Classification of each and every pharmacological drug Classification and moa for viva
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Given the massive scope of this request (all pharmacology drug classes) and my limited tool budget, I'll use the textbooks as a backbone and synthesize a comprehensive viva-ready table from my medical knowledge, which aligns with Katzung, Goodman & Gilman, and Lippincott — the standard references.
Here is a comprehensive classification of all major pharmacological drug classes with MOA, organized by body system for viva:
📋 Complete Drug Classification & MOA — Viva Reference
🫀 1. AUTONOMIC NERVOUS SYSTEM (ANS) DRUGS
A. Cholinergic (Parasympathomimetic) Drugs
| Class | Drugs | MOA |
|---|---|---|
| Direct-acting cholinomimetics | Acetylcholine, Carbachol, Bethanechol, Pilocarpine, Muscarine | Bind & activate muscarinic (M) and/or nicotinic (N) receptors directly |
| Anticholinesterases (reversible) | Neostigmine, Pyridostigmine, Physostigmine, Edrophonium, Rivastigmine, Donepezil | Inhibit acetylcholinesterase → ↑ ACh at synapse |
| Anticholinesterases (irreversible) | Organophosphates (Malathion, Parathion), Echothiophate | Covalently bind AChE → permanent inhibition until new enzyme synthesized |
B. Anticholinergic (Parasympatholytic) Drugs
| Class | Drugs | MOA |
|---|---|---|
| Muscarinic antagonists | Atropine, Scopolamine, Ipratropium, Tiotropium, Oxybutynin, Tolterodine, Benztropine, Glycopyrrolate | Competitively block muscarinic receptors (M1–M5) |
| Ganglionic blockers | Hexamethonium, Trimethaphan | Block nicotinic receptors at autonomic ganglia |
| NMJ blockers (non-depolarizing) | Tubocurarine, Atracurium, Vecuronium, Rocuronium, Pancuronium | Competitive antagonists at nicotinic NMJ receptors |
| NMJ blockers (depolarizing) | Succinylcholine | Persistent depolarization at NMJ → phase I (depolarizing) and phase II block |
C. Adrenergic (Sympathomimetic) Drugs
| Class | Drugs | MOA |
|---|---|---|
| Direct α+β agonists | Adrenaline (Epinephrine), Noradrenaline (Norepinephrine) | Activate α1, α2, β1, β2 adrenoreceptors |
| β1+β2 agonists | Isoprenaline (Isoproterenol) | Non-selective β agonist |
| α1 agonists | Phenylephrine, Methoxamine | Vasoconstriction via α1 |
| α2 agonists | Clonidine, Methyldopa, Brimonidine | Presynaptic α2 → ↓ NE release; central α2 → ↓ sympathetic outflow |
| β1 agonists | Dobutamine | Selective β1 → ↑ cardiac contractility |
| β2 agonists (SABA) | Salbutamol, Terbutaline | Selective β2 → bronchodilation, uterine relaxation |
| β2 agonists (LABA) | Salmeterol, Formoterol | Selective β2, prolonged duration |
| Indirect sympathomimetics | Amphetamine, Ephedrine | Displace stored NE from presynaptic terminals → ↑ NE in synapse |
| Mixed (direct + indirect) | Ephedrine | Both direct receptor activation + NE release |
D. Adrenergic Antagonists (Sympatholytics)
| Class | Drugs | MOA |
|---|---|---|
| Non-selective α blockers | Phentolamine, Phenoxybenzamine | Block α1+α2; phenoxybenzamine = irreversible |
| Selective α1 blockers | Prazosin, Terazosin, Doxazosin, Tamsulosin | Block α1 → vasodilation, ↓ urethral tone |
| Non-selective β blockers | Propranolol, Nadolol, Timolol, Sotalol | Block β1+β2 → ↓ HR, ↓ contractility, bronchoconstriction |
| Selective β1 blockers (cardioselective) | Metoprolol, Atenolol, Bisoprolol, Esmolol | Preferentially block β1 → ↓ HR, ↓ BP |
| β blockers with ISA | Pindolol, Acebutolol | Partial agonist activity; less resting bradycardia |
| α+β blockers | Labetalol, Carvedilol | Block α1+β1+β2 → vasodilation + ↓ cardiac output |
❤️ 2. CARDIOVASCULAR DRUGS
A. Antihypertensives
| Class | Drugs | MOA |
|---|---|---|
| ACE inhibitors | Enalapril, Lisinopril, Ramipril, Captopril | Inhibit ACE → ↓ Angiotensin II, ↓ aldosterone, ↑ bradykinin |
| ARBs | Losartan, Valsartan, Candesartan, Telmisartan | Block AT1 receptors → vasodilation, ↓ aldosterone |
| ARNIs | Sacubitril/Valsartan (Entresto) | Neprilysin inhibitor (↑ natriuretic peptides) + ARB |
| CCBs – Dihydropyridines | Amlodipine, Nifedipine, Felodipine | Block L-type Ca²⁺ channels in vascular smooth muscle → vasodilation |
| CCBs – Non-dihydropyridines | Verapamil, Diltiazem | Block L-type Ca²⁺ in heart + vessels → ↓ HR, ↓ AV conduction, vasodilation |
| Thiazide diuretics | Hydrochlorothiazide, Chlorthalidone, Indapamide | Inhibit Na⁺/Cl⁻ cotransporter in distal tubule → natriuresis |
| Direct vasodilators | Hydralazine, Minoxidil | Hydralazine: ↑ cGMP → vasodilation; Minoxidil: opens K⁺ channels |
| Central acting | Clonidine, Methyldopa | α2 agonist → ↓ central sympathetic outflow |
B. Anti-anginal Drugs
| Class | Drugs | MOA |
|---|---|---|
| Nitrates | GTN, Isosorbide mononitrate, Isosorbide dinitrate | Release NO → activate guanylyl cyclase → ↑ cGMP → venodilation (↓ preload), coronary vasodilation |
| β-blockers | Metoprolol, Atenolol | ↓ HR + contractility → ↓ O₂ demand |
| CCBs | Amlodipine, Verapamil | Vasodilation + ↓ HR/contractility |
| Potassium channel openers | Nicorandil | Opens K⁺ channels + nitrate-like action |
| Late INa current blocker | Ranolazine | Inhibit late Na⁺ current → ↓ intracellular Ca²⁺ overload → ↑ diastolic relaxation |
C. Antiarrhythmics (Vaughan Williams Classification)
| Class | Drugs | MOA |
|---|---|---|
| Class IA | Quinidine, Procainamide, Disopyramide | Block Na⁺ channels (intermediate kinetics) + K⁺ channels → ↑ QRS + QT |
| Class IB | Lidocaine, Mexiletine, Phenytoin | Block Na⁺ channels (fast off-rate) → prefer ischemic/depolarized tissue |
| Class IC | Flecainide, Propafenone | Block Na⁺ channels (slow off-rate) → marked ↑ QRS, minimal ↑ QT |
| Class II | Propranolol, Metoprolol, Esmolol | β-blockers → ↓ SA node automaticity, ↓ AV conduction |
| Class III | Amiodarone, Sotalol, Dronedarone, Ibutilide | Block K⁺ channels → ↑ action potential duration + refractory period → ↑ QT |
| Class IV | Verapamil, Diltiazem | Block Ca²⁺ channels → ↓ AV node conduction |
| Others | Adenosine, Digoxin, Magnesium | Adenosine: activate A1 receptors → hyperpolarize AV node; Digoxin: Na⁺/K⁺-ATPase inhibitor → vagal tone |
D. Heart Failure Drugs
| Class | Drugs | MOA |
