Peptic ulcer disease

Epidemiology:

Duodenal ulcer (DU) >> gastric ulcer GU (3 : 1)

Approx. 15% of the population will suffer from a DU

Aetiology:

One factor in the formation of a peptic ulcer is an imbalance between acid and pepsin against the mucosal defences (mucus, bicarbonate, PGs)

Another major factor is infection by Helicobacter pylori. DU pts with H. pylori infection secrete more acid after stimulation by gastrin and have more parietal cells in the stomach than healthy people with H. pylori.

NSAIDs certainly contribute to the formation of GUs but NOT DUs

Peptic ulceration is more common in pts with blood group O

Pathology:

GUs are found in any part of the stomach but are most common on the lesser curve

Most DUs are found in the duodenal cap; the surrounding mucosa appears inflamed, haemorrhagic or friable (duodenitis)

Histologically there is:

A break in the superficial epithelial cells penetrating down to the muscularis mucosa at the site of the ulcer

A fibrous base

An increase in inflammatory cells

H. pylori may be found scattered on the surface of the gastric mucosa or in the ectopic gastric mucosa in the duodenum

Associated active gastritis

Clinical features:

Very well localised epigastric pain

Pain is relieved by antacids

The pain of a DU classically occurs at night (as well as in the day) and is worse when the pt is hungry

Nausea may accompany the pain

Vomiting is infrequent but often relieves the pain

Anorexia/weight loss, particularly with GUs

Back pain suggests a penetrating posterior DU

Pts can present for the first time with haematemesis or malaena or a perforation

Investigations:

Serology or breath test to confirm H. pylori status. Further ix is only indicated in pts with persistent dyspepsia following successful eradication therapy, or in symptomatic pts who are H. pylori negative

Endoscopy:

To exclude GORD or cancer

All gastric ulcers should be biopsied

Peptic ulcer disease

Barium meal (double contrast):

Less commonly used than endoscopy in this situation

Treatment of peptic ulcers associated with H. pylori:

Successful eradication of H. pylori:

Results in healing rates of 90%

Prevents recurrence of the ulcer

Anti-secretory therapy:

Proton-pump inhibitor (PPI) (e.g. Omeprazole) or,

H₂-receptor antagonist (e.g. Ranitidine)

Continued for 4-8 weeks to ensure ulcer healing

Treatment of peptic ulcers NOT associated with H. pylori:

These are mainly due to NSAID ingestion

Treatment involves acid suppression and discontinuation of NSAIDs (if possible). This may be difficult in pts with severe arthritis, and PPIs, H₂-receptor antagonists or Misoprostol may be used concurrently with NSAIDs.

Proton-pump inhibitors (PPIs):

Omeprazole 20mg daily

Lansoprazole 30mg daily

Pantoprazole 40mg daily

H₂-receptor antagonist:

Ranitidine 300mg daily

Cimetidine 800mg daily

Famotidine 40mg daily

Nizatidine 300mg daily

Misoprostol:

Is a synthetic analogue of PGE₁

Inhibits gastric acid secretion

Is mainly used as a cytoprotective agent against NSAID –associated GUs, particularly in the elderly

Prophylaxis is 200mg 2-4x daily

The main side-effects are diarrhoea and abdominal pain

Surgical mx:

Since the introduction in the 1970s of H₂-receptor antagonists, surgery for peptic ulceration is rarely necessary and is reserved only for the complications:

Recurrent uncontrolled haemorrhage – ligation of the bleeding vessel

Perforation – oversown

Complications of peptic ulcers:

Haemorrhage (i.e. an upper GI bleed)

Perforation:

DU >> GU

Peptic ulcer disease

Gastric outflow obstruction:

The obstruction may be pre-pyloric or in the duodenum

In this situation, it occurs for two reasons:

An active ulcer with surrounding oedema

The healing of the ulcer has been followed by scarring

Vomiting (usually projectile and huge in volume)

Severe or persistent vomiting causes loss of acid from the stomach and a metabolic alkalosis occurs