Changes

*hypotensive shock (for example with blood loss, sepsis, endotoxaemia or fluid sequestration in colic)

*hypotensive shock (for example with blood loss, sepsis, endotoxaemia or fluid sequestration in colic)

*an increase in sympathetic tone (which might be related to physiological or psychological stresses) or  

*an increase in sympathetic tone (which might be related to physiological or psychological stresses) or  

*other severe disease states (such as disseminated intravascular coagulation).

*other severe disease states (such as [[DIC|disseminated intravascular coagulation]]).

Furthermore, any impairment of gastric motility (as seen with neurological imbalances, several types of colic and certain drugs) might be expected to increase the risk of ulceration.  Despite a lack of clarity, the final common pathway for EGUS appears to be the breaching of mucosal defences by acidic gastric contents.  Since horses secrete gastric HCl continuously, even in the fasted state,<ref>Campbell-Thompson, M.L, Merritt, A.M (1987) Effect of ranitidine on gastric acid secretion in young male horses.  ''Am J Vet Res'', 48:1511-1515.</ref> they are especially vulnerable to acid-associated damage.

Furthermore, any impairment of gastric motility (as seen with neurological imbalances, several types of colic and certain drugs) might be expected to increase the risk of ulceration.  Despite a lack of clarity, the final common pathway for EGUS appears to be the breaching of mucosal defences by acidic gastric contents.  Since horses secrete gastric HCl continuously, even in the fasted state,<ref>Campbell-Thompson, M.L, Merritt, A.M (1987) Effect of ranitidine on gastric acid secretion in young male horses.  ''Am J Vet Res'', 48:1511-1515.</ref> they are especially vulnerable to acid-associated damage.