GIT- PHARMACOLOGY

✅ Tetracyclines
Aluminum hydroxide, an antacid, can chelate tetracyclines in the gastrointestinal tract. This forms insoluble complexes, significantly impairing their absorption and reducing antibiotic effectiveness. That’s why tetracyclines should not be taken with antacids or dairy products containing calcium/magnesium.

Incorrect Options

❌ Cefoperazone
Absorption is not significantly affected by antacids.

❌ Erythromycin
Its absorption may be affected by gastric pH but not specifically by aluminum hydroxide chelation.

❌ Chloramphenicol
Absorption is not notably impaired by aluminum hydroxide.

❌ Penicillin
Penicillin absorption is also not significantly affected by aluminum hydroxide.

✅ Sodium bicarbonate
Sodium bicarbonate is a systemic antacid. When ingested, it neutralizes gastric acid but can also be absorbed into the bloodstream, leading to metabolic alkalosis. Chronic use may cause the so-called “milk-alkali syndrome” when taken with calcium supplements, resulting in alkalosis, hypercalcemia, and renal impairment.

Incorrect Options

❌ Magnesium hydroxide
A non-systemic antacid that is poorly absorbed. Its main side effect is diarrhea, not alkalosis.

❌ Aluminium hydroxide
Another non-systemic antacid, not absorbed significantly, but it may cause constipation and hypophosphatemia, not alkalosis.

❌ Calcium carbonate
This can rarely contribute to milk-alkali syndrome if taken excessively, but it is not the classic systemic antacid linked to metabolic alkalosis like sodium bicarbonate.

❌ None of them
Incorrect, since sodium bicarbonate clearly causes systemic alkalosis.

Step 1: Mechanism of antacids

• Antacids neutralize gastric acid in the stomach.

• Some are poorly absorbed (like aluminium hydroxide, magnesium hydroxide) → act locally, minimal systemic effects.

• Others can be absorbed (like sodium bicarbonate) → can alter systemic pH.

Step 2: Why sodium bicarbonate causes alkalosis

• Sodium bicarbonate reacts with HCl

• Excess bicarbonate can be absorbed into the blood.

• This leads to increased blood bicarbonate → metabolic alkalosis.

• Also produces CO₂ → gastric distension, belching.

Step 3: Why the others are wrong

• Aluminium hydroxide ❌ → Causes constipation, phosphate depletion; not systemic alkalosis.

• Calcium carbonate ❌ → Can cause the “milk-alkali syndrome” with hypercalcemia and alkalosis, but sodium bicarbonate is the classic answer for direct systemic alkalosis.

• Magnesium hydroxide ❌ → Causes diarrhea, acts locally; not systemic alkalosis.

• None of them ❌ → Wrong, because sodium bicarbonate clearly does.

Quick Clinical Pearl

👉 Sodium bicarbonate = “systemic alkalosis + belching”
👉 Magnesium hydroxide = diarrhea
👉 Aluminium hydroxide = constipation
👉 Calcium carbonate = hypercalcemia, milk-alkali syndrome

Correct Answer: Antacids neutralize gastric acid, temporarily raising the pH and reducing mucosal irritation ✅

Why this is correct:

• Antacids are weak bases (e.g., magnesium hydroxide, aluminum hydroxide, calcium carbonate).

• They act directly in the stomach lumen to neutralize gastric acid, raising pH.

• This reduces the acidity of refluxed gastric contents → less esophageal irritation → temporary symptom relief in GERD/Barrett esophagus.

Why the Others Are Incorrect

• Decrease gastric acid secretion by inhibiting proton pumps ❌ – That’s the mechanism of PPIs (e.g., omeprazole, esomeprazole), not antacids.

• Stimulate mucous production ❌ – Cytoprotective drugs like misoprostol or sucralfate do this, not antacids.

• Block histamine receptors ❌ – Mechanism of H₂ blockers (ranitidine, famotidine), not antacids.

• Enhance gastric emptying ❌ – Prokinetics (metoclopramide, domperidone) do this, not antacids.

Correct Answer: Hyoscine ✅

• Hyoscine (Scopolamine) is the classic prophylactic drug for motion sickness.

• It is a muscarinic receptor antagonist that blocks cholinergic transmission from the vestibular system to the vomiting center.

• Best used before travel to prevent symptoms.

