Pharmacology

Pharmacology is the single highest-yield-per-hour subject in the NEET PG and INI-CET universe. It is small enough to be finished cold in three to four weeks, yet it returns questions in numbers far out of proportion to its size — and it doubles as the answer key for half of Medicine, Anaesthesia, Dermatology, Microbiology and even Forensic Medicine. If you are short on time, Pharmacology is where you spend it. This mother page maps the whole subject the way it is actually tested, system by system, with the associations, numbers, traps and recent guideline shifts that examiners keep returning to.

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How Pharmacology Is Tested

Weightage and format

• NEET PG: Pharmacology typically contributes 12–16 questions out of 200 (roughly 6–8%), making it one of the three biggest pre/para-clinical scorers alongside Pathology and Medicine-linked PSM.
• INI-CET (AIIMS/PGI pattern): Pharmacology runs slightly higher in conceptual depth — expect 10–14 questions, with a heavy bias toward mechanism, receptor, and clinical-decision framing rather than rote recall.
• FMGE: Even larger fractional weight, more factual ("drug of choice", "side effect") in style.

Recurring question styles

Style	What it looks like	Example flavour
Drug of choice (DOC)	"Best initial drug for…"	DOC for status epilepticus, for MRSA, for absence seizures
Mechanism of action	"Acts by…"	Sacubitril = neprilysin inhibitor; ezetimibe blocks NPC1L1
Adverse effect / toxicity	"Characteristic toxicity of…"	Vincristine → neuropathy; bleomycin → pulmonary fibrosis
Antidote pairing	"Specific antidote for…"	Dabigatran → idarucizumab; methotrexate → leucovorin
Receptor / pathway	"Receptor targeted by…"	Varenicline = partial α4β2 nAChR agonist
Image / structure	enzyme cascade, dose-response curve	Graded vs quantal curve, therapeutic index
Assertion–Reason / multi-statement	INI-CET favourite	"Which statements about warfarin are true?"
Newest-drug recall	recently approved molecules	SGLT2i, GLP-1 RA, monoclonals, antivirals

The reliable scoring strategy is to over-prepare General Pharmacology, ANS, and Antimicrobials, because these three groups alone generate close to half of all pharmacology questions and underpin clinical-subject MCQs as well.

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General Pharmacology

This is the conceptual spine — pharmacokinetics (PK), pharmacodynamics (PD), and the lab/regulatory framework. INI-CET loves this section.

Pharmacokinetics: ADME high-yield

• Bioavailability (F): fraction reaching systemic circulation. IV = 100%. First-pass metabolism reduces oral F (propranolol, lignocaine, GTN, morphine, verapamil).
• Volume of distribution (Vd): high Vd = lipophilic, tissue-bound drugs (chloroquine, digoxin, TCAs — not dialysable). Low Vd = plasma-protein-bound, water-soluble (warfarin, aminoglycosides).
• Clearance and half-life: t½ = 0.693 × Vd / CL. Steady state reached in ~4–5 half-lives regardless of dose.
• Zero-order kinetics (constant amount removed): PEAT-W — Phenytoin, Ethanol, Aspirin (high dose), Theophylline, Warfarin (high dose). Trap: students forget aspirin shifts to zero-order at toxic doses.
• Metabolism phases: Phase I (oxidation/reduction/hydrolysis — CYP450) → Phase II (conjugation: glucuronidation, sulfation, acetylation). Prodrugs need activation: enalapril, levodopa, clopidogrel (CYP2C19), codeine (CYP2D6), cyclophosphamide.

CYP450 inducers vs inhibitors — perennial trap

Inducers (↓ drug levels)	Inhibitors (↑ drug levels)
CRAP-GPS: Carbamazepine, Rifampicin, Alcohol (chronic), Phenytoin, Phenobarbitone, Griseofulvin, smoking	Cimetidine, Ketoconazole, Erythromycin/clarithromycin, Grapefruit juice, Isoniazid, Valproate, Ritonavir, Ciprofloxacin

Trap: Valproate is an inhibitor (raises lamotrigine → SJS risk), while most other antiepileptics are inducers. Acute alcohol inhibits; chronic alcohol induces.

