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Related Concept Videos

Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

203
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...
203
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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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.
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...
642
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

380
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...
380
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

540
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.
540
Esophageal Varices-I: Introduction01:24

Esophageal Varices-I: Introduction

193
Esophageal varices are dilated, tortuous veins which are found mainly in the submucosa of the lower esophagus but which may also appear higher up or extend into the stomach. They develop due to increased pressure in the portal venous system, often as a result of liver cirrhosis. This condition scars and damages the liver, impeding normal blood flow through the portal vein. To compensate, blood seeks alternative pathways, forming fragile new vessels (varices) in the esophagus and stomach. These...
193
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

468
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.
468

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Risk factors for rebleeding in gastroduodenal ulcers.

Nobuhito Ito1, Kohei Funasaka2, Toshihisa Fujiyoshi3

  • 1Department of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Aichi, Japan.

Irish Journal of Medical Science
|July 11, 2023
PubMed
Summary
This summary is machine-generated.

Rebleeding after gastroduodenal ulcer hemostasis is a risk. A new Rebleeding-N score identifies patients at high risk based on transfusion, albumin levels, duodenal ulcers, and vessel size.

Keywords:
Endoscopic interventionGastrointestinal bleedingRebleedingRetrospective study

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Area of Science:

  • Gastroenterology
  • Endoscopic hemostasis
  • Peptic ulcer disease

Background:

  • Rebleeding after endoscopic hemostasis of gastroduodenal ulcers (GDU) is a significant predictor of mortality.
  • Limited research exists on risk stratification for post-hemostasis rebleeding in GDU patients.

Purpose of the Study:

  • To identify patient-specific factors associated with rebleeding after endoscopic hemostasis of bleeding GDU.
  • To develop and validate a risk score for stratifying rebleeding risk.

Main Methods:

  • Retrospective analysis of 587 patients with Forrest Ia-IIa bleeding GDU treated with endoscopic hemostasis.
  • Univariate and multivariate logistic regression to identify risk factors.
  • Development and internal validation of the Rebleeding Nagoya University (Rebleeding-N) score.

Main Results:

  • 11% of patients (64/587) experienced rebleeding.
  • Independent risk factors identified: blood transfusion, albumin < 2.5 g/dL, duodenal ulcer, and exposed vessel diameter ≥ 2 mm.
  • The Rebleeding-N score demonstrated good predictive ability (AUC 0.830) for stratifying rebleeding risk.

Conclusions:

  • Blood transfusion, low albumin, duodenal ulcer location, and large exposed vessel diameter are key predictors of rebleeding.
  • The Rebleeding-N score effectively stratifies rebleeding risk after endoscopic hemostasis for GDU.