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Here are comprehensive viva questions with answers for all 8 units as per the Tamil Nadu Dr. MGR Medical University (Second MBBS) Pharmacology syllabus:

PHARMACOLOGY VIVA QUESTIONS & ANSWERS

Tamil Nadu Dr. M.G.R. Medical University - II MBBS


UNIT 1 - GENERAL PHARMACOLOGY

Q1. Define pharmacology. A: Pharmacology is the science that deals with the study of drugs - their sources, physicochemical properties, dosage forms, mechanisms of action, absorption, distribution, metabolism, excretion, effects, uses, and adverse reactions.
Q2. What is a drug? Give examples. A: A drug is any substance that, when administered to a living organism, produces a biological effect. Examples: aspirin, penicillin, morphine.
Q3. What are the routes of drug administration? Which is fastest? A: Routes include:
  • Enteral: oral, sublingual, rectal
  • Parenteral: intravenous (IV), intramuscular (IM), subcutaneous (SC), intradermal
  • Others: inhalation, transdermal, topical, intrathecal The IV route is the fastest as it bypasses absorption.
Q4. What is bioavailability? A: Bioavailability is the fraction (percentage) of the administered drug that reaches the systemic circulation in unchanged form. IV bioavailability = 100%. Oral bioavailability is reduced by first-pass metabolism.
Q5. What is first-pass metabolism? Give examples of drugs with high first-pass effect. A: First-pass metabolism (presystemic metabolism) is the metabolism of a drug in the gut wall and liver before it reaches systemic circulation, reducing its bioavailability. Examples: morphine, propranolol, lignocaine, nitroglycerin, aspirin. These drugs are given by non-oral routes to avoid this.
Q6. What is plasma protein binding? What is its significance? A: Drugs bind reversibly to plasma proteins (mainly albumin). Significance:
  • Bound drug is pharmacologically inactive (only free drug acts)
  • Acts as a drug reservoir
  • Bound drug cannot be filtered by kidney
  • Drug-drug interaction can occur at protein binding sites (displacement)
Q7. What is Vd (volume of distribution)? A: Vd is a theoretical volume that the drug would need to occupy to explain the observed plasma concentration relative to the total dose administered. Vd = Amount of drug in body / Plasma drug concentration. High Vd = drug is extensively distributed to tissues (e.g., chloroquine). Low Vd = drug stays in plasma.
Q8. What is the half-life of a drug? A: Half-life (t½) is the time taken for the plasma concentration of a drug to fall to half its original value. It determines dosing frequency and time to steady state (4-5 half-lives). Example: digoxin t½ = 36-40 hours.
Q9. What are the phases of drug metabolism (biotransformation)? A:
  • Phase I (Nonsynthetic): Oxidation, reduction, hydrolysis - mediated by CYP450 enzymes in liver. Usually converts active drug to less active/inactive metabolite or creates reactive intermediate.
  • Phase II (Synthetic/Conjugation): Glucuronidation, sulfation, acetylation, methylation - makes metabolite water-soluble for excretion.
Q10. What is enzyme induction? Give examples. A: Enzyme induction is an increase in the synthesis of CYP450 enzymes, leading to faster metabolism of drugs and reduced drug effect. Examples of inducers: rifampicin, phenobarbitone, phenytoin, carbamazepine, alcohol (chronic). Clinical significance: rifampicin reduces efficacy of oral contraceptive pills.
Q11. What is enzyme inhibition? Give examples. A: Inhibition of CYP450 enzymes leads to reduced metabolism, increased plasma levels, and toxicity of co-administered drugs. Examples: ketoconazole, erythromycin, ciprofloxacin, cimetidine, grapefruit juice. Mnemonic: SICK - Sulfonamides, Isoniazid, Cimetidine, Ketoconazole.
Q12. What are receptors? Classify them. A: Receptors are macromolecular proteins that recognize and bind specific drugs/endogenous ligands and produce a response. Classification:
  1. Ionotropic (ligand-gated ion channels): Nicotinic ACh receptor, GABA-A
  2. G-protein coupled receptors (GPCR/metabotropic): Adrenergic, muscarinic, opioid
  3. Enzyme-linked receptors (tyrosine kinase): Insulin receptor, growth factors
  4. Nuclear receptors (intracellular): Steroid hormones, thyroid hormones, vitamin D
Q13. What is an agonist? What is an antagonist? A:
  • Agonist: A drug that binds to a receptor and produces a biological response (has both affinity and intrinsic activity). Example: salbutamol (β2 agonist).
  • Antagonist: A drug that binds to a receptor but produces no response, and blocks the agonist (has affinity but no intrinsic activity). Example: propranolol (β blocker).
Q14. Difference between competitive and non-competitive antagonism? A:
FeatureCompetitiveNon-competitive
BindingSame receptor site as agonistDifferent site (allosteric)
Effect of increasing agonistCan overcome antagonismCannot overcome
Log dose-response curveShifted right, parallelMaximum depressed
ExampleAtropine (blocks ACh), naloxonePhenoxybenzamine
Q15. What is tolerance? Tachyphylaxis? Dependence? A:
  • Tolerance: Reduced response to a drug on repeated administration requiring increased doses. Example: opioids, alcohol.
  • Tachyphylaxis: Rapid development of tolerance after just a few doses. Example: ephedrine (indirect sympathomimetic).
  • Dependence: Compulsive drug use despite harm. Physical dependence = withdrawal symptoms on stopping (opioids). Psychological dependence = craving.
Q16. What is idiosyncrasy? A: An abnormal, genetically determined qualitatively different response to a drug that is not seen in most individuals. Example: G6PD-deficient patients develop hemolysis with primaquine, sulfonamides; succinylcholine causes prolonged apnea in pseudocholinesterase-deficient patients.
Q17. What is the therapeutic index? A: Therapeutic Index (TI) = TD50 / ED50. It measures the safety margin of a drug. A high TI = safer drug (e.g., penicillin). A low TI = narrow safety margin, requires monitoring (e.g., digoxin, warfarin, lithium, theophylline, aminoglycosides).
Q18. What is plasma half-life and how does it relate to steady state? A: Steady state is achieved after 4-5 half-lives of continuous administration, when the rate of drug intake equals rate of elimination. Time to steady state is independent of dose and only depends on t½.

UNIT 2 - AUTONOMIC NERVOUS SYSTEM & PERIPHERAL NERVOUS SYSTEM

Q1. What is neurohumoral transmission? What are the steps? A: Neurohumoral transmission is the process by which nerve impulses are transmitted across synapses via chemical messengers (neurotransmitters). Steps:
  1. Synthesis of neurotransmitter
  2. Storage in vesicles
  3. Release into synaptic cleft (triggered by Ca²⁺)
  4. Binding to receptors on postsynaptic membrane
  5. Termination (reuptake, degradation, or diffusion)
Q2. What are the neurotransmitters of ANS? Where is each released? A:
  • Acetylcholine (ACh): Released at all preganglionic synapses (both sympathetic and parasympathetic), all parasympathetic postganglionic synapses, sympathetic postganglionic fibers to sweat glands, and NMJ.
  • Norepinephrine: Released at sympathetic postganglionic nerve endings (except sweat glands).
  • Epinephrine: Released from adrenal medulla into blood.
Q3. Classify cholinergic receptors with examples of drugs acting on them. A:
  • Muscarinic (M1-M5): On smooth muscle, cardiac muscle, exocrine glands. Agonists: pilocarpine, bethanechol. Antagonists: atropine, scopolamine.
  • Nicotinic (Nn): At autonomic ganglia. Agonist: nicotine. Antagonist: hexamethonium.
  • Nicotinic (Nm): At neuromuscular junction. Agonist: succinylcholine. Antagonists: tubocurarine, vecuronium.
Q4. What are the effects of muscarinic receptor stimulation? A: "SLUD" + others:
  • Salivation, Lacrimation, Urination, Defecation (diarrhea)
  • Bradycardia, hypotension
  • Bronchoconstriction, increased secretions
  • Miosis (pupil constriction), accommodation for near vision
  • Increased GI motility
Q5. What is atropine? What are its pharmacological effects? A: Atropine is a competitive muscarinic antagonist (alkaloid from Atropa belladonna). Effects (opposite to muscarinic stimulation):
  • Tachycardia
  • Mydriasis and cycloplegia
  • Reduced secretions (dry mouth, dry skin, anhidrosis)
  • Bronchodilation
  • Reduced GI motility (constipation)
  • Urinary retention
  • CNS: stimulation (high dose), sedation (moderate)
Q6. What are the uses and contraindications of atropine? A: Uses: organophosphate poisoning, preanaesthetic medication, bradycardia, peptic ulcer (reduces secretions), ophthalmic (mydriasis), antidote for mushroom (muscarine) poisoning. Contraindications: glaucoma, benign prostatic hyperplasia, pyloric stenosis, tachyarrhythmia.
Q7. Classify adrenergic receptors with their actions. A:
  • α1: Vasoconstriction, mydriasis, urinary sphincter contraction
  • α2: Presynaptic - reduces NE release; also in CNS (reduces sympathetic outflow)
  • β1: Tachycardia, increased contractility (heart), renin release
  • β2: Bronchodilation, vasodilation, uterine relaxation, glycogenolysis
  • β3: Lipolysis in fat cells
Q8. What is the mechanism and uses of adrenaline (epinephrine)? A: Adrenaline acts on α1, α2, β1, β2, β3 receptors. Effects: increased heart rate and force, bronchodilation, vasoconstriction (skin/viscera) + vasodilation (skeletal muscle). Uses: anaphylaxis (drug of choice), cardiac arrest, local anaesthetic adjuvant (prolongs action, reduces bleeding), acute severe asthma.
Q9. What are beta blockers? Classify them. Give uses. A: Beta blockers antagonize β-adrenergic receptors. Classification:
  • Non-selective (β1+β2): Propranolol, nadolol, timolol
  • Cardioselective (β1): Atenolol, metoprolol, bisoprolol
  • With intrinsic sympathomimetic activity (ISA): Pindolol, oxprenolol
  • With α-blocking activity: Labetalol, carvedilol Uses: hypertension, angina, arrhythmias, heart failure (carvedilol, bisoprolol), thyrotoxicosis, glaucoma (timolol), migraine prophylaxis, anxiety.
Q10. What are the adverse effects and contraindications of beta blockers? A: Adverse effects: bradycardia, heart block, bronchospasm (avoid non-selective in asthma), cold extremities, hypoglycaemia masking, fatigue, impotence. Contraindications: bronchial asthma, COPD, heart block, severe bradycardia, decompensated heart failure, Prinzmetal's angina.
Q11. What are organophosphate compounds? What is their mechanism of toxicity? A: Organophosphates (e.g., malathion, parathion, tabun) are irreversible inhibitors of acetylcholinesterase (AChE). They phosphorylate the active site of AChE, leading to accumulation of ACh at all cholinergic synapses (muscarinic + nicotinic + CNS).
Q12. What are the features and treatment of organophosphate poisoning? A: Features (SLUD + nicotinic + CNS):
  • Muscarinic: bradycardia, bronchospasm, increased secretions, miosis, diarrhea, urination
  • Nicotinic: muscle fasciculations, weakness, paralysis
  • CNS: anxiety, convulsions, coma Treatment:
  1. Atropine (large doses IV, reverses muscarinic effects) - drug of choice
  2. Pralidoxime (2-PAM) (reactivates AChE if given early, before "ageing")
  3. Supportive: airway, oxygen, diazepam for convulsions
Q13. What are neuromuscular blocking agents? Classify them. A: NMBAs block the NMJ, causing skeletal muscle paralysis. Used during general anaesthesia.
  • Depolarizing: Succinylcholine (suxamethonium) - causes initial fasciculations (Phase I block), then sustained depolarization. Short acting. Reversed by plasma cholinesterase.
  • Non-depolarizing: Tubocurarine, pancuronium, vecuronium, rocuronium, atracurium - competitive antagonism at nicotinic Nm receptors. Reversed by neostigmine.
Q14. What is succinylcholine? What are its side effects? A: Succinylcholine is a depolarizing NMB (mimics ACh). Side effects: muscle fasciculations, postoperative myalgia, hyperkalemia (dangerous in burns, crush injuries), raised intraocular and intragastric pressure, malignant hyperthermia (with halothane), prolonged apnea in pseudocholinesterase deficiency.
Q15. What are local anaesthetics? Give examples and mechanism. A: Local anaesthetics (LAs) block nerve conduction by blocking voltage-gated Na⁺ channels in the nerve membrane, preventing depolarization. Examples: lignocaine (lidocaine), bupivacaine, cocaine, benzocaine, procaine. Lignocaine is the most commonly used. Adrenaline is added to prolong action and reduce systemic toxicity. Order of blockade: pain > temperature > touch > pressure > motor.
Q16. What are the uses and toxicity of lignocaine? A: Uses: surface/infiltration/nerve block/epidural/spinal anaesthesia, ventricular arrhythmias (IV). Toxicity: CNS (dizziness, perioral tingling, convulsions) and CVS (hypotension, bradycardia, cardiac arrest) due to systemic absorption.
Q17. What are anticholinesterases? Classify with examples. A: Drugs that inhibit AChE, leading to ACh accumulation. Classification:
  • Reversible: Physostigmine, neostigmine, pyridostigmine, edrophonium
  • Irreversible: Organophosphates (parathion, malathion, DFP, nerve agents - tabun, sarin) Uses of reversible: myasthenia gravis (neostigmine, pyridostigmine), reversal of NMB (neostigmine), glaucoma (physostigmine), Alzheimer's (donepezil, rivastigmine), atropine poisoning reversal (physostigmine).

