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Gastritis-I: Introduction and Types

Gastritis-I: Introduction and Types

Gastritis, defined by the inflammation or irritation of the stomach lining or gastric mucosa, manifests in several distinct forms: acute, chronic, reactive, and a specific subtype known as autoimmune metaplastic atrophic gastritis.
Acute gastritis presents as a sudden inflammation triggered by various stressors to the stomach lining, such as exposure to corrosive agents, local irritants like aspirin and other NSAIDs, alcohol consumption, radiation therapy, physical trauma, severe burns, sepsis,...

Gastritis-II: Pathophysiology

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...

Gastritis III: Clinical Manifestations and Management

Gastritis III: Clinical Manifestations and Management

The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...

Peptic Ulcer

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...

Gastritis II: Pathophysiology

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...

Cholecystitis

Cholecystitis

Cholecystitis is inflammation of the gallbladder, most commonly caused by obstruction of the cystic duct. This blockage prevents bile from draining, leading to gallbladder distension, inflammation, and potentially serious complications. This condition may present acutely or chronically and can happen with or without gallstones.EtiologyAbout 95% of cholecystitis cases are calculous, caused by gallstones blocking the cystic duct, leading to bile accumulation and inflammation of the gallbladder...

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Updated: Jul 2, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Published on: October 18, 2018

Phlegmonous gastritis.

A I Miller, B Smith, A I Rogers

Gastroenterology

|February 1, 1975

Summary

This summary is machine-generated.

Phlegmonous gastritis is a rare infection. Early recognition in patients with abdominal pain, fever, and specific risk factors improves outcomes, as medical treatment alone has a 100% mortality rate.

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Area of Science:

Gastroenterology
Infectious Diseases

Background:

Phlegmonous gastritis is a rare, severe bacterial infection of the stomach wall.
It presents a diagnostic challenge due to its infrequent occurrence and varied symptoms.

Purpose of the Study:

To review documented cases of phlegmonous gastritis.
To identify clinical trends and aid in earlier diagnosis and improved patient outcomes.

Main Methods:

Systematic literature review of 23 cases since 1945.
Inclusion of two additional case studies.
Analysis of clinical presentation, diagnostic methods, treatment, and outcomes.

Main Results:

Key symptoms include acute upper abdominal pain, peritonitis, fever, and purulent ascites.
Risk factors include heavy ethanol intake, recent gastritis, or upper respiratory infection.
Preoperative diagnosis is uncommon; gastroscopy and gastric cultures can aid diagnosis.
Treatment involves surgery (resection or drainage) and systemic antibiotics.
Surgical mortality was 18.2%, while medical mortality was 100%.

Conclusions:

Phlegmonous gastritis requires high clinical suspicion in appropriate patient profiles.
Earlier diagnosis and prompt surgical intervention combined with antibiotics are crucial for reducing high morbidity and mortality rates.