Changes

   

   

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:

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,<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> 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