Why the Others Are Incorrect

• Aprepitant ❌ – NK₁ receptor antagonist, used for chemotherapy-induced nausea, not motion sickness.

• Cyclizine ❌ – An H₁ antihistamine that can treat motion sickness, but not as effective prophylactically as hyoscine.

• Diphenhydramine ❌ – H₁ antihistamine with antiemetic action, can help motion sickness, but again hyoscine is the standard prophylaxis.

• Properidol ❌ – Likely meant droperidol, a D₂ antagonist, used for postoperative nausea, not motion sickness.

Correct Answer: Esomeprazole ✅

• Esomeprazole is a proton pump inhibitor (PPI).

• It irreversibly inhibits the H⁺/K⁺ ATPase in gastric parietal cells → markedly reduces gastric acid secretion.

• It’s the most effective therapy for severe, persistent GERD symptoms like heartburn and acid regurgitation.

Why the Others Are Incorrect

• An antacid ❌ – Provides only short-term symptomatic relief; doesn’t prevent acid secretion.

• Dicyclomine ❌ – Anticholinergic, used for irritable bowel syndrome (IBS) spasms, not GERD.

• Granisetron ❌ – 5-HT₃ antagonist, antiemetic (esp. chemotherapy-induced nausea), not for acid suppression.

• Loperamide ❌ – Antidiarrheal opioid agonist; no effect on acid secretion.

Correct Answer: Magnesium hydroxide ✅

• Magnesium hydroxide is a saline osmotic laxative.

• It works by drawing water into the intestinal lumen → increases stool liquidity and promotes bowel movement.

• Very effective for drug-induced constipation, such as from verapamil (a calcium channel blocker).

Why the Others Are Incorrect

• Aluminum hydroxide ❌ – An antacid; actually causes constipation as a side effect.

• Diphenoxylate ❌ – Antidiarrheal (opioid agonist); would worsen constipation.

• Metoclopramide ❌ – Prokinetic (D₂ antagonist); improves gastric emptying but not an osmotic laxative.

• Ranitidine ❌ – H₂ receptor blocker; reduces gastric acid secretion, no effect on constipation.

Correct Answer: Metoclopramide ✅

• Metoclopramide is a prokinetic drug.

• Mechanism:

  • D₂ receptor antagonist → removes inhibitory dopaminergic effect on GI motility.

  • Enhances ACh release in the GI tract.

  • Increases gastric emptying and lower esophageal sphincter tone.

• Clinically used to prevent aspiration risk before anesthesia (esp. in emergency surgery).

Why the Others Are Incorrect

• Apomorphine ❌ – Dopamine agonist; induces vomiting (emetic), not gastric emptying.

• Hyoscine ❌ – Anticholinergic; decreases motility, used for motion sickness.

• Methylpolysiloxane ❌ – Antifoaming agent used in bloating/flatulence; no effect on gastric emptying.

• Promethazine ❌ – Antihistamine (H₁ blocker) with antiemetic properties; no prokinetic action.

Correct Answer: H⁺, K⁺, ATPase ✅

• Omeprazole is a proton pump inhibitor (PPI).

• It irreversibly inhibits the H⁺/K⁺-ATPase pump in gastric parietal cells → prevents final step of acid secretion.

• This markedly reduces gastric acid, promoting ulcer healing and relief of GERD symptoms.

Why the Others Are Incorrect

• Prostaglandins ❌ – Misoprostol (a prostaglandin analog) acts here, not omeprazole.

• Gastric secretion ❌ – Too general; PPIs specifically block acid secretion at the final step, not all gastric secretions.

• Pepsin secretion ❌ – Reduced indirectly (since pepsinogen activation requires acid), but not the direct target.

• Cholinergic action ❌ – Blocked by atropine (antimuscarinics), not PPIs.

• Antacids are basic compounds (e.g., aluminum hydroxide, magnesium hydroxide) that neutralize excess gastric acid in the stomach.

• They provide rapid symptomatic relief from heartburn, dyspepsia, or gastric irritation.

• The effect is short-term, as they do not heal ulcers or prevent acid secretion.

Incorrect Options:

• Aspirin ❌ – Can irritate the gastric mucosa and worsen symptoms.

• Milk ❌ – May temporarily buffer acid but stimulates gastric acid secretion, so relief is not reliable.

