Alcoholic cirrhosis
Introduction
Introduction The occurrence of alcoholic cirrhosis is related to the drinking mode, gender, genetic factors, nutritional status of the drinker and whether or not the hepatitis virus infection is associated. A large amount of drinking is more harmful than a small amount of drinking. Daily drinking is more harmful than intermittent drinking. Women who drink alcohol are more likely to develop alcoholic liver disease than men. Malnutrition, protein deficiency, combined with chronic hepatitis B or hepatitis C virus infection can increase the risk of cirrhosis. Long-term excessive drinking, history of liver cell recurrence of steatosis, necrosis and regeneration, eventually leading to liver fibrosis and cirrhosis.
Cause
Cause
The mechanism of alcoholic cirrhosis is:
1. Liver damage:
In the past, alcoholic liver injury was thought to be caused by malnutrition due to eating. And now studies have shown that even without nutritional defects, even in the presence of protein, vitamins and minerals, drinking can still lead to liver ultrastructural damage, liver fibrosis and cirrhosis.
2. Immune response disorder:
A, ethanol can activate lymphocytes. B. It can enhance the pathogenicity of hepatitis B and C viruses. C. Enhance the toxicity of liver damage caused by endotoxin. D, increased cytokines in alcoholic hepatitis, such as tumor necrosis factor (TNF), leukocyte pigment (TL) and so on. These cytokines are mainly derived from lymphocytes, monocytes, fibroblasts, and collagen, leading to liver fibrosis. TGF- is the most important cytokine that has been found to cause fibrosis. E, ethanol and metabolites have a direct impact on immune regulation, and history of immunological markers changes.
3, collagen metabolism disorder and sputum hardening formation:
A, lipid oversaturation promotes collagen formation. B, alcoholic liver disease patients with collagen synthesis key enzyme proline hydroxylase is activated. C. Alcohol can make fat storage cells become myofibroblasts, synthesize layer mucin, increase the mRNA content of collagen, and synthesize various collagens. D, the wine contains iron, drinking leads to increased intake and absorption, iron particles in the liver cells, iron can stimulate fiber proliferation, aggravate cirrhosis.
Examine
an examination
Related inspection
Indirect bilirubin on ammonia horse uric acid synthesis test serous effusion protein anti-histone protein antibody reflects liver cell damage test
Symptoms usually occur around the age of 50, with a male to female ratio of about 2:1, often dying around the age of 60. Early symptoms are often asymptomatic, weight loss, loss of appetite, abdominal pain, fatigue, burnout, dark urine, bleeding gums and nosebleeds (up to decompensation may occur jaundice, ascites, edema, skin and mucous membranes and upper digestive tract) Bleeding, etc.) Facial ash, poor nutrition, telangiectasia, spider mites, liver palm, parotid gland non-inflammatory swelling, palmar contracture, male breast development, testicular atrophy and pubic hair distribution in females, and anaerobic bacteria Primary peritonitis, hepatic encephalopathy, etc.
Alcoholic cirrhosis belongs to the type of portal cirrhosis, which has increased significantly in China in recent years, second only to cirrhosis after viral hepatitis. In the early stage of alcoholic cirrhosis, the regenerative nodules formed by the pseudolobes of the liver are small, and the surrounding fiber bundles are narrow and tidy. The B-mode ultrasound examinations often increase the diameter of the diameter lines, and the intrahepatic echoes are densely enhanced and slightly thickened. Other chronic liver diseases are not easy to distinguish. As the disease progresses, the liver cells are destroyed, liver cells regenerate and a large number of fibrous tissue hyperplasia. Ultrasound examination of the cut surface image can show numerous round or round-shaped hypoechoic nodules, diffusely distributed in the whole liver, and nodules are more cirrhotic after hepatitis. The size is small and uniform, and the size is mostly between 0.2 and 0.5 cm. The surrounding of the nodules is surrounded by fibrous tissue and has a grid-like strong echo.
