Cirrhosis of the liver

Cirrhosis of the liver is a chronic progressive disease characterized by defeat as parenchyma, and organ dystrophy with hepatic cell dystrophy, nodular regeneration of the hepatic tissue, development of connective tissue, diffuse restructuring of the lobed structure and vascular system of the liver, hyperplasia of the reticuloendothelial elements of the liver and spleen and clinical symptoms reflecting blood flow disorders On intrademporal portal tracts, biliary excretion, cholic outflow, functional disorders of the liver, signs of hypersplenoma. It occurs relatively often, more often in men, mainly in middle age and elderly.

Etiology. Cirrhosis can develop after viral hepatitis; Due to malnutrition (especially proteins, vitamins) and metabolic disorders (diabetes mellitus, thyrotoxicosis), chronic alcoholism; On the soil of the choleo-pelvis with prolonged compression or blockage of the bile ducts; As an outcome of toxic or toxic-allergic hepatitis; Due to constitutional-family predisposition; Chronic liver infiltration by some, substances with subsequent inflammatory reaction (hemochromatosis, hepatocerebral dystrophy); On a background of chronic infections, occasionally - parasitic invasions.

Allocate. Primary cirrhosis of the liver, as well as cirrhosis ,. In which liver damage is only one of many manifestations in the overall clinical picture of the disease: with tuberculosis, brucellosis, syphilis, endocrine-metabolic diseases, some intoxications, collagenoses. "Pathogenesis: Direct damage to the hepatic tissue by an infectious or toxic factor with prolonged exposure to immunological disorders, manifested in the acquisition of antigenic properties by the proteins of the liver and the production of antibodies to them." At the heart of primary (cholangiotic) biliary cirrhosis is long intrahepatic cholestasis. "In secondary biliary cirrhosis Violation of the outflow of bile from the extrahepatic bile ducts, cholangitis, the development of antibodies to the proteins of the epithelial cells of the bile ducts.Dystrophy and necrobiosis of the hepatocytes develop in all types of cirrhosis, a pronounced mesenchymal reaction, proliferation of the connective tissue, as a result of which the lobular structure of the liver, intrahepatic blood flow, lymph flow, Outflow of intrahepatic blood flow causes hypoxia and intensifies dystrophic changes in the liver parenchyma.Nature nerve regeneration of hepatocytes is also characteristic.

Morphological and clinical signs distinguish cirrhosis portal, postnecrotic, biliary (primary and secondary), mixed; By activity of the process - active, progressive and inactive; On the degree of functional disorders - compensated and decompensated. There are also small- and large-nodular cirrhosis and its mixed variant.

Symptoms, course. Along with the increase or decrease in the size of the liver, its denseness, concomitant splenomegaly (see Hepatolienal syndrome), symptoms of portal hypertension (see), jaundice (see) is characteristic. Often dull or aching pain in the region of the liver, intensifying after inaccuracies in diet and physical work; Dyspepsia, skin itching caused by delayed release and accumulation in the tissues of bile acids. When the patient is examined, the "liver signs" characteristic of cirrhosis are revealed: vascular telangiectasias (sprouts, spiders) on the skin of the upper body, palm artefact (hepatic palms), crimson tongue of the crimson color, hepatic tongue. Xanthelasms, xanthomas, fingers in the form of drumsticks are frequent, in men - gynecomastia, dysplasia of hair on the chin and in the armpits.

Often, anemia, leuko- and thrombocytopenia, increased ESR, hyperbilirubinemia, especially with biliary cirrhosis, are detected. When jaundice in the urine is found urobilin, bilirubin, the content of stercobilin in the stool is reduced. They note hyperglobulinemia, changes in the indices of protein, sedimentary samples (sulemic, thymol, etc.).

Diagnosis is established based on the clinical picture, laboratory data. Differential diagnostics with other chronic hepatopathies (chronic hepatitis, hepatosis, hemochromatosis, etc.), as well as clarification of the clinical and morphological form of the disease, provide puncture biopsy, echography and liver scanning. X-ray examination with a suspension of barium sulfate allows to reveal varicose veins of the esophagus, especially characteristic of portal and mixed cirrhosis. In doubtful cases, laparoscopy, splenoportography, angiography, computed tomography are used.

Postnecrotic cirrhosis develops as a result of extensive necrosis of hepatocytes (more often in patients who underwent severe forms of viral hepatitis B). The liver is moderately enlarged or reduced in size, signs of hepatic insufficiency are characteristic, weakness is expressed, disability is reduced, hypoproteinemia (mainly hypoalbuminemia), hypofibrinogenemia, hypoprothrombinemia is determined in the blood, and signs of hemorrhagic diathesis are not uncommon.

