The pathogenesis of portal hypertension

Pathogenesis. The pathogenesis of portal hypertension with different types of block portal system is not the same. It is especially difficult when intrahepatic block.
In 1861 took place showed that gleams intrahepatic branches of the portal vein cirrhosis become narrow, venules winding, there obliteration of capillaries hepatic vein. Since then it has accumulated a lot of material to study the cardiovascular system, liver cirrhosis. It was proved the presence of blood (intrahepatic) arterio-portal and Porto kafelnyh anastomoses. Developing group regenerates disrupt the structure of the liver lobules and squeeze the ramifications of the portal vein. Come significant hemodynamic disturbances with the development of high portal hypertension, pressure in the veins inside the liver reaches 600 mm of water. senior and more. It should be noted that hemodynamic disturbances and phenomena hypertension is clearly depend on the intensity nodular regeneration. It was also noted that small sites regenerates cause more extensive compression and therefore contribute to improving portal pressure.
However nodular regeneration causes the disorder and vascularization of the liver, which leads to deterioration of arterialization, oxygenation and nutrition liver cells, are very sensitive to oxygen starvation and increased pressure in the sinusoids. As soon as there comes a compression of the units of the branches of the hepatic veins enters into force a new factor: the blood from the hepatic artery penetrates into the ramifications of the portal vein on presinusoidal arterio-venous anastomoses, so the pressure of the hepatic artery starts transferred to the system of portal vein. As a result, the pressure in the sinusoids increases, and portal hypertension increases.
In addition to the influence nodular regeneration on intrahepatic circulation, is of great importance and disorganization vnutridiskovoe patterns. Occurs disorder vnutridiskovoe circulation due to necrosis in Central slices, fibrosis and expressed cellular infiltration along with the proliferation coppersky cells; the latter can go into the lumen of sinusoidal, narrowing them and to contribute thereby to raising the pressure in the portal system to poslablati oxygenation of liver cells.
Obstruction of blood flow through the system of portal vein and increase of portal pressure cause congestive increase and enlargement of the spleen. Occurs splenomegaly. Elaboration hyperplastic spleen products of its activity causes of the phenomenon of hypersplenism (anemia, leukopenia, thrombocytopenia). In the future join inflammatory changes that cause perispirit, fusion spleen with aperture and retroperitoneal fiber, which partly compensates for portal hypertension by strengthening Porto kabelnogo outflow, and on the other hand, leads to compaction hyperplastic tissue spleen, its fibroadenoma.
Portal hypertension causes the development of collaterals, both natural and new Porto kafelnyh relations, in particular through the coronary veins of the stomach to the venous plexus of the esophagus and then through unmatched and pollonarrua Vienna with the system top Vena cava. Expanded veins of the gastric cardia and esophagus, and into the esophagus, according to our data, the varicose veins reaches the level of the aortic arch and even higher. Varicose veins of the esophagus and stomach is the source of profuse bleeding, patients often leading to death. Still there is no consensus about the causes of bleeding. You should think that, apart from mechanical injury, is set to regurgitation of gastric contents into the esophagus. Resulting in the development of esophagitis, pitting lying in the submucosal layer varicose site. In addition, influenced by other factors, which will be discussed below.
When intrahepatic form of portal hypertension as a result of severe violations of the liver pervert the process of blood clotting. There bleeding on the one hand, and on the other, acute thrombosis of the portal vein and its main branches, leading to a sharp increase of portal pressure. It is also one of the causes of the terrible gastroezofagealna bleeding. In the developing anaemia and hypoxia liver is exacerbated by its failure, flash new foci of necrosis. This contributes to relapse fatal for the life of the patient bleeding in severe renal and hepatic failure, sometimes with the outcome in hepatic coma, from which the patients die.
In the development of Porto kafelnyh anastomoses with portal hypertension participate vv. epigastricae, forming caput Medusa syndrome Cruveillier - Baumgarten or without it and hemorrhoidal veins. Bleeding from the last sometimes reduces portal hypertension. Reckless surgical removal of such "hemorrhoids" contributes to the rapid strengthening of portal hypertension and can bring irreparable harm to the patient.
Much more complicated mechanism of development of cirrhosis with portal hypertension. The stasis in the portal vein and its system plays a major role in its development.
In addition to mechanical obstacles to blood flow in the portal vein, known role hypoproteinemia, developing or as a result of liver failure, or after a massive bleeding. It is proved that the origin of ascites important mineralocorticoids, in particular aldosterone. Inactivation of corticosteroids, in particular aldosterone implemented in physiological terms, liver, caused by its illness.
When intrahepatic form of portal hypertension violated choleresis and biliary excretion. It is associated with liver and is most sharply expressed in the biliary cirrhosis.
Unlike intrahepatic forms of pathogenesis out (up) hepatic forms of portal hypertension is more simple. Most often following the closing of the lumen (thrombus, thrombophlebitis, fleboscleros etc) portal vein or its ducts occurs hypertension gantries system (total or zone), stabilization her, then changed spleen, developing public communication, varicose veins appear hypersplenism and upset disorders, impaired liver function. Ascites, as a rule, no.
As for portal hypertension caused over (over)hepatic block portal system, it is most likely to occur due to the General blood circulation disorder syndrome Budd - Chiari, decompensated heart disease, constrictive pericarditis the.
As a result, the idea of portal hypertension can be schematically presented as such classification table:

Out (up) hepatic block:
Thrombosis of the portal vein or splenic vein; cavernomas these veins. Squeeze of these veins swelling or lymph nodes. Congenital obliteration - stenosis these veins; primary portal sclerosis. Splenic or liver arteriovenous fistula.
Inside the liver unit:
Cirrhosis of the liver. Parasitic infestation. Intrahepatic tumors. Congenital anomalies portal bed in the liver.
Over (over) hepatic block:
Syndrome Budd-Chiari. The compression of the hepatic veins swelling, scarring, lymph nodes.

Each of these blocks can be compensated, subcompensated and decompensated form. Such division is of importance in clinical practice. Extrahepatic block more often gives zonal hypertension, intrahepatic - more total, sometimes with zonal prevalence, nadpochechnymi is usually total.