Pharmacodynamics essentials

• Affinity = binding; efficacy/intrinsic activity = effect produced. Full agonist (IA = 1), partial agonist (0 < IA < 1, acts as antagonist in presence of full agonist), inverse agonist (IA = −1).
• Potency (dose for effect, shifts curve on x-axis) vs efficacy (max ceiling). A high-ceiling diuretic (furosemide) > thiazide in efficacy though thiazide may be equally "potent" at low end.
• Competitive antagonist → parallel rightward shift, surmountable, Emax unchanged. Non-competitive/irreversible → Emax ↓, not surmountable (phenoxybenzamine).
• Therapeutic index = LD50/ED50. Narrow-TI drugs need monitoring: digoxin, lithium, warfarin, phenytoin, theophylline, aminoglycosides, cyclosporine.
• Graded dose–response (individual, continuous) vs quantal (population, all-or-none → gives ED50, TD50, certain safety factor).

Drug development, trials, pharmacovigilance

• Phase 0 (microdosing) → Phase I (safety, healthy volunteers, ~20–80) → Phase II (efficacy, patients) → Phase III (large RCT, comparison) → Phase IV (post-marketing surveillance).
• Pharmacovigilance in India: PvPI (Pharmacovigilance Programme of India), coordinating centre IPC Ghaziabad; global database VigiBase (Uppsala, WHO-UMC). ADR causality by WHO-UMC scale / Naranjo algorithm.
• Schedule H, H1 (antibiotics/habit-forming, to curb AMR), X (narcotics) under Drugs & Cosmetics Act. Pregnancy categories now replaced by PLLR (Pregnancy and Lactation Labeling Rule) narrative format in the US.

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Autonomic Nervous System (ANS)

ANS is the most "examinable per page" topic. Master receptors and the cholinergic/adrenergic toxidromes and you bank 2–3 questions reliably.

Receptor map

Receptor	G-protein / mechanism	Key effect
α1	Gq → ↑IP3/DAG	vasoconstriction, mydriasis, prostate/bladder neck contraction
α2	Gi → ↓cAMP	presynaptic ↓NE; central sympatholysis (clonidine), platelet aggregation
β1	Gs → ↑cAMP	↑HR, contractility, renin
β2	Gs → ↑cAMP	bronchodilation, vasodilation, uterine relaxation, ↑glycogenolysis
β3	Gs	bladder relaxation (mirabegron), lipolysis
M1/M3	Gq	M3 = smooth muscle/gland secretion
M2	Gi	cardiac slowing
Nm / Nn	ligand-gated ion channel	skeletal NMJ / ganglia

Cholinergic pharmacology

• Organophosphate poisoning (irreversible AChE inhibitor): DUMBBELLS / SLUDGE toxidrome. Treatment = atropine (titrate to dry secretions/clear chest) + pralidoxime/2-PAM (reactivates enzyme before aging; give early). Carbamate poisoning — pralidoxime usually not needed.
• Reversible AChE inhibitors: physostigmine (crosses BBB → CNS/atropine toxicity antidote), neostigmine/pyridostigmine (don't cross BBB → myasthenia, reversal of non-depolarizing blockade), donepezil/rivastigmine/galantamine (Alzheimer's), edrophonium (short, was used in Tensilon test).
• Trap: physostigmine for anticholinergic (atropine, TCA-antimuscarinic) toxicity; neostigmine is the wrong answer there because it can't enter the CNS.