• Alcohol ❌ – Irritates the gastric mucosa and can increase acid production.

• Lemon juice ❌ – Acidic; worsens gastric irritation rather than relieving it.

• Ondansetron is a 5-HT3 (serotonin) receptor antagonist.

• It is widely used as a prophylactic antiemetic in post-operative nausea and vomiting (PONV) and in chemotherapy-induced nausea.

• Its mechanism involves blocking serotonin receptors in the chemoreceptor trigger zone (CTZ) and the gastrointestinal tract, reducing signals that trigger vomiting.

Incorrect Options:

• Metoclopramide ❌ – Dopamine antagonist; used for gastroparesis or general nausea, but less preferred in PONV due to extrapyramidal side effects.

• Bismuth subsalicylate ❌ – Used for diarrhea and mild gastrointestinal upset, not PONV.

• Dexamethasone ❌ – Can be used adjunctively for PONV, but not the primary antiemetic.

• Loperamide ❌ – Antidiarrheal; does not prevent nausea or vomiting

Antacids are substances that neutralize gastric acid, used for dyspepsia, gastritis, and peptic ulcer. Their effects and side effects depend on the ions they contain:

• Aluminium hydroxide:

  • Neutralizes acid, constipating effect, not diarrhea.

  • Rarely can lead to hypophosphatemia if used long-term.

• Magnesium salts (e.g., magnesium hydroxide):

  • Neutralize acid

  • Osmotic effect in the gut → may cause diarrhea ✅

• Sodium bicarbonate:

  • Rapidly neutralizes acid, but not preferred for chronic peptic ulcer due to risk of systemic alkalosis and sodium overload.

• Carbonate-containing antacids (like sodium bicarbonate):

  • Release CO₂, but not all antacids liberate carbon dioxide.

Option breakdown:

• Aluminium hydroxide gel causes systemic alkalosis – Incorrect: Minimal systemic absorption; usually causes constipation, not alkalosis.

• Aluminium hydroxide may cause diarrhea – Incorrect: It tends to cause constipation.

• Magnesium containing salt may cause diarrhea – Correct: Osmotic effect draws water into gut → diarrhea.

• Liberation of carbon dioxide is done by all antacids – Incorrect: Only carbonate/bicarbonate-containing antacids release CO₂.

• Sodium bicarbonate is useful in peptic ulcer – Incorrect: Rapid neutralization, but not suitable for chronic therapy due to systemic effects.

Key point:
Magnesium-based antacids are commonly associated with diarrhea, whereas aluminium-based ones tend to constipate, and combinations are often used to balance effects.

In barbiturate poisoning, an NG (nasogastric) tube can be used to administer activated charcoal, which binds to the barbiturates in the gastrointestinal tract and prevents further absorption. This is a standard initial management step in many cases of drug overdose, especially if the patient presents early.

Option breakdown:

• Decompression of gastrointestinal tract – Incorrect: NG tubes can be used for decompression in bowel obstruction or ileus, but here the goal is to neutralize the ingested poison.

• Prevention of aspiration – Incorrect: NG intubation does not directly prevent aspiration; airway protection would require endotracheal intubation.

• Administration of oral feeding – Incorrect: Not indicated in an emergency setting, especially during poisoning.

• Upper gastrointestinal hemorrhage – Incorrect: NG tubes may be used for lavage in GI bleeding, but this is not the purpose here.

• Administration of charcoal as antidote – Correct: Activated charcoal binds barbiturates and reduces systemic absorption, helping to manage poisoning.

Peptic ulcers form when there is an imbalance between gastric acid secretion and the protective mechanisms of the stomach lining. One of the major stimulators of gastric acid secretion is histamine acting on H₂ receptors present on parietal cells.

• H₂ receptor antagonists (like Famotidine, Ranitidine, Nizatidine, Cimetidine) block histamine binding on parietal cells.

• This reduces cAMP levels inside the parietal cells, leading to reduced activity of the H⁺/K⁺ ATPase proton pump, and thus decreased gastric acid secretion.

• This directly helps in healing and preventing peptic ulcers.

❌ Why the Other Options Are Incorrect:

• Metoclopramide → A prokinetic drug that enhances gastric emptying and treats nausea/vomiting, not for direct acid suppression.

• Sucralfate → Forms a protective physical barrier over ulcers but does not affect histamine receptors.

