Pathogenetic chain
The development of cirrhosis represents a closed pathological loop:
- Hepatocyte death stimulates their compensatory proliferation.
- Regenerative nodules (pseudolobules) form, which become isolated by connective tissue layers.
- Capillarization of sinusoids occurs, disrupting normal exchange between liver cells and blood.
- Hemodynamics changes: blood bypasses the nodules, forming intrahepatic portosystemic shunts.
- Parenchymal hypoxia develops, which provokes further necrosis, closing the "vicious circle".
Macroscopic forms
Morphologically, cirrhosis is classified according to the size of the regenerative nodules and the severity of connective tissue septa:
- Macronodular: nodules exceed 3 mm in diameter.
- Micronodular: nodules are small, frequently associated with alcohol-induced liver disease.
- Incomplete septal and mixed types.
Important: this classification is descriptive and has limited value for clinical prognosis.
General morphological changes
In addition to nodule formation, the following are observed in liver tissue:
- Various types of hepatocyte dystrophy (protein in viral hepatitis, fatty in toxic damage).
- Proliferation of cholangiooles.
- Cholestasis.
- Deformation of the organ with a nodular surface.
Briefly: answers to topical questions
What is the morphological essence of hepatic sinusoid capillarization?
The morphological essence of sinusoid capillarization consists in the transformation of permeable hepatic sinusoids into ordinary capillaries with a dense basement membrane. The process includes the following changes in the perisinusoidal space (Space of Disse):
- Matrix accumulation — excessive deposition of extracellular matrix components and formation of a dense collagen framework.
- Structural remodeling — appearance of a basement membrane and collagen fibers in the sinusoid walls, which are normally absent.
This creates a capillary-parenchymal block — a mechanical obstacle to metabolic exchange between blood and hepatocytes.
What are the precise morphometric criteria for micronodular liver cirrhosis?
The precise morphometric criterion for micronodular liver cirrhosis is the formation of regenerative nodules no more than 3 mm in diameter (usually about 1–3 mm). Additional morphological characteristics:
- Regenerative nodules — uniform in size (monomorphic), represented by small pseudolobules.
- Stroma — nodules are separated by thin layers of connective tissue (septa of uniform width) forming a fine reticular network.
This variant of parenchymal remodeling is considered characteristic of the early stage of cirrhosis formation.
What microscopic features distinguish a pseudolobule from a normal liver lobule?
A pseudolobule (regenerative nodule) in cirrhosis is characterized by a disruption of normal liver angioarchitecture. Its microscopic features include:
- Surrounding connective tissue — regenerative nodules are surrounded on all sides by connective tissue (septa).
- Disruption of the trabecular structure — the normal trabecular architecture of the liver is disrupted, and the radial orientation of liver trabeculae is lost.
- Central vein — absent within the nodule or displaced to the periphery.
- Hepatocyte regeneration — nodular regeneration of hepatocytes is observed within the pseudolobules; the regenerative nodules consist of dividing hepatocytes, large and sometimes multinucleated.
What is incomplete septal liver cirrhosis?
Incomplete septal liver cirrhosis is a variant of the disease in which typical pseudolobules are not defined, and signs of regeneration within nodules are not clearly expressed. Its main morphological features are:
- Septa — presence of thin, sometimes incomplete fibrous septa between large nodules.
- Connections — septa connect adjacent portal tracts.
- Blind ends — some septa may end blindly in the liver parenchyma.
Between which vessels do intrahepatic portosystemic shunts form in cirrhosis?
Intrahepatic portosystemic shunts in cirrhosis form between the branches of the portal and hepatic veins. The mechanism and consequences of their formation:
- Localization — these direct vessels form within the connective tissue layers (septa).
- Hemodynamics — due to impaired blood flow in the pseudolobules, blood rushes into the hepatic veins, bypassing the regenerative nodules.
- Pathogenesis — shunting causes microcirculation impairment, parenchymal hypoxia, and progressive dystrophy and necrosis of hepatocytes.
"Necrosis — Regeneration — Shunts". Necrosis triggers nodule growth, nodules compress vessels, blood is diverted into shunts, causing hypoxia and new necrosis.
Class and exam questions
What are pseudolobules?
These are regenerative nodules that lack the normal structure of a liver lobule and are surrounded on all sides by connective tissue.
Why does portal hypertension develop in cirrhosis?
Due to sinusoid capillarization and the formation of intrahepatic shunts, blood flow within the lobules is hindered, which increases pressure in the portal venous system.
Which cirrhosis is called macronodular?
The one in which regenerative nodules are greater than 3 mm in diameter.
What else to study on this topic
- Etiology of liver cirrhosis (viral, toxic, alcoholic factors).
- Mechanisms of portal hypertension development.
- Differential diagnosis of types of hepatocyte dystrophy.
- Clinical significance of morphological changes.
- The role of cholangiole proliferation in pathogenesis.
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