Adrenergic and antagonists

• Selective β1 blockers (cardioselective): BEAM-N — Betaxolol, Esmolol, Atenolol, Metoprolol, Nebivolol (also ↑NO). Nonselective: propranolol, timolol, nadolol.
• α-blockers: phenoxybenzamine (irreversible) + phentolamine for pheochromocytoma — always block α before β to avoid unopposed α crisis. "-osin" (prazosin, tamsulosin) for BPH/HTN; first-dose orthostatic hypotension.
• Epinephrine reversal: after α-blockade, adrenaline's β2 vasodilation predominates → BP falls (Dale's phenomenon).

Classic trap: in pheochromocytoma, never start a β-blocker first.

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Cardiovascular System (CVS)

A dense, clinically integrated group overlapping with Medicine. Focus on antihypertensives, heart failure, antiarrhythmics, anticoagulants, and lipids.

Heart failure — the modern quadruple therapy

Guideline-driven and frequently updated. GDMT "four pillars" for HFrEF:

1. ARNI (sacubitril/valsartan) or ACEi/ARB — sacubitril = neprilysin inhibitor, raises natriuretic peptides; do not combine with ACEi (angioedema), need 36-h washout.
2. Beta-blocker (carvedilol, bisoprolol, metoprolol succinate).
3. MRA (spironolactone, eplerenone).
4. SGLT2 inhibitor (dapagliflozin, empagliflozin) — now indicated in HF regardless of diabetes; works even in HFpEF (recent shift).

• Digoxin: inhibits Na/K-ATPase → ↑intracellular Ca; positive inotrope, used for rate control in AF. Toxicity ↑ by hypokalaemia, hypomagnesaemia, hypercalcaemia, renal failure. Antidote = digoxin-specific Fab (DigiFab). Yellow vision (xanthopsia), arrhythmias.

Antiarrhythmics (Vaughan-Williams)

Class	Mechanism	Examples	Pearl
Ia	Na block (moderate), ↑APD	quinidine, procainamide	cinchonism; lupus (procainamide)
Ib	Na block (fast), ↓APD	lignocaine, mexiletine	ventricular/digoxin arrhythmias
Ic	Na block (marked)	flecainide, propafenone	avoid in structural heart disease
II	β-blockers	metoprolol	rate control
III	K block, ↑APD	amiodarone, sotalol, dofetilide	amiodarone → thyroid, lung, liver, cornea, skin
IV	Ca-channel block	verapamil, diltiazem	AV nodal

• Adenosine: DOC for terminating PSVT (transient AV block; flushing, chest tightness, very short t½).

Anticoagulants / antiplatelets — antidote pairings

Drug	Mechanism	Reversal
Heparin (UFH)	activates antithrombin → ↓IIa, Xa	protamine
LMWH	mainly anti-Xa	protamine (partial)
Warfarin	inhibits VKORC1 (factors II, VII, IX, X, protein C/S)	vitamin K + FFP/4F-PCC
Dabigatran	direct thrombin (IIa)	idarucizumab
Rivaroxaban/apixaban	direct Xa	andexanet alfa
Clopidogrel/prasugrel	P2Y12 blocker	—
Ticagrelor	reversible P2Y12	—

Warfarin pearls: teratogenic (fetal warfarin syndrome), needs heparin bridging due to early protein C fall (skin necrosis), monitored by INR, countless CYP interactions.

Lipids

• Statins (HMG-CoA reductase) — first-line; myopathy/rhabdomyolysis (worse with fibrates—esp. gemfibrozil), ↑transaminases.
• Ezetimibe — blocks NPC1L1 intestinal cholesterol absorption.
• PCSK9 inhibitors (evolocumab, alirocumab) and inclisiran (siRNA, twice-yearly) — newest LDL-lowering; high-yield recent additions.
• Bempedoic acid (ATP-citrate lyase inhibitor) — for statin-intolerant.
• Fibrates → ↓TG (PPAR-α); niacin → ↑HDL but flushing (prevent with aspirin).