Portal cirrhosis occurs after viral hepatitis, as a result of alcoholism, malnutrition, less often due to other causes; Its peculiarity is a massive growth in the liver of connective tissue septums, a difficulty in blood flow through the intrahepatic branching of the portal vein. Symptoms are caused by portal hypertension (see), early ascites, varicose veins of the hemorrhoids, esophagus veins and cardiac section of the stomach, as well as subcutaneous peripodal veins diverging in different directions from the umbilical ring ("Medusa's head"). Jaundice and laboratory-biochemical changes occur relatively in a later period. The most frequent complications are profuse esophageal-gastric and repeated hemorrhoidal hemorrhages.

Biliary cirrhosis occurs on the ground of prolonged holostasis and is manifested by early jaundice, hyperbilirubinemia, skin itching, fever in a number of cases with chills. Serum increases the content of alkaline phosphatase and cholesterol, often alpha (two) and beta-globulin.

Mixed cirrhosis is most common, has common clinical and laboratory manifestations of all the three forms of cirrhosis listed above.

Compensated cirrhosis is characterized by satisfactory state of health of patients and in the presence of clinical-laboratory-morphological changes characteristic of cirrhosis-preservation of the basic functions of the liver. Decompensated hepatic cirrhosis manifests a general weakness. Jaundice, portal hypertension, hemorrhagic phenomena, laboratory changes, indicating a decrease in the functional capacity of the liver.

The course with inactive cirrhosis is slowly progressing (for many years and dozens of years), there are often periods of prolonged remission with a satisfactory well-being of patients, close to normal liver indicators. With active cirrhosis, the progression of the disease is rapid (several years), clinical and laboratory manifestations of the activity of the process (fever, hyperglobulinemia, increased ESR, shifts of protein sediment samples) are significant.

Unregulated lifestyle, systematic diet disorders, alcohol abuse contribute to the activation of the process in the liver.

The terminal period of the disease, regardless of the form of cirrhosis, is characterized by the progression of signs of functional liver failure with an outcome in the hepatic coma.

The prognosis is unfavorable with active cirrhosis, somewhat better (with respect to life expectancy and duration of survival) - with inactive, compensated. With secondary biliary cirrhosis, the prognosis is largely determined by the causes that caused plugging of the bile duct (tumor, stone, etc.) and the possibility of their elimination. The prognosis of patients with haemorrhages from the esophagus and stomach varices in the anamnesis worsens; Such patients live no more than 1-1,5 years and often die from repeated bleeding.

Treatment with active decompensated cirrhosis and the occurrence of complications is stationary. Assign bed rest, diet number 5. When the activity of the process is enhanced, glucocorticosteroid hormones are shown (prednisolone - 15-20 mg / day, etc.). With varicose veins of the esophagus - astringent and antacid preparations; With ascites - a salt-free diet, diuretics, spironolactones, in the absence of effect - paracentesis. With pronounced hypoalbuminemia - plasma, albumin IV. With decompensated cirrhosis, liver hydrolysates (sirepar, etc.), vitamins B1, B6, cocarboxylase, lipoic and glutamic acids are shown. At the first signs of hepatic encephalopathy, the intake of protein into the body is limited and liver failure, water-salt metabolism, hemorrhagic syndrome are treated. To reduce the painful itching, prescribe cholestyramine, which binds bile acids in the intestines and prevents them from being drawn back.

With biliary cirrhosis complicated by cholangitis, and with hepatic insufficiency, antibiotics of a wide spectrum of action are shown.

With secondary biliary cirrhosis-surgical treatment to remove obstruction or compression of the common bile duct.

In acute bleeding from esophageal varices - urgent hospitalization in a surgical hospital, hunger, stopping of tamponade bleeding with a special probe with two blown balloons or introduction through the esophagoscope into the bleeding veins of coagulating drugs, laser coagulation, the appointment of vi-kasol, the drip injection of pituitrin In / in, in some cases - urgent surgical treatment.

With inactive cirrhosis, dispensary supervision of patients is performed (at least 2 times per year), diet No. 5, regular 4-5 meals a day, and physical activity (especially in portal cirrhosis) are indicated. Alcoholic beverages are forbidden. Useful 1-2 times a year, courses of vitamin therapy, treatment with sirep, essenciape. In portal cirrhosis with significant varicose veins of the esophagus or persistent, unrecoverable ascites for the purpose of unloading the portal system, surgically impose a portocaval or splenorenal anastomosis surgically (or perform other types of operations). Patients with cirrhosis of the liver are limited in working capacity or are disabled and need to be transferred to a disability.

Prevention. Prevention of epidemic and serum hepatitis, rational nutrition, effective sanitary and technical supervision in industries associated with hepatotropic poisons, fighting alcoholism. Timely treatment of chronic hepatitis and diseases that occur with cholestasis.