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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...
Gastroesophageal Reflux Disease I: Meaning and Pathophysiology01:29

Gastroesophageal Reflux Disease I: Meaning and Pathophysiology

Gastroesophageal Reflux Disease (GERD) involves the recurrent backflow of the stomach or duodenal contents into the esophagus, leading to troublesome symptoms and potential esophageal mucosal damage. Although GERD is often referred to as a disease, it is more accurately described as a syndrome, as it encompasses a range of symptoms and complications rather than a singular pathological entity, impacting a large number of individuals as the most prevalent upper gastrointestinal problem. Roughly...
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...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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. Bicarbonate,...
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...

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Related Experiment Video

Updated: Jun 17, 2026

Simultaneous Laryngopharyngeal and Conventional Esophageal pH Monitoring
06:46

Simultaneous Laryngopharyngeal and Conventional Esophageal pH Monitoring

Published on: December 14, 2020

Rebound acid hypersecretion from a physiological, pathophysiological and clinical viewpoint.

Helge L Waldum1, Gunnar Qvigstad, Reidar Fossmark

  • 1Department of Gastroenterology and Liver Diseases, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway. helge.waldum@ntnu.no

Scandinavian Journal of Gastroenterology
|December 17, 2009
PubMed
Summary

Proton-pump inhibitors (PPIs) can cause rebound acid hypersecretion, worsening reflux disease. This review examines gastric acid secretion regulation to understand acid-related conditions better.

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Related Experiment Videos

Last Updated: Jun 17, 2026

Simultaneous Laryngopharyngeal and Conventional Esophageal pH Monitoring
06:46

Simultaneous Laryngopharyngeal and Conventional Esophageal pH Monitoring

Published on: December 14, 2020

Construction of a Wireless-Enabled Endoscopically Implantable Sensor for pH Monitoring with Zero-Bias Schottky Diode-based Receiver
08:25

Construction of a Wireless-Enabled Endoscopically Implantable Sensor for pH Monitoring with Zero-Bias Schottky Diode-based Receiver

Published on: August 27, 2021

Area of Science:

  • Gastroenterology
  • Physiology
  • Endocrinology

Background:

  • Dyspepsia after stopping proton-pump inhibitors (PPIs) suggests treatment may exacerbate reflux disease.
  • Understanding gastric acid secretion is crucial for managing acid-related conditions.

Purpose of the Study:

  • To review current knowledge on gastric acid secretion regulation.
  • To elucidate the pathogenesis of acid-related conditions.

Main Methods:

  • Review of three decades of studies on gastric acid secretion in rats and humans.
  • Inclusion of studies on gastrinoma patients.

Main Results:

  • Parietal cells have histamine and acetylcholine receptors; gastrin receptors are on ECL cells.
  • Gastrin regulates ECL cell mass, influencing histamine release and parietal cell mass.
  • PPIs cause rebound acid hypersecretion, unlike histamine-2 blockers which induce tolerance.

Conclusions:

  • Treatments should minimally disturb normal physiological processes.
  • Understanding acid secretion pathways is key to effective therapeutic strategies.