12 → impaired DNA synthesis
Features
- Megaloblastic anaemia
- Glossitis
- Neurological (subacute combined degeneration)
Loss of intrinsic factor blocks B12 absorption, causing anaemia and neuropathy. Feature Detail Cause ↓ intrinsic factor Anaemia Megaloblastic Applied
- Schilling test (historical)
- B12 injections
🔑KEY POINTS TO REMEMBER- Pernicious anaemia = B12 deficiency (↓ intrinsic factor).
- Megaloblastic anaemia + neuropathy.
- Treated with B12 injections.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Xerophthalmia is dryness of the eye due to vitamin A deficiency; Bitot’s spots are a characteristic sign.
Features
- Conjunctival & corneal dryness (xerosis)
- Bitot’s spots — foamy white patches
- Keratomalacia → corneal ulceration / blindness
Vitamin A lack dries and keratinises the eye surface, risking blindness. Stage Sign Early Night blindness Xerosis Dry eye Bitot’s White patches Applied
- Leading cause of childhood blindness
- Vitamin A supplementation
🔑KEY POINTS TO REMEMBER- Xerophthalmia = vitamin A deficiency eye disease.
- Bitot’s spots = foamy white conjunctival patches.
- Keratomalacia → blindness.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Vitamin K is essential for synthesis of clotting factors; warfarin is an anticoagulant that antagonises it.
Vitamin K
- Cofactor for γ-carboxylation of factors II, VII, IX, X (+ protein C, S)
- Needed for functional clotting factors
Warfarin
- Inhibits vitamin K epoxide reductase
- ↓ Active clotting factors → anticoagulation
- Monitored by PT / INR
Warfarin blocks vitamin K recycling, reducing active clotting factors. Agent Effect Vitamin K ↑ clotting factors Warfarin ↓ clotting factors Applied
- Warfarin therapy (INR monitoring)
- Vitamin K reverses warfarin
🔑KEY POINTS TO REMEMBER- Vitamin K γ-carboxylates factors II, VII, IX, X.
- Warfarin inhibits vitamin K epoxide reductase.
- Monitored by INR; reversed by vitamin K.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).