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Related Concept Videos

Gastritis II: Pathophysiology01:26

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...
Gastritis-I: Introduction and Types01:27

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,...
Barrett Esophagus-I: Introduction01:21

Barrett Esophagus-I: Introduction

Barrett's esophagus is a medical condition where the esophageal mucosa is significantly damaged by stomach acid or other digestive fluids, often due to long-term exposure associated with gastroesophageal reflux disease (GERD). In GERD, a weakened or abnormally relaxed lower esophageal sphincter allows stomach acid to flow persistently into the esophagus.
This constant acid exposure transforms the esophagus's pink mucosal lining (stratified squamous epithelium) into a type of lining more similar...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Peptic Ulcer Disease I: Introduction01:25

Peptic Ulcer Disease I: Introduction

Peptic ulcer disease (PUD) involves breaks in the gastrointestinal tract's mucosal lining, primarily in the stomach and duodenum, with less frequent occurrences in the lower esophagus or near the pylorus.Ulcers can be acute or chronic. Acute ulcers are short-lived with minimal inflammation and heal quickly after the irritant is removed. Chronic ulcers persist, may recur, and often cause scarring due to ongoing tissue damage. Superficial erosions affect only the mucosal layer and are called...
Peptic Ulcer01:27

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...

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Related Experiment Video

Updated: May 11, 2026

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
03:05

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia

Published on: February 16, 2024

Gastric cancer: overview.

Pelayo Correa1

  • 1Division of Gastroenterology, Vanderbilt University Medical Center, Nashville, TN 37232, USA. pelayo.correa@vanderbilt.edu

Gastroenterology Clinics of North America
|May 4, 2013
PubMed
Summary

This review details gastric cancer causes, focusing on Helicobacter pylori infection and host factors. It covers the precancerous process, clinical symptoms, and prevention methods for this common malignancy.

Area of Science:

  • Gastroenterology and Oncology

Background:

  • Gastric cancer remains a significant global health concern.
  • Helicobacter pylori infection is a primary risk factor.
  • Understanding multifactorial etiology is crucial for effective management.

Purpose of the Study:

  • To provide a comprehensive overview of gastric cancer.
  • To elucidate the role of Helicobacter pylori and host factors.
  • To discuss prevention strategies.

Main Methods:

  • Literature review of current research on gastric cancer.
  • Analysis of Helicobacter pylori biology and its interaction with host factors.
  • Examination of the precancerous cascade and clinical manifestations.

Main Results:

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Laparoscopic Radical Gastrectomy for Remnant Gastric Cancer
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Laparoscopic Radical Gastrectomy for Remnant Gastric Cancer

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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT

Published on: January 22, 2018

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Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
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Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia

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Laparoscopic Radical Gastrectomy for Remnant Gastric Cancer
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Laparoscopic Radical Gastrectomy for Remnant Gastric Cancer

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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT

Published on: January 22, 2018

  • Helicobacter pylori is the principal infectious agent in gastric cancer development.
  • Host genetic susceptibility and environmental factors interact with H. pylori.
  • The progression from infection to cancer involves distinct precancerous stages.

    • Conclusions:

    • Effective prevention strategies require targeting H. pylori and mitigating environmental risks.
    • Further research into host-pathogen interactions can inform personalized prevention.
    • Integrated approaches are necessary for gastric cancer control.