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Related Concept Videos

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...
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: Pathophysiology01:24

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...
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.
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...

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Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
11:48

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration

Published on: May 7, 2018

Aphthous ulcers as a multifactorial problem.

Ana Ujević1, Liborija Lugović-Mihić, Mirna Situm

  • 1Vukić Private Dental Clinic, Zagreb, Croatia.

Acta Clinica Croatica
|September 24, 2013
PubMed
Summary

Recurrent aphthous stomatitis (RAS) involves painful mouth ulcers with unknown causes but several contributing factors. Treatment includes corticosteroids and vitamin therapy, requiring a multidisciplinary medical approach.

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Area of Science:

  • Oral Medicine
  • Immunology
  • Pathology

Background:

  • Recurrent aphthous stomatitis (RAS) presents as recurring oral mucosal ulcerations.
  • RAS is considered a complex condition with multiple underlying pathological states rather than a single disease.
  • The exact etiology of RAS remains unknown, but several predisposing factors are identified.

Purpose of the Study:

  • To provide a comprehensive overview of Recurrent Aphthous Stomatitis (RAS).
  • To discuss the various clinical presentations and potential etiologies of RAS.
  • To highlight the importance of a multidisciplinary approach in managing RAS.

Main Methods:

  • Literature review of existing research on Recurrent Aphthous Stomatitis.
  • Analysis of predisposing factors including nutritional deficiencies (iron, folic acid, vitamin B), neutropenia, trauma, stress, metabolic and hormonal disorders, and immunodeficiency.
  • Categorization of clinical forms: small, large, and herpetiform aphthous ulcers.

Main Results:

  • Predisposing factors for RAS include anemia, neutropenia, local trauma, stress, metabolic/hormonal imbalances, and immunodeficiency.
  • RAS manifests in three distinct clinical forms: small, large, and herpetiform ulcers.
  • Current treatment strategies involve topical or systemic corticosteroids, immunostimulants, and vitamin supplementation.

Conclusions:

  • RAS is a multifactorial condition requiring a comprehensive understanding of its diverse presentations and triggers.
  • Effective management necessitates a collaborative, multidisciplinary approach involving various medical specialties.
  • Further research into the precise mechanisms of RAS is needed to optimize therapeutic interventions.