Internal Diseases and Therapy · MU Sofia

100. Liver cirrhosis – etiology, pathogenesis, clinical features

Covers liver cirrhosis as diffuse fibrosis with nodule formation, its common causes including viral hepatitis, alcohol, fatty liver and autoimmune diseases, and the pathogenic processes of hepatocyte death, stellate cell fibrosis and vascular change. It then lists the three major clinical syndromes and their signs, followed by treatment principles for the underlying cause and for complications. A trichrome-stained biopsy image is included.

Inside: 2 sections · 2 labelled pictures · 14 flashcards · 3 min

Topic 101 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 2 sections, about 487 words (3 min of reading), with 14 flashcards.

In this note

  1. Liver cirrhosis - etiology, pathogenesis, clinical features
  2. Principles in treatment of chronic liver disease

Liver cirrhosis - etiology, pathogenesis, clinical features

Liver cirrhosis is a diffuse process characterized by fibrosis and conversion of normal liver tissue into abnormal nodules, the main characteristics are:

  • Fibrous septa - broad fibrous deposits around multiple adjacent lobules
  • Parenchymal nodules - range in size

Trichrome-stained liver biopsy in cirrhosis: blue fibrous septa surround and separate pink regenerative nodules of hepatocytes.

Image: “Cirrhosis of the liver (trichrome stain) (5690946257)” by Ed Uthman from Houston, TX, USA, CC BY 2.0, via Wikimedia Commons.

It is the end stage process of liver damage that may have multiple causes, the most common being Hep B, C, alcoholic and nonalcoholic steatohepatitis. Additionally, autoimmune conditions such as primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis can lead to cirrhosis.

Pathogenesis

  • Three main processes, death of hepatocytes, ECM deposition and vascular reorganisation
  • Fibrosis is present in liver capsule, portal tracts and around central veins
  • Major source of fibrosis is the perisinusoidal stellate cells which transform to myofibroblasts and lay down collagen fibers
  • These stellate cells themselves produce growth factors for more stellate cells (transforming growth factor Beta)
  • Vascular injuries also occur in cirrhosis, with inflammation and thrombosis of portal veins, hepatic arteries and/or central veins, causing zones of parenchymal hypoperfusion causing atrophy.
  • We also see conversion of thin-walled sinusoids into higher pressure which increases speed of fluid movement and inhibits protein movement. Due to the lack of basement membrane in the sinusoids, collagen is deposited with increased ease which causes the stenosis of these vessels.

The major clinical syndromes of liver cirrhosis are hepatic failure, portal hypertension and cholestasis. Hepatic failure is generally the end point of progressive liver damage, either thanks to gradual or sudden destruction of hepatocytes, around 90% of hepatic function should be lost before we call it hepatic failure.

Clinical features are jaundice, hypoalbuminemia, hyperammonemia, palmar erythema, spider angiomas and hypogonadism and gynecomastia in men.

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