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Drugs Used in Acid‐Peptic Diseases (Agents that reduces intra‐gastric…
Drugs Used in Acid‐Peptic Diseases
Agents that reduces intra‐gastric acidity
Antacids
Weak bases: NaHCO3, CaCO3, Mg(OH)2, MgCO3, Mg2O8Si3, Al(OH)3
Antacids DO NOT prevent gastric acid production
Liquid antacid is better than tablet
Some antacid preparations contain
Simethicone
, an anti‐foaming
agent, easing the release of gas within the gastrointestinal tract via
burping or flatulence
All antacids affect the absorption of other medications, and therefore:
Antacids should NOT be given within 2 hours of other drugs like:
tetracyclin, fluroquinolone, itraconazole, iron, etc.
Patients with renal insufficiency should not take these agents long‐term
H2‐receptor Antagonists
(H2 Blocker)
Competitive inhibition of H2 receptors on parietal cells to suppress gastric acid secretion and pepsin concentration induced by
histamine, gastrin and acetylcholine
Most potent:
Famotidine
Side effects of old‐drug cimetidine, therefore, not prescribed
Proton Pump Inhibitors (PPI)
Prodrug:
Omeprazole
form covalent disulphide bond with H/K ATPase
Bioavailability of PPI is decreased 50% by food
Recommendation: PPI is given 1 hr before a meal (usually breakfast) once daily
may cause osteoporosis, gastric cancer
Mucosal protective agents
Sucralfate
Negatively charged sucrose sulfate binds
positively charged proteins at ulcer crater
forming a viscous, tenacious gel that prevents further acid attack
Side effects: constipation due to Al(OH)3; impairs absorption of other drugs
Misoprostol
Indications: prevention of NSAID‐induced peptic ulcers
Because other classes of drugs, especially H2-receptor antagonists and proton pump inhibitors, are more effective for the treatment of acute peptic ulcers, misoprostol is only indicated for use by people who are both taking NSAIDs and are at high risk for NSAID-induced ulcers
The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins
Binds to GPCR PGE2 receptors (analog of PGE1)
Low dose (cyto‐protective): promotes HCO3 and mucus secretion, enhances mucosal blood flow
High dose (anti‐secretory): inhibition gastric acid secretion
Adverse effects: abdominal pain, diarrhoea, abortion (uterine contraction), bone pain, hyperostosis (excessive growth of bone)
Limited use due to adverse effect profile, multiple daily dosing (non‐
compliance) and development of cyclooxygenase‐2‐selective NSAIDs
Bismuth Compounds
Bismuth subcitrate potassium – “quadruple therapy”
for eradication of H. pylori:
e.g. PPI + metronidazole + tetracycline + bismuth subcitrate
Bismuth forms a protective layer coating ulcer beds against acid & pepsin.
Stimulates mucus and bicarbonate secretion.
Direct anti‐microbial activity against H. pylori.
For traveler’s diarrhoea: bismuth possesses anti‐microbial effects and binds enterotoxins
Side effects: excellent safety profiles. Bismuth causes harmless
blackening of stool and darkening of tongue (reversible)
Triple‐Therapy for Helicobacter pylori eradication
Clarithromycin
Metronidazole
Omeprazole (a PPI)
1st line “Triple Therapy”: 1 PPI + 2 antibiotics (7‐14 days)
Mechanisms of PPI:
Direct anti‐microbial properties (minor)
Raising intra‐gastric pH (3.5‐5.5) ‐ lowering the MIC of antibiotics against H. pylori
After completion of triple therapy, PPI should be continued for 4‐6 weeks to ensure complete ulcer healing
2nd line “Quadruple Therapy”: Bismuth + 1 PPI + 2 antibiotics (10‐14 days)
Bismuth has direct antimicrobial activity against H. pylori