Peptic Ulcer Disease

 

• Background

  Pathophysiology

  • Erosion of the gastric or duodenal mucosa which extends into the submucosa or deeper. Due to imbalance of harmful factors – acid, pepsin – and protective factors – mucus bicarbonate layer, prostaglandins, and epithelial tight junctions.
  • Duodenal ulcers (DU) are commoner than gastric ulcers (GU).
  • DU are associated with gastric acid hypersecretion. Due to H. pylori infection in the gastric antrum → ↓somatostatin release → ↑gastrin release → ↑acid secretion.
  • GU are associated with normal or low acid. Due to NSAIDs → ↓prostaglandins → ↓mucin, ↓HCO3-. Alternatively, H. pylori infection → inflammation and damage to epithelial tight junctions.

  Causes and risk factors

  • Helicobacter pylori (80%), mainly duodenal.
  • NSAIDs (20%), mainly gastric.
  • Steroids
  • Alcohol, smoking.
  • Family history.
  • Stress (maybe).

• Signs and symptoms

  Epigastric pain after eating:

  • If gastric ulcer, shortly after.
  • If duodenal ulcer, somewhat later (2-3 hours) and is more likely to wake at night. May radiate through to back. Eating itself may initially relieve the pain.
  • In practice, it is difficult to reliably distinguish between the two from symptoms alone.

  Others:

  • Nausea
  • Epigastric tenderness.
  • Symptoms of complications: haematemesis or melena (bleeding ulcer), vomiting (gastric outlet obstruction).

• Investigations

  H. pylori testing:

  • 13C urea breath test or stool antigen test.
  • Stop PPIs 2 weeks before test.

  FBC:

  • May show iron-deficiency anaemia.

  Endoscopy:

  • 2 week referral if there are alarm signs for gastric or oesophageal cancer: >55 years old at onset (and persistent), persistent vomiting, dysphagia, weight loss, upper GI bleeding (or iron-deficiency anaemia), epigastric mass.
  • Biopsy: histology for cancer and CLO test (aka rapid urease test) for H. pylori.
  • Stop PPIs 2 weeks before test.

• Prevention and management

  Ulcer prevention in high risk patients:

  • PPIs if on long term steroids.
  • Avoid long-term NSAIDs if possible, but if necessary consider COX2 inhibitor (celecoxib) over other NSAIDs, and/or adjunct PPIs.

  Management of dyspepsia:

  1. Review meds (and maybe stop NSAIDs) and try lifestyle changes for 1 month e.g. stop smoking and alcohol. Endoscopy if there are alarm signs.
  2. H. pylori test and treat if PUD suspected (rather than GORD) i.e. epigastric pain predominates.

  H. pylori test and treat:

  • Test as described above.
  • If test +ve, give triple therapy: 2 months of PPI plus 1 week of {clarithromycin} + {amoxicillin or metronidazole}.
  • If test -ve, give 1-2 months of PPI.
  • Follow up endoscopy: only indicated if diagnosis was originally by endoscopy and it was a gastric ulcer, as gastric cancer can present with ulcer. Duodenal ulcers only need checking if unresponsive to treatment.

  Ulcer surgery:

  • Rarely needed these days, but historically was common.
  • Indications: ulcer refractory to medical treatment, bleeding ulcer, perforated ulcer, gastric outlet obstruction.
  • Commonest procedure is truncal vagotomy with pyloroplasty. Vagotomy denervates the pylorus, reducing acid secretion but also slowing emptying, hence the need for pyloroplasty, which involves relaxation of pylorus through cutting and resuturing.
  • Early complications: bleeding and bilious vomiting.
  • Late complications: dumping syndrome, diarrhoea, anaemia, osteomalacia. Dumping syndrome is rapid food entry into small bowel, causing fluid shifts into bowel and reactive hypoglycaemia; presents with distention and flushing/sweating.

• Complications

  • Upper GI bleed, which may be acute or chronic.
  • Perforation or penetration (e.g. gastrocolic fistula).
  • Gastric outlet obstruction (pyloric stenosis) due to scarring and oedema of pyloric ulcers.

• Perforated peptic ulcer

  Background

  • Erosion of an ulcer through wall of GI tract.
  • Commoner with anterior duodenal ulcers.

  Signs and symptoms

  Acute abdomen:

  • Severe pain: epigastric then quickly generalised.
  • Shock
  • Peritonitis, with patient lying still in pain.

  May vomit once or twice, but any more and consider acute pancreatitis as a more likely diagnosis.

  Investigations

  • Erect CXR: pneumoperitoneum. AXR may also be done, but is not as useful.
  • Abdo CT.

  Management

  1. 'Drip and suck': IV fluids, and NG tube to empty stomach.
  2. PPIs and antibiotics to relieve symptoms and prevent infection, and continued subsequently for H. pylori eradication.
  3. Peritoneal washout and surgical repair with a patch of omentum. Excision and biopsy if ulcer is gastric, as some are malignant. Sometimes repair is spontaneous and surgery is not needed.

• Gastritis

  Definition and pathophysiology

  • Strictly speaking, refers to inflammation of the gastric mucosa, but term is loosely used and sometimes describes non-inflammatory mucosal injury which may be more accurately described as gastropathy.
  • Has many of the same risk factors and causes as PUD – especially H. pylori, NSAIDs, and alcohol – and can be seen as a precursor to ulceration and, less commonly, malignancy. Other causes include ischaemia (e.g. in critical illness) and autoimmune disease.
  • May be acute or chronic, with the latter classified as atrophic or nonatrophic, as per histologic findings.

  Presentation

  • Epigastric pain.
  • Nausea and vomiting, with or without diarrhoea.
  • Upper GI bleeding.

  Diagnosis

  Gastroscopy: diagnosis technically requires biopsy, but often made based on appearance.

  Management

  As for PUD, including symptomatic relief with anti acid medications and H. pylori eradication if present.