|---|---|---|
| Cardiac glycosides | Digoxin | Inhibit Na⁺/K⁺-ATPase → ↑ intracellular Na⁺ → ↑ Ca²⁺ via NCX → ↑ contractility; also ↑ vagal tone |
| Inotropes | Dobutamine, Dopamine, Milrinone | Dobutamine: β1 agonist; Dopamine: dose-dependent D1/β1/α1; Milrinone: PDE3 inhibitor → ↑ cAMP |
| Diuretics | Furosemide, Spironolactone, Eplerenone | Furosemide: loop diuretic; Spirono/Eplerenone: aldosterone antagonist |
| SGLT2 inhibitors | Empagliflozin, Dapagliflozin | ↓ glucose/Na reabsorption → osmotic diuresis + direct cardiac/renal protection |
E. Lipid-lowering Drugs
| Class | Drugs | MOA |
|---|---|---|
| Statins (HMG-CoA reductase inhibitors) | Atorvastatin, Rosuvastatin, Simvastatin | Inhibit HMG-CoA reductase → ↓ cholesterol synthesis → ↑ LDL receptors on hepatocytes |
| Fibrates | Gemfibrozil, Fenofibrate | Activate PPAR-α → ↑ LPL → ↑ TG clearance; ↑ HDL |
| Bile acid sequestrants | Cholestyramine, Colestipol | Bind bile acids in gut → ↑ bile acid synthesis from cholesterol → ↓ LDL |
| PCSK9 inhibitors | Evolocumab, Alirocumab | Inhibit PCSK9 → prevent LDL receptor degradation → ↑ LDL uptake |
| Cholesterol absorption inhibitors | Ezetimibe | Block NPC1L1 transporter in intestine → ↓ dietary cholesterol absorption |
| Niacin (Nicotinic acid) | Niacin | Inhibits VLDL synthesis, ↓ TG, ↑ HDL; blocks adipose lipolysis via GPR109A |
F. Anticoagulants / Antiplatelets / Thrombolytics
| Class | Drugs | MOA |
|---|---|---|
| Heparins (UFH) | Unfractionated Heparin | Binds antithrombin III → inactivates thrombin (IIa) + Xa + IXa, XIa |
| LMWH | Enoxaparin, Dalteparin | Primarily inhibit Factor Xa > IIa via antithrombin III |
| Fondaparinux | Fondaparinux | Selective anti-Xa via antithrombin III |
| Vitamin K antagonists | Warfarin | Inhibit VKORC1 → ↓ activation of factors II, VII, IX, X, protein C, S |
| Direct thrombin inhibitors | Dabigatran, Bivalirudin, Argatroban | Directly inhibit thrombin (Factor IIa) |
| Direct Xa inhibitors | Rivaroxaban, Apixaban, Edoxaban | Directly inhibit Factor Xa |
| Antiplatelet – COX inhibitors | Aspirin | Irreversibly acetylate COX-1 → ↓ TXA2 synthesis → ↓ platelet aggregation |
| Antiplatelet – P2Y12 inhibitors | Clopidogrel, Ticagrelor, Prasugrel, Cangrelor | Block ADP-P2Y12 receptor → ↓ platelet activation (Clopidogrel/Prasugrel: irreversible; Ticagrelor: reversible) |
| GPIIb/IIIa inhibitors | Abciximab, Eptifibatide, Tirofiban | Block GPIIb/IIIa receptor → prevent fibrinogen binding → ↓ platelet cross-linking |
| Thrombolytics | Streptokinase, Alteplase (tPA), Tenecteplase | Convert plasminogen → plasmin → lyse fibrin clots |
🧠 3. CNS DRUGS
A. General Anesthetics
| Class | Drugs | MOA |
|---|---|---|
| Inhalational (volatile) | Halothane, Isoflurane, Sevoflurane, Desflurane | Potentiate GABA-A, inhibit NMDA receptors; alter membrane fluidity |
| Inhalational (gas) | Nitrous oxide | NMDA antagonist, opioid receptor activation |
| IV induction agents | Propofol | Positive allosteric modulator of GABA-A receptors |
| Barbiturates | Thiopental | Prolongs Cl⁻ channel opening at GABA-A; at high doses, direct channel activation |
| Ketamine | Ketamine | NMDA receptor antagonist (dissociative anesthesia) |
| Benzodiazepines (IV) | Midazolam, Diazepam | Increase frequency of Cl⁻ channel opening at GABA-A |
| Etomidate | Etomidate | Potentiate GABA-A; inhibits 11β-hydroxylase |
B. Local Anesthetics
| Class | Drugs | MOA |
|---|---|---|
| Esters | Procaine, Cocaine, Benzocaine, Tetracaine | Block voltage-gated Na⁺ channels (intracellularly) → prevent AP generation/propagation |
| Amides | Lidocaine, Bupivacaine, Ropivacaine, Prilocaine | Same MOA; metabolized by liver CYP enzymes |
C. Opioid Analgesics
| Class | Drugs | MOA |
|---|---|---|
| Strong agonists | Morphine, Oxycodone, Fentanyl, Methadone, Pethidine | Activate μ (mu) > κ, δ opioid receptors → ↑ K⁺ conductance + ↓ Ca²⁺ entry → ↓ neuronal excitability |
| Partial agonists | Buprenorphine | Partial μ agonist, κ antagonist |
| Mixed agonist-antagonist | Pentazocine, Nalbuphine | κ agonist + μ antagonist/partial agonist |
| Antagonists | Naloxone, Naltrexone | Competitive μ, κ, δ antagonists |
| Weak opioids | Codeine, Tramadol | Codeine: prodrug → morphine; Tramadol: weak μ agonist + inhibit NE/5-HT reuptake |
D. NSAIDs & Analgesics
| Class | Drugs | MOA |
|---|---|---|
| Non-selective COX inhibitors | Ibuprofen, Naproxen, Diclofenac, Indomethacin, Ketorolac | Inhibit COX-1 + COX-2 → ↓ prostaglandin synthesis |
| Selective COX-2 inhibitors | Celecoxib, Etoricoxib | Selective COX-2 inhibition → ↓ inflammation/pain with less GI toxicity |
| Paracetamol (Acetaminophen) | Paracetamol | Inhibits prostaglandin synthesis centrally (COX-3?); activates descending serotonergic pathways; endocannabinoid involvement |
| Glucocorticoids | Dexamethasone, Prednisolone | Induce lipocortin → inhibit phospholipase A2 → ↓ arachidonic acid → ↓ all eicosanoids |
E. Sedatives / Hypnotics / Anxiolytics
| Class | Drugs | MOA |
|---|---|---|
| Benzodiazepines | Diazepam, Lorazepam, Clonazepam, Alprazolam, Midazolam | Positive allosteric modulation of GABA-A → ↑ frequency of Cl⁻ channel opening |
| Z-drugs (non-BZD hypnotics) | Zolpidem, Zaleplon, Eszopiclone | Act on BZ1 (ω1) subunit of GABA-A → sedation without anxiolysis |
| Barbiturates | Phenobarbital, Pentobarbital | Increase duration of Cl⁻ channel opening; direct activation at high doses |
| Melatonin receptor agonists | Ramelteon, Melatonin | Agonize MT1/MT2 melatonin receptors → ↓ sleep latency |
| Orexin receptor antagonists | Suvorexant, Lemborexant | Block orexin (hypocretin) OX1/OX2 receptors → promote sleep |
| Buspirone | Buspirone | Partial agonist at 5-HT1A; D2 receptor partial agonist → anxiolytic without sedation/dependence |
F. Antidepressants
| Class | Drugs | MOA |
|---|---|---|
| SSRIs | Fluoxetine, Sertraline, Escitalopram, Citalopram, Paroxetine, Fluvoxamine | Selectively inhibit serotonin reuptake transporter (SERT) → ↑ synaptic 5-HT |
| SNRIs | Venlafaxine, Duloxetine, Desvenlafaxine | Inhibit SERT + NET → ↑ 5-HT + NE |
| TCAs | Amitriptyline, Imipramine, Clomipramine, Nortriptyline | Inhibit SERT + NET; also block H1, muscarinic, α1 receptors |
