Liver Cirrhosis

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Cirrhosis refers to the diffuse transformation of the liver into regenerative parenchymal nodules surrounded by fibrous bands.

It is a permanent scarring of the liver, that leads to an altering in its function and thus can also eventually lead to liver failure (it is important to note however that this is not always the case).

Histologically, cirrhosis is characterized by three findings:

1. marked distortion of hepatic architecture
2. scarring due to increased deposition of collagen and fibrous tissue
3. regenerative nodules surrounded by scar tissue

Etiology

Cirrhosis is triggered by chronic hepatitis and can have a number of causes, some of them are listed below.

• Alcohol-induced hepatitis: from long term alcohol abuse. The exact manner in which alcohol leads to chronic liver disease and cirrhosis is not known.
• Chronic hepatitis B infection: a viral infection that may become chronic in some cases, it is not curable but treatable.
• Chronic hepatitis C infection: a viral infection that becomes chronic majority of the time, it is curable with anti-viral.
• Cardiovascular diseases: for example congestive heart failure which causes blood to build up in your liver or chronic ischemia which prevents blood from reaching your liver.
• Genetic conditions: damage caused due to buildup of toxic substances for example glycogen storage diseases, Wilsons disease.
• Autoimmune diseases: for example autoimmune hepatitis that cause chronic liver inflammation.

Pathogenesis:

Due to any of the reasons listed above, there is liver injury which leads to hepatocellular necrosis or apoptosis. These dead cells release DAMPS (damage associated molecular patterns) and ROS (reactive oxygen species) which activate the quiescent Kupffer cells and stellate cells of the hepatic reticuloendothelial system. The stellate cells will differentiate into myofibroblasts and further stimulate the Kupffer cells to release cytokines, release chemokines to attract innate immune cells to the area. The immune cells cause inflammation which stimulates nodule formation as well.

Overall this leads to extracellular matrix production which leads to fibrosis of the liver. It is thought the fibrosis occurs in two stages, the first stage where there is transformation of the collagen in the ECM from non-cross-linked non-fibril-forming to more dense collagen that is able to cross link. The second stage is characterized by formation of sub-endothelial cross links of collagen, proliferation of myoepithelial cells, and distortion of hepatic architecture with the subsequent appearance of nodules. The first stage is thought to be reversible still, with the second one more advanced and irreversible. However cirrhosis is a dynamic process and even in the advanced stages, with intervention, there can be some improvements in clinical outcomes.

Clinical Manifestations:

The clinical manifestations of cirrhosis is similar to that of acute and chronic hepatitis.

There are constitutional symptoms including fatigue, loss of vigor and weight loss. GI symptoms include vomiting, nausea, jaundice.

Cirrhosis results in portal hypertension due to an increase in intrahepatic vascular resistance. Portal hypertension can cause:

• Ascites and increased risk of spontaneous bacterial peritonitis
• Increased risk of sepsis
• Splenomegaly with thrombocytopenia
• Encephalopathy
• Varices
• Increased risk of disseminated intravascular coagulation

to name a few.

Clinical manifestations of liver cirrhosis

Investigations:

To confirm liver cirrhosis doctors perform one or more of the following:

• Liver biopsy
• Liver function tests
• Ultrasound (or imaging in general) to look at the liver architecture

Management:

The main thing to do is to try and slow down the progression of the liver disease by treating the cause such as giving anti viral in case its caused by a virus or eliminating alcohol if its alcohol dependent, and by changing ones diet and lifestyle.

Symptoms are managed in various ways and in extreme cases, a liver transplant may be considered.