UNIT 3 - CENTRAL NERVOUS SYSTEM

Q1. Classify general anaesthetics. A:
  • Inhalational: Volatile liquids (halothane, isoflurane, sevoflurane, desflurane) and gases (nitrous oxide)
  • IV anaesthetics: Thiopentone sodium, propofol, ketamine, etomidate, midazolam
Q2. What is balanced anaesthesia? A: Use of a combination of drugs to achieve the components of anaesthesia (hypnosis/unconsciousness, analgesia, muscle relaxation, prevention of autonomic reflexes) while minimizing the adverse effects of any single agent.
Q3. What is the triad/components of general anaesthesia? A: 1. Loss of consciousness (hypnosis), 2. Analgesia, 3. Muscle relaxation
Q4. What is ketamine? Give its unique features. A: Ketamine is a dissociative anaesthetic (NMDA receptor antagonist). Unique features:
  • Produces "dissociative anaesthesia" (patient appears awake but is unresponsive)
  • Potent analgesic - useful for short procedures
  • Increases heart rate, BP, and cardiac output (sympathomimetic - safe in hemorrhagic shock)
  • Bronchodilator (useful in asthmatic patients)
  • Causes emergence delirium/hallucinations (minimized by benzodiazepines)
  • Increases intracranial and intraocular pressure (contraindicated in head injury, glaucoma)
Q5. Classify sedative-hypnotics. A:
  • Benzodiazepines: Diazepam, lorazepam, midazolam, alprazolam
  • Barbiturates: Phenobarbitone, thiopentone, pentobarbitone
  • Non-benzodiazepine hypnotics (Z drugs): Zolpidem, zaleplon, zopiclone
  • Others: Chloral hydrate, meprobamate
Q6. What is the mechanism of benzodiazepines? A: Benzodiazepines (BZDs) act on GABA-A receptors (ionotropic, Cl⁻ channel). They potentiate the effect of GABA by increasing the frequency of Cl⁻ channel opening, causing hyperpolarization and CNS depression. Note: barbiturates increase the duration of Cl⁻ channel opening.
Q7. What are the uses of benzodiazepines? A: Anxiety, insomnia, status epilepticus (IV diazepam/lorazepam), alcohol withdrawal, preanaesthetic medication, muscle relaxation (diazepam), procedural sedation, night terrors.
Q8. What is the antidote for benzodiazepine overdose? A: Flumazenil - a competitive BZD receptor antagonist. It reverses sedation, respiratory depression, and unconsciousness caused by BZDs.
Q9. Classify antiepileptic drugs with examples. A:
  • Sodium channel blockers: Phenytoin, carbamazepine, lamotrigine, valproate
  • GABA enhancers: Valproate, phenobarbitone, benzodiazepines, gabapentin, vigabatrin
  • Ca²⁺ channel (T-type) blockers: Ethosuximide (absence seizures)
  • Multiple mechanisms: Valproate (drug of choice for multiple seizure types)
Q10. What is phenytoin? Give its mechanism, uses, and adverse effects. A: Phenytoin blocks voltage-gated Na⁺ channels (stabilizes inactive state), reducing repetitive firing. Uses: all types of epilepsy except absence, trigeminal neuralgia, cardiac arrhythmias (IV). Adverse effects (unique): gingival hyperplasia, hirsutism, coarsening of facial features, megaloblastic anaemia (folate deficiency), teratogenicity (fetal hydantoin syndrome), nystagmus, ataxia, diplopia. It is a potent enzyme inducer.
Q11. What is valproate? Give its uses and adverse effects. A: Valproate blocks Na⁺ channels, enhances GABA, blocks T-type Ca²⁺ channels. Drug of choice for: generalized seizures, absence seizures, juvenile myoclonic epilepsy, mixed seizure disorders, bipolar disorder (mood stabilizer), migraine prophylaxis. Adverse effects: weight gain, hair loss (alopecia), tremor, hepatotoxicity, teratogenicity (neural tube defects - spina bifida), pancreatitis, thrombocytopenia.
Q12. Classify opioid analgesics. Give mechanism and uses. A: Classification:
  • Strong agonists: Morphine, fentanyl, methadone, meperidine (pethidine), heroin
  • Moderate agonists: Codeine, tramadol, oxycodone
  • Partial agonists: Buprenorphine
  • Antagonists: Naloxone, naltrexone
  • Mixed agonist-antagonists: Pentazocine, butorphanol Mechanism: Act on μ, κ, δ opioid receptors (Gi-coupled GPCRs) - hyperpolarization, reduced neuronal excitability, decreased neurotransmitter release. Uses: severe pain (cancer, post-op, MI), cough suppression (codeine), diarrhea (loperamide), pulmonary edema (morphine).
Q13. What are the adverse effects and antidote of morphine? A: Adverse effects: respiratory depression (most dangerous), constipation, nausea/vomiting, miosis, urinary retention, euphoria, physical dependence, histamine release, delayed gastric emptying. Constipation does not show tolerance. Antidote: naloxone (pure opioid antagonist), given IV; short half-life (30-60 min) - may need repeated doses.
Q14. Classify antipsychotics (neuroleptics). A:
  • Typical (First generation): Low potency: chlorpromazine, thioridazine. High potency: haloperidol, fluphenazine, trifluoperazine.
  • Atypical (Second generation): Clozapine, risperidone, olanzapine, quetiapine, aripiprazole, ziprasidone.
Q15. What is the mechanism of typical antipsychotics? What are extrapyramidal side effects (EPS)? A: Typical antipsychotics block D2 dopamine receptors (mesolimbic/mesocortical pathway). EPS:
  • Acute dystonia (within hours-days) - muscle spasms, torticollis; treat with biperiden/benztropine
  • Akathisia (days-weeks) - motor restlessness
  • Parkinsonism (weeks) - tremor, rigidity, bradykinesia; treat with anticholinergics
  • Tardive dyskinesia (months-years) - involuntary oro-facial movements; difficult to treat, switch to clozapine
Q16. What is Neuroleptic Malignant Syndrome (NMS)? A: A rare but life-threatening reaction to antipsychotics. Features: FEVER - Fever, Encephalopathy (altered consciousness), Vitals unstable, Elevated CK, Rigidity. Treatment: stop drug, dantrolene, bromocriptine, cooling, supportive care.
Q17. Classify antidepressants with examples. A:
  • TCAs (Tricyclics): Imipramine, amitriptyline, clomipramine - block reuptake of NE and 5-HT
  • SSRIs: Fluoxetine, sertraline, paroxetine, escitalopram - drug of choice for depression, safest
  • SNRIs: Venlafaxine, duloxetine
  • MAOIs: Phenelzine, tranylcypromine - tyramine interaction risk (cheese reaction)
  • Others: Mirtazapine, bupropion, trazodone
Q18. What is lithium? Give its uses, toxicity, and monitoring. A: Lithium is a mood stabilizer. Uses: bipolar disorder (both acute mania and prophylaxis), augmentation in resistant depression. Toxicity (low therapeutic index, monitor plasma levels): tremor, polyuria/polydipsia (nephrogenic DI), hypothyroidism, weight gain. Toxicity signs: nausea, vomiting, coarse tremor, ataxia, confusion, convulsions, coma. Therapeutic range: 0.6-1.2 mEq/L; >2 mEq/L = toxic.

UNIT 4 - CARDIOVASCULAR SYSTEM, BLOOD & DIURETICS

Q1. Classify antihypertensive drugs. A:
  • Diuretics: Thiazides (hydrochlorothiazide), loop diuretics (furosemide)
  • Beta blockers: Atenolol, metoprolol
  • CCBs: Amlodipine (dihydropyridine), verapamil, diltiazem
  • ACE inhibitors: Enalapril, lisinopril, ramipril
  • ARBs: Losartan, valsartan, telmisartan
  • Centrally acting: Methyldopa (drug of choice in pregnancy), clonidine
  • Alpha blockers: Prazosin, doxazosin
  • Vasodilators: Hydralazine, minoxidil, sodium nitroprusside (hypertensive emergency)
Q2. What is the mechanism of ACE inhibitors? What are their uses and adverse effects? A: ACE inhibitors block angiotensin-converting enzyme, preventing conversion of Angiotensin I → Angiotensin II (vasoconstrictor). Also prevent breakdown of bradykinin. Effects: vasodilation, reduced aldosterone (natriuresis). Uses: hypertension, heart failure (reduces mortality), diabetic nephropathy (renoprotection), post-MI. Adverse effects: dry cough (bradykinin accumulation - most common reason to switch to ARB), hyperkalemia, first-dose hypotension, angioedema (contraindication), teratogenicity (contraindicated in pregnancy).
Q3. Classify calcium channel blockers. What are their uses? A:
  • Dihydropyridines (DHP): Amlodipine, nifedipine, felodipine - act mainly on vascular smooth muscle (vasodilators); used for hypertension, angina, Raynaud's.
  • Non-DHPs:
    • Verapamil (phenylalkylamine) - cardiac > vascular; bradycardia, negative inotrope; used for arrhythmias (SVT), angina, hypertension.
    • Diltiazem (benzothiazepine) - intermediate; used for angina, arrhythmias. Note: Amlodipine causes reflex tachycardia and ankle edema.
Q4. What are cardiac glycosides? What is the mechanism of digoxin? A: Cardiac glycosides are derived from Digitalis (foxglove plant). Digoxin is the prototype. Mechanism:
  1. Inhibits Na⁺/K⁺-ATPase pump → intracellular Na⁺ rises → Na⁺-Ca²⁺ exchanger is inhibited → intracellular Ca²⁺ rises → increased contractility (positive inotropy).
  2. Increases vagal tone → slows heart rate (negative chronotropy) and conduction through AV node.
Q5. What are the uses and adverse effects of digoxin? A: Uses: heart failure (reduces symptoms), atrial fibrillation/flutter (controls ventricular rate). Adverse effects (narrow therapeutic index): GI (nausea, vomiting, diarrhea), CNS (visual disturbances - yellow-green halos, xanthopsia), cardiac (any arrhythmia - most dangerous, ventricular tachycardia). Toxicity enhanced by hypokalemia, hypomagnesemia, hypercalcemia. Antidote: Digibind (digoxin-specific antibody fragments).
Q6. Classify anti-anginal drugs and their mechanisms. A:
  • Nitrates (organic nitrates): GTN (nitroglycerin), isosorbide dinitrate/mononitrate. Mechanism: release NO → activates guanylyl cyclase → ↑ cGMP → vascular smooth muscle relaxation → venodilation (↓ preload) + arteriodilation (↓ afterload at high doses).
  • Beta blockers: Reduce heart rate and contractility (↓ O2 demand).
  • Calcium channel blockers: Reduce afterload and heart rate.
  • Combination: Nitrate + beta blocker (most effective for chronic stable angina).
Q7. What is nitrate tolerance? How is it prevented? A: Nitrate tolerance is reduced efficacy of nitrates on repeated use due to depletion of -SH groups and reduced NO generation. Prevention: provide a nitrate-free interval of 8-12 hours (usually at night for nocturnal chest pain relief in the morning). Sildenafil + nitrate = dangerous hypotension (absolute contraindication).
Q8. Classify antiarrhythmic drugs (Vaughan Williams classification). A:
  • Class I (Na⁺ channel blockers): Ia - quinidine, procainamide, disopyramide; Ib - lignocaine, mexiletine; Ic - flecainide, propafenone
  • Class II (Beta blockers): Atenolol, metoprolol, esmolol
  • Class III (K⁺ channel blockers - prolong AP): Amiodarone, sotalol, dofetilide
  • Class IV (Ca²⁺ channel blockers): Verapamil, diltiazem
  • Unclassified: Adenosine (drug of choice for acute SVT), digoxin
Q9. What are the adverse effects of amiodarone? A: Amiodarone has many serious adverse effects (iodine-containing):
  • Pulmonary toxicity (most serious - pulmonary fibrosis)
  • Thyroid dysfunction (hypo or hyperthyroidism)
  • Hepatotoxicity
  • Corneal microdeposits (blue-grey vision)
  • Photosensitivity, blue-grey skin discoloration
  • Peripheral neuropathy
  • Bradycardia, QT prolongation (torsades de pointes)
Q10. Classify diuretics with examples and mechanisms. A:
ClassSiteMechanismExample
OsmoticPCT, descending loopOsmotic retention of waterMannitol
Carbonic anhydrase inhibitorsPCTBlock CA → ↓ HCO3⁻ reabsorptionAcetazolamide
Loop diureticsThick ascending loop of HenleBlock Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2)Furosemide, bumetanide
ThiazidesDistal convoluted tubuleBlock Na⁺-Cl⁻ cotransporter (NCC)Hydrochlorothiazide, chlorthalidone
K⁺-sparingCollecting ductAldosterone antagonist or Na⁺ channel blockerSpironolactone, amiloride
Q11. What are the adverse effects of furosemide? A: Hypokalemia, hyponatremia, hypomagnesemia, hypovolemia, metabolic alkalosis, hyperuricemia (gout), ototoxicity (high doses/IV), hyperglycemia, dehydration. Mnemonic: OH DANG - Ototoxicity, Hyperuricemia, Dehydration, Alkalosis, Nephritis (interstitial), Glucose increased.
Q12. What are anticoagulants? Classify them. A:
  • Parenteral: Heparin (unfractionated - UFH), low molecular weight heparins (enoxaparin, dalteparin), fondaparinux, bivalirudin
  • Oral: Warfarin (vitamin K antagonist); DOACs: dabigatran (direct thrombin inhibitor), rivaroxaban, apixaban (factor Xa inhibitors)
  • Fibrinolytics (thrombolytics): Streptokinase, alteplase (tPA), tenecteplase
Q13. What is the mechanism of heparin and warfarin? What are their antidotes? A:
  • Heparin: Activates antithrombin III, which inhibits thrombin (IIa) and factor Xa. Antidote: Protamine sulfate.
  • Warfarin: Inhibits vitamin K epoxide reductase → prevents activation of vitamin K-dependent clotting factors (II, VII, IX, X) and proteins C and S. Antidote: Vitamin K (slow reversal) or Fresh Frozen Plasma/PCC (rapid reversal).
Q14. What are antiplatelet drugs? Give examples and mechanisms. A:
  • Aspirin: Irreversibly inhibits COX-1 (and COX-2) → reduces thromboxane A2 synthesis → reduces platelet aggregation. Low dose (75-150 mg) for antiplatelet effect.
  • Clopidogrel, ticagrelor, prasugrel: Block P2Y12 ADP receptor on platelets. Used with aspirin (DAPT) after ACS/stenting.
  • GPIIb/IIIa inhibitors: Abciximab, tirofiban, eptifibatide - block final common pathway of platelet aggregation.
  • Dipyridamole: Inhibits phosphodiesterase → increases cAMP → inhibits platelet aggregation. Also used with aspirin for secondary stroke prevention.

UNIT 5 - RESPIRATORY SYSTEM, GIT & AUTACOIDS

Q1. Classify antiasthmatic drugs. A:
  • Bronchodilators:
    • β2 agonists: Short-acting (SABA) - salbutamol (albuterol), terbutaline; Long-acting (LABA) - salmeterol, formoterol
    • Methylxanthines: Theophylline, aminophylline
    • Anticholinergics: Ipratropium (short), tiotropium (long)
  • Anti-inflammatory:
    • Inhaled corticosteroids (ICS): Budesonide, beclomethasone, fluticasone (mainstay of prophylaxis)
    • Leukotriene antagonists: Montelukast, zafirlukast
    • Mast cell stabilizers: Sodium cromoglycate
    • Omalizumab (anti-IgE monoclonal antibody)
Q2. What is the mechanism of salbutamol? What are its uses and adverse effects? A: Salbutamol is a selective β2 agonist. Mechanism: activates β2 receptors → ↑ cAMP → protein kinase A activation → bronchial smooth muscle relaxation (bronchodilation) + inhibition of mediator release. Uses: acute bronchospasm (reliever/rescue), exercise-induced asthma, preterm labor (tocolytic). Adverse effects: tremor, palpitations, tachycardia, hypokalemia (with high doses), hyperglycemia.
Q3. What is theophylline? Give mechanism and adverse effects. A: Theophylline is a methylxanthine. Mechanism: inhibits phosphodiesterase (PDE) → ↑ cAMP → bronchodilation + anti-inflammatory effect; also adenosine receptor antagonist. Adverse effects (narrow TI): GI (nausea, vomiting), CNS (insomnia, anxiety, headache, seizures), CVS (arrhythmias, tachycardia). Therapeutic plasma level: 10-20 mcg/mL.
Q4. Classify antihistamines. What is the difference between H1 and H2 blockers? A:
  • H1 antihistamines (1st gen): Diphenhydramine, chlorpheniramine, promethazine, cyclizine - cross BBB, cause sedation
  • H1 antihistamines (2nd gen): Cetirizine, loratadine, fexofenadine - non-sedating
  • H2 antihistamines: Ranitidine, famotidine, cimetidine - block H2 receptors in gastric parietal cells → reduce gastric acid secretion; used for peptic ulcer, GERD.
Q5. What are proton pump inhibitors? Give mechanism and uses. A: PPIs (omeprazole, pantoprazole, lansoprazole, rabeprazole, esomeprazole) irreversibly inhibit H⁺/K⁺-ATPase (proton pump) on parietal cells, producing maximum (near-complete) suppression of gastric acid. They are prodrugs activated in the acidic environment of the stomach. Uses: peptic ulcer disease, GERD, Zollinger-Ellison syndrome, H. pylori eradication (triple therapy), NSAID-induced ulcers.
Q6. What is H. pylori triple therapy? A: PPI + Clarithromycin + Amoxicillin for 7-14 days. If penicillin allergy: PPI + Clarithromycin + Metronidazole. Quadruple therapy (for clarithromycin-resistant cases): PPI + Bismuth + Metronidazole + Tetracycline.
Q7. What are laxatives? Classify with examples. A:
  • Bulk-forming: Ispaghula (psyllium), methylcellulose - mimic dietary fibre, safest
  • Osmotic: Lactulose (also reduces ammonia in hepatic encephalopathy), magnesium sulphate, polyethylene glycol
  • Stimulant/irritant: Bisacodyl, senna, castor oil - stimulate intestinal peristalsis
  • Stool softeners/lubricants: Liquid paraffin, docusate
Q8. What are antiemetics? Classify with mechanism. A:
  • D2 receptor antagonists: Metoclopramide (also 5-HT4 agonist - prokinetic), domperidone, prochlorperazine
  • 5-HT3 antagonists: Ondansetron, granisetron, palonosetron - best for chemotherapy-induced vomiting
  • Antihistamines (H1 blockers): Promethazine, cyclizine - useful for motion sickness
  • Anticholinergics: Scopolamine - motion sickness (transdermal patch)
  • NK1 receptor antagonist: Aprepitant - for chemotherapy-induced vomiting (delayed phase)
  • Corticosteroids: Dexamethasone - adjunct in chemo-induced vomiting
Q9. What are autacoids? Give examples. A: Autacoids are local hormones (endogenous chemical mediators) produced locally in tissues and act locally. They are not true hormones because they lack specific glands of origin. Examples:
  • Biogenic amines: Histamine, serotonin (5-HT), bradykinin
  • Lipid-derived: Prostaglandins, thromboxanes, leukotrienes, platelet-activating factor (PAF)
  • Peptides: Angiotensin II, substance P, endothelins
Q10. What are prostaglandins? What are their uses? A: Prostaglandins are eicosanoids synthesized from arachidonic acid via COX pathway. Uses:
  • PGE2 / Misoprostol (PGE1 analogue): Cervical ripening, labor induction, medical abortion (with mifepristone), peptic ulcer prevention (with NSAIDs)
  • PGF2α / Dinoprostone: Abortion, labor induction
  • PGI2 (Prostacyclin) / Epoprostenol: Pulmonary arterial hypertension, prevention of platelet aggregation
  • Latanoprost (PGF2α analogue): Glaucoma (increases uveoscleral outflow)
Q11. What are NSAIDs? What is their mechanism and classification? A: NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) inhibit cyclooxygenase (COX) enzymes → reduce prostaglandin synthesis → anti-inflammatory, antipyretic, analgesic effects. Classification:
  • Non-selective (COX-1 + COX-2): Aspirin, ibuprofen, naproxen, diclofenac, indomethacin, piroxicam
  • Selective COX-2 inhibitors (Coxibs): Celecoxib, etoricoxib, rofecoxib (withdrawn due to MI risk) Adverse effects: GI ulceration (COX-1 inhibition reduces cytoprotective PGs), renal impairment, bronchospasm (aspirin-sensitive asthma), platelet dysfunction, hypertension.

