Peptic Ulcer Disease

Peptic Ulcer Disease (PUD) is a common condition in UK general practice and hospital settings, encompassing both gastric and duodenal ulcers. It's a high-yield topic for finals due to its prevalence, diverse presentations, and life-threatening complications. Duodenal ulcers are more frequent and strongly linked to *Helicobacter pylori* infection (90-95%). Gastric ulcers are also associated with *H. pylori* but have a higher correlation with NSAID use and, crucially, carry a risk of malignancy. Therefore, all gastric ulcers require biopsy and follow-up endoscopy to confirm healing and exclude cancer.

Classic symptoms include epigastric pain, often described as 'gnawing' or 'burning'. While traditionally duodenal ulcer pain is relieved by food and gastric ulcer pain worsened, this distinction is unreliable in exams and practice.

**MLA Focus:** Recognising complications is paramount. Acute upper GI bleeding (haematemesis, melaena) and perforation (sudden, severe abdominal pain, 'board-like' rigidity, peritonitis) are surgical emergencies. Diagnosis is primarily by Oesophago-Gastro-Duodenoscopy (OGD), allowing direct visualisation, biopsy, and therapeutic intervention for bleeding. Non-invasive *H. pylori* testing (C13 urea breath test or stool antigen) is key for 'test and treat' strategies in primary care for dyspepsia in patients under 55 without alarm features. Management involves *H. pylori* eradication (triple therapy) and stopping causative agents like NSAIDs.

PUD results from an imbalance between aggressive factors (gastric acid, pepsin) and protective factors (mucus, bicarbonate, prostaglandins, mucosal blood flow).

*H. pylori*, a Gram-negative bacterium, colonises the gastric antrum. Its urease enzyme produces ammonia, neutralising acid and allowing survival. This leads to chronic inflammation, increasing gastrin secretion and thus acid production, predisposing to duodenal ulcers. If the infection spreads to the gastric body, it can lead to atrophy and reduced acid, but also impaired mucosal integrity, causing gastric ulcers.

NSAIDs inhibit cyclooxygenase (COX-1), which is crucial for prostaglandin synthesis. Prostaglandins maintain the protective gastric mucus barrier and blood flow. Their inhibition leaves the gastric mucosa vulnerable to acid, leading to ulceration. This is why NSAIDs are a major cause of gastric ulcers and upper GI bleeding.

Patients typically present with dyspepsia (epigastric pain, bloating, nausea, early satiety). The pain can be 'gnawing' or 'burning' and may radiate to the back.

**Red Flags/Complications (SBA/OSCE critical):**
- **Acute GI Bleeding:** Haematemesis (vomiting blood), melaena (black, tarry stools), syncope, dizziness, tachycardia, hypotension. Requires urgent ABCDE assessment, IV access, fluid resuscitation, and OGD.
- **Perforation:** Sudden onset, severe, generalised abdominal pain. On examination: 'board-like' rigid abdomen, guarding, rebound tenderness, absent bowel sounds. This is a surgical emergency.
- **Gastric Outlet Obstruction:** Due to chronic scarring (cicatrisation) at the pylorus. Presents with recurrent, projectile, non-bilious vomiting (often food eaten hours ago), early satiety, weight loss. A 'succussion splash' may be elicited on examination (listen over the epigastrium while rocking the patient).

**UK Finals/OSCE Pearls:**
- Always ask about NSAID use and *H. pylori* history.
- Differentiate between gastric and duodenal ulcers: gastric ulcers *always* need biopsy and follow-up OGD; duodenal ulcers typically do not unless symptoms persist.
- Consider differentials: GORD, gastritis, cholecystitis, pancreatitis, MI, gastric cancer.

**Bloods:**
- **FBC:** To check for anaemia (chronic blood loss) or acute drop in Hb (acute bleed).
- **U&Es:** Urea often disproportionately elevated in upper GI bleeding due to digestion of blood proteins.
- **Group and Save/Crossmatch:** Essential if bleeding is suspected.

**Diagnostic Gold Standard:**
- **OGD (Oesophago-Gastro-Duodenoscopy):** Allows direct visualisation of ulcers, biopsy (essential for gastric ulcers to exclude malignancy, CLO/RUT test for *H. pylori*), and therapeutic intervention for bleeding (e.g., adrenaline injection, clipping, thermal coagulation).

***H. pylori* Testing (Non-invasive):**
- **C13 Urea Breath Test:** Highly sensitive and specific. Patient ingests C13-labelled urea; if *H. pylori* is present, urease breaks it down into C13-labelled CO2, detected in breath. **Crucially, PPIs must be stopped 2 weeks prior, and antibiotics 4 weeks prior, to avoid false negatives.**
- **Stool Antigen Test:** Similar accuracy to breath test, useful for children or those unable to perform breath test. Same PPI/antibiotic cessation rules apply.

**Imaging:**
- **Erect Chest X-ray:** If perforation is suspected, look for free air under the diaphragm (pneumoperitoneum). This is a classic SBA finding.

**1. *H. pylori*-Positive Ulcers:**
- **Eradication Therapy (Triple Therapy):** 7-day course (NICE guidelines).
- **PPI** (e.g., Omeprazole 20mg BD or Lansoprazole 30mg BD) +
- **Amoxicillin** 1g BD +
- **Clarithromycin** 500mg BD (or **Metronidazole** 400mg BD if penicillin allergic or local resistance patterns dictate).
- **Confirmation of Eradication:** Urea breath test or stool antigen test 4-6 weeks *after* completing therapy (and stopping PPI for 2 weeks).

**2. *H. pylori*-Negative (NSAID-induced) Ulcers:**
- **Stop NSAID:** If possible.
- **Full-dose PPI:** For 1-2 months to allow healing.
- **If NSAID must continue:** Prescribe a concomitant PPI for gastroprotection (e.g., Omeprazole 20mg OD).

**3. Acute Bleeding (Emergency):**
- **ABCDE approach:** Resuscitation (IV fluids, blood products if needed).
- **IV PPI:** High-dose (e.g., Omeprazole 80mg bolus then 8mg/hr infusion).
- **Urgent OGD:** For endoscopic haemostasis (e.g., adrenaline injection, clips, thermal coagulation).

**4. Perforation (Emergency):**
- **Nil by mouth (NBM), IV fluids, IV antibiotics.**
- **Urgent Surgical Repair:** Typically an omental patch (Graham patch) to seal the perforation.