Gastritis is an inflammation of the mucosal lining of the stomach. It can occur suddenly (acute) or gradually (chronic). Gastritis can be caused by irritation or inflammation from excessive alcohol use or the use of certain medications such as aspirin or other anti inflammatory drugs. It may also be caused by H. pylori and other bacterial and viral infections, pernicious anemia, and bile reflux.
Gastric irritation from abuse of alcohol, coffee, and tobacco and from chemicals and drugs such as NSAIDs and, perhaps, corticosteroids is the main cause of acute gastritis. Acute gastritis may also develop during many febrile infections, such as typhoid, pneumonia, and diphtheria. H. pylori infection can present with acute gastritis. The gastric mucosa in acute gastritis is erythematous, often with erosions, and may be covered with a thick mucus. Symptoms of gastritis vary among individuals, and in many people there are no symptoms. The most common symptoms include epigastric pain or discomfort, nausea or indigestion, vomiting, a burning or gnawing feeling in the stomach between meals or at night, and a disagreeable taste. A corrosive type of gastritis, originating from the intake of strong chemicals such as lye, can lead to a localized or diffuse necrosis and permanent scarring.
Erosive hemorrhagic gastritis is characterized by multiple, diffuse erosions in an inflamed mucosa. Nausea, anorexia, pain, and gastric hemorrhage may occur. This acquires a special clinical significance with its tendency to cause severe, at times life-endangering, hemorrhages. Larger arteries extend quite frequently as far up as the epithelium and may become involved in some of the many small, but by no means superficial, erosions. Whenever the origin of gastrointestinal bleeding cannot be identified, the possibility of an erosive hemorrhagic gastritis must be seriously considered, especially in severely ill hospitalized patients. Endoscopy is important for the diagnosis, though during an episode of acute bleeding the mucosa may not be well visualized. At laparotomy the diagnosis may still be difficult, because, even when viewing the mucosa directly after gastrostomy, the small erosions (i.e., the source of the bleeding) may not be well seen macroscopically.
A similar type of hemorrhagic gastritis has been observed after partial resection of the stomach or after gastroenterostomy or ulcer. This should be kept in mind if the suspicion of a bleeding peptic “anastomotic ulcer” cannot be confirmed unequivocally by x-ray studies, endoscopically, or at laparotomy. Under such circumstances, vagotomy may be the best procedure to stop the bleeding. It has helped in many cases and, in any event, is preferable to an additional resection.
Chronic atrophic gastritis is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. This may be an aftermath of an acute gastritis, but many other possible etiologic factors of exogenous or endogenous origin need to be considered. Chronic atrophic gastritis has a close relationship to pernicious anemia and vitamin B12 deficiency. The relationship of chronic atrophic gastritis and, more specifically, pernicious anemia with malignancies has not been clarified. The characteristic features of chronic atrophic gastritis endoscopically are the disappearance of the folds and the thinness of the mucosa through which shines the vascular net, both arterial and venous. Microscopically, the chief and parietal cells are considerably reduced in size and number; the epithelial cells are transformed to a great extent into goblet cells, or undergo metaplastic changes. The clinical manifestations are rather nonspecific. Upper endoscopy with biopsies of the gastric body is used to establish the diagnosis.
With chronic hypertrophic gastritis the situation is clinically much the same, except that hyperacidity is present in most cases, and the distribution of the rugae and the “cobblestone” appearance of the mucosal surface, seen roentgenographically, provide more often the right clue for diagnosis; endoscopy is needed to make the unequivocal diagnosis. The rugae are strikingly thickened and, even at autopsy, do not flatten out when the wall is stretched. Ménétrier disease (also known as hypoproteinemic hypertrophic gastropathy) is a rare, acquired disorder of the stomach characterized by greatly thickened gastric folds and excessive mucus production, with resultant protein loss leading to diarrhea. Other conditions, such as lymphoma and Zollinger-Ellison syndrome, can cause hypertrophic mucosal folds in the stomach, and use of proton pump inhibitors can also be a cause. In Zollinger-Ellison syndrome, or gastrinoma, the elevated serum gastrin levels lead to parietal cell hypertrophy, prominently in the fundus and body of the stomach. The use of proton pump inhibitors results in gastric hypoacidity leading to increases in gastrin levels and, also, parietal cell hypertrophy.