UNIT 6 - ENDOCRINE PHARMACOLOGY

Q1. Classify oral hypoglycemic agents (OHAs). A:
  • Sulfonylureas: Glibenclamide, glipizide, glimepiride - stimulate insulin secretion (close K⁺-ATP channels on β cells). Risk of hypoglycaemia and weight gain.
  • Biguanides: Metformin - reduces hepatic glucose production (gluconeogenesis), increases insulin sensitivity. Drug of first choice in type 2 DM (especially obese patients). No hypoglycaemia. Lactic acidosis (rare). Contraindicated in renal failure, liver failure.
  • Thiazolidinediones (TZDs): Pioglitazone - activates PPARγ → increases insulin sensitivity. Risk of weight gain, edema, osteoporosis, bladder cancer.
  • Alpha-glucosidase inhibitors: Acarbose, voglibose - delay carbohydrate absorption. Flatulence.
  • DPP-4 inhibitors (Gliptins): Sitagliptin, vildagliptin - inhibit DPP-4 → increase incretin (GLP-1) levels → glucose-dependent insulin release.
  • SGLT2 inhibitors: Dapagliflozin, empagliflozin - block glucose reabsorption in PCT → glycosuria. Weight loss, BP reduction, renal/cardiac protection. Risk: urinary/genital infections, DKA.
  • GLP-1 receptor agonists: Liraglutide, semaglutide (injectable) - mimic GLP-1, weight loss, CV benefit.
Q2. What is metformin? Why is it the drug of choice in type 2 DM? A: Metformin is a biguanide. Mechanism: activates AMPK → reduces hepatic gluconeogenesis, increases peripheral glucose uptake, reduces intestinal glucose absorption. Advantages: does not cause hypoglycaemia, causes weight loss/neutral, reduces cardiovascular events (UKPDS), inexpensive. Contraindications: renal failure (GFR <30), liver failure, heart failure (risk of lactic acidosis), contrast procedures (hold 48h before and after).
Q3. Classify insulin preparations. A:
TypeOnsetDurationExample
Ultra-short acting (rapid)15 min3-4 hAspart, lispro, glulisine
Short acting (regular)30 min6-8 hRegular/soluble insulin
Intermediate acting1-2 h12-18 hNPH (isophane), lente
Long acting (basal)2-4 h20-24 hGlargine, detemir
Ultra-long acting6 h>42 hDegludec
Q4. What are corticosteroids? Classify with examples. A: Corticosteroids are steroid hormones produced by the adrenal cortex.
  • Glucocorticoids: Cortisol (natural), prednisolone, dexamethasone, betamethasone, budesonide, beclomethasone
  • Mineralocorticoids: Aldosterone (natural), fludrocortisone
  • Both (combined activity): Hydrocortisone (also used IV)
Q5. What are the uses of corticosteroids? A:
  • Anti-inflammatory/immunosuppressive: rheumatoid arthritis, SLE, inflammatory bowel disease, asthma, COPD exacerbation, allergic reactions
  • Replacement therapy: Addison's disease, congenital adrenal hyperplasia
  • Specific: dexamethasone in raised ICP, cerebral edema, septic shock (in combination), antenatal steroids for fetal lung maturity, organ transplant rejection prevention
  • Topical: skin conditions (eczema, psoriasis)
Q6. What are the adverse effects of long-term corticosteroid use? A: Mnemonic: BECLOMETHASONE
  • B: Blood sugar ↑ (steroid diabetes)
  • E: Electrolyte imbalance (↑ Na, ↓ K, ↓ Ca)
  • C: Cushing's syndrome (moon face, buffalo hump, central obesity, striae)
  • L: Lipid abnormalities
  • O: Osteoporosis (most serious long-term effect)
  • M: Myopathy (proximal)
  • E: Eye: glaucoma, posterior subcapsular cataract
  • T: Thin skin, Tendon rupture
  • H: Hypertension
  • A: Adrenal suppression (HPA axis suppression - never stop abruptly)
  • S: Susceptibility to infections
  • O: Oedema
  • N: Neuropsychiatric (insomnia, psychosis, euphoria)
  • E: (Peptic) Ulcer
Q7. What are thyroid drugs? Classify with mechanism. A:
  • Antithyroid drugs:
    • Thionamides: Carbimazole (prodrug → methimazole), propylthiouracil (PTU). Mechanism: inhibit thyroid peroxidase → block synthesis of T3 and T4. PTU also inhibits peripheral conversion of T4 → T3 (preferred in thyroid storm and pregnancy 1st trimester).
    • Radioactive iodine (¹³¹I): Destroys thyroid tissue.
    • Iodine/Iodides (Lugol's iodine): Wolff-Chaikoff effect (high iodine paradoxically inhibits thyroid) - used pre-operatively (reduces vascularity).
    • Beta blockers (propranolol): Symptom control in thyrotoxicosis, inhibit T4→T3 conversion.
  • Thyroid replacement: Levothyroxine (T4), liothyronine (T3)
Q8. What are sex hormones? What are oral contraceptives? A: Oral contraceptive pills (OCPs):
  • Combined OCP (estrogen + progestogen): Most effective. Mechanism: inhibit GnRH pulsation → suppress LH surge → prevent ovulation; cervical mucus thickening; endometrial atrophy. Examples: ethinyl estradiol + levonorgestrel. Side effects: DVT/thromboembolism (most serious), nausea, headache, hypertension, breakthrough bleeding. Contraindicated in smokers >35 years, history of VTE, migraine with aura, liver disease.
  • Mini-pill (Progestogen only pill): Suitable for breastfeeding women, those who cannot use estrogen.
  • Emergency contraception: Levonorgestrel (within 72h) or ulipristal acetate (within 120h).

UNIT 7 & 8 - CHEMOTHERAPY

Q1. What is chemotherapy? What are the ideal properties of an antimicrobial drug? A: Chemotherapy is the use of chemical substances to treat infections or malignancies without significantly harming the host. Ideal properties:
  1. Selective toxicity (targets microorganism, spares host)
  2. Bactericidal rather than bacteriostatic
  3. Broad spectrum
  4. Good oral bioavailability
  5. Good tissue penetration (including CNS)
  6. Minimal adverse effects
  7. No development of resistance
  8. Long half-life (convenient dosing)
Q2. What is the difference between bacteriostatic and bactericidal drugs? A:
BacteriostaticBactericidal
Inhibit bacterial growthKill bacteria
Require intact host immunityCan act without host immunity
Examples: tetracyclines, chloramphenicol, sulfonamides, erythromycin, clindamycinExamples: penicillins, cephalosporins, aminoglycosides, fluoroquinolones, metronidazole
Should not be combined with bactericidal (antagonism)Preferred in immunocompromised, endocarditis, meningitis
Q3. Classify penicillins with examples and uses. A:
  • Natural penicillins: Penicillin G (benzylpenicillin - IV), Penicillin V (oral) - streptococcal infections, syphilis
  • Anti-staphylococcal: Cloxacillin, flucloxacillin, oxacillin - beta-lactamase-resistant; used for S. aureus (MSSA)
  • Aminopenicillins: Ampicillin, amoxicillin - broader spectrum (gram-positive + some gram-negative like H. influenzae, E. coli)
  • Anti-Pseudomonal: Piperacillin, ticarcillin (+ with clavulanate)
  • Beta-lactam + inhibitor combinations: Amoxicillin-clavulanate (co-amoxiclav), Piperacillin-tazobactam
Q4. What is the mechanism of penicillin? What is the mechanism of resistance? A: Mechanism: Penicillins inhibit transpeptidase (penicillin-binding proteins, PBPs) → prevent cross-linking of peptidoglycan in bacterial cell wall → cell lysis (bactericidal). They are most effective against actively dividing bacteria. Resistance: Production of beta-lactamase (penicillinase) enzyme that hydrolizes the beta-lactam ring. Other mechanisms: altered PBPs (MRSA), reduced permeability, efflux pumps.
Q5. What are cephalosporins? Classify with generations. A: Cephalosporins are beta-lactam antibiotics.
  • 1st generation: Cephalexin, cefazolin - gram-positive coverage; surgical prophylaxis
  • 2nd generation: Cefuroxime, cefaclor - extended gram-negative coverage (H. flu, Moraxella)
  • 3rd generation: Ceftriaxone, cefotaxime, cefixime - better gram-negative, less gram-positive; meningitis, typhoid (ceftriaxone)
  • 4th generation: Cefepime - antipseudomonal + gram-positive
  • 5th generation: Ceftaroline - active against MRSA Note: 10% cross-reactivity between penicillin and cephalosporins (reduced with newer generations).
Q6. What are aminoglycosides? Give mechanism, uses, and toxicity. A: Examples: streptomycin, gentamicin, amikacin, tobramycin, neomycin. Mechanism: Bind irreversibly to 30S ribosomal subunit → misreading of mRNA → non-functional proteins → bactericidal. Uses: gram-negative infections (including Pseudomonas), synergy with beta-lactams for endocarditis, TB (streptomycin), topical infections. Toxicity: nephrotoxicity (proximal tubular damage), ototoxicity (cochlear - sensorineural hearing loss, and vestibular), neuromuscular blockade. Monitoring: trough levels; avoid with other nephrotoxic/ototoxic drugs. Contraindicated in pregnancy (fetal ototoxicity).
Q7. What are fluoroquinolones? Give mechanism, uses, and adverse effects. A: Examples: ciprofloxacin, ofloxacin, levofloxacin, moxifloxacin, norfloxacin. Mechanism: Inhibit bacterial DNA gyrase (topoisomerase II) and topoisomerase IV → prevent DNA replication and transcription → bactericidal. Uses: UTI (norfloxacin, ciprofloxacin), respiratory infections (levofloxacin, moxifloxacin), typhoid, anthrax, atypical pneumonia, gonorrhea. Adverse effects: GI upset, CNS (seizure risk in epileptics), tendinopathy/tendon rupture (especially Achilles), QT prolongation, phototoxicity, cartilage damage (avoid in children and pregnancy), dysglycemia.
Q8. What are tetracyclines? Give mechanism and uses. A: Examples: tetracycline, doxycycline, minocycline. Mechanism: Bind to 30S ribosomal subunit → block attachment of aminoacyl-tRNA → inhibit protein synthesis → bacteriostatic. Uses: rickettsial infections (drug of choice), Chlamydia (drug of choice), mycoplasma pneumonia, brucellosis (with streptomycin), acne vulgaris, cholera, atypical pneumonia, malaria (doxycycline prophylaxis), Lyme disease. Adverse effects: GI disturbance, photosensitivity, superinfection (candidiasis, C. difficile), teeth discoloration and enamel hypoplasia (contraindicated in children <8 years and pregnancy), hepatotoxicity (high dose IV), Fanconi syndrome (outdated tetracyclines).
Q9. What are macrolides? Give mechanism and uses. A: Examples: erythromycin, azithromycin, clarithromycin, roxithromycin. Mechanism: Bind to 23S rRNA of 50S ribosomal subunit → inhibit translocation (block elongation) → bacteriostatic (bactericidal at high doses). Uses: Alternative to penicillin in allergy, atypical pneumonia (Legionella, Mycoplasma, Chlamydia), H. pylori eradication (clarithromycin), whooping cough (azithromycin), community-acquired pneumonia. Azithromycin advantages: long half-life (3-5 days), once-daily 5-day course, excellent tissue penetration. Adverse effects: GI upset (most common), QT prolongation, hepatotoxicity (cholestatic jaundice), drug interactions (CYP450 inhibitors).
Q10. What are sulfonamides and trimethoprim? What is co-trimoxazole? A: Mechanism:
  • Sulfonamides: Structural analogue of PABA; competitively inhibit dihydropteroate synthase → block folate synthesis.
  • Trimethoprim: Inhibits dihydrofolate reductase (bacterial enzyme selectively) → blocks tetrahydrofolate synthesis. Both work sequentially on folate synthesis → sequential blockade → synergistic effect. Co-trimoxazole = Sulfamethoxazole + Trimethoprim (5:1 ratio). Uses: UTI, Pneumocystis jirovecii pneumonia (PCP) - drug of choice in prophylaxis and treatment, typhoid, MRSA (community-acquired).
Q11. What is the mechanism of metronidazole? Give its uses. A: Metronidazole is a nitroimidazole. Mechanism: Reduced by anaerobic/microaerophilic organisms to reactive intermediates that damage DNA. Uses: anaerobic infections (Bacteroides), Clostridioides difficile infection (oral), H. pylori eradication, Trichomoniasis (drug of choice), Giardiasis (drug of choice), Amoebiasis (intestinal and hepatic), bacterial vaginosis. Adverse effects: metallic taste (most common), nausea, disulfiram-like reaction with alcohol (avoid alcohol).
Q12. What are antitubercular drugs? Name first-line and second-line drugs. A:
  • First-line (RIPE/HRZE):
    • R - Rifampicin (inhibits RNA polymerase; enzyme inducer; turns urine/secretions orange)
    • I/H - Isoniazid (INH; inhibits mycolic acid synthesis; peripheral neuropathy prevented by pyridoxine B6)
    • P/Z - Pyrazinamide (disrupts membrane potential; hepatotoxic; hyperuricemia)
    • E - Ethambutol (inhibits arabinosyl transferase; optic neuritis - red-green colour vision loss)
    • S - Streptomycin (aminoglycoside; given IM; ototoxic)
  • Second-line: Fluoroquinolones (levofloxacin, moxifloxacin), kanamycin, capreomycin, linezolid, bedaquiline (MDR-TB), cycloserine, ethionamide
  • TB regimen: 2 months HRZE (intensive phase) + 4 months HR (continuation phase)
Q13. What are antimalarials? Classify with mechanism. A:
  • Chloroquine: Drug of choice for P. vivax/ovale/malariae (blood schizonticide); inhibits heme polymerization → toxic heme accumulates. Adverse effects: retinal toxicity (irreversible), pruritus, nausea. Resistance in P. falciparum.
  • Artemisinin and derivatives (artesunate, artemether): Drugs of choice for P. falciparum (severe malaria). Mechanism: endoperoxide bridge reacts with heme → free radicals.
  • ACT (Artemisinin Combination Therapy): Artemether + lumefantrine (Coartem) or artesunate + mefloquine - recommended by WHO for falciparum malaria.
  • Primaquine: Only drug active against liver stages (radical cure of P. vivax/ovale; kills gametocytes). Causes hemolytic anemia in G6PD-deficient patients.
  • Mefloquine: Blood schizonticide for falciparum. Neuropsychiatric side effects.
  • Quinine: For severe/complicated P. falciparum (IV); cinchonism (tinnitus, headache, visual disturbance).
  • Doxycycline, proguanil: Chemoprophylaxis.
Q14. What are antifungal drugs? Classify with mechanism. A:
  • Polyene macrolides (target ergosterol directly): Amphotericin B (gold standard for systemic fungal infections; nephrotoxic), Nystatin (topical only - oral thrush, vaginal candidiasis)
  • Azoles (inhibit ergosterol synthesis via CYP51/14-demethylase):
    • Imidazoles: Clotrimazole, miconazole (topical)
    • Triazoles: Fluconazole (candidiasis, cryptococcal meningitis), itraconazole, voriconazole (aspergillosis), posaconazole
  • Echinocandins (inhibit beta-1,3-glucan synthase - unique target, low side effects): Caspofungin, micafungin, anidulafungin - used for invasive candidiasis and aspergillosis
  • Other: Griseofulvin (inhibits microtubule - used for dermatophyte infections, onychomycosis); Terbinafine (inhibits squalene epoxidase - dermatophytes)
Q15. What are antiviral drugs? Give examples for HIV. A: HIV treatment - Antiretroviral therapy (ART):
  • NRTIs (Nucleoside Reverse Transcriptase Inhibitors): Zidovudine (AZT), lamivudine (3TC), tenofovir, emtricitabine - chain termination of viral DNA synthesis
  • NNRTIs (Non-nucleoside RTIs): Nevirapine, efavirenz - bind RT allosterically
  • PIs (Protease Inhibitors): Ritonavir, lopinavir, atazanavir - inhibit HIV protease; must be boosted with ritonavir
  • INSTIs (Integrase inhibitors): Raltegravir, dolutegravir - preferred first-line in current guidelines
  • CCR5 antagonist: Maraviroc
  • Standard regimen: 2 NRTIs + 1 INSTI (e.g., tenofovir + emtricitabine + dolutegravir = TLD - WHO preferred first-line)
Q16. What are anticancer drugs? Classify with examples. A:
  • Alkylating agents: Cyclophosphamide, chlorambucil, melphalan, busulfan - cross-link DNA strands; hemorrhagic cystitis (cyclophosphamide, prevent with mesna)
  • Antimetabolites: Methotrexate (DHFR inhibitor), 5-fluorouracil (5-FU), cytarabine (Ara-C), 6-mercaptopurine
  • Vinca alkaloids (antimitotic): Vincristine, vinblastine - inhibit microtubule polymerization; peripheral neuropathy (vincristine)
  • Taxanes: Paclitaxel, docetaxel - stabilize microtubules; prevent depolymerization
  • Platinum compounds: Cisplatin, carboplatin - cross-link DNA; nephrotoxic (cisplatin - prevent with hydration and amifostine), peripheral neuropathy, ototoxicity
  • Anthracyclines: Doxorubicin, daunorubicin - intercalate DNA, inhibit topoisomerase II; cardiomyopathy (dose-limiting)
  • Topoisomerase inhibitors: Irinotecan, topotecan (CPT-11, Topo I); etoposide (Topo II)
  • Monoclonal antibodies: Rituximab (anti-CD20, B-cell lymphoma), trastuzumab (anti-HER2, breast cancer), bevacizumab (anti-VEGF), cetuximab
  • Tyrosine kinase inhibitors: Imatinib (CML, BCR-ABL inhibitor), erlotinib, gefitinib (EGFR inhibitors)
  • Hormonal agents: Tamoxifen (ER antagonist, breast cancer), anastrozole/letrozole (aromatase inhibitors), leuprolide (prostate cancer)

