NRE Step 1 Biochemistry MCQs
12 sample questions from the 164 Biochemistry questions in NRE-1 Prep. Choose an answer to see why it is right and why each other option is wrong.
Practise all 164 Biochemistry questions in NRE-1 Prep
Sample Biochemistry questions
1. A 48-year-old man with chronic alcohol use is brought in confused and unsteady. He has nystagmus and bilateral lateral rectus weakness. Capillary glucose is 3.2 mmol/L. Which treatment should be given first?
Answer: IV thiamine, then glucose. This is Wernicke’s encephalopathy: confusion, ataxia and ophthalmoplegia. Thiamine is a cofactor for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase. Glucose given to a thiamine-deficient patient can precipitate or worsen Wernicke’s, so give IV thiamine (e.g. Pabrinex) before or with glucose — never delay correcting hypoglycaemia for long.
- IV dextrose, then thiamine: Glucose before thiamine can precipitate or worsen Wernicke encephalopathy.
- IV vitamin B12, then folate: B12 deficiency causes subacute combined degeneration, a different picture.
- Oral pyridoxine: B6 deficiency causes neuropathy and sideroblastic anaemia, not this triad.
2. Serum protein electrophoresis from a 68-year-old with back pain and anaemia shows a narrow, dense band in the gamma region and reduced other immunoglobulins. What does this band represent?
Answer: Monoclonal paraprotein. A sharp, narrow band (M-spike) means one clone of plasma cells makes one immunoglobulin — myeloma, MGUS, Waldenström or plasmacytoma. Immunoparesis (low other immunoglobulins) supports myeloma. A broad polyclonal increase occurs in chronic infection, liver cirrhosis (beta–gamma bridging) and autoimmune disease. Nephrotic syndrome shows low albumin and high alpha-2 (macroglobulin).
- Polyclonal gammopathy: A polyclonal rise gives a broad, diffuse gamma band (e.g. chronic infection or liver disease), not a narrow spike.
- Raised alpha-1 antitrypsin: Alpha-1 antitrypsin sits in the alpha-1 region and rises as an acute-phase protein, not in the gamma region.
- Raised beta-2 transferrin: Beta region; not a narrow gamma spike.
3. A man with recurrent sinus infections and chronic Giardia diarrhoea develops anaphylaxis during his first blood transfusion. Which immunoglobulin abnormality is most likely?
Answer: Selective IgA deficiency. Selective IgA deficiency is the commonest primary immunodeficiency (most are asymptomatic). IgA (secretory dimer with J chain and secretory component) protects mucosae, so deficiency gives sinopulmonary infections, giardiasis, coeliac disease and autoimmunity. Some patients make anti-IgA antibodies → anaphylaxis to blood products containing IgA — use washed red cells or IgA-deficient donors. Immunoglobulin functions: IgG — most abundant, crosses placenta, opsonises; IgM — pentamer, first response, best complement activator; IgA — mucosal, breast milk; IgE — mast cells, allergy, parasites; IgD — B-cell receptor.
- Hyper-IgM: Severe infections; not this reaction.
- IgG subclass deficiency: IgG subclass deficiency does not cause anaphylaxis with transfusion.
- C1-INH deficiency: C1-INH deficiency causes angioedema, not transfusion reactions.
4. A man who eats mainly polished white rice and drinks heavily has breathlessness, warm peripheries, bounding pulse, oedema and an enlarged heart. Which condition is this?
Answer: Wet beriberi. Thiamine pyrophosphate is a cofactor for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase (pentose phosphate pathway). Deficiency (polished rice diets, alcohol, hyperemesis, refeeding, bariatric surgery) causes: wet beriberi — peripheral vasodilatation, high-output cardiac failure, oedema (Shoshin = fulminant form with lactic acidosis); dry beriberi — symmetrical sensorimotor peripheral neuropathy; Wernicke–Korsakoff; infantile beriberi in breastfed infants of deficient mothers. Raised red-cell transketolase activation; dramatic response to IV thiamine. Give thiamine before glucose in at-risk patients.
- Dry beriberi: Dry beriberi causes neuropathy without heart failure.
- Pellagra: Pellagra causes the three Ds (dermatitis, diarrhoea, dementia).
- Wernicke encephalopathy: Wernicke encephalopathy causes ataxia, confusion and ophthalmoplegia.
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5. A 40-year-old Pakistani man has BMI 26 kg/m² and waist circumference 96 cm. How should his weight status be classified?
