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Related Concept Videos

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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Peptic Ulcer Disease II: Pathophysiology01:28

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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.
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Gastritis-II: Pathophysiology01:17

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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.
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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.
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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.
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The small intestine exhibits a unique histological structure that significantly enhances its function in digestion and nutrient absorption. These structures include circular folds, villi, and various specialized cells that collectively facilitate the digestion of food.
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Author Spotlight: Isolation and Characterization of Equine Submucosal Enteric Glia &#8212; Implications for Preventing Postoperative Complications in Colic Surgery
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Equine Intestinal Mucosal Pathobiology.

Anthony Blikslager1, Liara Gonzalez1

  • 1Center for Gastrointestinal Biology and Disease, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27607, USA;

Annual Review of Animal Biosciences
|November 17, 2017
PubMed
Summary

Equine intestinal mucosa repair is vital for horses prone to colic. Understanding mechanisms like epithelial restitution and tight junction function aids in developing better treatments for intestinal injury.

Keywords:
barrier functionenteroidhorseintestineischemiastem cell niche

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Area of Science:

  • Equine gastrointestinal physiology
  • Mucosal immunology
  • Pathobiology of equine colic

Background:

  • The equine intestinal mucosa maintains homeostasis and barrier function.
  • Horses are susceptible to colic, often involving ischemic injury to the mucosa due to strangulating obstruction.
  • The mucosal epithelium is vulnerable to ischemic damage due to its vascular architecture.

Purpose of the Study:

  • To review the pathobiology of equine mucosal repair.
  • To discuss mechanisms of mucosal repair and factors affecting it.
  • To highlight the role of inflammation and NSAIDs in mucosal healing.

Main Methods:

  • Review of existing literature on equine intestinal mucosal pathobiology.
  • Analysis of mechanisms of mucosal repair: villus contraction, epithelial restitution, tight junction closure.
  • Discussion of factors influencing repair, including ischemia, reperfusion, inflammation, and NSAIDs.

Main Results:

  • Reperfusion injury plays a minimal role in equine intestinal injury.
  • Inflammation significantly impacts mucosal repair processes.
  • Nonsteroidal anti-inflammatory drugs affect tight junction integrity during repair.
  • Enteroid models are crucial for studying equine mucosal regeneration and proliferation.

Conclusions:

  • Understanding equine mucosal repair mechanisms is critical for managing colic.
  • Factors like inflammation and NSAIDs must be considered in therapeutic strategies.
  • Further research using equine enteroids will advance knowledge of mucosal regeneration.