peptic ulcer


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peptic ulcer

  2. 2. PEPTIC ULCER <ul><li>An Ulcer is … </li></ul><ul><ul><li>Erosion in the lining of the stomach or the first part of the small intestine, an area called the duodenum. </li></ul></ul><ul><ul><li>Ulcers damage the mucosa of the alimentary tract, which extends through the muscularis mucosa into the sub mucosa or deeper. </li></ul></ul>
  3. 3. Ulcers that form in the stomach are called gastric ulcers; in the duodenum, they are called duodenal ulcers. Both types are referred to as peptic ulcers.
  5. 5. PATHOGENESIS OF PEPTIC ULCER DISEASE IMBALANCE : <ul><li>Acid </li></ul><ul><li>Pepsin </li></ul><ul><li>Helicobacter pylori </li></ul><ul><li>NSAIDS </li></ul><ul><li>Prostaglandins </li></ul><ul><li>Mucosal blood flow </li></ul><ul><li>Mucous gel layer </li></ul><ul><li>HCO 3 </li></ul><ul><li>Epithelial junctions </li></ul><ul><li>Regeneration of the epithelial layer </li></ul><ul><li>Epidermal growth factor </li></ul><ul><li>AGGRESSIVE FACTORS </li></ul><ul><li>DEFENSIVE FACTORS </li></ul>
  6. 6. HELICOBACTER PYLORI <ul><li>1981 - Robin Warren , M.D., an Australian pathologist, discovered numerous bacteria living in tissue taken during a stomach biopsy. </li></ul><ul><ul><li>Spiral urease-producing, Gram-negative bacteria always accompanied changes in the stomach lining </li></ul></ul>
  7. 7. HELICOBACTER PYLORI <ul><li>Gram negative, Spiral bacilli </li></ul><ul><li>Spirochetes </li></ul><ul><li>Do not invade cells – only mucous </li></ul><ul><li>Breakdown urea - ammonia </li></ul><ul><li>Break down mucosal defense </li></ul><ul><li>Chronic Superficial inflammation </li></ul>
  8. 8. SYMPTOMS OF H. PYLORI <ul><li>Abdominal pain </li></ul><ul><li>Feeling of Fullness </li></ul><ul><li>Indigestion </li></ul><ul><li>Feeling very hungry 1 to 3 hours after eating </li></ul><ul><li>Mild nausea </li></ul><ul><li>Pain Starts 2/3 hours after meals, or in the middle of the night </li></ul>
  9. 9. PHYSIOLOGY OF GASTRIC ACID SECRETION <ul><li>Gastric acid secretion is a complex, continuous process in which multiple central and peripheral factors contribute to a common endpoint secretion of H ⁺ by parietal cells. </li></ul><ul><li>Neuronal(acetylcholine,Ach),paracrine(histamine), and endocrine (gastrin) factors all regulate acid secretion. </li></ul><ul><li>Their specific receptors (M 3 ,H 2 ,and CCK 2 receptors, respectively)are on the basolateral membrane of parietal cells in the body and fundus of the stomach. </li></ul>
  10. 10. <ul><li>The H 2 receptor is a GPCR that activates the Gs- adenyl cyclase –cyclic AMP-PKA pathway. </li></ul><ul><li>Ach and gastrin signal through GPCRs that couple to the G q -PLC-IP 3 -Ca 2+ pathway in parietal cells . </li></ul><ul><li>In parietal cells , the cyclic AMP and the Ca 2+ dependant pathways activate H + ,K + -ATPase (the proton pump), which exchanges hydrogen and potassium ions across the parietal cell membrane </li></ul>
  12. 12. SYMPTOMS <ul><li>Burning abdominal pain </li></ul><ul><li>Haematemesis </li></ul><ul><li>Melena </li></ul><ul><li>Nausea or vomiting </li></ul><ul><li>Unexplained weight loss </li></ul><ul><li>Anorexia </li></ul><ul><li>Abdominal fullness </li></ul>
