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  1. Liver is the largest and most complex organ in the body. It’s located in the right upper part of the abdominal cavity below the diaphragm. Liver has 4 lobules: right, left, quadrate and caudate. Liver is covered by tough, fibrous capsule. It’s composed of 100000 branched and interconnected cells (lobules). Each lobule is surrounded by capillaries from hepatic portal veins and hepatic artery. The structure of unit of the liver is a hepatocyte.

  1. The principal functions of human liver are: to produce cholesterol, to convert glucose to glycogen, to maintain proper level of glucose in the blood, to produce bile, bile salts, bilirubin, hormones, proteins, lipids, Aeron and minerals, to recycle hemoglobin, to destroy toxic substances, to store vitamins (except vitamin C), to destroy unwanted proteins and change them into the urea, to take part in digestion.

  1. Causes of liver diseases are alcohol, infections, metabolic disorders, poisoning, obstruction deficiency disorders, inflammation of liver cells, accumulation of cholesterol.

  1. I know such liver diseases: hepatitis, cirrhosis, primary tumor, liver cancer, hepatoma, ascites, haemachromatosis, hepatic encephalopathy, gall stones.

Hepatitis is an inflammation of the liver, caused by viruses hepatitis A, B and C.

Cirrhosis is a damage of the liver with the formation of fibrous scar tissue.

Liver cancer is malignant tumor of the liver.

Gall stone is obstruction of bile flow in the bile duct.

Haemachromatosis is an accumulation of of Aeron in the liver.

  1. Main symptoms of liver disorders are jaundice, dull ache in upper right part of the abdomen, fluid in the peritoneum, melena (blood in stool), haematemesis (blood in the vomit), enlarged liver, dark urine, itching of the skin, excessive tiredness.

  1. Cirrhosis is a type of permanent and progressive liver damage that leads to the formation of fibrous scars and nodules in the liver. Causes that can provoke development of cirrhosis are alcohol abuse, viral hepatitis, autoimmune diseases, rare inherited diseases, drugs and chemicals.

  1. Early symptoms of cirrhosis include weakness, feeling of tiredness, loss of appetite, nausea and haematemesis (vomiting of blood), constipation or diarrhea.

Symptoms of advanced cirrhosis include jaundice, broken blood vessels, a hard liver, a swollen abdomen, and swollen ankles. Some man suffering from the disorder experience an enlargement of their breasts, loss pf pubic hair, and shrinking of the testicles.

  1. The treatment of cirrhosis includes steroids, immunosuppressive drugs if there is autoimmune disease and high protein diet with extra vitamins is needed and advisable. Antibiotics may be prescribed in case of infections.

  1. Traditionally, viral hepatitis had been classified into two epidemiologically distinct types: infectious hepatitis (hepatitis A) and serum hepatitis (hepatitis B). These distinctions were based on earlier observations that hepatitis A had a shorter incubation period, high contagious rate, and usually fecal-oral route of transmission, while hepatitis B had a longer incubation period, was less contagious, and was thought to be transmitted only the parenteral route.

  1. The typical morphologic lesions of both hepatitis A and B are often similar and consist of panlobular infiltration with mononuclear cells, hepatic cell necrosis, hyperplasia of Kupffer cells, and variable degrees of cholestasis. Hepatic cell regeneration is present, as evidenced by numerous mitotic figures, multinucleated cells, and “rosette” or “pseudoglandular” formation. The mononuclear infiltration consists primarily of small lymphocytes, although plasma cells and eosinophils occasionally are present. Liver cell damage consists of hepatic cell degeneration and necrosis, cell dropout, ballooning of cells, and acidophilic degeneration of hepatocytes (so-called Councilman-like bodies).

A more severe histologic lesion, bridging hepatic necrosis, also termed subacute or confluent necrosis or interface hepatitis, is occasionally observed in some patients with acute hepatitis. “Bridging” between lobules results from large areas of hepatic cell dropout, with collapse of

the reticulin framework. Characteristically, the bridge consists of condensed reticulum, inflammatory debris, and degenerating liver cells that span adjacent portal areas, portal to central veins, or central vein to central vein.

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