TOPIC 2. Hepatocellular Disease, Liver Failure, Cirrhosis & Hepatic Encephalopathy

One connected picture of disease mechanisms, clinical clues, investigations and management.

1. THE TOPIC IN ONE CONNECTED FLOW

Hepatocyte injury may cause an acute loss of liver function or, when persistent, fibrosis and cirrhosis. Cirrhosis changes portal blood flow and reduces important liver functions. Follow the sequence from the cause to clinical signs, investigations and treatment to understand why ascites, bleeding and encephalopathy develop.

CAUSE

Hepatitis B/C, alcohol, metabolic or drug-related injury

HEPATOCYTE DAMAGE

Inflammation and cell injury → ALT/AST rise

TWO PATHWAYS

Chronic fibrosis → cirrhosis; severe acute injury → acute liver failure

FUNCTIONAL EFFECT

Portal hypertension; reduced synthesis and ammonia clearance

CLINICAL CLUES

Ascites, varices, jaundice, bruising or confusion

CONFIRM & INTERPRET

Liver tests, INR, ultrasound, ascitic fluid and clinical assessment

ACT & PREVENT

Treat cause, manage complications, prevent recurrence and assess referral

2. KEY CLINICAL CONNECTIONS

Liver tests → clinical meaning

Marked ALT/AST rise → hepatocyte injury; low albumin + prolonged INR → impaired synthesis. Cholestatic ALP/GGT rise → assess bile-flow obstruction.

Portal hypertension → ascites and infection

Cirrhosis → increased portal resistance and sodium retention → ascites → diagnostic paracentesis. SAAG ≥1.1 g/dL → portal hypertensive ascites; ascitic PMN ≥250/mm³ → treat suspected SBP promptly.

Acute failure → emergency recognition

Acute severe liver injury + INR ≥1.5 + encephalopathy without pre-existing cirrhosis → acute liver failure → urgent liver-unit assessment; monitor glucose and neurological status.

Encephalopathy → treatment and prevention

Reduced ammonia handling + infection, GI bleeding, constipation, electrolyte disturbance or sedatives → altered attention/asterixis → correct trigger + lactulose; recurrent episodes → consider rifaximin.

3. AIM HIGH-YIELD INTEGRATION REVIEW

⭐ Injury ≠ function: ALT/AST indicate hepatocyte injury → albumin and PT/INR help assess synthetic function.

Examine for decompensation: Cirrhosis → portal hypertension → splenomegaly, ascites and variceal bleeding risk; focused history and examination identify complications.

⭐ Interpret ascitic fluid: Serum albumin − ascitic albumin = SAAG; ≥1.1 g/dL → portal hypertension; PMN ≥250/mm³ → suspected SBP.

Paracentesis changes care: New/worsening ascites → diagnostic tap and fluid report interpretation; large-volume drainage >5 L → consider IV albumin.

⭐ Acute liver failure is urgent: Acute injury + INR ≥1.5 + encephalopathy → risk of hypoglycemia and cerebral edema → urgent specialist management.

⭐ Grade encephalopathy clinically: Attention change, disorientation and asterixis → clinical West Haven grading; ammonia level alone does not grade severity.

Prevent recurrence: Find triggers → correct infection, bleeding, constipation or hypokalemia; lactulose reduces intestinal ammonia absorption → rifaximin may prevent recurrence.

Counsel and follow up: HBV/HCV-related cirrhosis → antiviral assessment and counselling; ongoing HCC surveillance and transplantation assessment when decompensated.

AIM Exam Trap: Elevated serum ammonia may support the assessment, but hepatic encephalopathy is diagnosed and graded clinically; assess alternative causes of altered consciousness.