  13. 13. DIAGNOSIS <ul><li>Endoscopy: </li></ul><ul><li>Flexible tube fitted with camera is threaded down the esophagus in to stomach to see the ulcer by physician </li></ul><ul><li>Barium meal: </li></ul><ul><li>Barium liquid is drunk making ulcer visible on X-ray </li></ul>
  14. 14. <ul><li>Test for diagnosing H.pylori </li></ul><ul><li>Breath test :by measuring the amount of co 2 in exhaled breath. </li></ul><ul><li>Blood test : by identifying H.pylori antibodies by ELISA test. </li></ul><ul><li>Stool test :stool sample tested with H.pylori antigen. </li></ul>
  15. 15. LIFE-STYLE MODIFICATION IN PUD <ul><li>Doubtful efficacy </li></ul><ul><ul><li>REST </li></ul></ul><ul><ul><li>RELAXATION </li></ul></ul><ul><ul><li>GOOD SLEEP </li></ul></ul><ul><ul><li>DIET INDICATION </li></ul></ul><ul><ul><ul><li>Balanced diet </li></ul></ul></ul><ul><ul><ul><li>Frequent small meal </li></ul></ul></ul><ul><ul><ul><li>fiber </li></ul></ul></ul><ul><ul><ul><li>vitamin E and dietary fatty acids </li></ul></ul></ul><ul><ul><ul><li>fat diet </li></ul></ul></ul><ul><ul><li>CONTRAINDICATION </li></ul></ul><ul><ul><ul><li>caffeine-containing beverages </li></ul></ul></ul><ul><ul><ul><li>spices </li></ul></ul></ul><ul><ul><ul><li>Alcohol </li></ul></ul></ul>
  16. 16. ANTI ULCER DRUGS <ul><li>REDUCTION OF GASTRIC ACID SECRETION </li></ul><ul><li>Histamine antagonist : Cimetidine, ranitidine </li></ul><ul><li>Proton pump inhibitors : omeprazole, pantaprazole </li></ul><ul><li>Acetyl choline antagonist : pirenzepine, propantheline </li></ul><ul><li>Prostaglandin analogue : misoprostol </li></ul>
  17. 17. ANTIULCER DRUGS <ul><li>Neutralization of gastric acid(antacids) Systemic : Sodium bicarbonate, Sodium citrate </li></ul><ul><li>Nonsystemic : Magnesium hydroxide , Aluminium hydroxides </li></ul><ul><li>Ulcer protectives : Sucralfate </li></ul><ul><li>Anti helicobacter pylori: amoxicillin, clarithromycin etc </li></ul>
  18. 18. HISTAMINE ANTAGONIST <ul><li>Cimetidine </li></ul><ul><li>.Histamine antagonists inhibit the action of histamine on the acid-producing cells of the stomach and reduce stomach acid </li></ul>
  19. 19. CIMETIDINE <ul><li>SIDE EFFECTS ; it include constipation , diarrhea, fatigue , headache, insomnia, muscle pain, and vomiting. Major side effects include confusion and hallucinations, gynacomastia (enlargement of the breasts); impotence. </li></ul><ul><li>USES: it is used in treatment of duodenal ulcer, </li></ul><ul><li>Gastric ulcer, stress ulcer, GERD, zollinger ellison syndrome </li></ul>
  20. 20. PROTON PUMP INHIBITORS <ul><li>  </li></ul><ul><li>Proton pump inhibitors act by irreversibly blocking the  hydrogen/potassium adenosine triphosphatase enzyme  system of the gastric parietal cells. </li></ul><ul><li>The proton pump is the terminal stage in gastric acid secretion </li></ul>
  21. 21. PROTON PUMP INHIBITORS <ul><li>OMEPRAZOLE </li></ul><ul><li>Omeprazole is inactive at neutral pH, but at pH<5 rearranges to two charged cationic forms(a sulphenic acid and a sulphenamide configurations)that react covalently with SH groups of the H + K + ATPase enzyme and inactivate it irreversibly, especially when two molecules of omeprazole react with one molecule of the enzyme </li></ul><ul><li>SIDE EFFECTS Stomach pain, Diarrhea,Constipation,Dizziness,Pain,Hives, Itching,seizures </li></ul>
