PGIMER Entrance Pharmacology Syllabus

Pharmacology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pharmacology in PGIMER Entrance, not a summary of it.

1. 1

   General Pharmacology

   4 topics

   • Pharmacokinetics
     • Absorption, bioavailability and distribution
     • Metabolism, clearance and half-life
   • Pharmacodynamics and receptor theory
   • Adverse drug reactions and drug interactions
   • Routes of administration and bioequivalence
2. 2

   Autonomic and CNS Pharmacology

   4 topics

   • Cholinergic and adrenergic drugs
   • Sedative-hypnotics and antiepileptics
   • Antipsychotics and antidepressants
   • Opioid analgesics and general anesthetics
3. 3

   Systemic and Chemotherapy Pharmacology

   5 topics

   • Antihypertensives and antianginal drugs
   • Diuretics and drugs for heart failure
   • Antimicrobial agents
     • Beta-lactams and protein synthesis inhibitors
     • Antitubercular and antiretroviral drugs
   • Anticancer drugs and immunosuppressants
   • Endocrine pharmacology and hypoglycemics

Pharmacology flashcards for PGIMER Entrance

25 of 55 cards from the Pharmacology deck — real questions with worked answers.

1. Define bioavailability (F) and state its value for an intravenous drug.

   Bioavailability is the fraction of an administered dose that reaches the systemic circulation in unchanged form. For an IV drug, F = 1 (100%) by definition.

2. What is the formula for volume of distribution (Vd)?

   Vd = Amount of drug in the body / Plasma drug concentration. It is an apparent volume relating total body drug to measured plasma concentration.

3. What is the relationship between clearance (CL), volume of distribution (Vd), and elimination half-life (t1/2)?

   t1/2 = 0.693 x Vd / CL. Half-life is directly proportional to Vd and inversely proportional to clearance.

4. Differentiate zero-order from first-order kinetics of drug elimination.

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

5. What is first-pass metabolism and which routes avoid it?

   First-pass metabolism is presystemic metabolism of an oral drug in the gut wall/liver before reaching systemic circulation, reducing bioavailability. Avoided by IV, sublingual, rectal (partial), transdermal, and inhalational routes.

6. How many half-lives are needed to reach steady-state concentration on repeated dosing?

   Approximately 4-5 half-lives (about 94-97% of steady state); the same applies for drug elimination after stopping.

7. List the four reactions of Phase I metabolism and the main enzyme system involved.

   Phase I reactions are oxidation, reduction, hydrolysis, and cyclization/decyclization, performed mainly by the hepatic cytochrome P450 (CYP) microsomal enzyme system.

8. What distinguishes Phase II metabolism from Phase I?

   Phase II is conjugation (glucuronidation, sulfation, acetylation, glutathione, methylation) that adds an endogenous polar group, producing usually inactive, water-soluble metabolites for excretion. Phase I introduces/exposes a functional group.

9. Define the therapeutic index (TI) and give its formula.

   Therapeutic index = TD50 / ED50 (or LD50/ED50 in animals). It measures drug safety; a higher TI indicates a wider safety margin.

10. Distinguish affinity from efficacy (intrinsic activity) at a receptor.

    Affinity is the tendency of a drug to bind to its receptor (governs potency/EC50). Efficacy/intrinsic activity is the ability of the bound drug to produce a response (full agonist =1, antagonist =0, partial agonist between 0 and 1).

11. How does a competitive (reversible) antagonist alter the agonist dose-response curve?

    It shifts the curve to the right (parallel) with no change in maximal response; the effect is surmountable by increasing agonist concentration.

12. How does a non-competitive (irreversible) antagonist alter the agonist dose-response curve?

    It reduces the maximal response (lowers the ceiling) and the effect is not fully surmountable by increasing agonist concentration.

13. Compare a partial agonist with a full agonist at the same receptor.

    A partial agonist has lower intrinsic activity, producing a submaximal response even at full occupancy; in the presence of a full agonist it can act as an antagonist by competing for receptors.

14. What is an inverse agonist?

    An inverse agonist binds the same receptor as an agonist but produces the opposite effect by reducing constitutive (baseline) receptor activity, e.g. beta-carbolines at GABA-A benzodiazepine site.

15. Name the four main receptor superfamilies by signal transduction speed.

    1) Ligand-gated ion channels (milliseconds), 2) G-protein coupled receptors (seconds), 3) Enzyme-linked/kinase-linked receptors (minutes), 4) Intracellular/nuclear (gene transcription) receptors (hours).

16. Classify adverse drug reactions into Type A and Type B with examples.

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

17. What is the difference between pharmacokinetic and pharmacodynamic drug interactions?

    Pharmacokinetic interactions alter absorption, distribution, metabolism, or excretion (changing drug concentration). Pharmacodynamic interactions alter the response at the site of action without changing concentration (additive, synergistic, or antagonistic effects).

18. Name two potent CYP450 enzyme inducers and two inhibitors.

    Inducers: rifampicin, phenytoin, carbamazepine, phenobarbitone, chronic alcohol. Inhibitors: ketoconazole, erythromycin/clarithromycin, cimetidine, ciprofloxacin, grapefruit juice.

19. Define bioequivalence.

    Two pharmaceutically equivalent products are bioequivalent when their rate and extent of absorption (bioavailability: Cmax, Tmax, AUC) are not statistically significantly different under the same conditions.

20. Which routes of administration produce the fastest onset of systemic drug action?

    Intravenous (instantaneous, 100% bioavailability) and inhalational routes give the fastest onset; IV gives immediate, controllable plasma levels.

21. Differentiate nicotinic and muscarinic cholinergic receptors.

    Nicotinic: ligand-gated ion channels at autonomic ganglia (NN) and neuromuscular junction (NM). Muscarinic (M1-M5): G-protein coupled, found on effector organs of parasympathetic system and sweat glands.

22. What are the muscarinic (cholinergic) effects summarized by SLUDGE/DUMBELS?

    Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis (and Miosis, Bronchospasm, Bradycardia). Reflects excess parasympathetic/muscarinic stimulation.

23. What is the antidote for organophosphate (irreversible anticholinesterase) poisoning?

    Atropine (blocks muscarinic effects) plus pralidoxime (2-PAM), a cholinesterase reactivator given before aging of the enzyme occurs.

24. Classify adrenergic receptors and their main second messengers.

    Alpha-1 (Gq, IP3/DAG - vasoconstriction), Alpha-2 (Gi, decrease cAMP - presynaptic inhibition), Beta-1/Beta-2/Beta-3 (Gs, increase cAMP - cardiac stimulation, bronchodilation, lipolysis).

25. Why is adrenaline (epinephrine) preferred over noradrenaline in anaphylaxis?

    Adrenaline stimulates alpha-1 (vasoconstriction, raises BP), beta-1 (cardiac output), and beta-2 (bronchodilation and mast cell stabilization), addressing all features of anaphylaxis.

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