Abstract
The common acid related diseases of the upper gastrointestinal tract could be considered as primarily due to the defect in barrier function either of the gastric mucosal or duodenal epithelium leading to the formation of gastric or duodenal ulcers. An attempt was made in this review to discuss the classification, pathophysiology, diagnosis and treatment of gastric ulcer in dogs. Early surgical advances in the management of peptic ulcers are emphasized that were then subsequently replaced by pharmacological treatment (histamine H2-receptor antagonists, proton pump inhibitors) and considered as the major strategy against the acid disorders.
Highlights
In narrow sense, gastric ulcer is a defect in the mucosa that penetrates the muscularis mucosa [1]
[34] Reported diarrhoea, progressive anorexia, 23-39% body weight loss, vomition, depression and lethargy associated with primary gastrointestinal lymphosarcoma induced gastric ulceration in 3 male Shepard dogs and one Boxer dog
Gastro diagnose (Merck) is a preparation of pentagastrin, when injected IM @ 6 microgm/Kg body weight. increases the gastric secretion in a dog suffering from gastric ulceration and perforation
Summary
Gastric ulcer is a defect in the mucosa that penetrates the muscularis mucosa [1]. The common underlying pathophysiological mechanism is stimulation of gastric acid secretion and inhibition of the gastric mucosal barrier properties. The multifactorial pathophysiological mechanism of gastric ulceration, stem from any processes, including physical damage to the gastric mucosa, impaired mucosal defense and chemical alteration to the mucosa and its repair process. Prostaglandins that are beneficial to the stomach are created through the COX1 pathway [25] Without these beneficial PG's blood flow and gastric mucous and bicarbonate production are reduced. Chemical insult to the gastric mucosa comes from endogenous compounds (HCl, bile acids, and pancreatic enzymes) or exogenous HCl. In Dogs, Helicobacter pylorus experimentally increases gastrin production by endocrine G cells, which increases production of the HCl by oxyntic cells. Concurrent hepatic diseases may have prolonged its duration of activity thereby increasing the severity of side effects including gastro intestinal ulceration
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