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Related Concept Videos

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...
Chronic Pancreatitis I: Introduction01:24

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
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 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 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: May 16, 2026

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

How and where does acute pancreatitis begin?

M L Steer1

  • 1Department of Surgery, Beth Israel Hospital, Boston, Mass. 02215.

Archives of Surgery (Chicago, Ill. : 1960)
|November 1, 1992
PubMed
Summary
This summary is machine-generated.

Gallstone-induced pancreatitis may stem from pancreatic duct obstruction. Studies reveal digestive enzyme zymogens and cathepsin B colocalization, suggesting early intra-acinar cell activation is key to acute pancreatitis development.

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Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct
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A Simple and Rapid Method for Simultaneous Isolation of Primary Islets and Primary Pancreatic Acinar Cells from Mice
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A Simple and Rapid Method for Simultaneous Isolation of Primary Islets and Primary Pancreatic Acinar Cells from Mice

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Last Updated: May 16, 2026

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

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

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A Simple and Rapid Method for Simultaneous Isolation of Primary Islets and Primary Pancreatic Acinar Cells from Mice
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A Simple and Rapid Method for Simultaneous Isolation of Primary Islets and Primary Pancreatic Acinar Cells from Mice

Published on: January 9, 2026

Area of Science:

  • Gastroenterology and Hepatology
  • Cell Biology
  • Pathology

Background:

  • Gallstone-induced pancreatitis is suspected to result from pancreatic duct obstruction.
  • Understanding the early cellular events is crucial for pancreatitis research.

Purpose of the Study:

  • To investigate the early events leading to acute pancreatitis using experimental models.
  • To explore the role of digestive enzyme zymogen activation in pancreatitis pathogenesis.

Main Methods:

  • Review of studies using diet-induced, secretagogue-induced, and duct obstruction-induced experimental pancreatitis models.
  • Morphologic evaluation of early lesions in duct ligation models.

Main Results:

  • Colocalization of digestive enzyme zymogens and lysosomal hydrolase cathepsin B was observed in all models.
  • Earliest lesions in hemorrhagic pancreatitis models occur within acinar cells.

Conclusions:

  • Intra-acinar cell activation of digestive enzyme zymogens by lysosomal hydrolases is a potential critical event in acute pancreatitis.
  • Early pancreatic duct ligation studies pinpoint acinar cells as the site of initial injury.