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Central Nervous System (CNS)

A favourite for DOC and adverse-effect questions. Antiepileptics, antiparkinsonian, antipsychotics, antidepressants, anaesthetics, and opioids dominate.

Antiepileptics

Indication	Drug of choice	Trap
Status epilepticus	IV lorazepam (or diazepam) → then phenytoin/fosphenytoin/levetiracetam	benzodiazepine first
Absence seizures	ethosuximide (or valproate)	T-type Ca channel
Generalized tonic-clonic	valproate, levetiracetam
Focal	carbamazepine, lamotrigine, levetiracetam
Pregnancy / safest	levetiracetam, lamotrigine	avoid valproate (NTDs)
Myoclonic	valproate, levetiracetam	avoid carbamazepine (worsens)

• Carbamazepine — SIADH/hyponatraemia, SJS with HLA-B*1502 (test in Asians), agranulocytosis.
• Valproate — teratogenic, hepatotoxic, weight gain, hyperammonaemia, tremor.
• Phenytoin — zero-order kinetics, gingival hyperplasia, hirsutism, megaloblastic anaemia, purple glove syndrome, cerebellar signs.
• Vigabatrin — irreversible GABA-transaminase inhibitor, visual field defects.

Parkinsonism

• Levodopa + carbidopa (carbidopa = peripheral DOPA-decarboxylase inhibitor, ↓peripheral side effects, doesn't cross BBB). On–off and wearing-off phenomena.
• COMT inhibitors (entacapone, tolcapone), MAO-B inhibitors (selegiline, rasagiline), dopamine agonists (pramipexole, ropinirole — impulse-control disorders), amantadine (dyskinesia).

Antipsychotics & antidepressants

• Typical (haloperidol, chlorpromazine) — D2 block → extrapyramidal symptoms (EPS), hyperprolactinaemia, NMS (rigidity, hyperthermia, ↑CK → treat with dantrolene + bromocriptine).
• Atypical — clozapine (agranulocytosis → monitor counts; reserved for refractory; also myocarditis, seizures, sialorrhoea), olanzapine/risperidone (metabolic syndrome, weight gain).
• SSRIs — first-line depression; serotonin syndrome (clonus, hyperthermia, autonomic instability) esp. with MAOIs/tramadol → treat with cyproheptadine. SSRI discontinuation syndrome (not with fluoxetine — long t½).
• TCAs — anticholinergic, cardiotoxic (QRS widening → sodium bicarbonate for overdose), the 3 C's: Coma, Convulsions, Cardiotoxicity.

Anaesthetics & opioids

• Inhalational potency = MAC; potency ∝ lipid solubility (Meyer-Overton). Low blood:gas coefficient = fast induction (desflurane, N2O). Halothane → hepatitis; all volatiles + succinylcholine → malignant hyperthermia (RYR1) → dantrolene.
• Ketamine — NMDA antagonist, dissociative, ↑BP/HR, bronchodilator, emergence reactions.
• Opioids — μ-receptor; pinpoint pupils, respiratory depression, constipation (no tolerance). Antidote naloxone. Tramadol → seizures/serotonin syndrome. Buprenorphine = partial agonist (ceiling effect).

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Antimicrobials

The biggest single chemotherapy block and a relentless source of DOC, resistance, and toxicity questions. Integrates heavily with Microbiology and Medicine.

Cell-wall & protein-synthesis inhibitors

Class	Mechanism	Signature toxicity
β-lactams (penicillins, cephalosporins, carbapenems)	inhibit transpeptidase (PBP)	hypersensitivity; cross-reactivity
Vancomycin	inhibits cell-wall (D-ala-D-ala)	Red man syndrome (infusion rate, not allergy), nephro/ototox
Aminoglycosides	30S, irreversible, bactericidal	nephro + ototoxicity, neuromuscular block
Tetracyclines	30S	teeth/bone deposition, photosensitivity (avoid <8 y, pregnancy)
Macrolides	50S	QT prolongation, CYP3A4 inhibition (erythro/clarithro)
Chloramphenicol	50S	aplastic anaemia, grey baby syndrome
Clindamycin	50S	C. difficile colitis
Linezolid	50S	thrombocytopenia, serotonin syndrome (MAOI), MRSA/VRE

