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What's Inside Each Set

🔴 SET 1 — Anti-Ulcer Drugs

🟠 SET 2 — Antiemetics

🟡 SET 3 — Antidiarrhoeals & Laxatives

🟢 SET 4 — Cough

🔵 SET 5 — Anti-Asthma

PHARMACOLOGY EXAM QUESTION BANK

Anti-Ulcers | Antiemetics | Anti-Diarrhoea/Constipation | Cough | Anti-Asthma

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🔴 PART A — MCQs (Multiple Choice Questions)

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SET 1 — ANTI-ULCER MCQs

• A) Omeprazole
• B) Esomeprazole
• C) Pantoprazole ✓
• D) Lansoprazole

Explanation: Pantoprazole has the least CYP2C19 inhibitory activity among PPIs, minimising interference with clopidogrel activation (which requires CYP2C19 for conversion to active metabolite). Omeprazole and esomeprazole are the strongest CYP2C19 inhibitors.

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• A) With the antacid simultaneously for synergistic effect
• B) At least 30 minutes before the antacid ✓
• C) Only at bedtime
• D) After meals only

Explanation: Sucralfate requires an acidic environment (pH <4) for polymerization into its protective gel. Antacids raise gastric pH and inactivate sucralfate. Space them at least 30 minutes apart.

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• A) Famotidine
• B) Omeprazole
• C) Cimetidine ✓
• D) Sucralfate

Explanation: Cimetidine uniquely blocks androgen receptors → anti-androgenic effects → gynaecomastia, impotence, decreased libido. No other H₂ blocker has this effect.

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• A) Magnesium hydroxide
• B) Calcium carbonate
• C) Aluminium hydroxide ✓ (in moderate doses) / actually all systemic absorbed ones
• D) Sodium bicarbonate ✓ (best answer in CKD context)

Exam-smart answer: D — Sodium bicarbonate. Causes systemic alkalosis and sodium load, harmful in CKD and hypertension. Aluminium can accumulate in severe CKD causing encephalopathy. NaHCO₃ also causes CO₂ gas and acid rebound.

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• A) They are direct-acting drugs that inhibit the pump immediately
• B) They work best when taken after a meal
• C) They are prodrugs activated in the acidic environment of parietal cell canaliculi ✓
• D) They competitively block H₂ receptors

Explanation: PPIs (omeprazole etc.) are benzimidazole prodrugs. They are acid-activated to form sulfenamide, which irreversibly binds cysteine residues of H⁺/K⁺-ATPase. Must be taken 30–60 min before meals so the pump is active.

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• A) Sucralfate
• B) Bismuth subcitrate
• C) Misoprostol ✓
• D) Omeprazole

Explanation: Misoprostol (PGE₁ analogue) has uterotonic properties causing cervical ripening and uterine contractions. It is a Category X in pregnancy for ulcer prophylaxis but used therapeutically for medical abortion (with mifepristone).

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• A) Stop the drug immediately and perform endoscopy
• B) Order stool occult blood test
• C) Reassure — this is a harmless side effect of bismuth ✓
• D) Start IV PPI therapy

Explanation: Bismuth compounds cause harmless blackening of stool (and tongue with liquids). This must be distinguished from melaena (digested blood). Melaena has a tarry consistency and offensive odour. Reassurance is correct if the patient is on bismuth.

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• A) PPI
• B) Bismuth
• C) Metronidazole
• D) Clarithromycin ✓

Explanation: Quadruple therapy = PPI + Bismuth + Tetracycline + Metronidazole. Clarithromycin is part of standard triple therapy (PPI + Clarithromycin + Amoxicillin), used when clarithromycin resistance is low.

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SET 2 — ANTIEMETIC MCQs

• A) Ondansetron
• B) Prochlorperazine
• C) Metoclopramide ✓
• D) Aprepitant

Explanation: Metoclopramide is the drug of choice for hyperemesis gravidarum AND vomiting associated with headache/migraine. Ondansetron is preferred for chemotherapy-induced vomiting. Prochlorperazine has higher EPS risk.

