Clinical meaning
Cirrhosis is the end-stage of chronic liver disease characterized by diffuse fibrosis, regenerative nodule formation, and distortion of hepatic architecture. Chronic injury (alcohol, viral hepatitis, NAFLD/NASH) activates hepatic stellate cells, which transform from quiescent vitamin A-storing cells into myofibroblasts that produce excessive collagen (types I and III), forming fibrous septa that disrupt normal lobular architecture. This creates portosystemic shunting, impaired hepatocyte function, and portal hypertension (hepatic venous pressure gradient >5 mmHg; clinically significant >10 mmHg). Consequences include synthetic failure (hypoalbuminemia, coagulopathy), impaired detoxification (hyperammonemia → hepatic encephalopathy), and portal hypertension complications (varices, ascites, splenomegaly).
Diagnosis & workup
Diagnostics & workup: - Liver biopsy: gold standard for diagnosis and staging (Metavir fibrosis score F0-F4; F4 = cirrhosis) - FibroScan (transient elastography): non-invasive assessment of liver stiffness; >12.5 kPa suggests cirrhosis - FIB-4 index: calculated from age, AST, ALT, and platelet count; non-invasive fibrosis assessment - Serum markers: AST/ALT ratio >1 suggests cirrhosis (reversed from hepatitis); low albumin, prolonged PT/INR, elevated bilirubin, thrombocytopenia (splenic sequestration) - Abdominal ultrasound: nodular liver surface, splenomegaly, ascites, portal vein dilation (>13 mm) - Upper endoscopy: screen for esophageal/gastric varices at diagnosis; every 2-3 years if none found - AFP every 6 months for HCC surveillance (with ultrasound) - Hepatic venous pressure gradient (HVPG): >10 mmHg = clinically significant portal hypertension