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Peptic Ulcer (peptic ulcer disease)

Peptic Ulcer (peptic ulcer disease). Shanghai Ren-Ji Hospital Shanghai Institute of Digestive Disease Wenzhong Liu. What is the peptic ulcer ?. Definition. Craters extending to below the muscularis mucosa of stomach (GU) or duodenum (DU). A products of self-digestion.

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Peptic Ulcer (peptic ulcer disease)

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  1. Peptic Ulcer (peptic ulcer disease) Shanghai Ren-Ji Hospital Shanghai Institute of Digestive Disease Wenzhong Liu

  2. What is the peptic ulcer ?

  3. Definition • Craters extending to below the muscularis mucosa of stomach (GU) or duodenum (DU). • A products of self-digestion.

  4. Epidemiology • Estimated life time prevalence :10% • Male: female =3- 4:1 • Ratio of DU: GU = 3:1 • DU emerges 10-20 years earlier than GU

  5. Etiology & Pathogenesis

  6. Barrier of Gastric Mucosa

  7. Etiology & Pathogenesis • Helicobacter pylori infection • NSAIDs & Aspirin • Acid/Pepsin • Smoking • Genetics • Psychological factors Nonsteroidal anti-inflammatory drugs, NSAIDs

  8. Etiology & Pathogenesis

  9. Aggressive Factors • Acid/Pepsin • H. pylori infection • NSAIDs • Smoking • Defensive Factors • Mucus-bicarbonate barrier • Barrier of apical membrane • Mucosal blood flow • Prostaglandins • Epithelial cell restitution Aggressive Factors  Defensive Factors  I II III Aggressive Factors + Defensive Factors

  10. Evolving Knowledge • Dictum • No acid, no ulcer • No acid, no Hp, no ulcer • No Hp, No NSAIDs, no ulcer

  11. Under Electromicroscopy

  12. Clinical Evidences That H.pylori Infection Plays Major Role in Peptic Ulcer • High prevalence of Hp infection in peptic ulcer. DU: 90-100%; GU:70-90% • Eradication of Hp improves healing of ulcer. Healing refractory ulcer  Shortening treatment course: 4 - 6 weeks 1-2 weeks

  13. Clinical Evidences That H.pylori Infection Plays Major Role in Peptic Ulcer • Eradication of Hp markedly reduces relapse and complication rates of ulcer.  50 - 70%/yr < 5%/yr • Prospective study shows that individuals infected with Hp has higher risk of developing peptic ulcer.  15 - 20%

  14. Why anti-secretory agents can heal H.pylori associated peptic ulcer? Anti-secretory agents Acid  Mucosal Barrier

  15. “Leaking Roof ” Hypothesis Mucosal Barrier

  16. The strongest evidence for the pathogenic role of H. pylori in peptic ulcer disease is the marked decrease in the recurrence rate of ulcers following the eradication of infection.

  17. “for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease”

  18. Why only a part of patients with H.pylori infection have peptic ulcer? H.pylori Virulence Host Factor Environment Factors IL-1B polymorphism

  19. NSAIDs & Peptic Ulcer

  20. Gastric acid plays a central role inNSAID-associated gastroduodenal damage Bicarbonate layer Surface epithelial cells

  21. NSAID Damage to the Gastric Mucosa Scanning electron micrographs of normal gastric mucosa (left) andmucosal surface (right) 16 minutes after administration of aspirin Baskin et al 1976

  22. Two Common Forms of Peptic Ulcer • H.pylori – associated: 70-85% • NSAIDs – associated: 10-25% Non-Hp, Non-NSAID Ulcer: 5-30%

  23. Acid /Pepsin • By definition, peptic ulcer is caused by autodigestion of acid and pepsin • Activity of pepsin is pH-depedent Pepsinogen pepsin pH< 4 Maintaining activity pH< 4 • Usual therapy toward suppression of acid

  24. The influence of pH on gastricpepsin activity 1 2 3 4 Adapted from Berstad 1970

  25. Smoking & Peptic Ulcer • Increasing incidence of peptic ulcer • Delaying healing of ulcer • Increasing relapse and complication • Mechanisms: Facilitating bile reflux Decreasing mucosal blood supply Inhibiting synthesis of PGs

  26. Genetics & Peptic Ulcer • Familial Clustering  Genetic factors  Environment factor : H. pylori infection

  27. Genetics & Peptic Ulcer • Concordance of peptic ulcer is more common in monozygotic that dizygotic twins. • Peptic ulcer occurs in a few rare inherited syndromes. Gastrinoma Mastocytosis

  28. Psychological Factor in Peptic Ulcer • Controversial • Possible mechanisms through vagal mechanisms, Stimulating acid secretion Decreasing mucosal blood supply

  29. Clinical Presentation • Symptoms are neither specific nor sensitive • Silent Ulcer Emergence of complications: bleeding, perforation Discovered by chance

  30. Clinical Presentation • Acid dyspepsia in DU Epigastric “ hunger ” pain or discomfort; Occurred 2-4 hours after meal,or at night; Relieved by food or antacids; • Acid dyspepsia in GU More severe pain; Occurred soon after meal; Less relieved by food or antacids;

  31. Physical Examination • Limited value in patients with uncomplicated ulcer. • Epigastric tenderness on deep palpitation in active stage. Sensitivity 50% Specificity 50%

  32. Atypical Ulcers • Giant Ulcer DU>2cm, GU>3cm • Pyloric Channel Ulcer Pain occurring shortly after meal.  Poor relief by antacids  Vomiting • Postbulbar Ulcers • Multiple Ulcers

  33. Laboratory Examination • Detection of H. pylori Infection Essential • Gastric Secretory Test For ruling out Zollinger-Ellison Syndrome • Determination of Serum Gastrin level For ruling out Zollinger-Ellison Syndrome • Fecal Occult Blood Test Nonspecific

  34. Detection of H. pylori Infection Direct smear PCR 13C- Breath test

  35. Warthin -Starry Stain Acridine orange stain

  36. Endoscopy versus Radiography • Endoscopy has a greater accuracy of establishing diagnosis than radiography. • Endoscopy can take biopsies for histology, ruling out malignancy, and detection of Hp. • Endoscopy can carry out therapy. • Cost • Risk

  37. Endoscopy Gastric ulcers

  38. Endoscopy Duodenal ulcer

  39. Peptic ulcers

  40. Staging of peptic ulcer under endoscopy

  41. Barium Radiogram

  42. Differential Diagnosis • Functional dyspepsia: By Endoscopy • Zollinger Ellison Syndrome (Gastrinoma) • Gastric Malignant Ulcer: Endoscopy + Biopsy • Biliary or pancreatic diseases: Ultrosonography, MRCP, ERCP

  43. Zollinger Ellison Syndrome • Clinical Characteristics  Peptic ulcer with Diarrhea Peptic ulceration in unusual location Multiple ulcers  Refractory ulcer Complications No H.pylori, no NSAIDs • Gastric Secretory Test Basic acid output > 15mEq/hour • Determination of Serum Gastrin level Fasting serum gastrin >500pg/ml

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