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• A) Ondansetron alone
• B) Metoclopramide + dexamethasone
• C) Ondansetron + Dexamethasone + Aprepitant ✓
• D) Promethazine + ondansetron

Explanation: Triple antiemetic therapy = 5-HT₃ antagonist (ondansetron) + corticosteroid (dexamethasone) + NK₁ antagonist (aprepitant). This covers both acute (ondansetron) and delayed (aprepitant) CINV phases.

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• A) Ondansetron
• B) Metoclopramide
• C) Hyoscine (Scopolamine) ✓
• D) Aprepitant

Explanation: Motion sickness is mediated via vestibular-cerebellar pathways using H₁ and muscarinic (M₁) receptors. Scopolamine (anticholinergic) and antihistamines (meclizine, promethazine) are effective. Ondansetron (5-HT₃) and metoclopramide (D₂) do NOT work for motion sickness.

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• A) Metoclopramide
• B) Prochlorperazine
• C) Domperidone ✓
• D) Haloperidol

Explanation: Domperidone is a peripheral D₂ antagonist that does NOT cross the blood–brain barrier. It controls nausea without worsening Parkinson's motor symptoms. All other D₂ antagonists (metoclopramide, prochlorperazine, haloperidol) cross the BBB and will block striatal dopamine → worsen parkinsonism.

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• A) Blocks D₂ receptors in the CTZ
• B) Blocks histamine H₁ receptors in the vestibular nucleus
• C) Blocks NK₁ receptors in the vomiting centre
• D) Blocks 5-HT₃ receptors on vagal afferents and in the CTZ ✓

Explanation: Chemotherapy damages gut enterochromaffin cells → release 5-HT → activates 5-HT₃ on vagal afferents → triggers vomiting. Ondansetron blocks this peripherally (gut) and centrally (CTZ).

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• A) It is a prodrug
• B) It has a half-life of ~40 hours and binds receptor differently ✓
• C) It blocks NK₁ receptors
• D) It stimulates 5-HT₄ receptors

Explanation: Palonosetron has t½ ≈ 40 hours (vs ondansetron 3–4 hrs), binds 5-HT₃ receptor with different allosteric properties, and is effective for both acute and delayed CINV, unlike earlier setrons.

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• A) Ondansetron
• B) Metoclopramide ✓
• C) Domperidone
• D) Hyoscine

Explanation: Acute dystonic reactions (including oculogyric crisis, torticollis, trismus) are EPS caused by D₂ blockade in the nigrostriatal pathway. Metoclopramide crosses the BBB and causes this. Treatment: IV/IM diphenhydramine or benztropine.

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SET 3 — ANTIDIARRHOEAL/LAXATIVE MCQs

• A) Loperamide
• B) Bismuth subsalicylate
• C) Diphenoxylate ✓
• D) Codeine

Explanation: Diphenoxylate can cross the BBB at high doses → euphoria/abuse. Atropine (subtherapeutic dose) causes unpleasant anticholinergic effects if high doses are taken recreationally, acting as a deterrent. This combination = Lomotil.

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• A) Oral vancomycin
• B) Loperamide ✓
• C) Cholestyramine
• D) Probiotics

Explanation: Loperamide reduces gut motility → prolongs retention of C. difficile toxins → risk of toxic megacolon. Contraindicated in infectious/inflammatory diarrhoea. Treat the underlying cause with metronidazole/oral vancomycin.

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• A) Lubricates the colon
• B) Directly kills gut bacteria
• C) Acidifies colon → converts NH₃ to NH₄⁺ → traps and eliminates ammonium ✓
• D) Stimulates gut motility via 5-HT₄ receptors

Explanation: Lactulose is fermented by colonic bacteria → lactic/acetic acid → ↓ colonic pH → NH₃ + H⁺ → NH₄⁺ (ionised, non-absorbable) → excreted in stool. Also osmotic laxative effect → rapid bowel evacuation of ammonia.

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• A) Lactulose
• B) Psyllium
• C) PEG (polyethylene glycol)
• D) Senna ✓

Explanation: Senna (and other anthraquinone glycosides like cascara) cause brown-black pigmentation of colonic mucosa (melanosis coli) due to apoptosis of colonic epithelial cells and subsequent phagocytosis by macrophages. Benign but indicates chronic stimulant laxative overuse.

