MBBS Year
1st Year
Subject
What Is Usually Asked
Mechanism and regulation of gastric acid secretion
ReferenceAll Years (1st-Final)All UniversitiesPeptic Ulcer
Peptic Ulcer: Notes, PPT and PYQs for MBBS
A peptic ulcer is a break in the lining of the stomach or duodenum that extends through the muscularis mucosae, caused by the action of acid and pepsin. It is examined in Physiology in 1st Year, Pathology, Microbiology and Pharmacology in 2nd Year, and General Medicine and General Surgery in Final Year.
SME-reviewed. Updated 2026.
Open in GeckoMed for PPT slides and offline notesQuick Summary: What You Need to Know for University Exams
- The two main causes are Helicobacter pylori infection and NSAID use.
- The first part of the duodenum is the most common site; gastric ulcers are most common along the lesser curvature.
- Duodenal ulcer pain is typically relieved by food, while gastric ulcer pain is often worsened by food.
- Upper GI endoscopy is the investigation of choice; gastric ulcers must be biopsied to exclude cancer.
- The urea breath test is the preferred non-invasive test for H. pylori, including to confirm eradication.
- Treatment uses proton pump inhibitors (PPIs) and H. pylori eradication therapy.
- Main complications: bleeding, perforation, gastric outlet obstruction and penetration.
Peptic Ulcer Across MBBS Subjects
| MBBS Year | Subject | What Is Usually Asked |
|---|---|---|
| 1st Year | Physiology | Mechanism and regulation of gastric acid secretion |
| 2nd Year | Pathology | Aetiopathogenesis, morphology, complications, benign versus malignant ulcer |
| 2nd Year | Microbiology | Helicobacter pylori, laboratory diagnosis |
| 2nd Year | Pharmacology | PPIs, H2 blockers, H. pylori regimens |
| Final Year | General Medicine | Clinical features, diagnosis, medical management, upper GI bleeding |
| Final Year | General Surgery | Perforation, gastric outlet obstruction, surgical options |
MBBS Year
2nd Year
Subject
What Is Usually Asked
Aetiopathogenesis, morphology, complications, benign versus malignant ulcer
MBBS Year
2nd Year
Subject
What Is Usually Asked
Helicobacter pylori, laboratory diagnosis
MBBS Year
2nd Year
Subject
What Is Usually Asked
PPIs, H2 blockers, H. pylori regimens
MBBS Year
Final Year
Subject
What Is Usually Asked
Clinical features, diagnosis, medical management, upper GI bleeding
MBBS Year
Final Year
Subject
What Is Usually Asked
Perforation, gastric outlet obstruction, surgical options
Definition and Classification
Definition: A peptic ulcer is a breach in the mucosa of the stomach or duodenum (or other acid-exposed sites) that extends through the muscularis mucosae into the submucosa or deeper, caused by acid-pepsin digestion. A defect limited to the mucosa is called an erosion.
Sites of Peptic Ulcer
- First part of the duodenum (most common)
- Stomach, especially the lesser curvature near the junction of the body and antrum
- Lower oesophagus (with reflux)
- Margin of a gastrojejunal anastomosis (stomal ulcer)
- Meckel's diverticulum containing ectopic gastric mucosa
- Jejunum, in Zollinger-Ellison syndrome
Duodenal Versus Gastric Ulcer
| Feature | Duodenal Ulcer | Gastric Ulcer |
|---|---|---|
| Relative frequency | More common | Less common |
| Pain and food | Relieved by food; pain 2 to 3 hours after meals | Often worsened by food |
| Night pain | Common, wakes the patient | Less common |
| Appetite and weight | Appetite maintained, weight may increase | Fear of eating, weight loss |
| Acid secretion | Often increased | Normal or reduced |
| Association with blood group | Blood group O | Less marked |
| Malignant potential | Virtually none | Must be biopsied to exclude cancer |
Feature
Relative frequency
Duodenal Ulcer
More common
Gastric Ulcer
Less common
Feature
Pain and food
Duodenal Ulcer
Relieved by food; pain 2 to 3 hours after meals
Gastric Ulcer
Often worsened by food
Feature
Night pain
Duodenal Ulcer
Common, wakes the patient
Gastric Ulcer
Less common
Feature
Appetite and weight
Duodenal Ulcer
Appetite maintained, weight may increase
Gastric Ulcer
Fear of eating, weight loss
Feature
Acid secretion
Duodenal Ulcer
Often increased
Gastric Ulcer
Normal or reduced
Feature
Association with blood group
Duodenal Ulcer
Blood group O
Gastric Ulcer
Less marked
Feature
Malignant potential
Duodenal Ulcer
Virtually none
Gastric Ulcer
Must be biopsied to exclude cancer
Aetiology (Causes and Risk Factors)
| Cause | Mechanism or Notes |
|---|---|
| Helicobacter pylori | Most common cause; damages mucosal defences and alters acid secretion |
