Post-necrotic liver cirrhosis
Etiology and pathogenesis. The process develops rapidly, sometimes taking literally months. The main triggers are the fulminant form of viral hepatitis B (VHB) and massive parenchymal necrosis due to toxic injury.
Macroscopic appearance. The organ is reduced in size and dense. The surface acquires a macronodular relief: the diameter of the nodules exceeds 3 mm. On cross-section, these nodules are separated by broad, dense grayish layers of connective tissue.
Microscopic appearance. The normal trabecular angio-architecture is completely destroyed. Regenerative nodules of various calibers are formed, tightly squeezed by fibrosis from all sides. The radial direction of the hepatic trabeculae disappears, and the central vein is either absent or displaced to the periphery of the nodule. In the broad connective tissue septa, approximated triads are identified—a classic trace of stromal collapse (collapse after hepatocyte death). Lymphomacrophage infiltration and actively proliferating bile ducts are also visible in the septa. The hepatocytes themselves are in a state of hydropic or ballooning degeneration, with numerous regenerating cells present.
Clinical and morphological features. Early hepatic failure comes to the fore, whereas portal hypertension joins only at late stages.
Portal liver cirrhosis
Etiology and pathogenesis. Forms slowly over a number of years, usually as the finale of chronic hepatitis (alcoholic or viral, more often VHC). The mechanism is based on the ingrowth of fibrous strands from portal tracts or central veins with their subsequent connection (septum formation). This is how small false lobules—pseudolobules—arise.
Macroscopic appearance. In early stages, the liver is enlarged, dense, with a micronodular surface (nodules do not exceed 3 mm). Due to concomitant fatty degeneration, the nodules acquire a bright yellow color, separated by thin grayish septa. In the finale of the disease, the organ may decrease in size, change color to brownish-red, and the nodule sizes begin to vary from 3 to 10 mm.
Microscopic appearance. Appears more uniform. The stroma is represented by a fine reticular network. Small monomorphic regenerative nodules separated by narrow septa are visible. Fatty and protein degeneration predominates in hepatocytes. In the septa, there are proliferating ducts and a cellular infiltrate, the composition of which is dictated by the etiology. In alcoholism, portal monolobular cirrhosis is characteristic (connective tissue is well detected by Van Gieson's picrofuchsin staining).
Clinical and morphological features. Early portal hypertension is characteristic, while hepatic failure becomes a late complication. Primary biliary cirrhosis (PBC) is singled out separately—it is considered "true" portal cirrhosis, and its basis is non-suppurative destructive cholangitis and cholangiolitis.
Comparative characteristics and terminology
In addition to the two main forms, there is mixed liver cirrhosis, which combines morphological features of both post-necrotic and portal types.
Analogous terms are often found in medical literature, but it is important to understand the nuances:
- Macronodular cirrhosis correlates closely with post-necrotic.
- Micronodular cirrhosis correlates with portal.
Important: These pairs of concepts demonstrate a strong connection, but are not full synonyms.
| Sign | Post-necrotic LC | Portal LC |
|---|---|---|
| Rate of development | Rapid (months) | Slow (years) |
| Frequent causes | Fulminant VHB, toxins | Chronic alcoholic hepatitis, VHC |
| Nodule size (macro) | Large (> 3 mm) | Small (up to 3 mm), up to 10 mm in the finale |
| Septa | Broad, dense | Thin, narrow |
| Specific markers | Approximated triads in septa | Pseudolobules, monomorphism |
| Early clinical syndrome | Hepatic failure | Portal hypertension |
Briefly: answers to topical questions
Which cells are the main source of collagen synthesis during the formation of fibrous septa in the liver?
The main source of collagen synthesis during the formation of fibrous septa in the liver are hepatic stellate cells (Ito cells) and fibroblasts of the portal tracts.
The following participate in the process of collagenogenesis:
- Hepatic stellate cells—under the action of cytokines, they transform into an activated phenotype (myofibroblasts), begin to intensively proliferate and produce extracellular matrix components, including fibrillar collagens types I and III.
- Fibroblasts—localized in the portal tracts and also participate in the formation of connective tissue.
What histological stains are used to detect connective tissue proliferation in liver cirrhosis?
Van Gieson's picrofuchsin staining is used to detect connective tissue proliferation in liver cirrhosis.
The presented materials indicate that in alcoholism, portal monolobular cirrhosis can be demonstrated by Van Gieson's picrofuchsin staining, which reveals connective tissue.
What complications are characteristic of portal hypertension syndrome in liver cirrhosis?
Complications associated with variceal veins and hemorrhages are characteristic of liver cirrhosis with portal hypertension.
Complications confirmed by sources include:
- varicose veins of the esophagus, stomach, and intestines;
- hemorrhage from varicose veins of the esophagus, stomach, and intestines;
- gastrointestinal and hemorrhoidal bleeding;
- rupture of esophageal varices, which is the cause of fatal bleeding in 7–20% of patients with liver cirrhosis;
- ascites, which can be complicated by spontaneous bacterial peritonitis.
What morphogenetic types of liver cirrhosis are distinguished in modern classification?
The presented materials distinguish the following forms of liver cirrhosis:
- post-necrotic liver cirrhosis;
- portal liver cirrhosis;
- mixed liver cirrhosis, exhibiting features of both postnecrotic and portal cirrhosis;
- biliary liver cirrhosis: primary biliary cirrhosis and secondary biliary cirrhosis.
Postnecrotic cirrhosis is characterized by a macronodular surface and varying-sized nodules exceeding 3 mm; the source also provides an example of postnecrotic multilobular cirrhosis.
Portal cirrhosis is characterized by a micronodular pattern, small monomorphic regenerative nodules, and, in alcoholism, portal monolobular cirrhosis.
Important: the sources indicate that the pairs "macronodular — postnecrotic" and "micronodular — portal" correlate, but are not completely synonymous.
For a quick memory hook on the clinical presentation: Portal cirrhosis starts with Portal hypertension (develops slowly). Post-Necrotic cirrhosis rapidly leads to hepatic Failure.
Class and exam questions
Why are closely spaced triads visible within septa in postnecrotic cirrhosis?
This is a characteristic histological feature resulting from stromal collapse following massive hepatic parenchymal necrosis.
What is the color of the liver in early portal cirrhosis and why?
It acquires a bright yellow color. This is due to the fact that this type frequently develops against the background of alcoholic liver disease and is accompanied by pronounced hepatocyte fatty degeneration.
Are the terms "micronodular" and "portal" absolute synonyms?
No. A close correlation exists between these terms (as well as between the pair "macronodular" and "postnecrotic"), but they are not exact equivalents.
What else to study on this topic
- Mechanism of pseudolobule formation in portal cirrhosis.
- Morphological presentation of primary biliary cirrhosis (PBC).
- Types of hepatocyte degeneration: hydropic, ballooning, fatty, and protein (parenchymatous).
- Van Gieson's picrofuchsin staining: principle of connective tissue detection.
- Mixed liver cirrhosis: features of the combination of morphological signs.
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