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Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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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.
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...
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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Mucosal Barrier of the Stomach01:25

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The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
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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.
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,...
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Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
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Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
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Inflammatory microenvironment in gastric premalignant lesions: implication and application.

Shengxiong Zhang1,2,3, Yang Shen4, Hao Liu4

  • 1Rehabilitation Department, Guangdong Work Injury Rehabilitation Hospital, Guangzhou, China.

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Summary

Gastric precancerous lesions (GPL) progress to gastric cancer (GC) driven by inflammation. Targeting inflammatory pathways, including those influenced by Helicobacter pylori, offers potential for early detection and treatment of GPL.

Keywords:
TCMantioxidantsgastric cancergastric precancerous lesionsinflammatory microenvironment

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Area of Science:

  • Gastroenterology
  • Oncology
  • Immunology

Background:

  • Gastric precancerous lesions (GPL) are a significant global health concern due to their potential progression to gastric cancer (GC).
  • The precise mechanisms by which the inflammatory microenvironment influences GPL progression to GC remain incompletely understood.
  • Chronic inflammation is a common feature of GPL, implicating it as a critical factor in disease advancement.

Purpose of the Study:

  • To review the role of the inflammatory microenvironment in GPL progression to GC.
  • To explore the implications for early detection and potential therapeutic strategies.
  • To highlight Helicobacter pylori as a key mediator in this process.

Main Methods:

  • Literature review focusing on inflammation, immune cells, and inflammatory molecules in GPL.
  • Analysis of the role of Helicobacter pylori in driving GC progression.
  • Examination of therapeutic strategies targeting inflammatory pathways.

Main Results:

  • Inflammation is a central driver in the progression of GPL to GC.
  • Helicobacter pylori significantly contributes to the inflammatory microenvironment and GC development.
  • Immune cells and inflammatory molecules play crucial roles in mediating GPL progression.

Conclusions:

  • Targeting inflammatory pathways presents a promising avenue for the early detection and treatment of GPL.
  • Traditional Chinese Medicine and natural antioxidants show potential for suppressing or reversing GPL progression due to their anti-inflammatory properties.
  • Further research into the inflammatory microenvironment is essential for developing innovative therapeutic approaches for GPL.