{"id":18849,"date":"2026-05-12T10:33:30","date_gmt":"2026-05-12T10:33:30","guid":{"rendered":"https:\/\/www.diginerve.com\/blogs\/?p=18849"},"modified":"2026-05-12T10:33:30","modified_gmt":"2026-05-12T10:33:30","slug":"important-biochemistry-questions-for-neet-pg","status":"publish","type":"post","link":"https:\/\/www.diginerve.com\/blogs\/important-biochemistry-questions-for-neet-pg\/","title":{"rendered":"Important Questions and Answers on Biochemistry for NEET PG 2026"},"content":{"rendered":"

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. <\/span>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, \u22121 for incorrect, 0 for unattempted, and time-bound sections of 40 questions each were described in the 2025 bulletin.<\/span><\/p>\n

These are original NEET-PG-style practice questions, not reproduced past-paper questions.<\/span><\/p>\n

Core NEET-PG Pattern MCQs: Biochemistry<\/b><\/h2>\n

Q1. A patient taking isoniazid develops seizures. Which coenzyme deficiency explains this?<\/b><\/p>\n

A. FAD<\/span>
\n<\/span>B. Pyridoxal phosphate<\/span>
\n<\/span>C. NAD<\/span>\u207a<\/span>
\n<\/span>D. Tetrahydrofolate<\/span><\/p>\n

Answer: B. Pyridoxal phosphate<\/b>
\n<\/span>INH causes vitamin B6 deficiency. PLP is needed for glutamate decarboxylase, which forms GABA.<\/span><\/p>\n

 <\/p>\n

Q2. Wernicke encephalopathy is due to a deficiency of the cofactor required for:<\/b><\/p>\n

A. Pyruvate carboxylase<\/span>
\n<\/span>B. Transketolase<\/span>
\n<\/span>C. Glutathione reductase<\/span>
\n<\/span>D. Xanthine oxidase<\/span><\/p>\n

Answer: B. Transketolase<\/b>
\n<\/span>Thiamine pyrophosphate is the cofactor for transketolase, pyruvate dehydrogenase, \u03b1-ketoglutarate dehydrogenase, and branched-chain \u03b1-ketoacid dehydrogenase.<\/span><\/p>\n

Read More\u00a0 – Important Physiology Questions for NEET PG 2026<\/a>
\n<\/strong><\/p>\n

Q3. An infant has vomiting, jaundice, hepatomegaly, cataract, and <\/b>E. coli<\/i><\/b> sepsis after milk feeding. Deficient enzyme?<\/b><\/p>\n

A. Galactokinase<\/span>
\n<\/span>B. Galactose-1-phosphate uridyltransferase<\/span>
\n<\/span>C. Aldolase B<\/span>
\n<\/span>D. Fructokinase<\/span><\/p>\n

Answer: B. Galactose-1-phosphate uridyltransferase<\/b>
\n<\/span>Classic galactosemia causes cataracts, liver dysfunction, and sepsis after lactose intake.<\/span><\/p>\n

 <\/p>\n

Q4. A child develops severe hypoglycemia, vomiting, and liver failure after drinking fruit juice. Which enzyme is deficient?<\/b><\/p>\n

A. Fructokinase<\/span>
\n<\/span>B. Aldolase B<\/span>
\n<\/span>C. Glucose-6-phosphatase<\/span>
\n<\/span>D. Galactokinase<\/span><\/p>\n

Answer: B. Aldolase B<\/b>
\n<\/span>Hereditary fructose intolerance causes the accumulation of fructose-1-phosphate, trapping phosphate and causing hypoglycemia.<\/span><\/p>\n

 <\/p>\n

Q5. A fasting child has hypoketotic hypoglycemia and dicarboxylic aciduria. Diagnosis?<\/b><\/p>\n

A. MCAD deficiency<\/span>
\n<\/span>B. Von Gierke disease<\/span>
\n<\/span>C. Pompe disease<\/span>
\n<\/span>D. Carnitine excess<\/span><\/p>\n

Answer: A. MCAD deficiency<\/b>
\n<\/span>Medium-chain acyl-CoA dehydrogenase deficiency impairs \u03b2-oxidation, causing low ketones during fasting.<\/span><\/p>\n

 <\/p>\n

Q6. The rate-limiting enzyme of glycolysis is:<\/b><\/p>\n

A. Hexokinase<\/span>
\n<\/span>B. Phosphofructokinase-1<\/span>
\n<\/span>C. Pyruvate kinase<\/span>
\n<\/span>D. Glucokinase<\/span><\/p>\n

