1. Epidemiology
   1. The population of the US, almost 25% are affected by the symptoms of dyspepsia including gastritis that contributes about 50% of patients who are diagnosed and referred by endoscopy procedure
   2. Patients are taking nonsteroidal anti-inflammatory drugs (NSAIDs), 10% to 20% of patients have reported with symptoms of dyspepsia though the occurrence may range from 5% to 50%.
   3. For autoimmune gastritis, the high-risk ancestry is the North European or Scandinavian
   4. In developing countries and is impacted by a multitude of factors, H pylori infection occurrence is higher such as strain virulence, environmental factors, age, geography, and socioeconomic status
2. Pathophysiology
   1. Gastritis are acute, or chronic gastritis affect the antrum or fundus or both, and it's an inflammatory disorder that affect the gastric mucosa.
   2. In acute gastritis, the surface epithelium erodes in a localized or diffused pattern and typically the erosions are superficial.
   3. Drugs or chemicals damage the protective mucosal barrier, such as nonsteroidal anti-inflammatory drugs (NSAIDs), that prevent the action of cyclooxygenase-1 (COX-1) that leads to gastritis due to the prostaglandins inhibitions that stimulate the primary secretion of mucus.
   4. In chronic gastritis, the degeneration and thinning of the gastric mucosa, elderly individuals are affected.
   5. Type A (fundal) or type b (antral) is the classification of chronic gastritis, depending on the location and pathogenesis of the lesions.
   6. When antrum is more affected, both types of chronic gastritis present and it’s called type AB or pangastritis.
   7. Extensive degeneration of the gastric mucosa in the body and fundus of the stomach, leading to gastric atrophy.
   8. Due to the loss of parietal cells and chief cells, acid secretion diminished, therefore, gastric secretion is impaired resulting in elevation plasma levels of gastrin.
   9. Chronic antral gastritis usually involves the antrum, and it occurs more in fundal gastritis.
   10. Due to the increase levels hydrochloric acid secretion, H. pylori can cause autoimmune atrophic gastritis and it’s affected the fundus.
   11. The gastric secretion can evaluate the presence of the intrinsic factor.
3. Clinical Presentation
   1. In acute gastritis, such as vague abdominal discomfort, bleeding, and epigastric tenderness are the clinical presentation
   2. Chronic gastritis shows vague symptoms such as anorexia, fullness, nausea, vomiting, and epigastric pain, gastric bleeding is the only clinical manifestation of gastritis.
4. Diagnosis
   1. A mucosal biopsy is necessary to distinguish between acute, chronic active, or chronic gastritis from gastropathy
   2. And the radiologic and endoscopic features may be the same and often clinical features are unreliable for predicting histologic findings
   3. Histologic findings can vary over a broad spectrum ranging from epithelial hyperplasia to extensive epithelial cell damage with infiltration by inflammatory cells
5. Treatment
   1. To promote healing, drugs to avoids are the use of antacids and to reduce acid secretion with an H2-receptor histamine antagonist and proton pump inhibitor
   2. The treatments depend on the etiology
   3. Eradication of H pylori therapy is one option, NSAIDs or alcohol exposure reduction, histamine-2 antagonists symptomatic treatment, and proton-pump inhibitors
   4. Progression to peptic ulcer disease if remains untreated, and complications may arise such as gastric carcinoma and gastric lymphoma