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ANTIULCER AGENTS.pptx
- 1. DRUGS USED FORPEPTIC ULCER AND GERD PRESENTED BY- SAYANTAN DUTTA ASSISTANT PROFESSOR FACULTY OF PHARMACEUTICAL SCIENCES RAMA UNIVERSITY KANPUR, UTTAR PRADESH
- 2. WHAT IS PEPTICULCER • Peptic ulcer - A sore of oesophagus, stomach, intestine. • It occurs in the part of gastrointestinal tract (g.i.t.) which is exposed to gastric and pepsin. • Etiology - imbalance between aggressive & defensive factor. . AGGRESSIVE FACTORS DEFENSIVE FACTORS Acid Gastric mucosa Pepsin Bicarbonate Bile Prostaglandins H. pylori Nitric oxide
- 3. FORMS OF PEPTICULCER- 1. Duodenal 2. Gastric 3. Stress 4. NSAIDs - Duodenal ulcer- Acid secretion is high in half of the patients. - Gastric ulcer- Acid secretion is normal or low, but defense is low. {Stomach secrete about 2.5 liter of gastric juice (parietal cells)} Gastric acid secretion is regulated by- a. Vagus pathway (Ach) b. Gastric pathway c. Local histamine - They activate H+ K+ ATPase (proton pump) on the parietal cells, which results into secretion of H+ into gastric lumen, where it combines with Cl- (drawn from the plasma) and forms HCl Causes- 1. H. Pylori 2. aspirin- NSIADs 3. stress Risk- 1. alcohol abuse 2. Improper diet 3. Empty stomach
- 4. CLASSIFICATION OF DRUGSFOR PEPTIC ULCER
- 5. H2 ANTIHISTAMINES • Cimetidine •Ranitidine • Famotidine • Roxatidine • Lafutidine Physiology- Histamine H2 receptor on parietal cell HCl. H2 blockers are competitive antagonist (famotidine partially strong). They volume and acidity of basal , nocturnal and food induced gastric acid secretion. Inhibition is dose dependent. They also reduce gastrin induced HCl release and also reduce pepsin release. Effect on animal cells- 1. cardiac stimulation= isolated guinea pig 2. Uterine relaxation = rat 3. Bronchial relaxation = sheep
- 7. INTERACTIONS OF CIMETIDINE 1.Inhibitis several CYP450 isoenzymes and reduces hepatic blood flow. 2. Inhibits metabolism of many drugs --- accumulate to toxic level ( theophylline, phenytoin, warfarin, sulfonylurea, metronidazole, etc. 3. Antacids reduce absorption of all H2 blockers. 4. Ketoconazole absorption by H2 blockers due to reduced gastric acidity. Uses- Promotes the healing of gastric and duodenal ulcer • Gastric ulcer- 50 to 75% • Duodenal ulcer- 70 to 90 % at 8 weeks • Prophylaxis of aspiration pneumonia • Peptic ulcer • Urticaria • Bleeding from stress ulcer • Gastroesophageal reflux disease • Nonulcer dyspepsia
- 8. ADVERSE EFFECTS • Headache •Dizziness • Bowel upset Generally mild • Dry mouth • CNS: confusion, restlessness • Rapid or high dose i.v. – bradycardia, cardiac arrhythmia, cardiac arrest • Cimetidine has androgenic action. • May cross placenta
- 9. PROTON PUMP INHIBITORS DRUGS •Omeprazole • Esomeprazole • Pantoprazole • Lansoprazole • Rabeprazole • Dexrabeprazole • Ilaprazole OMEPRAZOLE • Prototype of the class. Most effective in acid • Parietal cells secrete H+ with the help of H+ K+ ATPase – proton pump. • This is final step of acid secretion by any stimulus. • PPI are inactive prodrugs. • Accumulate in parietal cell quickly activates in acidic environment sulfenamide • The active form firmly binds H+ K+ ATPase by covalent bond and inhibits irreversibly the pump = gastric acid reduction • They are enteric coated to prevent premature activation. • PPI should be taken in empty stomach.