Answer: B. Phosphofructokinase-1<\/b>
\n<\/span>PFK-1 is activated by AMP and fructose-2,6-bisphosphate; inhibited by ATP and citrate.<\/span><\/p>\n

 <\/p>\n

Q7. Glucagon decreases glycolysis in liver mainly by lowering:<\/b><\/p>\n

A. Fructose-1,6-bisphosphate<\/span>
\n<\/span>B. Fructose-2,6-bisphosphate<\/span>
\n<\/span>C. Glucose-6-phosphate<\/span>
\n<\/span>D. Pyruvate<\/span><\/p>\n

Answer: B. Fructose-2,6-bisphosphate<\/b>
\n<\/span>Glucagon activates PKA, which activates fructose-2,6-bisphosphatase activity of PFK-2\/FBPase-2.<\/span><\/p>\n

 <\/p>\n

Q8. A child has lactic acidosis, neurologic symptoms, and increased alanine. Defect?<\/b><\/p>\n

A. Pyruvate dehydrogenase<\/span>
\n<\/span>B. Pyruvate carboxylase<\/span>
\n<\/span>C. Lactate dehydrogenase<\/span>
\n<\/span>D. Glucose-6-phosphatase<\/span><\/p>\n

Answer: A. Pyruvate dehydrogenase<\/b>
\n<\/span>PDH deficiency diverts pyruvate to lactate and alanine. Treatment may include a ketogenic diet and a thiamine trial.<\/span><\/p>\n

 <\/p>\n

Q9. Arsenic poisoning mainly affects enzymes requiring:<\/b><\/p>\n

A. Biotin<\/span>
\n<\/span>B. Lipoic acid<\/span>
\n<\/span>C. Vitamin K<\/span>
\n<\/span>D. Cobalamin<\/span><\/p>\n

Answer: B. Lipoic acid<\/b>
\n<\/span>Arsenic inhibits lipoic-acid-dependent enzyme complexes like PDH and \u03b1-ketoglutarate dehydrogenase.<\/span><\/p>\n

 <\/p>\n

Q10. Pyruvate carboxylase requires which vitamin-derived coenzyme?<\/b><\/p>\n

A. Biotin<\/span>
\n<\/span>B. Riboflavin<\/span>
\n<\/span>C. Niacin<\/span>
\n<\/span>D. Folate<\/span><\/p>\n

Answer: A. Biotin<\/b>
\n<\/span>Biotin is required for carboxylation reactions: pyruvate carboxylase, acetyl-CoA carboxylase, and propionyl-CoA carboxylase.<\/span><\/p>\n

 <\/p>\n

Q11. A neonate has hyperammonemia and high orotic acid without megaloblastic anaemia. Diagnosis?<\/b><\/p>\n

A. CPS-I deficiency<\/span>
\n<\/span>B. OTC deficiency<\/span>
\n<\/span>C. UMP synthase deficiency<\/span>
\n<\/span>D. HGPRT deficiency<\/span><\/p>\n

Answer: B. OTC deficiency<\/b>
\n<\/span>Ornithine transcarbamylase deficiency causes carbamoyl phosphate accumulation, which enters pyrimidine synthesis, increasing orotic acid.<\/span><\/p>\n

 <\/p>\n

Q12. Hyperammonemia with low orotic acid suggests deficiency of:<\/b><\/p>\n

A. Ornithine transcarbamylase<\/span>
\n<\/span>B. Carbamoyl phosphate synthetase I<\/span>
\n<\/span>C. UMP synthase<\/span>
\n<\/span>D. Argininosuccinate lyase<\/span><\/p>\n

Answer: B. Carbamoyl phosphate synthetase I<\/b>
\n<\/span>CPS-I deficiency causes severe hyperammonemia but does not increase orotic acid.<\/span><\/p>\n

 <\/p>\n

Q12. N-acetylglutamate activates:<\/b><\/p>\n

A. CPS-I<\/span>
\n<\/span>B. CPS-II<\/span>
\n<\/span>C. OTC<\/span>
\n<\/span>D. Arginase<\/span><\/p>\n

Answer: A. CPS-I<\/b>
\n<\/span>CPS-I is the first committed enzyme of the urea cycle and requires N-acetylglutamate.<\/span><\/p>\n

 <\/p>\n

Q13. A child has intellectual disability, musty body odour, fair skin, and eczema. Enzyme-deficient?<\/b><\/p>\n

