Antiulcer drugs

Antiulcer drugs

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  Antiulcer Drugs yogeeta M. Pharm PharmacologyIst year
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  Content • INTRODUCTION • PHYSIOLOGY •ETIOLOGY • CLASSIFICATION OF DRUGS • ANTIULCER DRUGS • REFERENCES
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   Introduction • Pepticulcers form when cells on the surface of the lining become inflamed and die. • Peptic ulcers are sores that develop in the lining of the stomach, lower esophagus, or small intestine. • They’re usually formed as a result of inflammation caused by the bacteria H. pylori, as well as from erosion from stomach acids.
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  • Antiulcer drugsare the drug which is used to treat or prevent ulcer of intestine or stomach. • These drugs act by either inhibiting acid production • or by killing the microorganism responsible for ulcer.
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   PHYSIOLOGY
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   Etiology • H.pylori • Drugs such as NSAID’S • Life style factors • Severe emotional or physiological stress • Having family history
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   Classification OfAntiulcer Agent 1) Reduction of gastric acid secretion • H2 antihistamines: Cimetidine, ranitidine, famotidine, roxatidine. • PPI’s : Omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole • Anticholinergics: Pirenzepine, propantheline, ox phenonium • Prostaglandin analogues:- Misoprostol.
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  2) Neutralization ofgastric acid (Antacids) • Systemic : Sodium bicarbonate, sodium citrate • Non-systemic (Local) : Mg hydroxide, Mg trisilicate, Al hydroxide gel, calcium) 3) Ulcer protectives: Sucralfate, CBS ( Colloidal Bismuth Sub- citrate) 4) Anti-H. pyloric drugs: Amoxicillin, clarithromycin, metronidazole, tinidazole, tetracycline
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  Fig: DRUGS USEDIN PEPTIC ULCER antacids acid • PPI • H2 blocker • prostaglandin • Sucralfate • CBS NEUTRALIZE SECRETION Protection
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  A . REDUCEGASTRIC SECRETION •H2- RECEPTOR BLOCKER (Cimetidine, Ranitidine, Famotidine, roxatidine) • MOA:inhibit acid secretion by blocking H2 receptors on the parietal cell • These agents inhibit gastric acid secretion by competitively blocking the binding of histamine to H2 receptors. decreases gastric acid secretion • They are taken orally and are well absorbed in the gastrointestinal tract. • They undergo first-pass metabolism in the liver. • Oral bioavailability : 50%
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  • Use: a) inpeptic ulcer b) Zollinger-Ellison syndrome c) GERD • Adverse effects: - Diarrhoea, dizziness, muscle pain, hypotension, gynaecomastia
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  • PROTON PUMPINHIBITOR (Omeprazole, Rabeprazole, pantoprazole) • MOA: act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme (H+K+ATPase) system of the gastric parietal cells.(sulfenamide) • USE: in peptic ulcer, GERD, Zollinger-Ellison syndrome. • Adverse effects: Nausea, abdominal pain, constipation, flatulence, Subacute myopathy, headaches, and skin rashes.
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  • Anticholinergic (pirenzepine, telenzepine) MOA:Inhibit acetylcholine action on muscarinic receptor-Decreases HCl secretion(M1 receptor blocker) (Have low efficacy and anticholinergic side effect) • Prostaglandin analogous (Misoprostol, Enprostol) MOA: Increase mucous and bicarbonate secretion, increase blood supply, Decrease HCl secretion • Contraindications: - It is contraindicated during pregnancy because it can increase uterine contractility. • Adverse effects: - Diarrhea and nausea are the most common adverse effects
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  B. Neutralization ofgastric acid • (Systemic: sod. Bicarbonate, Sod. Citrate) • (Non- systemic: Al(OH)3, Mg(OH)2 • MOA: Antacids are weak bases that react with (neutralize) gastric acid to form water and a salt, thereby diminishing gastric acidity. • They reduce gastric acidity and increase gastric mucosal protection. A single dose of antacid (taken 1 hour after meal) can neutralize the acid for 2 hours. • Sucralfate • CBS Antacid (Weak base) HCl Salt +H2O
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  • Sodium bicarbonate -Effective,rapid action onset but short acting . And has some disadvantages. -Used in acidosis. Contraindicated in patient with CCF and hypertension. • Magnesium hydroxide and aluminum hydroxide -They react slowly with HC1. They are combined together, because Aluminum causes constipation and Magnesium causes osmotic diarrhea. They can interact with other drugs, inhibiting their absorption. • Adverse effects. • Drug interaction. NaHCO3 + HCl = Co2 + NaCl
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  C. ULCER PROTECTIVE •(SUCRALFATE, CBS) • MOA: These compounds, known as cytoprotective compounds, have several actions that enhance mucosal protection mechanisms, thereby preventing mucosal injury, reducing inflammation, and healing existing ulcers. • Adverse effects: Constipation, dryness of mouth, abdominal discomfort.
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  D. Anti h.pylori drugs (Amoxicillin, metronidazole) • MOA: The antimicrobial agents acts on bacterial cell wall synthesis and bacterial protein synthesis. • Resistance to metronidazole occurs rapidly but not with amoxicillin. • Adverse effects: Epigastric pain, Hypersensitivity reactions,
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  References • Rang andDale,Pharmacology, 6th edition, 2007, pg.385 – 390. • Bertram G.Katzung, Basic & Clinical pharmacology, 11th edition, 2009, pg.1070 – 1076. • Goodman & Gilman's The Pharmacological Basis of Therapeutics. 5th edition, pg 1008-1010. • Lippincott's Illustrated Reviews Pharmacology, 4th Edition, pg.329 – 335. • K.D.Tripati, Essentials of Medical pharmacology, 6th edition,2008, pg.627 – 638.
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  Thank you