DOC quick reference

Organism / condition	Drug of choice
MRSA	vancomycin (or linezolid/daptomycin)
MSSA	cloxacillin/cefazolin
Pseudomonas	piperacillin-tazobactam / ceftazidime / cefepime
Atypical pneumonia (Mycoplasma/Legionella)	macrolide / doxycycline
Syphilis	benzathine penicillin G
Gonorrhoea	ceftriaxone (+ azithro for chlamydia co-treat)
Rickettsia	doxycycline
Anaerobes (below diaphragm)	metronidazole
ESBL	carbapenem
C. difficile	oral vancomycin / fidaxomicin (metronidazole now 2nd line)

Antitubercular (RIPE)

• Isoniazid — peripheral neuropathy (give pyridoxine), hepatitis, lupus; inhibits CYP. Rifampicin — orange secretions, hepatitis, potent CYP inducer (fails OCPs, warfarin). Pyrazinamide — hyperuricaemia/gout, hepatotoxic. Ethambutol — retrobulbar neuritis / colour vision loss (dose-related), least hepatotoxic.
• MDR/XDR-TB: shift to all-oral BPaLM regimen (bedaquiline, pretomanid, linezolid, moxifloxacin) — a major recent guideline change. Bedaquiline → QT prolongation.

Antifungal, antiviral, antimalarial, antiretroviral pearls

• Amphotericin B — binds ergosterol; nephrotoxicity, hypokalaemia, infusion fever (liposomal less toxic). Azoles inhibit ergosterol synthesis (CYP inhibition). Echinocandins (caspofungin) — β-glucan synthesis, candidaemia, well tolerated.
• Antivirals: acyclovir (HSV/VZV, crystalluria), oseltamivir (neuraminidase, influenza), tenofovir (renal/bone), remdesivir/molnupiravir/nirmatrelvir-ritonavir (Paxlovid) for COVID-19 (recent).
• Malaria (India NVBDCP): ACT-based for P. falciparum; primaquine for radical cure of vivax + falciparum gametocyte clearance — check G6PD first (haemolysis). Severe malaria → IV artesunate.
• HIV: first-line = TLD (tenofovir + lamivudine + dolutegravir) per current NACO/WHO. Know zidovudine (anaemia), didanosine/stavudine (pancreatitis, neuropathy — older), efavirenz (CNS/teratogenic), protease inhibitors (lipodystrophy, CYP).

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Endocrine

Diabetes — the rapidly evolving group

Class	Mechanism	Pearl
Biguanide (metformin)	↓hepatic gluconeogenesis (AMPK)	first-line; lactic acidosis, B12 deficiency, weight-neutral
Sulfonylureas	close K-ATP channel	hypoglycaemia, weight gain
SGLT2 inhibitors ("-gliflozin")	block proximal tubule glucose reabsorption	CV + renal protection, euglycaemic DKA, genital infections
GLP-1 RA ("-tide": semaglutide, liraglutide, tirzepatide=GIP/GLP-1)	incretin mimetic	weight loss, CV benefit; pancreatitis, MTC risk; recent star drugs
DPP-4 inhibitors ("-gliptin")	↑endogenous incretin	weight-neutral
Thiazolidinediones (pioglitazone)	PPAR-γ	fluid retention, fractures, bladder Ca caution
α-glucosidase inhibitors (acarbose)	↓carbohydrate absorption	flatulence

Recent shift: SGLT2i and GLP-1 RA are now chosen for CV/renal benefit, not just glucose. Tirzepatide (dual incretin) and oral semaglutide are favourite "new drug" MCQs.

