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Related Concept Videos

Acute Pancreatitis I: Introduction01:25

Acute Pancreatitis I: Introduction

Acute pancreatitis is the sudden inflammation of the pancreas caused by the early activation of digestive enzymes, leading to the autodigestion of pancreatic tissue. This results in local inflammation and, in severe cases, systemic complications.EtiologyUnderstanding the underlying causes is crucial, as identifying the etiology guides treatment and anticipates complications. Acute pancreatitis can be triggered by various factors, typically grouped into the following clinical categories.Biliary...
Acute Pancreatitis I: Introduction01:27

Acute Pancreatitis I: Introduction

Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
Acute Pancreatitis II: Clinical Manifestations and Management01:30

Acute Pancreatitis II: Clinical Manifestations and Management

Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Chronic Pancreatitis II: Collaborative Care01:29

Chronic Pancreatitis II: Collaborative Care

The management of chronic pancreatitis is multifaceted, involving a comprehensive approach that includes thorough assessment, diagnostic testing, and a variety of management strategies.
Assessment:
Chronic Pancreatitis I: Introduction01:25

Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...

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Related Experiment Video

Updated: Jun 13, 2026

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct
07:10

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Published on: April 1, 2022

Update in acute pancreatitis.

Bechien U Wu1, Darwin L Conwell

  • 1Center for Pancreatic Disease, Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. buwu@partners.org

Current Gastroenterology Reports
|April 29, 2010
PubMed
Summary
This summary is machine-generated.

Recent advances in acute pancreatitis research offer new insights into acinar cell function and immune responses. Clinical studies highlight improved severity assessment, complication management, and infection recognition for better patient outcomes.

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Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
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Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
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Related Experiment Videos

Last Updated: Jun 13, 2026

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct
07:10

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Published on: April 1, 2022

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
07:38

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection

Published on: May 10, 2024

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
06:35

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice

Published on: June 28, 2021

Area of Science:

  • Gastroenterology and Hepatology
  • Cell Biology
  • Immunology

Background:

  • Acute pancreatitis is a significant cause of hospitalization globally.
  • Existing research covers acinar cell pH, signaling, and immune responses.
  • Clinical management strategies are evolving.

Purpose of the Study:

  • To summarize recent advancements in acute pancreatitis research.
  • To highlight findings relevant to clinical practice.
  • To provide an overview of basic and clinical science progress.

Main Methods:

  • Literature review of recent publications on acute pancreatitis.
  • Synthesis of findings from basic science research (e.g., acinar cell function).
  • Analysis of clinical research on disease severity, complications, and management.

Main Results:

  • New insights into the acinar cell pH microenvironment and cell fate signaling.
  • Understanding of the innate immune response in acute pancreatitis.
  • Development of novel methods for assessing disease severity and managing complications.
  • Emphasis on early infection detection and recurrence prevention.
  • Evidence suggesting specialized centers benefit severe acute pancreatitis management.

Conclusions:

  • Recent research provides a deeper understanding of acute pancreatitis pathophysiology.
  • Clinical advancements offer improved diagnostic and therapeutic strategies.
  • A multidisciplinary approach and specialized care are crucial for managing severe cases.