Peptic Ulcer

Definition:
Mucosal laceration near acid bearing region of GIT (duodenum + lesser curvature of
stomach)
Site:
Duodenum + stomach + esophagus (in reflux) + jejunum (ZE syndrome) + Meckle’s
Etiology:
- H. Pylori (90% of duodenal + 70% of gastric)
- NSAIDS (30% gastric; inhibit both COX 1+ 2; 1 is imp for mucosal barrier: aspirin
esp)
- Hereditary (runs in families esp due to large partial mass + O blood group + unable to
secrete blood group antigen)
- Smoking (stimulate acid secretion)
- Others (COPD + cirrhosis + chronic renal failure)
- Steroids (high doses) + burns
- Alcohol + diet do not cause ulcers
Pathogenesis:
- Mucosal barrier damaged because of H. Pylori, NSAIDS, smoking, etc > pepsin +
acid affect mucosa
Mechanisms of physiological disruption
•
H. pylori
◦ Gastric ulcers
▪ H. pylori secretes urease → conversion of urea to NH3 → alkalinization of
acidic environment → survival of bacteria in gastric lumen
▪ Bacterial colonization and attachment to epithelial cells → release of cytotoxins
(e.g., cagA toxin) → disruption of the mucosal barrier and damage to underlying
cells
◦ Duodenal ulcers
▪ H. pylori inhibits somatostatin secretion → ↑ gastrin secretion → ↑ H+ secretion
→ excess H+ delivery to the duodenum 
▪ Direct spread of H. pylori to the duodenum → inhibition of duodenal HCO3-
(alkaline) secretion→ acidi cation and insuf cient neutralization of duodenal contents
• NSAIDs
◦ Inhibit COX-1 and COX-2 → decrease in prostaglandin  production → erosion of
the gastric mucosa
◦ Decrease mucosal blood ow (decrease alkalization)
◦ Inhibit mucosal cell proliferation

• Acid hypersecretion: acid hypersecretion (e.g., Zollinger-Ellison syndrome) and

increased gastrin production → ↑ H+ secretion and parietal cell mass → delivery of
excessive acid to the duodenum

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 Clinical Features:
1. Pain
• Site: Epigastrium
• Character: Burning
• Radiation: local (can point with one finger) if to back + inter-scapular + no
response to antacids or anti-ulcer drugs = posterior penetration into pancreas
• Time: gastric = 15-30 mins after eating ; duodenal = 2-3 hours + wakes up at
night
• Periodicity: (relapse in smokers) gastric = 2-3 months ; duodenal = 4-6 months
• Duration: gastric= weeks ; duodenal = 1-2 months
• Food: gastric = pain if eating; duodenal = pain if not eating
• Aggravating: smoking + a lot of coffee & tea + alcohol + eating in gastric
• Relieving: antacids + milk + vomiting in gastric + eating in duodenal
• 70% of patients with peptic ulcers do not experience symptoms
2. Vomiting
• Relives gastric pain ; forced
3. Others:
• Hematemesis due to perforation
• No pain but retrosternal burning + nausea
Complications:
1. Hemorrhage 15-25 % [self limiting]
2. Perforation 2-3% [peritoneal cavity]
3. Penetration [pancreas]
4. Pyloric obstruction [due to edema + spasm or fibrosis]
Investigation:
1. Endoscopy
• Best
• Detects H.
Pylori and malignancy
• All patients with gastric ulcers require initial biopsy + follow-up endoscopy +
biopsy after 6 weeks of therapy to confirm healing
• Malignant: large ulcer + greater curvature + definitive mass + friable + bleeds
easily
2. Barium meal (not often used anymore)
Gastric Duodenal
Site Lesser curvature (antrum) First part

Malignancy Yes Never

Frequency less common Most common
Age Males; 30-35 yo
Causes NSAIDS, bile reflux, H. Pylori H. Pylori, smoking, NSAIDS,
COPD, cirrhosis, chronic renal
failure
Pain With food (15-30 mins) With skipping meals (2-3 hrs after
eating)

Duration Weeks 1-2 months

Period 2-3 months 4-6 months