• Omeprazole → A proton pump inhibitor (PPI) that irreversibly inhibits the H⁺/K⁺ ATPase, reducing acid secretion, but not via H₂ receptor antagonism.

• Misoprostol → A PGE₁ analogue that increases mucous and bicarbonate secretion and decreases acid secretion, mainly useful for NSAID-induced ulcers, but not via H₂ receptors.

• Antacids are alkaline substances (e.g., magnesium hydroxide, aluminum hydroxide, calcium carbonate) that neutralize gastric acid immediately, giving quick relief from gastric irritation, heartburn, and dyspepsia.

• They act faster than other classes of acid-suppressing drugs (like H2 blockers or PPIs) though their effect is short-lived.

Incorrect answer explanations:

• Aspirin → An NSAID that worsens gastric irritation by inhibiting prostaglandins and damaging the gastric mucosa.

• Lemon juice → Acidic; increases irritation instead of relieving it.

• Milk → May give temporary soothing effect, but proteins and calcium later stimulate gastrin → increases acid secretion.

• Alcohol → Damages gastric mucosa and worsens irritation.

Step 1: Recall what peristalsis is

• Peristalsis = rhythmic, coordinated contractions of the GI tract that propel contents forward.

• Some drugs stimulate peristalsis (laxatives, prokinetics), while others inhibit peristalsis (antidiarrheals, opioids).

Step 2: Evaluate each option

Sorbitol
❌ An osmotic laxative. It draws water into the intestines → increases stool bulk → stimulates peristalsis.

Psyllium
❌ A bulk-forming laxative. It absorbs water, increases stool mass, and indirectly promotes peristalsis.

Lubiprostone
❌ A chloride channel activator. Increases intestinal fluid secretion → stimulates bowel motility → enhances peristalsis.

Castor oil
❌ A stimulant laxative. Hydrolyzed to ricinoleic acid, which directly irritates the intestinal mucosa and stimulates peristalsis.

Loperamide
✅ Correct.

• It is an opioid receptor agonist acting on the myenteric plexus in the intestine.

• Decreases acetylcholine release → reduces gut motility → inhibits peristalsis.

• Used as an antidiarrheal drug.

Misoprostol is a synthetic analogue of prostaglandin E₁ (PGE₁).

• Prostaglandins normally stimulate mucus and bicarbonate secretion and increase mucosal blood flow in the stomach, protecting it from acid.

• NSAIDs cause peptic ulcers mainly because they inhibit cyclooxygenase (COX), reducing prostaglandin synthesis.

• By replacing this lost prostaglandin activity, misoprostol prevents and helps heal NSAID-induced gastric ulcers.

It is often used prophylactically in patients who require long-term NSAID therapy.

Incorrect options:

• Vulvovaginitis → Misoprostol has no role; treatment depends on cause (fungal, bacterial, etc.).

• Aphthous mouth ulcers → These are usually self-limiting; topical corticosteroids or analgesics are used, not misoprostol.

• Alcoholic hematemesis → Most often due to esophageal varices or gastric erosions in alcoholics. Management involves endoscopic intervention, not misoprostol.

• Henoch-Schönlein purpura → An IgA-mediated small vessel vasculitis, treated with supportive care or steroids. Misoprostol is not relevant.

• Omeprazole (Correct)

  • A proton pump inhibitor (PPI).

  • Irreversibly inhibits the H⁺/K⁺ ATPase in parietal cells.

  • This is the final step in acid secretion, so inhibition is profound and long-lasting.

  • PPIs are the most effective drugs for suppressing gastric acid secretion and are widely used in peptic ulcer disease, GERD, and Zollinger–Ellison syndrome.

• Ranitidine

  • An H₂ receptor antagonist.

  • It reduces acid secretion by blocking histamine stimulation of parietal cells.

  • Effective, but weaker compared to PPIs.

• Misoprostol

  • A prostaglandin E₁ analog.

  • Inhibits acid secretion modestly while promoting mucus and bicarbonate secretion.

  • Mainly used for NSAID-induced ulcer prevention, not as potent as PPIs.

• Atropine

  • A muscarinic receptor antagonist.

  • Can reduce acid secretion by blocking vagal stimulation, but has widespread side effects and is not used clinically for this purpose.

• Bismuth subsalicylate

  • A mucosal protectant with antimicrobial activity (against H. pylori).