| MAOIs | Phenelzine, Tranylcypromine, Moclobemide (reversible) | Inhibit MAO-A/B → ↓ metabolism of 5-HT, NE, DA |
| NaSSA | Mirtazapine | Block presynaptic α2 autoreceptors → ↑ NE+5-HT release; also 5-HT2/3 + H1 antagonism |
| NDRIs | Bupropion | Inhibit NE + DA reuptake |
| SARIs | Trazodone | 5-HT2 antagonist + weak SERT inhibitor |
| Agomelatine | Agomelatine | MT1/MT2 agonist + 5-HT2C antagonist |
G. Antipsychotics
| Class | Drugs | MOA |
|---|---|---|
| Typical (FGAs) | Haloperidol, Chlorpromazine, Fluphenazine, Trifluoperazine | D2 receptor antagonism (mainly mesolimbic pathway) |
| Atypical (SGAs) | Clozapine, Olanzapine, Risperidone, Quetiapine, Aripiprazole, Ziprasidone | D2 + 5-HT2A antagonism (Aripiprazole: D2 partial agonist) → ↓ EPS, ↓ negative symptoms |
H. Mood Stabilizers
| Class | Drugs | MOA |
|---|---|---|
| Lithium | Lithium carbonate | Inhibit inositol monophosphatase → ↓ IP3/DAG signaling; modulate GSK-3β |
| Anticonvulsants | Valproate, Lamotrigine, Carbamazepine | Valproate: ↑ GABA; Lamotrigine: block Na⁺ channels + ↓ glutamate release; Carbamazepine: block Na⁺ channels |
I. Antiepileptics / Anticonvulsants
| Class | Drugs | MOA |
|---|---|---|
| Na⁺ channel blockers | Phenytoin, Carbamazepine, Oxcarbazepine, Lamotrigine, Lacosamide | Stabilize inactivated state of voltage-gated Na⁺ channels |
| GABA potentiators | Phenobarbital, Benzodiazepines, Tiagabine, Vigabatrin | ↑ GABA activity (various mechanisms) |
| Ca²⁺ channel blockers (T-type) | Ethosuximide | Block T-type Ca²⁺ channels in thalamic neurons → control absence seizures |
| AMPA receptor blockers | Perampanel | Block AMPA receptors → ↓ glutamatergic excitation |
| NMDA receptor modulators | Felbamate | Blocks NMDA + potentiates GABA-A |
| SV2A ligands | Levetiracetam | Binds synaptic vesicle protein SV2A → ↓ neurotransmitter release |
| Multiple MOA | Valproate, Topiramate | Valproate: ↑ GABA, ↓ Na⁺/Ca²⁺; Topiramate: Na⁺ block + GABA + AMPA antagonism + CA inhibition |
J. Antiparkinson Drugs
| Class | Drugs | MOA |
|---|---|---|
| Dopamine precursor | Levodopa (+ Carbidopa/Benserazide) | L-DOPA crosses BBB → converted to DA; carbidopa inhibits peripheral DOPA decarboxylase |
| DA agonists | Bromocriptine, Ropinirole, Pramipexole, Cabergoline | Directly stimulate D2 (and D3) receptors |
| MAO-B inhibitors | Selegiline, Rasagiline | Selectively inhibit MAO-B → ↓ DA breakdown |
| COMT inhibitors | Entacapone, Tolcapone | Inhibit COMT → ↓ peripheral metabolism of L-DOPA → prolong effect |
| Amantadine | Amantadine | NMDA antagonist + promotes DA release + anticholinergic |
| Anticholinergics | Benztropine, Trihexyphenidyl | Block muscarinic receptors → restore DA/ACh balance in striatum |
K. Drugs for Alzheimer's Disease
| Class | Drugs | MOA |
|---|---|---|
| AChE inhibitors | Donepezil, Rivastigmine, Galantamine | Inhibit AChE → ↑ ACh in synaptic cleft |
| NMDA antagonist | Memantine | Blocks NMDA receptors → ↓ excitotoxic Ca²⁺ influx |
🫁 4. RESPIRATORY DRUGS
| Class | Drugs | MOA |
|---|---|---|
| SABA | Salbutamol, Terbutaline | β2 agonist → activate adenylyl cyclase → ↑ cAMP → relax bronchial smooth muscle |
| LABA | Salmeterol, Formoterol, Indacaterol | Long-acting β2 agonist |
| SAMA | Ipratropium | Block M3 muscarinic receptors → ↓ bronchoconstriction |
| LAMA | Tiotropium, Glycopyrronium, Umeclidinium | Long-acting M3 antagonism |
| Inhaled corticosteroids | Budesonide, Fluticasone, Beclomethasone | Activate glucocorticoid receptors → ↓ inflammatory cytokines, ↓ IgE, ↓ mast cell mediators |
| Leukotriene antagonists | Montelukast, Zafirlukast | Block CysLT1 receptors → ↓ bronchoconstriction + mucus |
| 5-Lipoxygenase inhibitors | Zileuton | Inhibit 5-LOX → ↓ leukotriene synthesis |
| Mast cell stabilizers | Cromolyn, Nedocromil | Inhibit mast cell degranulation (stabilize Cl⁻ channels) |
| Theophylline | Theophylline | PDE inhibitor → ↑ cAMP + cGMP → bronchodilation; also adenosine antagonism |
| Anti-IgE | Omalizumab | Monoclonal Ab binds free IgE → ↓ mast cell/basophil activation |
| Anti-IL-5 | Mepolizumab, Benralizumab | Inhibit IL-5 (eosinophil survival factor) |
| Anti-IL-4/13 | Dupilumab | Blocks IL-4Rα → ↓ IL-4 + IL-13 signaling (Th2 response) |
| Antitussives | Codeine, Dextromethorphan | Central cough suppression; Dextromethorphan: NMDA antagonist + σ receptor |
| Mucolytics | Acetylcysteine, Ambroxol | Acetylcysteine: breaks disulfide bonds in mucus glycoproteins; Ambroxol: ↑ surfactant |
🍽️ 5. GASTROINTESTINAL DRUGS
| Class | Drugs | MOA |
|---|---|---|
| Proton Pump Inhibitors (PPIs) | Omeprazole, Esomeprazole, Pantoprazole, Rabeprazole | Irreversibly inhibit H⁺/K⁺-ATPase (proton pump) on parietal cells |
| H2 receptor antagonists | Ranitidine, Famotidine, Cimetidine | Block H2 receptors on parietal cells → ↓ gastric acid secretion |
| Antacids | Mg(OH)₂, Al(OH)₃, CaCO₃ | Neutralize HCl directly |
| Sucralfate | Sucralfate | Cross-links proteins on ulcer base → forms protective barrier; ↑ mucus/bicarb |
| Misoprostol | Misoprostol | PGE1 analogue → ↑ mucus/bicarb secretion, ↓ acid secretion, ↑ mucosal blood flow |
| Bismuth | Bismuth subcitrate | Bactericidal to H. pylori; forms protective coating |
| Prokinetics | Metoclopramide, Domperidone, Cisapride | Metoclopramide: D2 antagonist + 5-HT4 agonist; Domperidone: D2 antagonist (no CNS); Cisapride: 5-HT4 agonist |
| 5-HT3 antagonists (antiemetics) | Ondansetron, Granisetron, Palonosetron | Block 5-HT3 receptors in GIT + CTZ → ↓ vomiting reflex |
| NK1 antagonists (antiemetics) | Aprepitant, Rolapitant | Block substance P at NK1 receptors in CNS |
| Laxatives – Osmotic | Lactulose, PEG, Magnesium sulfate | ↑ osmotic pressure in colon → retain water → soften stool |
| Laxatives – Stimulant | Senna, Bisacodyl | Stimulate myenteric plexus → ↑ intestinal motility |
| Laxatives – Bulk-forming | Ispaghula (Psyllium), Methylcellulose | Absorb water → swell → ↑ stool bulk |
| Antidiarrheals | Loperamide, Diphenoxylate | μ opioid agonist in gut → ↓ peristalsis + ↑ sphincter tone |
| IBD drugs | Sulfasalazine, Mesalazine | Inhibit COX + 5-LOX in colon wall → ↓ prostaglandins + leukotrienes |
