Hepatic steatosis

Introduction The clinical manifestations of dystrophic cirrhosis appear as hepatic steatosis. Malnutration Cirrhosis is caused by chronic nutrient deficiencies. The causes of malnutrition, in addition to the lack of intake of individual patients, mostly due to other diseases limit food intake and absorption, such as small bowel bypass surgery, Birroth II type surgery. Patients can supplement a variety of vitamins, vitamins C, E and B vitamins, improve liver cell metabolism, prevent fatty changes and protect liver cells, can also take yeast tablets, supplement vitamin K, B12 and folic acid as appropriate.

Cause

Malnu tration Cirrhosis is caused by chronic nutritional deficiencies. Animal experiments have confirmed that simple malnutrition, especially protein, anti-fatty liver factors and B vitamin deficiency, can cause fatty liver, hepatocyte necrosis, degeneration and cirrhosis.

The mechanism by which malnutrition leads to cirrhosis may be:

1 When a cystine-containing protein is lacking, the source of cysteine and glutathione is reduced, and the production and activity of the enzyme in the liver cell are affected, and the liver cell is damaged by various factors to cause degeneration and necrosis.

2 Choline is a fat-promoting substance, and it can synthesize phospholipids in the liver with neutral fat, so that the liver fat is easily oxidized and used. If the amino acids necessary for choline or synthetic choline are severely deficient, fat will accumulate in the liver cells and become fatty liver. Steatosis of hepatocytes can reduce the resistance of hepatocytes to various harmful factors, and can also squeeze and compress the hepatic sinus due to the increase of cell volume, gradually causing ischemia, necrosis, fibrous tissue hyperplasia and cirrhosis.

The causes of malnutrition, except for the lack of intake of individual patients, are mostly due to other diseases that limit food intake and absorption, such as after small bowel bypass surgery.

Like other types of cirrhosis, dystrophic cirrhosis precedes the formation of hepatocyte injury such as steatosis, accompanied by inflammatory cell infiltration in the portal area and hepatic lobule, granuloma formation, and later development of liver fibrosis, and Alcoholic liver injury is similar, and liver fibrosis around the small vein is a sign of development of cirrhosis. Long-term repeated damage to the liver leads to cirrhosis, and the lesions and liver lesions are similar to alcoholic liver injury.

an examination

Related inspection

Liver function test liver ultrasound examination liver, gallbladder, spleen CT examination

Changes in sexual characteristics may occur 12 to 18 months after small bowel bypass surgery, such as decreased sexual desire, male breast development, female amenorrhea and secondary sexual characteristics. There is also loss of appetite, weakness, abdominal pain, nausea, vomiting. Signs of jaundice, hepatosplenomegaly, ascites, spider mites. The test showed elevated serum bile acid, elevated AST, normal ALT, prolonged prothrombin time, hypoalbuminemia, and liver biopsy showed hepatic steatosis and hepatitis.

Cirrhosis can occur in patients more than 7 years after small bowel bypass surgery. The formation of cirrhosis is hidden, clinical manifestations are not prominent, and occasionally die of cirrhosis and liver failure.

Differential diagnosis

Note the differentiation with other types of cirrhosis.

Changes in sexual characteristics may occur 12 to 18 months after small bowel bypass surgery, such as decreased sexual desire, male breast development, female amenorrhea and secondary sexual characteristics. There is also loss of appetite, weakness, abdominal pain, nausea, vomiting. Signs of jaundice, hepatosplenomegaly, ascites, spider mites. The test showed elevated serum bile acid, elevated AST, normal ALT, prolonged prothrombin time, hypoalbuminemia, and liver biopsy showed hepatic steatosis and hepatitis.

Cirrhosis can occur in patients more than 7 years after small bowel bypass surgery. The formation of cirrhosis is hidden, clinical manifestations are not prominent, and occasionally die of cirrhosis and liver failure.

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