Mucus gastric

Ulcer formation is the net result of a lack of homeostasis between factors within the gastrointestinal tract responsible for the breakdown of food (e.g., gastric acid and pepsin) and factors that promote epithelial defense and repair (e.g., bicarbonate, mucus secretion, and prostaglandins). 

Prostaglandins, one of the most important epithelial growth factors, inhibit gastric acid secretion and have numerous mucosal protective effects, the most important of which include the stimulation of both mucus and phospholipid production, promotion of bicarbonate secretion, and increased mucosal cell turnover. Damage to the mucosal defense system is the primary method by which HP or NSAIDs cause peptic ulcers. 

Mucus is produced by the mucus neck cells and by the surface epithelial cells of the stomach wall. A thick layer of mucus adheres to the wall of the stomach, forming the gastric mucosal barrier. The function of this barrier is to protect the gastric mucosa from injury — specifically, from the corrosive actions of HCl and pepsin. Together with bicarbonate ion released into the lumen of the stomach, mucus neutralizes the acid and maintains the mucosal surface at a nearly neutral pH. 

There is also a gradient from the low luminal pH through the mucus layer, under which gastric bicarbonate secretion maintains neutral conditions. Mechanically, this is explained by the acid secretion occurring like small finger-like ejections penetrating the thick gel-like mucus layer into the gastric lumen [27]. 

In the present review the gastric lumen is confined to the habitat above the mucus layer, for which the pH of fasting gastric juice is the major defense mechanism against bacterial colonization. This defense mechanism is henceforth denoted the gastric acid barrier. 

Galati EM, Pergolozzi S, Miceli N, Monforte MT and Tripodo MM. 2001. Study on the increment of production of gastric mucus in rats treated with Opuntiaficus-indica (L) Mill, cladodes. J Ethnopharmacol 83(3) 229—233. 

Gupta, B. L. (1989). The relationship of mucoid substances and ion and water transport, with new data on intestinal goblet cells and a model for gastric secretion. In Mucus and Related Topics, eds. Chantler, E. and Ratcliffe, N. A., The Company of Biologists, Cambridge, pp. 81-110. 

Burger, O., Weiss, E., Sharon, N., Tabak, M., Neeman, I., and Ofek, I. (2002). Inhibition of Helicobacter pylori adhesion to human gastric mucus by a high-molecular-weight constituent of cranberry juice. Grit. Rev. Food Sci. Nutr. 42, 279-284. 

In the area of a gastric or duodenal peptic ulcer, the mucosa has been attacked by digestive juices to such an extent as to expose the subjacent connective tissue layer (submucosa). This self-digestion occurs when the equilibrium between the corrosive hydrochloric acid and acid-neutralizing mucus, which forms a protective cover on the mucosal surface, is shifted in favor of hydrochloric acid. Mucosal damage can be promoted by Helicobacter pylori bacteria that colonize the gastric mucus. 

Gastric secretion. PG promote the production of gastric mucus and reduce the formation of gastric acid (p. 160). 

Bisphosphonates irritate esophageal and gastric mucus membranes tablets should be swallowed with a reasonable amount of water (250 mL) and the patient should keep in an upright position for 30 min following drug intake. 

Gastric juice is the product of several cell types. The parietal cells produce hydrochloric acid, chief cells release pepsinogen, and accessory cells form a mucin-containing mucus. 

Acetylsalicylic acid and related non-steroidal anti-inflammatory drugs (NSAIDs) selectively inhibit the cyclooxygenase activity of prostaglandin synthase [2] and consequently the synthesis of most eicosanoids. This explains their analgesic, antipyretic, and antirheumatic effects. Frequent side effects of NSAIDs also result from inhibition of eicosanoid synthesis. For example, they impair hemostasis because the synthesis of thromboxanes by thrombocytes is inhibited. In the stomach, NSAIDs increase HCl secretion and at the same time inhibit the formation of protective mucus. Long-term NSAID use can therefore damage the gastric mucosa. 

However the dosages that are needed to inhibit gastric acid secretion are higher than those for achieving cytoprotective effects, i.e. enhanced secretion of mucus and HCO3 . Its indication is mainly protection against NSAID-associated gastric ulceration. Only misoprostol 800 pg/day has been directly shown to reduce the risk of ulcer complications. 

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