Peptic Ulcer

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

Peptic Ulcer Disease

Objectives:(PUD)
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:

No
acid
No
OLD
TESTAMENT
ulcer

Chronic gastritis 90%

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

Genetic link: 3x more common in 1st a three- to four-fold increase in risk

degree relatives
more common with blood group O

of gastric ulcer
Less related to H. pylori than

associated with increased serum duodenal ulcers : about 80%

pepsinogen

10 - 20% of patients with a

H. pylori infection common,up to 95%

gastric ulcer have a concomitant

smoking is twice as common

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.