AIIMS PG (DM/MCh) Entrance Basic and Applied Sciences Flashcards

24 sample cards from the Basic and Applied Sciences deck

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

1. What neurotransmitter and receptor mediate the resting membrane potential restoration, and what is the typical neuronal resting membrane potential?

   The Na+/K+-ATPase maintains gradients; resting membrane potential is about -70 mV, closest to the K+ equilibrium potential.

2. Which hypothalamic hormones control anterior pituitary secretion of growth hormone?

   GHRH (growth hormone-releasing hormone) stimulates and somatostatin (GHIH) inhibits GH release.

3. What are the two hormones released by the posterior pituitary and where are they synthesized?

   Oxytocin and ADH (vasopressin); both are synthesized in the hypothalamus (supraoptic and paraventricular nuclei) and stored/released from the posterior pituitary.

4. What is the difference between saltatory and continuous conduction?

   Saltatory conduction occurs in myelinated axons where the action potential jumps node to node (nodes of Ranvier), making it fast; continuous conduction occurs in unmyelinated fibers and is slower.

5. What is the net ATP yield of complete aerobic oxidation of one glucose molecule (commonly cited)?

   Approximately 30-32 ATP (older texts: 36-38), via glycolysis, the TCA cycle, and oxidative phosphorylation.

6. Which enzyme is the rate-limiting (committed) step of glycolysis and how is it regulated?

   Phosphofructokinase-1 (PFK-1); activated by AMP and fructose-2,6-bisphosphate, inhibited by ATP and citrate.

7. What is the rate-limiting enzyme of cholesterol synthesis and the target of statins?

   HMG-CoA reductase, which converts HMG-CoA to mevalonate; inhibited competitively by statins.

8. What is the Cori cycle?

   Lactate produced by anaerobic glycolysis in muscle is transported to the liver and converted back to glucose via gluconeogenesis, then returned to muscle.

9. Distinguish transcription, translation, and replication in molecular genetics.

   Replication: DNA → DNA (DNA polymerase). Transcription: DNA → mRNA (RNA polymerase). Translation: mRNA → protein (ribosomes).

10. What is the difference between a missense, nonsense, and silent mutation?

    Missense: codon change yields a different amino acid. Nonsense: codon change yields a premature stop codon. Silent: codon change codes the same amino acid (no effect).

11. What is the principle of the polymerase chain reaction (PCR), and the three steps per cycle?

    PCR amplifies DNA in vitro. Steps: denaturation (~95°C), annealing of primers (~50-65°C), and extension by Taq polymerase (~72°C).

12. Define enzyme Km and Vmax in Michaelis-Menten kinetics.

    Vmax is the maximal reaction velocity at saturating substrate. Km is the substrate concentration at half Vmax; a low Km indicates high substrate affinity.

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

    Competitive: increases Km, Vmax unchanged. Noncompetitive: Km unchanged, decreases Vmax.

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

    Cardiac troponin (cTnI/cTnT); rises within 3-6 hours, peaks at ~24 hours, and remains elevated for 7-10 days.

15. Define zero-order and first-order pharmacokinetics.

    First-order: a constant fraction of drug is eliminated per unit time (rate proportional to concentration). Zero-order: a constant amount is eliminated per unit time (saturated enzymes), e.g., ethanol, phenytoin at high doses.

16. Write the formula for volume of distribution (Vd).

    Vd = Total amount of drug in the body / Plasma drug concentration; a high Vd indicates extensive tissue distribution.

17. Define the loading dose and maintenance dose formulas.

    Loading dose = (Target plasma concentration × Vd) / bioavailability (F). Maintenance dose rate = (Target concentration × Clearance) / F.

18. Differentiate a drug's potency from its efficacy.

    Potency is the amount of drug needed to produce an effect (related to EC50, position on dose-response curve). Efficacy is the maximal effect achievable (Emax/ceiling), regardless of dose.

19. What is the difference between a competitive antagonist and a noncompetitive (irreversible) antagonist on the agonist dose-response curve?

    Competitive antagonist: shifts curve right (decreased potency), Emax preserved, surmountable. Noncompetitive antagonist: lowers Emax (decreased efficacy), not surmountable.

20. Which adrenergic receptors mediate vasoconstriction, increased heart rate, and bronchodilation respectively?

    Alpha-1: vasoconstriction; Beta-1: increased heart rate/contractility; Beta-2: bronchodilation and vasodilation.

21. What is the mechanism and main use of atropine?

    A competitive muscarinic acetylcholine receptor antagonist; used to treat symptomatic bradycardia and organophosphate (cholinergic) poisoning, and to reduce secretions.

22. Which antibiotics inhibit the bacterial 30S vs the 50S ribosomal subunit?

    30S: aminoglycosides and tetracyclines. 50S: macrolides, clindamycin, chloramphenicol, linezolid, and streptogramins.

23. What is the mechanism of beta-lactam antibiotics, and the main resistance mechanism?

    They inhibit cell wall synthesis by binding penicillin-binding proteins (transpeptidases); resistance is chiefly via bacterial beta-lactamase (penicillinase) enzymes.

24. What is a Type A versus a Type B adverse drug reaction?

    Type A (Augmented): dose-dependent, predictable, related to pharmacology, common (e.g., bleeding with warfarin). Type B (Bizarre): dose-independent, unpredictable, idiosyncratic/immunologic, rarer (e.g., anaphylaxis).

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Basic and Applied Sciences flashcards FAQ