Secretion of acid by the parietal cells of the gastric glands is stimulated by factors such as the thought of food, distension of the stomach, and protein ingestion (Hammer & McPhee, 2014). Gastric acid hypersecretory states are responsible for the development and progression of GERD, PUD, and gastritis disorders (Phan, Benhammou, & Pisegna, 2015). Studies have consistently agreed about the proposed role of visceral hypersensitivity, motility dysfunctions, and central neural mechanisms in gastric acid hypersecretion in GERD (de Bortoli, Martinucci, Bellini et al. , 2013). In the cephalic phase, visceral hypersensitivity occurs due to overstimulation of M3 muscarinic receptors by acetylcholine released by vagal afferents (Phan et al ., 2015). In the gastric phase, visceral hypersensitivity occurs through overstimulation of cholecystokinin-2 (CCK-2) receptors expressed on ECL cells by gastrin. The process is sustained by stimulants such as histamine and PACAP, which are also responsible for recycling of pumps and synthesis of new proton pumps. cAMP. However, inhibition of Somatostatin secretion by Vagal ACh and the T H 1 cytokine interferon-γ leads to sustained acid production that causes hypergastremia. Transient lower oesophageal sphincter relaxations and other lower oesophageal sphincter pressure abnormalities cause reflux leading to injury to the mucosal wall.
In peptic ulcer disease (PUD), colonization of the duodenum by H pylori predisposes the mucosal wall to distal gastric cancer. According to Hammer and McPhee (2014) and Phan et al. (2015), hypersensitivity is made possible by the transformation of parietal cells upon stimulation. The cells’ tubulovesicular membranes fuse with the plasma membrane to form a canalicular membrane with microvilli, increasing the area of apical membrane 50-100 times, and increasing the secretion of HCl by H + -K + ATPase pumps into the lumen of the stomach (Hammer & McPhee, 2014). Metaplasia results in gastric secreting tumors ( Zollinger-Ellison syndrome ), significantly increasing the apical membrane area that is stimulated and hence hyper-secretion. Metaplasia increases visceral hypersensitivity to stimulants, and together with suppressed released of Somatostatin, form the primary causes of hypergastrinemia PUD.
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Gastritis disorders are primarily caused by H pylori and to a lesser extent by in all gastric Autoimmune mechanisms and Helicobacter heilmannii infection. Chronic gastritis results characterized by severe inflammation and atrophic gastritis decreases gastric acid secretion and production (Phan et al. , 2015). Gastritis with atrophic and metaplastic sequelae are characterized by a damaged mucosal membrane and reduces the area of the apical membrane exposed to stimulation. The outcome is impaired secretion and production of gastric acid, resulting in a hypogatremia state. H pylori may also induce antibodies that prevent activation of proton pumps within the parietal cells. However, where H pylori cause metaplasia, hyper-secretion occurs in a similar mechanism as in PUD.
References
de Bortoli, N., Martinucci, I., Bellini, M., Savarino, E., Savarino, V., Blandizzi, C., & Marchi, S. (2013). Overlap of functional heartburn and gastroesophageal reflux disease with irritable bowel syndrome. World Journal of Gastroenterology , 19(35), 5787-5797.
Hammer, G. G., & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.
Phan, J., Benhammou, J. N., & Pisegna, J. R. (2015). Gastric hypersecretory states: investigation and management. Current treatment options in gastroenterology , 13 (4), 386-397.
