NBEMS has listed NEET-PG 2026 tentatively on 30-08-2026, and says the exact dates will be confirmed in the Information Bulletin; candidates are advised to keep checking the official NBEMS website for the bulletin and application forms. For question practice, use the latest full NEET-PG scheme as the pattern anchor: CBT, single-best MCQs, 200 questions, English only, 3 hours 30 minutes, +4 for correct, −1 for incorrect, 0 for unattempted, and time-bound sections of 40 questions each were described in the 2025 bulletin.

These are original NEET-PG-style practice questions, not reproduced past-paper questions.

Core NEET-PG Pattern MCQs: Biochemistry

Q1. A patient taking isoniazid develops seizures. Which coenzyme deficiency explains this?

A. FAD
B. Pyridoxal phosphate
C. NAD⁺
D. Tetrahydrofolate

Answer: B. Pyridoxal phosphate
INH causes vitamin B6 deficiency. PLP is needed for glutamate decarboxylase, which forms GABA.

Q2. Wernicke encephalopathy is due to a deficiency of the cofactor required for:

A. Pyruvate carboxylase
B. Transketolase
C. Glutathione reductase
D. Xanthine oxidase

Answer: B. Transketolase
Thiamine pyrophosphate is the cofactor for transketolase, pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and branched-chain α-ketoacid dehydrogenase.

Read More  – Important Physiology Questions for NEET PG 2026

Q3. An infant has vomiting, jaundice, hepatomegaly, cataract, and E. coli sepsis after milk feeding. Deficient enzyme?

A. Galactokinase
B. Galactose-1-phosphate uridyltransferase
C. Aldolase B
D. Fructokinase

Answer: B. Galactose-1-phosphate uridyltransferase
Classic galactosemia causes cataracts, liver dysfunction, and sepsis after lactose intake.

Q4. A child develops severe hypoglycemia, vomiting, and liver failure after drinking fruit juice. Which enzyme is deficient?

A. Fructokinase
B. Aldolase B
C. Glucose-6-phosphatase
D. Galactokinase

Answer: B. Aldolase B
Hereditary fructose intolerance causes the accumulation of fructose-1-phosphate, trapping phosphate and causing hypoglycemia.

Q5. A fasting child has hypoketotic hypoglycemia and dicarboxylic aciduria. Diagnosis?

A. MCAD deficiency
B. Von Gierke disease
C. Pompe disease
D. Carnitine excess

Answer: A. MCAD deficiency
Medium-chain acyl-CoA dehydrogenase deficiency impairs β-oxidation, causing low ketones during fasting.

Q6. The rate-limiting enzyme of glycolysis is:

A. Hexokinase
B. Phosphofructokinase-1
C. Pyruvate kinase
D. Glucokinase

Answer: B. Phosphofructokinase-1
PFK-1 is activated by AMP and fructose-2,6-bisphosphate; inhibited by ATP and citrate.

Q7. Glucagon decreases glycolysis in liver mainly by lowering:

A. Fructose-1,6-bisphosphate
B. Fructose-2,6-bisphosphate
C. Glucose-6-phosphate
D. Pyruvate

Answer: B. Fructose-2,6-bisphosphate
Glucagon activates PKA, which activates fructose-2,6-bisphosphatase activity of PFK-2/FBPase-2.

Q8. A child has lactic acidosis, neurologic symptoms, and increased alanine. Defect?

A. Pyruvate dehydrogenase
B. Pyruvate carboxylase
C. Lactate dehydrogenase
D. Glucose-6-phosphatase

Answer: A. Pyruvate dehydrogenase
PDH deficiency diverts pyruvate to lactate and alanine. Treatment may include a ketogenic diet and a thiamine trial.

Q9. Arsenic poisoning mainly affects enzymes requiring:

A. Biotin
B. Lipoic acid
C. Vitamin K
D. Cobalamin

Answer: B. Lipoic acid
Arsenic inhibits lipoic-acid-dependent enzyme complexes like PDH and α-ketoglutarate dehydrogenase.

