Chronic gastritis

Chronic gastritis

    * Introduction
    * Causes and Risk Factors
    * Signs and symptoms
    * Diagnosis
    * Treatment
Chronic gastritis is a histological entity characterized by chronic inflammation of gastric mucosa. Gastritis can be classified according to causative agent: Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs, autoimmunity, allergic response and pathological mechanism by which may suggest the etiologic agent and clinical source. Other classifications are based on endoscopic appearance of gastric mucosa.
Chemical or reactive gastritis is caused by damage to gastric mucosa by reflux of bile and pancreatic secretions in the stomach, but may be caused by exogenous substances, including NSAIDs, acetilsalicilis acid, alcohol and chemotherapeutic agents. These chemicals cause damage to epithelial erosions and ulcers that are followed by regenerative hyperplasia detected as foveolara hyperplasia and capillary destruction with mucosal edema, hemorrhage and smooth muscle growth in the lamina propria.
No classification of gastritis allows a satisfactory description for all types of the disease. However calsificarea etiological model provides guidance to appropriate therapy. Frequently gastritis is a relatively minor manifestation of another disease prevalent and manifest in other organs or systemic immunosuppressive drugs such as gastritis people.
Approximately 35% of adults are infected with Helicobacter pylori, but the prevalence of infection in minority groups of immigrants from underdeveloped countries is much higher. Children aged 2-8 years in developing countries gain from an infection rate of 10% per year, while the U.S. rate of infection in children is less than 1% per year. This difference between rates of infection in children is responsible for the difference in epidemiology between developed and developing countries.
Mortality in chronic gastritis is closely related to immediate cause. Chronic gastritis as a primitive condition, such as Helicobacter pylori gastritis may progress from asymptomatic disease in some patients, while others reported dyspeptic symptoms. Evolution clinic can be exacerbated when patients develop complications such as infection with H. pylori and peptic ulcer, gastric malignancy. Environmental factors such as diet and living standards are important in determining the pathogenic mechanism prevailing in that country.
Pathogens. Pathophysiology of chronic gastritis complicating a systemic disease such as cirrhosis or uremia infefctie. Pathogenesis of the most important forms of gastritis include:
Chronic gastritis associated with Helicobacter pylori infection. Helicobacter pylori is a gram-negative bacterium that has the ability to colonize and infect the stomach. The bacterium survives in the mucous layer that covers the gastric epithelial surface and upper portions of gastric foveolelor. Infection is usually gained during childhood. Once oraganul was contaminated and the bacteria becomes stable in the gastric mucous layer is their intense inflammatory response to tissue.
This bacteria is associated with tissue damage and the presence of active and chronic histological gastritis. Host response to infection consists of T and B lymphocytes showing chronic gastritis, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear phagocytes which are bacteria. This active gastritis diagnosed polymorphonuclear leukocytes. Antral inflammation afeteaza interface between gastrin and somatostatin secretion, affecting cells in G and D. In particular, gastrin secretion is abnormal in people who are infected with Helicobacter pylori, the excessive release of gastrin-mediated food.
Infection with the bacterium associated chronic gastritis progresses with these two main mechanisms that have different clinical consequences: Antral-predominant gastritis, characterized by inflammation and antru limited to people with peptic ulcers usually demonstrate this pattern of gastritis Multifocal atrophic gastritis, characterized by involving the body and gastric antrum with progressive development of atrophic gastritis and gastric glands with partial reinlocuirea intestinal epithelium, intestinal metaplasia, those who develop gastric carcinoma and gastric ulcers usually demonstrate this pattern of gastritis.
Effect on gastric physiology by Helicobacter pylori. Increased gastric acid secretion and washes the precipitate bile salts, which normally inhibits gresterea bacteria. Progressive alteration of intestinal metaplasia duodenum promotes bacterial proliferation and resulting outbreaks suprainflamatie. This cycle increases the duodenal bulb inability to neutralize the acid in the stomach until the time when the bulb will change the structure and function was sufficient to develop an ulcer.