Thyroid, steroids, bone

• Hyperthyroidism: carbimazole/methimazole (1st line; aplasia cutis in pregnancy → use PTU in 1st trimester); agranulocytosis with both. PTU also blocks peripheral T4→T3 (thyroid storm). β-blocker for symptoms.
• Corticosteroids: Cushingoid effects, osteoporosis, hyperglycaemia, immunosuppression, HPA suppression (taper, don't stop abruptly). Mineralocorticoid potency: fludrocortisone >> others; dexamethasone has none.
• Bone: bisphosphonates (osteoclast inhibition; osteonecrosis of jaw, atypical femoral fracture, oesophagitis — take upright fasting); denosumab (RANKL mAb); teriparatide (PTH analogue, anabolic); romosozumab (sclerostin inhibitor, newer).

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Chemotherapy (Anticancer)

A high-yield block dominated by mechanism + organ-specific toxicity pairings and the new targeted/immuno agents.

Cytotoxics — signature toxicity (commonest trap)

Drug	Class	Hallmark toxicity
Vincristine	vinca alkaloid (M phase)	peripheral neuropathy (no myelosuppression)
Vinblastine	vinca	myelosuppression
Bleomycin	antibiotic (G2)	pulmonary fibrosis; minimal marrow tox
Doxorubicin	anthracycline	dilated cardiomyopathy (prevent with dexrazoxane)
Cyclophosphamide	alkylator	haemorrhagic cystitis (prevent with MESNA)
Cisplatin	platinum	nephrotoxicity, ototoxicity, peripheral neuropathy (amifostine protective)
Methotrexate	antifolate (S)	mucositis, marrow → rescue with leucovorin
5-FU	antimetabolite	mucositis, hand-foot syndrome, cerebellar
Busulfan	alkylator	pulmonary fibrosis, hyperpigmentation
Paclitaxel	taxane	neuropathy, hypersensitivity

• Tumour lysis syndrome: ↑K, ↑PO4, ↑uric acid, ↓Ca → prevent with hydration + rasburicase/allopurinol.

Targeted & immunotherapy (recent, high-yield)

• Imatinib — BCR-ABL TKI (CML, GIST c-KIT) — landmark targeted drug.
• -mabs: trastuzumab (HER2, cardiotoxic), rituximab (CD20), bevacizumab (VEGF — bleeding/HTN), cetuximab (EGFR).
• Immune checkpoint inhibitors: pembrolizumab/nivolumab (PD-1), atezolizumab (PD-L1), ipilimumab (CTLA-4) → immune-related adverse events (colitis, hypophysitis, thyroiditis, pneumonitis). Increasingly tested.
• CAR-T cell therapy — cytokine release syndrome (treat with tocilizumab, anti-IL-6R).

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Autacoids

Histamine, serotonin, prostaglandins, NSAIDs, and migraine drugs — a small but reliably tested group.

NSAIDs and eicosanoids

• Aspirin: irreversible COX inhibition. Low dose = antiplatelet (COX-1, TXA2). Overdose → mixed respiratory alkalosis + metabolic acidosis; tinnitus; Reye's syndrome in children with viral fever (avoid). Zero-order at high dose.
• COX-2 selective (celecoxib, etoricoxib): less GI ulceration but ↑CV/thrombotic risk (rofecoxib withdrawn — classic example).
• Prostaglandin uses: misoprostol (PGE1 — NSAID-ulcer prophylaxis, MTP with mifepristone, PPH), alprostadil (PDA patency, ED), latanoprost (PGF2α — glaucoma), dinoprostone (cervical ripening).
• Paracetamol: overdose → NAPQI hepatotoxicity → antidote N-acetylcysteine (replenishes glutathione).

