LESION
MECHANISM · RISK
FEATURES
CLUE
Cavernous hemangioma
most common benign
Dilated vascular channels
Usually incidental; adults
No biopsy — hemorrhage risk
Focal nodular hyperplasia
Hyperplastic response to an abnormal artery
Young women; well-circumscribed with a central stellate scar
No malignant potential
Oral contraceptives, anabolic steroids, GSD I; β-catenin-mutant subtype can turn malignant
Young women; subcapsular; may rupture and bleed (esp. pregnancy)
Often regresses after stopping estrogen
Chronic injury and regeneration: HBV (even without cirrhosis), HCV, alcohol, NAFLD, hemochromatosis, α1AT, Wilson, aflatoxin (TP53)
Weight loss, RUQ pain, decompensated cirrhosis; invades portal/hepatic veins (Budd-Chiari)
↑ AFP · arterial enhancement with washout · sorafenib
Tumor products
Erythrocytosis (EPO), hypoglycemia, hypercalcemia (PTHrP)
Rising Hb in a cirrhotic
HCC variant; DNAJB1-PRKACA fusion
Adolescents/young adults, no cirrhosis; layered fibrous bands; normal AFP
Better prognosis
Embryonal tumor
Children < 3; abdominal mass, ↑ AFP
Beckwith-Wiedemann, FAP, prematurity
Malignant endothelial tumor; vinyl chloride, arsenic, Thorotrast
Aggressive, hemorrhagic
CD31 ⁺
Metastases
most common malignancy
Portal and systemic spread
Multiple nodules; colon, breast, lung, pancreas, stomach
Multiple masses = metastases first
Hepatic vein / IVC thrombosis: polycythemia vera, hypercoagulable states, pregnancy, OCPs, HCC
Painful hepatomegaly, ascites, varices; centrilobular congestion; no JVD
Caudate lobe hypertrophy (separate drainage)
Right heart failure, constrictive pericarditis → backflow
Nutmeg liver (dark congested centrilobular zones); ↑ JVD; cardiac cirrhosis late
JVD distinguishes from Budd-Chiari
Sinusoidal obstruction syndrome
Endothelial injury to sinusoids/venules: stem cell transplant conditioning, pyrrolizidine alkaloids
Weight gain, painful hepatomegaly, jaundice within weeks
Veno-occlusive disease