The liver capsule is thickened and the echo is enhanced, but there is no common jagged change in cirrhosis after hepatitis, and the liver volume is often reduced. Ultrasound examination revealed that portal vein widening, portal collateral circulation and ascites were helpful in diagnosing cirrhotic portal hypertension, but the sensitivity was low. In portal cirrhosis, hepatic regenerative nodules compress peripheral branches of the portal vein, Disse gap, and fibrous tissue in the portal area, which cause the blood vessels to distort and occlude, increase the resistance of the hepatic artery and portal vein, slow down the portal vein blood flow, and even appear high liver. Blood flow. Color Doppler can show the main characteristics of blood circulation changes in the liver, and significantly improve the sensitivity and specificity of ultrasound diagnosis of alcoholic cirrhosis. Portal venous flow velocity was significantly lower in patients with cirrhosis, and hepatic artery pulsatility index (PI) was increased (1.28 ± 0.18, normal control 0.95 ± 0.17, P < 0.001 =. Hepatic vascular index refers to portal venous flow velocity / hepatic artery pulsation index With the index reduced to 12cm/s, the diagnostic sensitivity to cirrhosis is 97% and the specificity is 93%. The newly developed second harmonic imaging technology combined with a new acoustic contrast agent makes the liver The ultrasound diagnosis of sclerotherapy has improved to a new level. The Doppler time intensity curve of patients with cirrhosis after angiography is very different from that of normal and non-sclerosing liver disease groups. The angiography group showed an average start time of 18 s, followed by A steep rise, the average group and non-hardening group began to show an average of 52s and 39s, followed by a slower and slower rise. Studies have shown that the contrast agent reaches the hepatic vein less than 24, the diagnosis of cirrhosis With a sensitivity and specificity of 100%, this new non-invasive diagnosis of cirrhosis is expected to reduce the number of liver biopsy in the future. In patients with alcoholic cirrhosis, portal vein velocity is peaceful. Traffic associated with the degree of portal hypertension.
Diagnosis
Differential diagnosis
(1) Diabetic fatty liver:
No history of drinking, history of diabetes; combined with blood sugar, urine sugar detection is not difficult to identify.
(2) Hyperlipidemia fatty liver:
Determination of blood cholesterol, triglycerides, apolipoprotein can help diagnose, if there is no history of drinking can help to distinguish.
(3) Obese fatty liver:
First ask if there is a history of drinking, such as drinking time > 10 years, alcohol consumption > 60g / d, the possibility of alcoholic fatty liver is large. If there is no history of drinking or insufficient time course and quantity, if there is obesity, obesity fatty liver may be larger.
(4) Fatty liver after hepatitis:
More common in patients with acute viral hepatitis recovery or chronic hepatitis due to excessive calorie intake, high sugar and excessive restriction activities leading to weight gain and liver fat deposition. This type of fatty liver has a clear history of hepatitis, and most are advised not to drink alcohol.
(5) Use corticosteroids, drugs or long-term exposure to toxic chemicals:
(such as CCl4, chloroform, ethionine), lead to fatty liver, no history of drinking, a history of useful drugs.
(6) Acute fatty liver in pregnancy:
It has been called acute yellow liver atrophy in the past, and it is rare, with a high maternal and infant mortality rate (more than 75%). The cause is still unclear and more common in early pregnant women. 36 to 40 weeks of pregnancy, but it has also been reported in 30 weeks of pregnancy or a few days after delivery. Pathology: Liver puncture showed diffuse steatosis in the hepatic lobules, but no extensive necrosis of hepatocytes (this is easy to distinguish from acute hepatic necrosis caused by acute jaundice hepatitis). Hepatocytes are infiltrated by fat, and there is no area around the portal vein. This phenomenon, no inflammatory infiltration or necrotic areas. Ultrasound has a typical fatty liver wave pattern. The liver buds of the rehabilitation patients showed that the fat gradually disappeared and returned to normal from the edge of the hill. Similar changes in the liver, but also in the pancreas, bone marrow, kidney and brain. The surviving mother and baby generally recovered well.
(7) Malnutrition fatty liver:
More common in patients with inadequate food intake or digestive dysfunction and chronic wasting disease, no history of drinking, it is not difficult to distinguish.
