Presentation on theme: "Peptic Ulcer Disease Dr. Wael H. Mansy, MD Assistant Professor"— Presentation transcript:
1 Peptic Ulcer Disease Dr. Wael H. Mansy, MD Assistant Professor College of PharmacyKing Saud University
2 Peptic Ulcer Disease (PUD) Objectives:Define the following terms: peptic ulcer, gastric ulcer,Discuss the different etiologic factors of PUDList 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 PUDDiscuss the complications of PUDDiscuss the treatment of PUD
3 Peptic Ulcer Disease (PUD) DefinitionPeptic ulcerrefers 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 malignantduodenal ulcer : most often seen in first portion of duodenum (>95%)
9 Peptic Ulcer Disease Causes: 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
11 Helicobacter pylori: No acid No ulcer No HP No ulcer Most common infection in the world (20%)10% of men, 4% women develop PUDPositive in % of PUD patients.H.pylori related disorders:Chronic gastritis – 90%Peptic ulcer disease – %Gastric carcinoma – 70%Gastric lymphomaReflux Oesophagitis.Non ulcer dyspepsiaNo acidNo ulcerOLD TESTAMENTNo HPNo ulcerNEW TESTAMENT
12 Helicobacter pylori: Gram negative, Spiral bacilli Spirochetes Do not invade cells – only mucousBreakdown urea - ammoniaBreak down mucosal defenseChronic Superficial inflammation
13 Duodenal Ulcer Vs. Gastric Ulcer duodenal sites are 4x as common as gastric sitesmost common in middle age with peak yearsMale to female ratio—4:1Genetic link: 3x more common in 1st degree relativesmore common with blood group Oassociated with increased serum pepsinogenH. pylori infection common,up to 95%smoking is twice as commoncommon in late middle age.incidence increases with age.Male to female ratio—2:1More common with bl. group AUse of NSAIDs: associated with a three- to four-fold increase in risk of gastric ulcerLess related to H. pylori than duodenal ulcers : about 80%% 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
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 –TreatmentTriple therapy for 14 days is considered the ttt of choice.Proton Pump Inhibitor + clarithromycin and amoxicillinOmeprazole (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 dCan 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 listFantry, G. T. (2005, May 6). Peptic Ulcer Disease. Retrieved September 4th, 2006, fromGeneral Practice Notebook (2006). Peptic Ulcer. Retrieved September 10th, 2006, fromMicrobe Wiki (2006, August 16). Heliobacter. Retrieved September 10th, 2006, fromMoore, 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.