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• A) IBS-C in men; hepatotoxicity
• B) IBS-D in children; constipation
• C) IBS-D in women; ischaemic colitis ✓
• D) CINV; QTc prolongation

Explanation: Alosetron (5-HT₃ antagonist) slows colonic transit, specifically approved for women with severe IBS-D failing conventional therapy. Ischaemic colitis (Black Box Warning) and severe constipation led to initial withdrawal and now a REMS programme.

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• A) Bisacodyl
• B) Psyllium
• C) Methylnaltrexone (Relistor) ✓
• D) Lubiprostone (also correct but less specific)

Best answer: Methylnaltrexone — peripheral μ-opioid receptor antagonist that does NOT cross BBB → reverses opioid-induced constipation without affecting analgesia. Lubiprostone also approved for opioid-induced constipation.

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• A) Blocking 5-HT₃ receptors in the colon
• B) Lubricating stool with mineral oil
• C) Inhibiting Na⁺/K⁺-ATPase in colonocytes
• D) Activating guanylate cyclase-C → ↑ cGMP → ↑ CFTR Cl⁻ secretion ✓

Explanation: Linaclotide is a GC-C (guanylate cyclase-C) agonist. ↑ cGMP activates CFTR → ↑ Cl⁻ and HCO₃⁻ secretion → ↑ intestinal fluid → softer stool + faster transit. cGMP also acts on pain-sensing afferents → ↓ visceral pain in IBS-C.

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SET 4 — COUGH MCQs

• A) Prescribe codeine syrup
• B) Prescribe dextromethorphan syrup
• C) Prescribe promethazine + codeine combination syrup
• D) Advise against OTC antitussives; recommend honey and fluids ✓

Explanation: OTC antitussives are NOT recommended in children <4 years (FDA 2007 guidance; most guidelines extend caution to <12 years). Codeine is contraindicated <12 yrs. Honey (≥1 yr) has evidence for cough suppression. Safety first.

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• A) Enhanced antitussive effect
• B) Serotonin syndrome ✓
• C) QTc prolongation
• D) Respiratory depression

Explanation: Dextromethorphan weakly inhibits serotonin reuptake. Combined with MAOIs (which prevent serotonin degradation) → serotonin accumulation → serotonin syndrome (hyperthermia, agitation, clonus, autonomic instability). Strict contraindication.

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• A) Inhibiting phosphodiesterase
• B) Activating mucociliary transport
• C) Breaking disulphide bonds in mucus glycoproteins ✓
• D) Blocking M₃ receptors in bronchial glands

Explanation: NAC's free thiol (-SH) group reduces disulphide bonds (-S-S-) holding mucus gel together → depolymerises mucus → ↓ viscosity → easier expectoration.

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• A) Severe diarrhoea
• B) Bronchospasm only
• C) Oropharyngeal anaesthesia → choking + potential cardiovascular collapse ✓
• D) Acute dystonic reaction

Explanation: Benzonatate is a local anaesthetic (related to tetracaine). If chewed, it causes oropharyngeal anaesthesia → loss of gag reflex, choking, aspiration, as well as CNS toxicity (seizures) and cardiovascular collapse. Capsules must be swallowed whole.

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• A) Carbocisteine
• B) Erdosteine
• C) Acetylcysteine
• D) Ambroxol ✓

Explanation: Ambroxol is the active metabolite of bromhexine; it depolymerises mucus AND stimulates type II pneumocytes to produce surfactant. This additional property makes it useful in premature neonates and post-surgical respiratory care.

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SET 5 — ANTI-ASTHMA MCQs

• A) Good asthma control
• B) Salbutamol tolerance requiring dose increase
• C) Poor asthma control requiring step-up in controller therapy ✓
• D) Need to switch to ipratropium

Explanation: According to GINA guidelines, SABA use >2 days/week (excluding pre-exercise use) indicates inadequate asthma control. Step up — add or increase ICS. Overuse of SABA (>3 canisters/year) is associated with ↑ mortality.