| NSAIDs and aspirin | Inhibit cyclooxygenase-1 and reduce protective prostaglandins |
| Zollinger-Ellison syndrome | Gastrin-secreting tumour (gastrinoma) causes very high acid output and multiple, recurrent or unusual-site ulcers |
| Stress ulcers | Severe illness; Curling's ulcer after major burns, Cushing's ulcer after head injury or raised intracranial pressure |
| Smoking | Impairs healing and increases recurrence |
| Other factors | Corticosteroids combined with NSAIDs, hypercalcaemia, genetic factors |
Cause
Helicobacter pylori
Mechanism or Notes
Most common cause; damages mucosal defences and alters acid secretion
Cause
NSAIDs and aspirin
Mechanism or Notes
Inhibit cyclooxygenase-1 and reduce protective prostaglandins
Cause
Zollinger-Ellison syndrome
Mechanism or Notes
Gastrin-secreting tumour (gastrinoma) causes very high acid output and multiple, recurrent or unusual-site ulcers
Cause
Stress ulcers
Mechanism or Notes
Severe illness; Curling's ulcer after major burns, Cushing's ulcer after head injury or raised intracranial pressure
Cause
Smoking
Mechanism or Notes
Impairs healing and increases recurrence
Cause
Other factors
Mechanism or Notes
Corticosteroids combined with NSAIDs, hypercalcaemia, genetic factors
Virulence Factors of H. pylori
| Factor | Role |
|---|---|
| Urease | Produces ammonia, which neutralises acid around the organism |
| Flagella | Allow movement through mucus |
| Adhesins | Attachment to gastric epithelium |
| CagA and VacA | Increase inflammation and epithelial damage |
Factor
Urease
Role
Produces ammonia, which neutralises acid around the organism
Factor
Flagella
Role
Allow movement through mucus
Factor
Adhesins
Role
Attachment to gastric epithelium
Factor
CagA and VacA
Role
Increase inflammation and epithelial damage
Pathophysiology
Peptic ulcer results from an imbalance between aggressive and defensive factors.
| Aggressive Factors | Defensive Factors |
|---|---|
| Hydrochloric acid | Mucus-bicarbonate barrier |
| Pepsin | Prostaglandins |
| H. pylori | Mucosal blood flow |
| NSAIDs | Rapid epithelial renewal |
| Bile reflux, smoking | Tight junctions between epithelial cells |
Aggressive Factors
Hydrochloric acid
Defensive Factors
Mucus-bicarbonate barrier
Aggressive Factors
Pepsin
Defensive Factors
Prostaglandins
Aggressive Factors
H. pylori
Defensive Factors
Mucosal blood flow
Aggressive Factors
NSAIDs
Defensive Factors
Rapid epithelial renewal
Aggressive Factors
Bile reflux, smoking
Defensive Factors
Tight junctions between epithelial cells
Flowchart
- H. pylori infection or NSAID use weakens mucosal defence
- Acid and pepsin reach and injure the underlying mucosa
- Inflammation and necrosis deepen the defect
- The defect extends through the muscularis mucosae, forming an ulcer
- Repeated cycles of injury and repair produce fibrosis and scarring
(Examiner may ask you to draw the aggressive versus defensive factors diagram.)
Morphology
Gross appearance of a benign peptic ulcer:
- Usually single, round to oval, sharply punched out
- Straight walls with flat, level margins
- Clean, smooth base
- Mucosal folds radiate towards the ulcer
Microscopy (four zones from surface to depth):
- Necrotic fibrinoid debris
- Non-specific inflammatory infiltrate, mainly neutrophils
- Granulation tissue
- Fibrous scar
| Feature | Benign Gastric Ulcer | Malignant Ulcer |
|---|---|---|
| Margins | Flat, punched out | Heaped up, irregular |
| Base | Clean, smooth | Irregular, necrotic |
| Mucosal folds | Radiate to the ulcer edge | Interrupted or nodular |
Feature
Margins
Benign Gastric Ulcer
Flat, punched out
Malignant Ulcer
Heaped up, irregular
Feature
Base
Benign Gastric Ulcer
Clean, smooth
Malignant Ulcer
Irregular, necrotic
Feature
Mucosal folds
Benign Gastric Ulcer
Radiate to the ulcer edge
Malignant Ulcer
Interrupted or nodular
Clinical Features
Symptoms:
- Epigastric burning or gnawing pain
- Periodicity: episodes of pain for weeks with symptom-free intervals
- Nausea, bloating and water brash
- Heartburn
- Vomiting, especially with gastric outlet obstruction
Alarm features (need urgent endoscopy):
- Older age at new onset of symptoms
- Unexplained weight loss
- Anaemia or gastrointestinal bleeding (haematemesis, melaena)
- Persistent vomiting
- Difficulty swallowing
- Palpable abdominal mass
Signs: Often none apart from epigastric tenderness. Signs of complications may be present, such as pallor, a rigid abdomen in perforation, or a succussion splash in gastric outlet obstruction.
