- Joined
- Jan 18, 2012
- Messages
- 3,880
- Reaction score
- 1,676
What is the mechanism behind peptic ulcer formation secondary to hyperparathyroidism?
This has nothing to do with MEN-I (Wermer syndrome) btw. Kaplan QBank says increased PTH can lead to peptic ulcers, and they don't give a mechanism/explanation. They even have a vignette of a guy with an ulcer and hypercalcaemia, and I thought it was MEN-I, but it wasn't; they also went on to say that ZES tends to produce multiple, not isolated, ulcers.
The only thing I can think of is increased PTH --> hypercalcaemia --> pancreatitis --> islet delta-cell damage --> decreased somatostatin --> increased HCl secretion --> ulcers.
That actually sounds like a stretch to me, but the only reason I feel that mechanism is a possibility is because if DM can occur secondary to pancreatitis, and beta-cells are more numerous than delta-cells, then delta-cell numbers could definitely decline as well.
A more simple explanation is that it could just be due to decreased effectiveness of pancreatic bicarbonate secretion.
Any thoughts?
This has nothing to do with MEN-I (Wermer syndrome) btw. Kaplan QBank says increased PTH can lead to peptic ulcers, and they don't give a mechanism/explanation. They even have a vignette of a guy with an ulcer and hypercalcaemia, and I thought it was MEN-I, but it wasn't; they also went on to say that ZES tends to produce multiple, not isolated, ulcers.
The only thing I can think of is increased PTH --> hypercalcaemia --> pancreatitis --> islet delta-cell damage --> decreased somatostatin --> increased HCl secretion --> ulcers.
That actually sounds like a stretch to me, but the only reason I feel that mechanism is a possibility is because if DM can occur secondary to pancreatitis, and beta-cells are more numerous than delta-cells, then delta-cell numbers could definitely decline as well.
A more simple explanation is that it could just be due to decreased effectiveness of pancreatic bicarbonate secretion.
Any thoughts?