MORPHOLOGYStress-relatedgastricmucosalinjuryrangesfromshallowerosionscausedbysuperficialepithelialdamagetodeeperlesionsthatpenetratethedepthofthemucosa.Acuteulcersareroundedandtypicallylessthan1cmindiameter.Theulcerbasefrequentlyisstainedbrowntoblackbyacid-digestedextravasatedredcells.Unlikepepticulcers,whichariseinthesettingofchronicinjury,acutestressulcersarefoundanywhereinthestomachandareoftenmultiple.Theyaresharplydemarcated,withessentiallynormaladjacentmucosa,althoughtheremaybesuffusionofbloodintothemucosaandsubmucosaandsomeinflammatoryreaction.Thescarringandthickeningofbloodvesselsthatcharacterizechronicpepticulcersareabsent.Healingwithcompletereepithelializationoccursdaysorweeksaftertheinjuriousfactorsareremoved.
Most critically ill patients admitted to hospital intensive care units have histologic evidence of gastric mucosal damage. Ulcers are associated with nausea, vomiting, melena, and coffee-ground hematemesis. Bleeding from superficial gastric erosions or ulcers that may require transfusion develop in 1% to 4% of these patients. Other complications, including perforation, also may occur. Prophylaxis with proton pump inhibitors may blunt the impact of stress ulceration, but the most important determinant of outcome is the severity of the underlying condition.
The most common cause of chronic gastritis is infection with the bacillus Helicobacter pylori. Autoimmune http://ebooksmedicine.net gastritis, typically associated with gastric atrophy, represents less than 10% of cases of chronic gastritis but is the most common cause in patients without H. pylori infection. Chronic NSAID use is a third important cause of gastritis in some populations, as discussed later. Less common causes include radiation injury and chronic bile reflux.
The signs and symptoms associated with chronic gastritis typically are less severe but more persistent than those of acute gastritis. Nausea and upper-abdominal discomfort may occur, sometimes with vomiting, but hematemesis is uncommon.
The discovery of the association of H. pylori with peptic ulcer disease revolutionized the understanding of chronic gastritis. These spiral-shaped or curved bacilli are present in gastric biopsy specimens from almost all patients with duodenal ulcers and a majority of those with gastric ulcers or chronic gastritis. Acute H. pylori infection is subclinical in most cases; rather, it is the chronic gastritis that ultimately brings the afflicted person to medical attention. H. pylori infection most often presents as an antral gastritis with increased acid production. The increased acid production may give rise to peptic ulcer disease of the duodenum or stomach.
While in most cases H. pylori gastritis is limited to the antrum, in some individuals it progresses to involve the gastric body and fundus, resulting in reduced parietal cell mass and acid secretion. Reduced acid output results in hypergastrinemia, as in autoimmune atrophic gastritis. In addition, extension of the gastritis to the gastric body and fundus results in intestinal metaplasia and increased risk of gastric cancer.
In the United States, H. pylori infection is associated with poverty, household crowding, limited education, residence in areas with poor sanitation, and birth outside of the United States. Infection is typically acquired in childhood and may then persist for life. Improved sanitation in many areas likely explains why H. pylori infection rates among younger individuals today are markedly lower than they were in similarly aged individuals 30 years ago. In the United States, the prevalence of H. pylori infection is also higher in African Americans and Mexican Americans. Worldwide, colonization rates vary from less than 10% to more than 80% as a function of age, geography, and social factors.