Chronic hepatitis refers to a disease in which the liver is affected by viral infections, drug damage, alcohol abuse and other factors for a long time, resulting in chronic and persistent liver inflammation. If chronic hepatitis is not effectively controlled in time, cirrhosis may develop. This article will analyze the transition from chronic hepatitis to cirrhosis from the perspectives of pathogenesis, pathological changes and clinical manifestations.
First of all, the main causes of chronic hepatitis include a variety of factors such as chronic viral hepatitis, long-term alcohol abuse, drugs, toxicants, and metabolic abnormalities. These factors lead to liver cell damage, causing an inflammatory response. The inflammatory response stimulates liver cell proliferation and regeneration, but it also leads to liver cell death and fibrosis.
Second, when the liver is stimulated by long-term inflammation, a fibrotic reaction occurs. Fibrosis is a compensatory response to the structure and function of liver tissue, manifested by increased collagen deposition and structural distortion of the hepatic sinusoids. When the degree of fibrosis exceeds a certain level, more fibrous reticular structures are formed in the tissues, and cirrhosis is formed.
Cirrhosis is characterized by a reduced liver size, hard texture, superficial nodules, severe tissue structure disorders, and loss of function. The main mechanisms of cirrhosis include fibrosis due to inflammation, cell proliferation and cell death, and changes in the blood vessels and biliary tract inside the liver.
Inflammatory stimulation is one of the key factors in the development of cirrhosis. Long-term chronic inflammatory stimulation not only damages liver cells, but also activates a variety of inflammatory cells, such as hepatic stellate cells and inflammatory cells, which will release a large number of inflammatory factors and growth factors, induce liver fibrosis response, and accelerate the fibrosis process of liver tissue.
Cell proliferation is another important factor in the development of cirrhosis. When liver cells are damaged, they undergo a proliferative response to try to repair the damaged tissue. However, long-term damage and proliferative reactions can lead to cell cycle disorders and abnormal proliferation, increasing the risk of cell mutation and malignant transformation, thereby inducing complications such as liver cancer.
In addition, cirrhosis can cause structural and functional abnormalities in the blood vessels and biliary tracts inside the liver. Fibrosis narrows and occludes the lumen of blood vessels, leading to hepatic ischemia and affecting oxygen supply and nutrition to hepatocytes**. The biliary tract is eroded by fibrosis, which can lead to cholestasis and inflammation of the biliary tract, further exacerbating liver damage and fibrotic progression.
When chronic hepatitis progresses to cirrhosis, the patient's clinical presentation will also change. The clinical symptoms of cirrhosis are varied, including pain in the liver area, ascites, jaundice, malaise, and weight loss. In addition, cirrhosis may also be complicated by dilation and rupture of blood vessels inside the liver, leading to serious complications such as esophageal varices, abdominal wall umbilical hernia, and hepatic encephalopathy.
In conclusion, chronic hepatitis is one of the important pathogenesis of liver cirrhosis. Long-term inflammatory stimulation, fibrosis due to hepatocyte proliferation and cell death, and changes in the internal blood vessels and biliary tract are the main mechanisms of liver cirrhosis. Understanding the process of liver cirrhosis can help improve the awareness and prevention of chronic hepatitis. Therefore, early detection and ** chronic hepatitis is a key measure to prevent cirrhosis. At the same time, maintaining good living Xi and staying away from alcohol, viral infections and other harmful factors is also an important part of preventing liver cirrhosis. December Creation Incentive Program