Histamine & serotonin

• H1 antagonists: 1st gen (diphenhydramine, promethazine — sedating, antiemetic, antimuscarinic) vs 2nd gen (cetirizine, fexofenadine, loratadine — non-sedating, don't cross BBB).
• H2 blockers (ranitidine—largely withdrawn over NDMA, famotidine) for acid; PPIs (omeprazole) irreversibly block H/K-ATPase — long-term: hypomagnesaemia, B12 deficiency, C. difficile, fracture, rebound hyperacidity.
• 5-HT3 antagonists (ondansetron — chemo emesis, QT). Triptans (sumatriptan, 5-HT1B/1D agonist) for acute migraine — contraindicated in CAD; gepants (rimegepant) and CGRP mAbs (erenumab) are the newer migraine class (recent).

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Cross-Subject Integration Points

Pharmacology rarely sits alone in a paper. These overlaps recur:

• Medicine: HF quadruple therapy, antihypertensive choices in comorbidity (ACEi in DM nephropathy, avoid in bilateral RAS/pregnancy), anticoagulation, DKA, thyroid storm.
• Microbiology: mechanism of resistance (β-lactamase, efflux, altered PBP), DOC per organism, antibiotic-bacteria pairing.
• Anaesthesia: MAC, neuromuscular blockers, malignant hyperthermia, local anaesthetic toxicity (lignocaine max dose, intralipid for LA systemic toxicity).
• OBG: uterotonics (oxytocin, ergometrine—avoid in HTN, carboprost—avoid in asthma, misoprostol), tocolytics (nifedipine, atosiban), teratogens.
• Forensic Medicine: poisoning antidotes, drug schedules, NDPS Act, dependence.
• Dermatology: isotretinoin (teratogen, dyslipidaemia), dapsone (haemolysis/methaemoglobinaemia), biologics.
• Ophthalmology: glaucoma drugs, ethambutol/hydroxychloroquine retinal toxicity, mydriatics/miotics.

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Recent Update Themes (Current Exams)

Examiners chase what is new in guidelines. Prioritise:

• SGLT2 inhibitors & GLP-1 RA expanding beyond diabetes into HF and CKD; tirzepatide dual agonist.
• HF "four pillars" including ARNI and SGLT2i, and SGLT2i benefit in HFpEF.
• Newer anticoagulant reversal: idarucizumab, andexanet alfa.
• TB: all-oral BPaLM regimen for DR-TB; bedaquiline, pretomanid.
• HIV: dolutegravir-based TLD first line.
• Lipid lowering: PCSK9 inhibitors, inclisiran (siRNA), bempedoic acid.
• Migraine: CGRP antagonists (gepants, mAbs).
• Oncology: checkpoint inhibitors, CAR-T, antibody-drug conjugates.
• Drug withdrawals/safety: ranitidine (NDMA), rofecoxib (CV), regulatory pharmacovigilance via PvPI.
• COVID-era antivirals: nirmatrelvir-ritonavir, molnupiravir, remdesivir.

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Study Roadmap

Phased plan (3–4 weeks first pass)

1. Week 1 — General Pharmacology + ANS. These are conceptual and reusable everywhere; nail PK/PD, CYP, receptors, cholinergic/adrenergic. Highest ROI.
2. Week 2 — ANS antagonists, CVS, CNS. Build DOC tables; learn toxicity-by-drug.
3. Week 3 — Antimicrobials + Chemotherapy. Largest factual load; make DOC and toxicity grids.
4. Week 4 — Endocrine, Autacoids, integration + revision. Layer the recent-drug updates.

Method

• Drive learning through tables and one-liners, not paragraphs — pharmacology is association-heavy.
• Solve PYQs first, then topic; the same drugs recur (digoxin, amiodarone, MTX, INH, warfarin).
• Maintain a running antidote sheet and a toxicity sheet — two of the most question-dense formats.
• For INI-CET, add a depth pass on mechanism and receptor detail and multi-statement reasoning.