  • It does not significantly suppress acid secretion.

Cimetidine is an H₂ receptor blocker used to reduce gastric acid secretion, especially in conditions like peptic ulcers, GERD, and Zollinger-Ellison syndrome.

However, unlike other H₂ blockers (like ranitidine or famotidine), cimetidine has notable hormonal and drug interaction-related side effects.

🔬 Why Cimetidine Causes Gynecomastia:

• Cimetidine inhibits cytochrome P450 enzymes → interferes with the metabolism of sex hormones

• Also blocks androgen (testosterone) receptors and inhibits estradiol metabolism

• This leads to:

  • Increased estrogen effect

  • Decreased testosterone action

• Result → Gynecomastia in men (swelling of breast tissue)

💡 It’s reversible upon discontinuation of the drug.

❌ Why the Other Options Are Incorrect:

• Bloating ❌
  → Not a common or characteristic side effect of cimetidine.

• Pneumonia ❌
  → While proton pump inhibitors (like omeprazole) may slightly increase the risk of pneumonia, it’s not a typical adverse effect of cimetidine.

• Alertness ❌
  → Cimetidine may cause confusion in elderly patients, not increased alertness.

• Diarrhea ❌
  → Though GI upset is possible, gynecomastia is more specific and characteristic.

🔍 Clinical Pearl:

Cimetidine also interferes with the metabolism of other drugs (like warfarin, phenytoin, theophylline) due to CYP450 inhibition — making it a less favorable option in many cases compared to newer H₂ blockers.

Extrapyramidal side effects (EPSEs) are drug-induced movement disorders that include dystonia, akathisia, parkinsonism, and tardive dyskinesia. These occur due to dopamine D2 receptor blockade in the nigrostriatal pathway of the brain, which is essential for regulating motor activity.

Metoclopramide is a dopamine D2 receptor antagonist primarily used as an antiemetic and prokinetic agent. While effective for nausea, vomiting, and gastroparesis, it crosses the blood-brain barrier and can block D2 receptors in the basal ganglia, leading to extrapyramidal symptoms, especially with prolonged use or high doses.

Why the Other Options Are Incorrect:

• Benztropine: ❌ Not a cause—actually used to treat extrapyramidal symptoms. It’s an anticholinergic agent that restores dopamine-acetylcholine balance in the basal ganglia.

• Benzodiazepine: ❌ These are GABA-A receptor agonists, used for anxiety, seizures, and muscle relaxation. They do not block dopamine receptors and don’t cause EPSEs.

• Clozapine: ❌ An atypical antipsychotic with very low affinity for D2 receptors. It is least likely among antipsychotics to cause extrapyramidal symptoms. It may cause agranulocytosis and sedation, but not EPSEs.

• Procyclidine: ❌ Like benztropine, it is an anticholinergic drug used to manage or prevent extrapyramidal side effects caused by antipsychotic medications.

When we discuss “quickest treatment for ulcers”, there can be two interpretations:

1. Quickest symptom relief → Antacids (because they act immediately).

2. Quickest healing of the ulcer → Proton Pump Inhibitors (PPIs) like Omeprazole, because they profoundly and consistently inhibit gastric acid secretion, creating the ideal environment for mucosal healing.

The question is likely referring to ulcer healing, not just temporary relief of pain, so Omeprazole is the correct answer for long-term effectiveness.

Mechanism of Omeprazole:

• Irreversibly inhibits the H+/K+ ATPase proton pump in the gastric parietal cells.

• This is the final step of acid secretion, so PPIs are the most potent acid-suppressing drugs available.

• Result: Profound reduction in gastric acidity, promoting rapid healing of duodenal and gastric ulcers.

Onset and Duration:

• Takes a few hours to start working, but the effect lasts 24–48 hours per dose.

• Maximum benefit after a couple of days, which is still much faster for actual ulcer healing than H2 blockers or misoprostol.

Why the Correct Option is Right:

• Omeprazole provides the most effective suppression of acid secretion and accelerates ulcer healing faster than H2 blockers or mucosal protectants.

Why the Other Options are Wrong:

• Antacid: Gives quick symptom relief but does not heal ulcers effectively.

• H2 antagonists: Reduce acid secretion but less potent than PPIs.

• Misoprostol: Prevents NSAID-induced ulcers but is not primary for healing existing ulcers.