Answer: Obese (Asian cut-off), central obesity. BMI = weight (kg) / height (m)². WHO standard: 18.5–24.9 normal, 25–29.9 overweight, ≥ 30 obese. South Asians develop diabetes and CVD at lower BMI and have more visceral fat, so lower thresholds are used: WHO Asian action points — ≥ 23 increased risk, ≥ 27.5 high risk; many South Asian guidelines define overweight ≥ 23 and obesity ≥ 25. Waist (central obesity): South Asian men ≥ 90 cm, women ≥ 80 cm (IDF). Metabolic syndrome (IDF): central obesity plus two of raised triglycerides, low HDL, raised BP, raised fasting glucose. Management: diet, activity, behavioural therapy, drugs (orlistat, GLP-1 agonists), bariatric surgery.
- Overweight; waist irrelevant: Waist circumference adds to cardiometabolic risk.
- Normal — BMI under 30: South Asians have lower cut-offs; BMI 25 or more is obese.
- Overweight (WHO global cut-off only): Asian cut-offs classify him as obese.
6. A 3-day-old boy, well at birth, becomes lethargic and starts vomiting after protein feeds, then hyperventilates and has seizures. Ammonia is 450 µmol/L, there is respiratory alkalosis, and urinary orotic acid is high. What is the diagnosis?
Answer: OTC deficiency. Urea cycle: NH₃ + CO₂ → carbamoyl phosphate (CPS I, mitochondrial, needs N-acetylglutamate) → + ornithine → citrulline (OTC) → argininosuccinate → arginine → urea + ornithine. OTC deficiency is the commonest urea cycle disorder (X-linked; boys present neonatally, carrier girls may present later with protein-induced episodes). Hyperammonaemia stimulates the respiratory centre → respiratory alkalosis (an important clue vs organic acidaemias, which cause metabolic acidosis). Orotic acid ↑ distinguishes OTC from CPS I deficiency (orotic acid low). Treatment: stop protein, IV glucose (stop catabolism), ammonia scavengers (sodium benzoate, sodium phenylbutyrate), arginine, haemodialysis if very high; long-term low-protein diet, liver transplant.
- CPS I deficiency: In CPS I deficiency orotic acid is low.
- Hereditary orotic aciduria: Hereditary orotic aciduria does not cause hyperammonaemia.
- Argininosuccinic aciduria: Orotic acid usually normal or mild.
7. The bicarbonate buffer has a pKa of 6.1, far from blood pH 7.4. Why is it still the most important extracellular buffer?
Answer: Open system (lungs, kidneys). Henderson–Hasselbalch: pH = 6.1 + log ([HCO₃⁻] / (0.03 × PaCO₂ in mmHg)); at pH 7.4 the ratio HCO₃⁻:dissolved CO₂ is about 20:1 (24 : 1.2). Although its pKa is not ideal, the bicarbonate system is powerful because it is present in high concentration and is open: the lungs rapidly change PaCO₂ (minutes) and the kidneys reclaim/generate HCO₃⁻ (days). Other buffers: haemoglobin (main intracellular buffer for CO₂; histidine imidazole groups), proteins, phosphate (intracellular and urinary; pKa 6.8), ammonia (urinary). pH depends on the ratio, not absolute values — compensation restores the ratio.
- Its pKa equals blood pH: Its pKa is 6.1, not 7.4.
- It has the highest pKa: A high pKa is not what makes it effective.
- It is the only buffer: Many other buffers exist, such as proteins and phosphate.
8. A child has recurrent pancreatitis, eruptive xanthomas, lipaemia retinalis and creamy plasma after standing overnight; triglycerides are very high. Which defect is likely?
Answer: Lipoprotein lipase defect. Familial chylomicronaemia (type I hyperlipoproteinaemia): lipoprotein lipase or ApoC-II deficiency (AR) → chylomicrons accumulate → very high triglycerides, creamy supernatant layer on refrigerated plasma, pancreatitis, eruptive xanthomas, hepatosplenomegaly, lipaemia retinalis; no increased atherosclerosis risk. Treatment: very low-fat diet, medium-chain triglycerides. Type IIa (familial hypercholesterolaemia): LDL receptor — tendon xanthomas, premature CAD. Type III: ApoE2 — palmar xanthomas.
- LDL receptor defect: LDL receptor defects cause high LDL and tendon xanthomas.
- ApoE2 homozygosity: ApoE2 homozygosity causes dysbetalipoproteinaemia.
- Abetalipoproteinaemia: Abetalipoproteinaemia causes low lipids.
9. A 20-year-old has hyperextensible skin, hypermobile joints, easy bruising and wide atrophic ‘cigarette-paper’ scars. Which molecule is most commonly defective in the classical type?
