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

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Presentation on theme: "Peptic Ulcer Disease Dr. Wael H. Mansy, MD Assistant Professor College of Pharmacy King Saud University."— Presentation transcript:

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

2 Peptic Ulcer Disease (PUD) Objectives: 1.Define the following terms: peptic ulcer, gastric ulcer, 2.Discuss the different etiologic factors of PUD 3.List the role of H.pylori as the main cause of PUD. 4.Describe the role of each of these specific cells in the immune response. 5.Discuss the different diagnostic methods of PUD 6.Discuss the complications of PUD 7.Discuss the treatment of PUD

3 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%) Peptic Ulcer Disease (PUD) Definition

4 Normal Esophagus & Stomach

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

6 A) Normal B) Increased Attack * Hyperacidity Etiology of PUD A) Normal B) Increased Attack * Hyperacidity*Pepsin.*NSAIDs. C) Weak defense * Helicobacter pylori * Stress, drugs, smoking

7 Peptic ulcer disease

8 Peptic Ulcer Disease Pathogenesis :

9 The causes of peptic ulcer disease include the following:  Infection with the bacteria Helicobacter pylori occurs 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 Peptic Ulcer Disease Causes:

10 ETIOLOGIC FACTORS OF PUD

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

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

14 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 Peptic Ulcer Disease Manifestations:

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

16 Urease Breath Test.

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

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 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 or Lansoprazole (Prevacid): 30 mg PO bid for 14 d or Rabeprazole (Aciphex): 20 mg PO bid for 14 d or Esomeprazole (Nexium): 40 mg PO qd for 14 d plus Clarithromycin (Biaxin): 500 mg PO bid for 14 and Amoxicillin (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. PUD –Treatment

20 Reference list  Fantry, G. T. (2005, May 6). Peptic Ulcer Disease. Retrieved September 4th, 2006, from  General Practice Notebook (2006). Peptic Ulcer. Retrieved September 10th, 2006, from  Microbe Wiki (2006, August 16). Heliobacter. Retrieved September 10th, 2006, from  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,  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.


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