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Related Concept Videos

Pyloric Obstruction01:11

Pyloric Obstruction

Pyloric obstruction, also referred to as gastric outlet obstruction, is a condition characterized by narrowing or blockage at the pylorus—the muscular valve regulating the flow of stomach contents into the duodenum. When this passage becomes impaired, the stomach cannot effectively empty its contents into the small intestine. This disruption leads to a range of gastrointestinal symptoms, including early satiety, bloating, epigastric pain, postprandial nausea, persistent vomiting, and...
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-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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...
Esophageal Achalasia01:27

Esophageal Achalasia

Esophageal achalasia is a chronic neurogenic disorder characterized by impaired relaxation of the lower esophageal sphincter (LES) and absent or ineffective peristalsis in the distal esophagus. This leads to a functional obstruction without a physical blockage, despite significant disruption of esophageal motility.EtiologyAchalasia is caused by degeneration of the myenteric (Auerbach's) plexus, specifically the loss of inhibitory ganglion cells that produce vasoactive intestinal peptide (VIP)...
Gastric Emptying01:16

Gastric Emptying

Gastric emptying occurs when the stomach gradually releases chyme into the duodenum. When the stomach is distended, it triggers the release of gastrin, a hormone that promotes gastric acid secretion to aid in digestion. Additionally, stomach distension contributes to peristaltic waves that propel gastric contents toward the pyloric region. The gastroenteric reflex, on the other hand, primarily stimulates peristalsis in the intestines, facilitating the movement of contents further along the...
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,...

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Gastric Point of Care Ultrasound in Adults: Image Acquisition and Interpretation
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When does gastric atrophy develop in Japanese children?

Seiichi Kato1, Shogo Kikuchi, Shigemi Nakajima

  • 1Department of Pediatrics, Tohoku University School of Medicine, Aoba-ku, and Tohoku Koseinenkin Hospital, Sendai, Japan. skato@tohoku-knhp.ne.jp

Helicobacter
|July 31, 2008
PubMed
Summary

Helicobacter pylori infection in children can cause gastric atrophy, but age did not correlate with atrophy severity in this study. Early H. pylori eradication may prevent future gastric cancer.

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Area of Science:

  • Pediatric Gastroenterology
  • Oncology
  • Infectious Diseases

Background:

  • Long-term Helicobacter pylori infection is linked to gastric atrophy, intestinal metaplasia, and increased gastric cancer risk.
  • Gastric atrophy has been observed in Japanese children with H. pylori infection, primarily in the antrum.
  • Limited data exists on the specific ages of children affected by H. pylori-induced gastric atrophy.

Purpose of the Study:

  • To investigate the association between age and the grade of gastric atrophy in children with H. pylori infection.
  • To analyze the prevalence of gastric atrophy and intestinal metaplasia in relation to age in pediatric H. pylori cases.

Main Methods:

  • Retrospective analysis of 131 children (79 boys) diagnosed with H. pylori infection.
  • Histological evaluation of gastric antrum in all patients and corpus in 46 patients.
  • Assessment of gastric atrophy grades (0-3) and intestinal metaplasia.

Main Results:

  • Grade 2 and 3 antral atrophy was found in 14 children with a mean age of 12.1 years.
  • Two children (aged 11 and 14) had grade 2 corpus atrophy; no grade 3 corpus atrophy was observed.
  • No significant age difference was found across different grades of antral or corpus atrophy (p > 0.59).
  • Intestinal metaplasia was absent in patients with grade 2 or 3 atrophy.

Conclusions:

  • While age did not correlate with atrophy severity in this retrospective study, findings suggest H. pylori eradication in childhood may be crucial.
  • Early intervention in high-risk gastric cancer regions could prevent H. pylori-induced gastric atrophy and subsequent malignancy.