Cirrhosis I: Introduction

Cirrhosis develops from chronic liver injury that triggers progressive fibrosis and structural remodeling. Common causes include chronic alcohol use, hepatitis B and C infections, and nonalcoholic fatty liver disease. Other causes encompass autoimmune liver diseases like autoimmune hepatitis, inherited metabolic disorders such as Wilson disease, and prolonged exposure to hepatotoxic substances.

Cirrhosis replaces healthy liver tissue with fibrotic scar tissue and regenerative nodules, distorting the liver's normal architecture. These structural alterations lead to compromised liver function and increased portal pressure. The progressive damage impairs the liver's ability to perform its vital metabolic, synthetic, and detoxification roles.

Micronodular cirrhosis features small, uniform nodules less than 3 millimeters in diameter, typically associated with alcoholic liver disease. Macronodular cirrhosis displays larger, irregularly shaped nodules separated by prominent fibrous bands, often linked to chronic hepatitis infections. Mixed cirrhosis combines both small and large nodules, reflecting advanced or evolving liver pathology.

Cirrhosis presents with general symptoms including fatigue, loss of appetite, and weight loss. These occur alongside gastrointestinal symptoms such as nausea, vomiting, tender hepatomegaly, and jaundice. The combination of these symptoms reflects the progressive decline in liver function and metabolic capacity.

Advanced cirrhosis produces extrahepatic signs including palmar erythema, spider angiomas, and muscle wasting. Men may develop gynecomastia and testicular atrophy, while women experience menstrual irregularities. Enlargement of the parotid and lacrimal glands also occurs, reflecting systemic effects of hepatic dysfunction and portal hypertension.

Autoimmune liver diseases like autoimmune hepatitis trigger chronic inflammation and hepatocyte loss, activating fibrogenic pathways that lead to cirrhosis. Inherited metabolic disorders such as hemochromatosis, Wilson disease, and alpha-1 antitrypsin deficiency cause progressive liver damage through abnormal accumulation or deficiency of essential proteins, ultimately resulting in cirrhosis.

Chronic inflammation from sustained liver injury activates fibrogenic pathways, leading to hepatocyte loss and progressive fibrosis. Regardless of the underlying cause—whether viral hepatitis, alcohol, or metabolic dysfunction—all pathways converge on chronic inflammation as the central mechanism driving scar tissue formation and cirrhosis ii pathophysiology.