Key Tips for MGR University Viva:
  • Always know the mechanism + uses + adverse effects for any drug asked
  • For antibiotics, know the spectrum and resistance mechanisms
  • Be ready to write prescriptions for common conditions (peptic ulcer, hypertension, malaria, TB, diabetes)
  • Know drug doses for emergency drugs (atropine, adrenaline, morphine, digoxin)
  • Know important drug interactions (warfarin, MAOIs, antiepileptics)
  • Practical viva often tests prescription writing, spotter identification, and dose calculation

Generate a pdf of this pls

Reading File
Running Command

ls /home/daytona/workspace/ 2>/dev/null || mkdir -p /home/daytona/workspace

Running Command

mkdir -p /home/daytona/workspace/pharmacology-viva && python3 -c "from reportlab.platypus import SimpleDocTemplate; print('reportlab OK')" && python3 -c "from fpdf import FPDF; print('fpdf OK')"

Writing File

~/pharmacology-viva/generate_pdf.py

from reportlab.platypus import (
    SimpleDocTemplate, Paragraph, Spacer, Table, TableStyle,
    PageBreak, HRFlowable
)
from reportlab.lib.pagesizes import A4
from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle
from reportlab.lib.units import cm
from reportlab.lib import colors
from reportlab.lib.enums import TA_CENTER, TA_LEFT, TA_JUSTIFY

OUTPUT = "/home/daytona/workspace/pharmacology-viva/Pharmacology_Viva_QA_MGR_University.pdf"

doc = SimpleDocTemplate(
    OUTPUT,
    pagesize=A4,
    rightMargin=2*cm, leftMargin=2*cm,
    topMargin=2.5*cm, bottomMargin=2.5*cm,
    title="Pharmacology Viva Q&A - MGR University",
    author="Orris AI"
)

styles = getSampleStyleSheet()

# Custom styles
TITLE_STYLE = ParagraphStyle(
    'CustomTitle',
    parent=styles['Title'],
    fontSize=20,
    textColor=colors.HexColor('#1a237e'),
    spaceAfter=6,
    spaceBefore=6,
    alignment=TA_CENTER,
    fontName='Helvetica-Bold'
)

SUBTITLE_STYLE = ParagraphStyle(
    'Subtitle',
    parent=styles['Normal'],
    fontSize=11,
    textColor=colors.HexColor('#3949ab'),
    spaceAfter=4,
    alignment=TA_CENTER,
    fontName='Helvetica'
)

UNIT_HEADING = ParagraphStyle(
    'UnitHeading',
    parent=styles['Heading1'],
    fontSize=14,
    textColor=colors.white,
    backColor=colors.HexColor('#1a237e'),
    spaceBefore=16,
    spaceAfter=8,
    fontName='Helvetica-Bold',
    leftIndent=-10,
    rightIndent=-10,
    borderPad=6,
)

QUESTION_STYLE = ParagraphStyle(
    'Question',
    parent=styles['Normal'],
    fontSize=10,
    textColor=colors.HexColor('#b71c1c'),
    fontName='Helvetica-Bold',
    spaceBefore=8,
    spaceAfter=2,
    leftIndent=0,
)

ANSWER_STYLE = ParagraphStyle(
    'Answer',
    parent=styles['Normal'],
    fontSize=9.5,
    textColor=colors.HexColor('#1a1a1a'),
    fontName='Helvetica',
    spaceBefore=2,
    spaceAfter=4,
    leftIndent=12,
    leading=14,
    alignment=TA_JUSTIFY,
)

BULLET_STYLE = ParagraphStyle(
    'Bullet',
    parent=styles['Normal'],
    fontSize=9.5,
    textColor=colors.HexColor('#1a1a1a'),
    fontName='Helvetica',
    spaceBefore=1,
    spaceAfter=1,
    leftIndent=24,
    bulletIndent=12,
    leading=13,
)

TIP_STYLE = ParagraphStyle(
    'Tip',
    parent=styles['Normal'],
    fontSize=9.5,
    textColor=colors.HexColor('#1b5e20'),
    fontName='Helvetica-Oblique',
    spaceBefore=4,
    spaceAfter=4,
    leftIndent=12,
    leading=13,
)

SECTION_LABEL = ParagraphStyle(
    'SectionLabel',
    parent=styles['Normal'],
    fontSize=11,
    textColor=colors.HexColor('#e65100'),
    fontName='Helvetica-Bold',
    spaceBefore=10,
    spaceAfter=4,
    leftIndent=0,
)

def Q(text):
    return Paragraph(text, QUESTION_STYLE)

def A(text):
    return Paragraph(text, ANSWER_STYLE)

def B(text):
    return Paragraph(f"• {text}", BULLET_STYLE)

def unit_header(text):
    return Paragraph(f"  {text}", UNIT_HEADING)

def section(text):
    return Paragraph(text, SECTION_LABEL)

def tip(text):
    return Paragraph(text, TIP_STYLE)

def hr():
    return HRFlowable(width="100%", thickness=0.5, color=colors.HexColor('#9e9e9e'), spaceAfter=4, spaceBefore=4)

def table_2col(data, col_widths=None):
    if col_widths is None:
        col_widths = [7*cm, 9.5*cm]
    tbl = Table(data, colWidths=col_widths)
    tbl.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,0), colors.HexColor('#1a237e')),
        ('TEXTCOLOR', (0,0), (-1,0), colors.white),
        ('FONTNAME', (0,0), (-1,0), 'Helvetica-Bold'),
        ('FONTSIZE', (0,0), (-1,-1), 9),
        ('ROWBACKGROUNDS', (0,1), (-1,-1), [colors.HexColor('#f5f5f5'), colors.white]),
        ('GRID', (0,0), (-1,-1), 0.4, colors.HexColor('#bdbdbd')),
        ('VALIGN', (0,0), (-1,-1), 'TOP'),
        ('LEFTPADDING', (0,0), (-1,-1), 6),
        ('RIGHTPADDING', (0,0), (-1,-1), 6),
        ('TOPPADDING', (0,0), (-1,-1), 4),
        ('BOTTOMPADDING', (0,0), (-1,-1), 4),
    ]))
    return tbl

def table_generic(data, col_widths=None):
    if col_widths is None:
        col_widths = [3.8*cm, 4*cm, 4*cm, 4*cm]
    tbl = Table(data, colWidths=col_widths)
    tbl.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,0), colors.HexColor('#283593')),
        ('TEXTCOLOR', (0,0), (-1,0), colors.white),
        ('FONTNAME', (0,0), (-1,0), 'Helvetica-Bold'),
        ('FONTSIZE', (0,0), (-1,-1), 9),
        ('ROWBACKGROUNDS', (0,1), (-1,-1), [colors.HexColor('#e8eaf6'), colors.white]),
        ('GRID', (0,0), (-1,-1), 0.4, colors.HexColor('#9fa8da')),
        ('VALIGN', (0,0), (-1,-1), 'TOP'),
        ('LEFTPADDING', (0,0), (-1,-1), 5),
        ('RIGHTPADDING', (0,0), (-1,-1), 5),
        ('TOPPADDING', (0,0), (-1,-1), 4),
        ('BOTTOMPADDING', (0,0), (-1,-1), 4),
    ]))
    return tbl

story = []

# ── COVER PAGE ────────────────────────────────────────────────────────────────
story.append(Spacer(1, 3*cm))
story.append(Paragraph("PHARMACOLOGY", TITLE_STYLE))
story.append(Paragraph("VIVA QUESTIONS & ANSWERS", TITLE_STYLE))
story.append(Spacer(1, 0.4*cm))
story.append(Paragraph("Tamil Nadu Dr. M.G.R. Medical University", SUBTITLE_STYLE))
story.append(Paragraph("II MBBS — All Units", SUBTITLE_STYLE))
story.append(Spacer(1, 1.5*cm))

cover_box = Table(
    [["Units Covered"],
     ["Unit 1: General Pharmacology"],
     ["Unit 2: Autonomic & Peripheral Nervous System"],
     ["Unit 3: Central Nervous System"],
     ["Unit 4: CVS, Blood & Diuretics"],
     ["Unit 5: Respiratory System, GIT & Autacoids"],
     ["Unit 6: Endocrine Pharmacology"],
     ["Unit 7 & 8: Chemotherapy"]],
    colWidths=[12*cm]
)
cover_box.setStyle(TableStyle([
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story.append(cover_box)
story.append(Spacer(1, 2*cm))
story.append(Paragraph("Compiled for Viva Voce Preparation", TIP_STYLE))
story.append(PageBreak())

# ═══════════════════════════════════════════════════════════════════════════════
# UNIT 1 - GENERAL PHARMACOLOGY
# ═══════════════════════════════════════════════════════════════════════════════
story.append(unit_header("UNIT 1 — GENERAL PHARMACOLOGY"))
story.append(Spacer(1, 0.2*cm))

qa1 = [
    ("Q1. Define pharmacology.",
     "Pharmacology is the science that deals with the study of drugs — their sources, physicochemical properties, dosage forms, mechanisms of action, absorption, distribution, metabolism, excretion, effects, uses, and adverse reactions."),
    ("Q2. What is a drug? Give examples.",
     "A drug is any substance that, when administered to a living organism, produces a biological effect. Examples: aspirin, penicillin, morphine."),
    ("Q3. What are the routes of drug administration? Which is fastest?",
     None),
    ("Q4. What is bioavailability?",
     "Bioavailability is the fraction (percentage) of the administered drug that reaches the systemic circulation in unchanged form. IV bioavailability = 100%. Oral bioavailability is reduced by first-pass metabolism."),
    ("Q5. What is first-pass metabolism? Give examples.",
     "First-pass metabolism (presystemic metabolism) is the metabolism of a drug in the gut wall and liver before it reaches systemic circulation, reducing its bioavailability. Examples: morphine, propranolol, lignocaine, nitroglycerin, aspirin. These drugs are often given by non-oral routes to avoid this effect."),
    ("Q6. What is plasma protein binding? What is its significance?",
     None),
    ("Q7. What is Vd (volume of distribution)?",
     "Vd is a theoretical volume that the drug would need to occupy to explain the observed plasma concentration relative to the total dose administered. Vd = Amount of drug in body / Plasma drug concentration. High Vd = drug is extensively distributed to tissues (e.g., chloroquine). Low Vd = drug stays in plasma."),
    ("Q8. What is the half-life of a drug?",
     "Half-life (t½) is the time taken for the plasma concentration of a drug to fall to half its original value. It determines dosing frequency and time to steady state (4-5 half-lives). Example: digoxin t½ = 36-40 hours."),
    ("Q9. What are the phases of drug metabolism (biotransformation)?",
     None),
    ("Q10. What is enzyme induction? Give examples.",
     "Enzyme induction is an increase in synthesis of CYP450 enzymes, leading to faster metabolism of drugs and reduced drug effect. Inducers: rifampicin, phenobarbitone, phenytoin, carbamazepine, alcohol (chronic). Clinical example: rifampicin reduces efficacy of oral contraceptive pills."),
    ("Q11. What is enzyme inhibition? Give examples.",
     "Inhibition of CYP450 enzymes leads to reduced metabolism, increased plasma levels, and toxicity of co-administered drugs. Examples: ketoconazole, erythromycin, ciprofloxacin, cimetidine, grapefruit juice."),
    ("Q12. What are receptors? Classify them.",
     None),
    ("Q13. What is an agonist? What is an antagonist?",
     None),
    ("Q14. Difference between competitive and non-competitive antagonism?",
     None),
    ("Q15. What is tolerance? Tachyphylaxis? Dependence?",
     None),
    ("Q16. What is idiosyncrasy?",
     "An abnormal, genetically determined qualitatively different response to a drug not seen in most individuals. Example: G6PD-deficient patients develop hemolysis with primaquine/sulfonamides; succinylcholine causes prolonged apnea in pseudocholinesterase-deficient patients."),
    ("Q17. What is the therapeutic index?",
     "Therapeutic Index (TI) = TD50 / ED50. A high TI = safer drug (e.g., penicillin). A low TI = narrow safety margin requiring monitoring (e.g., digoxin, warfarin, lithium, theophylline, aminoglycosides)."),
    ("Q18. What is steady state and how does half-life relate to it?",
     "Steady state is achieved after 4-5 half-lives of continuous administration, when rate of drug intake = rate of elimination. Time to steady state depends only on t½, not on dose."),
]