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• A) It can be used as a rescue inhaler due to its potency
• B) Its onset is rapid (3–5 min) making it ideal for acute attacks
• C) It can be used as monotherapy in asthma
• D) It has a slow onset (20–30 min) and should never be used without ICS in asthma ✓

Explanation: Salmeterol has partial agonist activity with slow onset — NOT suitable for acute bronchospasm. FDA black box warning: LABAs must NOT be used as monotherapy in asthma (associated with increased asthma deaths in the SMART trial). Always combine with ICS.

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• A) Rifampicin
• B) Omeprazole
• C) Ciprofloxacin ✓
• D) Salbutamol

Explanation: Ciprofloxacin inhibits CYP1A2 → ↓ theophylline metabolism → toxic plasma levels. Therapeutic range is 10–20 mg/L. At 35 mg/L, seizures and arrhythmias occur. Other inhibitors: erythromycin, cimetidine, fluvoxamine. Rifampicin DECREASES levels.

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• A) Omalizumab
• B) Montelukast ✓
• C) Salmeterol
• D) Cromoglicate

Explanation: Aspirin/NSAID-exacerbated respiratory disease (AERD) — COX inhibition shunts arachidonic acid toward the 5-LOX pathway → excess LTC₄/LTD₄ → bronchoconstriction. Montelukast (CysLT₁ antagonist) directly blocks this pathway. Drug of choice in AERD.

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• A) Omalizumab
• B) Mepolizumab
• C) Benralizumab
• D) Tezepelumab ✓

Explanation: Tezepelumab blocks TSLP (thymic stromal lymphopoietin) — the most upstream cytokine in airway inflammation, present across all asthma endotypes (eosinophilic, allergic, and non-eosinophilic). Others target specific downstream pathways (IgE, IL-5) and require specific biomarker criteria.

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• A) Bronchodilation via β₂ receptor activation
• B) Inhibition of phosphodiesterase
• C) Inhibition of mast cell degranulation → prevention of mediator release ✓
• D) 5-HT₃ receptor blockade in bronchi

Explanation: Cromoglicate is a mast cell stabiliser. Taken prophylactically 15–20 min before exercise, it prevents mast cell degranulation triggered by osmotic changes in airway surface fluid during exercise. It is purely preventive with NO bronchodilator activity.

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• A) Blocking β₂ receptors
• B) Inhibiting phosphodiesterase
• C) Antagonising calcium → relaxing bronchial smooth muscle ✓
• D) Blocking leukotriene receptors

Explanation: Mg²⁺ competes with Ca²⁺ in smooth muscle contraction. Ca²⁺ is required for smooth muscle contraction via calmodulin–myosin light chain kinase pathway. By blocking Ca²⁺ entry, Mg²⁺ causes bronchodilation. Dose: 1.2–2 g IV over 20 min.

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• A) Formoterol has slower onset
• B) Formoterol has shorter duration
• C) Formoterol should not be used as a reliever
• D) Formoterol has fast onset (3–5 min) and can be used as both reliever and maintenance (MART strategy) ✓

Explanation: Formoterol is a full agonist at β₂ receptors with fast onset (unlike salmeterol which is a partial agonist with slow onset). This allows its use in the MART (Maintenance And Reliever Therapy) strategy with budesonide/formoterol.

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🟠 PART B — SAQs (Short Answer Questions)

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SAQ 1

Model Answer:

• PPIs (e.g., omeprazole, lansoprazole) are prodrugs — inactive at neutral pH
• In the acidic secretory canaliculi of parietal cells, they are protonated → converted to active sulfenamide
• Sulfenamide irreversibly (covalent) binds to cysteine residues on the H⁺/K⁺-ATPase (proton pump)
• This blocks the final step of acid secretion regardless of stimulus (histamine, gastrin, ACh)
• Effect lasts 24–36 hrs despite short plasma t½ (1–2 hrs) — new pump synthesis needed for recovery
• Maximal suppression achieved after 3–4 days of daily dosing
• Must be taken 30–60 min before meals (pumps must be active/stimulated for drug to work)

⭐ Exam point: PPIs do NOT directly block receptors — they block the pump itself. Pantoprazole is preferred with clopidogrel (least CYP2C19 inhibition).

