Changes

   

   

It is clear that the aetiopathogenesis of EGUS is multifactorial(Josnsen 2006).  What remains uncertain, is how these various risk factors interact to produce lesions in different regions of the equine gastric mucosa.  Based on extrapolation from other species, it is conceivable that a reduction in mucosal blood flow might result from:

It is clear that the aetiopathogenesis of EGUS is multifactorial.<ref name="Jonssen">Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref> What remains uncertain, is how these various risk factors interact to produce lesions in different regions of the equine gastric mucosa.  Based on extrapolation from other species, it is conceivable that a reduction in mucosal blood flow might result from:

*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 (DIC)).

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

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 the

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.

==Clinical syndrome==

==Clinical syndrome==