30. Treatment of gastric and duodenal ulcers Flashcards
what can gastric and duodenal ulcers be grouped into and why?
peptic ulcers
though they differ in terms of presentation and epidemiology, their treatment is the same
what does the carbon-urea breath test do and how does it work?
detects the presence of H. pylori
the patient is given a lot of urea because H. pylori metabolises urea to nitrogen. if there are increased levels of nitrogen, H. pylori infection is present
what does the stool antigen test do?
tests for H. pylori antigens in the stool of the patient
what % of duodenal and gastric ulcers are due to H. pylori?
duodenal - 98-100%
gastric - 70-80%
what is H. pylori?
a motile spirochete that is able to move around (due to its flagella)
it is a commensal bacteria that is present in the stomach
how does H. pylori cause ulceration?
- a mucus layer protects the stomach epithelium from the acidic environment
- H. pylori can dissolve our mucus layer using urease enzyme allowing H. pylori to access epithelia –> epithelial cell death (exotoxins are released –> increased inflammation)
- eventually there is damage to the mucus layer, epithelial layer and interstitial layer –> ulceration
what is the link between acidity and ulceration?
increased acidity –> peptic ulcer
increased acidity also –> increased cell production of protons –> even greater acidity –> further ulceration
how are H. pylori infections treated?
amoxicillin and clarithromycin antibiotics
what is used to reduce acid production?
proton pump inhibitor for 7 days
what might you give alongside amoxicillin and clarithromycin?
quinolone or tetracycline if the H. pylori infection doesn’t go away
give an example of a proton pump inhibitor and outline why they are necessary
omeprazole
- parietal cells produce H+ via proton pumps
- the main regulators of this are the cholinergic system and the histaminergic system
- parietal cells are also influenced by other cells in the stomach: cells in the fundus release somatostatin (reduce parietal cell activity) and gastrin (increase parietal cell activity)
- proton pump inhibitors are necessary for reducing the activity of proton pumps and reducing stomach acidity
what is the second most common cause of peptic ulcers?
prolonged NSAID usage
in what ways are NSAIDs and H. pylori similar?
- NSAIDs can be directly cytotoxic
- they reduce mucus production
- this leads to a breakdown of the mucus barrier –> epithelia exposure –> ulceration
in what ways are NSAIDs different to how H. pylori causes ulceration?
- NSAIDs may increase the likelihood of bleeding (acts as an anti-platelet agent)
- this can worsen the symptoms
give an example of a histamine H2 receptor antagonist and outline what they do
ranitidine
- H2 receptor stimulation on parietal cells increases acid secretion due to increased activity of the proton pump
- an antagonist can be used to treat NSAID-induced peptic ulcers
- H2 receptor antagonists work together with proton pump inhibitors to reduce proton pump activity