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Portal hypertension: pathogenesis
Last reviewed: 23.04.2024
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The main pathogenetic factors of portal hypertension are the following:
- Mechanical obstruction of outflow of blood.
With subhepatic and posthepatic portal hypertension, an obstruction to blood flow is due to thrombosis, obliteration, or (pressure from outside large vessels (portal vein, hepatic veins).
The postsynusoidal intrahepatic block is caused by the obliteration of the terminal branches of the hepatic vein or (pressure by their regeneration nodes, the centrolobular formation of fibrous tissue (for example, hyaline central sclerosis in chronic alcoholic hepatitis, etc.) The disturbance of blood flow in the hepatic sinusoids is due to the proliferation of connective tissue inside the lobule of the liver , proliferation of endotheliocytes.
Presinusoidal intrahepatic block is associated with infiltration and fibrosis in portal and periportal areas.
- Increased blood flow in portal veins.
This may be due to the difficulty of outflow of blood from the liver to the hepatic veins, the presence of arterio-venous fistulas, myeloproliferative diseases, cirrhosis, etc.
- Increased resistance (resistance) of portal vessels.
In the portal venous system there are no valves and any structural changes in it cause an increase in pressure. In patients with cirrhosis of the liver, resistance to blood flow may increase in different sections of the intrahepatic vascular bed.
The increase in vascular resistance is due to the presence of regeneration nodes that compress the hepatic and portal veins, as well as the formation of collagen around the sinusoids, terminal hepatic venules, a violation of the liver architectonics.
- Formation of collaterals between the portal of the portal vein and the systemic blood flow.
The development of these anastomoses is a consequence of portal hypertension.
With prehepatic portal hypertension, port-portal anastomoses develop. They restore the flow of blood from the portal system located below the block to the intrahepatic branches of the portal vein.
With intrahepatic and extrahepatic portal hypertension, porto-caval anastomoses develop, which ensure the outflow of blood from the portal vein system into the basins of the upper and lower hollow veins bypassing the liver.
Particularly important are the anastomoses in the cardiac region of the stomach and esophagus, since bleeding from these veins is a serious complication of portal hypertension.
- The development of ascites, the most important symptom of portal hypertension, is due to the following factors:
- increased lymphoma in the liver in connection with the blockade of the outflow of venous blood from the liver. Lymph seeps through the lymphatic vessels of the liver capsule directly into the abdominal cavity or enters through the lymphatic ducts in the area of the liver gates in the thoracic duct. The throughput of the lymphatic duct becomes inadequate and lymphatic stasis develops, contributing to swelling of the fluid into the abdominal cavity;
- the fall of the colloid-osmotic pressure of the plasma, which is associated with a violation of protein synthesis in the liver; decrease in colloid osmotic pressure promotes the outflow of water into the extravascular space, i.e. Into the abdominal cavity;
- increased activity of the renin-angiotensin-aldosterone system;
- impaired renal function (decreased renal blood flow, glomerular filtration, increased sodium reabsorption) due to impaired venous outflow from the kidneys or a decrease in blood flow to the kidneys;
- increase in the content of estrogen in the blood in connection with a decrease in their destruction in the liver; estrogens have antidiuretic effect.
- Splenomegaly is a consequence of portal hypertension. Splenomegaly is caused by stagnant phenomena, as well as growth in the spleen of connective tissue and hyperplasia of the cells of the reticulo-histiocytic system.
- Portal hypertension with the development of porto-caval anastomoses gradually leads to hepatic (port-systemic) encephalopathy.
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