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Related Concept Videos

Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Cirrhosis I: Introduction01:23

Cirrhosis I: Introduction

Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Diseases of the Liver and Gallbladder01:26

Diseases of the Liver and Gallbladder

Liver and gallbladder diseases are a significant health concern, with prominent conditions including cirrhosis, hepatitis, non-alcoholic fatty liver disease (NAFLD), and gallstones. Jaundice is a common manifestation of liver and biliary disease.
Cirrhosis is characterized by the scarring of hepatic lobules in the liver, which are replaced by fibrous tissue, affecting the liver's normal functioning. NAFLD, on the other hand, is caused by an excessive build-up of fat in the liver, not related to...
Ascites01:19

Ascites

DefinitionAscites is the buildup of fluid inside the peritoneal cavity. It occurs when fluid moves out of the vascular system faster than the peritoneal lymphatics can remove it. This fluid shift is most commonly seen in liver cirrhosis but can also appear in several other systemic disorders.EtiologyCirrhosis remains the leading cause of ascites. Other conditions that can contribute include:Heart failureConstrictive pericarditisAbdominal cancersNephrotic syndromeSevere protein–calorie...
Gross Anatomy of the Liver01:17

Gross Anatomy of the Liver

The liver, the largest gland within the human body, is a firm and reddish-brown organ. This wedge-shaped structure weighs approximately 1.5 kg and occupies a significant portion of the right hypochondriac and epigastric regions. It extends more to the right of the body's midline than to the left.
Located under the diaphragm, the liver is almost entirely ensconced within the rib cage, providing it with substantial protection. Except for the superior most bare area, the liver's surface is covered...

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Related Experiment Video

Updated: May 14, 2026

A Simple Composite Phenotype Scoring System for Evaluating Mouse Models of Cerebellar Ataxia
07:33

A Simple Composite Phenotype Scoring System for Evaluating Mouse Models of Cerebellar Ataxia

Published on: May 21, 2010

The ataxic cirrhotic

Tim Ambrose1, Nishchay Chandra

  • 1Department of Gastroenterology, Royal Berkshire Hospital, Reading, UK.

Clinical Medicine (London, England)
|January 25, 2013
PubMed
Summary

No abstract available in PubMed .

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Last Updated: May 14, 2026

A Simple Composite Phenotype Scoring System for Evaluating Mouse Models of Cerebellar Ataxia
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A Simple Composite Phenotype Scoring System for Evaluating Mouse Models of Cerebellar Ataxia

Published on: May 21, 2010