Peptic ulcer disease and Gastritis

Question 1

Define

Answer 1

• Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin
• Most commonly gastric and duodenal

Question 2

Causes

Answer 2

imbalance between damaging action of acid and pepsin and mucosal protective mechanisms

Question 3

Risk factors

Answer 3

• strong association with H. pylori

(95% duodenal and 80% gastric) - mechanism still unclear

• Duodenal: H. pylori, drugs (NSAIDs, steroids, SSRI)
• Gastric: H. pylori, NSAIDs, reflux if duodenal contents, stress

Question 4

Epidemiology

Answer 4

COMMON, 1-4/1000
More common in males
Duodenal: mean age 30 years, 4 fold commoner than gastric Gastric: 50 years, mainly elderly

Question 5

Symptoms

Answer 5

• Epigastric pain
• Relieved by antacids
• ± Bloating, fullness after meals, heatburb, decreased weight

Symptoms have a variable relationship to food intake:

• Gastric - pain is worse soon after eating
• Duodenal - pain is worse several hours after eating (and relieves right after food)

Patients may present with complications e.g. haematemesis, melaena

Question 6

Signs

Answer 6

There may be NO physical findings

Epigastric tenderness

Signs of complications e.g. anaemia

Question 7

Investigations

Answer 7

Bloods:

• FBC (for anaemia)
• Serum amylase (to exclude pancreatitis)
• U&Es
• Clotting screen
• LFT
• Cross-match if active bleeding
• Secretin test (if Zollinger-Ellison syndrome suspected) - IV secretin causes a rise in serum gastrin in ZE patients but not in normal patients)

Endoscopy:

• Biopsies of gastric ulcers can be taken to rule out malignancy
• Duodenal ulcers do NOT need to be biopsied

Rockall Scoring:

• Scores the severity after a GI bleed
• Score < 3 carries good prognosis
• Score > 8 carries high risk of mortality

Testing for H. pylori:

• C13-urea breath test :
• Radio-labelled urea is given by mouth
• C13 is detected in the expelled air

Serology:

• IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication

Campylobacter-like organism (CLO) test:

• Gastric biopsy is placed with a substrate of urea and a pH indicator
• If H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red

Question 8

Management

Answer 8

Acute:

• Fluid resuscitation needed if the ulcer is perforated or bleeding (IV colloids/crystalloids)
• Close monitoring of vital signs
• Endoscopy
• Surgical treatment
• NOTE: patients with upper GI bleeding should be treated with IV PPIs at presentation until the cause of bleeding is identified

Endoscopy:

If the ulcer is bleeding, haemostasis can be achieved with:

• Injection sclerotherapy
• Laser coagulation
• Electrocoagulation

Surgery:

• Indicated if the ulcer has perforated or if the bleeding ulcer can’t be controlled

Helicobacter pylori eradication:

• Triple therapy for 1-2 weeks
• Various combinations may be recommended - usually a combination of 2 antibiotics + PPI (e.g. clarithromycin + amoxicillin + omeprazole)

If peptic ulcer disease is NOT associated with H. pylori:

• Treat with PPIs or H2 antagonists
• Stop NSAID use
• Use misoprostol (prostoglandin E1 analogue) if NSAID use is necessary

Question 9

Complications

Answer 9

Rate of major complication = 1 % per year

Major complications:

• Haemorrhage (haematemesis, melaena, iron-deficiency anaemia)
• Perforation
• Obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)

Question 10

Prognosis

Answer 10

• Overall lifetime risk = 10%
• Outlook is generally good because peptic ulcers associated with H. pylori can be cured by eradication