Liver Cirrhosis

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In cirrhosis the liver is diffusely replaced by nodules of hepatocytes separated by fibrosis.
In cirrhosis the normal architecture of the liver is diffusely replaced by nodules of regenerated
liver cells, separated by bands of collagenous fibrosis.
An irreversible form of chronic liver disease, cirrhosis is the end-stage of many processes. It has three key characteristics, namely long-standing destruction of liver cells, associated chronic inflammation that stimulates fibrosis, and regeneration of hepatocytes to cause nodules.
Fibrosis is caused by growth factors liberated from inflammatory cells, Kupffer cells, and hepatocytes.
The inflammatory cells may be part of the disease process (e.g. in hepatitis) or may be recruited in response to liver cell necrosis. Myofibroblast-like cells, derived from the fat-storing Ito cells
are responsible for secreting collagen.
Nodules of hepatocytes form as part of the normal capacity of hepatocytes to divide and regenerate
in response to damage.

Cirrhosis is best classified according to the cause of liver damage
The best way to classify cirrhosis is by its aetiology.
The main causes of cirrhosis are conditions known to result in chronic liver cell
necrosis with fibrosis and regeneration. In early classifications two types of cirrhosis were described,
based on the size of the regenerative nodules:
micronodular cirrhosis nodules are small, ranging in size up to 3 mm; macronodular cirrhosis
nodules are larger than 3 mm, ranging in size up to 2 cm.
This classification has little clinical relevance, although there is some inconsistent association with cause.

Cirrhosis results in liver failure and portal hypertension
The main consequences of cirrhosis are:
Reduced hepatocyte function (decreased synthesis of proteins, failure of detoxification).
Disturbance of blood flow through the liver, causing portal hypertension.
Reduced immune competence and increased susceptibility to infection.
Increased risk of development of hepatocellular carcinoma.
Increased risk of development of portal vein thrombosis.
Acute liver failure frequently develops in cirrhosis
Importantly, patients with chronic liver failure are at risk of an abrupt deterioration in condition
that leads to acute liver failure. The main precipitating factors are alcohol binge, development of intercurrent infection, gastrointestinal bleed (e.g. from oesophageal varices), portal vein thrombosis,
and development of carcinoma of the liver.
These consequences are manifest by a group of distinctive clinical features in a typical patient
with cirrhosis.

In clinical practice, cirrhosis is encountered in one of two ways. It may develop in patients who are
under follow-up for known chronic liver disease (e.g. chronic hepatitis or alcoholic liver disease),
or it may first present as end-stage disease, having been entirely sub-clinical in its evolution.
Clinical stigmata of cirrhosis.

Cirrhosis gives rise to clinical stigmata caused by failure of liver metabolism as well as those caused
by portal hypertension. Testicular atrophy, spider naevi and gynaecomastia are the result of impaired
metabolism of endogenous oestrogens. Ascites and oedema are caused by low serum albumen. Varices,
splenomegaly and caput medusae are caused by portal hypertension. Bruising is caused by
failure to synthesize clotting factors.

Cirrhosis may develop as a consequence of biliary obstruction
Biliary cirrhosis is the result of long-standing obstruction of bile ducts, leading to the
development of obstructive jaundice, liver cell necrosis, and fibrosis with regenerative nodules.
The main causes are primary biliary cirrhosis; unrelieved obstruction of the main extrahepatic
bile ducts, also termed secondary biliary cirrhosis;and sclerosing cholangitis.
Primary biliary cirrhosis is associated with anti-mitochondrial antibodies
Primary biliary cirrhosis (PBC) is characterized by chronic destruction of intrahepatic bile ducts.
The incidence is ten times higher in women than in men, and it is an important cause of chronic liver disease and cirrhosis in women over the age of 50 years.
As disease progresses, there is fibrosis and proliferation of small bile ducts at the periphery
of the portal tracts. In the final stages of disease cirrhosis develops.
There is gradual progression over about 10 years.
Primary sclerosing cholangitis is the result of inflammation and fibrosis of bile ducts
and leads to cirrhosis

Primary sclerosing cholangitis (PSC) causes progressive obstruc-tive jaundice and is characterized
by chronic inflammation and fibrosis of bile ducts.
It is associated with the presence of inflammatory bowel disease, 60% of patients with PSC having ulcerative colitis, and about 5% of patients with ulcerative colitis developing PSC.

Patients develop cholestatic jaundice with progression to cirrhosis over a period of about 10 years.
Early in the course of biliary obstruction there is oedema and expansion of intrahepatic
portal tracts, with portal tract fibrosis.
Bile droplets develop in biliary canaliculi, which may rupture and cause death of adjacent hepatocytes (so-called bile infarcts).
Over a long period of time, liver cell death,regeneration and fibrosis result in cirrhosis.

Clinically, in the early stages of disease, patients develop pruritus and mild hyperbilirubinaemia
due to inflammatory destruction of intrahepatic bile ducts.
It is only many years later that patients develop true cirrhosis with fibrosis and
regenerative nodules of liver cells. For most of the duration of the disease, patients have
no histological changes of cirrhosis.
Although immune phenomena are involved, the aetiology of primary biliary cirrhosis is uncertain.
Liver biopsy is performed to evaluate the stage of the disease; early disease reveals
obliteration of bile ducts from portal tracts, associated with small granulomas. There is infiltration
of portal tracts by lymphoid cells, with destruction of adjacent hepatocytes in a manner similar to that
of piecemeal necrosis. As disease progresses, there is fibrosis and proliferation of small bile
ducts at the periphery of the portal tracts.
In the final stages of disease cirrhosis develops.

Primary sclerosing cholangitis is the result of inflammation and fibrosis of bile ducts
and leads to cirrhosis.
PSC affects both intrahepatic and extrahepatic bile ducts. Large intrahepatic and extrahepatic
ducts develop fibrous strictures with segmental dilatation.
Radiological examination after injection of contrast agent up the common bile duct back into the liver
(endoscopic retrograde cholangiogram) reveals a 'beaded' appearance of affected ducts.
Medium-sized ducts, and ducts in portal tracts, show inflammation and a pattern of concentric fibrosis around ducts, whereas small bile ducts in portal tracts are replaced by collagenous scar (vanishing bile ducts).
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