Alcoholic cirrhosis
Introduction
Introduction to alcoholic cirrhosis Alcoholic cirrhosis is cirrhosis caused by long-term heavy drinking. It is the terminal stage of alcoholic liver and belongs to the type of portal cirrhosis. In recent years, the incidence rate in China has increased significantly, accounting for about 7% of liver cirrhosis, which is second only to cirrhosis after viral hepatitis. Long-term excessive drinking, especially when drinking high-calorie wines, causes hepatocytes to repeatedly undergo fatty degeneration, necrosis and regeneration, eventually leading to cirrhosis. 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. basic knowledge The proportion of sick people: the incidence rate of alcoholics is about 10% Susceptible people: long-term heavy drinkers Mode of infection: non-infectious Complications: primary peritonitis upper gastrointestinal hemorrhage hepatic encephalopathy hepatorenal syndrome
Cause
Cause of alcoholic cirrhosis
Cause
Long-term excessive drinking, history of liver cell recurrence of steatosis, necrosis and regeneration, eventually leading to liver fibrosis and cirrhosis. Alcoholic liver disease in the pathological manifestations of trilogy: alcoholic fatty liver alcoholic hepatitis alcoholic liver Hardened, and the three often overlap.
The mechanism
Liver injury
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.
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.
Collagen metabolism disorder and sclerosis
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.
Prevention
Alcoholic cirrhosis prevention
1. Diet should provide adequate nutrition, food should be diversified, supply high-priced protein containing amino acids, multi-vitamins, low-fat, less slag diet, to prevent rough multi-fiber food damage to the esophageal vein, causing major bleeding.
2. Patients with high blood ammonia or poor liver function should limit protein intake to avoid hepatic coma. Those with ascites should enter a low-salt or salt-free diet.
3. Daily measurement of abdominal circumference and measurement of urine volume, abdominal obesity is a great way to identify fatty liver.
4. Pay attention to the changes of bleeding, cyanosis, fever, and neuropsychiatric symptoms, and get in touch with the doctor in time.
5. Supplementing selenium and nourishing the liver, supplementing selenium can make the activity of glutathione peroxidase in the liver reach normal level, and play a good role in nourishing liver and protecting liver. Selenium malt powder and schisandra are the ingredients of body Hengjian Yanggan tablets It has a good effect on nourishing the liver and protecting the liver, and has a good effect on nourishing the liver and protecting the liver.
Complication
Alcoholic cirrhosis complications Complications Primary peritonitis Upper gastrointestinal bleeding Hepatic encephalopathy Hepatorenal syndrome
1) Infection: The most common form of primary peritonitis. The incidence rate is about 3~10%, the abdomen has tenderness, rebound tenderness, ascites is exudate, and peripheral blood is increased.
2) Upper gastrointestinal bleeding: Esophageal varices bleeding and hepatic gastrointestinal mucosal ulcer bleeding.
3) Hepatic encephalopathy: On the basis of cirrhosis, patients with hepatic encephalopathy can be induced by excessive protein intake, gastrointestinal bleeding, infection, and electrolyte imbalance.
4) Hepatorenal syndrome: manifested as oliguria, anuria, azotemia, low sodium, high potassium, hepatic coma, hypotension shock.
Symptom
Alcoholic cirrhosis symptoms Common symptoms Abdominal hepatosplenomegaly Liver palm jaundice spider fatigue liver shrinkage
Symptoms usually occur around the age of 50. The ratio of male to female is about 2:1. It usually dies around 60 years old. It is often asymptomatic in the early stage. Afterwards, weight loss, loss of appetite, abdominal pain, fatigue, fatigue, dark urine, bleeding gums and Nasal bleeding, etc. (to decompensation may occur jaundice, ascites, edema, skin and mucous membranes and upper gastrointestinal bleeding, etc.). Facial ash, poor nutrition, telangiectasia, spider mites, liver palm, parotid gland non-inflammatory swelling , palm contracture, male breast development, testicular atrophy and pubic hair distribution in women, and anaerobic bacteria caused by primary peritonitis, hepatic encephalopathy.
1. Compensation period (generally Child-Pugh A grade): It can have clinical manifestations of hepatitis, and can also conceal the onset. There may be mild fatigue, abdominal distension, mild swelling of the liver and spleen, mild jaundice, liver palm, spider mites. Imaging, biochemistry, or blood tests have evidence of hepatocyte synthesis dysfunction or portal hypertension (such as hypersplenism and esophageal varices), or histology consistent with cirrhosis, but no esophageal varices bleeding, Serious complications such as ascites or hepatic encephalopathy.