| Biologics for IBD | Infliximab, Adalimumab, Vedolizumab | Anti-TNF-α (Infliximab/Adalimumab); Vedolizumab: anti-α4β7 integrin |
🩸 6. ENDOCRINE / METABOLIC DRUGS
A. Diabetes Drugs
| Class | Drugs | MOA |
|---|---|---|
| Insulin | Regular, NPH, Glargine, Detemir, Lispro, Aspart | Binds insulin receptor (RTK) → GLUT4 translocation → glucose uptake; ↑ glycogen + fat synthesis |
| Biguanides | Metformin | Inhibit mitochondrial Complex I → activate AMPK → ↓ hepatic gluconeogenesis; ↑ insulin sensitivity |
| Sulfonylureas | Glibenclamide, Glipizide, Glimepiride | Block ATP-sensitive K⁺ channels on β cells → depolarization → ↑ Ca²⁺ → insulin secretion |
| Meglitinides | Repaglinide, Nateglinide | Same as sulfonylureas (KATP blockers) but short-acting, meal-time |
| Thiazolidinediones (TZDs) | Pioglitazone, Rosiglitazone | Activate PPAR-γ → ↑ insulin sensitivity in adipose/muscle |
| DPP-4 inhibitors (Gliptins) | Sitagliptin, Saxagliptin, Vildagliptin, Linagliptin | Inhibit DPP-4 → ↑ GLP-1 + GIP half-life → ↑ insulin, ↓ glucagon (glucose-dependent) |
| GLP-1 receptor agonists | Liraglutide, Semaglutide, Exenatide, Dulaglutide | Activate GLP-1R → ↑ glucose-dependent insulin, ↓ glucagon, ↓ gastric emptying, ↓ appetite |
| SGLT2 inhibitors | Empagliflozin, Dapagliflozin, Canagliflozin | Block SGLT2 in proximal tubule → ↑ urinary glucose excretion |
| α-glucosidase inhibitors | Acarbose, Miglitol | Inhibit intestinal α-glucosidase → ↓ carbohydrate digestion + glucose absorption |
B. Thyroid Drugs
| Class | Drugs | MOA |
|---|---|---|
| Thyroid hormones | Levothyroxine (T4), Liothyronine (T3) | Bind nuclear thyroid receptors → regulate gene transcription for metabolism |
| Thionamides | Propylthiouracil (PTU), Carbimazole/Methimazole | Inhibit thyroid peroxidase (TPO) → ↓ T3/T4 synthesis; PTU also inhibits peripheral T4→T3 conversion |
| Iodides (high-dose) | Lugol's iodine, Potassium iodide | Wolff-Chaikoff effect: excess iodide acutely suppresses thyroid hormone synthesis |
| Radioactive iodine | ¹³¹I | Concentrated in thyroid → β-radiation destroys follicular cells |
C. Adrenocorticosteroids
| Class | Drugs | MOA |
|---|---|---|
| Glucocorticoids | Cortisol, Prednisolone, Dexamethasone, Methylprednisolone | Bind GR → translocate to nucleus → transactivation/transrepression → ↓ NF-κB → ↓ cytokines/inflammation; ↑ gluconeogenesis |
| Mineralocorticoids | Fludrocortisone, Aldosterone | Bind MR → ↑ Na⁺ reabsorption + K⁺ excretion in collecting duct |
| Aldosterone antagonists | Spironolactone, Eplerenone | Competitive MR antagonists → ↑ K⁺ retention, natriuresis |
| Adrenal enzyme inhibitors | Metyrapone, Ketoconazole, Aminoglutethimide | Block steroidogenesis enzymes → ↓ cortisol (used in Cushing's) |
D. Sex Hormones & Related
| Class | Drugs | MOA |
|---|---|---|
| Estrogens | Ethinylestradiol, Estradiol | Bind ERα/ERβ → regulate female reproductive gene transcription |
| Progestins | Levonorgestrel, Medroxyprogesterone, Norethindrone | Bind PR → maintain endometrium, ↓ LH surge, thicken cervical mucus |
| Combined OCP | Ethinylestradiol + Progestin | ↓ FSH/LH (negative feedback) → ↓ ovulation |
| SERMs | Tamoxifen, Raloxifene, Clomiphene | Tissue-specific ER modulators; Tamoxifen: ER antagonist in breast; Clomiphene: ER antagonist in hypothalamus → ↑ GnRH/FSH |
| Aromatase inhibitors | Anastrozole, Letrozole, Exemestane | Inhibit aromatase → ↓ estrogen synthesis |
| GnRH analogues | Leuprolide, Goserelin | Continuous use → pituitary GnRH-R downregulation → ↓ LH/FSH (medical castration) |
| Androgens | Testosterone, Danazol | Bind AR → virilizing effects; Danazol: weak androgen + ↓ FSH/LH |
| Anti-androgens | Flutamide, Bicalutamide, Spironolactone, Finasteride | Flutamide/Bicalutamide: AR antagonists; Finasteride: inhibit 5α-reductase → ↓ DHT |
💉 7. DIURETICS
| Class | Drugs | MOA |
|---|---|---|
| Carbonic anhydrase inhibitors | Acetazolamide | Inhibit CA in proximal tubule → ↓ HCO₃⁻ reabsorption → ↓ Na⁺/water reabsorption |
| Loop diuretics | Furosemide, Torsemide, Bumetanide, Ethacrynic acid | Inhibit Na⁺/K⁺/2Cl⁻ cotransporter (NKCC2) in thick ascending loop of Henle |
| Thiazides | HCTZ, Chlorthalidone, Indapamide | Inhibit NCC (Na⁺/Cl⁻ cotransporter) in DCT |
| K⁺-sparing (aldosterone antagonist) | Spironolactone, Eplerenone | Block aldosterone receptor in collecting duct |
| K⁺-sparing (ENaC blockers) | Amiloride, Triamterene | Block ENaC (epithelial Na⁺ channel) in collecting duct |
| Osmotic diuretics | Mannitol | Freely filtered, not reabsorbed → ↑ tubular osmolality → ↑ urine output |
| ADH antagonists (Vaptans) | Tolvaptan, Conivaptan | Block V2 receptors in collecting duct → ↓ aquaporin-2 insertion → aquaresis |
🦠 8. ANTIMICROBIALS
A. Antibacterials
| Class | Drugs | MOA |
|---|---|---|
| Penicillins | Amoxicillin, Ampicillin, Piperacillin, Nafcillin, Cloxacillin | Bind PBPs → inhibit transpeptidation → ↓ cell wall cross-linking → bactericidal |
| Cephalosporins (1st–5th gen) | Cephalexin, Cefazolin (1st); Cefuroxime (2nd); Ceftriaxone, Cefotaxime (3rd); Cefepime (4th); Ceftaroline (5th) | Same as penicillins (β-lactam → PBP inhibition) |
| Carbapenems | Meropenem, Imipenem, Ertapenem | Broadest β-lactam; resistant to most β-lactamases |
| Monobactams | Aztreonam | β-lactam active only against Gram-negative aerobes |
| β-lactamase inhibitors | Clavulanic acid, Sulbactam, Tazobactam, Avibactam | Suicide inhibitors of β-lactamases → restore penicillin activity |
| Glycopeptides | Vancomycin, Teicoplanin | Bind D-Ala-D-Ala terminus of peptidoglycan precursor → inhibit transpeptidase/transglycosylase |
| Aminoglycosides | Gentamicin, Amikacin, Tobramycin, Streptomycin, Neomycin | Bind 30S ribosome (16S rRNA) → misreading of mRNA → abnormal proteins → membrane damage |
| Tetracyclines | Tetracycline, Doxycycline, Minocycline, Tigecycline | Bind 30S ribosome → block aminoacyl-tRNA from binding A site |
| Macrolides | Erythromycin, Azithromycin, Clarithromycin | Bind 50S ribosome (23S rRNA) → block translocation (transpeptidation) |
| Chloramphenicol | Chloramphenicol | Bind 50S ribosome → inhibit peptidyl transferase |
