Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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 to M3...
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...
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 Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Worldwide prevalence and burden of gastroparesis-like symptoms as defined by the United European Gastroenterology (UEG) and European Society for Neurogastroenterology and Motility (ESNM) consensus on gastroparesis.

United European gastroenterology journal·2022
Same author

Editorial: refractory reflux sensitivity-A place for baclofen? Authors' reply.

Alimentary pharmacology & therapeutics·2022
Same author

Exploring the pathophysiology of LARS after low anterior resection for rectal cancer with high-resolution colon manometry.

Neurogastroenterology and motility·2022
Same author

Functional bowel disorders with diarrhoea: Clinical guidelines of the United European Gastroenterology and European Society for Neurogastroenterology and Motility.

United European gastroenterology journal·2022
Same author

Clinical trial: a controlled trial of baclofen add-on therapy in PPI-refractory gastro-oesophageal reflux symptoms.

Alimentary pharmacology & therapeutics·2022
Same author

Zhizhu Kuanzhong Capsule in treating patients with functional dyspepsia postprandial distress syndrome: study protocol for a multicenter, randomized, double-blind, placebo-controlled, parallel-group clinical trial.

Trials·2022

Related Experiment Video

Updated: Jul 5, 2026

The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management
06:40

The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management

Published on: June 29, 2019

Pathogenesis of dyspepsia.

Kostas Mimidis1, Jan Tack

  • 1Department of Pathophysiology, University Hospital Gasthuisberg, KU Leuven, Leuven, Belgium.

Digestive Diseases (Basel, Switzerland)
|May 9, 2008
PubMed
Summary
This summary is machine-generated.

Functional dyspepsia (FD) is a common gut disorder with unclear causes. Research explores various factors like gut motility, sensitivity, genetics, and infections contributing to FD pathogenesis.

More Related Videos

Effects of Desmodium caudatum on Gastrointestinal Hormones and Intestinal Flora in Rats with Gastritis
03:48

Effects of Desmodium caudatum on Gastrointestinal Hormones and Intestinal Flora in Rats with Gastritis

Published on: March 1, 2024

Surgical Models of Gastroesophageal Reflux with Mice
05:19

Surgical Models of Gastroesophageal Reflux with Mice

Published on: August 25, 2015

Related Experiment Videos

Last Updated: Jul 5, 2026

The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management
06:40

The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management

Published on: June 29, 2019

Effects of Desmodium caudatum on Gastrointestinal Hormones and Intestinal Flora in Rats with Gastritis
03:48

Effects of Desmodium caudatum on Gastrointestinal Hormones and Intestinal Flora in Rats with Gastritis

Published on: March 1, 2024

Surgical Models of Gastroesophageal Reflux with Mice
05:19

Surgical Models of Gastroesophageal Reflux with Mice

Published on: August 25, 2015

Area of Science:

  • Gastroenterology
  • Digestive Health
  • Functional Gastrointestinal Disorders

Background:

  • Functional dyspepsia (FD) is a prevalent and heterogeneous gastrointestinal disorder.
  • The exact pathogenesis of FD remains largely unknown despite ongoing research.
  • Understanding FD etiology is crucial for developing effective treatments.

Purpose of the Study:

  • To provide a comprehensive overview of the pathogenetic factors and pathophysiologic mechanisms underlying functional dyspepsia.
  • To synthesize current knowledge on the multifactorial nature of FD.
  • To highlight potential targets for therapeutic interventions in FD.

Main Methods:

  • Review of existing scientific literature on functional dyspepsia.
  • Analysis of proposed pathophysiologic mechanisms including gastric emptying, accommodation, duodenal sensitivity, and motility.
  • Examination of implicated pathogenetic factors such as genetics, H. pylori, infections, and psychosocial elements.

Main Results:

  • FD pathogenesis involves a complex interplay of factors.
  • Key mechanisms include delayed gastric emptying, impaired gastric accommodation, visceral hypersensitivity, and altered duodenal sensitivity.
  • Contributing factors encompass genetic predisposition, Helicobacter pylori infection status, prior gastrointestinal infections, and psychosocial influences.

Conclusions:

  • Functional dyspepsia arises from a combination of genetic, infectious, and environmental factors influencing gut physiology.
  • Altered gastrointestinal motility and sensitivity are central to FD symptom generation.
  • Further research into these mechanisms is essential for advancing FD management.