GASTRITIS • This diagnosis is – Overused when it is applied loosely to any transient upper abdominal complaint in the absence of validating evidence, – missed because most persons with chronic gastritis are asymptomatic.
• Gastritis is simply defined as inflammation of the gastric mucosa. • By far the majority of cases are chronic gastritis, but occasionally, distinct forms of acute gastritis are encountered
Acute Gastritis • Acute mucosal inflammatory process, usually of a transient nature. • The inflammation may be accompanied by hemorrhage into the mucosa and, in more severe circumstances, by sloughing of the superficial mucosal epithelium (erosion). • This severe erosive form of the disease is an important cause of acute gastrointestinal bleeding.
Etiology • Acute gastritis is frequently associated with: Heavy use of NSAIDs aspirin – – – – – – – – – –
Excessive alcohol consumption Heavy smoking Treatment with cancer chemotherapeutic drugs Uremia Systemic infections (e.g., salmonellosis) Severe stress (e.g., trauma, burns, surgery) Ischemia and shock Suicide attempts with acids and alkali Mechanical trauma (e.g., nasogastric intubation) Reflux of bilious material after distal gastrectomy
Pathogenesis • One or more of the following influences leading to imbalance between defensive and offensive factors: – disruption of the adherent mucous layer, – stimulation of acid secretion with hydrogen ion backdiffusion into the superficial epithelium, – decreased production of bicarbonate buffer by superficial epithelial cells, – reduced mucosal blood flow, – direct damage to the epithelium – Acute infection with H. pylori
Morphology • Acute gastritis ranges from extremely localized (as in NSAID-induced) to diffuse, and from superficial inflammation to involvement of the entire mucosal thickness with hemorrhage and focal erosions. • Concurrent erosion and hemorrhage are readily visible by endoscopy and termed acute erosive gastritis. • All variants are marked by mucosal edema and an inflammatory infiltrate of neutrophils and possibly by chronic inflammatory cells. • Regenerative replication of epithelial cells in the gastric pits is usually prominent.
Clinical Features • Depending on the severity of the anatomic changes, acute gastritis may be entirely asymptomatic, may cause variable epigastric pain with nausea and vomiting, or may present as overt hematemesis, melena, and potentially fatal blood loss. • Overall, it is one of the major causes of hematemesis, particularly in alcoholics. • In 25% of persons who take daily NSAID for rheumatoid arthritis develop acute gastritis at some time in their course, many with occult or overt bleeding.
Chronic Gastritis • Chronic gastritis is defined as the presence of chronic inflammatory changes in the mucosa; – mucosal atrophy – epithelial metaplasia.
Etiopathogenesis • most important etiologic association is chronic infection by the bacillus H. pylori. • This organism is a worldwide pathogen that has the highest infection rates in developing countries. • In areas where the infection is endemic, it seems to be acquired in childhood and persists for decades.
H. pylori • Noninvasive, non-spore-forming, S-shaped gram-negative rod measuring approximately 3.5 μm × 0.5 μm. • Gastritis; as a result of combined influence of bacterial enzymes and release of chemicals by recruited neutrophils. • After exposure to H. pylori, gastritis may develop in; – (1) an antral-type with high acid production and higher risk for the development of duodenal ulcer, and – (2) a pangastritis with multifocal mucosal atrophy, with low acid secretion and increased risk for adenocarcinoma.
• Chronic gastritis by H. pylori usually improve when treated with antibiotics and proton pump inhibitors. • Relapses are associated with reappearance of organism
Morphology
• Regardless of the cause; lymphocytic and plasma cell infiltrate in the lamina propria • Occasionally neutrophilic inflammation • Inflammation may be accompanied by variable gland loss and mucosal atrophy. • When present, H. pylori organisms are found nestled within the mucus layer overlying the superficial mucosal epithelium • In the autoimmune variant, loss of parietal cells is particularly prominent.
Morphology
• Two additional features are of note: • Intestinal metaplasia refers to the replacement of gastric epithelium with columnar and goblet cells of intestinal variety; • significant, because carcinomas seem to arise from dysplasia of this metaplastic epithelium.
• H. pylori-induced proliferation of lymphoid tissue within gastric mucosa; • implicated as a precursor of gastric lymphoma.
1. Intestinal metaplasia (Goblet cells) Arrow 2. H. pylori-induced proliferation of lymphoid tissue
Chronic gastritis, showing partial replacement of the gastric mucosal epithelium by intestinal metaplasia (upper lef), and inflammation of the lamina propria containing lymphocytes and plasma cells (right).
Helicobacter pylori gastritis. A Steiner silver stain demonstrates the numerous darkly stained Helicobacter organisms along the luminal surface of the gastric epithelial cells.
Autoimmune gastritis (Type A chronic gastritis) • Involves mainly the body-fundic mucosa • Circulating antibodies against parietal cell and Intrinsic factor present and may be associated with other autoimmune diseases • Depletion of parietal cells leads to impaired synthesis of intrinsic factors and diffuse gastric atrophy and intestinal metaplasia – Hypochlorhydria/achlorhydria – Some patients develop Pernicious anemia (Megaloblastic anemia)