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Pathophysiology of Gastritis

Pathophysiology of Gastritis

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Published by Florsean Mae Sala

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Published by: Florsean Mae Sala on Sep 16, 2012
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07/01/2014

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Pathophysiology
Acute gastritis has a number of causes, including certain drugs; alcohol; bile; ischemia; bacterial, viral, and fungal infections; acutestress (shock); radiation; allergy and food poisoning; and direct trauma. The common mechanism of injury is an imbalance betweenthe aggressive and the defensive factors that maintain the integrity of the gastric lining (mucosa).Acute erosive gastritis can result from the exposure to a variety of agents or factors. This is referred to as reactive gastritis. Theseagents/factors include nonsteroidal anti-inflammatory medications (NSAIDs), alcohol, cocaine, stress, radiation, bile reflux, andischemia. The gastric mucosa exhibits hemorrhages, erosions, and ulcers. NSAIDs, such as aspirin, ibuprofen, and naproxen, are themost common agents associated with acute erosive gastritis. This results from oral or systemic administration of these agents eitherin therapeutic doses or in supratherapeutic doses.Because of gravity, the inciting agents lie on the greater curvature of the stomach. This partly explains the development of acutegastritis distally on or near the greater curvature of the stomach in the case of orally administered NSAIDs. However, the majormechanism of injury is the reduction in prostaglandin synthesis. Prostaglandins are chemicals responsible for maintainingmechanisms that result in the protection of the mucosa from the injurious effects of the gastric acid. Long-term effects of suchingestions can include fibrosis and stricture.Bacterial infection is another cause of acute gastritis. The corkscrew-shaped bacterium called
H pylori 
is the most common cause of gastritis. Complications result from a chronic infection rather than from an acute infection. The prevalence of 
H pylori 
in otherwisehealthy individuals varies depending on age, socioeconomic class, and country of origin. The infection is usually acquired inchildhood. In the Western world, the number of people infected with
H pylori 
increases with age. Evidence of 
H pylori 
infection canbe found in 20% of individuals younger than 40 years and in 50% of individuals older than 60 years. How the bacterium istransmitted is not entirely clear. Transmission is likely from person to person through the oral-fecal route or through the ingestion of contaminated water or food. This is why the prevalence is higher in lower socioeconomic classes and in developing countries.
H pylori 
is associated with 60% of gastriculcersand80%ofduodenalulcers.
H pylori 
gastritis typically starts as an acute gastritis in the antrum, causing intense inflammation, and over time, it may extend toinvolve the entire gastric mucosa resulting in chronic gastritis.  The acute gastritis encountered with
H pylori 
is usually asymptomatic. The bacterium imbeds itself in the mucous layer, a protectivelayer that coats the gastric mucosa. It protects itself from the acidity of the stomach through the production of large amounts of urease, an enzyme that catalyzes the breakdown of urea to the alkaline ammonia and carbon dioxide. The alkaline ammonianeutralizes the gastric acid in the immediate vicinity of the bacterium conferring protection.
H pylori 
also has flagella that enable it to move and help it to penetrate the mucous layer so that it comes into contact with gastricepithelial cells. It also has several adhesions that help it to adhere to these cells. It produces inflammation by activating a number of toxins and enzymes that activate IL-8, which eventually attracts polymorphs and monocytes that cause acute gastritis.Antigen-presenting cells activate lymphocytes and other mononuclear cells that lead to chronic superficial gastritis. The infection isestablished within a few weeks after the primary exposure to
H pylori 
. It produces inflammation via the production of a number of toxins and enzymes. The intense inflammation can result in the loss of gastric glands responsible for the production of acid. This isreferred to as atrophic gastritis.Consequently, gastric acid production drops. The virulence genotype of the microbe is an important determinant for the severity of the gastritis and the formation of intestinal metaplasia, the transformation of gastric epithelium. Thistransformation can lead to gastric cancer.  Reactive gastropathy is the second most common diagnosis made on gastric biopsy specimens after
H pylori 
gastritis. This entity isbelieved to be secondary to bile reflux and was originally reported after partial gastrectomy (Billroth I or II). It is now considered torepresent a nonspecific response to a variety of other gastric irritants.
Helicobacter heilmanii 
is a gram-negative, tightly spiraled, helical-shaped organism with 5-7 turns. The prevalence of 
H heilmanii 
isextremely low (0.25-1.5%). The source of 
H heilmanii 
infection is unclear, but animal contact is thought to be the means of transmission.Tuberculosis is a rare cause of gastritis, but an increasing number of cases have developed because of patients who areimmunocompromised. Gastritis caused by tuberculosis is generally associated with pulmonary or disseminated disease.

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