Liver cirrhosis

Cirrhosis - a chronic progressive disease of the liver with the involvement of other organs and systems of the body, characterized by degeneration of the liver cells, nodular regeneration of liver tissue, diffuse development of connective tissue and reconstruction of lobular and vascular architectonics of the liver.
Cirrhosis - polietiologic disease. It arises have a value of infectious disease (especially epidemic hepatitis), lack of food proteins and vitamins (such as kwashiorkor), alcoholism, intoxication heliotrope, chloroform, carbon tetrachloride, phosphorus, arsenic, as well as increased sensitivity to medicines - antibiotics, sulfa drugs and other, resulting develop necrosis of liver cells.
Cause of cirrhosis of the liver can be blocked bile passages inflammation (cholangitis).
Pathogenesis. A major factor in the pathogenesis of liver cirrhosis is a necrosis of liver parenchyma of different length. The decay products of liver cells called in the circle of inflammation and necrosis in the further development of connective tissue. Along with scarring occur nodules liver tissue regeneration that constrict the blood vessels of the liver, primarily hepatic vein that leads to disturbance of blood outflow and increased pressure in the portal vein (portal hypertension). Developing scars and regeneration units, in turn, can cause ischemic necrosis of individual sections of the hepatic parenchyma. Thus, the progression of the cirrhotic process occurs on the type of chain reaction: necrosis - regeneration - reconstruction of the vascular bed - ischemia parenchyma - necrosis.

Healthy liver
cirrhosis of the liver
Liver cirrhosis

Pathological anatomy. There are three different morphological type of liver cirrhosis: postnecrotic, portal (septal) and biliary.
Postnecrotic cirrhosis is characterized by units of various sizes, separated by connective tissue fibers. Macroscopically liver resembles a bunch of grapes. During periods of exacerbation of the process are found necrosis of liver cells in the centers of segments and units. Gets formed and end, dystrophic stage postnecrotic cirrhosis.
Portal cirrhosis is characterized by the development of connective tissue partitions, dismembering segments, resulting in the formation of atypical built nodules of the liver tissue is "false slices". Macroscopically: the liver is reduced, its surface a fine-grained or finely tuberous.
The morphological picture of biliary cirrhosis expressed violation of bile secretion: advanced and crowded bile ducts and capillaries. Inflammation along omologului and vnutriposelkovykh ducts leads to the development of fibrosis, and further morphological picture is almost the portal cirrhosis of the liver. Macroscopically: the liver has a green color, enlarged, its surface is long stays smooth.
Classification. Cirrhosis should be characterized positions: morphological (A), etiological (B) and functional (In) (decision V pan-American Congress of gastroenterology, Cuba, 1956).
A. Morphological characteristics of cirrhosis: portal, postnecrotic and biliary.
B. etiological position distinguish cirrhosis evolving as a result of nutritional deficiency, alcohol, viral hepatitis and cholestasis.
B. Functional characteristics of cirrhosis of liver failure liver cells (jaundice, coma), portal hypertension (ascites, an enlarged spleen, varicose veins of the esophagus, stomach). The diagnosis must specify and activity of the process (progression, steady state, and devolution).
According to these principles of classification of the conclusion of cirrhosis should be similar to the following expression: postnecrotic cirrhosis in the outcome of the epidemic hepatitis, is actively progressing with pronounced symptoms of portal hypertension.

Cirrhosis (gr. kirros - ocher-yellow) - chronic diseases of the liver with the involvement of other organs and systems of the body, characterized by degeneration of the liver cells, nodular regeneration of liver tissue, diffuse connective tissue proliferation and reconstruction of lobular and vascular architectonics of the liver. Develops in the primary outcome of inflammatory and dystrophic processes in the liver. In connection with the development of liver failure are manifestations of metabolic disorders; because in almost every case of cirrhosis in the liver in one degree or another creates difficulty for the passage of blood growing intrahepatic portal hypertension Genesis.
Modern understanding of the term "liver cirrhosis allows us to distinguish the "true" cirrhosis from fibrous modified liver, for example when decompensated heart diseases, cardiosclerosis and adhesive pericardite, or from MS who-humongo hepatitis on the grounds of acquired syphilis. Incorrect terms are "atrophic", "hypertrophic" cirrhosis of the liver. In any cirrhosis of the liver atrophy and necrosis, usually combined with hypertrophy and hyperplasia of the parenchyma. The term "hypertrophy" liver cannot serve as a criterion for differentiating between different types of cirrhosis, as most of cirrhosis passes a stage of hepatomegaly and not always in the future, there comes a decrease in the size of the liver, especially when there is a significant growth of fibrous tissue, and excessive accumulation of fat in the parenchyma of the body.