for q, a_text in qa1:
    story.append(Q(q))
    if q == "Q3. What are the routes of drug administration? Which is fastest?":
        story.append(A("Routes include:"))
        story.append(B("Enteral: oral, sublingual, rectal"))
        story.append(B("Parenteral: IV, IM, SC, intradermal"))
        story.append(B("Others: inhalation, transdermal, topical, intrathecal"))
        story.append(A("The IV route is the fastest as it bypasses absorption completely."))
    elif q == "Q6. What is plasma protein binding? What is its significance?":
        story.append(A("Drugs bind reversibly to plasma proteins (mainly albumin). Significance:"))
        story.append(B("Bound drug is pharmacologically inactive (only free drug acts)"))
        story.append(B("Acts as a drug reservoir"))
        story.append(B("Bound drug cannot be filtered by kidney"))
        story.append(B("Drug-drug interaction can occur at protein binding sites (displacement)"))
    elif q == "Q9. What are the phases of drug metabolism (biotransformation)?":
        story.append(A("Phase I (Nonsynthetic): Oxidation, reduction, hydrolysis — mediated by CYP450 enzymes in liver."))
        story.append(A("Phase II (Synthetic/Conjugation): Glucuronidation, sulfation, acetylation, methylation — makes metabolite water-soluble for excretion."))
    elif q == "Q12. What are receptors? Classify them.":
        story.append(A("Receptors are macromolecular proteins that recognize and bind specific drugs/endogenous ligands and produce a response. Classification:"))
        story.append(B("Ionotropic (ligand-gated ion channels): Nicotinic ACh receptor, GABA-A"))
        story.append(B("G-protein coupled receptors (GPCR): Adrenergic, muscarinic, opioid"))
        story.append(B("Enzyme-linked receptors (tyrosine kinase): Insulin receptor, growth factors"))
        story.append(B("Nuclear receptors (intracellular): Steroid hormones, thyroid hormones, vitamin D"))
    elif q == "Q13. What is an agonist? What is an antagonist?":
        story.append(A("Agonist: Binds to a receptor and produces a biological response (has affinity + intrinsic activity). Example: salbutamol (beta-2 agonist)."))
        story.append(A("Antagonist: Binds to a receptor but produces no response, and blocks the agonist (has affinity, no intrinsic activity). Example: propranolol (beta blocker)."))
    elif q == "Q14. Difference between competitive and non-competitive antagonism?":
        tdata = [
            ['Feature', 'Competitive', 'Non-competitive'],
            ['Binding site', 'Same as agonist', 'Allosteric (different site)'],
            ['Effect of increasing agonist', 'Can overcome antagonism', 'Cannot overcome'],
            ['Dose-response curve', 'Shifted right, parallel', 'Maximum depressed'],
            ['Example', 'Atropine, naloxone', 'Phenoxybenzamine'],
        ]
        story.append(Spacer(1,4))
        story.append(table_generic(tdata, col_widths=[4*cm, 5*cm, 5.5*cm]))
        story.append(Spacer(1,4))
    elif q == "Q15. What is tolerance? Tachyphylaxis? Dependence?":
        story.append(B("Tolerance: Reduced response on repeated administration requiring increased doses (e.g., opioids, alcohol)."))
        story.append(B("Tachyphylaxis: Rapid development of tolerance after just a few doses (e.g., ephedrine)."))
        story.append(B("Dependence: Compulsive drug use despite harm. Physical dependence = withdrawal symptoms on stopping. Psychological dependence = craving."))
    elif a_text:
        story.append(A(a_text))
    story.append(hr())

story.append(PageBreak())

# ═══════════════════════════════════════════════════════════════════════════════
# UNIT 2 - ANS & PERIPHERAL NERVOUS SYSTEM
# ═══════════════════════════════════════════════════════════════════════════════
story.append(unit_header("UNIT 2 — AUTONOMIC & PERIPHERAL NERVOUS SYSTEM"))
story.append(Spacer(1, 0.2*cm))

u2_items = [
    ("Q1. What is neurohumoral transmission?",
     "The process by which nerve impulses are transmitted across synapses via chemical messengers. Steps: (1) Synthesis of neurotransmitter, (2) Storage in vesicles, (3) Release into synaptic cleft (Ca2+-triggered), (4) Binding to receptors, (5) Termination (reuptake, degradation, or diffusion)."),
    ("Q2. What are the neurotransmitters of ANS?",
     None),
    ("Q3. Classify cholinergic receptors with examples.",
     None),
    ("Q4. What are the effects of muscarinic receptor stimulation?",
     None),
    ("Q5. What is atropine? Give pharmacological effects.",
     None),
    ("Q6. What are the uses and contraindications of atropine?",
     None),
    ("Q7. Classify adrenergic receptors with their actions.",
     None),
    ("Q8. What is the mechanism and uses of adrenaline?",
     "Adrenaline acts on alpha1, alpha2, beta1, beta2, beta3 receptors. Effects: increased heart rate and force, bronchodilation, vasoconstriction (skin/viscera) + vasodilation (skeletal muscle). Uses: anaphylaxis (drug of choice), cardiac arrest, adjuvant in local anaesthetics (prolongs action, reduces bleeding), acute severe asthma."),
    ("Q9. What are beta blockers? Classify and give uses.",
     None),
    ("Q10. Adverse effects and contraindications of beta blockers?",
     None),
    ("Q11. What are organophosphates? Mechanism of toxicity?",
     "Organophosphates (malathion, parathion) are irreversible inhibitors of acetylcholinesterase (AChE). They phosphorylate the active site of AChE, leading to accumulation of ACh at all cholinergic synapses (muscarinic + nicotinic + CNS)."),
    ("Q12. Features and treatment of organophosphate poisoning?",
     None),
    ("Q13. What are neuromuscular blocking agents? Classify.",
     None),
    ("Q14. What is succinylcholine? Side effects?",
     None),
    ("Q15. What are local anaesthetics? Mechanism?",
     None),
    ("Q16. Uses and toxicity of lignocaine?",
     "Uses: surface/infiltration/nerve block/epidural/spinal anaesthesia, ventricular arrhythmias (IV). Toxicity: CNS (dizziness, perioral tingling, convulsions) then CVS (hypotension, bradycardia, cardiac arrest) due to systemic absorption."),
    ("Q17. What are anticholinesterases? Classify.",
     None),
]

for q, a_text in u2_items:
    story.append(Q(q))
    if q == "Q2. What are the neurotransmitters of ANS?":
        story.append(B("Acetylcholine (ACh): Released at all preganglionic synapses (sympathetic + parasympathetic), all parasympathetic postganglionic synapses, sympathetic fibers to sweat glands, and NMJ."))
        story.append(B("Norepinephrine: Released at sympathetic postganglionic nerve endings (except sweat glands)."))
        story.append(B("Epinephrine: Released from adrenal medulla into blood."))
    elif q == "Q3. Classify cholinergic receptors with examples.":
        story.append(B("Muscarinic (M1-M5): On smooth muscle, cardiac, exocrine glands. Agonists: pilocarpine, bethanechol. Antagonists: atropine, scopolamine."))
        story.append(B("Nicotinic (Nn): At autonomic ganglia. Agonist: nicotine. Antagonist: hexamethonium."))
        story.append(B("Nicotinic (Nm): At neuromuscular junction. Agonist: succinylcholine. Antagonists: tubocurarine, vecuronium."))
    elif q == "Q4. What are the effects of muscarinic receptor stimulation?":
        story.append(A("Mnemonic: SLUD + others"))
        story.append(B("Salivation, Lacrimation, Urination, Defecation (diarrhea)"))
        story.append(B("Bradycardia, hypotension"))
        story.append(B("Bronchoconstriction, increased secretions"))
        story.append(B("Miosis (pupil constriction), accommodation for near vision"))
        story.append(B("Increased GI motility"))
    elif q == "Q5. What is atropine? Give pharmacological effects.":
        story.append(A("Atropine is a competitive muscarinic antagonist (alkaloid from Atropa belladonna). Effects (opposite to muscarinic stimulation):"))
        story.append(B("Tachycardia"))
        story.append(B("Mydriasis and cycloplegia"))
        story.append(B("Reduced secretions (dry mouth, dry skin, anhidrosis)"))
        story.append(B("Bronchodilation"))
        story.append(B("Reduced GI motility (constipation)"))
        story.append(B("Urinary retention"))
        story.append(B("CNS: stimulation (high dose)"))
    elif q == "Q6. What are the uses and contraindications of atropine?":
        story.append(A("Uses: organophosphate poisoning, preanesthetic medication, bradycardia, peptic ulcer, ophthalmic (mydriasis), antidote for muscarine/mushroom poisoning."))
        story.append(A("Contraindications: glaucoma, benign prostatic hyperplasia, pyloric stenosis, tachyarrhythmia."))
    elif q == "Q7. Classify adrenergic receptors with their actions.":
        tdata = [
            ['Receptor', 'Main Actions'],
            ['alpha-1', 'Vasoconstriction, mydriasis, urinary sphincter contraction'],
            ['alpha-2', 'Reduces NE release (presynaptic); reduces sympathetic outflow (CNS)'],
            ['beta-1', 'Tachycardia, increased contractility, renin release'],
            ['beta-2', 'Bronchodilation, vasodilation, uterine relaxation, glycogenolysis'],
            ['beta-3', 'Lipolysis in fat cells'],
        ]
        story.append(Spacer(1,4))
        story.append(table_generic(tdata, col_widths=[3*cm, 12*cm]))
        story.append(Spacer(1,4))
    elif q == "Q9. What are beta blockers? Classify and give uses.":
        story.append(A("Beta blockers antagonize beta-adrenergic receptors. Classification:"))
        story.append(B("Non-selective (beta1+beta2): Propranolol, nadolol, timolol"))
        story.append(B("Cardioselective (beta1): Atenolol, metoprolol, bisoprolol"))
        story.append(B("With ISA: Pindolol, oxprenolol"))
        story.append(B("With alpha-blocking activity: Labetalol, carvedilol"))
        story.append(A("Uses: hypertension, angina, arrhythmias, heart failure (carvedilol, bisoprolol), thyrotoxicosis, glaucoma (timolol), migraine prophylaxis, anxiety."))
    elif q == "Q10. Adverse effects and contraindications of beta blockers?":
        story.append(A("Adverse effects: bradycardia, heart block, bronchospasm, cold extremities, hypoglycemia masking, fatigue, impotence."))
        story.append(A("Contraindications: bronchial asthma, COPD, heart block, severe bradycardia, decompensated heart failure, Prinzmetal's angina."))
    elif q == "Q12. Features and treatment of organophosphate poisoning?":
        story.append(A("Features: Muscarinic (SLUD, bradycardia, bronchospasm, miosis) + Nicotinic (muscle fasciculations, weakness, paralysis) + CNS (anxiety, convulsions, coma)."))
        story.append(A("Treatment:"))
        story.append(B("Atropine (large doses IV, reverses muscarinic effects) — drug of choice"))
        story.append(B("Pralidoxime / 2-PAM (reactivates AChE if given early, before 'ageing')"))
        story.append(B("Supportive: airway, oxygen, diazepam for convulsions"))
    elif q == "Q13. What are neuromuscular blocking agents? Classify.":
        story.append(A("NMBAs block the NMJ, causing skeletal muscle paralysis. Used during general anaesthesia."))
        story.append(B("Depolarizing: Succinylcholine — causes initial fasciculations (Phase I block), then sustained depolarization. Short acting. Reversed by plasma cholinesterase."))
        story.append(B("Non-depolarizing: Tubocurarine, pancuronium, vecuronium, rocuronium, atracurium — competitive antagonism at nicotinic Nm receptors. Reversed by neostigmine."))
    elif q == "Q14. What is succinylcholine? Side effects?":
        story.append(A("Succinylcholine is a depolarizing NMB (mimics ACh). Side effects: muscle fasciculations, postoperative myalgia, hyperkalemia (dangerous in burns/crush injuries), raised intraocular and intragastric pressure, malignant hyperthermia (with halothane), prolonged apnea in pseudocholinesterase deficiency."))
    elif q == "Q15. What are local anaesthetics? Mechanism?":
        story.append(A("LAs block nerve conduction by blocking voltage-gated Na+ channels in nerve membrane, preventing depolarization. Examples: lignocaine (most used), bupivacaine, cocaine, procaine. Adrenaline is added to prolong action. Order of blockade: pain > temperature > touch > pressure > motor."))
    elif q == "Q17. What are anticholinesterases? Classify.":
        story.append(A("Drugs that inhibit AChE, leading to ACh accumulation. Classification:"))
        story.append(B("Reversible: Physostigmine, neostigmine, pyridostigmine, edrophonium"))
        story.append(B("Irreversible: Organophosphates (parathion, malathion, DFP, nerve agents — tabun, sarin)"))
        story.append(A("Uses of reversible: myasthenia gravis, reversal of NMB (neostigmine), glaucoma (physostigmine), Alzheimer's (donepezil, rivastigmine)."))
    elif a_text:
        story.append(A(a_text))
    story.append(hr())

story.append(PageBreak())

