Peptic Ulcer Disease

1. Peptic Ulcer Disease Dr. Wael H. Mansy, MD Assistant Professor College of Pharmacy King Saud University

2. Peptic Ulcer Disease (PUD) Objectives: • Define the following terms: peptic ulcer, gastric ulcer, • Discuss the different etiologic factors of PUD • List the role of H.pylori as the main cause of PUD. • Describe the role of each of these specific cells in the immune response. • Discuss the different diagnostic methods of PUD • Discuss the complications of PUD • Discuss the treatment of PUD

3. Peptic Ulcer Disease (PUD) Definition • Peptic ulcer • refers to erosion of the mucosa lining any portion of the G.I. tract. • It is defined as : A circumscribed ulceration of the gastrointestinal mucosa occurring in areas exposed to acid and pepsin and most often caused by Helicobacter pylori infection. (Uphold & Graham, 2003) • gastric ulcer : the ulcer that occurs in the stomach lining ,some of them may be malignant • duodenal ulcer : most often seen in first portion of duodenum (>95%)

4. Normal Esophagus & Stomach

5. Peptic Ulcer Disease Pathogenesis : Protective factors vs. hostile factors

6. Etiology of PUDA) NormalB) Increased Attack *Hyperacidity *Pepsin. *NSAIDs. C) Weak defense *Helicobacter pylori*Stress, drugs, smoking

7. Peptic ulcer disease

8. Peptic Ulcer Disease Pathogenesis :

9. Peptic Ulcer Disease Causes: • The causes of peptic ulcer disease include the following: • Infection with the bacteria Helicobacter pylorioccurs in 80 to 95% of patients with peptic ulcer disease. H. pylori infection impairs the protective mechanisms of the G.I. tract against low pH and digestive enzymes and leads to ulceration of the mucosa. • Stress — Emotional, trauma, surgical. • Injury or death of mucus-producing cells. • Excess acid production in the stomach. The hormone gastrin stimulates the production of acid in the stomach; therefore, any factors that increase gastrin production will in turn increase the production of stomach acid. • Drugs: Chronic use of aspirins and NSAIDs, or Corticosteroids

10. ETIOLOGIC FACTORS OF PUD

11. No acid No ulcer OLD TESTAMENT No ulcer No HP NEW TESTAMENT Helicobacter pylori: • Most common infection in the world (20%) • 10% of men, 4% women develop PUD • Positive in 70-100% of PUD patients. • H.pylori related disorders: • Chronic gastritis – 90% • Peptic ulcer disease – 95-100% • Gastric carcinoma – 70% • Gastric lymphoma • Reflux Oesophagitis. • Non ulcer dyspepsia

12. Helicobacter pylori: • Gram negative, Spiral bacilli • Spirochetes • Do not invade cells – only mucous • Breakdown urea - ammonia • Break down mucosal defense • Chronic Superficial inflammation

13. Duodenal Ulcer Vs. Gastric Ulcer • duodenal sites are 4x as common as gastric sites • most common in middle age with peak 30-50 years • Male to female ratio—4:1 • Genetic link: 3x more common in 1st degree relatives • more common with blood group O • associated with increased serum pepsinogen • H. pylori infection common,up to 95% • smoking is twice as common • common in late middle age. • incidence increases with age. • Male to female ratio—2:1 • More common with bl. group A • Use of NSAIDs: associated with a three- to four-fold increase in risk of gastric ulcer • Less related to H. pylori than duodenal ulcers : about 80% • 10 - 20% of patients with a gastric ulcer have a concomitant duodenal ulcer

14. Peptic Ulcer Disease Manifestations: Manifestations of peptic ulcer disease: • Episodes of remission and exacerbation • Pain that for duodenal ulcers is often relieved by eating or antacids • G.I. bleeding and possible hemorrhage (20 to 25% of patients) • Perforation of ulcers with significant mortality • Obstruction of G.I. tract

15. PUD - Diagnosis • Endoscopy • Barium meal – contrast x-ray • Biopsy – bacteria & malignancy • H.Pylori: • Endoscopy cytology • Biopsy – Special stains • Culture - difficult • Urease Breath test.

16. Urease Breath Test.

17. PUD – Complications • Bleeding – Chronic, Acute, Massive • Fibrosis, Stricture obstruction – pyloric stenosis. • Perforation – Peritonitis- emergency. • Gastric carcinoma. (not duodenal carcinoma)

18. Non-pharmacological Treatment of Peptic ulcer 1-Avoid spicy food. 2-Avoid xanthin containing beverges. 3-Avoid Alcohol. 4-Avoid Smoking. 5-Avoid heavy meals. 6-Encourage small frequent low caloric meals. 7-Avoid ulcerating drugs e.g. NSAIDs, corticosteroids, xanthines and parasympathomimetics

19. PUD –Treatment Triple therapy for 14 days is considered the ttt of choice. • Proton Pump Inhibitor + clarithromycin and amoxicillin • Omeprazole (Prilosec): 20 mg PO bid for 14 d orLansoprazole (Prevacid): 30 mg PO bid for 14 d orRabeprazole (Aciphex): 20 mg PO bid for 14 d orEsomeprazole (Nexium): 40 mg PO qd for 14 d plusClarithromycin (Biaxin): 500 mg PO bid for 14 andAmoxicillin (Amoxil): 1 g PO bid for 14 d • Can substitute Flagyl 500 mg PO bid for 14 d if allergic to Penicillin. • In the setting of an active ulcer, continue on proton pump inhibitor therapy for additional 2 weeks. • Goal: complete elimination of H. Pylori. Once achieved reinfection rates are low.

20. Reference list • Fantry, G. T. (2005, May 6). Peptic Ulcer Disease. Retrieved September 4th, 2006, from www.emedicine.com/med/topic1776.htm • General Practice Notebook (2006). Peptic Ulcer. Retrieved September 10th, 2006, from www.gpnotebook.co.uk/simplepage.cfm?ID=630849536 • Microbe Wiki (2006, August 16). Heliobacter. Retrieved September 10th, 2006, from www.microbewiki.kenyon.edu/index.php/Helicobacter • Moore, R. A. (1995). Helicobacter pylori and peptic ulcer: A systematic review of effectiveness and an overview of the economic benefits of implementing what is known to be effective. Oxford: Cortecs Limited and Health Technology Evaluation Association. • Pounder, R. (1994). Peptic ulceration. Medicine International, 22:6, 225-30. • Rodney, W.M. (2005, Summer). H. Pylori eradication options for peptic ulcer. Nurse Practitioners Prescribing Reference,12(2), 150. • Uphold, C. R. & Graham, M. V. (2003). Clinical Guidelines in Family Practice (4th ed.). Gainesville, FL: Barmarrae Books, Inc.