Gastritis: Endoscopic Biopsy and Classification

• Gastritis is the inflammation of the gastric mucosa, caused by chemicals, infectious agents, radiation, or immunological factors.
• Gastritis can manifest as pangastritis, antral, or corpus-specific issues, and it may be focal, diffuse, superficial, or affect the entire mucosal thickness.

Endoscopic Gastric Mucosal Biopsy

• It's used for identifying and monitoring various gastric conditions like gastritis, peptic ulcer disease, and gastric neoplasms.
• H pylori presence can be determined in the stomach using this biopsy.
• The grade, extent, and topography of gastritis and atrophy-related lesions can be assessed to determine the risk of gastric carcinoma.
• Biopsies are commonly taken from the body, antrum, and endoscopically visible lesions.
• Biopsies should be collected from five locations: greater and lesser curvatures in the antrum and corpus, and the incisura.
• Samples should be submitted in separate containers.

Classification of Gastritis

• Gastritis can be classified into acute and chronic types.
• Other classifications include:
  • Aetiological: e.g., H pylori, mycobacterial, gastric syphilis, or fungal gastritis.
  • Morphological: e.g., acute, erosive/hemorrhagic, lymphocytic, eosinophilic, or granulomatous gastritis.
  • Mechanisms of injury: e.g., chemical or reactive gastropathy (reflux of bile & pancreatic secretion, alcohol, NSAIDs, chemotherapeutic drugs), and immune-mediated gastritis (autoimmune gastritis).

Acute Gastritis

• Frequently accompanied by acute mucosal injury, such as hemorrhagic or non-hemorrhagic, erosive or non-erosive.
• May result from disorders with various causes and diverse histologic patterns.
• Causes include drugs, uremia, ischemia, shock, corrosive agents, radiation, sepsis, trauma, certain infections, acute alcoholism, severe burns, alkaline reflux, bile reflux, major surgery, increased intracranial pressure, respiratory failure, portal hypertension, congestive heart failure, and multiorgan failure.

Acute Hemorrhagic, Erosive Gastritis

• Characterized by necrosis, acute inflammatory response, and hemorrhage.

• Erosion can extend into deeper tissue and form an ulcer.

• Complications can include major physiologic disturbances like sepsis, extensive burn injury, head injury, severe trauma, and multiorgan failure.

• Associated with aspirin, NSAID, alcohol intake and ischemic injuries, which directly damage the mucosa.

• Breakdown of the mucosal barrier permits acid-induced injury.

• Major factors implicated are hyperchlorhydria and decreased mucosal protection, such as decreased mucous secretion or mucosal blood flow.

• Acute gastritis often presents as abdominal discomfort and pain, heartburn, nausea, vomiting, and haematemesis.

• Bleeding begins 3 to 7 days after a stressful event, ranging from occult blood to massive hemorrhage.

Specific Forms of Acute Hemorrhagic Gastritis

• Curling ulcer: develops in severe burn patients within 24-72 hours, likely due to ischemia.
• Cushing ulcer: occurs after accidental or surgical CNS trauma, increased vagal tone leads to increased acid secretion in cerebral injury.

Morphology of Acute Hemorrhagic Gastritis

• Typically appears as multiple lesions in the stomach, predominantly in the oxyntic mucosa.
• It can cause widespread petechial hemorrhages or submucosal bleeding.
• Lesions vary from 1-25mm across and may appear as sharply punched-out ulcers.
• Curling and Cushing ulcers tend to be deep and single.

Chronic Gastritis

• Histopathologic condition marked by inflammation of the gastric mucosa.
• Composed of a heterogeneous group of disorders, each with unique location, causes and resulting complications.
• It's defined by an elevation of lymphocytes and plasma cells in the lamina propria.
• Can range from a mild superficial lesion to severe atrophy.
• The main symptom is dyspepsia, though many are asymptomatic.
• Usually associated with active inflammation (congestion, edema, neutrophils), atrophy (decrease in normal glandular cells), and intestinal metaplasia (replacement of the surface, foveolae, and glandular epithelial cells with intestinal goblet cells).

Types of Intestinal Metaplasia

• Type I (complete): small intestinal type cells with brush borders and goblet cells with acidic mucin, with no malignancy risk.
• Type II (incomplete): colonic type goblet cells with sialomucin, doesn't increase malignancy risk.
• Type III (incomplete): colonic type goblet cells with sulfomucin, associated with potential increased risk of malignancy.

Pathogenesis of Chronic Gastritis

• There are 3 forms:
• Fundic or autoimmune chronic gastritis "Type A": inflammation restricted to the body and fundus, associated with Pernicious anemia, parietal cell and intrinsic factor antibodies, reduced gastric secretion, and increased gastrin secretion; adenocarcinoma risk is 0.5% per year.
• Diffuse antral chronic gastritis "Type B": involves the antrum and is associated with H pylori, peptic duodenitis, chronic peptic ulcers in the duodenum and prepyloric region, hyperchlorhydria, and no parietal or intrinsic antibodies; adenocarcinoma risk is low.
• Multifocal chronic atrophic gastritis "Type AB": associated with H pylori, gastric ulcers, and is at the highest risk for developing gastric adenocarcinoma.

H Pylori-Associated Gastritis

• H pylori is commonly the main cause of chronic gastritis.
• Approximately half the world’s population is affected by H pylori, with a prevalence of 70-90% in developing countries.
• Infection is more common in lower socioeconomic levels, and those affected are largely asymptomatic.
• H pylori colonizes and infects the gastric mucosa, with infections usually begin in childhood.
• Associated with tissue damage, active and chronic gastritis.
• The interaction of H pylori with surface mucosa leads to interleukin-8 release, which recruits polymorphs.
• Gastric epithelial cells express class II molecules, which present H pylori antigens, boosting cytokine release .
• Neutrophilic infiltration leads to elevated leukotriene levels, esp. leukotriene B4, is cytotoxic to gastric epithelium.
• Neutrophilic infiltration reduces quickly, but chronic inflammatory cells resolves more slowly.

Virulence Factors of H Pylori

• Vacuolating toxin A "VacA": H pylori strains that produce VacA are more likely to cause peptic ulcers.
• Coagulating antigen A "CagA": associated with a greater risk of adenocarcinoma and peptic ulcers.
• Strains lacking cagA can still cause adenocarcinoma and peptic ulcers.

Methods for Detecting H Pylori

• Histomorphology: from endoscopic biopsy using H&E, Giemsa, or Warthin-Starry stain; immunohistochemistry.
• Rapid urease test: detects urease produced by the organism acting on urea to generate NH3, with 85% sensitivity.
• Urea breath test: radioactive carbon measured in expired CO2, with 95% sensitivity.
• Serology test: detects H pylori antibodies
• Fecal antigen test: 90% sensitivity.

Diseases Associated with H Pylori Infection

• Gastric adenocarcinoma
• Malignant lymphoma arising in MALT
• Duodenal ulcer and nonulcer dyspepsia
• Gastric ulcer