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Pathology - Gastritis
Acute hemorrhagic gastritis • Resulting from a sudden injury to the gastric hmucosa. Acute gastritis frequently results from a significant alcohol binge, although any acute medical condition that diminishes stomach blood flow may potentially induce it. • Endoscopy reveals many punctate erosions that exude blood. • Severe cases may result in substantial upper gastrointestinal hemorrhage. Histology reveals neutrophilic infiltration of the stomach mucosa accompanied by hemorrhage and mucosal necrosis. • Acute gastritis typically cures swiftly and without complications.
Chemical/reactive gastritis • Induced by any minor damage to the stomach mucosa. • Primarily observed in the antrum associated with bile reflux or non-steroidal anti-inflammatory medicines (NSAIDs). • Endoscopic examination reveals erythema of the stomach mucosa. • Histological analysis indicates vascular congestion, foveolar hyperplasia, and smooth muscle proliferation. Inflammation is negligible or nonexistent. Reactive gastritis typically resolves without complications upon removal of the causative agent.
Iron pill gastritis • Induced by the corrosive properties of consumed iron supplements. • Histological examination reveals acute inflammation accompanied by erosion or ulceration of the stomach mucosa. Yellow-brown iron pigment may be observed.
Helicobacter gastritis • A prevalent etiology of gastritis, typically antral-predominant. • Predominantly caused by Helicobacter (H.) pylori, a curved flagellated Gram-negative bacillus. H. heilmannii, characterized by its tighter coiling, constitutes less than 1% of instances. Histology reveals a substantial lymphoid inflammatory infiltrate in the lamina propria, accompanied by neutrophilic infiltration of the superficial mucosa. • The organisms can be identified with normal stains, but are more effectively visible with specific stains that accentuate the bacteria. In most instances, gastritis is resolved by eliminating the organism. • A minority of untreated instances may lead to complications such as peptic ulceration, gastric cancer, or gastric marginal zone B-cell lymphoma.
Autoimmune gastritis • Resulting from an autoimmune assault on parietal cells within the fundic glands. • Histological examination reveals infiltration of the mucosal tissue by lymphocytes and plasma cells. The infiltrate targets fundic glands, resulting in the loss of chief and parietal cells. Pyloric and intestinal metaplasia is prevalent. • Elevated risk of stomach neuroendocrine tumors and carcinoma. • Certain patients may also produce antibodies against intrinsic factor, resulting in vitamin B12 deficiency and megaloblastic anemia.
Acute hemorrhagic gastritis • Resulting from a sudden injury to the gastric hmucosa. Acute gastritis frequently results from a significant alcohol binge, although any acute medical condition that diminishes stomach blood flow may potentially induce it. • Endoscopy reveals many punctate erosions that exude blood. • Severe cases may result in substantial upper gastrointestinal hemorrhage. Histology reveals neutrophilic infiltration of the stomach mucosa accompanied by hemorrhage and mucosal necrosis. • Acute gastritis typically cures swiftly and without complications.
Chemical/reactive gastritis • Induced by any minor damage to the stomach mucosa. • Primarily observed in the antrum associated with bile reflux or non-steroidal anti-inflammatory medicines (NSAIDs). • Endoscopic examination reveals erythema of the stomach mucosa. • Histological analysis indicates vascular congestion, foveolar hyperplasia, and smooth muscle proliferation. Inflammation is negligible or nonexistent. Reactive gastritis typically resolves without complications upon removal of the causative agent.
Iron pill gastritis • Induced by the corrosive properties of consumed iron supplements. • Histological examination reveals acute inflammation accompanied by erosion or ulceration of the stomach mucosa. Yellow-brown iron pigment may be observed.
Helicobacter gastritis • A prevalent etiology of gastritis, typically antral-predominant. • Predominantly caused by Helicobacter (H.) pylori, a curved flagellated Gram-negative bacillus. H. heilmannii, characterized by its tighter coiling, constitutes less than 1% of instances. Histology reveals a substantial lymphoid inflammatory infiltrate in the lamina propria, accompanied by neutrophilic infiltration of the superficial mucosa. • The organisms can be identified with normal stains, but are more effectively visible with specific stains that accentuate the bacteria. In most instances, gastritis is resolved by eliminating the organism. • A minority of untreated instances may lead to complications such as peptic ulceration, gastric cancer, or gastric marginal zone B-cell lymphoma.
Autoimmune gastritis • Resulting from an autoimmune assault on parietal cells within the fundic glands. • Histological examination reveals infiltration of the mucosal tissue by lymphocytes and plasma cells. The infiltrate targets fundic glands, resulting in the loss of chief and parietal cells. Pyloric and intestinal metaplasia is prevalent. • Elevated risk of stomach neuroendocrine tumors and carcinoma. • Certain patients may also produce antibodies against intrinsic factor, resulting in vitamin B12 deficiency and megaloblastic anemia.
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