2. Decompensation period (generally Child-Pugh B, C): Liver function damage and portal hypertension syndrome.
1) Systemic symptoms: fatigue, weight loss, dull complexion, less urine, lower extremity edema.
2) Digestive tract symptoms: anorexia, abdominal distension, gastrointestinal dysfunction, or even malabsorption syndrome, liver-derived diabetes, symptoms such as polyuria and polyphagia.
3) bleeding tendency and anemia: bleeding gums, nasal discharge, purpura, anemia.
4) Endocrine disorders: spider mites, liver palm, skin pigmentation, female menstrual disorders, male breast development, parotid swelling.
5) Hypoproteinemia: edema of both lower extremities, oliguria, ascites, and hepatic pleural effusion.
6) Portal hypertension: ascites, pleural effusion, splenomegaly, hypersplenism, portal collateral circulation, esophageal varices, abdominal wall varices.
Examine
Alcoholic cirrhosis
First, laboratory inspection
1. Blood routine: Hemoglobin, platelets, and white blood cells are reduced.
2. Liver function test: mild abnormality in the compensatory period, decreased serum protein in decompensated period, elevated globulin, and inverted A/G. Prothrombin time is prolonged and prothrombin activity is decreased. Transaminase and bilirubin are elevated. Total cholesterol and cholesterol are reduced, and blood ammonia can be elevated. Amino acid metabolism disorder, branch / aroma ratio imbalance. Urea nitrogen and creatinine increased. Electrolyte disorder: low sodium, low potassium.
3. Etiology: HBV-M or HCV-M or HDV-M negative.
4. Fibrosis examination: PIIIP value increased, prolyl hydroxylase (PHO) increased, monoamine oxidase (MAO) increased, and serum laminin (LM) increased.
5. Ascites examination: those who have recently had ascites and the rapid increase of the original ascites should be treated with abdominal puncture, ascites for routine examination, adenosine deaminase (ADA) determination, bacterial culture and cytology. In order to increase the positive rate of culture, ascites culture should be carried out at the bedside, using blood culture bottles for aerobic and anaerobic culture.
Second, imaging examination
1. X-ray examination: angiography of the esophagus and fundus sputum, showing changes in worm-like or varicose veins in the esophageal gastric vein.
2. B-type and color Doppler ultrasonography: in the early stage of alcoholic cirrhosis, the regenerated nodules formed by the pseudo-lobes of the liver are small, the surrounding fiber bundles are narrow and tidy, and the B-mode ultrasound examinations often increase the diameters. The intrahepatic echo is densely enhanced and slightly thickened, which is not easy to distinguish from other chronic liver diseases. 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.
3. CT examination: the proportion of the liver leaves is abnormal, the density is reduced, the nodular changes, the hilar widening, splenomegaly, ascites.
Third, endoscopy: can determine the presence or absence of esophageal varices, the positive rate is higher than the X-ray examination of barium meal, can understand the extent of varicose veins, and assess the risk of bleeding. Esophageal varices are the most reliable indicator for the diagnosis of portal hypertension. In the case of concurrent upper gastrointestinal bleeding, emergency gastroscopy can identify the location and cause of bleeding, and hemostasis treatment.
Fourth, liver biopsy examination: liver biopsy can confirm the diagnosis.
V. Laparoscopy: It can directly observe the abdominal organs and tissues such as liver and spleen, and can take biopsy under direct vision, which is valuable for those who have difficulty in diagnosis.
Sixth, portal vein pressure measurement: hepatic vein wedge pressure and free pressure were measured by jugular vein cannulation, the difference between the two is hepatic venous pressure gradient (HVPG), reflecting portal pressure. Normally less than 5mmHg, greater than 10mmHg is portal hypertension.
Diagnosis
Diagnosis and identification of alcoholic cirrhosis
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 was raised to a level. The Doppler time intensity curve of patients with cirrhosis after angiography was significantly different from that of the normal group and the non-sclerosing liver disease group. The angiography group showed an average start time of 18 s, followed by a The steeper 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 biopsies in the future. In patients with alcoholic cirrhosis, portal venous flow velocity and mean The amount associated with the degree of portal hypertension.