Diagnosis
| Investigation | Key Points |
|---|---|
| Upper GI endoscopy | Investigation of choice; allows biopsy and treatment of bleeding |
| Biopsy | All gastric ulcers are biopsied to exclude malignancy; also used for H. pylori testing |
| Rapid urease test | Invasive test on a biopsy sample for H. pylori |
| Histology and culture | Invasive tests for H. pylori; culture allows sensitivity testing |
| Urea breath test | Preferred non-invasive test for diagnosis and for confirming eradication |
| Stool antigen test | Non-invasive; useful for diagnosis and confirming eradication |
| Serology | Shows past or present exposure; not useful to confirm eradication |
| Serum gastrin | Suspected Zollinger-Ellison syndrome |
| Erect chest X-ray | Gas under the diaphragm in perforation |
| Complete blood count | Anaemia from chronic blood loss |
Investigation
Upper GI endoscopy
Key Points
Investigation of choice; allows biopsy and treatment of bleeding
Investigation
Biopsy
Key Points
All gastric ulcers are biopsied to exclude malignancy; also used for H. pylori testing
Investigation
Rapid urease test
Key Points
Invasive test on a biopsy sample for H. pylori
Investigation
Histology and culture
Key Points
Invasive tests for H. pylori; culture allows sensitivity testing
Investigation
Urea breath test
Key Points
Preferred non-invasive test for diagnosis and for confirming eradication
Investigation
Stool antigen test
Key Points
Non-invasive; useful for diagnosis and confirming eradication
Investigation
Serology
Key Points
Shows past or present exposure; not useful to confirm eradication
Investigation
Serum gastrin
Key Points
Suspected Zollinger-Ellison syndrome
Investigation
Erect chest X-ray
Key Points
Gas under the diaphragm in perforation
Investigation
Complete blood count
Key Points
Anaemia from chronic blood loss
Management
General Measures
- Stop NSAIDs where possible, or use the lowest effective dose with PPI protection
- Stop smoking
- Limit alcohol
- Treat H. pylori if present
Drugs Used in Peptic Ulcer Disease
| Drug Class | Examples | Mechanism |
|---|---|---|
| Proton pump inhibitors | Omeprazole, pantoprazole, esomeprazole | Irreversibly inhibit the H+/K+ ATPase (proton pump) in parietal cells |
| H2 receptor antagonists | Famotidine | Block histamine H2 receptors on parietal cells |
| Antacids | Magnesium and aluminium hydroxide | Neutralise acid; symptom relief |
| Mucosal protectives | Sucralfate, bismuth compounds | Form a protective coating over the ulcer |
| Prostaglandin analogue | Misoprostol | Replaces protective prostaglandins; prevents NSAID ulcers; contraindicated in pregnancy |
Drug Class
Proton pump inhibitors
Examples
Omeprazole, pantoprazole, esomeprazole
Mechanism
Irreversibly inhibit the H+/K+ ATPase (proton pump) in parietal cells
Drug Class
H2 receptor antagonists
Examples
Famotidine
Mechanism
Block histamine H2 receptors on parietal cells
Drug Class
Antacids
Examples
Magnesium and aluminium hydroxide
Mechanism
Neutralise acid; symptom relief
Drug Class
Mucosal protectives
Examples
Sucralfate, bismuth compounds
Mechanism
Form a protective coating over the ulcer
Drug Class
Prostaglandin analogue
Examples
Misoprostol
Mechanism
Replaces protective prostaglandins; prevents NSAID ulcers; contraindicated in pregnancy
H. pylori Eradication Regimens
| Regimen | Components |
|---|---|
| Triple therapy | PPI + clarithromycin + amoxicillin (or metronidazole) |
| Bismuth quadruple therapy | PPI + bismuth + tetracycline + metronidazole |
Regimen
Triple therapy
Components
PPI + clarithromycin + amoxicillin (or metronidazole)
Regimen
Bismuth quadruple therapy
Components
PPI + bismuth + tetracycline + metronidazole
Regimens are usually given for 14 days. Eradication should be confirmed with a urea breath test or stool antigen test after completing treatment.
