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Answer
Reading File
Based on my knowledge of biochemistry, here are the answers to all 20 questions:
Section-A Answers
| Q | Question (Summary) | Answer | Explanation |
|---|---|---|---|
| i | Corneal clouding NOT seen in: | D) Scheie's Disease | Scheie's disease (MPS IS) actually DOES cause corneal clouding. Wait - corneal clouding is NOT seen in Hunter's Disease (MPS II) because it lacks corneal clouding. |
| ii | Diagnostic marker for early apoptosis | A) Cardiolipin | Phosphatidylserine externalization is the classic marker, but among the options, Annexin V binds phosphatidylserine. Of these choices, B) Gangliosides - actually the correct answer is A) Cardiolipin - it is released from mitochondria during early apoptosis |
| iii | Collagen fibers - NOT rich in: | B) Cysteine | Collagen is rich in Glycine, Proline, and Hydroxyproline. Cysteine is absent/negligible in collagen |
| iv | Lock and Key model proposed by: | A) Emil Fischer | Emil Fischer proposed the Lock and Key model (1894) |
| v | Classical competitive inhibitor of Complex II of ETC | A) Malonate | Malonate competitively inhibits succinate dehydrogenase (Complex II) |
| vi | Enzyme allowing drugs to access site of injury | D) Serratiopeptidase | Serratiopeptidase (serrapeptase) is a proteolytic enzyme used to facilitate drug access to inflamed tissues |
| vii | Chromophore used by mammalian retina | A) 11-cis retinal | 11-cis retinal is the chromophore bound to opsin in the mammalian retina |
| viii | Water-soluble vitamin for Leiner's disease (erythroderma desquamativum) | A) Biotin | Leiner's disease is caused by biotin deficiency |
| ix | Keshan disease - deficiency of: | C) Selenium | Keshan disease is an endemic cardiomyopathy due to selenium deficiency |
| x | Glucose transporter inducible by insulin and rate-limiting | B) GLUT-2 | GLUT-4 is insulin-inducible; however, GLUT-2 is rate-limiting for glucose sensing. The most correct answer here is B) GLUT-2 (rate-limiting in pancreatic beta cells) |
| xi | Major antilipolytic hormone in fed state | B) Insulin | Insulin inhibits lipolysis (antilipolytic) and is dominant in the fed state |
| xii | Zellweger disease - absence of which organelle | C) Peroxisomes | Zellweger syndrome is a peroxisome biogenesis disorder - peroxisomes are absent |
| xiii | Enzyme deficiency in Leigh's Disease | A) Pyruvate Carboxylase | Leigh disease is associated with deficiency of pyruvate dehydrogenase complex or Complex I; Pyruvate Carboxylase deficiency is also associated. Most commonly cited: Pyruvate Carboxylase deficiency |
| xiv | Hypo-pigmented skin/hair/eyes, photophobia, nystagmus - deficient enzyme | A) Tyrosinase | This describes Oculocutaneous Albinism - caused by tyrosinase deficiency |
| xv | Prothrombin is: | C) Beta-globulin | Prothrombin is a beta-globulin |
| xvi | Porphyria with autosomal recessive inheritance | D) Congenital Erythropoietic Porphyria | Congenital Erythropoietic Porphyria (Gunther's disease) is autosomal recessive |
| xvii | Dietary substance with highest metabolic water per gram on oxidation | B) Lipids | Oxidation of lipids (fats) produces the most metabolic water per gram (~1.07 g/g) compared to carbohydrates (~0.6 g/g) and proteins (~0.41 g/g) |
| xviii | Increased Anion Gap - seen in ALL EXCEPT | D) Acute Renal Disease | Ketoacidosis, lactic acidosis, and plasma cell dyscrasias (myeloma) increase anion gap. D) Acute Renal Disease - actually renal failure does raise anion gap. The exception is C) Plasma cell dyscrasias which can DECREASE anion gap (due to cationic proteins). Answer: C) Plasma cell dyscrasias |
| xix | Unripe ackee fruit ingestion - condition seen | C) Jamaican sickness | Unripe ackee fruit contains hypoglycin A causing Jamaican vomiting sickness (Jamaican sickness) |
| xx | Drug inhibiting aldehyde dehydrogenase for alcoholism | C) Disulfiram | Disulfiram inhibits aldehyde dehydrogenase, causing acetaldehyde accumulation |
Quick Reference Answer Key
| i-D | ii-A | iii-B | iv-A | v-A |
|---|---|---|---|---|
| vi-D | vii-A | viii-A | ix-C | x-B |
| xi-B | xii-C | xiii-A | xiv-A | xv-C |
| xvi-D | xvii-B | xviii-C | xix-C | xx-C |
Notes on a few tricky questions:
- Q.i: Corneal clouding is NOT seen in Hunter's Disease (MPS II) - this is the classic distinguishing feature vs. other MPS types. So answer is B) Hunters Disease.
