168. Alcoholic liver damage: types, macro- and microscopic signs, complications, outcomes.

Types of alcoholic liver damage:

Fatty hepatosis (steatosis).

Alcoholic hepatitis (acute, chronic).

Alcoholic cirrhosis of the liver.

Macro and microscopic signs:

For fatty hepatosis: The liver with steatosis is large, yellow or red-brown, its surface is smooth. Fat related to triglycerides is determined in hepatocytes. Obesity of hepatocytes can be pulverized, small and large droplets. A drop of lipids pushes relatively intact organelles to the periphery of the cell, which becomes ring-shaped. With pronounced fatty infiltration, liver cells die, fat droplets merge and form extracellularly located fatty cysts, around which a cellular reaction occurs, connective tissue grows.

For alcoholic hepatitis: Liver changes in acute and chronic alcoholic hepatitis are different.

Acute alcoholic hepatitis. The liver is dense and pale, with reddish patches and often with scarring. Microscopic picture: necrosis of hepatocytes, infiltration of necrosis zones and portal tracts by neutrophils, the appearance of a large amount of alcoholic hyaline (Mallory bodies) in the cytoplasm of hepatocytes and extracellularly. Alcoholic hyaline is a fibrillar protein synthesized by hepatocytes under the influence of ethanol, which leads liver cells to death.

Chronic alcoholic hepatitis is often manifested by persistent, very rarely by active chronic hepatitis. In chronic persistent alcoholic hepatitis, hepatocyte obesity, sclerosis and abundant histiolymphocytic infiltration of the portal stroma are found. Active chronic alcoholic hepatitis is characterized by protein (hydropic, balloon) dystrophy and necrosis of hepatocytes along the periphery of lobules, the structure of which is impaired. In addition, diffuse histiolymphocytic infiltration of wide and sclerosed portal tracts is expressed, and infiltrate cells penetrate to the periphery of the lobules, surrounding and destroying hepatocytes (stepwise necrosis).

For alcoholic cirrhosis: Alcoholic CP is small—nodular, monolobular. The disease is characterized by progressive liver fibrosis, in which thin layers of connective tissue (septa) invade the acinus from both the central veins and the portal tracts, crushing the parenchyma into small, identical-sized (monomorphic) fragments. These fragments are surrounded on all sides by connective tissue, the radial orientation of the beams is disrupted in them, there is no central vein, and nodular regeneration of hepatocytes is noted. They are called false lobules or regenerate nodes.

Complications:

Steatosis: transition to steatohepatitis, portal hypertension, cirrhosis of the liver, intrahepatic cholestasis.

Hepatitis: jaundice, intoxication, hepatic encephalopathy, liver failure.

Cirrhosis: Acute and chronic liver failure, hepatic encephalopathy, jaundice, renal failure, ascites and edema, cancer.

Outcomes:

With steatosis, it is possible to restore liver tissue with the exclusion of alcohol and proper therapy, however, if time is lost, cirrhosis of the liver is formed. Death from liver and kidney failure, peritonitis, anemia, liver cancer.