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Peptic ulcer (defination, cause, tratment)

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peptic ulcer

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Peptic ulcer (defination, cause, tratment)

  1. 1. Presented by: Mohd akhtar M.Pharm. (Pharmacology)
  2. 2.  Anatomy of Stomach  Acid Peptic Disorders  Peptic ulcer disease  Comparison of Gastric & Duodenal ulcers  Risk factors  Symptoms  Physiology of Acid secretion  Treatment of peptic ulcer  Summary
  3. 3. Muscularis Serosa Mucosa Submucosa FundicFundic regionregion Esophagus Duodenum AntrumAntrum Layers Parieta l cells BodyBody Pyloric sphincter Chief cells Gastric pit
  4. 4.  Peptic Ulcers • Gastric ulcer • Duodenal Ulcer  Gastro Esophageal Reflux Disease (GERD)  Dyspepsia  Stress Ulcers  Gastric Cancers
  5. 5.  Peptic ulcer refers to an erosion of the mucosal layer anywhere in the GI tract; however, it usually refers to erosions in the stomach or duodenum.  Over 80% of peptic ulcers are caused by Infection with the bacterium Helicobacter pylori.
  6. 6. Pathophysiology of Peptic UlcerPathophysiology of Peptic Ulcer Disease (PUD)Disease (PUD) Mucosal Defenses • Bicarbonate • Mucus • Prostaglandin • Growth factor • Mucosal regeneration Luminal Aggressors • H. pylori • NSAIDs • Acid • Pepsin
  7. 7. DUODENAL GASTRIC INCIDENCE More common Less common ANATOMY First part of duodenum – anterior wall Lesser curvature of stomach DURATION Acute or chronic Chronic MALIGNANCY Rare Benign or malignant
  8. 8.  HELICOBACTER PYLORI Infection  Non Steroidal Anti-inflammatory Drugs  Steroid therapy  Smoking  Excess alcohol intake  Genetic factors  Zollinger Ellison syndrome – rare syndrome caused by gastrin-secreting tumour  Blood group O  Hyperparathyroidism
  9. 9.  Nausea – Vomiting – Anorexia  Epigastric pain after meal and during meal  Intolerance of fatty food  Heartburn  Loss of weight  Oral flatulence, bloating  Pain radiating to the back
  10. 10. Feldman: Sleisenger & Fortran’s Gastrointestinal and Liver Disease, 7th ed.
  11. 11.  Gastrointestinal hemorrhage  Chronic iron deficiency anemia  Pyloric stenosis  Perforation  peritonitis
  12. 12.  Bacteria  Gram Negative spiral bacterium  40% of patients >60 years are +ve for H.pylori  Transmitted: possibly person to person  Most common cause of antral gastritis  Mechanism of gastric injury  Adherence to epithelial cells  Infects mucosa of stomach > inflammatory response > gastritis > increased gastrin secretion > gastric metaplasia > damage to mucosa > ulceration  Cytotoxin
  13. 13.  Inhibits prostaglandin synthesis (COX inhibition)  Disrupts functional mucosal integrity  ↓ mucosal blood flow  ↓ cell regeneration  Direct GI irritation  Antiplatelet effect (causing bleeding)  ↑ acid (basal and maximal stimulation) secretion
  14. 14. ProglumideACh PGE2 Histamine Gastrin Adenyl cyclase _ + ATP cAMP Protein Kinase (Activated) Ca++ + Ca++ Proton pump K+ H+ Gastric acid Parietal cell Lumen of stomach AntacidOmeprazole Ranitidine H2M3 Misoprostol _ _ _ _ + PGE receptor + + Gastrin receptor+ + + Cl- K+
  15. 15.  Promotion of ulcer healing.  Symptomatic relief of pain.  Prevention of recurrence (relapse).  Prevention of complications
  16. 16. I. Gastric hyposecretory drugs  Proton pump inhibitors  H2 receptor blockers  Muscarinic receptor blockers II. Eradication of H. pylori infections  To prevent relapse III. Mucosal cytoprotective agents  Sucralfate  Colloidal bismuth  Prostaglandin analogues IV. Neutralizing agents (antacids)
  17. 17. 1. Proton pump inhibitors 2. H2 receptor blockers 3. Muscarinic receptor blockers
  18. 18.  Mechanism of action Irreversible inhibition of proton pump (H+/ K+ ATPase) that is responsible for final step in gastric acid secretion from the parietal cell. PP inhibitors include:  Omperazole  Lansoprazole  Pantoprazole  Rabeprazole
  19. 19.  They are prodrugs – taken orally.  Are given as enteric coated capsules  They are activated in the acidic medium of the secretory parietal cell canaliculus.  They are inactivated if (combined with H2 receptor blockers).  Have long duration of action (> 18 -24 hr).  Bioavailability is reduced by food.  Given 1 hr before meal.