# ═══════════════════════════════════════════════════════════════════════════════
# UNIT 3 - CNS
# ═══════════════════════════════════════════════════════════════════════════════
story.append(unit_header("UNIT 3 — CENTRAL NERVOUS SYSTEM"))
story.append(Spacer(1, 0.2*cm))

u3 = [
    ("Q1. Classify general anaesthetics.",
     None),
    ("Q2. What is balanced anaesthesia? What is the triad of GA?",
     "Balanced anaesthesia = combination of drugs to achieve the triad of GA while minimizing adverse effects of any single agent. Triad: (1) Loss of consciousness (hypnosis), (2) Analgesia, (3) Muscle relaxation."),
    ("Q3. What is ketamine? Unique features?",
     None),
    ("Q4. Classify sedative-hypnotics.",
     None),
    ("Q5. What is the mechanism of benzodiazepines?",
     "BZDs act on GABA-A receptors (ionotropic, Cl- channel). They potentiate GABA by increasing the FREQUENCY of Cl- channel opening, causing hyperpolarization and CNS depression. (Note: barbiturates increase the DURATION of Cl- channel opening.)"),
    ("Q6. Uses and antidote of benzodiazepines?",
     None),
    ("Q7. Classify antiepileptic drugs.",
     None),
    ("Q8. Phenytoin — mechanism, uses, adverse effects?",
     None),
    ("Q9. Valproate — uses and adverse effects?",
     None),
    ("Q10. Classify opioid analgesics. Mechanism and uses?",
     None),
    ("Q11. Adverse effects and antidote of morphine?",
     None),
    ("Q12. Classify antipsychotics (neuroleptics).",
     None),
    ("Q13. Mechanism of typical antipsychotics? What are EPS?",
     None),
    ("Q14. What is Neuroleptic Malignant Syndrome (NMS)?",
     "Rare but life-threatening reaction to antipsychotics. Features (FEVER mnemonic): Fever, Encephalopathy (altered consciousness), Vitals unstable, Elevated CK, Rigidity. Treatment: stop drug, dantrolene, bromocriptine, cooling, supportive care."),
    ("Q15. Classify antidepressants.",
     None),
    ("Q16. What is lithium? Uses, toxicity, and monitoring?",
     None),
]

for q, a_text in u3:
    story.append(Q(q))
    if q == "Q1. Classify general anaesthetics.":
        story.append(B("Inhalational: Volatile liquids (halothane, isoflurane, sevoflurane, desflurane) and gases (nitrous oxide)"))
        story.append(B("IV anaesthetics: Thiopentone sodium, propofol, ketamine, etomidate, midazolam"))
    elif q == "Q3. What is ketamine? Unique features?":
        story.append(A("Ketamine is a dissociative anaesthetic (NMDA receptor antagonist). Unique features:"))
        story.append(B("Produces 'dissociative anaesthesia' (patient appears awake but unresponsive)"))
        story.append(B("Potent analgesic — useful for short procedures"))
        story.append(B("Increases HR, BP, cardiac output (sympathomimetic — safe in hemorrhagic shock)"))
        story.append(B("Bronchodilator (useful in asthmatic patients)"))
        story.append(B("Causes emergence delirium/hallucinations (minimized by benzodiazepines)"))
        story.append(B("Increases ICP and IOP — CONTRAINDICATED in head injury, glaucoma"))
    elif q == "Q4. Classify sedative-hypnotics.":
        story.append(B("Benzodiazepines: Diazepam, lorazepam, midazolam, alprazolam"))
        story.append(B("Barbiturates: Phenobarbitone, thiopentone, pentobarbitone"))
        story.append(B("Non-BZD hypnotics (Z drugs): Zolpidem, zaleplon, zopiclone"))
        story.append(B("Others: Chloral hydrate, meprobamate"))
    elif q == "Q6. Uses and antidote of benzodiazepines?":
        story.append(A("Uses: anxiety, insomnia, status epilepticus (IV diazepam/lorazepam), alcohol withdrawal, preanaesthetic medication, muscle relaxation (diazepam), procedural sedation."))
        story.append(A("Antidote: Flumazenil — competitive BZD receptor antagonist; reverses sedation and respiratory depression caused by BZDs."))
    elif q == "Q7. Classify antiepileptic drugs.":
        story.append(B("Sodium channel blockers: Phenytoin, carbamazepine, lamotrigine, valproate"))
        story.append(B("GABA enhancers: Valproate, phenobarbitone, benzodiazepines, gabapentin, vigabatrin"))
        story.append(B("T-type Ca2+ channel blockers: Ethosuximide (absence seizures)"))
        story.append(B("Multiple mechanisms: Valproate (drug of choice for multiple seizure types)"))
    elif q == "Q8. Phenytoin — mechanism, uses, adverse effects?":
        story.append(A("Mechanism: Blocks voltage-gated Na+ channels (stabilizes inactive state), reducing repetitive firing."))
        story.append(A("Uses: all epilepsy except absence seizures, trigeminal neuralgia, cardiac arrhythmias (IV)."))
        story.append(A("Unique adverse effects: gingival hyperplasia, hirsutism, coarsening of facial features, megaloblastic anaemia (folate deficiency), teratogenicity (fetal hydantoin syndrome), nystagmus, ataxia. Also a potent enzyme inducer."))
    elif q == "Q9. Valproate — uses and adverse effects?":
        story.append(A("Uses: drug of choice for generalized seizures, absence seizures, juvenile myoclonic epilepsy, mixed seizure disorders, bipolar disorder (mood stabilizer), migraine prophylaxis."))
        story.append(A("Adverse effects: weight gain, hair loss (alopecia), tremor, hepatotoxicity, teratogenicity (neural tube defects — spina bifida), pancreatitis, thrombocytopenia."))
    elif q == "Q10. Classify opioid analgesics. Mechanism and uses?":
        story.append(B("Strong agonists: Morphine, fentanyl, methadone, pethidine, heroin"))
        story.append(B("Moderate agonists: Codeine, tramadol, oxycodone"))
        story.append(B("Partial agonists: Buprenorphine"))
        story.append(B("Antagonists: Naloxone, naltrexone"))
        story.append(B("Mixed agonist-antagonists: Pentazocine, butorphanol"))
        story.append(A("Mechanism: Act on mu, kappa, delta opioid receptors (Gi-coupled GPCRs) — hyperpolarization, reduced neuronal excitability."))
        story.append(A("Uses: severe pain (cancer, post-op, MI), cough suppression (codeine), diarrhea (loperamide), acute pulmonary edema (morphine)."))
    elif q == "Q11. Adverse effects and antidote of morphine?":
        story.append(A("Adverse effects: respiratory depression (most dangerous), constipation (no tolerance), nausea/vomiting, miosis (pin-point pupils), urinary retention, euphoria, physical dependence, histamine release."))
        story.append(A("Antidote: Naloxone (pure opioid antagonist, IV). Short half-life (30-60 min) — may need repeated doses."))
    elif q == "Q12. Classify antipsychotics (neuroleptics).":
        story.append(B("Typical (1st gen) — Low potency: chlorpromazine, thioridazine; High potency: haloperidol, fluphenazine, trifluoperazine"))
        story.append(B("Atypical (2nd gen): Clozapine, risperidone, olanzapine, quetiapine, aripiprazole, ziprasidone"))
    elif q == "Q13. Mechanism of typical antipsychotics? What are EPS?":
        story.append(A("Mechanism: Block D2 dopamine receptors (mesolimbic/mesocortical pathway)."))
        story.append(A("Extrapyramidal Side Effects (EPS):"))
        story.append(B("Acute dystonia (hours-days): muscle spasms, torticollis — treat with biperiden/benztropine"))
        story.append(B("Akathisia (days-weeks): motor restlessness"))
        story.append(B("Parkinsonism (weeks): tremor, rigidity, bradykinesia — treat with anticholinergics"))
        story.append(B("Tardive dyskinesia (months-years): involuntary oro-facial movements — switch to clozapine"))
    elif q == "Q15. Classify antidepressants.":
        story.append(B("TCAs (Tricyclics): Imipramine, amitriptyline, clomipramine — block reuptake of NE and 5-HT"))
        story.append(B("SSRIs: Fluoxetine, sertraline, paroxetine, escitalopram — drug of choice; safest"))
        story.append(B("SNRIs: Venlafaxine, duloxetine"))
        story.append(B("MAOIs: Phenelzine, tranylcypromine — tyramine/cheese reaction risk"))
        story.append(B("Others: Mirtazapine, bupropion, trazodone"))
    elif q == "Q16. What is lithium? Uses, toxicity, and monitoring?":
        story.append(A("Uses: Bipolar disorder (both acute mania and prophylaxis), augmentation in resistant depression."))
        story.append(A("Toxicity (low TI): tremor, polyuria/polydipsia (nephrogenic DI), hypothyroidism, weight gain. Toxic signs: nausea, vomiting, coarse tremor, ataxia, confusion, convulsions, coma."))
        story.append(A("Therapeutic range: 0.6-1.2 mEq/L; >2 mEq/L = toxic. Monitor renal and thyroid function regularly."))
    elif a_text:
        story.append(A(a_text))
    story.append(hr())

story.append(PageBreak())

# ═══════════════════════════════════════════════════════════════════════════════
# UNIT 4 - CVS, BLOOD & DIURETICS
# ═══════════════════════════════════════════════════════════════════════════════
story.append(unit_header("UNIT 4 — CARDIOVASCULAR SYSTEM, BLOOD & DIURETICS"))
story.append(Spacer(1, 0.2*cm))

u4 = [
    ("Q1. Classify antihypertensive drugs.",
     None),
    ("Q2. Mechanism of ACE inhibitors? Uses and adverse effects?",
     None),
    ("Q3. Classify calcium channel blockers.",
     None),
    ("Q4. What are cardiac glycosides? Mechanism of digoxin?",
     None),
    ("Q5. Uses and adverse effects of digoxin?",
     None),
    ("Q6. Classify anti-anginal drugs and mechanisms.",
     None),
    ("Q7. What is nitrate tolerance? How is it prevented?",
     "Nitrate tolerance = reduced efficacy on repeated use due to depletion of -SH groups and reduced NO generation. Prevention: provide a nitrate-free interval of 8-12 hours (usually at night). IMPORTANT: Sildenafil + nitrate = dangerous hypotension (absolute contraindication)."),
    ("Q8. Classify antiarrhythmic drugs (Vaughan Williams).",
     None),
    ("Q9. Adverse effects of amiodarone?",
     None),
    ("Q10. Classify diuretics with mechanisms.",
     None),
    ("Q11. Adverse effects of furosemide?",
     "Hypokalemia, hyponatremia, hypomagnesemia, hypovolemia, metabolic alkalosis, hyperuricemia (gout), ototoxicity (high doses/IV), hyperglycemia, dehydration."),
    ("Q12. Classify anticoagulants.",
     None),
    ("Q13. Mechanism of heparin and warfarin? Antidotes?",
     None),
    ("Q14. What are antiplatelet drugs? Examples and mechanisms?",
     None),
]

for q, a_text in u4:
    story.append(Q(q))
    if q == "Q1. Classify antihypertensive drugs.":
        story.append(B("Diuretics: Thiazides (hydrochlorothiazide), loop diuretics (furosemide)"))
        story.append(B("Beta blockers: Atenolol, metoprolol"))
        story.append(B("CCBs: Amlodipine (DHP), verapamil, diltiazem"))
        story.append(B("ACE inhibitors: Enalapril, lisinopril, ramipril"))
        story.append(B("ARBs: Losartan, valsartan, telmisartan"))
        story.append(B("Centrally acting: Methyldopa (DOC in pregnancy), clonidine"))
        story.append(B("Alpha blockers: Prazosin, doxazosin"))
        story.append(B("Vasodilators: Hydralazine, minoxidil, sodium nitroprusside (hypertensive emergency)"))
    elif q == "Q2. Mechanism of ACE inhibitors? Uses and adverse effects?":
        story.append(A("Mechanism: Block ACE, preventing Angiotensin I -> Angiotensin II. Also prevent breakdown of bradykinin -> vasodilation, reduced aldosterone."))
        story.append(A("Uses: hypertension, heart failure (reduces mortality), diabetic nephropathy (renoprotection), post-MI."))
        story.append(A("Adverse effects: DRY COUGH (bradykinin accumulation — most common, reason to switch to ARB), hyperkalemia, first-dose hypotension, angioedema (contraindication), teratogenicity."))
    elif q == "Q3. Classify calcium channel blockers.":
        story.append(B("Dihydropyridines (DHP): Amlodipine, nifedipine — mainly vascular smooth muscle; hypertension, angina. Causes reflex tachycardia and ankle edema."))
        story.append(B("Verapamil (phenylalkylamine): Cardiac > vascular; bradycardia, negative inotrope; arrhythmias (SVT), angina, hypertension."))
        story.append(B("Diltiazem (benzothiazepine): Intermediate; angina, arrhythmias."))
    elif q == "Q4. What are cardiac glycosides? Mechanism of digoxin?":
        story.append(A("Derived from Digitalis (foxglove plant). Digoxin is the prototype."))
        story.append(A("Mechanism: (1) Inhibits Na+/K+-ATPase pump -> intracellular Na+ rises -> Na+-Ca2+ exchanger inhibited -> intracellular Ca2+ rises -> positive inotropy. (2) Increases vagal tone -> slows HR (negative chronotropy) and AV conduction."))
    elif q == "Q5. Uses and adverse effects of digoxin?":
        story.append(A("Uses: Heart failure (reduces symptoms), atrial fibrillation/flutter (controls ventricular rate)."))
        story.append(A("Adverse effects (narrow TI): GI (nausea, vomiting, diarrhea), CNS (yellow-green halo vision, xanthopsia), Cardiac (any arrhythmia — most dangerous)."))
        story.append(A("Toxicity enhanced by: hypokalemia, hypomagnesemia, hypercalcemia. Antidote: Digibind (digoxin-specific antibody fragments)."))
    elif q == "Q6. Classify anti-anginal drugs and mechanisms.":
        story.append(B("Nitrates (GTN, ISDN, ISMN): Release NO -> cGMP -> vascular smooth muscle relaxation -> venodilation (reduces preload) + arteriodilation (reduces afterload)."))
        story.append(B("Beta blockers: Reduce HR and contractility (reduce O2 demand)."))
        story.append(B("Calcium channel blockers: Reduce afterload and HR."))
        story.append(B("Combination: Nitrate + beta blocker is most effective for chronic stable angina."))
    elif q == "Q8. Classify antiarrhythmic drugs (Vaughan Williams).":
        story.append(B("Class I (Na+ channel blockers): Ia — quinidine, procainamide; Ib — lignocaine; Ic — flecainide"))
        story.append(B("Class II (Beta blockers): Atenolol, metoprolol, esmolol"))
        story.append(B("Class III (K+ channel blockers — prolong AP): Amiodarone, sotalol"))
        story.append(B("Class IV (Ca2+ channel blockers): Verapamil, diltiazem"))
        story.append(B("Unclassified: Adenosine (DOC for acute SVT), digoxin"))
    elif q == "Q9. Adverse effects of amiodarone?":
        story.append(B("Pulmonary toxicity — most serious (pulmonary fibrosis)"))
        story.append(B("Thyroid dysfunction (hypo or hyperthyroidism) — iodine-containing drug"))
        story.append(B("Hepatotoxicity"))
        story.append(B("Corneal microdeposits (blue-grey vision)"))
        story.append(B("Photosensitivity, blue-grey skin discoloration"))
        story.append(B("QT prolongation — torsades de pointes"))
        story.append(B("Peripheral neuropathy"))
    elif q == "Q10. Classify diuretics with mechanisms.":
        tdata = [
            ['Class', 'Site of Action', 'Mechanism', 'Example'],
            ['Osmotic', 'PCT, descending loop', 'Osmotic retention of water', 'Mannitol'],
            ['CA inhibitors', 'PCT', 'Block CA -> reduce HCO3- reabsorption', 'Acetazolamide'],
            ['Loop', 'Thick ascending loop of Henle', 'Block NKCC2 cotransporter', 'Furosemide, bumetanide'],
            ['Thiazides', 'Distal convoluted tubule', 'Block NCC cotransporter', 'Hydrochlorothiazide'],
            ['K+-sparing', 'Collecting duct', 'Aldosterone antagonist or Na+ channel blocker', 'Spironolactone, amiloride'],
        ]
        story.append(Spacer(1,4))
        story.append(table_generic(tdata, col_widths=[3.2*cm, 4*cm, 5*cm, 3.5*cm]))
        story.append(Spacer(1,4))
    elif q == "Q12. Classify anticoagulants.":
        story.append(B("Parenteral: Heparin (UFH), LMWHs (enoxaparin, dalteparin), fondaparinux, bivalirudin"))
        story.append(B("Oral anticoagulants: Warfarin (vitamin K antagonist)"))
        story.append(B("DOACs: Dabigatran (direct thrombin inhibitor), rivaroxaban, apixaban (factor Xa inhibitors)"))
        story.append(B("Fibrinolytics (thrombolytics): Streptokinase, alteplase (tPA), tenecteplase"))
    elif q == "Q13. Mechanism of heparin and warfarin? Antidotes?":
        story.append(A("Heparin: Activates antithrombin III, which inhibits thrombin (IIa) and factor Xa. Antidote: PROTAMINE SULFATE."))
        story.append(A("Warfarin: Inhibits vitamin K epoxide reductase -> prevents activation of vitamin K-dependent clotting factors (II, VII, IX, X) and proteins C and S. Antidote: VITAMIN K (slow) or FFP/PCC (rapid reversal)."))
    elif q == "Q14. What are antiplatelet drugs? Examples and mechanisms?":
        story.append(B("Aspirin: Irreversibly inhibits COX-1 -> reduces TXA2 synthesis -> reduces platelet aggregation. Low dose 75-150 mg."))
        story.append(B("Clopidogrel, ticagrelor, prasugrel: Block P2Y12 ADP receptor. Used as DAPT after ACS/stenting."))
        story.append(B("GPIIb/IIIa inhibitors: Abciximab, tirofiban — block final common pathway of aggregation."))
        story.append(B("Dipyridamole: Inhibits phosphodiesterase -> increases cAMP -> inhibits platelet aggregation."))
    elif a_text:
        story.append(A(a_text))
    story.append(hr())

story.append(PageBreak())