| Lincosamides | Clindamycin | Bind 50S ribosome → block peptide bond formation |
| Oxazolidinones | Linezolid, Tedizolid | Bind 50S ribosome → inhibit 70S initiation complex formation |
| Fluoroquinolones | Ciprofloxacin, Levofloxacin, Moxifloxacin, Norfloxacin | Inhibit DNA gyrase (Gram−) + Topoisomerase IV (Gram+) → block DNA replication |
| Sulfonamides | Sulfamethoxazole, Sulfadiazine | Competitive antagonists of PABA → inhibit dihydropteroate synthase → ↓ folate synthesis |
| Trimethoprim | Trimethoprim | Inhibit dihydrofolate reductase (DHFR) → ↓ THF → ↓ DNA synthesis |
| Nitrofurantoin | Nitrofurantoin | Reduced by bacterial nitrofuran reductase → reactive intermediates → damage DNA/ribosomal proteins |
| Metronidazole | Metronidazole | Reduced by anaerobes to reactive nitro-radical → strand breaks in bacterial DNA |
| Rifamycins | Rifampicin, Rifabutin | Inhibit bacterial DNA-dependent RNA polymerase → ↓ transcription |
| Polymyxins | Polymyxin B, Colistin | Act as cationic detergents → disrupt outer membrane of Gram-negative bacteria |
| Daptomycin | Daptomycin | Inserts into Gram-positive membrane → K⁺ efflux → membrane depolarization → cell death |
| Fusidic acid | Fusidic acid | Inhibit elongation factor G (EF-G) → block translocation of ribosome |
| Fosfomycin | Fosfomycin | Inhibit MurA (UDP-GlcNAc enolpyruvyl transferase) → ↓ peptidoglycan precursor synthesis |
B. Antitubercular Drugs
| Drug | MOA |
|---|---|
| Isoniazid (INH) | Inhibit InhA (enoyl-ACP reductase) → ↓ mycolic acid synthesis (prodrug activated by KatG) |
| Rifampicin | Inhibit RNA polymerase |
| Pyrazinamide | Disrupts membrane potential in acidic environment (exact MOA unclear; disrupts fatty acid synthesis) |
| Ethambutol | Inhibit arabinosyl transferase → ↓ arabinogalactan → ↓ cell wall |
| Streptomycin | 30S ribosome → misreading |
| Bedaquiline | Inhibit mycobacterial ATP synthase |
| Linezolid | 50S ribosome inhibitor |
C. Antifungals
| Class | Drugs | MOA |
|---|---|---|
| Polyenes | Amphotericin B, Nystatin | Bind ergosterol in fungal membrane → form pores → ↑ permeability → cell lysis |
| Azoles | Fluconazole, Itraconazole, Voriconazole, Posaconazole, Ketoconazole | Inhibit CYP51 (lanosterol 14α-demethylase) → ↓ ergosterol synthesis → ↑ toxic sterols |
| Echinocandins | Caspofungin, Micafungin, Anidulafungin | Inhibit β-1,3-glucan synthase → ↓ fungal cell wall synthesis |
| Allylamines | Terbinafine | Inhibit squalene epoxidase → ↓ ergosterol, accumulate toxic squalene |
| Flucytosine | 5-Fluorocytosine | Converted to 5-FU within fungi → inhibit thymidylate synthase + RNA synthesis |
| Griseofulvin | Griseofulvin | Bind β-tubulin → ↓ microtubule polymerization → ↓ fungal mitosis |
D. Antivirals
| Class | Drugs | MOA |
|---|---|---|
| Nucleoside reverse transcriptase inhibitors (NRTIs) | Zidovudine (AZT), Lamivudine, Tenofovir, Abacavir, Emtricitabine | Competitive inhibitors of HIV reverse transcriptase; lack 3'-OH → chain termination |
| Non-nucleoside RT inhibitors (NNRTIs) | Efavirenz, Nevirapine, Rilpivirine | Non-competitive inhibitors of HIV RT |
| Protease inhibitors (PIs) | Ritonavir, Lopinavir, Darunavir, Atazanavir | Inhibit HIV aspartyl protease → immature non-infective virions |
| Integrase inhibitors (INSTIs) | Raltegravir, Elvitegravir, Dolutegravir, Bictegravir | Inhibit HIV integrase → prevent viral DNA integration into host genome |
| CCR5 antagonist | Maraviroc | Block CCR5 co-receptor → HIV cannot enter CD4⁺ cell |
| Fusion inhibitors | Enfuvirtide (T-20) | Bind gp41 → prevent viral-cell membrane fusion |
| Anti-herpetics | Acyclovir, Valacyclovir, Famciclovir, Ganciclovir | Thymidine kinase phosphorylates prodrug → active triphosphate → inhibit viral DNA polymerase + chain termination |
| Anti-influenza | Oseltamivir, Zanamivir | Inhibit neuraminidase → ↓ viral release from host cells |
| Anti-HCV (DAAs) | Sofosbuvir, Daclatasvir, Ledipasvir | NS5B polymerase inhibitors + NS5A inhibitors → ↓ HCV replication |
| Hepatitis B | Entecavir, Tenofovir | Nucleoside/nucleotide analogues → inhibit HBV DNA polymerase |
E. Antiparasitic Drugs
| Class | Drugs | MOA |
|---|---|---|
| Antimalarials | Chloroquine, Hydroxychloroquine | Accumulate in parasite food vacuole → inhibit heme polymerization → toxic free heme accumulates |
| Artemisinin, Artesunate, Artemether | Endoperoxide bridge reacts with Fe²⁺ → free radicals → damage parasite membranes | |
| Mefloquine | Disrupt parasite membrane function (exact MOA unclear) | |
| Primaquine | Oxidative damage to parasite (radical metabolites); eradicates liver hypnozoites | |
| Proguanil, Pyrimethamine | Inhibit dihydrofolate reductase of Plasmodium | |
| Atovaquone | Inhibit mitochondrial electron transport chain | |
| Anthelmintics | Mebendazole, Albendazole | Bind β-tubulin → ↓ microtubule polymerization → ↓ glucose uptake |
| Ivermectin | Potentiate glutamate-gated Cl⁻ channels (invertebrate-specific) → paralysis of parasite | |
| Praziquantel | ↑ Ca²⁺ permeability → spastic paralysis; disrupts tegument of cestodes/trematodes | |
| Diethylcarbamazine (DEC) | Immobilize microfilariae + enhance immune killing | |
| Antiprotozoals | Metronidazole | Reactive nitro-radicals → DNA strand breaks (anaerobes + protozoa) |
| Nitazoxanide | Inhibit pyruvate-ferredoxin oxidoreductase (PFOR) | |
| Miltefosine | Disrupt parasite lipid metabolism + signal transduction (Leishmania) |
🔬 9. IMMUNOSUPPRESSANTS / IMMUNOMODULATORS
| Class | Drugs | MOA |
|---|---|---|
| Calcineurin inhibitors | Cyclosporine, Tacrolimus | Bind cyclophilin/FKBP12 → complex inhibits calcineurin → ↓ NFAT → ↓ IL-2 transcription → ↓ T-cell activation |
| mTOR inhibitors | Sirolimus (Rapamycin), Everolimus | Bind FKBP12 → complex inhibits mTORC1 → ↓ T/B cell proliferation |
| Antiproliferatives | Mycophenolate mofetil, Azathioprine | MMF: inhibit IMPDH → ↓ guanosine synthesis (lymphocyte-selective); Aza: antimetabolite (6-MP prodrug) → ↓ DNA synthesis |
| Corticosteroids | Prednisolone, Dexamethasone | ↓ NF-κB → ↓ IL-1, IL-2, TNF; ↓ lymphocyte proliferation + migration |
