Gastric ulcer formation of a variety of factors
The occurrence of peptic ulcer disease is the invasion of the gastrointestinal tract mucosa of factors than mucosal factors in self-defense capability to protect results. Invasion main factors include gastric acid, pepsin and Helicobacter pylori, in addition to bile salts, non-autologous anti-inflammatory drugs and so on. Protective factors are mainly a bicarbonate barrier mucus, mucosal barriers. Peptic ulcer is a multi-etiology, mechanisms of complex diseases frequently occurring reason, its formation can be said to a variety of pathogenic factors effects. Clinical findings of the stomach, duodenal ulcers, mostly for chronic ulcers, and stress ulcer is another clinically significant acute ulcers.
1, the pathogenesis of gastric ulcer
The basis of patients with gastric ulcer gastric acid and pepsin secretion in normal volume and is similar to the majority of ulcer patients but lower than the amount of postprandial gastric acid secretion, so the majority of peptic ulcer disease in the pathogenesis of gastric acid may not be due to the increased but because of mucosal defense machine to move destroyed.
Helicobacter pylori infection is likely to remain a major cause of peptic ulcer disease. Occurred in the stomach ulcers and distal gastric antrum pyloric canal ulcer more with Helicobacter pylori infection. In addition, the taking of non-autologous anti-inflammatory drug is a major defense mechanism of gastric mucosa damage common causes. Non-self-anti-inflammatory drugs inhibit the prostaglandin cyclooxygenase, inhibiting prostaglandin production, thereby reducing the secretion of mucus and bicarbonate, to reduce gastrointestinal mucosal blood flow, leading to a decline in mucosal defense capabilities.
Bile reflux may also be one of the causes stomach ulcers. Bile reflux into the stomach to alkaline, leading to reverse the proliferation of hydrogen ions into the gastric mucosa increased and may induce increased antral gastrin secretion, while bile salts can directly damage gastric mucosa, causing ulcers.
2, the pathogenesis of duodenal ulcer
First of all, the majority of H. pylori infection is a major cause of duodenal ulcer. Helicobacter pylori itself does not directly encroach upon the gastrointestinal tract organization, but through its formation of bacterial toxins, enzymes or physical destruction of inflammatory mucosal defense mechanisms, including the reduction of bicarbonate secretion, mucus changes in the composition and structure, inducing epithelial cell degeneration, etc., and by promoting the release of gastrin and other ways to increase gastric acid and pepsinogen secretion. In susceptible persons, decreased mucosal defense mechanisms, the epithelium susceptible to gastric acid and pepsin, and other invasion factors damage, leading to ulcer disease.
Second, the increased gastric acid and pepsin in the pathogenesis of duodenal ulcer is also important reasons. About one-third or so of gastric acid secretion in patients with duodenal ulcer was significantly higher than normal, its causes may include: the promotion of gastric acid secretion of factors too strong, such as the G-cell hyperplasia or hyperfunction; pairs of gastrin and so promote acid secretion increased the sensitivity of the material, such as the parietal cells of patients with gastrin affinity than normal high; inhibit gastric acid secretion factors weakened, such as the D cells, the reduction or reduction of somatostatin release. These changes may be more with Helicobacter pylori infection.
In addition, about less than 10% of duodenal ulcer patients with H. pylori-negative, its incidence may be related to drinking, smoking and non-self-serving body of anti-inflammatory drugs and other factors.
Comments
Leave a Reply
WordPress ·