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SAQ 2

Model Answer:

• Central: Blocks D₂ receptors in the CTZ → antiemetic
• Peripheral: Blocks D₂ in gut + activates 5-HT₄ → ↑ ACh release from myenteric plexus → ↑ LOS tone + ↑ gastric emptying + ↑ intestinal peristalsis = prokinetic

1. Nausea/vomiting (post-op, drug-induced, mild CINV)
2. Hyperemesis gravidarum (drug of choice)
3. Headache/migraine-associated vomiting (drug of choice)
4. Gastroparesis (diabetic + post-surgical)
5. GERD (augments LOS tone)

• EPS: Acute dystonia, akathisia, tardive dyskinesia (long-term) — D₂ blockade in nigrostriatal pathway
• Hyperprolactinaemia → galactorrhoea, menstrual irregularities, gynaecomastia (D₂ blockade in tuberoinfundibular pathway)
• Sedation, fatigue
• Restlessness

⭐ Exam point: Pretreat with diphenhydramine/benztropine to reduce EPS. Domperidone is preferred in Parkinson's as it doesn't cross BBB.

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SAQ 3

Model Answer:

• Lactulose = dual use: laxative + hepatic encephalopathy (↓ ammonia absorption)
• Bisacodyl suppository: onset 15–60 min (vs oral 6–12 hrs)
• Senna long-term → melanosis coli (anthraquinone pigment)
• Linaclotide contraindicated in children <6 yrs (dehydration risk)

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SAQ 4

Model Answer:

1. Inhibits phosphodiesterase (PDE) → ↑ cAMP → bronchodilation + ↓ mast cell degranulation
2. Adenosine receptor antagonism → bronchodilation + CNS stimulation (explains CNS toxicity)
3. At low doses: Activates HDAC-2 → ↑ corticosteroid sensitivity (anti-inflammatory; useful in steroid-resistant asthma)
4. ↑ Diaphragm contractility → useful in COPD and respiratory failure

• Narrow therapeutic index: Target = 10–20 mg/L
• Metabolised by CYP1A2 and CYP3A4
• Half-life varies: 3–5 hrs in healthy adults; up to 24 hrs in liver disease/heart failure
• Smoking ↓ t½ (CYP1A2 induction); stopping smoking → levels rise → toxicity risk
• Aminophylline = theophylline + ethylenediamine (IV use; 80% theophylline content)

• ↑ Levels: Erythromycin, Ciprofloxacin, Cimetidine, Allopurinol, Oral contraceptives
• ↓ Levels: Rifampicin, Phenytoin, Carbamazepine, Smoking, Phenobarbitone

• 10–20: Nausea, vomiting, headache, insomnia
• 20–30: Tachycardia, arrhythmias, tremor

• 30: Seizures, life-threatening arrhythmias (may occur without warning nausea)

⭐ Exam point: Seizures from theophylline toxicity may occur WITHOUT prior nausea/vomiting — monitor levels carefully, especially when CYP inhibitors are added.

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SAQ 5

Model Answer:

1. Salbutamol (nebulised/IV) — β₂ agonist → ↑ cAMP → bronchodilation. Continuous or back-to-back nebulisation. Also used IV in life-threatening asthma.
2. Ipratropium bromide (nebulised) — Muscarinic M₃ antagonist → ↓ bronchoconstriction. Synergistic with salbutamol. Add in moderate-severe attack.
3. Systemic corticosteroids — IV hydrocortisone (100 mg qds) or oral prednisolone (40–50 mg). Onset delayed 4–6 hrs (gene transcription). Suppress airway inflammation, restore β₂ receptor responsiveness.
4. Oxygen — Target SpO₂ 94–98%. Hypoxaemia is the main cause of death.

1. IV Magnesium sulphate (1.2–2 g over 20 min) — Antagonises Ca²⁺ in bronchial smooth muscle → relaxation. Safe, effective add-on.
2. IV Aminophylline — PDE inhibitor → ↑ cAMP bronchodilation. Narrow TI; monitor levels. Rarely used now.

⭐ Key: Antibiotics NOT routinely given (most acute asthma is viral/inflammatory not bacterial). MgSO₄ is now standard in severe attacks.

