The gastric injury that occurs in uremic patients and those infected with urease-secreting H. pylori may be due to inhibition of gastric bicarbonate transporters by ammonium ions.
Reduced mucin and bicarbonate secretion have been suggested as factors that explain the increased susceptibility of older adults to gastritis.
Hypoxemia and decreased oxygen delivery may account for an increased incidence of gastropathy and acute gastritis at high altitudes.
Ingestion of harsh chemicals, particularly acids or bases, either accidentally or in a suicide attempt, leads to severe gastric mucosal damage as a result of direct injury to epithelial and stromal cells. Direct cellular damage also contributes to gastritis induced by excessive alcohol consumption, NSAID use, and radiation therapy. Agents that inhibit DNA synthesis or the mitotic apparatus, including those used in cancer chemotherapy, may cause generalized mucosal damage due to insufficient epithelial renewal.
MORPHOLOGYHistologically,gastropathyandmildacutegastritismaybedifficulttorecognize,sincethelaminapropriashowsonlymoderateedemaandslightvascularcongestion.Thesurfaceepitheliumisintact,buthyperplasiaoffoveolarmucuscellsistypicallypresent.Neutrophils,lymphocytes,andplasmacellsarenotprominent.
Thepresenceofneutrophilsabovethebasementmembraneincontactwithepithelialcellsisabnormalinallpartsofthegastrointestinaltractandsignifiesactiveinflammation,or,atthissite,gastritis(ratherthangastropathy).Thetermactive inflammation ispreferredoveracuteinflammationthroughouttheluminalgastrointestinaltract,sinceactiveinflammationmaybepresentinbothacuteandchronicdiseasestates.Withmoreseveremucosaldamage,erosionsandhemorrhagedevelop.Hemorrhagemaymanifestasdarkpunctaeinanotherwisehyperemicmucosa.Concurrentpresenceoferosionandhemorrhageistermed acute erosive hemorrhagic gastritis.
Stress-related gastric injury occurs in patients with severe trauma, extensive burns, intracranial disease, major surgery, serious medical disease, and other forms of severe physiologic stress. More than 75% of critically ill patients develop endoscopically visible gastric lesions during the first 3 days of their illness. In some cases, the associated ulcers are given specific names based on location and clinical associations. Examples are as follows:
Stress ulcers affecting critically ill patients with shock, sepsis, or severe trauma.
Curling ulcers occur in the proximal duodenum and are associated with severe burns or trauma.
Cushing ulcers arise in the stomach, duodenum, or esophagus of those with intracranial disease and have a high incidence of perforation.
The pathogenesis of stress-related gastric mucosal injury is most often due to local ischemia. This may be caused by systemic hypotension or reduced blood flow resulting from stress-induced splanchnic vasoconstriction. Upregulation and increased release of the vasoconstrictor endothelin-1 also contributes to ischemic gastric mucosal injury, while increased COX-2 expression appears to be protective. Cushing ulcers are thought to be caused by direct stimulation of vagal nuclei resulting acid hypersecretion. Systemic acidosis may also contribute to mucosal injury by lowering the intracellular pH of mucosal cells.