Answer: Type V collagen. Ehlers–Danlos syndromes: heterogeneous collagen disorders — classical (COL5A1/2 — type V collagen): skin hyperextensibility, atrophic scars, joint hypermobility; vascular (COL3A1 — type III collagen): thin translucent skin, arterial/bowel/uterine rupture — most dangerous; hypermobile type (commonest, gene unknown). Contrast: Marfan (fibrillin-1), osteogenesis imperfecta (type I), Alport (type IV), scurvy (impaired hydroxylation).
- Type I collagen only: Type I collagen defects cause osteogenesis imperfecta.
- Fibrillin-1: Fibrillin-1 defects cause Marfan syndrome.
- Elastin: Elastin defects cause Williams syndrome or cutis laxa.
10. A 25-year-old with a strong family history has stable mild fasting hyperglycaemia (6.5–7.5 mmol/L) since childhood with HbA1c around 6.5%, no complications. Which enzyme is mutated?
Answer: Glucokinase. Glucokinase (hexokinase IV): high Km, not inhibited by product — glucose sensor in β-cells and liver. Heterozygous inactivating mutations (GCK-MODY, MODY 2) raise the glucose set-point → mild, stable fasting hyperglycaemia, rarely complications; usually no treatment needed (except possibly pregnancy). HNF-1α (MODY 3, commonest): progressive, glycosuria, very sensitive to sulfonylureas; HNF-4α (MODY 1): macrosomia, neonatal hypoglycaemia; HNF-1β (MODY 5): renal cysts, genital anomalies.
- Hexokinase I: Hexokinase I is not the β-cell glucose sensor.
- HNF-1α: HNF-1α MODY is progressive and sulfonylurea-sensitive.
- Insulin receptor: Insulin receptor defects cause severe insulin resistance.
11. In acute intermittent porphyria, which enzyme is deficient and which drug class commonly precipitates attacks?
Answer: Porphobilinogen deaminase; enzyme inducers. Haem synthesis: ALA synthase (rate-limiting, mitochondrial; B6 needed; induced by drugs) → ALA dehydratase (lead) → PBG deaminase (AIP — acute neurovisceral attacks: abdominal pain, neuropathy, psychiatric, hyponatraemia, port-wine urine; triggers — enzyme inducers (barbiturates, phenytoin, carbamazepine), alcohol, fasting, OCP; no photosensitivity) → … uroporphyrinogen decarboxylase (porphyria cutanea tarda — blisters on sun-exposed hands, hepatitis C, alcohol, iron) → ferrochelatase (lead; erythropoietic protoporphyria). AIP treatment: IV haem arginate, glucose; avoid triggers.
- ALA dehydratase; antibiotics: ALA dehydratase is inhibited by lead.
- Ferrochelatase; antacids: Ferrochelatase is involved in lead poisoning and protoporphyria.
- Uroporphyrinogen decarboxylase; statins: UROD deficiency causes PCT.
12. During fasting, muscle sends nitrogen and carbon to the liver for gluconeogenesis and urea synthesis mainly as which amino acid?
Answer: Alanine. Glucose–alanine cycle: muscle transaminates pyruvate to alanine (taking amino groups from branched-chain amino acid breakdown) → alanine travels to liver → transaminated back to pyruvate (ALT) for gluconeogenesis, while nitrogen enters the urea cycle; glucose returns to muscle. Glutamine is the other main nitrogen carrier (to gut and kidney). Cori cycle: lactate from muscle/RBCs → liver gluconeogenesis. Purely ketogenic amino acids: leucine and lysine.
- Leucine: Leucine is ketogenic and not the main carrier.
- Lysine: Lysine is purely ketogenic.
- Tryptophan: Tryptophan is a precursor of serotonin and niacin.
Topics covered
Vitamins, Bioenergetics, Acid–base, Vitamin deficiency, Glucose regulation, Lipoproteins, Amino acid disorders, Minerals, Mineral metabolism, Carbohydrate metabolism, Enzymes in diagnosis, Haemoglobinopathies, Trace elements, Requirements, Obesity, Glycogen storage, Purine metabolism, Amino acid metabolism, Lipid metabolism, Nutrition, Immunoglobulins, Lipid storage disorders, Balanced diet, Molecular techniques, Mutations, Hormone action, Ehlers–Danlos syndrome, Thiamine-dependent enzymes, Nucleotide metabolism, Liver function, Proteins, Lipids & eicosanoids, Molecular biology, Hormones, Porphyrins, Plasma proteins, Lipids, Steroid synthesis, Enzyme kinetics, Haem synthesis
Frequently asked questions
How many NRE Step 1 Biochemistry questions are in the bank?
There are 164 Biochemistry questions in NRE-1 Prep, each with an explanation for every option.
Are these past paper questions?
No. Every question is original, written by us and mapped to the published PMDC NRE syllabus.
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