Complications include infection with Helicobacter pylori: And development of gastric lymphoma of MALT type, especially in people who have gastric intestinal metaplasia Bacterial infection-chronic atrophic gastritis is a precursor Intestinal metaplasia, gastric and duodenal ulcer gastric allows Persistent inflammation-associated bacteria in the body and allow the accumulation of mutations in gastric epithelial cells, leading to increased risk of malignant transformation and progression to adenocarcinoma.
Gstrita granulomatous infection. It is a rare entity. Tuberculosis can affect the stomach and cause granulomas. Fungi can also cause granulomas and necrosis, more of ALS patients who are immunosuppressed.
Gastritis in patients who are immunosuppressed. Cytomegalovirus infection of the stomach is seen in immunosuppressed patients. Infection and eosinophilic inclusions histologically typical small intracytoplasmic inclusions are seen. The mechanism detects an inflammatory infiltrate in the lamina propria. Viral inclusions are present in gastric epithelial cells and the endothelial and mesenchymal. Severe necrosis and ulceration may result. Herpes simplex infection basophilia determine cellular inclusions in epithelial cells. Mycobacterial infection with Mycobacterium avium-intracellulare are characterized by diffuse infiltrates in the lamina propria often forming granulomas.
Autoimmune gastritis. This type of gastritis is associated with serum antibodies and anti-intrinsic factor antiparietali. Gastric body shows progressive atrophy and patients will develop pernicious anemia. Autoimnua gastritis associated with serum antibodies to determine the intrinsic factor deficiency. Atrophic gastritis is limited to the stomach.
Chronic reactive chemical gastropathy. This type of chronic gastritis is associated with prolonged consumption of aspirin or NSAIDs. It develops and when the ball reflueaza intestinal contents in the stomach, most often in patients with gastrectomy in the surgical lesions develop near the stoma. The mechanism involving the gastric epithelium is due to the effect of constituents of bile. Lisolecitina and bile acids can disrupt gastric mucosal barrier allowing diffusion of hydrogen ions and cell damage. Pancreatic juice aggravate cellular damage. In contrast to other gastropatii chronic inflammation of the gastric mucosa is typically lower in chemical gastropathy.
Noninfectioase chronic granulomatous gastritis. Noninfectioase diseases are the main cause of gastric granulomas and include Crohn's disease, sarcoidosis, and isolated granulomatous gastritis. Gastric involvement in Crohn's disease showed 33% of cases. Granulomas have been described in association with gastric malignancy, including carcinoma and malignant lymphoma. Similar sarcoidosis granulomas may be seen in people who consume cocaine.
Lymphocytic gastritis. It is a type of chronic gastritis with dense infiltration in surface and foveolar epithelium by T lymphocytes similar histopathology Because celiac disease, lymphocytic gastritis was alleged to be due to intraluminal antigens. In patients with lymphocytic gastritis were found high antibody titers against Helicobacter pylori infection and in studies of bacteria occurs after eradication. Some cases develop after gluten intolerance, and drugs such as ticlopidine.
Eosinophilic gastritis. Large amounts of eosinophils are observed in parasitic infections such as those triggered by Eustoma rotundatum and anisakiaza. Eosinophilic gastritis may be part of eosinophilic gastroenteritis. Although entrepre stomach is affected, this condition can affect any segment of the gastrointestinal tract and can be segmented. Patients often have peripheral blood eosinophilia. Cases in children are frequently due to allergy to soy or milk. Eosinophilic gastroenteritis may be encountered in patients with scleroderma, polymyositis and dermatomyositis.
Radiation gastritis. Low-dose radiation causes reversible mucosal lesions while high doses cause irreversible damage mediated by ischemic atrophy and ulceration. Reversible changes consist of degenerative events in epithelial cells and nonspecific chronic inflammatory infiltrate in the lamina propria. High doses of radiation cause irreversible damage to the gastric mucosa with gland atrophy bows, mucosal erosions and capillary bleeding.
Ischemic gastritis. It is considered to be the result of thrombus formation in atherosclerotic celiac and superior mesenteric arteries.