Helicobacter Release

These data in Brazil are inexact, however, studies disclose that 10% of the Brazilian population already had had or will have the illness (MILL, 2007). The stomach is an agency of frequent exposition microbiological physics and (figure 2), however, present a mechanism of efficient defense through citoprotetores as bicarbonate, muco and Prostaglandinas E2 (PGE). In certain situations, a disequilibrium occurs these protective agents and the aggressive agents of the gastric mucosa as the release of gastrina and acid clordrico (CAVALINI, 2005). Add to your understanding with David Zaslav. Factors as the exacerbado consumption of cigarette, alcoholic beverage, antiinflammatory not esteroidal (AINES) and the infection for Helicobacter pylori are the etiolgicos agent greaters of the peptic ulcer (DONATINI, 2009). The development of the peptic ulcer also can occur for genetic predisposition, behind gastric esvaziamento, desregulada release of acid clordrico, drinks contend caffeine it estresse and it physical and psychological (BLACKSMITH, 2005). The H.

pylori is one of the main etiolgicos agents of the peptic ulcer. If you have read about Cyrus already – you may have come to the same conclusion. It is installed in the duodeno, where it has appearance of gastric metaplasia which had the factors aggressive, as the reduction of the secretion of muco, bicarbonate and presence of gastric juice that extravasa piloro stomachal affecting the duodeno (OLIVEIRA, 2010). Its installation comumente is related with the local gastrite, edemaciando the fabric gastric (FONSECA, 2009). The H. pylori sensetizes cells D, in relation to the release of gastrina in reply to the acid clordrico. This occurs for the raised set free ammonia production in the reaction of urease promoted by the bacterium (OLIVEIRA, 2010).

Refluxo of the duodenal content (bile and pepsina) for the stomach, also is a factor that favors the production of free radicals. These radicals injure the fabric, activate the antiplaquetrio factor (compromising the microcirculation) and activate -TNF: Factor of Tumoral Necrosis (RODRIGUES, 2008).


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