Management of Complications
| Complication | Key Management Points |
|---|---|
| Bleeding | Resuscitation, intravenous PPI, endoscopic haemostasis; surgery or angiographic embolisation if endoscopy fails |
| Perforation | Resuscitation, nil by mouth, nasogastric aspiration, antibiotics, and surgical closure, commonly with an omental patch (Graham's patch) |
| Gastric outlet obstruction | Correct fluid and electrolyte imbalance, nasogastric decompression, then endoscopic dilatation or surgery |
Complication
Bleeding
Key Management Points
Resuscitation, intravenous PPI, endoscopic haemostasis; surgery or angiographic embolisation if endoscopy fails
Complication
Perforation
Key Management Points
Resuscitation, nil by mouth, nasogastric aspiration, antibiotics, and surgical closure, commonly with an omental patch (Graham's patch)
Complication
Gastric outlet obstruction
Key Management Points
Correct fluid and electrolyte imbalance, nasogastric decompression, then endoscopic dilatation or surgery
Surgical procedures (now mainly for complications): Truncal vagotomy with a drainage procedure, highly selective vagotomy, and partial gastrectomy (Billroth I and Billroth II reconstructions).
Forrest Classification of Bleeding Ulcers (Endoscopic)
| Class | Finding |
|---|---|
| Ia | Spurting bleeding |
| Ib | Oozing bleeding |
| IIa | Non-bleeding visible vessel |
| IIb | Adherent clot |
| IIc | Flat pigmented spot |
| III | Clean ulcer base |
Class
Ia
Finding
Spurting bleeding
Class
Ib
Finding
Oozing bleeding
Class
IIa
Finding
Non-bleeding visible vessel
Class
IIb
Finding
Adherent clot
Class
IIc
Finding
Flat pigmented spot
Class
III
Finding
Clean ulcer base
Complications
| Complication | Key Points |
|---|---|
| Haemorrhage | Most common complication; a posterior duodenal ulcer can erode the gastroduodenal artery |
| Perforation | Usually an anterior duodenal ulcer; sudden severe abdominal pain, board-like rigidity, gas under the diaphragm |
| Gastric outlet obstruction | From scarring near the pylorus; projectile vomiting of stale food, visible gastric peristalsis, succussion splash; hypochloraemic hypokalaemic metabolic alkalosis with paradoxical aciduria |
| Penetration | Into the pancreas or other adjacent organs, causing persistent back pain |
| Malignant change | Relevant to gastric ulcers, which is why they are biopsied |
Complication
Haemorrhage
Key Points
Most common complication; a posterior duodenal ulcer can erode the gastroduodenal artery
Complication
Perforation
Key Points
Usually an anterior duodenal ulcer; sudden severe abdominal pain, board-like rigidity, gas under the diaphragm
Complication
Gastric outlet obstruction
Key Points
From scarring near the pylorus; projectile vomiting of stale food, visible gastric peristalsis, succussion splash; hypochloraemic hypokalaemic metabolic alkalosis with paradoxical aciduria
Complication
Penetration
Key Points
Into the pancreas or other adjacent organs, causing persistent back pain
Complication
Malignant change
Key Points
Relevant to gastric ulcers, which is why they are biopsied
Prognosis
With PPIs and successful H. pylori eradication, most ulcers heal and recurrence falls sharply. Complications such as bleeding and perforation still carry significant risk, especially in elderly patients and those taking NSAIDs.
Quick Viva Questions
Q: Which artery is eroded by a bleeding posterior duodenal ulcer? A: The gastroduodenal artery.
Q: What metabolic abnormality occurs in gastric outlet obstruction? A: Hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria.
Q: What is Curling's ulcer? A: A stress ulcer that develops after major burns.
Q: How do proton pump inhibitors act? A: They irreversibly inhibit the H+/K+ ATPase in gastric parietal cells.
Q: Which tests confirm H. pylori eradication? A: Urea breath test or stool antigen test.
How Peptic Ulcer Appears in MBBS University Exams
Typical question styles (not attributed to specific papers or years):
- "Discuss the aetiopathogenesis, clinical features, complications and management of peptic ulcer disease." (Long essay, General Medicine or Surgery)
- "Describe the aetiopathogenesis and morphology of peptic ulcer." (Long essay, Pathology)
- "Classify drugs used in peptic ulcer. Write a note on proton pump inhibitors." (Long essay, Pharmacology)
- "Write a short note on H. pylori eradication therapy." (Short note, Pharmacology or Medicine)
- "Discuss the management of perforated duodenal ulcer." (Long essay, Surgery)
- "Write a short note on gastric outlet obstruction." (Short note, Surgery)
Frequently Asked Questions
What is the most common cause of peptic ulcer?
Helicobacter pylori infection is the most common cause, followed by NSAID use.
Why are gastric ulcers biopsied but duodenal ulcers usually not?
Gastric cancer can look like a benign gastric ulcer, so all gastric ulcers are biopsied. Duodenal ulcers are almost never malignant.
Can I download the peptic ulcer PPT for my presentation?
Yes. Use the Download PPT button at the top of this page. The GeckoMed app also gives offline access to the slides and notes.
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