Liver in Disease

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The liver has a limited set of responses to damage.
Following damage to the liver, several patterns of histological abnormality can be identified, which are the result of a limited set of pathological responses to damage. There may be fatty change, cholestasis, liver cell necrosis, fibrosis, or storage of abnormal material.
The histological diagnosis of liver disease requires evaluation of these abnormalities,
and their correlation with clinical features and biochemical tests.
Liver disease may be investigated by imaging, blood tests and liver biopsy.

Fatty change is most commonly caused by metabolic stresses and alcohol
Fatty change is a common response of the liver to diverse adverse stimuli.
The main causes are:
Metabolic stress, e.g. hypoxia, kwashiorkor and diabetes mellitus.
Toxins (the most common being alcohol)
Reye's syndrome causes extensive micro-vesicular fatty change.
Fatty liver of pregnancy.
Macroscopically the fatty liver is enlarged and, instead of appearing deep red, it is pale.
Histologically, fat can be seen in hepatocytes.

Cholestasis may be intrahepatic or extrahepatic in origin.
Many of the conditions causing conjugated hyperbilirubinaemia lead to the development
of cholestasis. Clinically this is charac-terized by conjugated hyperbilirubinaemia and
a great increase in the serum levels of alkaline phosphatase, an enzyme normally
located on the cell membranes of the biliary canaliculi. Two groups are recognized.
Intrahepatic cholestasis is caused by diseases affecting bile secretion in the liver,
due either to abnormalities of liver cells and biliary canaliculi, or to disease of
intrahepatic bile ducts.
Because they are generally managed by physicians, these conditions are sometimes loosely
grouped as medical jaundice. Changes are apparent on liver biopsy in this type of jaundice.
Extrahepatic cholestasis is caused by blockage of the main bile ducts outside
the liver. As many of the conditions responsible are amenable to operative
intervention, this type of problem is some-times referred to as surgical jaundice.
Extrahepatic obstruction causes distinct changes within the liver.

Bile can be seen dilating canalculi, predominantly in the centrilobular zones, as bile thrombi.
In addition to plugging of biliary canaliculi by bile, a characteristic feature of this type of
cholestasisis is oedema of the portal tracts which are expanded. In long-standing
cases there is proliferation of small bile ducts around the periphery of portal tracts.
Bile may leak from canaliculi associated with hydropic degeneration of hepatocytes
to cause small so-called bile infarcts or lakes.
Liver cell regeneration occurs following hepatocyte necrosis
The cells of Ito are the source of collagen-secreting cells in liver fibrosis
Necrosis of liver cells can be seen in several patterns
Six main patterns of liver cell death are seen, each of which can be related to the cause of liver damage:
1 Single liver cells die by the process of apoptosis.
2 Death of liver cells scattered throughout the lobule, both singly and in small groups (spotty necrosis) is seen with toxic damage and viral infections.
3 Death of liver cells confined to certain zones (zonal necrosis) is seen with certain diseases. For example, the centrilobular area (zone 3) is affected in paracetamol (acetaminophen) toxicity.
4 Piecemeal necrosis describes death of liver cells in a scattered pattern immediately next to the portal-tract connective tissue. This pattern is a characteristic of chronic active hepatitis.
5 Extensive patterns of necrosis that bridge between central veins, or between portal tracts and central
veins, is termed bridging necrosis.
6 Massive necrosis describes necrosis of the majority of hepatocytes. This occurs with fulminant hepatic damage and is seen in some cases of viral and toxin-induced damage.
Centrilobular (zone 3) necrosis caused by paracetamol.

Following overdose of paracetamol (acetaminophen),toxic metabolites are generated in centrilobular
hepatocytes, causing necrosis of this part of the lobule.
Confluent necrosis of centrilobular areas (zone 3) is seen, with surviving hepatocytes around portal areas (zone 1) .

The liver may be involved in several storage diseases
The liver stores several substances that may become pathological in disease states.
In haemochromatosis and haemosiderosis there is excessive iron storage, and excessive copper
deposition is seen in Wilson's disease.
Abnormal storage of metabolic products in the liver may be seen in some of the inborn errors of
metabolism. Glycogen deposition occurs in some of the glycogen storage diseases
and lipids are stored in multi-system disorders of metabolism, e.g. Gaucher's disease and Niemann-Pick disease.

Liver glycogenosis.
In glycogenosis Types IV, III, II and I, liver cells accumulate excess glycogen. Here,
liver cells from a case of Type III glycogenosis (debrancher deficiency) show striking vacuolation
of hepatocytes and liver nuclei due to the accumulation of glycogen.
True infarction of the liver is rare.
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