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🔵 PART C — LAQs (Long Answer Questions)

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LAQ 1

Model Answer:

I. Classification of Anti-Ulcer Drugs (2 marks)

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II. Proton Pump Inhibitors (PPIs) (8 marks)

• Oral bioavailability ~65% (first pass hepatic metabolism)
• Absorbed in small intestine (enteric-coated to prevent degradation in stomach)
• Plasma t½ = 1–2 hours
• Duration of action = 24–36 hours (irreversible binding)
• Extensively protein bound (>95%)
• Hepatic metabolism via CYP2C19 and CYP3A4
• Accumulate in acidic parietal cell canaliculi (trapped by protonation)

• PPI (prodrug) → enters blood → accumulates in parietal cell secretory canaliculi → protonated (activated) in acid → forms sulfenamide (active form)
• Sulfenamide: covalent bond with Cys813 and Cys892 of H⁺/K⁺-ATPase α subunit
• Irreversibly blocks the pump → complete cessation of acid secretion from that cell
• Only affects actively secreting pumps → maximum effect with meal-stimulated pumps
• Recovery requires synthesis of new pump protein (18–24 hrs)
• Full effect after 3–4 days of daily dosing

• Peptic ulcer disease (gastric + duodenal)
• GERD / erosive oesophagitis
• Zollinger-Ellison syndrome (high doses; e.g., omeprazole 60–120 mg/day)
• NSAID-induced ulcer prevention
• H. pylori eradication (as part of combination therapy)
• Upper GI bleeding (IV omeprazole 80 mg bolus + 8 mg/hr for 72 hrs post-endoscopy)
• Stress ulcer prophylaxis (ICU patients)

• Clopidogrel: Omeprazole/esomeprazole inhibit CYP2C19 → ↓ clopidogrel activation → ↓ antiplatelet effect → use pantoprazole instead
• ↑ Diazepam, warfarin, phenytoin levels (CYP2C19 inhibition)
• ↓ Absorption of: ketoconazole, itraconazole, iron, ampicillin esters (require acid)

• Short-term: headache, diarrhoea, nausea, abdominal pain
• Long-term:
  • Hypomagnesaemia (impairs Mg²⁺ absorption) → tetany, arrhythmias
  • Hypocalcaemia → osteoporosis, fractures (↓ Ca²⁺ absorption)
  • Vitamin B₁₂ deficiency (requires acid for release from food proteins)
  • C. difficile colitis (↑ risk — loss of acid barrier)
  • Community-acquired pneumonia (↑ risk)
  • Acute interstitial nephritis (rare, idiosyncratic)
  • Fundic gland polyps (benign, regress on stopping)

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III. H. pylori Eradication (2 marks)

PPI (bid) + Clarithromycin (500 mg bid) + Amoxicillin (1 g bid)

PPI (bid) + Bismuth + Tetracycline + Metronidazole (all qid)

• Pre-treatment: Urea breath test or stool antigen test (most sensitive non-invasive)
• Post-treatment: Urea breath test (wait ≥4 weeks after stopping PPI to avoid false negatives)

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LAQ 2

Model Answer:

I. Classification of Bronchodilators (2 marks)

• Short-acting (SABAs): Salbutamol, Terbutaline
• Long-acting (LABAs): Salmeterol, Formoterol, Indacaterol

• Short-acting (SAMAs): Ipratropium bromide
• Long-acting (LAMAs): Tiotropium, Aclidinium

• ICS: Beclomethasone, Budesonide, Fluticasone
• Leukotriene antagonists: Montelukast, Zafirlukast
• Biologics: Omalizumab, Mepolizumab, Tezepelumab

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II. Pharmacology of β₂-Agonists (5 marks)

• Bind β₂ receptors (Gs-coupled) → activate adenylyl cyclase → ↑ cAMP → activates PKA
• PKA phosphorylates myosin light chain kinase (MLCK) → inactivation → smooth muscle relaxation → bronchodilation
• Additionally: inhibit mast cell mediator release, ↑ mucociliary clearance

