Peptic Ulceration Flashcards
What does this include?
Duodenal + Gastric ulcers
What is the pathogenesis?
The stomach is a battle ground between the forces of attack (acid and helicobacter pylori) and defence (mucosal barrier - contains bicarbonate)
Increased damage or impaired defences lead to peptic ulceration
Which are more common: gastric or duodenal ulcers?
Duodenal ulcers (4 fold commoner than gastric ulcers)
What are the causes of duodenal ulcers?
H. pylori (90%)
Drugs
Increased gastric acid secretion (minor risk factor)
What are the causes of gastric ulcers?
H. pylori (80%)
Smoking
NSAIDs
What are some other causes of ulcers?
Zollinger-Ellison syndrome: gastrin secreting pancreatic tumour which causes recurrent poor healing duodenal ulcers
Hyperparathyroidism
Alcohol excess
Crohn’s disease
PMH of liver disease (peptic ulcer is more frequent in patients with liver cirrhosis)
What is the presentation of peptic ulceration?
Epigastric pain (may be relived by antacids)
Nocturnal/hunger pain (more common in DU)
Back pain (may suggest penetration of a posterior DU)
Nausea and occasionally vomiting
Weight loss and anorexia
Only sign may be epigastric tenderness
If the ulcer bleeds, patients may present with haematemesis and/or melaena or anaemia
What investigation is required?
Upper GI endoscopy to exclude malignancy (multiple biopsies)
Gastric ulcers may sit over a gastric carcinoma => repeat endoscopy indicated at 8 weeks
What is the treatment/management?
Lifestyle changes
H. pylori eradication therapy
PPIs
H2 receptor antagonists
If NSAIDs are also involved: stop if possible, or should continue to receive other protective agents following eradication therapy
Complications are treated as they arise
Surgery is only indicated in complicated PUD
If upper GI ulcers are diagnosed in a young patients: Crohn’s disease is in the differential diagnosis
What are the complications of a peptic ulcer?
Bleeding: acute = haemorrhage (melaena and haematemesis), chronic = anaemia
Perforation: peritonitis
Healing by fibrosis: obstruction (fibrotic stricture/gastric outlet obstruction)
How does h. pylori cause increased acid production?
Produces urease: ammonia produced which buffers gastric acid locally resulting in an increased acid production
How do we test for h. pylori, non-invasively?
Serology: IgG against H. pylori (might not currently have it, could just have been exposed in the past)
Urea breath test (current status)
Stool antigen test: ELISA (current status) note that for this the patient needs to be off PPI for 2 weeks
How do we test for h. pylori, invasively (requires endoscopy)?
Histology: gastric biopsies stained from the bacteria
Culture of gastric biopsies
Rapid slide urease test (CLO)
How do we treat h. pylori?
Triple therapy for 7 days
-Clarithromycin 500mg bd
-Amoxycillin 1g bd (tetracycline is given if penicillin allergy)
-PPI: e.g. omeprazole 20mg bd
Effective in 90%
Resistance to antibiotics and poor compliance are the main reasons for failure
What does h. pylori cause?
Peptic ulceration
Gastritis
Stomach cancer