A. Tyrosinase<\/span>
\n<\/span>B. Phenylalanine hydroxylase<\/span>
\n<\/span>C. Homogentisate oxidase<\/span>
\n<\/span>D. Cystathionine \u03b2-synthase<\/span><\/p>\n

Answer: B. Phenylalanine hydroxylase<\/b>
\n<\/span>Classic PKU causes increased phenylalanine and decreased tyrosine.<\/span><\/p>\n

 <\/p>\n

Q14. Maple syrup urine disease is due to a deficiency of:<\/b><\/p>\n

A. Branched-chain \u03b1-ketoacid dehydrogenase<\/span>
\n<\/span>B. Phenylalanine hydroxylase<\/span>
\n<\/span>C. Homogentisate oxidase<\/span>
\n<\/span>D. Propionyl-CoA carboxylase<\/span><\/p>\n

Answer: A. Branched-chain \u03b1-ketoacid dehydrogenase<\/b>
\n<\/span>Increased leucine, isoleucine, and valine cause sweet-smelling urine and neurologic symptoms.<\/span><\/p>\n

 <\/p>\n

Q15. A patient has lens subluxation, marfanoid habitus, osteoporosis, and thrombosis. Most likely enzyme deficiency?<\/b><\/p>\n

A. Cystathionine \u03b2-synthase<\/span>
\n<\/span>B. Homogentisate oxidase<\/span>
\n<\/span>C. Tyrosinase<\/span>
\n<\/span>D. Histidase<\/span><\/p>\n

Answer: A. Cystathionine \u03b2-synthase<\/b>
\n<\/span>Homocystinuria causes thromboembolism and downward\/inward lens dislocation.<\/span><\/p>\n

 <\/p>\n

Q16. Megaloblastic anaemia with increased orotic acid but normal ammonia is due to:<\/b><\/p>\n

A. OTC deficiency<\/span>
\n<\/span>B. UMP synthase deficiency<\/span>
\n<\/span>C. CPS-I deficiency<\/span>
\n<\/span>D. Dihydrofolate reductase deficiency<\/span><\/p>\n

Answer: B. UMP synthase deficiency<\/b>
\n<\/span>Hereditary orotic aciduria is treated with uridine.<\/span><\/p>\n

 <\/p>\n

Q17. Self-mutilation, chorea, and hyperuricemia suggest a deficiency of:<\/b><\/p>\n

A. Adenosine deaminase<\/span>
\n<\/span>B. HGPRT<\/span>
\n<\/span>C. Xanthine oxidase<\/span>
\n<\/span>D. PRPP synthetase<\/span><\/p>\n

Answer: B. HGPRT<\/b>
\n<\/span>Lesch-Nyhan syndrome is X-linked and causes a purine salvage defect.<\/span><\/p>\n

 <\/p>\n

Q18. Allopurinol inhibits:<\/b><\/p>\n

A. HGPRT<\/span>
\n<\/span>B. Xanthine oxidase<\/span>
\n<\/span>C. Adenosine deaminase<\/span>
\n<\/span>D. Ribonucleotide reductase<\/span><\/p>\n

Answer: B. Xanthine oxidase<\/b>
\n<\/span>It reduces uric acid formation from hypoxanthine and xanthine.<\/span><\/p>\n

 <\/p>\n

Q19. Primaquine-induced hemolysis with bite cells is classically due to a deficiency of:<\/b><\/p>\n

A. Pyruvate kinase<\/span>
\n<\/span>B. G6PD<\/span>
\n<\/span>C. Hexokinase<\/span>
\n<\/span>D. Aldolase<\/span><\/p>\n

Answer: B. G6PD<\/b>
\n<\/span>G6PD deficiency decreases NADPH, reducing glutathione regeneration and causing oxidative hemolysis.<\/span><\/p>\n

