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Circulatory disorders of the liver



The total volume of blood flowing through the liver in 1 min is approximately 1.5 L; 75% of this volume is delivered by the portal vein and 25% by the hepatic artery. Thus, although the blood brought a. hepatica, oxygenated more (95%) than blood v. portae (85%), the portal vein supply covers about 70% of the liver's oxygen demand. In the hepatic sinusoids, a mixture of arterial and venous blood occurs, and the intensity of blood flow is controlled by peculiar sphincters at both ends. Thus, the flow of arterial blood into the sinusoids can be intermittent with subsequent fluctuations in the intrasinus proportions of arterial and venous (portal) blood.

Blockage of the hepatic artery. That's great rarity. If the main trunk of this artery is ligated, an extensive heart attack develops. However, adequate collateral circulation can prevent it. For the same reason, blockage of smaller intrahepatic arterial branches occurs without serious consequences. Nevertheless, large focal infarction occurs in the liver, for example, with periarteritis nodosa (polyarteritis nodosa), as well as acute bacterial endocarditis.

Obstruction of the portal vein. The normal blood pressure in the portal vein is about 7 mmHg. ("0.9 kPa). The most important consequence of obstruction of this vein, regardless of the location and cause of the blockage, is portal hypertension. The volume of portal blood flow may decrease after blockage of the following vessels: hepatic veins, hepatic sinusoids, intrahepatic branches of the portal vein, and finally, the main trunk of the portal vein. The most common and important cause of obstruction is cirrhosis. Other causes are schistosomiasis of the liver (see chapter 14), congenital fibrosis of the liver (see below) and damage to this organ by metastases or a primary malignant tumor. The blood pressure in the portal vein can increase temporarily with acute hepatitis, viral or alcoholic, due to compression of the sinusoids by swollen hepatocytes.

Obstruction of the portal vein as such is rare and can occur with thrombosis of this vein, which sometimes occurs spontaneously, but is more often a complication of the following conditions: umbilical sepsis in the neonatal period, intraperitoneal sepsis, direct tumor invasion into the portal vein, myeloproliferative diseases, splenectomy, portal hypertension . Portal vein obstruction without thrombosis is the result of compression by tumors growing in or near the portal area of ​​the liver.

The effect of complete obstruction of the portal vein depends on localization. If this is only the main trunk of a vein, nothing threatening the patient’s life will happen. However, if the process captures the opening of the splenic vein, then the blood will not be able to pass through the splenic and gastroesophageal anastomoses. In this case, venous infarction of the intestine develops. Overlapping the portal vein branch is sometimes accompanied by a red liver infarction, especially if venous congestion is associated with this, although some researchers do not consider it a true heart attack. They believe that there is an overflow of blood with sinusoids and atrophy of hepatocytes from compression by sinusoids.

Obstruction of the hepatic veins. Obstruction of the main hepatic veins, leading to the development of Budd-Chiari syndrome (G. Budd, H. Chiari), is rare. Spontaneous thrombosis of these vessels sometimes occurs in myeloproliferative diseases, in particular in patients with true polycythemia (see chapter 12), as well as in individuals with migrating thrombophlebitis. Such thrombosis can be observed in women during pregnancy, in the postpartum period, or in the case of prolonged use of steroid contraceptives.
Sometimes obstruction of the hepatic veins occurs due to endophlebitis of unknown etiology. By closing the veins, they are predisposed to squeezing the tumor from the outside, as well as spreading through the venous trunks, for example, hepatocellular carcinoma.

Intense venous congestion in the liver is accompanied by dilatation of sinusoids, perivenular congestion and hemorrhage, atrophy and necrosis of hepatocytes. Pain in the abdomen appears, severe ascites develops. Palpation of the liver is painful. If portocaval venous shunts are ineffective, then a lethal outcome associated with hepatocellular insufficiency occurs.

V enozn o-o to k to yuz and about it I am a disease of a liver. It is found in Jamaica and other tropical countries, develops as a result of the use of various infusions from local plants and herbs. The active agents are alkaloids of the pyrolysidine group contained in plants of the genera Senecio (godson), Crotalaria and Heliotropium. Initially, changes are noted around the terminal hepatic venules, gradually obliterating due to fibrosis. Then the process spreads to larger branches of the hepatic veins. In acute cases, death occurs from liver failure, but in the chronic course of the disease there may be cirrhosis. Venous-occlusive disease occurs after irradiation of the liver, the use of immunosuppressive drugs, oral steroid contraceptives and antitumor agents.

Circulatory damage to the liver of systemic origin. Acute circulatory insufficiency, and about. A decrease in perfusion (natural blood supply) of the liver occurs due to a decrease in both arterial and portal venous blood flow and manifests itself as part of the general circulatory failure. First, the microvasculature is damaged, then hepatocyte necrosis develops, causing an acute inflammatory reaction with polymorphic nuclear leukocytes infiltration. Biochemical blood tests show an increase in the activity of serum aminotransferases. Serum bilirubin levels also increase.

Venous congestion. With rapidly growing (acute) systemic venous congestion (congestion in the pulmonary circulation), the liver enlarges and becomes painful on palpation. Macroscopically, a large amount of dark venous blood is noted in the section. Under the microscope, the sinusoids are sharply expanded, hyperemic, congestion is especially pronounced in the terminal hepatic (central) venules and perivenular sections of the sinusoids. In chronic systemic venous congestion, macro- and microscopic changes are expressed in the development of the "muscat liver" (see chapter 3). In this case, hepatocyte loss occurs due to compression by hyperemic sinusoids and prolonged hypoxia. Clinically, there may be slight jaundice, a moderate, and sometimes noticeable, increase in plasma aminotransferase activity, as well as a decrease in liver inactivation of all kinds of drugs. With prolonged venous congestion, mass death of perivenular liver cells can occur, in some cases compensatory hepatocyte hyperplasia occurs with the formation of nodules and minimally expressed fibrosis. Such changes are called nodular regenerative hyperplasia. In some cases, patients develop the so-called replacement, or cardiac, sclerosis ("cardiac liver fibrosis"). In this case, sections of perivenular sclerosis are connected by fibrous layers with portal tracts. Changes can have a diffuse nature with a violation of the architectonics of the liver, which resembles similar processes in cirrhosis. Such changes accompany tricuspid valve insufficiency.

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Circulatory disorders of the liver

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