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Pharmacology 3% exam weight

Must-know formulas

Part of the INI CET (AIIMS PG) study roadmap. Pharmacology topic pharma-007 of Pharmacology.

By Last updated 3% exam weight

Must-know formulas

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your INI CET Pharmacology paper.

Pharmacology is the science of drug action, split into pharmacokinetics (what the body does to a drug — ADME: Absorption, Distribution, Metabolism, Excretion) and pharmacodynamics (what the drug does to the body — receptor interaction, agonist/antagonist activity, dose–response).

Must-know formulas

  • Half-life: t½ = 0.693 × Vd / CL
  • Loading dose: LD = (Vd × Ctarget) / F
  • Maintenance dose: MD = (CL × Ctarget × τ) / F
  • Therapeutic index: TI = TD50 / ED50 (higher TI = wider safety margin)
  • Steady-state Css: Css = (F × Dose) / (CL × τ)

High-yield exam pointers

  • Zero-order kinetics drugs saturate metabolism — phenytoin, ethanol, high-dose aspirin.
  • Competitive antagonists shift the dose–response curve rightward; Emax is preserved.
  • CYP450 inducers (rifampicin, phenytoin, carbamazepine) lower plasma levels of co-administered drugs; inhibitors (ketoconazole, erythromycin, cimetidine) raise them.
  • Only the free (unbound) fraction is pharmacologically active; protein-bound drug is a reservoir.

🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months of preparation.

Pharmacokinetics — ADME in clinical practice

Absorption depends on route, formulation, and first-pass hepatic loss. Oral bioavailability (F) is reduced for drugs like nitroglycerin, lidocaine, and propranolol because of extensive hepatic first-pass metabolism. Distribution is governed by Vd, lipid solubility, and plasma protein binding (albumin for acidic drugs, α1-acid glycoprotein for basic drugs).

Metabolism occurs in two phases. Phase I (CYP450-mediated oxidation, reduction, hydrolysis) usually activates or detoxifies the parent compound. Phase II conjugates the metabolite with glucuronate, sulfate, or acetate to form water-soluble excretable products. Excretion is mainly renal; drugs with low renal clearance require dose reduction in CKD.

Pharmacodynamics — Receptors and responses

Receptors are classified into four superfamilies: G-protein coupled (β-adrenoceptors, muscarinic M1–M5), ion channel / ionotropic (nicotinic ACh receptor, NMDA), enzyme-linked (insulin receptor, receptor tyrosine kinases), and nuclear / intracellular (steroid, thyroid, vitamin D receptors).

Agonists possess both affinity (Kd) and intrinsic efficacy. Partial agonists produce a submaximal response even at full receptor occupancy. Competitive antagonists increase EC50 but spare Emax; non-competitive antagonists reduce Emax irreversibly.

Order of kinetics

FeatureFirst-orderZero-order
RateProportional to concentrationConstant, saturable
ConstantVariable, dose-dependent
ExamplesMost drugs at therapeutic dosesPhenytoin, ethanol, high-dose aspirin

Pharmacokinetic calculations — worked pattern

For a target theophylline concentration of 10 mg/L, Vd = 0.45 L/kg in a 70 kg adult, CL = 0.04 L/kg/h, τ = 12 h, F = 1:

  • Vd = 31.5 L → LD ≈ 315 mg
  • MD ≈ 168 mg every 12 h

Common exam traps

  • Confusing TD50 with LD50 in the TI formula.
  • Omitting F when calculating an oral loading dose.
  • Assuming CYP450 induction always reduces effect — for prodrugs (codeine → morphine, enalapril → enalaprilat), induction increases active metabolite and can cause toxicity.

🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for INI CET candidates on a longer study timeline.

Adverse drug reactions and clinical reasoning

Type A (augmented) reactions are dose-dependent and predictable — bleeding with warfarin, hypoglycemia with sulfonylureas. Type B (bizarre) reactions are idiosyncratic and unpredictable — malignant hyperthermia with halothane, Stevens-Johnson syndrome with lamotrigine. Type B reactions carry high mortality but low incidence and dominate the “drug of choice in renal/hepatic failure” vignette style.

Drug interactions — CYP450 map for INI CET

CYP isoformSubstratesInhibitorsInducers
CYP3A4Statins, calcium channel blockers, cyclosporineKetoconazole, erythromycin, ritonavir, grapefruit juiceRifampicin, carbamazepine, phenytoin, St John’s wort
CYP2D6Codeine, metoprolol, tricyclicsQuinidine, fluoxetine, paroxetine— (poorly inducible)
CYP2C9Warfarin (S-isomer), phenytoinFluconazole, amiodaroneRifampicin

Dose adjustment in organ dysfunction

  • Renal failure: dose = normal dose × (patient’s CLcr / normal CLcr) for renally cleared drugs (aminoglycosides, digoxin, vancomycin).
  • Hepatic failure: avoid drugs with high first-pass extraction; titrate warfarin, morphine, and propranolol carefully.
  • Elderly: reduced hepatic mass, renal blood flow, and lean body mass; start low, go slow.

Connected topics for integrated revision

  • NSAIDs — COX-1 vs COX-2 selectivity links to gastric mucosal toxicity and cardiovascular risk.
  • Antimicrobials — bactericidal vs bacteriostatic synergy (β-lactam + aminoglycoside) vs antagonism (β-lactam + tetracycline in meningitis).
  • Anticancer chemotherapy — cell-cycle specificity (S-phase: methotrexate, 5-FU; M-phase: vincristine, paclitaxel) connects to toxicity profiles.

Common mistakes revisited

  1. Mixing up potency (EC50) with efficacy (Emax).
  2. Forgetting that receptor desensitization explains tachyphylaxis with β2-agonists and nitrates.
  3. Reporting Vd as a real anatomical volume — it is an apparent value that can exceed total body water for lipophilic drugs.

Practice prompts

  1. A 60 kg patient with status epilepticus needs a phenytoin loading dose of 15 mg/kg IV. Vd = 0.65 L/kg, target Cp = 15 mg/L. Calculate the actual IV dose and explain why this drug cannot be given IM or in dextrose.
  2. A patient on warfarin starts rifampicin for TB. Predict the INR change within 2 weeks and the underlying CYP interaction. What INR monitoring schedule is appropriate?

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