The cause of disease
(1) viral hepatitis
? Hepatitis B virus infection is the most common cause, followed by hepatitis C virus infection. From viral hepatitis to cirrhosis, it can be as short as several months and as long as several decades. Hepatitis caused by hepatitis A virus and hepatitis E virus infection generally does not develop into cirrhosis. (BCD in the middle develops into cirrhosis, and AE in the head and tail does not develop into cirrhosis)
(2) Alcohol
? Long-term heavy drinking leads to liver cell damage, fat deposition and liver fibrosis, which gradually develops into cirrhosis. Malnutrition, HBV or HCV infection and drugs that damage the liver will increase the risk of alcoholic cirrhosis. Women who drink alcohol are more likely to suffer from alcoholic liver disease than men.
(3) cholestasis
Bile cirrhosis can develop from biliary obstruction inside and outside the liver and persistent cholestasis of any cause. According to the causes of cholestasis, it can be divided into primary and secondary biliary cirrhosis.
circulation system disease
Hepatic vein occlusion (or inferior vena cava occlusion), chronic cardiac insufficiency and constrictive pericarditis (cardiogenic) can cause long-term liver congestion, hepatocyte degeneration and fibrosis, and eventually develop into congestion cirrhosis.
(5) Drugs or chemical poisons
Long-term use of drugs that damage the liver and exposure to chemical poisons such as carbon tetrachloride, phosphorus and arsenic will cause toxic hepatitis and eventually evolve into cirrhosis.
(6) Immune diseases
Autoimmune hepatitis and various rheumatic immune diseases involving the liver can develop into cirrhosis.
(7) Parasitic infection
Schistosomiasis infection still exists in southern China. Mature eggs are swallowed by macrophages in the liver and evolve into fibroblasts, forming fibrous nodules. Because eggs are mainly deposited near the portal vein branches of the liver, fibrosis often hinders portal vein perfusion, and portal hypertension is a prominent feature of liver cirrhosis. Clonorchis sinensis is parasitic in the bile duct inside and outside the human liver, and biliary obstruction and inflammation (liver fluke disease) caused by Clonorchis sinensis can gradually develop into cirrhosis.
(8) Genetic and metabolic diseases
? Due to genetic or congenital enzyme defects, some metabolites are deposited in the liver, causing hepatocyte necrosis and connective tissue proliferation. Mainly includes:
1. Copper metabolism disorder? Hepatolenticular degeneration (HLD) is an autosomal recessive disease of copper metabolism. Its pathogenic gene is located in 13q 14.3, and the product encoded by this gene is P-ATPase which transports copper ions. Due to the dysfunction of enzymes, copper is deposited in the body, which damages organs such as liver and brain and causes diseases.
2. Hemochromatosis is due to the gene abnormality on chromosome 6, which leads to the increase of iron absorption in food by small intestinal mucosa, and too much iron is deposited in the liver, causing fibrous tissue proliferation and organ dysfunction.
3,-antitrypsin deficiency-antitrypsin is a low molecular weight glycoprotein synthesized by the liver. Due to gene defect, the normal -AT is obviously reduced, while the abnormal -AT has small molecular weight and low solubility, which makes the liver unable to be discharged into the blood, accumulates in the liver in large quantities, damages the liver tissue, and causes cirrhosis.
Other diseases such as galactosemia, hemophilia, tyrosine metabolism disorder and hereditary hemorrhagic telangiectasia can also lead to cirrhosis.
(9) malnutrition
? Fatty liver caused by long-term insufficient or unbalanced food nutrition, dyspepsia caused by various chronic diseases, obesity or diabetes can all develop into cirrhosis.
(10) The reason is unknown.
Some patients can't explain the occurrence of cirrhosis with the current etiology, which is also called cryptogenic cirrhosis. It should be noted that before the above causes are ascertained, it is not easy to draw the conclusion of cirrhosis with unknown causes, so as not to affect the etiological treatment of cirrhosis.
Pathogenesis and pathology
The basic characteristics of the development of liver cirrhosis are hepatocyte necrosis, regeneration, liver fibrosis, intrahepatic vascular proliferation and circulatory disorder.
The liver has a strong regenerative ability. Normal liver resection 70%-80% can still maintain normal physiological function; After normal liver lobectomy for about one year, the residual liver can be restored to its original weight. Various reasons lead to degeneration or necrosis of liver cells. If the cause persists, it is difficult for regenerated hepatocytes to restore normal liver structure and form irregular nodules.
Inflammation and other pathogenic factors activate hepatic stellate cells, and collagen synthesis increases and degradation decreases. The total collagen content can be increased to 3- 10 times of the normal value, and deposited in the Disse space, which leads to the widening of the space, the formation of basement membrane under the endothelial cells of the hepatic sinus, the reduction or even disappearance of the fenestration on the endothelial cells, and the formation of a diffuse barrier, which is called hepatic sinus capillarization. The villi on the surface of liver cells flatten to form a barrier, and the transport of substances in liver sinuses to liver cells is blocked through the wall of liver sinuses, which directly interferes with the function of liver cells, resulting in the dysfunction of liver cell synthesis, narrowing of liver sinuses, blocked blood flow and increased intrahepatic resistance, which directly affects the hemodynamics of portal vein, causes hypoxia and nutrient supply disorder of liver cells, aggravates the necrosis of liver cells, and enables the initiator to continue to play its role.
The fiber bundles in portal area and hepatic capsule extend to the central vein of hepatic lobule, and these fiber intervals surround regenerative nodules or re-divide residual hepatic lobules into pseudolobules, forming typical histopathological morphology of liver cirrhosis. At the same time, the development of hepatic fibrosis is accompanied by significant and abnormal vascular proliferation, which makes the three major vascular systems of intrahepatic portal vein, hepatic vein and hepatic artery lose their normal relationship and appear communicating anastomotic branches, which is not only the pathological basis of portal hypertension, but also an important mechanism to aggravate hepatocyte malnutrition and promote the development of cirrhosis.
Lin Biao
Liver cirrhosis usually has a hidden onset and a slow course of development. Clinically, liver cirrhosis can be roughly divided into compensatory stage and decompensated stage.
(1) compensation period
Most patients have no symptoms or mild symptoms, and may have abdominal discomfort, fatigue, loss of appetite, indigestion, diarrhea and other symptoms, mostly intermittent, often accompanied by fatigue, mental stress or other diseases, which can be relieved by rest and digestion drugs. The nutritional status of patients is acceptable, and whether the liver is significant depends on different types of cirrhosis. Spleen is often slightly or moderately swollen due to portal hypertension. Liver function test is normal or slightly abnormal.
(2) decompensated period
1. Liver function defect
(1) Dyspepsia: anorexia, nausea, anorexia and abdominal distension. It is aggravated after meals, and diarrhea is easy after eating meat, which is mostly related to gastrointestinal congestion and edema, digestive absorption disorder and intestinal flora imbalance during portal hypertension.
(2) Malnutrition: generally poor, emaciation and fatigue, listlessness, even bedridden due to weakness, and the patient's skin is dry or edema.