ALCOHOLIC HEPATITIS

Alcoholic hepatitis exhibits the following. Liver cell necrosis, single or scattered foci of cells undergo swelling (ballooning) and necrosis, more frequently in the centrolobular regions of the lobule. Mallory bodies, scattered hepatocytes accumulate tangled skeins of cytokeratin intermediate filaments and other proteins, visible as eosinophilic cytoplasmic inclusions. These may also be seen in primary biliary cirrhosis, Wilson's disease, chronic cholestatic syndromes, focal nodular hyperplasia, and hepatocellular carcinoma. Neutrophilic reaction, neutrophils permeate the lobule and accumulate around degenerating liver cells, particularly those having Mallory bodies. Lymphocytes and

macrophages also enter portal tracts and spill into the lobule. Fibrosis-alcoholic hepatitis is almost always accompanied by a brisk sinusoidal and perivenular fibrosis; occasionally periportal fibrosis may predominate, particularly with repeated bouts of heavy alcohol intake. Fat may be present or entirely absent.

CIRRHOSIS

Cirrhosisof the liver is a diffuse disease having the following 4 features:

1. It involves the entire liver.

2. The normal lobular architecture of hepatic parenchyma is disorganized.

3. There is formation of nodules separated from one another by irregular bands of connective tissue.

4. It occurs following hepatocellular necrosis of varying etiology so that there are alternate areas of necrosis and regenerative nodules.

The fibrosis once developed is irreversible.

Morphological classification

There are 3 morphological types of cirrhosis — micronodular (the nodules are usually regular and small, less than 3 mm in diameter), macronodular (the nodules are of variable size and are generally large than 3 mm in diameter) and mixed (some part of the liver show micronodular appearance while other parts show macronodular pattern). Each of these forms may

have an active and inactive form. An active form is characterized by hepatocellular necrosis and inflammatory reaction, a process that closely resembles chronic active hepatosis. An inactive form, vise verse, has no evidence of continuing hepatocellular necrosis and has sharply-defined nodules of surviving hepatic parenchyma without any significant inflammation.

Etiologic classification

1. Alcoholic cirrhosis (the most common, 60—70%).

2. Post-necrotic cirrhosis (10%).

3. Biliary cirrhosis (5—10%).

4. Pigment cirrhosis in hemochromatosis (5%).

5. Cirrhosis in Wilson's disease.

6. Cirrhosis in α-l antitrypsin deficiency.

7. Cardiac cirrhosis.

8. Indian childhood cirrhosis.

9. Miscellaneous forms of cirrhosis.

10. Cryptogenic cirrhosis (10—15%).

Pathology. Irrespective of type of cirrhosis morphological changes are similar. Macroscopically the liver is small, having distorted shape with irregular and coarse scars and nodules of varying size. The cut surface shows scars and nodules varying in diameter from 3 mm to a few centimeters.

Microscopically, the features are following: 1. Abnormal lobular architecture can be identified and central veins are hard to find.

2. The fibrous septa dividing the variable-sized nodules are generally thick.

3. Active liver cell necrosis is observed. Fibrous septa contain prominent mononuclear inflammatory cell infiltrate even with follicles. Often there is extensive proliferation of bile ductules derived from collapsed liver lobules.

4. Liver cells vary considerably in size and multiple large nuclei are common in regenerative nodules. Fatty degeneration may be present.






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