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Those with autoimmune atrophic gastritis (Type A gastritis) are statistically more likely to develop gastric carcinoma (a form of stomach cancer), Hashimoto's thyroiditis, and achlorhydria. Type A gastritis primarily affects the fundus (body) of the stomach and is more common with pernicious anemia . [ 1 ]
Gastric ulcers may develop; it is unclear if they are the causes or the consequences. Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics.
Biopsy of the stomach in Ménétrier disease; the substantial pit hyperplasia makes the large rugal folds appear to be covered by myriad polyps resembling hyperplastic polyps. The muscularis propria is the folded structure at the bottom center.
Antibodies to intrinsic factor and parietal cells cause the destruction of the oxyntic gastric mucosa, in which the parietal cells are located, leading to the subsequent loss of intrinsic factor synthesis. Without intrinsic factor, the ileum can no longer absorb the B 12. [40] Atrophic gastritis is often a precursor to gastric cancer. [39]
The usual appearance of portal hypertensive gastropathy on endoscopy is a mosaic-like or reticular pattern in the mucosa. Red spots may or may not be present. The pattern is usually seen throughout the stomach. [2] A similar pattern can be seen with a related condition called gastric antral vascular ectasia (GAVE), or watermelon stomach.
Reactive gastropathy is morphologically distinct entity [3] [4] that can be separated from gastritis, which by definition has a significant inflammatory component.. As a reactive gastropathy may mimic a (true) gastritis symptomatically and visually in an endoscopic examination, it may incorrectly be referred to as a gastritis.
In the absence of treatment, H. pylori infection usually persists for life. [181] Infection may disappear in the elderly as the stomach's mucosa becomes increasingly atrophic and inhospitable to colonization. Some studies in young children up to two years of age have shown that infection can be transient in this age group. [182] [183]
The symptoms of gastroparesis are best understood in the context of the physiology of gastric emptying (GE). The stomach functions as a reservoir for food and nutritional content, which are broken down to produce chyme. Chyme is then released into the duodenum at a controlled rate to allow for maximum nutrient absorption.