Peptic ulcer

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My Presentation , Surgery II, KFU,2011

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Peptic ulcer

  1. 1. Peptic Ulcer Fatimah Abdullah 6th year MS, KFU
  2. 2. Objectives Definition. Pathophysiology. Etiology. Clinical Picture. Management.
  3. 3. Break in the gastrointestinal mucosaexposed to the aggressive action of acid-peptic juices. Common sites are the first part of the duodenum and the lesser curve of the stomach.
  4. 4. The gastroduodenal mucosal integrity isdetermined by protective (defensive) &damaging (aggressive) factors.
  5. 5. • Bicarbonate • Helicobacter pylori• Mucus layer • NSAIDs• Prostaglandins • Pepsins• Mucosal blood flow • Bile acids• Epithelial renewal • Smoking and alcoholDefensive Aggressive Mucosal damage  erosions & ulcerations
  6. 6. H. Pylori Infection NSAIDs Smoking & Alcohol Acid Hypersecretion StressFamily History of PUD.
  7. 7. Duodenal Ulcer Gastric ulcer Age Any age specially 30-40 middle age 50-60 Sex More in male More in maleOccupation Stress job eg. Manager Same Pain Epigastric , discomfort Epi. Can radiate to back Onset 2-3 hours after eating & Immediately after midnight eating Agg.by Hunger Eating
  8. 8. Duodenal Ulcer Gastric ulcerRelived by Eating Lying down or vomitingDuration 1-2 months Few weeksVomiting Uncommon Common(to relieve the pain)Appetite Good Pt. afraid to eatDiet Good , eat to relieve the pain Avoid fried foodWeight No wt. loss wt. LossHematemesis 40% 60%Melena 60% 40%
  9. 9. Stool fecal occult blood.CBC   CBL.Rapid Urease test, ureabreath test  H. Pylori.Upper GI Endoscopy.Barium meal X-Ray.
  10. 10. Any patient >50 y/o with new onset of symptoms In all patients with “Alarmingsymptoms” endoscopy is required. Dysphagia. Weight loss. Vomiting. Anorexia. Hematemesis or Melena.
  11. 11. Life Style Change.Medical.Surgical.
  12. 12. Discontinue NSAIDsSmoking cessation. Alcohol cessation. Stress reduction.
  13. 13. AntacidsH2-receptor blocking agents.Proton pump inhibitors.Cytoprotective and antisecretory drugs.Antibiotics.
  14. 14. H. pylori Eradication Therapy:• Triple therapy:  Proton pump inhibitor .  2 Antibiotics: • Metronidazole + Clarithromycin. • Clarithromycin + Amoxicillin. » In some regimens, H2-receptor blockers, e.g. ranitidine, are used instead of PPI.
  15. 15. Indications: Failure of medical treatment. Development of complications High level of gastric secretion and combined duednal and gastric ulcer. Principle: Reduce acid and pepsin secretion.
  16. 16. Vagotomy: Truncal Vagotomy with drainage. Highly selective Vagotomy. Combination of vagal denervation (vagotomy) + anterctomy.
  17. 17. Truncal vagotomy with drainage:Resect the major trunk of the vagus tothe stomach this will lead to: Decrease acid and pepsin secretion. Impair antral motility and drainage. – Two types of drainage: Pyloroplasty. Gastrojejnostomy.
  18. 18. Highly selective vagotomy: • It is a parietal cells vagotomy. • It can be done with or without drainage. • It is done by cut a branch of vagus of the body and the fundus this will lead to decrease HCl production.
  19. 19. Combination of vagotomy+anterctomy: Combination of vagal denervation & removal of the major area of gastric production.
  20. 20. Gastrointestinal continuity is restored bygastroduodenal (Billroth 1) anastomosisOR gastrojejunal (Billroth 2)anastomosis.
  21. 21. Dehiscence.Stenosis of anastomosis.Bleeding.Injury to neighbour tissues.Dumping syndrome
  22. 22. HemorrhagePerforation peptic ulcerGastric outlet obstruction

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