PA24.{2,4} | Alcoholic Liver Disease, Cirrhosis & Hepatic Failure — Summary & Reflection

REFLECT

Return to the case in the Hook block: the 44-year-old man with 15 years of heavy drinking, ascites, jaundice, confusion, and uncorrectable coagulopathy.

Now map each finding to the mechanism you have just studied:
• Ascites — which two processes are acting simultaneously?
• Confusion (ammonia 140 µmol/L) — what is happening at the astrocyte level?
• Uncorrectable coagulopathy despite vitamin K administration — what does this tell you about the type of synthetic failure?
• The "shrunken nodular liver" on ultrasound — which stage of alcoholic liver disease has this man reached, and why is it irreversible?

If you were the intern on call tonight, what single blood test would give you the fastest real-time index of how much functional liver remains?

KEY TAKEAWAYS

Alcoholic liver disease follows a three-stage spectrum:
• Stage 1 — Hepatic steatosis: macrovesicular fat accumulation (↑NADH, ↓β-oxidation); fully reversible; no inflammation.
• Stage 2 — Alcoholic hepatitis: hepatocyte ballooning + Mallory-Denk bodies + neutrophilic infiltrate + perivenular fibrosis; AST:ALT >2:1 clue; may reverse with abstinence.
• Stage 3 — Alcoholic cirrhosis: micronodular pattern; irreversible bridging fibrosis + regenerative nodules; architecture destroyed.

NAFLD/NASH is the metabolic-syndrome counterpart — histologically similar, metabolically different aetiology.

Cirrhosis — defined by diffuse bridging fibrosis + regenerative nodules destroying lobular architecture. Causes: alcohol, HBV/HCV, NASH, haemochromatosis, Wilson, autoimmune, biliary.

Hepatic failure — acute (fulminant) or chronic/acute-on-chronic. Complications and mechanisms:
• Jaundice → failed bilirubin conjugation
• HE → ammonia accumulation → astrocyte swelling → asterixis
• Coagulopathy → ↓hepatic clotting factors (II, V, VII, X) → ↑PT/INR (Factor VII shortest t½)
• Ascites/oedema → ↓albumin + portal hypertension
• Feminisation/spider naevi → ↑oestrogens (failed inactivation)
• HRS → splanchnic vasodilatation → renal vasoconstriction → functional renal failure
• Hepatopulmonary syndrome → intrapulmonary shunts → hypoxaemia + platypnoea
• SBP/sepsis → ↓immune clearance + bacterial translocation

Child-Pugh score classifies severity using bilirubin, albumin, PT/INR, ascites, encephalopathy (Class A/B/C).