TRC: Proton pump inhibitors for ulcers

Proton pump inhibitors

Proton pump inhibitors for ulcers

Secretion of H+ into the lumen results from activation of the parietal cell H+/K+ATPase (proton pump). Activation of the proton pump is brought about by activation of histamine, gastrin, or muscarinic receptors. Inhibition of the proton pump by proton pump inhibitors (PPIs) is the most effective mechanism to reduce acid secretion.

Previously, there were serious concerns about the potential side effects of PPIs as a result of their superb acid-reducing capacity. Serum gastrin levels could increase and enterochromaffin-like cell hyperplasia could occur (and was indeed observed in gastric carcinoid tumours in animal models).

However, this has not appeared to be the case in humans during the 15 years of clinical and endoscopic surveillance while using PPIs. Theoretically, the risk of gastrointestinal and nosocomial infections is increased during PPI therapy, but in daily practice this has also not occurred.

PPIs (omeprazol, pantoprazol and rabeprazol) should be taken on an empty stomach to facilitate absorption. Ulcer patients should be told that pain relief does not correlate with endoscopic evidence of healing and that the drugs should be continued for the duration of 7 to 14 days, as indicated.

Which effect is NOT related to PPI therapy?

Extra info: Due to reduced gastric acid and increased pH after PPI therapy, there is an increase in gastrin secretion (as part of a feedback loop) and increase in local bacteria. PPIs are also potent inhibitors of the CYP450 system.

Option explanation:

serum gastrin increases

increase in small bowel bacterial growth

cytochrome P450 interactions

gallstone formation

Maintenance therapy with PPIs should be considered in patients with

Extra info: The severity of all three of the diseases warrants maintenance therapy with a PPI.

Option explanation:

Barrett oesophagus

oesophageal ulceration (endoscopy)

grade 3 oesophagitis

all three diseases