溃疡Ulcer · 腺胃 · 消化系统 · NTP ntp-0274
诊断要点:腺胃溃疡应根据病变的范围和分布进行诊断和分级。水肿、炎症和邻近上皮的增生不应单独诊断,除非它们是病变的显著组成部分。
病变描述
在小鼠和F344/N大鼠的NTP研究中,腺胃溃疡的自发性发生并不常见。溃疡主要见于受处理的大鼠,并已被实验性诱导作为人类溃疡的模型。溃疡(Figure 1、Figure 2)定义为整个上皮层厚度丧失,深达或穿透基底膜和黏膜肌层,而糜烂(见Stomach, Glandular Stomach - Erosion)为上皮的部分厚度丧失。相比之下,如果坏死上皮仍然存在且至少部分附着于其下的固有层,则诊断为上皮坏死而非溃疡。细菌感染可继发于糜烂或溃疡,原因包括灌胃操作造成的局部创伤或坏死/缺血。大鼠胃内的固有细菌通常仅见于附着于最靠近管腔的黏膜表面,而不见于胃小凹内。发生糜烂/溃疡后,细菌可进入黏膜和胃壁的更深部位。产生糜烂和溃疡的化合物可通过影响黏膜血流、黏膜细胞动力学、黏液或酸/碳酸氢盐分泌,或维持黏液屏障而发挥作用。高脂饮食、慢性泛酸缺乏、生糖氨基酸缺乏、血小板活化因子、胆汁盐反流增加以及外分泌胰腺功能降低与溃疡发生相关,但仅在迷走神经支配完整时如此。溃疡的介质可能是花生四烯酸代谢的脂氧合酶途径的代谢产物。白三烯阻断剂类药物可预防某些致溃疡物引起的溃疡。
诊断与分级建议(NTP 共识)
腺胃溃疡应根据病变的范围和分布进行诊断和分级。水肿、炎症和邻近上皮的增生不应单独诊断,除非它们是病变的显著组成部分。如果坏死上皮仍然存在且至少部分附着于其下的固有层,则诊断为上皮坏死而非溃疡。相关链接:Stomach, Glandular Stomach - Erosion
图谱


英文原文
展开 NTP 官方英文描述与建议
Comment:
Spontaneous occurrence of ulceration of the glandular stomach is uncommon in NTP studies in mice and F344/N rats. Ulceration is seen primarily in treated rats and has been experimentally induced as a model for ulcer in humans. An ulcer ( Figure 1 and Figure 2 ) is defined as the loss of the entire epithelial thickness down to or through the basement membrane and muscularis mucosa, whereas an erosion (see Stomach, Glandular Stomach - Erosion ) is a partial thickness loss of epithelium. In comparison, necrosis of epithelium is diagnosed instead of ulceration if the necrotic epithelium is still present and at least partially attached to the underlying lamina propria. Bacterial infections can occur secondary to erosion or ulceration due to local trauma from a gavage procedure or necrosis/ischemia. Indigenous bacteria in the stomach of the rat are normally found adherent to only the most luminal mucosa but not in the gastric pits. Following erosion/ulceration, bacteria can gain access to deeper portions of the mucosa and stomach wall. Compounds that produce erosions and ulcers can act via effects on mucosal blood flow, mucosal cell kinetics, mucus or acid/bicarbonate secretion, or maintenance of the mucus barrier. High-fat diets, chronic pantothenic acid deficiency, deficiency of gluconeogenic amino acids, platelet-activating factor, increased reflux of bile salts, and reduced exocrine pancreatic function are associated with ulceration but only with intact vagal innervations. The mediators of ulceration may be metabolites of the lipooxygenase pathway of arachidonic acid metabolism. Pharmaceutical agents that are leukotriene blockers prevent ulceration by some ulcerogens.
Recommendation:
Ulceration of the glandular stomach should be diagnosed and graded based upon the extent and distribution of the lesion. Edema, inflammation, and hyperplasia of the adjacent epithelium should not diagnosed separately unless they are a prominent component of the lesion. Necrosis of epithelium is diagnosed instead of ulceration if the necrotic epithelium is still present and at least partially attached to the underlying lamina propria. Related Links: Stomach, Glandular Stomach - Erosion
来源与引用
原始条目:https://ntp.niehs.nih.gov/atlas/nnl/alimentary-system/stomach-glandular-stomach/Ulcer
图谱总目录:NTP Nonneoplastic Lesion Atlas。 内容属美国联邦政府作品(公有领域),可引用;引用时请标注来源。
建议引用格式:NTP Nonneoplastic Lesion Atlas. Ulcer (stomach-glandular-stomach). LabSmart 中文版:
https://www.labsmart.cn/ntp/stomach-glandular-stomach-ulcer.html
中文图谱总页(可展开对照全部 595 条):https://www.labsmart.cn/ntp-atlas.html#stomach-glandular-stomach-ulcer