Morphological changes
The basis of Cirrhosis hepatis is a diffuse restructuring of liver angioarchitecture. Key features:
- Disruption of lobular and trabecular architecture.
- Formation of parenchymal nodules isolated by connective tissue septa.
- Profound disorganization of the vascular, lymphatic, and biliary systems, including the formation of pathological anastomoses.
Clinical presentation
The disease manifests with multi-organ involvement. Three clinical courses are distinguished:
- Mild (20%): vague complaints, early diagnosis is difficult.
- Prominent symptoms (60%): patients seek medical attention on their own.
- Latent (20%): diagnosis is established only at autopsy.
Early subjective signs include weakness, fatigue, loss of appetite, and abdominal pain.
Hepatosplenic syndrome and hypersplenism
A characteristic sign is enlargement of the liver and spleen. The organs have a firm consistency upon palpation. Important to remember: in the terminal stage with severe hepatic failure, the size of the liver may decrease.
Hypersplenism manifests as a decrease in blood cell counts (anemia, leukopenia, thrombocytopenia) with normal or increased bone marrow activity.
Briefly: answers to topical questions
What macroscopic forms of liver cirrhosis are distinguished by nodule size?
Based on the size of regenerative nodules, four macroscopic forms of liver cirrhosis are distinguished.
- Micronodular — regeneration nodules measure up to 3 mm.
- Macronodular — characterized by regenerative nodules of varying sizes exceeding 3 mm in diameter.
- Mixed — combines features of micro- and macronodular involvement.
- Incomplete septal — distinguished in the classification alongside other forms, based on the characteristics of the septa.
What are the main etiological factors causing liver cirrhosis?
The main etiological factors causing liver cirrhosis are chronic hepatitis of various origins and toxic exposures.
- Viral infections — the outcome of viral hepatitis ranks first among causes.
- Toxic factors — alcohol abuse, exposure to drugs and chemicals.
- Genetic and metabolic disorders — hemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency, nutritional deficiency.
- Biliary tract pathology — cholelithiasis, primary sclerosing cholangitis.
- Vascular pathology — congestive heart failure, Budd-Chiari syndrome.
- Autoimmune processes — autoimmune hepatitis.
What clinical manifestations are characteristic of portal hypertension syndrome in cirrhosis?
Portal hypertension syndrome in cirrhosis is characterized by the development of portosystemic anastomoses, splenomegaly, and fluid accumulation in the abdominal cavity.
- Ascites — accumulation of free fluid due to hepatic sinusoid overload and splanchnic vasodilation.
- Varicose veins — formation of portosystemic anastomoses in the esophagus, cardiac stomach, anterior abdominal wall, and hemorrhoidal plexus.
- Splenomegaly — enlargement of the spleen with the development of cyanotic induration and hypersplenism (leukopenia, thrombocytopenia).
- Bleeding — profuse gastrointestinal bleeding from ruptured varicose veins.
What microscopic changes characterize a pseudolobule (regenerative nodule) in cirrhosis?
The microscopic picture of a pseudolobule (regenerative nodule) in cirrhosis is characterized by the restructuring of normal liver tissue angioarchitecture.
- Structural disruption — normal trabecular and lobular architecture of the liver is disrupted.
- Hepatocyte changes — hepatocytes show fatty and protein degeneration.
- Nodule environment — regenerative nodules are surrounded on all sides by connective tissue septa.
- Changes in septa — cellular infiltrate and proliferation of bile ducts are determined in the septa.
What stages of morphogenesis does the liver undergo during the formation of cirrhosis?
Stereotypical morphological changes develop in the liver during the formation of cirrhosis.
- Cellular damage — degeneration, intracellular accumulations, apoptosis, and necrosis of hepatocytes.
- Inflammation — inflammatory cell infiltration.
- Fibrosis — Ito cells begin to synthesize collagen; collagen accumulates in the space of Disse, sinusoid capillarization develops, and connective tissue septa are formed.
- Regeneration — focal or nodular regeneration of hepatocytes.
- Cirrhotic transformation — the parenchyma is divided into nodules of regenerating hepatocytes surrounded by connective tissue; pseudolobules are formed.
For primary biliary cirrhosis, sources distinguish ductular, ductal, fibrotic, and cirrhotic stages.
P-P-P: Parenchyma (nodules), Restructuring (architecture), Portal (hypertension).
Class and exam questions
Why does the organ decrease in size in liver cirrhosis?
A decrease in liver size is characteristic of advanced stages of the disease accompanied by severe hepatic failure.
What is hypersplenism in cirrhosis?
This is a condition in which the peripheral blood count shows a decrease in leukocytes, platelets, and erythrocytes, despite their normal or increased content in the bone marrow.
Is cirrhosis always accompanied by jaundice?
No, not always. Cirrhosis with massive parenchymal necrosis can in some cases occur without jaundice.
What else to study on this topic
- Classification of cirrhosis by etiological principle.
- Pathogenesis of arteriovenous shunt formation.
- Mechanisms of hemorrhagic syndrome development in cirrhosis.
- The role of hereditary factors in the development of the disease.
- Differential diagnosis of causes of portal hypertension.
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