Budd-Chiari syndrome pathophysiology

Jump to navigation Jump to search

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: Mazia Fatima, MBBS [2]

Overview

Occlusion of at least two hepatic veins leads to Budd-Chiari syndrome. Single hepatic vein occlusion is usually silent. Obstruction in the venous drainage from liver results in venous congestion causing hepatomegaly. Patients may develop postsinusoidal portal hypertension. Stasis of blood and congestion cause hypoxic damage in the hepatocytes, affecting liver function. This can result in centrilobular fibrosis, nodular regenerative hyperplasia and ultimately cirrhosis. Hepatocellular necrosis results from increased sinusoidal pressure. Budd-Chiari syndrome is commonly associated with atrophy of peripheral regions and enlargement of the caudate lobe because blood is directly shunted through it into the inferior vena cava. Genes associated with increased expression in the pathogenesis of Budd-Chiari syndrome include matrix metalloproteinase 7, superior cervical ganglion 10 (SCG10), proliferating cell nuclear antigen gene, c-myc oncogene, tumor protein p53 gene, thrombospondin-1 gene.

Pathogenesis

Genetics

Gross Pathology

Microscopic Pathology

References

  1. 1.0 1.1 1.2 Martens P, Nevens F (2015). "Budd-Chiari syndrome". United European Gastroenterol J. 3 (6): 489–500. doi:10.1177/2050640615582293. PMC 4669515. PMID 26668741.
  2. Paradis V, Bièche I, Dargère D, Cazals-Hatem D, Laurendeau I, Saada V, Belghiti J, Bezeaud A, Vidaud M, Bedossa P, Valla DC (2005). "Quantitative gene expression in Budd-Chiari syndrome: a molecular approach to the pathogenesis of the disease". Gut. 54 (12): 1776–81. doi:10.1136/gut.2005.065144. PMC 1774794. PMID 16162682.
  3. Dragoteanu M, Balea IA, Piglesan CD (2014). "Nuclear medicine dynamic investigations in the diagnosis of Budd-Chiari syndrome". World J Hepatol. 6 (4): 251–62. doi:10.4254/wjh.v6.i4.251. PMC 4009481. PMID 24799994.

Template:WS Template:WH