| Biologic DMARDs | Methotrexate (low dose), Hydroxychloroquine, Sulfasalazine, Leflunomide | MTX: inhibit DHFR; HCQ: lysosomal pH alteration; Leflunomide: inhibit DHODH (pyrimidine synthesis) |
| Anti-TNF agents | Infliximab, Adalimumab, Etanercept, Certolizumab | Neutralize TNF-α → ↓ inflammation in RA, IBD, psoriasis |
| IL-6 inhibitors | Tocilizumab, Sarilumab | Block IL-6 receptor |
| IL-1 inhibitors | Anakinra, Canakinumab | Block IL-1 receptor or IL-1β |
| JAK inhibitors | Tofacitinib, Baricitinib, Upadacitinib | Inhibit JAK1/JAK3 → ↓ STAT signaling → ↓ cytokine cascade |
| CD20 inhibitors | Rituximab, Ocrelizumab | Anti-CD20 monoclonal Ab → B-cell depletion |
🧬 10. ANTICANCER / CHEMOTHERAPY
| Class | Drugs | MOA |
|---|---|---|
| Alkylating agents | Cyclophosphamide, Ifosfamide, Busulfan, Melphalan, Chlorambucil | Form covalent cross-links in DNA (N7 of guanine) → ↓ replication/transcription |
| Nitrosoureas | Carmustine, Lomustine | Alkylate + carbamylate DNA; lipid soluble → cross BBB |
| Platinum compounds | Cisplatin, Carboplatin, Oxaliplatin | Form intra/interstrand DNA cross-links → block replication |
| Antimetabolites – Folate | Methotrexate, Pemetrexed | Inhibit DHFR → ↓ THF → ↓ purine/pyrimidine synthesis |
| Antimetabolites – Pyrimidine | 5-Fluorouracil (5-FU), Capecitabine, Cytarabine, Gemcitabine | 5-FU: inhibit thymidylate synthase + incorporate into RNA; Cytarabine/Gemcitabine: chain termination |
| Antimetabolites – Purine | 6-Mercaptopurine, 6-Thioguanine, Fludarabine, Cladribine | False purine nucleotides → inhibit purine synthesis + chain termination |
| Vinca alkaloids | Vincristine, Vinblastine, Vinorelbine | Bind β-tubulin → inhibit microtubule polymerization → M-phase arrest |
| Taxanes | Paclitaxel, Docetaxel, Cabazitaxel | Stabilize microtubules → prevent depolymerization → M-phase arrest |
| Topoisomerase II inhibitors | Etoposide, Teniposide, Doxorubicin, Daunorubicin | Inhibit Topo II → ↑ DNA strand breaks |
| Topoisomerase I inhibitors | Irinotecan, Topotecan | Inhibit Topo I → single-strand DNA breaks |
| Anthracyclines | Doxorubicin, Epirubicin, Idarubicin | Intercalate DNA + inhibit Topo II + free radical generation |
| Hormonal therapy | Tamoxifen, Anastrozole, Leuprolide, Bicalutamide | See Sex Hormones section above |
| Tyrosine kinase inhibitors | Imatinib, Erlotinib, Gefitinib, Lapatinib, Imatinib | Inhibit specific TKs (BCR-ABL, EGFR) → ↓ cancer cell proliferation/survival |
| VEGF inhibitors | Bevacizumab, Sunitinib, Sorafenib | Anti-VEGF (Bevacizumab: monoclonal Ab); Sunitinib/Sorafenib: multi-kinase inhibitors including VEGFR |
| mTOR inhibitors | Everolimus, Temsirolimus | ↓ mTORC1 → ↓ cancer cell proliferation |
| PARP inhibitors | Olaparib, Niraparib | Inhibit PARP-1 → prevent DNA repair → synthetic lethality in BRCA-mutant tumors |
| CDK 4/6 inhibitors | Palbociclib, Ribociclib, Abemaciclib | Block CDK4/6 → prevent Rb phosphorylation → cell cycle arrest in G1 |
| Immune checkpoint inhibitors | Pembrolizumab, Nivolumab (anti-PD-1); Atezolizumab (anti-PD-L1); Ipilimumab (anti-CTLA-4) | Block inhibitory checkpoints → restore T-cell anti-tumor activity |
| Proteasome inhibitors | Bortezomib, Carfilzomib | Inhibit 26S proteasome → ↑ pro-apoptotic proteins → cell death (myeloma) |
| BCL-2 inhibitors | Venetoclax | Inhibit BCL-2 → ↑ apoptosis in CLL cells |
🦴 11. DRUGS FOR BONE / CALCIUM METABOLISM
| Class | Drugs | MOA |
|---|---|---|
| Bisphosphonates | Alendronate, Risedronate, Zoledronic acid, Pamidronate | Inhibit farnesyl pyrophosphate synthase (FPPS) in osteoclasts → ↓ osteoclast activity → ↓ bone resorption |
| SERMs | Raloxifene | ERα agonist in bone → ↓ bone resorption |
| Anti-RANKL | Denosumab | Anti-RANKL monoclonal Ab → ↓ osteoclast differentiation/activation |
| PTH analogues | Teriparatide, Abaloparatide | Intermittent PTH1R activation → ↑ osteoblast activity → anabolic bone effect |
| Calcitonin | Salmon calcitonin | Bind CT receptors on osteoclasts → ↓ bone resorption; also analgesic effect |
| Calcium + Vitamin D | Ca²⁺ carbonate/citrate + Cholecalciferol/Ergocalciferol | Replace deficiencies; Vitamin D → enhance intestinal Ca absorption + bone mineralization |
| Romosozumab | Romosozumab | Anti-sclerostin antibody → ↑ Wnt signaling → ↑ bone formation + ↓ resorption |
🧪 12. GOUT DRUGS
| Class | Drugs | MOA |
|---|---|---|
| Xanthine oxidase inhibitors | Allopurinol, Febuxostat | Inhibit xanthine oxidase → ↓ uric acid synthesis |
| Uricosuric agents | Probenecid, Benzbromarone | Inhibit URAT1 transporter in proximal tubule → ↓ uric acid reabsorption → ↑ urinary excretion |
| Colchicine | Colchicine | Bind β-tubulin → ↓ neutrophil migration + degranulation; inhibit NLRP3 inflammasome |
| IL-1 inhibitors | Canakinumab, Anakinra | Block IL-1β → ↓ acute gout inflammation |
| Rasburicase | Rasburicase | Recombinant uricase → converts uric acid → allantoin (soluble) |
| NSAIDs/Corticosteroids | Indomethacin, Prednisolone | Anti-inflammatory (acute gout) |
🔑 Quick MOA Memory Anchors (Viva Tips)
| Mechanism | Remember |
|---|---|
| Na⁺ channel block | Local anesthetics, Antiepileptics (phenytoin, CBZ), Class I antiarrhythmics |
| K⁺ channel block | Class III antiarrhythmics (amiodarone, sotalol) → prolong QT |
| Ca²⁺ channel block | CCBs (nifedipine = vessels; verapamil = heart), T-type Ca²⁺ = ethosuximide |
| GABA potentiation | BZDs (↑ frequency), Barbiturates (↑ duration), at high doses barbs = direct activation |
| cAMP ↑ | β2 agonists (adenylyl cyclase), PDE inhibitors (theophylline, milrinone, sildenafil) |
| Irreversible inhibitors | Aspirin (COX), Phenoxybenzamine (α), Organophosphates (AChE), Omeprazole (H⁺/K⁺-ATPase) |
| Prodrugs | Codeine→Morphine; Clopidogrel→active thiol; Enalapril→Enalaprilat; Prednisone→Prednisolone; Capecitabine→5-FU |
This table covers all major pharmacological drug classes used in clinical medicine, following the system-based approach used in Katzung and Goodman & Gilman. For viva, focus on:
- Class name + prototype drug
- MOA at receptor/enzyme/channel level
- Key adverse effects (for follow-up viva questions)
Want me to add a specific section on adverse effects, drug interactions, or any particular class in more depth?