Last-week revision strategy

• Revise only tables, mnemonics, and your error log — no new topics.
• Re-read the antidote/toxicity/DOC triad daily; these are guaranteed marks.
• Skim the recent-drug list the night before — examiners love newly approved molecules.
• Do 2–3 timed PYQ/mock blocks to keep recall fast under pressure.

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High-Yield Tables

Specific antidotes (must memorize)

Poison / drug	Antidote
Organophosphate	atropine + pralidoxime
Paracetamol	N-acetylcysteine
Opioids	naloxone
Benzodiazepines	flumazenil
Heparin	protamine
Warfarin	vitamin K / 4F-PCC
Dabigatran	idarucizumab
Rivaroxaban/apixaban	andexanet alfa
Digoxin	digoxin-specific Fab
Methotrexate	leucovorin (folinic acid)
Iron	desferrioxamine
Lead	EDTA / DMSA / dimercaprol
Methanol/ethylene glycol	fomepizole (or ethanol)
Cyanide	hydroxocobalamin / sodium thiosulfate
Methaemoglobinaemia	methylene blue
β-blocker / CCB overdose	glucagon / high-dose insulin
Malignant hyperthermia / NMS	dantrolene
Serotonin syndrome	cyproheptadine

Teratogenic drugs

Drug	Defect
Warfarin	fetal warfarin syndrome, nasal hypoplasia
Valproate / carbamazepine	neural tube defects
Phenytoin	fetal hydantoin syndrome
ACEi/ARB	renal dysgenesis, oligohydramnios
Isotretinoin	CNS, craniofacial, cardiac
Thalidomide	phocomelia
Tetracycline	teeth/bone staining
Lithium	Ebstein anomaly
Methotrexate	multiple
Aminoglycosides	ototoxicity

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Mnemonics

• Zero-order kinetics — "PEAT-W": Phenytoin, Ethanol, Aspirin (high dose), Theophylline, Warfarin (high dose).
• CYP inducers — "CRAP-GPS": Carbamazepine, Rifampicin, Alcohol(chronic), Phenobarb, Phenytoin, Griseofulvin, smoking.
• Cardioselective β1 blockers — "BEAM-N": Betaxolol, Esmolol, Atenolol, Metoprolol, Nebivolol.
• Cholinergic excess — "DUMBBELLS": Diarrhoea, Urination, Miosis, Bradycardia/Bronchorrhoea, Emesis, Lacrimation, Lethargy, Salivation.
• Narrow therapeutic index — "Watch Diligently, Lest Patients Take Anxiety, Cry": Warfarin, Digoxin, Lithium, Phenytoin, Theophylline, Aminoglycosides, Cyclosporine.
• HF four pillars — "ABMS": ARNI, Beta-blocker, MRA, SGLT2i.

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Rapid-Fire One-Liners

1. DOC for status epilepticus — IV lorazepam first; not phenytoin.
2. Sacubitril is a neprilysin inhibitor; never combine with ACEi (angioedema).
3. Ethambutol → retrobulbar neuritis / loss of colour vision; isoniazid → neuropathy (give pyridoxine).
4. Vincristine → neuropathy; bleomycin → pulmonary fibrosis; doxorubicin → cardiomyopathy.
5. Cyclophosphamide haemorrhagic cystitis is prevented by MESNA.
6. Idarucizumab reverses dabigatran; andexanet alfa reverses factor-Xa inhibitors.
7. Red man syndrome with vancomycin is an infusion-rate reaction, not true allergy.
8. First-trimester hyperthyroidism → use PTU (methimazole = aplasia cutis).
9. SGLT2 inhibitors cause euglycaemic DKA and now benefit HF and CKD irrespective of diabetes.
10. Physostigmine (crosses BBB) treats anticholinergic toxicity; neostigmine does not.
11. First-line MDR-TB is the all-oral BPaLM regimen (bedaquiline, pretomanid, linezolid, moxifloxacin).
12. First-line HIV = TLD (tenofovir + lamivudine + dolutegravir).