30. Treatment of gastric and duodenal ulcers Flashcards Preview

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Flashcards in 30. Treatment of gastric and duodenal ulcers Deck (15)
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1
Q

what can gastric and duodenal ulcers be grouped into and why?

A

peptic ulcers

though they differ in terms of presentation and epidemiology, their treatment is the same

2
Q

what does the carbon-urea breath test do and how does it work?

A

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

3
Q

what does the stool antigen test do?

A

tests for H. pylori antigens in the stool of the patient

4
Q

what % of duodenal and gastric ulcers are due to H. pylori?

A

duodenal - 98-100%

gastric - 70-80%

5
Q

what is H. pylori?

A

a motile spirochete that is able to move around (due to its flagella)

it is a commensal bacteria that is present in the stomach

6
Q

how does H. pylori cause ulceration?

A
  • 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
7
Q

what is the link between acidity and ulceration?

A

increased acidity –> peptic ulcer

increased acidity also –> increased cell production of protons –> even greater acidity –> further ulceration

8
Q

how are H. pylori infections treated?

A

amoxicillin and clarithromycin antibiotics

9
Q

what is used to reduce acid production?

A

proton pump inhibitor for 7 days

10
Q

what might you give alongside amoxicillin and clarithromycin?

A

quinolone or tetracycline if the H. pylori infection doesn’t go away

11
Q

give an example of a proton pump inhibitor and outline why they are necessary

A

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
12
Q

what is the second most common cause of peptic ulcers?

A

prolonged NSAID usage

13
Q

in what ways are NSAIDs and H. pylori similar?

A
  • NSAIDs can be directly cytotoxic
  • they reduce mucus production
  • this leads to a breakdown of the mucus barrier –> epithelia exposure –> ulceration
14
Q

in what ways are NSAIDs different to how H. pylori causes ulceration?

A
  • NSAIDs may increase the likelihood of bleeding (acts as an anti-platelet agent)
  • this can worsen the symptoms
15
Q

give an example of a histamine H2 receptor antagonist and outline what they do

A

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