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Pharmacology 3% exam weight

Pharmacodynamics Describes What a Drug Does to the

Part of the INI CET (AIIMS PG) study roadmap. Pharmacology topic pharma-004 of Pharmacology.

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Pharmacodynamics Describes What a Drug Does to the

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Pharmacodynamics describes what a drug does to the body: receptor binding, the resulting biochemical signal, and the magnitude of effect at a given dose. Two drugs can share affinity for one receptor but differ wildly in efficacy — a distinction INI CET rewards with direct MCQs.

  • Potency = EC50/ED50 (position of the curve on the dose axis); efficacy = Emax (height of the curve).
  • Therapeutic Index = TD50 / ED50 — higher TI means wider safety margin (e.g., penicillins high; digoxin, lithium, warfarin low).
  • Competitive antagonists shift the dose-response curve rightward in parallel; non-competitive antagonists lower the maximum (unsurmountable).
  • GPCR coupling rule of thumb: Gs → ↑cAMP, Gi → ↓cAMP, Gq → ↑IP3 / DAG / Ca²⁺.

🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

Receptor Occupancy and the Two Theories

Clark’s occupancy theory assumes response is proportional to the fraction of receptors occupied: Response = [D] / (KD + [D]). Stephenson and Ariëns corrected this by separating affinity (binding, governed by KD) from intrinsic activity / efficacy (ability to trigger a response once bound). This is why a partial agonist can occupy 100% of receptors yet produce only a submaximal effect, and why an inverse agonist produces an opposite effect below baseline.

Agonist Spectrum

Ligand typeAffinityIntrinsic activityNet clinical effect
Full agonistYes+1Maximal response
Partial agonistYes0 < α < 1Submaximal; antagonises full agonist
Competitive antagonistYes0No effect alone; right-shifts curve
Inverse agonistYesNegativeOpposite of basal activity

Dose-Response Curve Interpretation

Curve featureWhat changesWhat it means
Left shift of EC50More potentLess drug needed
Higher plateauMore efficaciousGreater maximum effect
Parallel right shiftCompetitive antagonismSurmountable with dose
Lower plateauNon-competitive antagonismUnsurmountable

Spare receptors mean Emax is reached at occupancy well below 100%, which is why low-dose competitive antagonists can be clinically silent until spare reserve is consumed.

🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for students on a longer study timeline.

Worked Calculation — Therapeutic Index

A drug has ED50 = 10 mg and TD50 (toxic dose in 50% of animals) = 300 mg. TI = 300 / 10 = 30. A narrow-TI drug like digoxin may have TI < 2 in animal screens, explaining why serum-level monitoring is mandatory.

Trap: the question stem often asks “which is safer, drug A or B?” — answer using the ratio, not the absolute TD50. A drug with TD50 = 1000 mg and ED50 = 100 mg (TI = 10) is safer than one with TD50 = 200 mg, ED50 = 50 mg (TI = 4), even though absolute toxicity looks worse.

Common Exam Traps

  1. Potency ≠ efficacy — morphine is less potent than fentanyl but comparable in maximum analgesic effect.
  2. Irreversible antagonists (phenoxybenzamine on α-receptors; aspirin acetylates COX) cannot be overcome by adding more agonist.
  3. Hill equation — n > 1 implies positive cooperativity (e.g., haemoglobin-O2 binding); n < 1 implies negative cooperativity or heterogeneity; n = 1 is classical occupancy.
  4. Receptor regulation — down-regulation (hours-days, decreased receptor number, e.g., β-receptors with chronic β-agonist) is distinct from desensitization / tachyphylaxis (rapid phosphorylation-mediated uncoupling, e.g., β-arrestin recruitment).
  5. Inverse agonists (e.g., famotidine, β-carbolines at GABA-A) only reduce activity below basal — useful when a receptor has constitutive activity.

Adjacent Topics Worth Linking

  • Pharmacokinetics (Topic 3) governs how much drug reaches the receptor; pharmacodynamics governs what happens once it arrives.
  • Adverse drug reactions and drug interactions (later topics) are largely predicted by TI and receptor selectivity.
  • Signal-transduction cascades feed into autonomic and CNS pharmacology — pair every GPCR ligand with its second messenger.

Practice Prompts

  1. A curve shifts right with no change in maximum response after adding an antagonist. Identify the antagonist type and predict the effect of doubling agonist dose.
  2. Calculate TI for Drug X (ED50 = 5 mg, LD50 = 250 mg) and Drug Y (ED50 = 50 mg, LD50 = 2000 mg), and state which is safer.

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