Definition
Cirrhosis is the end-stage scarring (fibrosis) of the liver resulting from chronic liver disease. It is
a progressive condition where healthy liver tissue is replaced by fibrotic tissue, impairing liver
function.
It includes a triad of pathological changes i.e. degeneration of hepatocytes, regenerative
(nodular) hyperplasia of remaining or surviving hepatocytes and fibrosis.
Pathophysiology
1. Chronic Injury: Persistent liver injury triggers an inflammatory response.
2. Fibrosis Formation: Stellate cells in the liver become activated, depositing collagen and
extracellular matrix.
3. Loss of Normal Architecture (Fibrosis formation): Fibrotic bands distort the hepatic
architecture, forming nodules and obstructing blood flow.
4. Portal Hypertension: Increased resistance in the liver leads to high portal vein pressure,
causing complications like ascites and varices.
5. Loss of Hepatocyte Function: Reduced ability to synthesize proteins (e.g., albumin,
clotting factors) and detoxify metabolites.
Causes
Cirrhosis has multiple etiologies, including:
1. Alcoholic Liver Disease: Chronic alcohol abuse is a leading cause.
2. Chronic Viral Hepatitis: Hepatitis B, C, and D infections contribute to inflammation
and scarring.
3. Non-Alcoholic Fatty Liver Disease (NAFLD): Associated with obesity, diabetes, and
metabolic syndrome.
4. Autoimmune Liver Diseases: Conditions like autoimmune hepatitis, primary biliary
cholangitis (PBC), or primary sclerosing cholangitis (PSC).
5. Genetic Disorders: Hemochromatosis, Wilson’s disease, and alpha-1 antitrypsin
deficiency.
6. Other Causes:
o Drug-induced liver damage.
o Chronic exposure to toxins.
o Biliary obstruction (e.g., gallstones, tumors).
Clinical Features
Cirrhosis may be asymptomatic in early stages (compensated cirrhosis) but progresses to more
severe symptoms (decompensated cirrhosis).
Cirrhosis is the end-stage scarring (fibrosis) of the liver resulting from chronic liver disease. It is
a progressive condition where healthy liver tissue is replaced by fibrotic tissue, impairing liver
function.
It includes a triad of pathological changes i.e. degeneration of hepatocytes, regenerative
(nodular) hyperplasia of remaining or surviving hepatocytes and fibrosis.
Pathophysiology
1. Chronic Injury: Persistent liver injury triggers an inflammatory response.
2. Fibrosis Formation: Stellate cells in the liver become activated, depositing collagen and
extracellular matrix.
3. Loss of Normal Architecture (Fibrosis formation): Fibrotic bands distort the hepatic
architecture, forming nodules and obstructing blood flow.
4. Portal Hypertension: Increased resistance in the liver leads to high portal vein pressure,
causing complications like ascites and varices.
5. Loss of Hepatocyte Function: Reduced ability to synthesize proteins (e.g., albumin,
clotting factors) and detoxify metabolites.
Causes
Cirrhosis has multiple etiologies, including:
1. Alcoholic Liver Disease: Chronic alcohol abuse is a leading cause.
2. Chronic Viral Hepatitis: Hepatitis B, C, and D infections contribute to inflammation
and scarring.
3. Non-Alcoholic Fatty Liver Disease (NAFLD): Associated with obesity, diabetes, and
metabolic syndrome.
4. Autoimmune Liver Diseases: Conditions like autoimmune hepatitis, primary biliary
cholangitis (PBC), or primary sclerosing cholangitis (PSC).
5. Genetic Disorders: Hemochromatosis, Wilson’s disease, and alpha-1 antitrypsin
deficiency.
6. Other Causes:
o Drug-induced liver damage.
o Chronic exposure to toxins.
o Biliary obstruction (e.g., gallstones, tumors).
Clinical Features
Cirrhosis may be asymptomatic in early stages (compensated cirrhosis) but progresses to more
severe symptoms (decompensated cirrhosis).
