Acute gastritis: etiology and morphology
Acute inflammation of the gastric mucosa develops under the influence of various damaging factors.
Main causes:
- Acute intoxications: consumption of alcohol surrogates, chemical burns, as well as endogenous intoxication (e.g., in uremia).
- Infectious diseases: salmonellosis, cholera.
Depending on the nature of the damage, several morphological forms of inflammation are distinguished: catarrhal, hemorrhagic, and fibrinous. Less common is corrosive (necrotic) gastritis, which usually occurs against the background of chemical burns or the intake of alcohol surrogates.
Most often, the acute process has a favorable outcome — the normal structure of the mucosal membrane is completely restored. However, in the necrotic form, severe complications are possible: massive hemorrhage from eroded (destroyed) vessels of the submucosal layer or perforation of the stomach wall, leading to peritonitis (inflammation of the peritoneum).
Chronic gastritis: essence of the pathology
Chronic gastritis is a long-standing inflammation of the mucosa, which is necessarily accompanied by a disruption of cell renewal.
It is important to understand that this is exclusively a morphological phenomenon. The disease has no specific clinical picture, so an accurate diagnosis can be made only on the basis of pathomorphological examination. For this, a biopsy is performed from two zones: the body and the antrum of the stomach.
A natural outcome of prolonged inflammation is the atrophy of the gastric glands. Functionally, this manifests as secretory insufficiency, up to the complete cessation of gastric juice production (achylia).
Activity assessment and the Sydney system
The generally accepted diagnostic standard is the Modified Sydney Classification (1996). It involves a comprehensive assessment of the disease in three areas: etiology, topography of the lesion, and morphological changes.
A key parameter is the activity of chronic gastritis. It is determined by the presence of neutrophilic leukocytes in the epithelial layer or the lamina propria of the mucosa.
Features of infiltration:
- Neutrophils can penetrate into the surface and foveolar epithelium.
- Accumulating in the lumen of the gastric pits, they form characteristic microscopic structures — pit abscesses.
- There is a strict correlation: in 90% of observations, the number of neutrophils in the mucosa directly reflects the degree of colonization by the bacterium Helicobacter pylori.
OLGA classification
The OLGA (Operative Link for Gastritis Assessment) system was developed to improve the Sydney classification. Its main goal is the accurate assessment of the risk of malignancy (malignant transformation) and the prediction of the reversibility of detected changes.
Key innovations of the OLGA system:
- Refined concept of atrophy. Now, atrophy includes not only a physical decrease in the number of glands, but also intestinal metaplasia. This is due to the fact that metaplastic cells lose the ability to perform the secretory function characteristic of this zone of the stomach.
- Separation of concepts:
- The grade of chronic gastritis reflects the severity of inflammatory infiltration.
- The stage of chronic gastritis is an integral assessment of mucosal atrophy in all examined parts of the stomach.
- Clinical significance. Patients diagnosed with stage III or IV chronic gastritis fall into the high-risk group: the probability of developing intestinal-type gastric cancer is increased 6-fold.
Briefly: answers to topical questions
What etiological types of chronic gastritis (A, B, C) are distinguished in the modern classification?
The modern classification distinguishes three main etiopathogenetic forms of chronic gastritis: autoimmune, infectious, and chemical.
- Autoimmune (type A) develops against the background of systemic autoimmune pathologies with the production of autoantibodies to parietal cells, predominantly affecting the body of the stomach.
- Bacterial (type B) is associated with Helicobacter pylori infection, most often localized in the antrum.
- Chemical (type C) is caused by chronic chemical irritation of the mucosa upon exposure to bile, nonsteroidal anti-inflammatory drugs, or glucocorticoids.
What types of intestinal metaplasia (complete and incomplete) occur in chronic gastritis?
In chronic gastritis, two main types of intestinal metaplasia occur: complete and incomplete.
- Complete metaplasia (type I) — the cellular composition of the mucosa is as close as possible to the small intestine, including properly formed goblet and absorptive brush-border cells.
- Incomplete metaplasia (type II) — characterized by the appearance of goblet cells containing vacuoles with a mixture of sialo- and sulfomucins, often adjacent to epithelial dysplasia and early cancer.
What infectious diseases and pathogens can cause the development of acute gastritis?
The development of acute gastritis can be caused by infectious diseases and microorganisms:
- Cholera and salmonellosis are listed among the infectious causes of acute gastritis.
- Emphysematous gastritis is caused by gas-forming microorganisms; typical pathogens are Escherichia coli and Clostridium welchii.
- Phlegmonous gastritis is caused by non-gas-forming microorganisms; among the typical pathogens are alpha-hemolytic streptococcus, Staphylococcus aureus, Escherichia coli, Clostridium welchii, and Streptococcus pneumoniae.
To avoid confusing criteria in the OLGA system, use the rule of identical letters: Grade evaluates the Severity of inflammation (infiltration), and Stage evaluates the Shrinkage of glands (atrophy).
Class and exam questions
Can a diagnosis of "chronic gastritis" be made solely on the basis of patient complaints?
No, this is exclusively a morphological diagnosis. It has no specific clinical manifestations and is confirmed only by pathomorphological examination of biopsy specimens from the body and antrum of the stomach.
What is the morphological marker of chronic gastritis activity?
The marker of activity is the presence of neutrophilic leukocytes in the lamina propria or the epithelium of the mucosa. Their accumulations in the gastric pits are called pit abscesses.
Why does the OLGA system equate intestinal metaplasia with atrophy?
Because cells that have undergone intestinal metaplasia lose their normal specialization and can no longer perform the secretory function characteristic of this zone of the stomach.
What are the dangers of corrosive (necrotic) gastritis?
It can lead to severe complications: massive hemorrhage from eroded (destroyed) vessels of the submucosal layer or perforation of the stomach wall with the subsequent development of peritonitis.
What else to study on this topic
- Gastric ulcer (peptic ulcer disease) and its morphogenesis
- Gastric cancer: intestinal type and other histological variants
- Mechanisms of development of mucosal intestinal metaplasia
- Pathogenesis of secretory insufficiency (achylia)
- Morphological differences of catarrhal, hemorrhagic, and fibrinous inflammation
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