Pyloric duct ulcers often lack the periodic and rhythmic pain of typical ulcers, postprandial epigastric pain is common, poor response to antacids, easy vomiting or pyloric obstruction, and more complications such as perforation or bleeding. Etiology: 1. Since bile reflux flows through here first, the bile salt component in bile can damage the gastric mucosal barrier, plus the longer residence time of chyme here, the local pressure increases and the blood circulation is relatively poor. In the past, this disease was rare, but with the popularity of endoscopy and the attention of endoscopists, the incidence of this disease was found to be not low. 2, because the ulcer occurs at the end of the stomach and duodenal junction, and its pathophysiology is similar to that of duodenal ulcer, stomach acid generally increases, and the abdominal pain of some pyloric duct ulcers is similar to DU; however, the abdominal pain of several patients is stubborn, and the relief is not obvious after eating, even if taking acid suppressants is not as significant as DU; another part of patients have abdominal pain immediately after meals, probably because eating that causes frequent peristalsis of the gastric pylorus to intensify chyme on This may be due to the direct stimulation of the ulcer surface on the narrow channel by the frequent peristalsis of the pylorus caused by eating. Therefore, the abdominal pain of pyloric duct ulcer does not have the periodicity and regularity of a typical ulcer. At the same time, the disease has a tendency to recur, which is related to the contraction dysfunction of the smooth muscle of the pyloric duct and the ulcer surface does not heal easily. 3, the gastroduodenal mucosa is often exposed to high concentrations of gastric acid, in addition to pepsin, microorganisms, bile salts, ethanol, drugs and other harmful substances. However, under normal circumstances, the gastroduodenal mucosa can resist the damaging effects of these aggressive factors and maintain the integrity of the mucosa. This is because the gastroduodenal mucosa has a series of defense repair and restoration mechanisms, including mucus bicarbonate barrier, mucosal barrier, mucosal blood flow, cell renewal, prostaglandins, and epidermal growth factor. Peptic ulcers occur as a result of a loss of balance between invasive factors that have a damaging effect on the gastroduodenal mucosa and the mucosa’s own defense-repair factors. GU and DU differ in their pathogenesis, with the former being primarily a weakening of defense and repair factors and the latter being primarily a strengthening of invasive factors. Peptic ulcer is a disease caused by multiple etiologies, i.e., the etiology and pathogenesis may not be the same between patients, but only the clinical manifestations are similar.