Budd-Chiari syndrome pathophysiology

Budd-Chiari syndrome Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Budd-Chiari syndrome from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Budd-Chiari syndrome pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Budd-Chiari syndrome pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Budd-Chiari syndrome pathophysiology
CDC on Budd-Chiari syndrome pathophysiology
Budd-Chiari syndrome pathophysiology in the news
Blogs on Budd-Chiari syndrome pathophysiology
Directions to Hospitals Treating Type page name here
Risk calculators and risk factors for Budd-Chiari syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Please help WikiDoc by adding content here. It's easy! Click here to learn about editing.

Overview

Any obstruction of the venous vasculature of the liver is referred to as Budd-Chiari syndrome, from the venules to theright atrium. This leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates. The increased portal pressure causes: 1) increased filtration of vascular fluid with the formation of protein-rich ascites in the abdomen; and 2) collateral venous flow through alternative veins leading to gastric varices and hemorrhoids. Obstruction also causes hepatic necrosis and eventual centrilobular fibrosis due to ischemia. Renal failure may occur, perhaps due to the body sensing an "underfill" state and subsequent activation of the renin-angiotensin pathways and excess sodium retention.