Peptic ulcer
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Peptic ulcer



My Presentation , Surgery II, KFU,2011

My Presentation , Surgery II, KFU,2011



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Peptic ulcer Peptic ulcer Presentation Transcript

  • Peptic Ulcer Fatimah Abdullah 6th year MS, KFU
  • Objectives Definition. Pathophysiology. Etiology. Clinical Picture. Management.
  • 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.
  • The gastroduodenal mucosal integrity isdetermined by protective (defensive) &damaging (aggressive) factors.
  • • Bicarbonate • Helicobacter pylori• Mucus layer • NSAIDs• Prostaglandins • Pepsins• Mucosal blood flow • Bile acids• Epithelial renewal • Smoking and alcoholDefensive Aggressive Mucosal damage  erosions & ulcerations
  • H. Pylori Infection NSAIDs Smoking & Alcohol Acid Hypersecretion StressFamily History of PUD.
  • 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 Hunger Eating
  • 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%
  • Stool fecal occult blood.CBC   CBL.Rapid Urease test, ureabreath test  H. Pylori.Upper GI Endoscopy.Barium meal X-Ray.
  • 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.
  • Life Style Change.Medical.Surgical.
  • Discontinue NSAIDsSmoking cessation. Alcohol cessation. Stress reduction.
  • AntacidsH2-receptor blocking agents.Proton pump inhibitors.Cytoprotective and antisecretory drugs.Antibiotics.
  • 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.
  • 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.
  • Vagotomy: Truncal Vagotomy with drainage. Highly selective Vagotomy. Combination of vagal denervation (vagotomy) + anterctomy.
  • 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.
  • 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.
  • Combination of vagotomy+anterctomy: Combination of vagal denervation & removal of the major area of gastric production.
  • Gastrointestinal continuity is restored bygastroduodenal (Billroth 1) anastomosisOR gastrojejunal (Billroth 2)anastomosis.
  • Dehiscence.Stenosis of anastomosis.Bleeding.Injury to neighbour tissues.Dumping syndrome
  • HemorrhagePerforation peptic ulcerGastric outlet obstruction