Q10. Pyruvate carboxylase requires which vitamin-derived coenzyme?

A. Biotin
B. Riboflavin
C. Niacin
D. Folate

Answer: A. Biotin
Biotin is required for carboxylation reactions: pyruvate carboxylase, acetyl-CoA carboxylase, and propionyl-CoA carboxylase.

Q11. A neonate has hyperammonemia and high orotic acid without megaloblastic anaemia. Diagnosis?

A. CPS-I deficiency
B. OTC deficiency
C. UMP synthase deficiency
D. HGPRT deficiency

Answer: B. OTC deficiency
Ornithine transcarbamylase deficiency causes carbamoyl phosphate accumulation, which enters pyrimidine synthesis, increasing orotic acid.

Q12. Hyperammonemia with low orotic acid suggests deficiency of:

A. Ornithine transcarbamylase
B. Carbamoyl phosphate synthetase I
C. UMP synthase
D. Argininosuccinate lyase

Answer: B. Carbamoyl phosphate synthetase I
CPS-I deficiency causes severe hyperammonemia but does not increase orotic acid.

Q12. N-acetylglutamate activates:

A. CPS-I
B. CPS-II
C. OTC
D. Arginase

Answer: A. CPS-I
CPS-I is the first committed enzyme of the urea cycle and requires N-acetylglutamate.

Q13. A child has intellectual disability, musty body odour, fair skin, and eczema. Enzyme-deficient?

A. Tyrosinase
B. Phenylalanine hydroxylase
C. Homogentisate oxidase
D. Cystathionine β-synthase

Answer: B. Phenylalanine hydroxylase
Classic PKU causes increased phenylalanine and decreased tyrosine.

Q14. Maple syrup urine disease is due to a deficiency of:

A. Branched-chain α-ketoacid dehydrogenase
B. Phenylalanine hydroxylase
C. Homogentisate oxidase
D. Propionyl-CoA carboxylase

Answer: A. Branched-chain α-ketoacid dehydrogenase
Increased leucine, isoleucine, and valine cause sweet-smelling urine and neurologic symptoms.

Q15. A patient has lens subluxation, marfanoid habitus, osteoporosis, and thrombosis. Most likely enzyme deficiency?

A. Cystathionine β-synthase
B. Homogentisate oxidase
C. Tyrosinase
D. Histidase

Answer: A. Cystathionine β-synthase
Homocystinuria causes thromboembolism and downward/inward lens dislocation.

Q16. Megaloblastic anaemia with increased orotic acid but normal ammonia is due to:

A. OTC deficiency
B. UMP synthase deficiency
C. CPS-I deficiency
D. Dihydrofolate reductase deficiency

Answer: B. UMP synthase deficiency
Hereditary orotic aciduria is treated with uridine.

Q17. Self-mutilation, chorea, and hyperuricemia suggest a deficiency of:

A. Adenosine deaminase
B. HGPRT
C. Xanthine oxidase
D. PRPP synthetase

Answer: B. HGPRT
Lesch-Nyhan syndrome is X-linked and causes a purine salvage defect.

Q18. Allopurinol inhibits:

A. HGPRT
B. Xanthine oxidase
C. Adenosine deaminase
D. Ribonucleotide reductase

Answer: B. Xanthine oxidase
It reduces uric acid formation from hypoxanthine and xanthine.

Q19. Primaquine-induced hemolysis with bite cells is classically due to a deficiency of:

A. Pyruvate kinase
B. G6PD
C. Hexokinase
D. Aldolase

Answer: B. G6PD
G6PD deficiency decreases NADPH, reducing glutathione regeneration and causing oxidative hemolysis.

Last-Minute High-Yield Biochemistry One-Liners

Suggested practice mode: attempt the 50 MCQs in 45 minutes, then spend another 45 minutes only on explanations and wrong-answer notes.