  20. 20. PPIs are quite safe but may occur: GIT disturbances: nausea, vomiting, diarrhoea  Achlorhydria: increase the risk of enteric infections due to Shigella, salmonella  Hypergastrinaemia  Gastric hyperplasia
  21. 21.  Mechanism of action They competitively and reversibly block to H2 receptors on the parietal cells thus reduce gastric secretion. They include: H2 Receptor inhibitors include:  Cimetidine  Ranitidine  Famotidine  Nizatidine
  22. 22.  Good oral absorption  Plasma half life (1-3 h).  Duration (4-12 h).  First pass metabolism (50% Except Nizatidine 100 % bioavailability).  Given before meals.  Metabolized by liver.  Excreted mainly in urine.  Cross placenta & excreted in milk
  23. 23. These are extremely safe drugs but may occur:  nausea, vomiting,  bradycardia and hypotension (rapid I.V.)  Gynecomasteia, impotence in male  Galactorrhea in female on long term use of cimitidine  Decrease metabolism of oral anticoagulant, phenytoin, benzodiazepines.
  24. 24. Acid (control) H2 Block PPI
  25. 25.  Mechanism of action  Blocks M3 receptors on the parietal cells.  Selectively inhibit gastric acid secretion  Decreased gastric motility  Delayed gastric emptying Muscarinic blockers:  Oxyphenonium  Dicyclomine  Pirenzepine  Telenzepine
  26. 26. Treatment Combined therapy is usually used.  Clarithromycin, tetracycline, amoxicillin  Proton pump inhibitors or H2 receptor blockers  Bismuth compounds  Metronidazole Resistance may develop to antibiotics so the better eradication is obtained using proton pump inhibitors, clarithromycin & Amoxicillin.
  27. 27. The BEST among all the Triple therapy regimen is Omeprazole/Lansoprazole - 20/30 mg bd Clarithromycin - 500 mg bd Amoxycillin/Metronidazole -1gm/500 mg bd Given for 14 days followed by P.P.I for 4 – 6 weeks. Short regimens for 7 – 10 days not very effective.
  28. 28. REGIMEN DOSE DURATION Bismuth Metronidazole Tetracycline 525 mg qid 250 mg tid 500 mg qid 2 weeks omeprazole Metronidazole Clarithromycin 20 mg bid 500 mg bid 500 mg bid 1 week omeprazole Amoxacillin Clarithromycin 20 mg bid 500 mg qid 500 mg bid 1 week omeprazole Bismuth Metronidazole Amoxacillin or / Tetracycline 20 mg bid 525 mg qid 500 mg qid 500 mg qid week
  29. 29. 1. Sucralfate 2. Prostaglandin analogs 3. Colloidal bismuth  Bismuth subcitrate  Tripotassium dicitrato bismuthate
  30. 30.  Sucralfate (aluminum hydroxide + sucrose)  Form a sticky like gel over ulcer crater to protect gastrointestinal mucosa and stimulates prostaglandin synthesis  It promote mucosal repair and ulcer healing  It has no acid neutralising action and delay gastric emptying  Dose: 1 g QID
  31. 31.  Misoprostol is a prostaglandin E1 analog that stimulates the secretion of mucus and bicarbonates and inhibits acid secretion to a minor degree.  The drug has significant side effects, primarily mild to moderate diarrhoea  Is too costly to be used by most patients.
  32. 32. Drugs used to relief gastric pain associated with hypersecretion of HCL and neutralize the gastric acid. Mechanism of Action Neutralization of HCL Inhibition of pepsin (inactive at PH 5) 1. Systemic Antacids Sodium bicarbonate Calcium Carbonate 2. Non Systemic Antacids Aluminum Hydroxide Gel Magnesium Trisilicate
  33. 33.  Sodium bicarbonate  Calcium Carbonate NaHCO3 + HCL → NaCL + CO2 Disadvantages  Rebound hyperacidity  Stomach distension due to CO2 liberation → pain sensation  Sodium load → salt and water retention ( # in cardiac patients)  Systemic alkalosis
  34. 34.  Aluminum Hydroxide Gel  Magnesium Trisilicate Al (OH)3 + HCL → HCL3 + H2O Advantages  Longer duration of action.  Gradual neutralization of HCL → No rebound hyperacidity.  Adsorbs pepsin.  No stomach distention
  35. 35.  Due to the benign nature of duodenal ulcers  When patients with duodenal ulcers require surgery, it is usually one of three procedures:  Vagotomy,  Vagotomy with antrectomy,  Pyloroplasty
  36. 36.  A peptic ulcer is a break in superficial epithelial cells penetrating down to muscularis mucosa  Duodenal > gastric ulcers  H pylori is a predominant risk factor  H pylori diagnosed by c urea breath test, stool antigen or if validated serology, treated with PAC500 or PMC250 regimen  Complications of PUD can lead to acute emergency of upper GI bleed

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