Duodenal ulcers are due to defects in the mucosal and muscular layers of the duodenum caused by a variety of factors. Although it is similar to gastric ulcer in terms of clinical manifestations and medications, it is significantly different in terms of onset, age, gender, and pathogenesis. It is a chronic ulcer that is only found in the contact area of the gastrointestinal tract and gastric juice, also known as ulcer disease, which is called “stomach pain”, “heart pain” and “stomach pain” in Chinese medicine. Etiology 1, genetic genes Genetic factors play a more important role in the susceptibility of the disease, based mainly on: (i) the high incidence of the patient’s family; (ii) the relevance of genetic markers (blood group and blood group secretory material, HLA antigen, high pepsinogen), the incidence of duodenal ulcer in the siblings of patients with duodenal ulcer is 2.6 times higher than the general population; more noteworthy is the incidence of duodenal ulcer in single The incidence of duodenal ulcer in siblings of singleton twins is 50%, and the incidence of duodenal ulcer in siblings of doubleton twins is also increased. The pathogenesis of duodenal ulcer is not a single well-defined process, but a complex, interactive formation of factors; caused by a malfunction in the balance between damaging factors and defenses. 3, weakened defense mechanism of duodenal mucosa duodenum through specific pH-sensitive receptors, acidification reaction, feedback delayed gastric emptying, keeping the pH in the duodenum close to neutral, and duodenal mucosa can absorb luminal hydrogen ions and not damaged by bile salts, duodenal ulcer patients, this feedback delayed gastric emptying and inhibition of gastric acid is weakened, and gastric emptying accelerated, so that the lumen of the duodenal bulb The increased acid load in the lumen of the duodenal bulb causes mucosal damage that can lead to ulcer formation. Prostaglandin E not only has the effect of inhibiting gastric acid, but more importantly has a direct protective effect on the mucosa and promotes ulcer healing. The content of prostaglandin E in the duodenal mucosa of patients with duodenal ulcer is significantly lower than that of normal controls, which reduces the protective effect of the duodenal mucosa. 4, Helicobacter pylori infection Helicobacter pylori infection and the development of peptic ulcer is closely related, eradication of Hp treatment can significantly reduce the recurrence rate of ulcer, Hp infection is the main cause of gastric sinusitis, is an important factor causing peptic ulcer, Hp is a microaerobic gram-negative bacillus, spiral-shaped, human gastric mucosa epithelial cells is its natural colonization site, Hp can survive in the acidic gastric juice is due to its The most reliable way to detect Hp in mucosal tissue is to combine bacterial culture and histological staining, and a simpler and faster method to detect Hp is the endoscopic biopsy tissue urease test, which has a sensitivity of 88% to 93% and a specificity of 99% to 100%. Hp is a common bacterial infection in humans, and its prevalence is related to age, race, economy and hygiene. Hp can be transmitted from person to person by the oral-fecal or oral-oral route, and virtually all patients with duodenal ulcers have Hp infection. Patients with acute duodenal ulcers and Hp infection reactively secrete more acid and release more gastrin after eating than patients with uninfected ulcers. When gastric acid secretion increases, the duodenal bulb is hyperacidified, causing foci of gastric epithelial metaplasia within the duodenal bulb, creating conditions for Hp to transplant from the gastric sinus mucosa to the duodenal bulb, where Hp survives and multiplies and acute duodenitis occurs, and ulceration occurs under the induction of other ulcerogenic factors, but this mechanism of duodenal ulcerogenesis remains to be further confirmed. Although all the above factors are related to duodenal ulcers, acid remains the most important, and medical and surgical treatment reduces gastric acid secretion, which results in ulcer healing, and excessive acid secretion causes ulcer formation, and animal experiments with chronic histamine stimulation producing excessive acid can form the same duodenal ulcers as in humans. Clinical manifestations The main clinical manifestation of duodenal ulcer is pain in the upper abdomen, which can be dull, burning, distending or severe, or it can be a vague discomfort only when hungry. Typically, the pain is mild or moderate and persistent below the glabella, and can be relieved by acidulants or food. About 2/3 of the pains are rhythmical: epigastric pain starts 1 to 3 hours after breakfast and continues until after lunch if no medication or food is taken. The pain returns 2 to 4 hours after eating and must also be relieved by eating. About half of the patients have midnight pain, and the patient can often wake up in pain. Rhythmic pain mostly lasts for a few weeks and can recur as it relieves for months.