PA24.{5,7} | Portal Hypertension & Hepatocellular Carcinoma — Summary & Reflection

REFLECT

Consider a 52-year-old farmer from rural Odisha with known HBV carrier status who comes to your outpatient clinic. He has mild jaundice, a palpable firm liver edge, mild splenomegaly, and minimal ankle oedema. His AFP is 28 ng/mL and ultrasound shows a 1.8 cm hypoechoic nodule in the right lobe with a cirrhotic background.

Reflect on the following:
1. Which aetiological factors — including environmental ones relevant to his region — could have contributed to both his cirrhosis and his liver nodule?
2. Using the SAAG framework, how would you distinguish whether any future ascites is from portal hypertension or from peritoneal metastases if the nodule turns out to be HCC?
3. If this patient were to develop haematemesis tonight, trace the exact anatomical pathway from his cirrhotic liver to the rupturing vessel.
4. What single preventive intervention, if given to his 6-year-old grandson today, would most reduce the grandson's lifetime risk of HCC?

KEY TAKEAWAYS

Portal Hypertension — Key Points:
• Defined as portal venous pressure > 12 mmHg; driven by increased resistance and a secondary hyperdynamic circulation.
• Causes classified as prehepatic (portal vein thrombosis), intrahepatic (cirrhosis — commonest; schistosomiasis; NCPF), posthepatic (Budd-Chiari, RHF, constrictive pericarditis).
• Porto-systemic collaterals form at four sites: oesophago-gastric (varices → haematemesis), umbilical (caput medusae), rectal (haemorrhoids), retroperitoneal.
• Ascites = portal hydrostatic pressure + hypoalbuminaemia + RAAS. SAAG ≥ 1.1 g/dL confirms portal hypertension aetiology.
• Complications: variceal haemorrhage (#1 cause of death), splenomegaly/hypersplenism, ascites, hepatic encephalopathy.

HCC — Key Points:
• Major aetiologies: chronic HBV (integrates DNA, direct oncogenesis), HCV (via cirrhosis), aflatoxin B1 (TP53 codon-249 mutation, synergistic with HBV), any cirrhosis, NASH.
• Pathogenesis: chronic injury → regeneration → dysplasia → HCC; key mutations: TERT promoter, TP53, Wnt/β-catenin.
• Gross types: unifocal (massive), multifocal, diffuse; vascular invasion of portal vein is characteristic.
• Micro: trabecular > pseudoglandular > solid; intracellular bile = pathognomonic of hepatocellular origin.
• AFP: elevated in 70%; > 400 ng/mL in a cirrhotic + mass = HCC. Screen cirrhotics 6-monthly with USS ± AFP.
• Fibrolamellar variant: young, non-cirrhotic, normal AFP, lamellar fibrosis, DNAJB1–PRKACA fusion.
• Complications: haemoperitoneum (rupture), PVTT, paraneoplastic syndromes, pulmonary/bone metastases.