Peptic ulcers are defects in the ga

Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer.
In the event of acid and pepsin entering the epithelial cells, additional mechanisms are in place to reduce injury. Within the epithelial cells, ion pumps in the basolateral cell membrane help to regulate intracellular pH by removing excess hydrogen ions. Through the process of restitution, healthy cells migrate to the site of injury. Mucosal blood flow removes acid that diffuses through the injured mucosa and provides bicarbonate to the surface epithelial cells.

Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs, H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, mucosal blood flow, cellular restitution, and epithelial renewal.

The gram-negative spirochete H pylori was first linked to gastritis in 1983. Since then, further study of H pylori has revealed that it is a major part of the triad, which includes acid and pepsin, that contributes to primary peptic ulcer disease. The unique microbiologic characteristics of this organism, such as urease production, allows it to alkalinize its microenvironment and survive for years in the hostile acidic environment of the stomach, where it causes mucosal inflammation and, in some individuals, worsens the severity of peptic ulcer disease.

When H pylori colonizes the gastric mucosa, inflammation usually results. The causal association between H pylori gastritis and duodenal ulceration is now well established in the adult and pediatric literature.

Результаты (английский) 3:

消化性溃疡是在胃或十二指肠粘膜，穿过粘膜肌层缺损。胃和十二指肠上皮细胞分泌粘液以响应上皮衬里的刺激，并作为胆碱能刺激的结果。对胃和十二指肠粘膜浅部存在的凝胶层的形成，这是不透水的胃酸和胃蛋白酶。其他的胃和十二指肠细胞分泌的氢，它有助于在缓冲酸，在于粘膜附近。的E型前列腺素（PGE）有重要的保护作用，因为PGE增加碳酸氢盐和粘液层的生产。
如酸和胃蛋白酶进入上皮细胞，额外的机制来减少损伤。在上皮细胞，在基底细胞膜离子泵帮助去除多余的氢离子调节细胞内pH值。通过恢复原状，健康细胞迁移到损伤部位。黏膜血流量，消除酸扩散通过受伤的粘膜表面的上皮细胞提供碳酸氢盐。

正常条件下，胃酸分泌和胃粘膜的防御之间存在的生理平衡。黏膜损伤，因此，消化性溃疡时发生的积极因素和防御机制之间的平衡被破坏。积极的因素，如非甾体类抗炎药，幽门螺杆菌感染，酒精，胆盐，酸和胃蛋白酶，可以通过允许氢离子的后扩散和随后的上皮细胞损伤改变粘膜防御。防御机制包括细胞间连接紧密，粘液，粘膜血流量，细胞恢复，和上皮细胞的更新。

革兰氏阴性螺旋体幽门螺杆菌首次在1983胃炎联系。从那时起，幽门螺杆菌的进一步研究表明，它是黑社会的一个重要组成部分，它包括酸和胃蛋白酶，导致原发性消化性溃疡病。该生物的独特的微生物学特征，如脲酶生产，允许其碱性的微环境和生存在胃的酸性环境下年的敌意，它会导致粘膜炎症，在一些个人，加重消化性溃疡病的严重程度。

当幽门螺杆菌感染的胃黏膜炎症，通常结果。幽门螺旋杆菌胃炎和十二指肠溃疡之间的因果关系现在已经建立在成人和儿童文学。