Overview
Peptic Ulcer Disease (PUD)
1. Clinical Overview
Summary
Peptic Ulcer Disease (PUD) refers to ulceration of the gastric or duodenal mucosa resulting from an imbalance between mucosal protective factors (Mucus, Bicarbonate, Prostaglandins, Blood flow) and aggressive factors (Acid, Pepsin). The two major causes are Helicobacter pylori infection and NSAID use, which together account for the vast majority of cases. Duodenal ulcers (DU) are more common than Gastric ulcers (GU). Patients present with epigastric pain, which may be described as burning or gnawing. DU pain classically improves with food ("Hunger pain"), while GU pain may be worsened by food. Complications include Haemorrhage, Perforation, and Gastric Outlet Obstruction. Diagnosis is confirmed by OGD (Upper GI Endoscopy) with biopsy for H. pylori and exclusion of malignancy in GU. Treatment involves PPI therapy, H. pylori eradication, and cessation of culprit medications (NSAIDs). [1,2,3]
Clinical Pearls
"H. pylori + NSAIDs = Cause Most Ulcers": Always test for H. pylori. Always ask about NSAID use (Including OTC/Low-dose aspirin).
"Duodenal = Hungry, Gastric = Worse with Food": DU pain relieved by eating. GU pain may worsen after meals.
"Biopsy Gastric Ulcers": Gastric ulcers need biopsy to exclude malignancy. Repeat OGD at 6-8 weeks to confirm healing.
"Eradicate H. pylori": Triple therapy (PPI + Amoxicillin + Clarithromycin) for 7-14 days. Confirm eradication.
2. Epidemiology
Demographics
| Factor | Notes |
|---|---|
| Prevalence | Lifetime prevalence ~5-10%. Decreasing due to H. pylori eradication and PPI use. |
| Age | DU: Younger adults (30-50). GU: Older adults (50-70). |
| Sex | Male > Female (Especially DU). |
| Location | DU: Anterior wall of duodenal bulb. GU: Lesser curve of stomach (Incisura angularis). |
Aetiological Factors
| Cause | Proportion |
|---|---|
| Helicobacter pylori | ~80-90% of DU. ~60-70% of GU. |
| NSAIDs (Including Low-Dose Aspirin) | Second most common. Higher risk with Cox-1 inhibitors. |
| Hypersecretory States | Zollinger-Ellison Syndrome (Gastrinoma). Rare. |
| Stress Ulcers (Curling/Cushing) | ICU patients. Burns. Head injury. |
| Other | Smoking, Alcohol, Crohn's disease, CMV, Cocaine. |
3. Pathophysiology
Mucosal Defence vs Aggression
| Protective Factors | Aggressive Factors |
|---|---|
| Mucus-Bicarbonate barrier | Gastric Acid (HCl) |
| Epithelial tight junctions | Pepsin |
| Prostaglandins (PGE₂) | H. pylori |
| Mucosal blood flow | NSAIDs |
| Epithelial regeneration | Bile acids |
H. pylori Mechanism
- Infection: Colonises gastric antrum under mucus layer.
- Urease Production: Converts urea to ammonia → Buffers local pH → Survival.
- Inflammation: Chronic gastritis → Reduced somatostatin → Increased gastrin → Increased acid → DU.
- Cytotoxins: CagA and VacA → Epithelial damage → GU.
NSAID Mechanism
- Systemic Prostaglandin Inhibition: NSAIDs inhibit COX-1 → Reduced PGE₂ → Reduced mucus/Bicarbonate → Reduced blood flow → Mucosal vulnerability.
- Topical Injury: Direct epithelial damage from acidic NSAIDs.