# ═══════════════════════════════════════════════════════════════════════════════
# UNIT 5 - RS, GIT, AUTACOIDS
# ═══════════════════════════════════════════════════════════════════════════════
story.append(unit_header("UNIT 5 — RESPIRATORY SYSTEM, GIT & AUTACOIDS"))
story.append(Spacer(1, 0.2*cm))

u5 = [
    ("Q1. Classify antiasthmatic drugs.",
     None),
    ("Q2. Mechanism, uses and adverse effects of salbutamol?",
     None),
    ("Q3. What is theophylline? Mechanism and adverse effects?",
     None),
    ("Q4. Classify antihistamines. H1 vs H2 blockers?",
     None),
    ("Q5. What are proton pump inhibitors? Mechanism and uses?",
     None),
    ("Q6. What is H. pylori triple therapy?",
     "PPI + Clarithromycin + Amoxicillin for 7-14 days. If penicillin allergy: PPI + Clarithromycin + Metronidazole. Quadruple therapy (clarithromycin-resistant): PPI + Bismuth + Metronidazole + Tetracycline."),
    ("Q7. Classify laxatives with examples.",
     None),
    ("Q8. Classify antiemetics with mechanism.",
     None),
    ("Q9. What are autacoids? Give examples.",
     None),
    ("Q10. What are prostaglandins? Uses?",
     None),
    ("Q11. What are NSAIDs? Mechanism and classification?",
     None),
]

for q, a_text in u5:
    story.append(Q(q))
    if q == "Q1. Classify antiasthmatic drugs.":
        story.append(A("Bronchodilators:"))
        story.append(B("Beta-2 agonists: SABA — salbutamol, terbutaline; LABA — salmeterol, formoterol"))
        story.append(B("Methylxanthines: Theophylline, aminophylline"))
        story.append(B("Anticholinergics: Ipratropium (short), tiotropium (long)"))
        story.append(A("Anti-inflammatory:"))
        story.append(B("ICS: Budesonide, beclomethasone, fluticasone (mainstay of prophylaxis)"))
        story.append(B("Leukotriene antagonists: Montelukast, zafirlukast"))
        story.append(B("Mast cell stabilizers: Sodium cromoglycate"))
        story.append(B("Omalizumab (anti-IgE monoclonal antibody)"))
    elif q == "Q2. Mechanism, uses and adverse effects of salbutamol?":
        story.append(A("Mechanism: Selective beta-2 agonist. Activates beta-2 receptors -> increases cAMP -> bronchial smooth muscle relaxation (bronchodilation) + inhibits mediator release."))
        story.append(A("Uses: Acute bronchospasm (reliever/rescue), exercise-induced asthma, preterm labor (tocolytic)."))
        story.append(A("Adverse effects: Tremor, palpitations, tachycardia, hypokalemia (high doses), hyperglycemia."))
    elif q == "Q3. What is theophylline? Mechanism and adverse effects?":
        story.append(A("Theophylline is a methylxanthine. Mechanism: Inhibits phosphodiesterase (PDE) -> increases cAMP -> bronchodilation + anti-inflammatory; also adenosine receptor antagonist."))
        story.append(A("Adverse effects (narrow TI, therapeutic range 10-20 mcg/mL): GI (nausea, vomiting), CNS (insomnia, anxiety, seizures), CVS (arrhythmias, tachycardia)."))
    elif q == "Q4. Classify antihistamines. H1 vs H2 blockers?":
        story.append(B("H1 antihistamines 1st gen: Diphenhydramine, chlorpheniramine, promethazine — cross BBB, cause SEDATION"))
        story.append(B("H1 antihistamines 2nd gen: Cetirizine, loratadine, fexofenadine — NON-SEDATING"))
        story.append(B("H2 antihistamines: Ranitidine, famotidine, cimetidine — block H2 receptors in gastric parietal cells -> reduce gastric acid; used for peptic ulcer, GERD"))
    elif q == "Q5. What are proton pump inhibitors? Mechanism and uses?":
        story.append(A("Examples: Omeprazole, pantoprazole, lansoprazole, rabeprazole, esomeprazole."))
        story.append(A("Mechanism: Irreversibly inhibit H+/K+-ATPase (proton pump) on parietal cells -> near-complete suppression of gastric acid. They are prodrugs activated in acidic environment."))
        story.append(A("Uses: Peptic ulcer disease, GERD, Zollinger-Ellison syndrome, H. pylori eradication, NSAID-induced ulcer prevention."))
    elif q == "Q7. Classify laxatives with examples.":
        story.append(B("Bulk-forming: Ispaghula (psyllium), methylcellulose — safest"))
        story.append(B("Osmotic: Lactulose (also for hepatic encephalopathy), magnesium sulphate, PEG"))
        story.append(B("Stimulant/irritant: Bisacodyl, senna, castor oil"))
        story.append(B("Stool softeners/lubricants: Liquid paraffin, docusate"))
    elif q == "Q8. Classify antiemetics with mechanism.":
        story.append(B("D2 antagonists: Metoclopramide (+ 5-HT4 agonist = prokinetic), domperidone, prochlorperazine"))
        story.append(B("5-HT3 antagonists: Ondansetron, granisetron — best for chemotherapy-induced vomiting"))
        story.append(B("Antihistamines (H1 blockers): Promethazine, cyclizine — motion sickness"))
        story.append(B("Anticholinergics: Scopolamine (transdermal) — motion sickness"))
        story.append(B("NK1 antagonist: Aprepitant — delayed-phase chemo-induced vomiting"))
        story.append(B("Corticosteroids: Dexamethasone — adjunct in chemo-induced vomiting"))
    elif q == "Q9. What are autacoids? Give examples.":
        story.append(A("Autacoids are local hormones (endogenous chemical mediators) produced locally in tissues and act locally. They lack specific glands of origin."))
        story.append(B("Biogenic amines: Histamine, serotonin (5-HT), bradykinin"))
        story.append(B("Lipid-derived: Prostaglandins, thromboxanes, leukotrienes, PAF"))
        story.append(B("Peptides: Angiotensin II, substance P, endothelins"))
    elif q == "Q10. What are prostaglandins? Uses?":
        story.append(B("PGE1 analogue — Misoprostol: Cervical ripening, labor induction, medical abortion (with mifepristone), peptic ulcer prevention (with NSAIDs)"))
        story.append(B("PGF2alpha — Dinoprostone: Abortion, labor induction"))
        story.append(B("PGI2 — Epoprostenol: Pulmonary arterial hypertension, anti-platelet aggregation"))
        story.append(B("Latanoprost (PGF2alpha analogue): Glaucoma (increases uveoscleral outflow)"))
    elif q == "Q11. What are NSAIDs? Mechanism and classification?":
        story.append(A("Mechanism: Inhibit cyclooxygenase (COX) enzymes -> reduce prostaglandin synthesis -> anti-inflammatory, antipyretic, analgesic effects."))
        story.append(B("Non-selective (COX-1 + COX-2): Aspirin, ibuprofen, naproxen, diclofenac, indomethacin"))
        story.append(B("Selective COX-2 inhibitors (Coxibs): Celecoxib, etoricoxib"))
        story.append(A("Adverse effects: GI ulceration (COX-1 inhibition reduces cytoprotective PGs), renal impairment, bronchospasm (aspirin-sensitive asthma), platelet dysfunction, hypertension."))
    elif a_text:
        story.append(A(a_text))
    story.append(hr())

story.append(PageBreak())

# ═══════════════════════════════════════════════════════════════════════════════
# UNIT 6 - ENDOCRINE
# ═══════════════════════════════════════════════════════════════════════════════
story.append(unit_header("UNIT 6 — ENDOCRINE PHARMACOLOGY"))
story.append(Spacer(1, 0.2*cm))

u6 = [
    ("Q1. Classify oral hypoglycemic agents (OHAs).",
     None),
    ("Q2. Why is metformin the drug of first choice in type 2 DM?",
     None),
    ("Q3. Classify insulin preparations.",
     None),
    ("Q4. Classify corticosteroids with examples.",
     None),
    ("Q5. Uses of corticosteroids?",
     None),
    ("Q6. Adverse effects of long-term corticosteroid use?",
     None),
    ("Q7. Classify thyroid drugs with mechanism.",
     None),
    ("Q8. What are oral contraceptive pills?",
     None),
]

for q, a_text in u6:
    story.append(Q(q))
    if q == "Q1. Classify oral hypoglycemic agents (OHAs).":
        story.append(B("Sulfonylureas: Glibenclamide, glipizide, glimepiride — stimulate insulin secretion. Risk: hypoglycemia, weight gain."))
        story.append(B("Biguanides: Metformin — reduces hepatic gluconeogenesis, increases insulin sensitivity. DOC in type 2 DM."))
        story.append(B("Thiazolidinediones (TZDs): Pioglitazone — activates PPARgamma -> increases insulin sensitivity."))
        story.append(B("Alpha-glucosidase inhibitors: Acarbose, voglibose — delay carbohydrate absorption. Side effect: flatulence."))
        story.append(B("DPP-4 inhibitors (Gliptins): Sitagliptin, vildagliptin — increase GLP-1 levels -> glucose-dependent insulin release."))
        story.append(B("SGLT2 inhibitors: Dapagliflozin, empagliflozin — block glucose reabsorption in PCT -> glycosuria. Cardiac/renal protection."))
        story.append(B("GLP-1 receptor agonists: Liraglutide, semaglutide — mimic GLP-1, cause weight loss, CV benefit."))
    elif q == "Q2. Why is metformin the drug of first choice in type 2 DM?":
        story.append(A("Advantages: Does not cause hypoglycemia, causes weight loss/neutral effect, reduces cardiovascular events (UKPDS trial), inexpensive, well-established safety profile."))
        story.append(A("Mechanism: Activates AMPK -> reduces hepatic gluconeogenesis, increases peripheral glucose uptake, reduces intestinal glucose absorption."))
        story.append(A("Contraindications: Renal failure (GFR <30 mL/min), liver failure, heart failure (risk of lactic acidosis), hold 48h before/after contrast procedures."))
    elif q == "Q3. Classify insulin preparations.":
        tdata = [
            ['Type', 'Onset', 'Duration', 'Example'],
            ['Ultra-short (rapid)', '15 min', '3-4 h', 'Aspart, lispro, glulisine'],
            ['Short acting (regular)', '30 min', '6-8 h', 'Regular/soluble insulin'],
            ['Intermediate acting', '1-2 h', '12-18 h', 'NPH (isophane), lente'],
            ['Long acting (basal)', '2-4 h', '20-24 h', 'Glargine, detemir'],
            ['Ultra-long acting', '6 h', '>42 h', 'Degludec'],
        ]
        story.append(Spacer(1,4))
        story.append(table_generic(tdata, col_widths=[4.5*cm, 2.5*cm, 2.5*cm, 6*cm]))
        story.append(Spacer(1,4))
    elif q == "Q4. Classify corticosteroids with examples.":
        story.append(B("Glucocorticoids: Cortisol (natural), prednisolone, dexamethasone, betamethasone, budesonide, beclomethasone"))
        story.append(B("Mineralocorticoids: Aldosterone (natural), fludrocortisone"))
        story.append(B("Both: Hydrocortisone (used IV for emergencies)"))
    elif q == "Q5. Uses of corticosteroids?":
        story.append(B("Anti-inflammatory/immunosuppressive: RA, SLE, IBD, asthma, COPD exacerbation, allergic reactions"))
        story.append(B("Replacement therapy: Addison's disease, congenital adrenal hyperplasia"))
        story.append(B("Specific uses: dexamethasone in raised ICP/cerebral edema; antenatal steroids for fetal lung maturity"))
        story.append(B("Organ transplant rejection prevention"))
        story.append(B("Topical: eczema, psoriasis"))
    elif q == "Q6. Adverse effects of long-term corticosteroid use?":
        story.append(A("Mnemonic: BECLOMETHASONE"))
        tdata = [
            ['Letter', 'Adverse Effect'],
            ['B', 'Blood sugar increased (steroid diabetes)'],
            ['E', 'Electrolyte imbalance (Na+ up, K+ down, Ca2+ down)'],
            ['C', "Cushing's syndrome (moon face, buffalo hump, striae)"],
            ['O', 'Osteoporosis (most serious long-term effect)'],
            ['M', 'Myopathy (proximal)'],
            ['E', 'Eye: glaucoma, posterior subcapsular cataract'],
            ['H', 'Hypertension'],
            ['A', 'Adrenal suppression (never stop abruptly!)'],
            ['S', 'Susceptibility to infections'],
            ['N', 'Neuropsychiatric (insomnia, psychosis, euphoria)'],
        ]
        story.append(Spacer(1,4))
        story.append(table_generic(tdata, col_widths=[1.5*cm, 14*cm]))
        story.append(Spacer(1,4))
    elif q == "Q7. Classify thyroid drugs with mechanism.":
        story.append(A("Antithyroid drugs:"))
        story.append(B("Thionamides: Carbimazole (prodrug -> methimazole), PTU — inhibit thyroid peroxidase -> block T3/T4 synthesis. PTU also inhibits peripheral T4->T3 conversion (preferred in thyroid storm and pregnancy 1st trimester)."))
        story.append(B("Radioactive iodine (131I): Destroys thyroid tissue"))
        story.append(B("Iodine/Iodides (Lugol's iodine): Wolff-Chaikoff effect — paradoxical inhibition; used pre-operatively."))
        story.append(B("Propranolol: Symptom control in thyrotoxicosis, inhibits T4->T3 conversion."))
        story.append(A("Thyroid replacement: Levothyroxine (T4), liothyronine (T3)"))
    elif q == "Q8. What are oral contraceptive pills?":
        story.append(B("Combined OCP (estrogen + progestogen): Most effective. Inhibit GnRH pulsation -> suppress LH surge -> prevent ovulation; thicken cervical mucus; endometrial atrophy. Side effects: DVT/thromboembolism (most serious), nausea, headache, hypertension. Contraindicated in smokers >35 years, VTE history, migraine with aura, liver disease."))
        story.append(B("Mini-pill (Progestogen only): For breastfeeding women, those who cannot use estrogen."))
        story.append(B("Emergency contraception: Levonorgestrel (within 72h) or ulipristal acetate (within 120h)."))
    elif a_text:
        story.append(A(a_text))
    story.append(hr())

story.append(PageBreak())

