Peptic Ulcer Disease

Dr. Wael H. Mansy, MD Assistant Professor College of Pharmacy King Saud University 2009

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

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%)

Normal
Esophagus & Stomach

Peptic Ulcer Disease Pathogenesis :

Protective factors vs. hostile factors

Etiology of PUD A) Normal B) Increased Attack *Hyperacidity

*Pepsin. *NSAIDs.

C) Weak defense *Helicobacter pylori *Stress, drugs, smoking

Peptic ulcer disease

Peptic Ulcer Disease

Pathogenesis :

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

ETIOLOGIC FACTORS OF PUD

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%

No acid No ulcer
OLD TESTAMENT

Peptic ulcer disease 95-100%

Gastric carcinoma 70% Gastric lymphoma

Reflux Oesophagitis.
Non ulcer dyspepsia

No HP

No ulcer

NEW TESTAMENT

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

Duodenal Ulcer Vs. Gastric Ulcer

duodenal sites are 4x as common as common in late middle age. gastric sites

incidence increases with age.

most common in middle age with Male to female ratio2:1 peak 30-50 years Male to female ratio4:1 More common with bl. group A

Use of NSAIDs: associated with a

Genetic link: 3x more common in 1st three- to four-fold increase in risk of degree relatives more common with blood group O associated pepsinogen H. pylori infection common,up to 95% smoking is twice as common with increased gastric ulcer

Less related to H. pylori than

serum duodenal ulcers : about 80% 10 - 20% of patients with a gastric

ulcer have a concomitant duodenal

ulcer

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

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

Urease Breath Test.

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

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

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 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.

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.