NEET PG Biochemistry Flashcards

24 sample cards from the Biochemistry deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Which enzyme synthesizes RNA primers in replication, and which removes them?

   Primase synthesizes RNA primers. In prokaryotes, DNA polymerase I removes primers (5'-3' exonuclease) and fills the gap; ligase seals the nicks.

2. What is the role of telomerase, and why is it relevant to aging and cancer?

   Telomerase is a reverse transcriptase with an RNA template that extends telomeres at chromosome ends, compensating for end-replication shortening. It is active in stem cells and most cancers but low in normal somatic cells.

3. What DNA repair mechanism is defective in xeroderma pigmentosum, and what is the result?

   Nucleotide excision repair (NER), which fixes UV-induced pyrimidine dimers. Defect causes extreme UV sensitivity and very high skin cancer risk.

4. Which DNA repair defect underlies hereditary nonpolyposis colorectal cancer (Lynch syndrome)?

   Defective DNA mismatch repair (e.g., MSH2, MLH1), leading to microsatellite instability and increased colorectal/endometrial cancer risk.

5. What is the direction of transcription and which enzyme carries it out in eukaryotes for mRNA?

   Transcription proceeds 5' to 3' (reading template 3' to 5'); RNA polymerase II transcribes mRNA. No primer is required. (Pol I makes rRNA, Pol III makes tRNA/5S rRNA.)

6. What are the three main post-transcriptional modifications of eukaryotic mRNA?

   5' 7-methylguanosine cap, 3' poly-A tail, and splicing to remove introns (joining exons via the spliceosome).

7. What is the wobble hypothesis in translation?

   The third (3') base of the codon (first/5' base of the anticodon) can form non-standard base pairs, allowing one tRNA to recognize multiple codons and explaining codon degeneracy.

8. What is the function of the lac operon and how is it regulated?

   It controls lactose metabolism in E. coli. The repressor blocks transcription; allolactose (inducer) inactivates the repressor (positive: lactose present). Low glucose raises cAMP, which with CAP activates transcription (catabolite repression).

9. What is the principle of the polymerase chain reaction (PCR), and what are its three steps?

   PCR exponentially amplifies a target DNA sequence using primers and a thermostable polymerase (Taq). Steps: denaturation (~95C), annealing (~50-65C), and extension (~72C), repeated in cycles.

10. Differentiate Southern, Northern, and Western blots by their target molecules.

    Southern blot detects DNA, Northern blot detects RNA, and Western blot detects protein (using antibodies). Southwestern detects DNA-binding proteins.

11. What molecular technique is used to detect chromosomal translocations/gene amplification on intact cells, and how does it work?

    FISH (fluorescence in situ hybridization) uses fluorescent DNA probes that hybridize to specific sequences, visualized directly on chromosomes or interphase nuclei.

12. Compare transition vs transversion mutations.

    A transition is a purine-to-purine or pyrimidine-to-pyrimidine substitution; a transversion is a purine-to-pyrimidine substitution (or vice versa). Transitions are more common.

13. Define nonsense, missense, and silent mutations.

    Nonsense mutation creates a premature stop codon; missense changes one amino acid to another; silent mutation changes the codon but encodes the same amino acid (due to degeneracy).

14. How do you recognize autosomal dominant vs autosomal recessive inheritance on a pedigree?

    Autosomal dominant: appears in every generation (vertical transmission), affected can be heterozygous, no skipping, both sexes affected. Autosomal recessive: skips generations (horizontal), parents often unaffected carriers, increased with consanguinity.

15. What features distinguish X-linked recessive inheritance on a pedigree?

    Mostly affected males, no male-to-male transmission, transmitted through carrier mothers; affected males pass the allele to all daughters (carriers) but no sons.

16. What is the Michaelis-Menten equation and what does Km represent?

    V = (Vmax[S])/(Km + [S]). Km is the substrate concentration at half Vmax and is inversely related to enzyme-substrate affinity (low Km = high affinity).

17. How do competitive and noncompetitive inhibitors affect Km and Vmax?

    Competitive inhibitor: increases apparent Km, Vmax unchanged (overcome by more substrate). Noncompetitive inhibitor: decreases Vmax, Km unchanged.

18. Match these B vitamins to their active coenzyme forms: B1, B2, B3, B6.

    B1 (thiamine) -> TPP; B2 (riboflavin) -> FAD/FMN; B3 (niacin) -> NAD+/NADP+; B6 (pyridoxine) -> pyridoxal phosphate (PLP).

19. What deficiency causes beriberi and Wernicke-Korsakoff syndrome, and what is the coenzyme role?

    Thiamine (B1) deficiency. TPP is a cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, branched-chain ketoacid dehydrogenase, and transketolase. Causes wet/dry beriberi and Wernicke-Korsakoff in alcoholics.

20. What are the active forms of vitamin D and the role of vitamin K?

    Vitamin D is activated by 25-hydroxylation (liver) then 1-alpha-hydroxylation (kidney) to calcitriol [1,25-(OH)2-D3]. Vitamin K is a cofactor for gamma-carboxylation of clotting factors II, VII, IX, X and proteins C and S.

21. What clinical syndromes result from vitamin A deficiency and vitamin E deficiency?

    Vitamin A deficiency: night blindness, xerophthalmia, Bitot spots, keratomalacia. Vitamin E deficiency: hemolytic anemia and neurologic deficits (spinocerebellar ataxia, areflexia) from oxidative damage.

22. Which cardiac biomarker is most specific for myocardial infarction and what is its time course?

    Cardiac troponin I/T — most specific; rises in 3-6 hours, peaks at ~24 hours, and stays elevated 7-10 days. CK-MB rises similarly but normalizes in 2-3 days, useful for detecting reinfarction.

23. In liver disease, what does an AST:ALT (De Ritis) ratio greater than 2 suggest?

    Alcoholic liver disease (AST > ALT, ratio >2). In most viral/other hepatitis, ALT > AST. Markedly elevated ALT/AST suggests hepatocellular injury, while elevated ALP/GGT suggests cholestasis.

24. Which enzyme is the most sensitive and specific marker for acute pancreatitis, and how does it compare with amylase?

    Serum lipase — more sensitive and specific, rises early and stays elevated longer (up to 8-14 days). Amylase rises early but is less specific and normalizes faster.

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