  22. 22. ACETYL CHOLINE ANTAGONIST <ul><li>PIRENZEPINE </li></ul><ul><li>MECHANISM: </li></ul><ul><li>It selectively block M1 muscaranic recptors and inhibits gastric secretion. </li></ul><ul><li>Because of their relatively poor efficacy, side effects, and risk of blood disorders, they are rarely used today </li></ul>
  23. 23. AGENTS THAT ENHANCE MUCOSAL DEFENSE <ul><li>Prostaglandin Analogs: </li></ul><ul><li>prostaglandins are produced in the gastric </li></ul><ul><li>mucosa and appear to serve a protective role by inhibiting acid secretion and promoting mucus </li></ul><ul><li>and bicarbonate secretion. </li></ul><ul><li>In addition, PGs inhibits gastrin production, increase mucosal blood flow and probably have an ill defined cytoprotective action. </li></ul><ul><li>DRUGS : Misoprostol </li></ul>
  24. 24. MISOPROSTOL <ul><li>MECHANISM: </li></ul><ul><li>Misoprostol acts upon gastric parietal cells , inhibiting the secretion of gastric acid via G-protein coupled receptor-mediated inhibition of adenylate cyclase , which leads to decreased intracellular cyclic AMP levels and decreased </li></ul><ul><li>pump activity at the apical surface of the parietal cell </li></ul><ul><li>Side effects </li></ul><ul><li>Diarrhea. </li></ul><ul><li>Other common side effects include: abdominal pain, nausea, flatulence, headache, dyspepsia, vomiting, and constipation. </li></ul>
  25. 25. ULCER PROTECTIVES <ul><li>SUCRALFATE </li></ul><ul><li>MECHANISM: </li></ul><ul><li>Sucralfate is a locally acting substance that in an acidic environment (pH < 4), reacts with hydrochloric acid in the stomach to form a cross-linking, viscous , paste-like material capable of acting as an acid buffer for as long as 6 to 8 hours after a single dose . It also attaches to proteins on the surface of ulcers, such as albumin and fibrinogen , to form stable insoluble complexes. These complexes serve as protective barriers at the ulcer surface, preventing further damage from acid , pepsin , and bile . </li></ul>
  26. 26. <ul><li>Side effects </li></ul><ul><li>The most common side effects seen are constipation . Less commonly reported include flatulence, cephalalgia (headache), xerostomia (dry mouth). </li></ul><ul><li>USES: </li></ul><ul><li>It is used in treatment of </li></ul><ul><li>Gastritis, </li></ul><ul><li>Stress ulcers. </li></ul>
  27. 27. SODIUM BICARBONATE (ANTACID) <ul><li>It is water soluble, acts instantaneously, but duration of action is short. It is a potent neutralizer , pH may raises above 7. </li></ul><ul><li>Adverse reactions </li></ul><ul><li>It causes systemic alkalosis, gastric distention, rebound acidity and milk-alkali syndrome </li></ul><ul><li>Uses </li></ul><ul><li>It is restricted to casual treatment of heartburn and to treat acidosis </li></ul>
  28. 28. ANTI H.PYLORI DRUGS <ul><li>Anti microbials that have been found clinically effective against H.pylori are: amoxicillin, clarithromycin, tetracycline and metronidazole. </li></ul><ul><li>A combination regimen is preferred, using gastric acid inhibitors and antibiotics. </li></ul><ul><li>Example: </li></ul><ul><li>A proton pump inhibitor or H2 blocker + amoxicillin + clarithromycin or metronidazole </li></ul>
  29. 29. CONCLUSION
  30. 30. <ul><li>Avoid stress </li></ul><ul><li>Avoid contamination </li></ul>