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StomachGastric Secretions, Motility, Digestion and Vomiting
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Specific receptors for histamine, acetylcholine and gastrin located in the basolateral membrane of the parietal cell stimulate acid secretion. However, somatostatin, epidermal growth factor, β-adrenergic agonists and enteroglucagon inhibit acid secretion, presumably by an indirect mechanism as specific receptors for these factors have not yet been identified. Histamine binds to H2 receptors at the basolateral membrane of the parietal cell to stimulate acid secretion. The parietal cells also contain a muscarinic receptor, which increases acid secretion when vagal stimulation releases acetylcholine. Some species possess gastrin receptors in the gastric parietal cells, but in humans, gastrin receptors may be absent. However, gastrin is a potent stimulant of acid secretion in humans, and its effects appear to be mediated by the release of histamine from other cells in the gastric glands binding to H2 receptors in the parietal cell to stimulate acid production.
Gastric Lipase
Published in Margit Hamosh, Lingual and Gastric Lipases: Their Role in Fat Digestion, 2020
The studies on the physiology of gastric secretion show a lack of interaction between acid and pepsinogen secretion in isolated gastric glands.95 Hersey et al.,95 using the isolated gastric gland preparation of rabbit mucosa, report that despite the apparent correlation between acid and pepsinogen secretion observed in vivo, their in vitro results indicate that stimulation of acid and pepsinogen secretion are independent events. They summarize that this independence is evidenced by (1) the existence of specific stimuli, e.g., isoproterenol for pepsinogen and histamine for acid, (2) the finding that inhibition of acid formation (by thiocyanate) does not influence pepsinogen secretion, and (3) a failure to observe interactions when acid and pepsinogen secretion are coactivated by cell-specific agents. Thus, although there are common secretagogues such as cholinergic agents, forskolin, and adenosine cyclic nucleotides, the stimulation by these agents is considered as separate and independent at the cellular level. The investigators conclude that “the lack of functional interactions, therefore, indicates that any observed correlation between acid and pepsinogen secretions is fortuitous or reflects coordination at a level of integration above the isolated gastric gland.” Although lipase secretion was not examined in the above-cited study, the data on pepsinogen probably apply also to lipase since we also observed a lack of stimulation of lipase release from isolated rabbit gastric glands by even high concentrations of histamine (Figure 14 and Reference 17).
Endoscopic screening for upper gastrointestinal malignancy
Published in David Westaby, Martin Lombard, Therapeutic Gastrointestinal Endoscopy A problem-oriented approach, 2019
The epidemiological link between H. pylori infection and gastric cancer is now convincing. The World Health Organization consensus committee have concluded that there is sufficient evidence of the aetiological role. Virtually all infected patients will develop gastritis, leading to destruction and atrophy of gastric glands and other specialized cells. They are replaced by atrophic mucosa with intestinal metaplasia. The prevalence of atrophic gastritis increases by 2% annually in patients with Helicobacter infection, compared with 0.3% in the uninfected. There are many confounding factors, as treatment of patients who are infected with long-term acid suppression causes an increase in gastritis and intestinal metaplasia (Fig. 5.7). The hypothesis is that acid suppression changes the pattern of infection, with an antral gastritis being transformed to a gastric body gastritis, and this further suppresses acid secretion, increases inflammation and leads to atrophic gastritis. A large case control study in rural Japan showed by unconditional logistic regression analysis that H. pylori infection was associated with an increased odds ratio of 11 for men and 7 for women for the development of atrophic gastritis. In this study, diet, smoking and lifestyle were not related to atrophic gastritis. H. pylori infection also causes increased gastric cell proliferation and impaired secretion of vitamin C – factors that are improved after eradication of infection.