4. Clinical Presentation
Symptoms
| Symptom | DU | GU |
|---|---|---|
| Epigastric Pain | Burning, Gnawing. Relieved by food/Antacids ("Hunger pain"). Worse 2-3 hours after meals and at night. | Burning. May worsen with food. |
| Nausea / Vomiting | Less common | More common |
| Weight Loss | Rare | May occur (Due to food avoidance) |
| Bloating | ||
| Asymptomatic | Some patients, Especially NSAID users |
Complications (Red Flags)
| Complication | Clinical Features |
|---|---|
| Haemorrhage | Haematemesis (Fresh blood or "Coffee-ground"). Melaena. Haemodynamic instability. |
| Perforation | Sudden severe epigastric pain. Peritonitis. Board-like rigidity. Sepsis. Free air on X-ray. |
| Gastric Outlet Obstruction | Projectile vomiting (Undigested food). Succussion splash. Weight loss. Chronic DU scarring or GU obstruction. |
| Penetration | Ulcer erodes into adjacent organ (Pancreas – Back pain). |
Examination Findings
| Finding | Notes |
|---|---|
| Epigastric Tenderness | Common but non-specific. |
| Peritonism | If perforated. Guarding, Rigidity. |
| Pallor | If anaemic (Chronic bleeding). |
| Melaena on PR | |
| Succussion Splash | Gastric outlet obstruction (Retained gastric contents). |
5. Investigations
OGD (Upper GI Endoscopy)
| Notes |
|---|
| Gold Standard for diagnosis. |
| Visualises ulcer, Assesses size, Location, Stigmata of recent bleeding. |
| Biopsy: Mandatory for Gastric ulcers (Exclude malignancy). Take multiple biopsies from ulcer edge and antrum/Body (For H. pylori). |
| Duodenal ulcers: Biopsy not routine for malignancy but sample for H. pylori. |
H. pylori Testing
| Test | Notes |
|---|---|
| CLO Test (Rapid Urease Test) | On biopsy. Rapid. Detects urease. |
| Histology | On biopsy. Can see organisms. |
| Urea Breath Test (UBT) | Non-invasive. ¹³C-urea. Post-eradication test of choice. |
| Stool Antigen Test | Non-invasive. Alternative. |
| Serology (IgG) | Less useful (Remains positive after eradication). Not recommended. |
Note: Stop PPI ≥2 weeks and Antibiotics ≥4 weeks before testing (False negatives).
Blood Tests
| Test | Notes |
|---|---|
| FBC | Anaemia (Chronic blood loss). |
| U&Es | Urea elevated (GI bleed). |
| Group and Save / Crossmatch | If bleeding. |
| Fasting Gastrin | If Zollinger-Ellison suspected (Refractory ulcers, Multiple ulcers, Unusual location). |
Imaging
| Test | Notes |
|---|---|
| Erect CXR | If perforation suspected → Free air under diaphragm (Pneumoperitoneum). |
| CT Abdomen | If clinical suspicion of perforation/Complication with negative CXR. |
6. Management
Management Algorithm
SUSPECTED PEPTIC ULCER DISEASE
(Epigastric pain, Dyspepsia)
↓
CHECK FOR ALARM SYMPTOMS
┌────────────────┴────────────────┐
NO ALARM SYMPTOMS ALARM SYMPTOMS PRESENT
↓ (GI bleed, Weight loss,
H. PYLORI TEST Dysphagia, Age >55)
(UBT or Stool Ag) ↓
**URGENT OGD (2WW)**
↓
H. PYLORI RESULT
┌────────────────┴────────────────┐
POSITIVE NEGATIVE
↓ ↓
**ERADICATION THERAPY** Review medications (NSAIDs?)
+ PPI PPI trial
(See Triple Therapy below) Consider OGD if refractory
↓
H. PYLORI ERADICATION THERAPY
┌──────────────────────────────────────────────────────────┐
│ **FIRST-LINE: Triple Therapy (7-14 Days)** │
│ - PPI (Full dose BD) + │
│ - Amoxicillin 1g BD + │
│ - Clarithromycin 500mg BD │
│ │
│ **If Penicillin Allergy:** │
│ - PPI + Clarithromycin + Metronidazole 400mg BD │
│ │
│ **Second-Line (If First-Line Fails):** │
│ - Quadruple Therapy (Bismuth-based) or │
│ - PPI + Amoxicillin + Metronidazole + Levofloxacin │
│ │
│ **Confirm Eradication:** │
│ - Urea Breath Test (≥4 weeks after treatment, ≥2 weeks │
│ off PPI) │
└──────────────────────────────────────────────────────────┘
↓
PPI THERAPY
┌──────────────────────────────────────────────────────────┐
│ - DU: PPI for 4 weeks (Or until H. pylori eradicated) │
│ - GU: PPI for 8 weeks │
│ - Repeat OGD at 6-8 weeks for GU to confirm healing │
│ and exclude malignancy │
└──────────────────────────────────────────────────────────┘
↓
STOP NSAIDS
- Discontinue if possible
- If NSAID essential: Use lowest dose, Shortest duration,
Cox-2 selective (Celecoxib), Co-prescribe PPI
↓
LIFESTYLE ADVICE
- Smoking cessation
- Reduce alcohol
- Avoid late-night eating
Acute GI Bleed Management
| Step | Action |
|---|---|
| Resuscitation | ABCDE. IV access. Fluids. Crossmatch. |
