Peptic Ulcer Disease

1. Peptic Ulcer Disease Buyucan, Cueto, Cunanan, Dadgardoust

2. Peptic Ulcer Disease Ulcer - break in the mucosal surface > 5 mm in size with a depth to the submucosa Doudenal Ulcer PUD Gastric Ulcer

3. Peptic Ulcer Disease Mucosal Defense and Repair Aggressive Agents Preepithelial Epithelial Subepithelial Hydrochloric Acid Pepsinogen

4. Peptic Ulcer Disease Mucosal Defense and Repair Aggressive Agents

5. Peptic Ulcer Disease Mucosal Defense and Repair Aggressive Agents

6. Peptic Ulcer Disease Aggressive Agents Mucosal Defense and Repair

7. Peptic Ulcer Disease Major Causes • H. Pylori Infection • NSAID Induced

8. Peptic Ulcer Disease Complications • GI Bleeding • Perforation • Gastric Outlet obstruction

9. Peptic Ulcer Disease Increased Acid secretion and/ o rDecreased Mucosal Defenses Mucosal Injury/ Ulceration GI Bleeding

10. Incidence and Epidemiology • Peptic ulcers are the most common source of upper GI bleeding accounting up to ~50% of cases • 2 most common causes of PUD: Helicobacter pylori infection and NSAID use. • As the prevalence of H. pylori infection decreases and NSAID use increases, the relative contribution of each factor to the incidence of PUD will change. References: Harrison’s Principles of Internal Medicine 17th edition Wong, et al. Changing trends in peptic ulcer prevalence in a tertiary care setting in the Philippines: A seven-year study. Journal of Gastroenterology and Hepatology, Vol 20, Number 4, April 2005: 628-632(5)

11. Incidence and Epidemiology • DUODENAL ULCERS • 6-15% of the Western population • Incidence declined steadily from 1960 to 1980 and has remained stable since then >50% over visits have decreased over the past 30 years • The declining global prevalence is due to declining prevalence of Helicobacter pylori infections • Eradication of H. pylori has greatly reduced the recurrence rates after initial therapy

12. GASTRIC ULCERS • Tend to occur later in life than duodenal lesions, with peak incidence reported in the 6th decade • More than half of GUs occur in males • Less common than duodenal ulcers, perhaps due to higher likelihood of Gus being silent and presenting only after a complication develops

13. Clinical Manisfestation • Abdominal pain • Burning or gnawing discomfort at epigatrium • Ill-defined, aching sensation, hunger pain • Occurs 90mins – 3 hrs after meal, empty stomach, early morning • Relieved by foods or antacids

14. Nausea, vomiting, weight loss • Epigastric tenderness • Right of midline (20%) Other posible manifestation • GI bleeding • Bloody or dark tarry stools • Coffee ground emesis • Chest pain • Fatigue

15. Perforation • Sudden, severe, generalized abdominal pain • Tender, boardlike abdomen

16. Diagnosis of PUD

17. Barium Studies • Still commonly used as a first test for documenting an ulcer • 80% sensitivity : single contrast barium study • 90% sensitivity: double contrast barium study • Sensitivity is low for small ulcers (<0.5 cm) • Duodenal ulcers appear as a well demarcated crater most often seen at the bulb • Gastric ulcers may either be benign or malignant

18. Barium Studies • Benign gastric ulcer appears as a discrete crater with radiating mucosal folds originating from the mucosal margin • Ulcers >3 cm are more often malignant Radiographic studies that show a gastric ulcer must be followed by endoscopy and biopsy. Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

19. Endoscopy • Most sensitive and specific • Direct visualization of the mucosa • Photographic documentation of the defect • Tissue biopsy to rule out malignancy or H. pylori. • Helpful in identifying lesions too small to detect by radiographic examination, evaluation of atypical radiographic abnormalities, or to determine if an ulcer is a source of blood loss Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

20. Detection of H. pylori • NON-INVASIVE • Serology • Detection of antibodies in the serum • Urea Breath Test • Simple, rapid, early follow up • Stool antigen • Sensitive, specific, and inexpensive Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

21. Detection of H. pylori • INVASIVE (Endoscopy/Biopsy required) • Rapid urease • Simple, false negative with recent use of PPIs, antibiotics, or bismuth compounds • Histology • Provides histologic information • Culture • Time-consuming, expensive Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

22. Treatment of PUD

23. Objectives • Pain relief • Healing • Prevention of complications • Prevention of recurrences

24. Antacids • Rarely used as a primary therapeutic agents but are instead used for symptomatic relief • Mixture of aluminum hydroxide and magnesium hydroxide • Eg. Maalox, Mylanta Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

25. H2 Receptor Antagonists • Inhibit basal and stimulated acid secretion • Often used for treatment of active ulcers (4-6 weeks) in combination with an antibiotic directed at eradicating H. pylori. • Eg. Cimetidine, Ranitidine, Famotidine, Nizatidine Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

26. Proton Pump Inhibitors • Substituted benzimidazole derivatives that covalently bind and irreversibly inhibit H+K+-ATPase • Eg. Omeprazole, Esomeprazole, Lansoprazole, Rabeprazole, Pantoprazole Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

27. Cytoprotective Agents • Sucralfate • Insoluble in water • Viscous paste within the stomach and duodenum, binding primarily to sites of active ulceration • Bismuth-containing compounds • Ulcer coating; prevention of further pepsin/HCl-induced damage; binding of pepsin; and stimulation of PGs, bicarbonate, and mucous secretion • Prostaglandin Analogues • Enhancement of mucosal defense and repair • Eg. Misoprostol Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

28. THERAPY FOR H. pylori • Eradication of H. pylori is the primary goal

29. Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.