Gastro-protective effect of Artemisia Sieberi essential oil against ethanol-induced ulcer in rats as revealed via biochemical, histopathological and metabolomics analysis
Published in Biomarkers, 2022
Naglaa M. Ammar, Heba A. Hassan, Rania F. Ahmed, Abd El-Nasser G. El-Gendy, Ahmed M. Abd-ElGawad, Abdel Razik H. Farrag, Mohamed A. Farag, Abdelsamed I. Elshamy, Sherif M. Afifi
Histological examination of the stomach from rats of the control group showed the normal structure of the mucosal layer, with an intact epithelial layer (Figure 1(A)). In contrast, histopathological investigation of sections from ulcer group showed sloughed off a superficial layer, inflammatory cells infiltration. Necrosis of gastric glands can be observed. Moderate erosion of the superficial epithelium with denuded epithelial cells, mild haemorrhages in lamina propria, very few inflammatory cells were detected (Figure 1(B)). Pre-treatment with omeprazole showed the mucosal layer appeared nearly to normal structure (Figure 1(C)). On the other hand, ulcer group pre-treated with 100 mg/kg of AS-EO showed an improvement of superficial epithelium structure. Mild haemorrhages in lamina propria, very few inflammatory cells were detected (Figure 1(D)). In some cases of the stomach from ulcer group pre-treated with 100 mg/kg of AS-EO, the microscopic investigation indicated mild erosion of the mucosal layer that associated with mild haemorrhages (Figure 1(E)). Pre-treatment ulcer group with 200 mg/kg of AS-EO exhibited mild erosion in the mucosal layer (Figure 1(F)). Moreover, ulcer group pre-treated with 200 mg/kg of AS-EO showed that the superficial epithelium layer was restored more or less to control one (Figure 1(G)).
Protective effects of a standardized extract (HemoHIM) using indomethacin- and ethanol/HCl-induced gastric mucosal injury models
Published in Pharmaceutical Biology, 2019
Da-Ae Kwon, Yong Sang Kim, Sin Hwa Baek, Seul-Ki Kim, Hyun Kyu Kim, Sung-Kee Jo, Uhee Jung, Hae-Ran Park, Hak Sung Lee
For the determination of gastric lesion area, the inner surface of the stomach was photographed and analyzed using Image J software (NIH ImageJ, NIH, Bethesda, MD). Lesion area (%) was determined for the lesion area of the stomach tissue. The inhibition ratio was calculated as follows: Inhibition ratio (%) = {(control lesion area - sample lesion area)/control lesion area}) × 100. For histopathological analysis, the stomachs were fixed in 10% neutral formalin and fixed overnight. Sections of the gastric glands were sliced at a thickness of 5 μm and stained with hematoxylin and eosin (H&E). The stained sections were examined under microscope for any damage or change in morphology of the particular tissue.
The clinicopathological characteristics of gastric cancer and precancerous conditions in gastric DLBCL and MALT lymphoma patients: a multi-center retrospective study
Published in Annals of Medicine, 2023
Yun Feng, Tian-Jiao Duan, Qing Huang, Zhi-Yi Li, Ya-Ping Liu, Miao-Sha Luo, Gui-Fang Lu, Wen Shi, Zhi-Yong Zhang, Hong-Xia Li
Atrophy and intestinal metaplasia can be diagnosed by gastroscopy or pathology alone. Diagnosis of gastric cancer and low-grade intraepithelial neoplasia must be confirmed by histopathological examination of a biopsy or surgical specimens. Endoscopic manifestations of atrophic gastritis include the pale appearance of gastric mucosa, thinning of the gastric mucosa, increased visibility of vasculature, and loss of gastric folds [15,16]. The degree of atrophic gastritis is assessed using the Kimura-Takemoto classification system or Operative Link for Gastritis Assessment (OLGA) classification [15–17]. The pathological diagnosis of atrophic gastritis is based on the loss of normal glandular epithelium gastric glands [15,16]. Intestinal metaplasia is manifested as a gray-white flat bulge on white light endoscopy, and regular vessels with ridge/tubular or tubulovillous glands, particularly with a light blue crest on magnified narrow band imaging, mostly on an atrophic background [18]. The degree of intestinal metaplasia is assessed using the Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM) system [15,16]. The pathological manifestations of intestinal metaplasia are divided into complete intestinal metaplasia and incomplete intestinal metaplasia. Complete intestinal metaplasia resembles the small intestinal epithelium, while incomplete intestinal metaplasia resembles the colonic epithelium [19]. The classification of gastric cancer and intraepithelial neoplasia was defined by World Health Organization [20]. Low-grade intraepithelial neoplasia has limited architectural abnormalities and only mild to moderate cytological atypia, with hyperchromatic, elongated, pseudostratified nuclei [21].