- 10. Mechanism of action Omeprazolesulfenic acid sulfenamide H+ K+ ATPase gastric acid reduction. Activ+ Covalent bond
- 11. PROTON PUMP INHIBITORS ADVERSEEFFECTS Generally well tolerated. • Prolonged use acid suppression = bacterial growth increases. • Nausea, loose stool, headache, abdominal pain, joint pain. • Accelerated osteoporosis among elderly patients. • Long term use- vitamin B12 deficiency due to reduced absorption of acid. DRUG INTERACTIONS • Oxidation inhibits of diazepam, warfarin, phenytoin. • Inhibits CYP2C19. • Reduced absorption of ketoconazole and iron salts. • Clarithromycin inhibits omeprazole metabolism and increase its plasma concentration
- 12. USES OF PROTONPUMP INHIBITORS • Peptic ulcer- in patients who are not responding to H2 blockers. • Drug induced ulcer- PPI drugs are required for NSAID usage. • Stress ulcer- intravenous pantoprazole/ rabeprazole are effective for stress ulcer. • Gastroesophageal reflux disease (GERD)- ulcer relieved fast and pain gets reduced. • Zollinger Ellison syndrome- it is a gastric hypersecretory state due to gastrinoma, a rare tumor secreting gastrin, which presents with difficult to heal ulcer. • Aspiration pneumonia- for prophylaxis of aspiration pneumonia due to prolonged anaesthia.
- 13. PROSTAGLANDIN ANALOGUE (MISOPROSTOL) •PGE2 and PGI2 = produced in gastric mucosa. • Protect ulcer by reducing acid secretion and increasing mucus + HCO3- secretion. • Decrease gastrin release , increase mucosal blood flow and cytoprotective. • Misoprostol is longer acting synthetic PGE1 derivative. • food and antacid may reduced its absorption and bioavailability. Adverse effects = diarrhoea and abdominal cramps. • PG has stimulant effect and increase uterine contraction. • Not suitable of used in pregnancy.
- 14. ANTACIDS • Weak basethat neutralize acid. • Also inhibits formation of pepsin. ( as pepsinogen converted to pepsin at acidic pH.) • Duration of action is about 30 to 60 minutes. Types = 1. systemic which gets absorbed. = sodium bicarbonate 2. non- systemic acts only on stomach = Al / Mg hydroxide.
- 15. ANTACIDS. SYSTEMIC • Rapid butshort acting. • CO2 is released. • NaHCO3 +HCl NaCl + H20 + CO2 • Demerits: large dose induce alkalosis. • Produce CO2 in stomach distension, discomfort. • Short lasting acid rebound occurs. NON- SYSTEMIC • Insoluble compound. • React with HCl form. • CaCO3 + 2HCl CaCl2 + H2O. • No acid base disturbance occurs. • However small amounts that are absorbed have the same alkalinizing effects as NaHCO3.
- 16. ANTACID COMBINATIONS: • Acombination of two or more antacid is frequently used. • Superior effect. • Fast ( Mag. Hydrox.) and slow (Alum. Hydrox.) acting components gives prompt as well as sustained effect. • Mag. Salts have laxative while alum salts are constipating annul each others action. • Gastric emptying is least effected. • Dose can be reduced = systemic toxicity is minimized.
- 17. DRUG INTERACTIONS: Antacids reducethe absorption of many drugs: tetracyclines, iron salts, fluroquinone, ketoconazole. Uses • Employed for only for intercurrent pain relief, dyspepsia and acidity. • Nonulcer dyspepsia • Heartburn. • Faster symptom relief of GERD.
- 19. ANTI H. pyloriDRUGS Gram negative bacteria. Survive in stomach. Attaches to the surface of the epithelium beneath mucus. Secretes urease convert urea to ammonia. Ammonia produce neutral microenvironment around the bacteria and promotes back diffusion of H+ ions. For faster activity anti- H. pylori drugs + PPI are used.
- 20. Lansoprazole 30mg +amoxicilline 1000mg + clarithromycin 500mg = twice daily = 14 days CBS 120mg QID + tetracycline 500 mg QID + metronidazole 400mg TDS + omeprazole 20mg BD Quadruple therapy US FDA approved regimen
- 21. DRUGS USED TOTREAT GERD • Reflux is very common problem. • Some cases have anatomical defect but majority are functional. • Repeated reflux may lead to esophagitis, erosion, ulcer, pain on swallowing and increases the risk of esophageal carcinoma.
- 22. REFERENCES Tripathi KD, Essentialsof medicals pharmacology, JAYPEE Brothers medicalpublishers (P) Ltd., Drugs for peptic ulcer and gastroesophageal reflux disease, 695-708.