Macroscopic picture and cellular reaction of the parenchyma
Upon visual assessment of the gross specimen, the affected organ is described by the classical term "big red liver".
At the microscopic level, the main pathological processes unfold within the hepatic lobules (acini). There is abundant inflammatory infiltration of the parenchyma. The cellular composition of the infiltrate is specific: it is represented predominantly by lymphocytes and macrophages, whereas the admixture of conventional leukocytes remains small.
An important role in the local reaction is played by stellate reticuloendothelial cells (Kupffer cells). In response to the viral aggression, their pronounced hyperplasia and focal proliferation occur. Along with damage, signs of recovery — regenerating hepatocytes — can be found in the micropreparations. An additional microscopic sign is often intrahepatic cholestasis (cholestasis).
Degeneration and necrosis of hepatocytes
Viral damage leads to profound metabolic disorders in liver cells, which morphologically manifests as degenerative changes. Histological preparations reveal two main types of degeneration: ballooning and hydropic (the latter is visualized with particular detail using electron microscopy).
The extreme degree of cell damage is their death. Viral hepatitis B is characterized by a wide spectrum of necrotic changes in hepatocytes, which are classified according to prevalence and localization:
- Spotty necrosis (spotty necrosis) — small foci of liver cell death accompanied by local lymphomacrophagic infiltration.
- Periportal and centrilobular necrosis — localized in the corresponding zones of the hepatic acinus.
- Bridging necrosis — forms strands of dead tissue between various structures of the lobule.
- Submassive and massive necrosis — indicate extremely severe organ damage.
Apoptosis and specific markers
In addition to necrosis, hepatocyte death actively occurs via apoptosis. The main histological marker of this process in viral damage is the formation of Councilman bodies.
These structures are shrunken apoptotic bodies detected by standard hematoxylin and eosin staining of micropreparations. The detection of Councilman bodies is a crucial diagnostic criterion confirming the viral etiology of liver damage.
Fulminant form and severe complications
In some cases, viral hepatitis B acquires a rapidly progressive (fulminant) course. Clinically, this condition manifests as acute liver failure. The morphological substrate of such pathology is the development of extensive submassive and massive necrosis of the parenchyma.
The severe course of the disease and its outcome in liver cirrhosis lead to the development of life-threatening complications:
- Neurological: hepatic encephalopathy.
- Hemorrhagic: bleeding from esophageal varices, as well as gastrointestinal and hemorrhoidal bleeding.
- Infectious: accession of secondary flora with the development of sepsis, bowel phlegmon, or spontaneous bacterial peritonitis (ascites-peritonitis).
Prevention principles
To prevent the spread of infection, comprehensive prevention is applied, the purpose of which is to interrupt the natural and artificial routes of virus transmission.
The main method of regulating the epidemic process is recognized to be vaccination. Plasma and recombinant (engineered) vaccines are used for immunization. The vaccination is included in the childhood immunization schedule and is also mandatory for at-risk groups.
Briefly: answers to topical questions
What does the liver look like macroscopically in acute and chronic courses of viral hepatitis B?
The macroscopic picture of the liver depends on the form and stage of the disease. In the acute course, the organ looks like a "big red liver". In the fulminant form (stage of yellow atrophy), the liver is flabby, reduced in size, with a wrinkled capsule, and on cross-section the tissue has a mottled, predominantly yellow color. In the chronic course resulting in post-necrotic cirrhosis, the liver is reduced, dense, with a macronodular surface. On cross-section, the parenchyma is represented by nodes greater than 3 mm in diameter, separated by dense, wide grayish connective tissue septa.
What specific marker cells are detected in the parenchyma in chronic viral hepatitis B?
In chronic viral hepatitis B, specifically altered cells are detected in the liver parenchyma, serving as morphological markers of the infection. These include:
- Ground-glass hepatocytes — cells with a specific alteration of the cytoplasm resembling ground glass, caused by the accumulation of HBsAg in the endoplasmic reticulum.
- Hepatocytes with "sanded" nuclei — cells containing HBcAg in their nuclei in the form of vacuoles with small eosinophilic inclusions.
By which morphological features is the histologic activity index (HAI) assessed in hepatitis?
The histologic activity index (HAI) in chronic hepatitis is assessed by semiquantitative analysis of biopsies using a scoring system. The following morphological criteria are used to calculate the index:
- Periportal and bridging necrosis — scored from 0 to 10 points.
- Intralobular focal necrosis and hepatocyte degeneration — scored from 0 to 4 points.
- Inflammatory infiltrate — severity of infiltration in the portal tracts (from 0 to 4 points).
- Fibrosis — stage of connective tissue proliferation (from 0 to 4 points).
What stages of liver fibrosis are distinguished in the progression of viral hepatitis B?
With the progression of chronic viral hepatitis B, the stages of fibrosis are assessed according to the METAVIR scale. The following stages are distinguished:
- F0 — no fibrosis.
- F1 (mild fibrosis) — stellate enlargement of portal tracts without septum formation.
- F2 (moderate fibrosis) — enlargement of portal tracts with rare portoportal septa.
- F3 (severe fibrosis) — numerous portocentral septa without cirrhosis.
- F4 — liver cirrhosis.
To memorize the types of necrosis in order of increasing severity, use the chain: Spotty → Periportal / Centrilobular → Bridging → Submassive → Massive. And the marker of apoptosis is easy to remember: the virus destroys the cell, leaving a Councilman body.
Class and exam questions
Which cells predominate in the inflammatory infiltrate in hepatitis B?
The infiltrate within the acini consists predominantly of lymphocytes and macrophages. The admixture of conventional leukocytes in it is negligible.
What are Councilman bodies and how to detect them?
These are specific apoptotic bodies formed during hepatocyte death. They serve as a marker of viral damage and are clearly visible in micropreparations upon standard hematoxylin and eosin staining.
What morphological substrate is characteristic of fulminant hepatitis?
The rapidly progressive form leading to acute liver failure is based on extensive submassive and massive necrosis of the liver parenchyma.
How do Kupffer cells react to viral injury?
Stellate reticuloendothelial cells (Kupffer cells) respond to injury with marked hyperplasia and focal proliferation.
What else to study on this topic
- Chronic hepatitis B (CHB): features of the morphological picture.
- Interaction of viral hepatitis B with delta infection (HDV).
- Vaccine prophylaxis: types of plasma and recombinant vaccines.
- Pathogenesis of hepatic encephalopathy development in severe course.
- Mechanisms of hemorrhage formation from varices.
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