Etiology. Prevails among the liver cirrhosis of viral, post-hepatitis ("Botkin") cirrhosis. Progressive active liver cirrhosis mainly viral etiology. The frequency of the outcome of the epidemic of hepatitis cirrhosis ranges from 1.5 to 2.4% (the A. F. of Bluger, X. X. Mansurov, E. M. Tareev).
With the direct transition of acute hepatitis to cirrhosis develops more often SKD option, and in the later period (8-10 years) of the portal, but there and then. Protracted cholangiolitis form rather leads to the biliary cirrhosis of the liver. Proven Exodus epidemic of hepatitis b hemochromatosis (see) and the gepatolentikuliarnaya degeneration (see). Cirrhosis may develop in congenital syphilis and occasionally when brucellosis. Doubtful corrigenda role malaria, tuberculosis.
Among non-communicable etiological factors prominent place is occupied by alcohol intoxication. In the development of such cirrhosis, no doubt, an important role plays the background of nutritional deficiency. However, there is no reason to completely deny specific impact of alcohol on liver cells. As a result of biochemical disturbances in the liver, increases the synthesis of fatty acids with possible simultaneously decreased activity cycle citric acid and oxidation of fatty acids [Lieber and Davidson (C. Lieber, S. Davidson)]. Even with the full power of prolonged alcohol intoxication liver experimental animals causes a change in the activity of enzymatic processes, for example glycolytic enzymes cycle, and protein content in separate fractions of liver homogenates (X. X. Mansurov et al.). Finally, it is possible that alcohol intoxication, causing persistent Qatar gastrointestinal tract, lead to liver damage harmful substances that are absorbed from the intestine, or, on the contrary, due to the fact that alcohol intoxication prevents absorption from the intestine of vitamins and proteins necessary for the normal functioning of the liver tissue (A. L. Myasnikov).
Malnutrition (lack in the diet of protein, b vitamins), a major etiologic factor of cirrhosis. In some countries of Africa and Asia still found kwashiorkor (see) as a consequence of protein starvation by eating mostly vegetable carbohydrate food. In the USSR alimentary cirrhosis of the liver, including alcohol, according to E. M. Tareeva, is about 10% of all liver cirrhosis. Alimentary hepatic impairment may be associated with chronic lesions of the gastrointestinal tract - gastroenterocolites, colitis (especially ulcerative), pancreatitis, peptic ulcer disease, etc.
Toxic substances (CCl4, trinitrotoluene, phosphorus), causing necrotic changes in repeated and long-term effects on the liver, can lead to the development of postnecrotic cirrhosis. These include massive necrosis of the liver caused by hypersensitivity to this or that drug - chlorpromazine, tuberculostatic drugs, sulfonamides, antibiotics, arsenic, chloroform, Atofina and other Toxic liver cirrhosis may occur when food poisoning toxins - seeds heliotrope, mushrooms.
The same damaging the liver factor depending on intensity and duration of exposure can lead to the formation of different morphological variants of cirrhosis: portal (or septal), postnecrotic and biliary. The delimitation of options on the basis of clinical and functional methods of research, even when using the most advanced sets of biochemical tests cannot be carried out with full confidence. Needle biopsy and laparoscopy are the main methods lifetime identification of morphological variants of cirrhosis. However, the possibility of needle biopsy for this purpose are limited, especially for establishing cases of postnecrotic cirrhosis of the liver with the large sizes of regeneration units. Therefore, despite the variety of options, cirrhosis should be treated as a single nosological unit, and you try to identify each case must have the appropriate documentation biopsies, laparoscopic observations.
Pathogenesis. In the development of chronic hepatitis and postnecrotic cirrhosis important weight distribution liver disease in the acute phase of illness. A role also belongs to the reactivity of the organism, the ability of the liver to regenerate. In the progression of chronic hepatitis and cirrhosis, along with violations of the considerable role belongs to the circulatory disorders of the liver, contributing to the development of liver failure. According to 3. A. Bondar with al., the degree of vascularization of cirrhosis is about three times smaller than normal.
In chronic liver diseases, Shaffner and Popper (F. Schaffner, N. Popper) using an electron microscope showed increasing changes in spaces of the thesis, eventually leading to the development of the primary membrane and capillarization of sinusoidal. As a result, the circulation of normal open enters closed, decreases also effective hepatic blood flow, which contributes to the development of liver failure.
In the pathogenesis of chronic hepatitis and postnecrotic cirrhosis specification is subject to the influence of chronic infection (viremia) and some immunological mechanisms. As in favor of the first and second there is some clinical and experimental data.