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Related Concept Videos

Gastritis-I: Introduction and Types01:27

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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.
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Gastritis-II: Pathophysiology01:17

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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.
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In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
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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
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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...
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Gastritis II: Pathophysiology01:26

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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...
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Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
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Epidemic gastritis with hypochlorhydria.

E J Ramsey, K V Carey, W L Peterson

    Gastroenterology
    |June 1, 1979
    PubMed
    Summary

    A sudden decrease in stomach acid (hypochlorhydria) occurred in healthy volunteers and a Zollinger-Ellison syndrome patient, possibly due to infection. Acid levels and gastritis improved over time in most subjects.

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    Area of Science:

    • Gastroenterology
    • Infectious Diseases

    Background:

    • Studies on gastric acid secretion can reveal unexpected physiological responses.
    • Zollinger-Ellison syndrome provides a model for studying extreme acid secretion conditions.

    Observation:

    • A significant number of healthy volunteers and one patient with Zollinger-Ellison syndrome experienced profound hypochlorhydria.
    • Mild illness with epigastric pain preceded the hypochlorhydria in some subjects.
    • Gastric biopsies showed severe fundal and antral gastritis despite normal-appearing parietal cells.

    Findings:

    • Gastric permeability to hydrogen, sodium, and lithium remained normal during hypochlorhydria.
    • Serum gastrin levels were typically normal, but serum pepsinogen concentrations were consistently elevated.
    • Parietal cell antibodies were absent in all subjects.
    • Acid secretion and gastritis severity improved in most subjects over several months.
    • An infectious cause is suspected but not confirmed by current diagnostic tests.

    Implications:

    • This suggests a potential infectious trigger for acute hypochlorhydria and gastritis.
    • Elevated pepsinogen may serve as a biomarker for this condition.
    • Further research is needed to identify the infectious agent and understand the mechanism of gastric acid suppression.