Introduction

• Acute inflammation of the gastric mucosa with variable disruption of the gastric mucosal barrier.
• Cause: ingestion of irritant substances, drugs, dietary factors, foreign body, possibly infectious agents.
• Signs: anorexia, vomiting, dehydration, anterior abdominal pain.
• Diagnosis: history, signs, radiography.
• Treatment: fluid therapy if needed, metoclopramide, sucralfate, cimetidine.
• Prognosis: usually good but depends on underlying cause.

Pathogenesis

Etiology

• Ingestion of irritant substances such as:
  • Acids.
  • Alkalis.
  • Corrosives.
• Drugs, such as aspirin and other NSAIDs, corticosteroids.
• Dietary factors including overeating and eating contaminated foods.
• Foreign body.
• Helicobacter Helicobacter spp infection remains controversial.
• Parasites, eg Physaloptera, are occasional causes.
• Viral agents may be involved.

Predisposing factors

• Indiscriminate eating behavior.

Pathophysiology

• Acute inflammation → disordered gastric motility → delayed gastric outflow and vomition.
• Acute gastritis is common in dogs compared with cats due to the latters' fastidious eating habits.

• Etiological agent damages gastric mucosal barrier.
• Inflammation follows with stimulation of submucosal mast cells and histamine release.
• Histamine stimulates hydrochloric acid and pepsinogen secretion.
• Excess acid and pepsin → further inflammation.
• Persistence of the vicious cycle → gastric ulceration.
• Inflammation stimulates afferent nerves with inputs to the vomiting center in the medulla.
• Inflammation may also contribute to increases in intragastric pressure → vomition.

Timecourse

• Hours to days.

Diagnosis

Treatment

Prevention

Outcomes