Acute and chronic gastritis - etiology, pathogenesis, types; microscopic & gross pathomorphology
Acute gastritis
This is transient mucosal inflammation that may be asymptomatic or cause epigastric pain, nausea and vomiting.
The stomach is a highly acidic environment, gastritis can occur when either the protective mechanisms of the stomach fail, or there is an increase in acid production. Protection mechanisms include:
- Foveolar cells produce Mucin which prevents direct contact with the epithelium
- Bicarbonate ion secretion by epithelial cells create neutral layer
- Rich vascular supply delivers oxygen, bicarbonates and nutrients, while removing acid that has diffused into the lamina propria
Disruption to any of these elements (e.g. reduced mucin synthesis due to age) increases susceptibility, as do drugs such as NSAIDs which reduce bicarbonate availability, and ingestion of harsh chemical elements.
On histologic examination, mild acute gastritis is largely invisible, as there is only slight edema and vascular congestion, scattered neutrophils may be present , and any neutrophils in contact with the epithelial cells is abnormal in all parts of the GI system and signifies active inflammation. In more extensive inflammation erosion may be present with purulent exudates and hemorrhage.
Chronic gastritis
Signs and symptoms typically less severe but more persistent than acute form. Nausea and upper abdominal pain can present. Most common cause is infection of H.pylori (see below) with atrophic gastritis due to autoimmune causes making up most of the remaining cases.
Mnemonic: chronic gastritis type A = Autoimmune: antibodies to parietal cells and intrinsic factor, body and fundus, Achlorhydria, pernicious Anaemia. Type B = Bacterial (H. pylori): antrum-predominant, neutrophils with lymphoid follicles; leads to peptic ulcer, adenocarcinoma and MALT lymphoma.
H. Pylori increase the acid secretion and weaken defences in the stomach and as such increase risk of gastritis and ulcers. H. Pylori create urease, elevating local gastric pH and therefore allows it to survive, while simultaneously releasing toxins which increase gastric secretions.
Giemsa stain, gastric biopsy: numerous small, curved (S-shaped) H. pylori rods lie in the mucus layer on the surface and pit epithelium.
Image: “Helicobacter Pylori, Stomach Biopsy, Giemsa Stain (5435867593)” by Ed Uthman from Houston, TX, USA, CC BY 2.0, via Wikimedia Commons.
Over time chronic gastritis can become pangastritis with multifocal atrophic gastritis and increased risk of adenocarcinoma.