Contents
Discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin.
Etiology
Helicobacter pylori infection:
Gram-negative, motile spiral rod found in 90% of duodenal ulcers and 70% to 90% of gastric ulcers

Non-steroidal anti-inflammatory drugs (NSAIDs):
#2 M/C cause of PUD. The secretion of prostaglandin normally protects the gastric mucosa. NSAIDs block prostaglandin synthesis by inhibiting COX-1 enzyme resulting in a decrease in gastric mucus and bicarbonate production and a decrease in mucosal blood flow.

Hypersecretory environments:
Multiple gastroduodenal, jejunal, or esophageal ulcers
- Zollinger Ellison syndrome
- Systemic mastocytosis
- Cystic fibrosis
- Hyperparathyroidism
- Antral G cell hyperplasia
Social factors:
- Smoking
- Alcohol (irritate gastric mucosa and induce acidity)
Malignancy:
- Gastric cancer
- Lymphomas
- Lung cancers
Stress:
- After acute illness
- Multiorgan failure
- Ventilator support
- Extensive burns (Curling’s ulcer)
- Head injury (Cushing’s ulcer)
Pathophysiology
Mucosal break of the upper gastrointestinal tract due to acid peptic digestion resulting in ulcer formation which extends beyond the muscularis mucosae into the submucosa.

Modified Johnson Classification system:
Based on location of the ulcer
- Type I (M/C): Lesser curvature; Associated with acid hypersecretion:
- Type II: Prepyloric + duodenal
- Type III: Prepyloric only
- Type IV: Proximal gastroesophageal ulcer
- M/C bleeds, usually from left gastric artery
- Type V: Diffuse occurrence. Associated with the chronic use of NSAIDs (such as ibuprofen)

Presentation
Signs and symptoms of peptic ulcer disease may vary depending upon the location of the disease and age.
Epigastric pain:
Usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer; on the other hand, the pain with a duodenal ulcer tends to occur 2-3 hours after a meal.

Duodenal ulcers:
Duodenal ulcers are more common than gastric ulcers.
- M/C site: 1st part of duodenum
- Anterior duodenal ulcer presentation: Perforation
- Posterior duodenal ulcer presentation: Bleeding (M/C presentation)
- Usually due to gastroduodenal artery
Associated features:
- Loss of appetite
- Weight loss
Alarming features:
- Evidence of overt or occult gastrointestinal bleeding: Hematemesis, melena, anaemia, heme-positive stool
- Symptom of impending perforation: Severe persistent epigastric pain
- Symptom of obstruction: Persistent vomiting
- Malignancy: anorexia, unintended weight loss
Complicatoins
- Upper GI bleeding (15–20%): Manifests as bloody or coffee-ground emesis and/or bloody or tarry stools
- Perforated peptic ulcer (PPU) (2–10%): Manifests as a sudden, severe, piercing epigastric pain followed by rapidly developing symptoms of diffuse peritonitis
- Gastric outlet obstruction (GOO): Results from permanent scarring/edema and inflammation associated with an ulcer located in the pylorus or duodenal bulb manifesting as gastric retention, nausea, and profuse vomiting; some patients develop hypokalemia and alkalosis.
Diagnosis
Non-invasive Helicobacter pylori testing:
- Urea breath test: A solution containing portions of 13C-labeled or 14C-labeled urea are consumed by the patient. The urea is hydrolyzed by bacterial urease to labeled CO2, which is measured in the expired air after 30 minutes.
- Stool antigen test
Esophagogastroduodenoscopy (EGD):
Gold standard
- Sharply demarcated circular mucosal defect or an irregular cavity with infiltrated edges
- Gastric ulcers: Lesser curvature or in prepyloric region
- Duodenal ulcers: Anterior wall of bulb

Differential diagnosis:
Other causes of dyspepsia, nausea and vomiting, and epigastric pain

Management
Medical management:

- Triple therapy: Proton pump inhibitor (PPI) + clarithromycin + amoxicillin/metronidazole (7-14 days)
- PPIs work synergistically with antibiotics to eradicate H. pylori
- Due to increasing antibiotic resistance, the efficacy of triple therapy has fallen below 70% in many countries.
- Bismuth-containing quadruple therapy (for clarithromycin resistance):
- PPI + bismuth + tetracycline + nitroimidazole (metronidazole/tinidazole) for 14 days
or
PPI + clarithromycin + amoxicillin + nitroimidazole
- PPI + bismuth + tetracycline + nitroimidazole (metronidazole/tinidazole) for 14 days
Surgical management:
Indicated if the patient is unresponsive to medical treatment, noncompliant, or at high risk of complications
- Duodenal ulcers:
- Highly selective vagotomy or truncal vagotomy with antrectomy
- Pyloric stenosis:
- Truncal vagotomy + pyloroplasty or vagotomy + antrectomy
- Gastric ulcers:
- Gastric body: Partial gastrectomy + gastroduodenal anastomosis without vagotomy
- Prepyloric region or gastric + duodenal ulcers: Vagotomy + antrectomy
- Subcardial region: Partial gastrectomy including pyloric region
Complications of vagotomy & gastric reconstruction:
Highly selective vagotomy has least amount of complications but the highest recurrence rate, whereas truncal vagotomy + antrectomy has the highest reduction in acid secretion with the most vagal complications
- Nutritional complications: Iron deficiency (M/C complication overall), vitamin B12, calcium deficiency
- Internal hernia: Stemmer’s hernia, Peterson’s hernia
- Dumping syndrome (postgastric surgery syndrome)
Summary:
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