This document provides an overview of peptic ulcer disease. It defines peptic ulcers as painful open sores or ulcers in the lining of the esophagus, stomach, or duodenum, which are most often caused by infection with Helicobacter pylori bacteria. The document discusses the etiology, risk factors, signs and symptoms, complications, diagnosis, and treatment of peptic ulcers. Treatment options include antibiotics to treat H. pylori infections, acid blockers to reduce stomach acid production, antacids to neutralize acid, and lifestyle modifications to avoid exacerbating factors. Hospitalization may be required for severe, unresponsive cases or if complications like hemorrhaging occur.

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Vitebsk State Order of Peoples’ Friendship Medical University
Department of Polyclinic Therapy
Report
Theme: Peptic Ulcer Disease
Prepared by Student:
Dinoosh De Livera
Group 49, 5th Course
Overseas Students Training Faculty
Vitebsk, VSMU
2016

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Peptic Ulcer Disease
Introduction:
Peptic ulcer disease is a formation of painful open sores or ulcers in the inside lining of the
esophagus (esophageal ulcers), stomach (gastric ulcers) or first part of the small intestine
called duodenum (duodenal ulcers). Most of the peptic ulcers are caused by infection with a
type of bacteria called Helicobacter Pylori (H Pylori).
Definition:
General chronic relapsing disease characterized by seasonal exacerbations with ulceration of
stomach wall and duodenum.
Ulcer:- Disruption of the mucosal integrity of stomach / duodenum leading to local defect /
extravasation due to active inflammation.
Etiology:
Peptic ulcers occur due to the erosion of inner surface of esophagus, stomach or duodenum. A
bacterial infection of Helicobacter Pylori (H Pylori) which usually lives in the mucus layer of
digestive tract may causeinflammation ofinnerlayer producingulcers.Longtermuse ofcertain
anti inflammatory drugs such as Aspirin, Ibuprofen etc can leads to ulcer formation.
The Main Etiological Agents are:
 Helicobacter pylori (95% - duodenal ulcers, 70% - stomach ulcers)
 NSAIDS, Steroids, Stress, Burns, Hyperparathyroidism
Risk Factors:
• Infection of H Pylori bacterium
• Long term intake of NSAIDs such as Aspirin, Ibuprofen etc
• Family history of peptic ulcers
• Smoking
• Alcohol consumptions
• Age 50 years or older
PredisposingFactors:
 Hereditary (Blood type O, high pepsinogen)
 Environmental (Irregular meals, Alcoholism, Smoking)

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Classification:
According to Localization:
1. Gastric (Cardiac, Subcardiac, Lesser & Greater Curvature, Corpus, Pylorus, Prepylorus)
2. Duodenal (Bulbar, Postbulbar)
3. Gastroduodenal
According to Stage:
1. Exacerbation
2. Remission
 Complete
 Incomplete
According to Complication:
1. Hemorrhage
2. Perforation
3. Penetration
4. Malignization
5. Pyloric stenosis
6. Reactive gastritis
7. Reactive pancreatitis
8. Perivisceritis
History:
 Seasonal Pain (Spring & Summer)
 Irregular food Intake
 Past family history
 Smoking
 Stress
MainSigns& Symptoms:
• Burning, Gnawing, Hunger-like pain in the epigastrium relieved by food and antacids
• Bloating and abdominal fullness
• Heartburn
• Nausea and vomiting
• Dark or black colored stool
• Unexplained weight loss
• Loss of appetite
• Vomiting of blood

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Gastric ulcer- “Early pain” – Epigastrium above umbilicus, Inconsistent pattern, 1-2 hours after
meal, eating may increase or decrease pain
Duodenal/Pre-pyloric- “Late pain” – Epigastrium, Right of median line (Right hypochondrium),
Consistent Pain Pattern, Absent when waking, relieved by food, recurs 2-4 hours after meals,
pain awakes patient at night, absent when waking, appears midmorning (hunger pain)
Cardiac- Xiphoid process
Vomiting- At height/max pain – relieves it, acid taste & smell
Heartburn – Periodic / seasonal, during exacerbation
Other symptoms: Weight loss, Eructation, Regurgitation, Salivation, Increased Appetite,
Citophobia, Hematemesis, Melena, Burping, Hiccuping.
PhysicalExamination
Wasting, Pallid skin & mucosa (hemorrhage), Brown abdominal pigmentation, Mendel’s test,
Vasilenko symptom (Splashing sound in the right medial line), hypersecretion between meals.
Complications
1. Perforation: Perforation caused by the erosion of wall of the gastrointestinal tract, is a
serious complication which may leads to acute peritonitis. This hole in digestive tract
may leads to spillage of gastric or intestinal content in to abdominal cavity.
2. Obstruction of Gastric outlet due to pyloric stenosis: Due to the scarring and swelling
around pyloric canal the gastric outlet becomes narrow and obstructed. Patient will
experience severe vomiting.
3. Stomach cancer (Malignization): peptic ulcers if left untreated may leads to stomach
cancer. Gastrointestinal bleeding: bleeding from the ulcers is the most common
complication. If large amount of blood loss occurs it can be a life threatening situation.
4. Penetration
5. Reactivegastritis
6. Reactivepancreatitis
7. Perivisceritis

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Diagnosis
1. CBC – Anemia
2. Occult blood in faeces – Positive
3. X ray ofupperdigestivetract (Double contrast barium xray): In this procedure you have
to swallow a contrast liquid and the x-ray technician visualizes the upper digestive tract
making an ulcer more visible.
4. Endoscopy (Gastroduodenoscopy): In this procedure doctor passes a hollow tube
equipped with a lens through your mouth into your esophagus, stomach and small
intestine. This procedure helps in detecting ulcers and small tissue samples can also be
removed for further examination in lab.
5. Gastric secretory function test
6. Tests to identify Helicobacter Pylori (H Pylori):
• Urea breath test
• Culture taken from endoscopic biopsy
• Measurement of antibody levels in blood
• Stool antigen test
• Histological examinations
Treatment:
Conservative Treatment:
1. Muscarinic antagonists (Atropine)
2. PG receptor agonists (Misoprostol)
3. Sucralfate, Bismuth subsalicylate
4. Antacids (Aluminium hydroxide, Magnesium hydroxide, Calcium carbonate, Almagel)
5. Proton pump inhibitors (Omeprazole, Lanoprazole)
6. H2 receptor antagonists (Cimetidine, Rnitidine, Famotidine, Nizatidine)
Lifestyle modifications: Changes or elimination of substances causing ulcer can help prevent
peptic ulcers such as smoking, drinking alcohol, stress etc.
Antibiotics: Antibiotics are used to treat H Pylori infection. A combination of antibiotics can be
used to kill the bacteria.
Acid blockers: Proton pump inhibitors are the drugs that blocks the production of acid in
stomach thereby prevents ulcer formation. These drugs include Pantoprazole, Omeprazole,
Lansoprazole, Rabeprazole etc.

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Drugs to reduceacid production: Histamine (H-2) blockers reduce the amount of stomach acid
released into your digestive tract thereby reducing ulcer pain and promoting healing. H-2
blockers include Ranitidine, Famotidine, Cimetidine etc.
Antacids to neutralize stomach acid: These drugs neutralize the existing stomach acid content
and can provide instant relief from ulcer pain. It includes sucralfate, misoprostol, bismuth
subsalicylate etc.
Indicationsfor hospitalization:
1. Worsening (no response to/ineffective conservative treatment)
2. Severe form
3. Surgical treatment (Complications)
4. Indication for emergency admission _ hemorrhage