Gastritis results from mucosal injury. When neutrophils are present, the lesion is referred to as acute gastritis. When cell injury and regeneration are present but inflammatory cells are rare or absent, the term gastropathy is applied. Agents that cause gastropathy include nonsteroidal anti-inflammatory drugs, alcohol, bile, and stress-induced injury. Acute mucosal erosion or hemorrhage, such as Curling ulcers or lesions following disruption of gastric blood flow, for example, in portal hypertension, can also cause gastropathy that typically progresses to gastritis. The term hypertrophic gastropathy is applied to a specific group of diseases exemplified by Ménétrier disease and Zollinger-Ellison syndrome (discussed later).
Both gastropathy and acute gastritis may be asymptomatic or cause variable degrees of epigastric pain, nausea, and vomiting. In more severe cases, there may be mucosal erosion, ulceration, hemorrhage, hematemesis, melena, or, rarely, massive blood loss.
The gastric lumen is strongly acidic, with a pH close to 1—more than 1 million times more acidic than the blood. This harsh environment contributes to digestion but also has the potential to damage the mucosa. Multiple mechanisms have evolved to protect the gastric mucosa (
Fig.
15.13 ). Mucin secreted by surface foveolar cells forms a thin layer of mucus that prevents large food particles from directly touching the epithelium. The mucus layer also promotes formation of an “unstirred” layer of fluid over the epithelium that protects the mucosa; it has a neutral pH as a result of secretion of bicarbonate ions by surface epithelial cells. Finally, the rich blood supply of the gastric mucosa efficiently buffers and removes protons that back-diffuse into the lamina propria. Gastropathy, acute
Damaging Forces: Gastric acidity Peptic enzymes Defensive Forces: Surface mucus secretion Bicarbonate secretion into mucus Mucosal blood flow Apical surface membrane transport Epithelial regenerative capacity Prostaglandin synthesis
Fig. 15.13 Mechanismsofgastricinjuryandprotection.Thisdiagramillustratestheprogressionfrommildformsofinjurytoulcerationthatmayoccurwithacuteorchronicgastritis.Ulcersincludelayersofnecroticdebris(N), inflammation(I), andgranulationtissue(G); scarring(S), whichdevelopsovertime,ispresentonlyinchroniclesions.
INJURIOUS EXPOSURES OR IMPAIRED DEFENSES H. pylori infection NSAID Aspirin Tobacco Alcohol Gastric hyperacidity Duodenal-gastric reflux Ischemia Shock Delayed gastric emptying Host factors http://ebooksmedicine.net gastritis, and chronic gastritis can occur after disruption of any of these protective mechanisms. The main causes include:
Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX)-dependent synthesis of prostaglandins E2 and I2, which stimulate nearly all of the above defense mechanisms including mucus and bicarbonate secretion, mucosal blood flow, and epithelial restitution. Although COX-1 plays a larger role than COX-2, both isoenzymes contribute to mucosal protection. Thus, while the risk for development of NSAID-induced gastric injury is greatest with nonselective inhibitors, such as aspirin, ibuprofen, and naproxen, selective COX-2 inhibition, for example, by celecoxib, can also result in gastropathy or gastritis.