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Antiulcer Drugs
yogeeta
M. Pharm
Pharmacology Ist year
Content
• INTRODUCTION
• PHYSIOLOGY
• ETIOLOGY
• CLASSIFICATION OF DRUGS
• ANTIULCER DRUGS
• REFERENCES
 Introduction
• Peptic ulcers 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.
• Antiulcer drugs are 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.
 PHYSIOLOGY
 Etiology
• H. pylori
• Drugs such as NSAID’S
• Life style factors
• Severe emotional or physiological stress
• Having family history
 Classification Of Antiulcer 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.
2) Neutralization of gastric 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
Fig: DRUGS USED IN PEPTIC ULCER
antacids acid
• PPI
• H2 blocker
• prostaglandin
• Sucralfate
• CBS
NEUTRALIZE SECRETION
Protection
A . REDUCE GASTRIC 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%
• Use:
a) in peptic ulcer
b) Zollinger-Ellison syndrome
c) GERD
• Adverse effects:
- Diarrhoea, dizziness, muscle pain, hypotension, gynaecomastia
• PROTON PUMP INHIBITOR
(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.
• 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
B. Neutralization of gastric 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
• 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
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.
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,
References
• Rang and Dale,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.
Thank you

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Antiulcer drugs

  • 2. Content • INTRODUCTION • PHYSIOLOGY • ETIOLOGY • CLASSIFICATION OF DRUGS • ANTIULCER DRUGS • REFERENCES
  • 3.  Introduction • Peptic ulcers 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.
  • 4. • Antiulcer drugs are 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.
  • 6.  Etiology • H. pylori • Drugs such as NSAID’S • Life style factors • Severe emotional or physiological stress • Having family history
  • 7.  Classification Of Antiulcer 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.
  • 8. 2) Neutralization of gastric 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
  • 9. Fig: DRUGS USED IN PEPTIC ULCER antacids acid • PPI • H2 blocker • prostaglandin • Sucralfate • CBS NEUTRALIZE SECRETION Protection
  • 10. A . REDUCE GASTRIC 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%
  • 11. • Use: a) in peptic ulcer b) Zollinger-Ellison syndrome c) GERD • Adverse effects: - Diarrhoea, dizziness, muscle pain, hypotension, gynaecomastia
  • 12. • PROTON PUMP INHIBITOR (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.
  • 13. • 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
  • 14. B. Neutralization of gastric 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
  • 15. • 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
  • 16. 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.
  • 17. 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,
  • 18. References • Rang and Dale,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.