Profilaxis use of antibiotics
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Excellent data from Katzung's and Sabiston's. Here is the comprehensive viva-ready guide:
🛡️ Prophylactic Use of Antibiotics — Complete Viva Guide
📌 Definition
Antibiotic prophylaxis = administration of antimicrobials to prevent infection (not treat an established one), given to a patient at risk before a colonization or infective event occurs.
🔑 General Principles of Antibiotic Prophylaxis
- Agent must be active against the likely pathogen (not unnecessarily broad)
- Must achieve concentrations above MIC at the target site at time of incision/exposure
- Single dose is sufficient for most procedures → reduces toxicity + resistance
- Administer parenterally 30–60 min before incision (not earlier, not later)
- Repeat dose if procedure lasts >2–6 hours (depending on drug half-life)
- Use least expensive effective agent when all else is equal
- Reserve newer broad-spectrum agents for therapy of resistant infections, not prophylaxis
Common Errors in Prophylaxis
- Wrong antibiotic selection
- First dose too early or too late
- Failure to repeat for prolonged procedures
- Excessive post-operative duration
- Inappropriate use of broad-spectrum agents
🏥 PART A: SURGICAL PROPHYLAXIS
Drug of choice in most surgeries = Cefazolin (covers staphylococci + gram-negative rods) β-lactam allergy → Clindamycin (gram+) or Vancomycin (MRSA risk) or Fluoroquinolone/Aminoglycoside (gram−)
| Type of Surgery | Target Pathogens | Drug of Choice |
|---|---|---|
| Cardiac (median sternotomy, bypass, pacemaker) | Staphylococci, enteric GNRs | Cefazolin / Cefuroxime |
| Thoracic (non-cardiac, thoracotomy, lobectomy) | Staphylococci, streptococci, GNRs | Cefazolin |
| Vascular (abdominal + lower extremity) | Staphylococci, GNRs | Cefazolin |
| Neurosurgery (craniotomy) | Staphylococci | Cefazolin |
| Orthopedic (hardware insertion, joint replacement) | Staphylococci | Cefazolin |
| Head & Neck (entry into oropharynx) | S. aureus, oral flora | Cefazolin + Metronidazole |
| Gastroduodenal | S. aureus, oral flora, GNRs | Cefazolin |
| Biliary tract (high-risk: age >70, jaundice, CBD stones) | S. aureus, enterococci, GNRs | Cefazolin |
| Colorectal – Elective | Enteric GNRs, anaerobes | Oral erythromycin + neomycin (with bowel prep) |
| Colorectal – Emergency/Obstruction | Enteric GNRs, anaerobes | Cefoxitin / Cefotetan / Cefazolin + Metronidazole |
| Appendectomy (non-perforated) | Enteric GNRs, anaerobes | Cefoxitin / Cefotetan / Cefazolin + Metronidazole |
| Hysterectomy | GNRs, anaerobes, enterococci, GBS | Cefazolin / Cefotetan / Cefoxitin |
| Cesarean section | GNRs, anaerobes, GBS | Cefazolin (given after cord clamping) |
| Urological (with bacteriuria risk) | GNRs, enterococci | Fluoroquinolone / Cefazolin |
| Bariatric / Pancreaticoduodenectomy | GNRs, S. aureus | Cefazolin |
| Laparoscopic – Elective low-risk | — | None needed |
| Laparoscopic – High-risk | GNRs, anaerobes | Cefazolin / Cefoxitin |
Vancomycin substituted for cefazolin in hospitals with high MRSA/MRSE rates
💊 PART B: NON-SURGICAL (MEDICAL) PROPHYLAXIS
| Infection Prevented | Indication | Drug of Choice | Efficacy |
|---|---|---|---|
| Infective Endocarditis | Dental/oral/upper respiratory procedures in at-risk patients (prosthetic valves, prior IE, congenital HD, cardiac transplant) | Amoxicillin 2g PO 30–60 min before; PCN allergy → Cephalexin / Clindamycin / Azithromycin | Proposed effective |
| Rheumatic Fever (2° prevention) | History of rheumatic fever / rheumatic heart disease | Benzathine Penicillin G IM monthly (or Penicillin V / Sulfadiazine oral) | Excellent |
| Tuberculosis (LTBI) | Positive TST or IGRA without active TB | Isoniazid 6–9 months; or Rifampicin 4 months; or INH + Rifapentine (3-HP weekly × 12) | Excellent |
| Meningococcal infection | Close contacts of case; asplenia | Rifampicin / Ciprofloxacin / Ceftriaxone (single dose) | Excellent |
| H. influenzae type B | Close contacts of case in unimmunized children | Rifampicin | Excellent |
| PCP (Pneumocystis jirovecii) | HIV (CD4 <200), leukemia, transplant, high-dose steroids | Co-trimoxazole (TMP-SMX) DS daily; alt: Dapsone / Atovaquone / Pentamidine | Excellent |
| MAC (M. avium complex) | HIV with CD4 <50/μL not on ART | Azithromycin weekly; alt: Clarithromycin / Rifabutin | Excellent |
| Toxoplasmosis | HIV + Toxoplasma IgG positive + CD4 <100/μL | Co-trimoxazole (TMP-SMX) | Good |
| Group B Streptococcal (neonatal) | GBS-colonized mothers with risk factors (preterm, prolonged ROM, fever, prior GBS baby) | Ampicillin / Penicillin IV intrapartum | Excellent |
| UTI (recurrent) | ≥3 episodes/year | Co-trimoxazole / Nitrofurantoin (low-dose nightly or post-coital) | Excellent |
| Recurrent Otitis Media | ≥3 episodes in 6 months | Amoxicillin (low-dose) | Good |
| Malaria – chloroquine-sensitive | Travel to endemic areas | Chloroquine weekly | Excellent |
| Malaria – chloroquine-resistant | Travel to resistant areas | Mefloquine / Doxycycline / Atovaquone-Proguanil (Malarone) | Excellent |
| HIV PEP (post-exposure) | Needle-stick / sexual exposure | Tenofovir/Emtricitabine + Raltegravir or Dolutegravir (within 72 hrs, × 28 days) | Good |
| HIV PrEP | HIV-negative at high risk | Tenofovir/Emtricitabine (daily) | Excellent |
| Pertussis | Close contacts of case | Azithromycin (or Erythromycin) | Excellent |
| Plague | Close contacts | Doxycycline / Ciprofloxacin | Excellent |
| Pneumococcal infection | Sickle cell disease, asplenia (children) | Penicillin V daily | Excellent |
| Anthrax | Suspected exposure | Ciprofloxacin / Doxycycline × 60 days | Proposed |
| Diphtheria | Unimmunized contacts | Penicillin / Erythromycin | Proposed |
| Neonatal ophthalmia (N. gonorrhoeae) | All newborns | Erythromycin 0.5% eye ointment | Excellent |
| Candida | Leukemia, neutropenia, transplant | Fluconazole / Posaconazole / Echinocandin | Excellent |
| CMV | High-risk transplant | Valganciclovir / Letermovir | Excellent |
| Herpes Simplex (recurrent genital) | ≥4 episodes/year | Acyclovir / Valacyclovir (daily suppression) | Excellent |
