Gastric ulcers occur when aggressive factors in gastric juice – such as acid and digestive enzymes – overpower the protective factors in the stomach lining1. As horses have evolved to be continually feeding, acid is continually secreted into the stomach; this means that prolonged periods without food to neutralise that acid can lead to ulceration. When horses are denied free access to feed or fail to eat, ulcers can develop rapidly1.
Two types of gastric ulcer The equine stomach is covered by two different types of epithelium.
Squamous Ulceration The dorsal region is covered by squamous epithelium and ulcers occur here as a direct result of extended exposure to acid secretions. Many equine stomach ulcers occur in the area near to the oesophagus2. In foals the developing cell lining is thinner than in adults, making foals especially prone to gastric ulceration3.
Glandular Ulceration The ventral region is covered in glandular epithelium and ulcers occur here when the protective mucus layer is compromised e.g. due a side-effect of certain medications, enabling acid erosion of the stomach wall4.
Murray MJ, Eichorn ES. Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall confinement with ad libitum access to hay on gastric ulceration in horses. Am J Vet Res 1996; 57: 1599-1603.
Widenhouse TV, Lester, Merritt AM. Effect of hydrochloric acid, pepsin, or taurocholate on bioelectric properties of gastric squamous mucosa in horses. Am J Vet Res 2002; 63: 744-749.
Murray MJ. Gastroduodenal ulceration in foals. Equine Vet Ed 1999; 11: 199-207.
MacAllister CG, Morgan SJ, Borne AT et al. Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses. J Am Med Assoc 1993; 202: 71-77.