• Aspirin: Contraindicated as it worsens ulcers.

Answer Breakdown:

• Best for symptom relief: Antacids.

• Best for fastest ulcer healing: PPIs (Omeprazole) → gold standard therapy.

• Metoclopramide is a prokinetic drug.

• Mechanism:

  • D₂ receptor antagonist → removes inhibitory dopaminergic effect on GI motility.

  • Enhances ACh release in the GI tract.

  • Increases gastric emptying and lower esophageal sphincter tone.

• Clinically used to prevent aspiration risk before anesthesia (esp. in emergency surgery).

Why the Others Are Incorrect

• Apomorphine ❌ – Dopamine agonist; induces vomiting (emetic), not gastric emptying.

• Hyoscine ❌ – Anticholinergic; decreases motility, used for motion sickness.

• Methylpolysiloxane ❌ – Antifoaming agent used in bloating/flatulence; no effect on gastric emptying.

• Promethazine ❌ – Antihistamine (H₁ blocker) with antiemetic properties; no prokinetic action.

Cimetidine is an H₂ receptor antagonist that reduces gastric acid secretion by blocking histamine-mediated stimulation of parietal cells.
However, it is notorious for its antiandrogenic and enzyme-inhibiting side effects.

🔹 Mechanism of Adverse Effects

1. Antiandrogenic Effects:

   • Cimetidine inhibits binding of dihydrotestosterone (DHT) to androgen receptors.

   • It also inhibits estradiol metabolism, causing gynecomastia, impotence, and decreased libido in men.

2. Drug Interactions:

   • Cimetidine is a potent inhibitor of cytochrome P450 (CYP450) enzymes.

   • Increases serum levels of drugs like warfarin, phenytoin, diazepam, and theophylline.

❌ Incorrect Options

• Ranitidine: ❌ Same class but does not inhibit androgen receptors or CYP450 significantly.

• Omeprazole: ❌ A proton pump inhibitor; minimal hormonal effects.

• Sucralfate: ❌ Acts locally to coat ulcers; no hormonal or CYP interactions.

• Misoprostol: ❌ Prostaglandin analog; causes diarrhea, not gynecomastia.

This patient has peptic ulcer disease worsened by aspirin (an NSAID).
NSAIDs inhibit cyclooxygenase (COX) → ↓ prostaglandin synthesis → ↓ mucus and bicarbonate secretion + ↑ acid injury to gastric mucosa.

Misoprostol, a PGE₁ analog, restores the protective prostaglandin function — making it ideal for NSAID-induced gastric mucosal protection.

🔹 Mechanism of Action

• Binds to prostaglandin receptors (EP₃) on parietal cells → ↓ cAMP → ↓ H⁺ secretion.

• Enhances mucus and bicarbonate secretion and increases mucosal blood flow.

• Prevents and heals NSAID-induced ulcers, especially in chronic users like this patient.

❌ Incorrect Options

• Sucralfate: ❌ Forms a protective barrier over ulcers but does not prevent NSAID injury; requires acidic pH and can interfere with absorption of other drugs.

• Ranitidine / Cimetidine: ❌ H₂ blockers reduce acid secretion but do not restore lost prostaglandins.

• Omeprazole: ❌ Proton pump inhibitor; effective for healing ulcers, but Misoprostol specifically prevents NSAID-induced mucosal damage by replacing prostaglandin function.

Verapamil, a calcium channel blocker, is well-known for causing constipation as a side effect by reducing intestinal smooth muscle contractility.
To manage this, an osmotic laxative such as magnesium hydroxide can be used safely and effectively.

🔹 Mechanism of Action:

• Magnesium hydroxide is a saline osmotic laxative.

• It retains water in the intestinal lumen by osmotic effect, increasing stool volume and stimulating peristalsis.

• Results in softened stool and bowel movement typically within 1–6 hours (depending on dose).

❌ Incorrect Options

• Aluminum hydroxide: ❌ An antacid, actually causes constipation, not relief.

• Diphenoxylate: ❌ An anti-diarrheal opioid analog — worsens constipation.

• Metoclopramide: ❌ A prokinetic/antiemetic, works on the upper GI tract, not effective for constipation.

• Ranitidine: ❌ An H₂ receptor blocker (anti-ulcer drug), no laxative effect.