| Risk Stratification | Glasgow-Blatchford Score (Pre-endoscopy). Rockall Score (Post-endoscopy). |
| Urgent OGD | Within 24 hours. |
| Endoscopic Therapy | Injection (Adrenaline), Thermal (Heater probe, APC), Mechanical (Clips). |
| PPI Infusion | High-risk stigmata: Omeprazole 80mg IV bolus then 8mg/hr infusion for 72 hours. |
| Rebleed / Failure | Interventional radiology (Embolisation) or Surgery. |
Perforation Management
| Step | Action |
|---|---|
| Resuscitation | IV Fluids. NBM. NG tube. Analgesia. |
| Antibiotics | Broad-spectrum (Gram-negatives, Anaerobes). |
| Surgery | Laparoscopic or Open. Omental patch repair (Graham patch). Peritoneal lavage. |
7. Complications
| Complication | Incidence | Notes |
|---|---|---|
| Haemorrhage | ~15-20% | Most common. Posterior DU erodes gastroduodenal artery. GU erodes left gastric artery. |
| Perforation | ~5% | Anterior DU more common. Peritonitis. Free air. Surgical emergency. |
| Gastric Outlet Obstruction | ~2% | Chronic scarring (Pyloric stenosis). Vomiting. Weight loss. |
| Penetration | Rare | Into pancreas (Back pain), Liver, Colon. |
8. Prognosis and Outcomes
| Factor | Notes |
|---|---|
| H. pylori Eradication | ~90%+ with triple therapy. Greatly reduces recurrence. |
| PPI Healing Rates | >90% healing at 8 weeks for uncomplicated ulcers. |
| Recurrence | Low if H. pylori eradicated and NSAIDs stopped. |
| Mortality (Bleeding) | ~5-10%. Higher in elderly, Comorbidities. |
| Mortality (Perforation) | ~5-25%. Depends on delay, Comorbidities. |
9. Evidence and Guidelines
Key Guidelines
| Guideline | Organisation | Key Recommendations |
|---|---|---|
| Dyspepsia and GORD | NICE NG42 | Test and treat H. pylori. PPI therapy. OGD for alarm symptoms. |
| GI Bleeding | NICE NG141 | OGD within 24 hours. Endoscopic therapy. PPI infusion for high-risk. |
10. Patient and Layperson Explanation
What is a Peptic Ulcer?
A peptic ulcer is a sore that develops on the lining of your stomach (Gastric ulcer) or the first part of your small bowel (Duodenal ulcer). It happens when the protective lining is damaged, Often by a germ called Helicobacter pylori or by painkillers like Ibuprofen.
What are the symptoms?
- Burning pain in the upper tummy.
- Pain may come and go. Often improves after eating (Duodenal ulcer) or may worsen (Gastric ulcer).
- Bloating, Nausea.
What are the warning signs?
See a doctor urgently if you have:
- Vomiting blood (Bright red or looks like coffee grounds).
- Black tarry stools.
- Sudden severe tummy pain.
- Unexplained weight loss.
How is it treated?
- Antibiotics: If H. pylori is found, A course of antibiotics and acid-reducing medication cures the infection.
- PPI: Tablets like Omeprazole reduce acid and help the ulcer heal.
- Stop NSAIDs: If painkillers are the cause, Switching to a safer alternative is important.
Can it come back?
With successful H. pylori treatment and avoiding NSAIDs, Most ulcers heal completely and do not return.
11. References
Primary Sources
- National Institute for Health and Care Excellence. Gastro-oesophageal reflux disease and dyspepsia in adults (NG42). 2014 (Updated 2019).
- Malfertheiner P, et al. Management of Helicobacter pylori infection – the Maastricht V/Florence Consensus Report. Gut. 2017;66(1):6-30. PMID: 27707777.
- Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017;390(10094):613-624. PMID: 28242110.
12. Examination Focus
Common Exam Questions
- Main Causes: "What are the two main causes of peptic ulcer disease?"
- Answer: Helicobacter pylori infection and NSAID use.
- Pain Pattern: "How does the pain of DU differ from GU?"
- Answer: DU: Relieved by food ("Hunger pain"), Worse at night. GU: May be worsened by food.
- H. pylori Eradication: "What is the first-line treatment for H. pylori?"
- Answer: Triple Therapy: PPI (BD) + Amoxicillin 1g BD + Clarithromycin 500mg BD for 7-14 days.
- Repeat OGD: "Why is repeat OGD needed for gastric ulcers?"
- Answer: To confirm healing and exclude malignancy (GU can be malignant).
Viva Points
- Test and Treat: Non-invasive H. pylori test (UBT or Stool Ag) for dyspepsia without alarms.
- Stop PPI 2 Weeks Before Testing: To avoid false negative H. pylori tests.
- Posterior DU Bleeds Gastroduodenal Artery: Massive haemorrhage.
- Anterior DU Perforates: Free air on erect CXR.
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.