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
| Feature | First-order | Zero-order |
|---|---|---|
| Rate | Proportional to concentration | Constant, saturable |
| t½ | Constant | Variable, dose-dependent |
| Examples | Most drugs at therapeutic doses | Phenytoin, 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 isoform | Substrates | Inhibitors | Inducers |
|---|---|---|---|
| CYP3A4 | Statins, calcium channel blockers, cyclosporine | Ketoconazole, erythromycin, ritonavir, grapefruit juice | Rifampicin, carbamazepine, phenytoin, St John’s wort |
| CYP2D6 | Codeine, metoprolol, tricyclics | Quinidine, fluoxetine, paroxetine | — (poorly inducible) |
| CYP2C9 | Warfarin (S-isomer), phenytoin | Fluconazole, amiodarone | Rifampicin |
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
- Mixing up potency (EC50) with efficacy (Emax).
- Forgetting that receptor desensitization explains tachyphylaxis with β2-agonists and nitrates.
- Reporting Vd as a real anatomical volume — it is an apparent value that can exceed total body water for lipophilic drugs.
Practice prompts
- 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.
- 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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Sources & verification
- Official INI CET (AIIMS PG) syllabus & pattern: https://www.aiimsexams.ac.in/
- Editorial methodology: research → draft → fact-verify → curate pipeline
- Reviewed by Pushkar Saini · last updated
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