• Onset: 3–5 min inhaled; Duration: 4–6 hrs
• Rescue reliever — use for breakthrough symptoms
• ADRs: Tremor, tachycardia, hypokalaemia (K⁺ shift into cells), hyperglycaemia
• Tachyphylaxis with overuse (receptor downregulation)

• LABAs must ALWAYS be combined with ICS in asthma (FDA black box warning — SMART trial: LABA monotherapy → ↑ asthma deaths)
• In COPD: LABAs can be used without ICS (first-line)
• Salbutamol drives K⁺ into cells → used for emergency hyperkalaemia management

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III. Inhaled Corticosteroids (ICS) (4 marks)

1. Bind intracellular glucocorticoid receptors (GR) → GR-drug complex → translocates to nucleus
2. Trans-repression: ↓ NF-κB and AP-1 activity → ↓ transcription of IL-4, IL-5, IL-13, TNF-α, eotaxin
3. Trans-activation: ↑ Lipocortin-1 synthesis → ↓ phospholipase A₂ → ↓ prostaglandins, leukotrienes
4. ↓ Mucosal oedema, ↓ eosinophil recruitment, ↓ goblet cell hyperplasia
5. ↑ β₂ receptor synthesis → restore/maintain bronchodilator responsiveness

• Most effective long-term controller in asthma
• Reduce exacerbations, hospitalisations, and asthma mortality
• NOT bronchodilators — DO NOT relieve acute bronchospasm

• Local: Oropharyngeal candidiasis (Candida albicans), dysphonia (hoarseness) — use spacer, rinse mouth
• Systemic (high dose/long-term): HPA suppression, growth retardation in children, osteoporosis, cataracts, glaucoma, easy bruising

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IV. Stepwise Asthma Management (GINA 2023) (4 marks)

• SABA-only treatment at Step 1 no longer preferred (increased mortality risk)
• ICS-formoterol as reliever across all steps (MART = Maintenance And Reliever Therapy)

• Anti-IgE (Omalizumab): allergic asthma, high IgE
• Anti-IL-5 (Mepolizumab, Benralizumab): eosinophilic asthma (eos ≥150–300)
• Anti-IL-4Rα (Dupilumab): type 2 asthma
• Anti-TSLP (Tezepelumab): any severe uncontrolled asthma

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LAQ 3

Model Answer:

I. Physiological Basis of Vomiting (1 mark)

• CTZ (chemoreceptor trigger zone) — Area postrema, outside BBB; senses drugs, toxins, metabolic changes (D₂, 5-HT₃, NK₁ receptors)
• Vestibular apparatus — motion sickness (H₁, M₁ receptors)
• Vagal afferents from gut — 5-HT₃ receptors
• Higher cortical centres (anticipatory nausea)

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II. Classification with Mechanisms (6 marks)

• Metoclopramide: D₂ block (CTZ) + 5-HT₄ agonism (gut) → antiemetic + prokinetic
• Domperidone: Peripheral D₂ only (doesn't cross BBB) → no EPS; safe in Parkinson's
• Prochlorperazine: Phenothiazine; D₂ block; used in vertigo/labyrinthitis

• Ondansetron, Granisetron, Palonosetron
• Block 5-HT₃ on vagal afferents and CTZ
• Most effective for CINV; no effect on motion sickness

• Aprepitant, Fosaprepitant
• Block substance P/NK₁ in vomiting centre
• Specifically effective for delayed CINV

• Promethazine, Meclizine, Cyclizine, Diphenhydramine
• Block H₁ in vestibular nucleus + vomiting centre; also anticholinergic
• Best for motion sickness; sedating

• Hyoscine (Scopolamine): M₁ block; most effective for motion sickness; transdermal patch

• Dexamethasone: Mechanism unclear (↓ prostaglandins, ↓ 5-HT release); adjunct in CINV

• Dronabinol, Nabilone: CB₁ receptor agonists; refractory CINV

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III. Drug of Choice by Scenario (3 marks)

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IV. Key Adverse Effects (2 marks)

⭐ Exam emphasis: Know the five receptor types at the CTZ/vomiting centre, which drug blocks which receptor, and match the drug to the clinical context. The Parkinson's-domperidone link and hyperemesis-metoclopramide link are high-yield.

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📋 QUICK MCQ REVISION GRID

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