# ═══════════════════════════════════════════════════════════════════════════════
# UNIT 7 & 8 - CHEMOTHERAPY
# ═══════════════════════════════════════════════════════════════════════════════
story.append(unit_header("UNIT 7 & 8 — CHEMOTHERAPY"))
story.append(Spacer(1, 0.2*cm))

u78 = [
    ("Q1. Bacteriostatic vs bactericidal drugs?",
     None),
    ("Q2. Classify penicillins with examples and uses.",
     None),
    ("Q3. Mechanism of penicillin and mechanism of resistance?",
     "Mechanism: Inhibit transpeptidase (PBPs) -> prevent cross-linking of peptidoglycan in bacterial cell wall -> cell lysis (bactericidal). Most effective against actively dividing bacteria. Resistance: Production of beta-lactamase (penicillinase) that hydrolyzes the beta-lactam ring; altered PBPs (MRSA); reduced permeability; efflux pumps."),
    ("Q4. Classify cephalosporins by generations.",
     None),
    ("Q5. Aminoglycosides — mechanism, uses, toxicity?",
     None),
    ("Q6. Fluoroquinolones — mechanism, uses, adverse effects?",
     None),
    ("Q7. Tetracyclines — mechanism, uses, adverse effects?",
     None),
    ("Q8. Macrolides — mechanism and uses?",
     None),
    ("Q9. Sulfonamides and trimethoprim? What is co-trimoxazole?",
     None),
    ("Q10. Mechanism of metronidazole? Uses?",
     None),
    ("Q11. Antitubercular drugs — first-line and second-line?",
     None),
    ("Q12. Classify antimalarials with mechanisms.",
     None),
    ("Q13. Classify antifungal drugs with mechanisms.",
     None),
    ("Q14. Antiretroviral (HIV) drugs — classify with examples.",
     None),
    ("Q15. Classify anticancer drugs with examples.",
     None),
]

for q, a_text in u78:
    story.append(Q(q))
    if q == "Q1. Bacteriostatic vs bactericidal drugs?":
        tdata = [
            ['Bacteriostatic', 'Bactericidal'],
            ['Inhibit bacterial growth', 'Kill bacteria'],
            ['Require intact host immunity', 'Can act without host immunity'],
            ['Antagonize bactericidal drugs', 'Preferred in meningitis, endocarditis, immunocompromised'],
            ['Tetracyclines, chloramphenicol, sulfonamides, erythromycin, clindamycin', 'Penicillins, cephalosporins, aminoglycosides, fluoroquinolones, metronidazole'],
        ]
        story.append(Spacer(1,4))
        story.append(table_generic(tdata, col_widths=[7.5*cm, 8*cm]))
        story.append(Spacer(1,4))
    elif q == "Q2. Classify penicillins with examples and uses.":
        story.append(B("Natural penicillins: Pen G (IV), Pen V (oral) — streptococcal infections, syphilis"))
        story.append(B("Anti-staphylococcal: Cloxacillin, flucloxacillin — beta-lactamase-resistant; MSSA"))
        story.append(B("Aminopenicillins: Ampicillin, amoxicillin — broader spectrum (gram+ve + H. influenzae, E. coli)"))
        story.append(B("Anti-Pseudomonal: Piperacillin, ticarcillin"))
        story.append(B("Beta-lactam + inhibitor combos: Amoxicillin-clavulanate (co-amoxiclav), Piperacillin-tazobactam"))
    elif q == "Q4. Classify cephalosporins by generations.":
        story.append(B("1st gen: Cephalexin, cefazolin — gram+ve coverage; surgical prophylaxis"))
        story.append(B("2nd gen: Cefuroxime, cefaclor — extended gram-ve (H. flu, Moraxella)"))
        story.append(B("3rd gen: Ceftriaxone, cefotaxime, cefixime — better gram-ve; meningitis, typhoid"))
        story.append(B("4th gen: Cefepime — antipseudomonal + gram+ve"))
        story.append(B("5th gen: Ceftaroline — active against MRSA"))
    elif q == "Q5. Aminoglycosides — mechanism, uses, toxicity?":
        story.append(A("Examples: Streptomycin, gentamicin, amikacin, tobramycin, neomycin."))
        story.append(A("Mechanism: Bind irreversibly to 30S ribosomal subunit -> misreading of mRNA -> non-functional proteins -> BACTERICIDAL."))
        story.append(A("Uses: gram-negative infections (including Pseudomonas), synergy with beta-lactams for endocarditis, TB (streptomycin)."))
        story.append(A("Toxicity: NEPHROTOXICITY (proximal tubular damage), OTOTOXICITY (sensorineural hearing loss and vestibular toxicity), neuromuscular blockade. Monitor trough levels. Contraindicated in pregnancy."))
    elif q == "Q6. Fluoroquinolones — mechanism, uses, adverse effects?":
        story.append(A("Examples: Ciprofloxacin, ofloxacin, levofloxacin, moxifloxacin, norfloxacin."))
        story.append(A("Mechanism: Inhibit bacterial DNA gyrase (topoisomerase II) and topoisomerase IV -> prevent DNA replication -> BACTERICIDAL."))
        story.append(A("Uses: UTI (norfloxacin, ciprofloxacin), respiratory infections (levofloxacin, moxifloxacin), typhoid, anthrax, atypical pneumonia."))
        story.append(A("Adverse effects: GI upset, CNS (seizure risk in epileptics), tendinopathy/tendon rupture (Achilles), QT prolongation, phototoxicity, cartilage damage (avoid in children and pregnancy)."))
    elif q == "Q7. Tetracyclines — mechanism, uses, adverse effects?":
        story.append(A("Examples: Tetracycline, doxycycline, minocycline."))
        story.append(A("Mechanism: Bind to 30S ribosomal subunit -> block attachment of aminoacyl-tRNA -> inhibit protein synthesis -> BACTERIOSTATIC."))
        story.append(A("Uses: Rickettsial infections (DOC), Chlamydia (DOC), Mycoplasma pneumonia, brucellosis, acne vulgaris, cholera, atypical pneumonia, malaria prophylaxis (doxycycline), Lyme disease."))
        story.append(A("Adverse effects: GI disturbance, photosensitivity, superinfection, teeth discoloration and enamel hypoplasia (CONTRAINDICATED in children <8 years and pregnancy), hepatotoxicity."))
    elif q == "Q8. Macrolides — mechanism and uses?":
        story.append(A("Examples: Erythromycin, azithromycin, clarithromycin."))
        story.append(A("Mechanism: Bind to 23S rRNA of 50S ribosomal subunit -> inhibit translocation (block elongation) -> BACTERIOSTATIC."))
        story.append(A("Uses: Alternative to penicillin in allergy, atypical pneumonia (Legionella, Mycoplasma, Chlamydia), H. pylori eradication (clarithromycin), whooping cough (azithromycin), community-acquired pneumonia."))
        story.append(A("Azithromycin advantage: long half-life (3-5 days), once-daily 5-day course. Adverse effects: GI upset, QT prolongation, hepatotoxicity."))
    elif q == "Q9. Sulfonamides and trimethoprim? What is co-trimoxazole?":
        story.append(A("Sulfonamides: Structural analogue of PABA; inhibit dihydropteroate synthase -> block folate synthesis."))
        story.append(A("Trimethoprim: Inhibits dihydrofolate reductase (bacterial) -> blocks tetrahydrofolate synthesis."))
        story.append(A("Sequential blockade of folate synthesis -> SYNERGISTIC effect."))
        story.append(A("Co-trimoxazole = Sulfamethoxazole + Trimethoprim (5:1 ratio). Uses: UTI, Pneumocystis jirovecii pneumonia (PCP) — DOC for prophylaxis and treatment, typhoid, community-acquired MRSA."))
    elif q == "Q10. Mechanism of metronidazole? Uses?":
        story.append(A("Mechanism: Nitroimidazole. Reduced by anaerobic organisms to reactive intermediates that damage DNA."))
        story.append(A("Uses: Anaerobic infections (Bacteroides), C. difficile infection (oral), H. pylori eradication, Trichomoniasis (DOC), Giardiasis (DOC), Amoebiasis (intestinal and hepatic), bacterial vaginosis."))
        story.append(A("Important: Disulfiram-like reaction with ALCOHOL — patient must avoid alcohol."))
    elif q == "Q11. Antitubercular drugs — first-line and second-line?":
        story.append(A("First-line drugs (HRZE + S):"))
        story.append(B("R — Rifampicin: Inhibits RNA polymerase; enzyme inducer; turns urine/secretions orange."))
        story.append(B("H — Isoniazid (INH): Inhibits mycolic acid synthesis; peripheral neuropathy prevented by pyridoxine (B6)."))
        story.append(B("Z — Pyrazinamide: Disrupts membrane potential; hepatotoxic; causes hyperuricemia."))
        story.append(B("E — Ethambutol: Inhibits arabinosyl transferase; optic neuritis — red-green colour vision loss."))
        story.append(B("S — Streptomycin: Aminoglycoside; given IM; ototoxic."))
        story.append(A("Second-line (MDR-TB): Fluoroquinolones (levofloxacin, moxifloxacin), bedaquiline, linezolid, kanamycin, capreomycin."))
        story.append(A("TB regimen: 2 months HRZE (intensive phase) + 4 months HR (continuation phase)."))
    elif q == "Q12. Classify antimalarials with mechanisms.":
        story.append(B("Chloroquine: DOC for P. vivax/ovale/malariae; inhibits heme polymerization. Adverse effects: retinal toxicity, pruritus."))
        story.append(B("Artemisinins (artesunate, artemether): DOC for P. falciparum (severe malaria); free radicals damage parasite."))
        story.append(B("ACT (Artemisinin Combination Therapy): Artemether + lumefantrine (Coartem) — WHO recommended for falciparum malaria."))
        story.append(B("Primaquine: Only drug active against liver stages (radical cure of P. vivax/ovale; kills gametocytes). Causes hemolysis in G6PD-deficient patients."))
        story.append(B("Quinine: For severe/complicated P. falciparum (IV); cinchonism (tinnitus, headache, visual disturbance)."))
        story.append(B("Doxycycline, proguanil: Chemoprophylaxis."))
    elif q == "Q13. Classify antifungal drugs with mechanisms.":
        story.append(B("Polyene macrolides (bind ergosterol directly): Amphotericin B (gold standard for systemic fungal infections; nephrotoxic), Nystatin (topical only)."))
        story.append(B("Azoles (inhibit ergosterol synthesis via CYP51): Imidazoles: clotrimazole, miconazole (topical); Triazoles: fluconazole (candidiasis, cryptococcal meningitis), voriconazole (aspergillosis)."))
        story.append(B("Echinocandins (inhibit beta-1,3-glucan synthase): Caspofungin, micafungin — invasive candidiasis, aspergillosis. Low side effects."))
        story.append(B("Griseofulvin: Inhibits microtubule; dermatophyte infections (onychomycosis)."))
        story.append(B("Terbinafine: Inhibits squalene epoxidase; dermatophytes."))
    elif q == "Q14. Antiretroviral (HIV) drugs — classify with examples.":
        story.append(B("NRTIs: Zidovudine (AZT), lamivudine (3TC), tenofovir, emtricitabine — chain termination of viral DNA synthesis."))
        story.append(B("NNRTIs: Nevirapine, efavirenz — bind RT allosterically."))
        story.append(B("PIs: Ritonavir, lopinavir, atazanavir — inhibit HIV protease; boosted with ritonavir."))
        story.append(B("INSTIs: Raltegravir, dolutegravir — preferred first-line (current guidelines)."))
        story.append(A("WHO preferred first-line regimen: TLD = Tenofovir + Lamivudine + Dolutegravir."))
    elif q == "Q15. Classify anticancer drugs with examples.":
        story.append(B("Alkylating agents: Cyclophosphamide, chlorambucil, busulfan — cross-link DNA; hemorrhagic cystitis (cyclophosphamide, prevent with mesna)."))
        story.append(B("Antimetabolites: Methotrexate (DHFR inhibitor), 5-fluorouracil (5-FU), cytarabine."))
        story.append(B("Vinca alkaloids: Vincristine, vinblastine — inhibit microtubule polymerization; peripheral neuropathy (vincristine)."))
        story.append(B("Taxanes: Paclitaxel, docetaxel — stabilize microtubules; prevent depolymerization."))
        story.append(B("Platinum compounds: Cisplatin, carboplatin — cross-link DNA; nephrotoxic, ototoxic, peripheral neuropathy."))
        story.append(B("Anthracyclines: Doxorubicin, daunorubicin — intercalate DNA; CARDIOMYOPATHY (dose-limiting)."))
        story.append(B("Monoclonal antibodies: Rituximab (anti-CD20), trastuzumab (anti-HER2, breast cancer), bevacizumab (anti-VEGF)."))
        story.append(B("Tyrosine kinase inhibitors: Imatinib (CML, BCR-ABL), erlotinib, gefitinib (EGFR)."))
        story.append(B("Hormonal agents: Tamoxifen (ER antagonist, breast cancer), anastrozole/letrozole (aromatase inhibitors), leuprolide (prostate cancer)."))
    elif a_text:
        story.append(A(a_text))
    story.append(hr())

story.append(PageBreak())

# ── KEY TIPS ──────────────────────────────────────────────────────────────────
story.append(unit_header("KEY TIPS FOR MGR UNIVERSITY VIVA"))
story.append(Spacer(1, 0.3*cm))
tips = [
    "Always know the MECHANISM + USES + ADVERSE EFFECTS for any drug asked.",
    "For antibiotics, know the SPECTRUM and RESISTANCE mechanisms.",
    "Be ready to write PRESCRIPTIONS for common conditions: peptic ulcer, hypertension, malaria, TB, diabetes.",
    "Know important DRUG INTERACTIONS: warfarin + NSAIDs; MAOIs + tyramine; rifampicin + OCP; sildenafil + nitrates.",
    "Know drug DOSES for emergency drugs: atropine, adrenaline (epinephrine), morphine, digoxin.",
    "Practical viva tests: PRESCRIPTION WRITING, SPOTTER identification, and DOSE CALCULATION.",
    "Remember antidotes: opioids (naloxone), BZDs (flumazenil), heparin (protamine), warfarin (vitamin K/FFP), atropine (physostigmine), organophosphates (atropine + pralidoxime), digoxin (Digibind).",
    "Drugs contraindicated in pregnancy: tetracyclines, aminoglycosides, fluoroquinolones, warfarin, ACE inhibitors, valproate.",
    "Know drugs that are enzyme INDUCERS (Rifampicin, Phenytoin, Carbamazepine, Phenobarbitone) vs INHIBITORS (Ketoconazole, Erythromycin, Ciprofloxacin, Cimetidine).",
]
for t in tips:
    story.append(tip(f"• {t}"))
    story.append(Spacer(1, 3))

story.append(Spacer(1, 1*cm))
story.append(Paragraph("Best of luck for your Viva! — Compiled by Orris AI", SUBTITLE_STYLE))

# BUILD
doc.build(story)
print("PDF generated successfully:", OUTPUT)
Running Command

cd /home/daytona/workspace/pharmacology-viva && python3 generate_pdf.py 2>&1

Running Command

ls -lh /home/daytona/workspace/pharmacology-viva/Pharmacology_Viva_QA_MGR_University.pdf

Your PDF is ready! Here's the download link:

Pharmacology Viva QA MGR University

PDF Document · PDF

What's included in the PDF:
  • A cover page with all unit names listed
  • All 8 units of the MGR University II MBBS Pharmacology syllabus
  • Questions in red bold and answers in clean body text
  • Bullet-point answers where applicable
  • Color-coded tables (for classifications like diuretics, insulin, antiarrhythmics, bacteriostatic vs bactericidal, etc.)
  • A final "Key Tips for MGR Viva" page with exam-focused reminders

Thank you so much!!

You're welcome! Good luck with your viva! 🎉
A few last-minute tips as you prepare:
  • Read the question carefully — examiners often ask "give an example" or "what is the antidote," so keep those handy.
  • Speak the mechanism first — examiners appreciate when you lead with mechanism before uses and side effects.
  • Know your mnemonics — SLUD (muscarinic effects), HRZE (TB drugs), RIPE, and the BECLOMETHASONE adverse effects list are great time-savers.
  • Practise prescription writing daily — it's a common practical viva component at MGR.
All the best for your exams! 💊📚

Can u please do the same for pathology and microbiology in separate pdfs

Searching the Web

MGR University II MBBS Pathology Microbiology syllabus units topics 2023

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