The document discusses peptic ulcer disease (PUD), which refers to erosion of the gastrointestinal mucosa exposed to acid and pepsin. PUD is most often caused by Helicobacter pylori infection, which impairs the GI tract's protective mechanisms. Other causes include stress, injury to mucus-producing cells, excess acid production, and chronic NSAID use. Symptoms vary by location but can include abdominal pain, nausea, and vomiting blood. Diagnosis involves tests to detect H. pylori such as a urea breath test, and endoscopy may be used. Treatment focuses on eliminating H. pylori using antibiotic combinations, and reducing acid with proton pump inhibitors, H2 blockers, or

1. Pratik Rahate

2. Introduction
 The term ‘peptic ulcer’ describes a condition in which there is a
discontinuity in the entire thickness of the gastric or duodenal mucosa that
persists as a result of acid and pepsin in the gastric juice.
 Oesophageal ulceration due to acid reflux is generally classified under
GORD. This definition excludes carcinoma and lymphoma, which may
also cause gastric ulceration, and also excludes other rare causes of
gastric and duodenal ulceration such as Crohn's disease, viral
infections and amyloidosis. About 10% of the population in developed
countries is likely to be affected at some time by peptic ulcer, with the
prevalence for active ulcer disease being about 1% at any particular
point in time.
 Peptic ulcer disease often presents to clinicians as dyspepsia. However,
not all patients with dyspepsia have peptic ulcer disease.

3. Epidemiology
 The incidence of duodenal ulcer is now declining, which follows the decline
in H. pylori infection. However, hospital admission rates for gastro-
intestinal bleeding associated with gastric and duodenal ulcers are rising,
especially in older patients.
 This is probably a consequence of increased prescriptions for low-dose
aspirin, NSAIDs, antiplatelets, anticoagulants and selective serotonin
reuptake inhibitors (SSRI).
 Infection by H. pylori, a spiral bacterium of the stomach, remains an
important epidemiological factor in causing peptic ulcer.
 Most H. pylori infections are acquired by oral–oral and oral–faecal
transmission. The most important risk factors for H. pylori infection are low
social class, overcrowding and home environment during childhood, for
example, bed sharing.

4. Aetology
 Aetology of peptic ulcer disease is multifactorial.
• 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.
• Chronic use of NSAIDs • Smocking • Alcohol and diet • Hypercalcemia (↑gastric secretion)
• Excess acid production in the stomach.
The old hypothesis that ulceration is caused simply by hyperacidity is not tenable. About 70% of gastric
ulcers and 50% of duodenal ulcers are not associated with abnormally high acid production.
• Genetic factor: The lifetime prevalence of developing ulcer disease in first-degree relatives of ulcer
patients is about three times greater than the general population. 20-50% of duodenal ulcer reported a
positive family history.
• Ulcers are also more common in blood group O subjects and in those who do not secrete blood group
antibodies into gastric secretions.

5. Classification of peptic ulcer
 Peptic ulcers classified based on region or location of illness
 Stomach (called gastric ulcer)
 Duodenum (called duodenal ulcer)
 Esophagus (called Esophageal ulcer)
 Meckel's Diverticulum (called Meckel's Diverticulum ulcer)

6. 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.
 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%)

7. Symptoms of peptic ulcer
 Symptoms of peptic ulcer very with location of the ulcer and the patient
age.
 Abdominal discomfort
 Pain or nausea (pain is located in the epogastrium; not radiate) Waterbrash
 Waterbrash
 Loss of appetite and weight loss
 Hematemesis (vomiting of blood) Rarely, ulcer lead to a gastric or duodenal
perforation. Hematemesis

8. Normal
Esophagus & Stomach

9. Peptic ulcer disease

10. 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:

11.  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
Duodenal Ulcer Vs. Gastric Ulcer

12. • Radiological Diagnosis: Barium x-ray or upper GI series is a
widely used for diagnosis. Barium x-ray is difficult to analysis and
less sensitive and accurate.
• Laboratory test:
– Noninvasive urea breath test.
– Patient with refractory or recurrent peptic ulcer may have
underlying H. pylori infection, histopathology investigation may
req.
– Serologic test for detecting H. pylori (levels of IgG and IgA
ELISA test)
– Stool antigen test for non-invasive detecting the presence of H.
pylori.
• Endoscopic diagnosis
Diagnosis of Peptic Ulcer

13. • Antibiotics for eradication of H. pylori, if present
(amoxicillin, clarithromycin)
• Antacids (magnesium hydroxide, aluminum
hydroxide)
• H2 receptor antagonists (ranitidine, cimetidine) •
Proton-pump inhibitors (omeprazole)
• Mucosal protective agents (bismuth, sucralfate)
Drugs for Treatment of Peptic Ulcer Disease

14. Antibiotic medications.
Doctors use combinations of antibiotics to treat H. pylori because one
antibiotic alone isn't always sufficient to kill the organism. Antibiotics
prescribed for treatment of H. pylori include amoxicillin (Amoxil),
clarithromycin (Biaxin) and metronidazole (Flagyl). Combination drugs that
include two antibiotics together with an acid suppressor or cytoprotective
agent (Helidac, Prevpac) have been designed specifically for the treatment
of H. pylori infection.
Acid blockers.
Acid blockers — also called histamine (H-2) blockers — reduce the amount
of hydrochloric acid released into digestive tract, which relieves ulcer pain
and encourages healing. Acid blockers work by keeping histamine from
reaching histamine receptors. Histamine is a substance normally present in
body. When it reacts with histamine receptors, the receptors signal acid-
secreting cells in stomach to release hydrochloric acid. Available by
prescription or over-the-counter (OTC), acid blockers include the
medications ranitidine (Zantac), famotidine (Pepcid), cimetidine (Tagamet)
and nizatidine (Axid).
Antacids.
An antacid may be taken in addition to an acid blocker or in place of one.
Instead of reducing acid secretion, antacids neutralize existing stomach acid
and can provide rapid pain relief.

15. 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
Non-pharmacological Treatment of
Peptic ulcer

16. 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

17.  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.
Reference list