Peptic Ulcers Flashcards
Potential causes of peptic ulcer disease?
Cause is an imbalance between damaging action of acid and pepsin and mucosal protective mechanisms.
There is a strong correlation with Helicobacter pylori infection, but it is unclear how the organism causes formation of ulcers.
Common:
•Very strong association with H. pylori (present in 95% of duodenal and 70–80% of gastric ulcers)
•NSAID use.
Rare:
•Zollinger–Ellison syndrome.
Describe the epidemiology of peptic ulcer disease:
•Incidence?
•Is it more common in males or females?
•Prevalence?
Common.
Annual incidence is about 1–4/1000.
More common in males.
Duodenal ulcers have a mean age in the thirties, while gastric ulcers have a mean age in the fifties.
H. pylori is usually acquired in childhood and the prevalence is roughly equivalent to age in years.
How would a patient with peptic ulcer disease present?
•Describe timing of symptoms.
Epigastric abdominal pain relieved by antacids.
Symptoms have a variable relationship to food:
•If worse soon after eating, more likely to be gastric ulcers.
•If worse several hours later, more likely to be duodenal.
May present with complications, eg haematemesis, melaena
What would be found on examination of a patient with peptic ulcers?
May be no physical findings.
Epigastric tenderness.
Signs of complications
(e.g. anaemia, succession splash in pyloric stenosis).
What investigations would you perform on a patient with Peptic Ulcers?
Bloods: •FBC (for anaemia) •amylase (to exclude pancreatitis) •U&Es •clotting screen (if GI bleeding) •LFT •cross-match if actively bleeding •Secretin test if Zollinger–Ellison syndrome is suspected: —IV secretin causes a rise in serum gastrin in ZE patients.
Endoscopy:
•Four quadrant gastric ulcer biopsies to rule out malignancy;
•duodenal ulcers need not be biopsied.
Rockall scoring:
•For severity after a GI bleed.
—Less than 3 carries good prognosis,
—>8 have a high risk of mortality.
Testing for H. pylori:
•13C-Urea breath test: Radio-labelled urea given by mouth and detection of 13C in the expired air.
Serology:
•IgG antibody against H. pylori, confirms exposure but not eradication.
Stool antigen test. Campylobacter-like organism 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 (yellow to red).
Histology of biopsies: Difficult to visualize H. pylori so of limited value.
How would you manage a patient with peptic ulcers?
•Acutely?
•H. pylori related?
•H. pylori non-related?
Acute:
•Resuscitation if perforated or bleeding (IV colloids/crystalloids),
•Close monitoring of vital signs,
•Proceeding endoscopic or surgical treatment.
Patients with upper GI bleeding:
Treated with IV PPI (e.g. omeprazole or pantoprazole) at presentation until the cause of bleeding is confirmed.
Patients with actively bleeding peptic ulcers or ulcers with high-risk stigmata (e.g. visible vessel or adherent clot) should continue IV PPI. Switch to oral PPI If there is no rebleeding within 24 hours.
Endoscopy:
Haemostasis by injection sclerotherapy, laser or electrocoagulation.
Surgery:
If perforated or ulcer-related bleeding cannot be controlled.
H. pylori eradication with triple therapy for 1–2 weeks:
•Various combinations are recommended made up of one proton pump inhibitors and two antibiotics
—(e.g. clarithromycin + amoxicillin, metronidazole + tetracycline).
If not associated with H. pylori:
•Treat with PPIs or H2-antagonists.
•Stop NSAID use (especially diclofenac),
•Use misoprostol (prostaglandin E1 analogue), if NSAID use is necessary.
What are the possible complications of Peptic Ulcer Disease?
Rate of major complication is 1% per year including:
•Haemorrhage (haematemesis, melaena, iron-deficiency anaemia),
•Perforation,
•Obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis).
What is the prognosis of peptic ulcer disease?
Overall lifetime risk around 10%.
Generally good as peptic ulcers associated with H. pylori can be cured by eradication.
What is the definition of peptic ulcer disease?
Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin. Most commonly gastric and duodenal.
(can also occur in oesophagus and Meckels diverticulum)
Describe pathogenesis of Peptic Ulcer Disease.
•H. pylori related?
•Other factors?
H. pylori is acquired in childhood via oral-oral or faecal-oral spread.
Organism lives within gastric epithelium undetected by host.
H. pylori produces the enzyme urease.
—converts urea to ammonia
—raises surrounding pH providing protection from stomach acid.
H.pylori causes chronic gastritis in adulthood, may or may not be symptomatic.
—in some adults this infection this causes peptic ulceration.