🦷 Special Focus: Infective Endocarditis Prophylaxis
High-Risk Cardiac Conditions (require prophylaxis):
- Prosthetic cardiac valves (including TAVI)
- Previous infective endocarditis
- Congenital heart disease (unrepaired cyanotic, repaired within 6 months, repaired with residual defects)
- Cardiac transplant with valvulopathy
Procedures Requiring Prophylaxis:
- Dental procedures involving gingival manipulation, mucosal perforation, periapical region
- NOT required for: respiratory/GI/GU procedures unless active infection present
Regimen:
| Situation | Drug | Dose |
|---|---|---|
| Standard | Amoxicillin | 2g PO, 30–60 min before |
| Unable to take oral | Ampicillin | 2g IM/IV |
| PCN allergy | Cephalexin / Cefazolin | 2g PO / 1g IV |
| PCN allergy + unable to take cephalosporins | Clindamycin | 600mg PO/IV |
| PCN allergy | Azithromycin / Clarithromycin | 500mg PO |
🦠 Wound Classification & Prophylaxis Need (Surgery)
| Wound Class | Description | Infection Risk | Prophylaxis |
|---|---|---|---|
| Class I – Clean | No hollow organ entered, no inflammation | 1–2% | Usually none (give if prosthesis/immunocompromised) |
| Class II – Clean-contaminated | Controlled hollow organ entry (GI, biliary, GU) | 5–15% | Yes |
| Class III – Contaminated | Open wound, spillage, GI breach | 15–30% | Yes (therapeutic intent) |
| Class IV – Dirty/Infected | Established infection, perforated viscus | >30% | Therapeutic (not prophylaxis) |
🧠 Key Viva Points to Remember
| Scenario | Key Answer |
|---|---|
| Drug of choice for most surgical prophylaxis | Cefazolin |
| Why give before incision, not after? | Must achieve MIC at tissue before bacterial contamination |
| Duration of surgical prophylaxis | Single dose for most; max 24 hours |
| Cesarean section timing | After umbilical cord clamping |
| Colorectal elective surgery | Oral neomycin + erythromycin with bowel prep |
| Most important non-surgical prophylaxis | TB (INH), PCP (TMP-SMX), Rheumatic fever (Benzathine PenG), IE (Amoxicillin) |
| When to use vancomycin instead of cefazolin | High MRSA prevalence institution |
| PEP for HIV needle-stick | TDF/FTC + Raltegravir within 72 hours, for 28 days |
| PrEP for HIV | TDF/FTC daily |
| Rheumatic fever 2° prophylaxis | Benzathine PenG IM monthly for years (duration depends on age + RHD) |
Sources: Katzung's Basic & Clinical Pharmacology 16e, Sabiston Textbook of Surgery, Red Book 2021, Barash Clinical Anesthesia 9e
Moa of busulfants
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I have sufficient data from Katzung and Goodman & Gilman. Here is a focused, viva-ready answer:
☢️ Busulfan — Classification & Mechanism of Action
📦 Classification
| Category | Detail |
|---|---|
| Drug class | Alkylating agent |
| Subclass | Alkyl sulfonate (also called methanesulfonate) |
| Chemical nature | Bifunctional alkylating agent — has two reactive methanesulfonate groups |
| Type | Cell-cycle non-specific (acts on non-dividing + dividing cells) |
⚙️ Mechanism of Action
Step-by-step:
-
Bifunctional alkylation: Busulfan has two methanesulfonate (–CH₂–O–SO₂–CH₃) groups at each end of a 4-carbon chain (tetramethylene dimethanesulfonate)
-
Carbonium ion formation: In aqueous solution, each end undergoes hydrolysis → generates a highly reactive carbonium ion (carbocation)
-
DNA alkylation at N7 of guanine: The carbonium ion forms a covalent bond with the N7 position of guanine in DNA
-
Interstrand + intrastrand cross-links: Because it is bifunctional (two reactive ends), it can:
- Cross-link two guanines on opposite strands (interstrand) → most cytotoxic
- Cross-link guanines on the same strand (intrastrand)
- Also alkylates adenine and crosslinks with proteins
-
Consequences of cross-linking:
- Inhibits DNA replication and transcription
- DNA cannot be unzipped → cell cannot divide
- Triggers apoptosis (programmed cell death)
-
Selective myelosuppression: Busulfan has a unique selectivity for hematopoietic progenitor cells (especially myeloid lineage) compared to other alkylating agents → used as conditioning regimen in bone marrow transplantation
🔬 Unique Features vs Other Alkylating Agents
| Feature | Busulfan |
|---|---|
| Chemical class | Alkyl sulfonate (NOT nitrogen mustard) |
| Selectivity | Highly selective for myeloid stem cells |
| Cross-resistance | Lacks cross-resistance with other classical alkylating agents (nitrogen mustards) |
| Metabolism | Eliminated via glutathione conjugation (catalyzed by GSTA1); does NOT require hepatic activation (unlike cyclophosphamide) |
| Route | Oral and IV |
💊 Clinical Uses
| Indication | Role |
|---|---|
| CML (Chronic Myeloid Leukemia) | Historically first-line (now replaced by imatinib/TKIs) |
| Bone Marrow Transplant conditioning | High-dose busulfan to ablate bone marrow before stem cell transplant |
| Myeloproliferative disorders | Polycythemia vera, essential thrombocythaemia |
⚠️ Adverse Effects (Unique to Busulfan)
| Toxicity | Mechanism |
|---|---|
| Myelosuppression (prolonged) | Destruction of hematopoietic stem cells |
| Pulmonary fibrosis ("Busulfan lung") | Idiosyncratic lung toxicity — delayed, progressive |
| Skin hyperpigmentation ("Bronze skin") | Unique to busulfan |
| Adrenal insufficiency | Rare but characteristic |
| Seizures | At high doses (conditioning regimens) → prophylax with phenytoin/levetiracetam |
| Infertility / premature menopause | Gonadotoxicity |
| Hepatic veno-occlusive disease (VOD/SOS) | Especially at high-dose conditioning |
| Cataracts | With prolonged use |
🧠 Viva One-Liner
Busulfan is a bifunctional alkyl sulfonate that generates reactive carbonium ions, forming covalent cross-links at the N7 position of guanine in DNA → inhibiting DNA replication → apoptosis. It selectively ablates myeloid progenitors and is uniquely characterized by pulmonary fibrosis, skin pigmentation, and adrenal insufficiency as adverse effects.
Source: Katzung's Basic & Clinical Pharmacology 16e; Goodman & Gilman's Pharmacological Basis of Therapeutics
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