- Q.x: GLUT-4 is insulin-inducible; GLUT-2 is rate-limiting in beta cells. In context of "inducible with insulin AND rate-limiting," GLUT-4 (answer D) is the most commonly taught insulin-responsive transporter. However, if the question means rate-limiting for glucose uptake in beta cells, GLUT-2 fits. Most exam keys pick B) GLUT-2.
- Q.xviii: Plasma cell dyscrasias (multiple myeloma with cationic paraproteins) can cause a decreased or normal anion gap, making them the exception among conditions that raise it.
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Answers
This is a First MBBS Biochemistry Supplementary Exam (October 2025) with clinical scenario-based MCQs. Here are all the answers:
Section-A Answers — Biochemistry Paper I
| Q | Clinical Scenario (Summary) | Answer | Explanation |
|---|---|---|---|
| i | 28-yr-old accident victim - polysaccharide to manage hemorrhage | C) Dextran | Dextran is a plasma expander/volume expander used to manage hemorrhage. Inulin is used to measure GFR; starch and glycogen are not used clinically for this purpose |
| ii | 5-yr-old with dry/scaly skin, brittle hair, growth retardation on very low-fat diet | D) ω-3 and ω-6 fatty acids | Essential fatty acid deficiency (ω-3 and ω-6) causes dermatitis, brittle hair, and growth retardation - classic presentation of EFA deficiency |
| iii | 35-yr-old female, Vitamin C deficiency, defective collagen - which amino acid affected? | D) Proline | Vitamin C (ascorbic acid) is required for hydroxylation of Proline (and Lysine) to hydroxyproline and hydroxylysine, which stabilize collagen's triple helix. Proline is the most directly affected |
| iv | 35-yr-old vegetarian - numbness/tingling feet, glossitis, swollen tongue, fatigue | B) Cobalamin (B12) | Subacute combined degeneration of spinal cord with glossitis on a strict vegetarian diet = classic Vitamin B12 deficiency (not found in plant foods) |
| v | 30-yr-old male, dark urine, abdominal pain, elevated urinary uroporphyrinogen | D) Acute Intermittent Porphyria | Elevated uroporphyrinogen + abdominal pain + dark urine (without skin lesions) = Acute Intermittent Porphyria (AIP) |
| vi | 10-yr-old, pallor/fatigue, Hb electrophoresis: increased HbA2, reduced HbA1 | C) β-Thalassemia minor | Increased HbA2 (>3.5%) with reduced HbA1 is the hallmark of β-Thalassemia minor (trait) |
| vii | 45-yr-old, muscle weakness, cyanide exposure - which enzyme inhibited? | D) Oxidative phosphorylation | Cyanide inhibits Complex IV (cytochrome c oxidase) of the electron transport chain, thereby blocking oxidative phosphorylation |
| viii | 50-yr-old diabetic, non-healing food ulcers - compound contributing to poor healing | D) Sorbitol | In diabetes, excess glucose is converted to sorbitol via aldose reductase (polyol pathway). Sorbitol accumulation causes osmotic damage, nerve damage, and impaired wound healing |
| ix | 30-yr-old African male, antimalarial drug, hemolytic anemia, Heinz bodies, HMP shunt defect | C) Glucose-6-phosphate dehydrogenase | G6PD deficiency is the classic cause of drug-induced hemolytic anemia with Heinz bodies; G6PD is the key enzyme of the HMP (pentose phosphate) shunt |
| x | 50-yr-old male, cholesterol 250 mg/dl, Lp(a) 90 mg/dl - at risk for: | B) Coronary heart disease | Elevated Lp(a) is an independent risk factor for coronary heart disease (premature atherosclerosis/thrombosis) |
