This document discusses the pathophysiology of peptic ulcers. It notes that peptic ulcers are lesions in the stomach or duodenum caused by stomach acid and pepsin. Risk factors include H. pylori infection in 80-95% of cases, as well as stress, NSAIDs, alcohol, and diet. Symptoms include abdominal pain, nausea, weight loss, vomiting blood, or perforation of the ulcer. Treatment involves eradicating H. pylori with antibiotics if present, and using antacids, H2 blockers, or PPIs to reduce stomach acid and promote healing.

1. By - Abhijit A. Gaikwad
Subject : Pathophisiology
Roll No 220 (SYPD)

2.  Peptic Ulcer
1. Peptic Ulcer is a lesion in the lining (mucosa) of the digestive
tract, typically in the stomach or duodenum, caused by the
digestive action of pepsin and stomach acid.
2. Lesion may subsequently occur into the lamina propria and
submucosa to cause bleeding. – Most of peptic ulcer occur
either in the duodenum, or in the stomach – Ulcer may also occur
in the lower esophagus due to reflexing of gastric content –
Rarely in certain areas of the

4.  Epidemiology
Peptic ulcers are common and it has been estimated that up to 10%
of the population has an ulcer and annual incidence of symptomatic
peptic ulcer about 0.3%
• Duodenal ulcers are four times as common as gastric ulcers and
occur mainly in the duodenal cap
• Gastric ulcers occurs mostly in the lesser curvature of the stomach.
These are benign, some time develop as a tumors (5%)
• Gastric malignancy is common in Japan, Chile, Finland and Iceland
than other world countries (because of environmental and diet
factor).

5.  Etiology
Etiology 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 , trauma .
 Injury or death of mucus-producing cells
 Chronic use of NSAIDs
 Alcohol and diet
 Hypercalcemia (↑gastric secretion)

6.  Signs And Symptoms
1. Symptoms of peptic ulcer with location of the ulcer and the patient age
2. Abdominal discomfort
3. Pain or nausea .
4. Loss of appetite and weight loss
5. Hematemesis (vomiting of blood) Rarely, ulcer lead to a gastric or
duodenal perforation.
6. Manifestations of peptic ulcer diseases
7. Episodes of remission and exacerbation
8. Pain that for duodenal ulcers is often relieved by eating or antacids
9. G.I. bleeding and possible hemorrhage (20 to 25% of patients)
10. Perforation of ulcers with significant mortality
11. Obstruction of G.I. tract

7.  Pathophisiology
1. Duodenal ulcer:
1. Due to increased gastric juice secretion + Rapid emptying of stomach
into duodenum
* Causes:
1. Increased vagus nerve stimulation.
2. Increased number of parietal cell (as in tall thin patient).
3. Increase hormonal stimulation (Z.E syndrome) Gastrinoma Gastrin.
4. Increase the responsiveness of parietal cells to secretory stimuli.
5. psychosomatic stimuli.
2. Gastric ulcer.
1. Due to decreased mucosal defense mechanisms or increasing damaging
forces causes PUD.

8.  Classification Of Peptic Ulcer
Gastric ulcer is further classified into 3 subtypes
depending upon their location:
1. Type 1: Ulcer present at the body of stomach without
involving duodenum, pylorus or prepyloric region and not
associated with hypersecretion of gastric acid
2. Type 2: Ulcer present at the body of stomach combined
with duodenum and associated with gastric acid
hypersecretion
3. Type 3: Ulcer close to pylorus and associated with gastric
acid hypersecretion

9.  Diagnosis
1. 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
2. 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.

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

11.  Abnormalities of GI
1. Anorexia – Loss of appetite
2. Hematemesis – Vomiting blood (could be red or altered “coffee
ground”)
3. Melaena – Passing of black tarry, offensive stool (usually due to
upper GI bleeding)
4. Hematochezia – Passing blood through rectum (PR bleeding)
5. Gastritis – Inflammation of the gastric mucosa
6. A peptic ulcer is an abnormal area of mucosa that has been
damaged by the pepsin and hydrochloric acid of gastric juice,
with consequent inflammation of the underlying and surrounding
tissue.

12.  Abnormalities of GI
7. Erosion may subsequently occur into the lamina
propria and submucosa to cause bleeding.
8. Most of peptic ulcer occur either in the duodenum, or
in the stomach.
9. Ulcer may also occur in the lower oesophagus due to
reflexing of gastric content.
10. Rarely in certain areas of the small intestine

13.  Management
Management of peptic ulcer The
objectives of management are to:
1. relieve pain and discomfort
2. accelerate healing
3. prevent recurrence and complications