 <\/p>\n

Last-Minute High-Yield Biochemistry One-Liners<\/strong><\/h2>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
Topic<\/b><\/td>\nMust-know answer<\/b><\/td>\n<\/tr>\n
G6PD function<\/span><\/td>\nNADPH production in the HMP shunt<\/span><\/td>\n<\/tr>\n
Thiamine enzymes<\/span><\/td>\nPDH, \u03b1-KGDH, BCKD, transketolase<\/span><\/td>\n<\/tr>\n
Biotin enzymes<\/span><\/td>\nCarboxylases<\/span><\/td>\n<\/tr>\n
B12 marker<\/span><\/td>\nMethylmalonic acid \u2191<\/span><\/td>\n<\/tr>\n
Folate marker<\/span><\/td>\nHomocysteine \u2191, MMA normal<\/span><\/td>\n<\/tr>\n
OTC deficiency<\/span><\/td>\nHyperammonemia + orotic acid \u2191<\/span><\/td>\n<\/tr>\n
UMP synthase deficiency<\/span><\/td>\nOrotic acid \u2191 + megaloblastic anemia + normal ammonia<\/span><\/td>\n<\/tr>\n
MCAD deficiency<\/span><\/td>\nHypoketotic hypoglycemia<\/span><\/td>\n<\/tr>\n
Von Gierke<\/span><\/td>\nG6Pase deficiency<\/span><\/td>\n<\/tr>\n
McArdle<\/span><\/td>\nMuscle glycogen phosphorylase deficiency<\/span><\/td>\n<\/tr>\n
Pompe<\/span><\/td>\nLysosomal acid \u03b1-glucosidase deficiency<\/span><\/td>\n<\/tr>\n
PKU<\/span><\/td>\nPhenylalanine hydroxylase deficiency<\/span><\/td>\n<\/tr>\n
MSUD<\/span><\/td>\nBCKD deficiency<\/span><\/td>\n<\/tr>\n
Alkaptonuria<\/span><\/td>\nHomogentisate oxidase deficiency<\/span><\/td>\n<\/tr>\n
Homocystinuria<\/span><\/td>\nCBS deficiency; thrombosis<\/span><\/td>\n<\/tr>\n
Lesch-Nyhan<\/span><\/td>\nHGPRT deficiency<\/span><\/td>\n<\/tr>\n
AIP<\/span><\/td>\nPorphobilinogen deaminase deficiency<\/span><\/td>\n<\/tr>\n
Lead poisoning<\/span><\/td>\nALA dehydratase + ferrochelatase inhibition<\/span><\/td>\n<\/tr>\n
Apo C-II<\/span><\/td>\nActivates LPL<\/span><\/td>\n<\/tr>\n
Apo E<\/span><\/td>\nRemnant uptake<\/span><\/td>\n<\/tr>\n
Apo B100<\/span><\/td>\nLDL receptor binding<\/span><\/td>\n<\/tr>\n
Southern blot<\/span><\/td>\nDNA<\/span><\/td>\n<\/tr>\n
Northern blot<\/span><\/td>\nRNA<\/span><\/td>\n<\/tr>\n
Western blot<\/span><\/td>\nProtein<\/span><\/td>\n<\/tr>\n
Sanger sequencing<\/span><\/td>\nddNTP chain termination<\/span><\/td>\n<\/tr>\n
Competitive inhibition<\/span><\/td>\nKm \u2191, Vmax same<\/span><\/td>\n<\/tr>\n
Noncompetitive inhibition<\/span><\/td>\nVmax \u2193, Km same<\/span><\/td>\n<\/tr>\n
Uncompetitive inhibition<\/span><\/td>\nKm \u2193, Vmax \u2193<\/span><\/td>\n<\/tr>\n
Vitamin C<\/span><\/td>\nCollagen hydroxylation<\/span><\/td>\n<\/tr>\n
Vitamin K<\/span><\/td>\n\u03b3-carboxylation of clotting factors<\/span><\/td>\n<\/tr>\n
Vitamin A<\/span><\/td>\nVision + epithelial differentiation<\/span><\/td>\n<\/tr>\n
Vitamin D<\/span><\/td>\nCalcium\/phosphate homeostasis<\/span><\/td>\n<\/tr>\n
Statins<\/span><\/td>\nHMG-CoA reductase inhibitors<\/span><\/td>\n<\/tr>\n
Liver cannot use ketones<\/span><\/td>\nLacks thiophorase<\/span><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Suggested practice mode:<\/b> attempt the 50 MCQs in 45 minutes, then spend another 45 minutes only on explanations and wrong-answer notes.<\/span><\/p>\n","protected":false},"excerpt":{"rendered":"

NBEMS has listed NEET-PG 2026 tentatively on 30-08-2026, and says […]<\/p>\n","protected":false},"author":16,"featured_media":18850,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[123],"tags":[975,976],"class_list":["post-18849","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-neet-pg","tag-biochemistry-neet-pg","tag-neet-pg-biochemistry-questions"],"yoast_head":"\nImportant Questions and Answers on Biochemistry for NEET PG 2026 - Your Guide At Every Step to Become The Top Doctor<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.diginerve.com\/blogs\/important-biochemistry-questions-for-neet-pg\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Important Questions and Answers on Biochemistry for NEET PG 2026 - 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