Peptic Ulcer Disease (PUD) Flashcards
Define PUD
A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter with depth to the submucosa (i.e. erodes into submucosa)
What is the pathophysiology of PUD?
Occurs when there is an imbalance between gastric acid secretion and protective mechanisms (bicarbonate and mucus secretion)
What is the aetiology of PUD?
Most common:
- H. pylori infection → chronic gastritis
(bacteria, increases acid secretion and decreases mucus production)
- NSAIDs
(inhibit COX-1 and COX-2 → decrease in PGE2 which normally decreases gastric acid secretion and increases HCO3- and mucus secretion)
Others:
- Smoking
- Alcohol
- Rare: Zollinger-Ellison syndrome (a gastrin-secreting neuroendocrine tumour that increases acid production)
What are the risk factors for PUD?
- H. pylori infection (present in 95% of duodenal and 70–80% of gastric ulcers)
- NSAID use
- Smoking
- Increasing age
- Excessive alcohol consumption
What is the epidemiology of PUD?
- Common
- More common in males (but similar occurrence in males and females)
- Duodenal ulcer mean age: 30s
- Gastric ulcer mean age: 50s
- H. pylori is usually acquired in childhood
- Duodenal ulcers more common than gastric ulcers
What are the presenting symptoms of PUD?
BOTH:
- Epigastric pain
- Pain relief by antacids
(BUT approx. 70% are asymptomatic)
PEPTIC ULCER:
- Pain increases shortly after eating → weight loss
DUODENAL ULCER:
- Pain increases 2–5 hours after eating
- Pain on an empty stomach (hunger pain) that is relieved with food intake → weight gain
(with a duodenal ulcer, you don’t get pain right after eating because the pyloric sphincter closes while food is in the stomach)
What are the presenting signs of PUD?
- Epigastric tenderness
May be signs of upper GI bleeding:
- Haematemesis
- Melaena
- Anaemia (e.g. pallor)
Signs of other complications:
- Succession splash heard on auscultation - suggests pyloric stenosis (retained gastric content)
This occurs in PUD because:
- acute PUD → inflammation and oedema
- chronic PUD → scarring and fibrosis)
What investigations would you do if you were suspecting PUD and what would you expect to see?
1st investigations:
- H. pylori urea breath test or stool antigen test
(H. pylori has urease so can break C-13 radio-labelled urea given by mouth into radio-labelled CO2 which is detected in expired air)
- OGD + gastric ulcer biopsy (to rule out malignancy)
(duodenal ulcer does not need to be biopsied because risk of malignancy is very low)
- FBC (to look for anaemia due to GI bleeding)
Other investigations:
- H. pylori antibody test (confirms exposure not eradication)
- Blood amylase (should be low - excludes pancreatitis)
- Secretin test for Zollinger-Ellison syndrome (IV secretin causes a rise in serum gastrin in ZE patients but not controls)
If GI bleed:
- Rockall Scoring to assess severity of bleed (< 3 = good prognosis, > 8 = high risk of mortality)
- Clotting screen (blood test)
What is the management for PUD?
IF GI BLEED:
- Fluid resuscitation needed if the ulcer is perforated or bleeding
- Close monitoring of vital signs
- Treat with IV PPI
Therapeutic endoscopy → haemostasis by:
- adrenaline injection (to constrict bleeding vessel)
- electrocoagulation
Surgery:
- If perforated or ulcer-related bleeding cannot be controlled
ULCER ASSOCIATED WITH H. PYLORI:
- 1 week triple therapy = 2 antibiotics + PPI
(e. g. clarithromycin + amoxicillin + PPI)
ULCER NOT ASSOCIATED WITH H. PYLORI:
Using NSAIDs:
- 8 week PPI or H2 antagonist therapy
- Stop taking NSAID if possible
If NSAID use is necessary:
- Use misoprostol (prostaglandin E1 analogue)
- Switch to a COX-2 selective NSAID
- Always prescribe NSAID with PPI
Not using NSAIDs:
- 4-8 week PPI or H2 antagonist therapy
What are the complications of PUD?
GI bleeding:
- Haematemesis
- Melaena
- Anaemia
- Perforation
- Pyloric stenosis (due to scarring)
What is the prognosis of PUD?
- Overall lifetime risk is approx. 10%
- Generally good prognosis as peptic ulcers associated with H. pylori can be cured by eradication
