GI ulcers

[obiwan]

i can't seem to find a good answer for this question in the various text but just wondering what is exactly the reason behind increased acid production with duodenal ulcers while there is normal gastric acid secretion by gastric ulcers? my only guess is that the duodenum is secreting alkaline juice so h.pylori needs acid for colonization of mucosa.

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[agranulocytosis]

I believe you are correct. I remember my prof saying the difference lies with the bacteria's tropism for an acidic environment.

 

[Mediculous]

i can't seem to find a good answer for this question in the various text but just wondering what is exactly the reason behind increased acid production with duodenal ulcers while there is normal gastric acid secretion by gastric ulcers? my only guess is that the duodenum is secreting alkaline juice so h.pylori needs acid for colonization of mucosa.

I think that with gastric ulcers, H. pylori damages antral G cells, which decreases gastrin stimulation of acid production in the parietal cell.

According to MicroCards, regarding increased gastric acid in duodenal ulcers: when antral D cells are damaged by H. pylori they produce less somatostatin, which leads to less inhibition of gastrin from G cells which leads to more stimulation of parietal cells, culminating with acid hypersecretion, which in turn damages the duodenal mucosa.

This article supports the d cell explanation: http://www.ncbi.nlm.nih.gov/pubmed/8500723

That's the first time I've heard of D cells in the antrum, since they aren't explicitly mentioned in the 3rd ed. of BRS physio in the illustration of stomach cells on p.231. Wikipedia has a diagram with them included, though. Thank you, wikipedia.

 

[LUBDUBB]

i can't seem to find a good answer for this question in the various text but just wondering what is exactly the reason behind increased acid production with duodenal ulcers while there is normal gastric acid secretion by gastric ulcers? my only guess is that the duodenum is secreting alkaline juice so h.pylori needs acid for colonization of mucosa.

I don't think the pathogenesis of H.pylori is crystal clear enough to explain the heterogeneity of clinical presentations. For one, I don't think it's very well understood why the bacteria lives in the stomach and NOT in the duodenum, even though it produces duodenal ulcers.

 

[LUBDUBB]

For those still interested in this thread.....I came accross costanzo's simplified explanation:

Gastric ulcers:
H+ secretion is dec because H+ leaks back through the damaged mucosa

Duodenal ulcers:
H+ secretion is inc; excess H+ is delivered to duodenum, damaging its mucosa.
H. pylori inhibits somatostatin --> therefore inc H+stim; and h.pylori inhibits intestinal HCO3 secretion, leaving the duodenal mucosa vulnerable to acid.

Don't ask me where she gets her mechanisms; the reference is p. 218 BRS physio 4th ed.