Antacids and Mucosal Protectants

Antacids Intro - Neutralizing Ninjas

• Weak bases; chemically neutralize gastric HCl.
• Result: ↑ gastric pH, ↓ pepsin activity (inactive > pH 4). Do NOT coat ulcers.
• Mechanism: $HCl + Antacid \rightarrow Salt + H_2O (+ CO_2 \text{ if carbonate})$
• Rapid onset, short duration. Symptomatic relief: dyspepsia, heartburn, GERD.
• Classification:
  • Systemic: Absorbed. E.g., Sodium Bicarbonate ($NaHCO_3$).
    • ⚠️ Risks: Systemic alkalosis, fluid overload, milk-alkali syndrome.
  • Non-systemic: Poorly absorbed. E.g., Aluminium Hydroxide ($Al(OH)_3$), Magnesium Hydroxide ($Mg(OH)_2$), Calcium Carbonate ($CaCO_3$).
    • Longer action, local effects.

⭐ Systemic antacids like Sodium Bicarbonate can cause systemic alkalosis, while non-systemic antacids like Aluminium Hydroxide and Magnesium Hydroxide do not.

Antacid Agents - The Stomach Soothers

• MOA: Weak bases; directly neutralize gastric HCl, raising pH. Symptomatic relief.
• Onset: Rapid (minutes); Duration: Short (1-3 hrs). Best taken 1 & 3 hrs post-meals & at bedtime.

-   ↓ Absorption (chelation/pH change): Tetracyclines, Fluoroquinolones, Ketoconazole, Itraconazole, Iron.
-   Administer antacids **1-2 hours** apart from other drugs.

⭐ Chronic use of Calcium Carbonate can lead to milk-alkali syndrome (hypercalcemia, alkalosis, renal impairment).

Mucosal Shields - Gut Guardians

• Sucralfate
  • Forms a viscous, sticky polymer in acidic environments (pH < 4), selectively binding to necrotic ulcer tissue.
  • Creates a physical barrier against acid, pepsin, and bile.
  • Stimulates prostaglandin synthesis and growth factors.
  • Minimal systemic absorption.
  • Adverse Effects: Constipation (most common), aluminum toxicity in renal failure.
  • Drug Interactions: Decreases absorption of phenytoin, digoxin, fluoroquinolones, ketoconazole. Administer other drugs 2 hours apart.

⭐ Sucralfate polymerizes and binds to necrotic ulcer tissue in an acidic environment (pH < 4), forming a protective barrier; its efficacy is reduced by co-administration with antacids, H2-blockers, or PPIs.

• Colloidal Bismuth Compounds (e.g., Bismuth Subsalicylate)

  • Coats ulcers and erosions, creating a protective layer.
  • Antimicrobial action (including H. pylori).
  • Stimulates prostaglandin, mucus, and bicarbonate secretion.
  • Adverse Effects: Harmless blackening of stool and tongue. Salicylate toxicity (rare).

• Misoprostol

  • Synthetic prostaglandin E1 (PGE1) analog.
  • MOA: ↓acid secretion, ↑mucus and bicarbonate secretion, ↑mucosal blood flow.
  • Primary Use: Prevention of NSAID-induced gastric ulcers.
  • Dose: e.g., 200 mcg QID.
  • Adverse Effects: Diarrhea, abdominal pain, uterine contractions.
  • ⚠️ Contraindicated in pregnancy (abortifacient).

High‑Yield Points - ⚡ Biggest Takeaways

• Antacids (Al(OH)₃, Mg(OH)₂) neutralize gastric acid; Al(OH)₃ causes constipation, Mg(OH)₂ causes diarrhea.
• Calcium carbonate risks hypercalcemia, rebound hyperacidity, and milk-alkali syndrome.
• Sodium bicarbonate can cause systemic alkalosis; avoid in cardiac/renal disease.
• Sucralfate forms a protective coat on ulcer base, requires acidic pH for activation, and chelates other drugs.
• Bismuth subsalicylate offers antimicrobial action and coats ulcers; causes black stools and tongue.
• Misoprostol (PGE₁ analog) protects against NSAID-induced ulcers; it's a potent abortifacient, contraindicated in pregnancy.