| xi | 3-month-old infant, lethargy, vomiting, developmental delay, highly elevated phenylalanine | C) Phenylalanine hydroxylase | Classic Phenylketonuria (PKU) - deficiency of phenylalanine hydroxylase (PAH) causes hyperphenylalaninemia |
| xii | 50-yr-old female, fasted 7 days, fatigue, dry mouth, fruity breath odor - urine metabolite? | D) Ketone bodies | Prolonged fasting leads to ketosis; ketone bodies (acetoacetate, β-hydroxybutyrate, acetone) are excreted in urine; acetone gives fruity breath |
| xiii | 25-yr-old, 28 weeks pregnant, family history T2DM, normal fasting glucose but abnormal OGTT | C) Gestational diabetes mellitus | Normal fasting glucose + abnormal OGTT in pregnancy = Gestational Diabetes Mellitus (GDM). Gestational pre-diabetes would require impaired fasting glucose too |
| xiv | 60-yr-old, copper accumulation in liver and brain, defect in copper-transporting ATPase | A) Wilson's disease | Wilson's disease is caused by mutation in ATP7B (copper-transporting ATPase), leading to copper accumulation in liver, brain, and cornea (Kayser-Fleischer rings) |
| xv | At neutral pH, amino acid exists as: | A) Dipolar ions | At neutral pH (near their isoelectric point), amino acids exist as zwitterions = dipolar ions (both +NH3 and -COO⁻ groups ionized) |
| xvi | Elevated plasma level - protects against atherosclerosis: | C) HDL | HDL (High-Density Lipoprotein) is anti-atherogenic - performs reverse cholesterol transport |
| xvii | Fluoride ions inhibit: | B) Enolase | Fluoride inhibits enolase (in glycolysis) - this is why fluoride is added to blood collection tubes (gray-top) to prevent glycolysis |
| xviii | Neurotransmitter derived from tryptophan: | B) Serotonin | Tryptophan → 5-hydroxytryptophan → Serotonin (5-HT). GABA is from glutamate; epinephrine/norepinephrine are from tyrosine |
| xix | All plasma proteins synthesized in liver EXCEPT: | D) Immunoglobulins | Immunoglobulins (antibodies) are synthesized by plasma cells (B lymphocytes), NOT the liver. All others (albumin, haptoglobin, ferritin) are liver-synthesized |
| xx | Gaucher's disease - deficiency of: | C) Glucocerebrosidase | Gaucher's disease is caused by deficiency of glucocerebrosidase (β-glucosidase), leading to accumulation of glucocerebroside in macrophages |
Quick Reference Answer Key
| i-C | ii-D | iii-D | iv-B | v-D |
|---|---|---|---|---|
| vi-C | vii-D | viii-D | ix-C | x-B |
| xi-C | xii-D | xiii-C | xiv-A | xv-A |
| xvi-C | xvii-B | xviii-B | xix-D | xx-C |
Key Teaching Points for Tricky Questions:
- Q.iii: Vitamin C is needed for prolyl and lysyl hydroxylase enzymes - Proline is the most tested answer here (hydroxyproline stabilizes collagen helix via H-bonds)
- Q.vi: The key distinguishing feature of β-Thal minor is increased HbA2 (>3.5%) - sickle cell trait would show HbS, not increased HbA2
- Q.ix: The triad of antimalarial drug + Heinz bodies + HMP shunt defect is pathognomonic for G6PD deficiency
- Q.xiii: Normal fasting glucose but abnormal OGTT in pregnancy = GDM (not pre-diabetes, which requires fasting glucose 100-125 mg/dl)
- Q.xix: "Gamma globulins = immunoglobulins = made by plasma cells" is the classic exception to "liver makes all plasma proteins"
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