Liver Cirrhosis

Writer:

Prof. Dr. Satish Kumar Panda, MD (Ay), PhD

Principal, Kritika Ayurvedic Medical College & Hospital, Bareilly, Uttar Pradesh.

Table of Contents

  1. Definition & Pathophysiology
  2. Etiology (Causes of Cirrhosis)
  3. Clinical Features
  4. Diagnosis & Investigations
  5. Child-Pugh & MELD Scoring
  6. Complications
  7. Management & Treatment
  8. Prognosis
  9. Key Takeaways & Mnemonics

1. Definition & Pathophysiology

What is Liver Cirrhosis?

  • Cirrhosis is the end-stage of chronic liver disease, characterized by:
  • Fibrosis (scar tissue replacing healthy liver parenchyma).
  • Regenerative nodules (required for diagnosis).
  • Portal hypertension (increased pressure in the portal vein).

Key Pathophysiological Changes

  1. Hepatocyte Injury → Chronic inflammation (e.g., viral hepatitis, alcohol).
  2. Activation of Stellate Cells → Excessive collagen deposition (fibrosis).
  3. Distorted Liver Architecture
  • Impaired liver function (↓ detoxification, ↓ protein synthesis).
  • Increased vascular resistancePortal HTN.
  1. Compensated vs. Decompensated Cirrhosis
  • Compensated: Liver functions normally despite fibrosis (asymptomatic or mild fatigue).
  • Decompensated: Liver failure (jaundice, ascites, variceal bleeding, encephalopathy).

2. Etiology (Causes of Cirrhosis) – Mnemonic: “VW HAPPENS”

CategorySpecific CausesKey Features
Viral HepatitisHCV, HBV, HDVHCV most common worldwide; HBV linked to HCC.
Alcohol (ASH)Chronic alcoholismAST:ALT >2:1, ↑GGT, ↑MCV.
NASHObesity, diabetesMetabolic syndrome, no alcohol history.
AutoimmunePBC, PSC, AIHPBC (AMA+), PSC (IBD association), AIH (ANA/ASMA+).
Genetic/MetabolicHemochromatosis, Wilson’s, A1ATHemochromatosis (↑ferritin), Wilson’s (Kayser-Fleischer rings).
VascularBudd-Chiari, PVTHepatic vein thrombosis (Budd-Chiari), portal vein obstruction.
Drugs/ToxinsMethotrexate, acetaminophenDirect hepatotoxicity.

3. Clinical Features

Early (Compensated) Cirrhosis

  • Fatigue, weakness, weight loss.
  • Physical signs:
  • Palmar erythema, spider angiomas (↑estrogen).
  • Dupuytren’s contracture (alcohol-related).
  • Clubbing, leukonychia (hypoalbuminemia).

Late (Decompensated) Cirrhosis

ComplicationSymptoms/Signs
Portal HTNAscites, splenomegaly, varices (esophageal, rectal).
AscitesAbdominal distension, shifting dullness.
Variceal BleedingHematemesis, melena, shock.
Hepatic EncephalopathyConfusion, asterixis, coma.
Hepatorenal SyndromeOliguria, ↑creatinine.
HCC (Hepatocellular Carcinoma)RUQ mass, ↑AFP.

4. Diagnosis & Investigations

Laboratory Tests

  • LFTs: AST > ALT (alcohol/NASH), ↑bilirubin, ↓albumin.
  • CBC: Thrombocytopenia (hypersplenism), anemia.
  • Coagulation: Prolonged PT/INR (↓ clotting factors).
  • Etiology-specific tests:
  • Viral serology (HCV Ab, HBsAg).
  • Autoantibodies (AMA for PBC, ANA/ASMA for AIH).
  • Ferritin/TIBC (hemochromatosis), ceruloplasmin (Wilson’s).

Imaging

  • Ultrasound: Nodular liver, ascites, splenomegaly.
  • FibroScan (Elastography): Measures liver stiffness.
  • CT/MRI: Detects HCC, vascular abnormalities.

Liver Biopsy (Gold Standard)

  • Shows bridging fibrosis + regenerative nodules.

5. Child-Pugh & MELD Scoring (Prognosis)

Child-Pugh Score

Parameter1 Point2 Points3 Points
Bilirubin (mg/dL)<22-3>3
Albumin (g/dL)>3.52.8-3.5<2.8
INR<1.71.7-2.3>2.3
AscitesNoneMildSevere
EncephalopathyNoneGrade 1-2Grade 3-4
  • Class A (5-6): Good prognosis (85% 2-year survival).
  • Class B (7-9): Moderate (60% survival).
  • Class C (10-15): Poor (35% survival, transplant needed).

MELD Score

  • Predicts 3-month mortality in cirrhosis.
  • Formula:
  MELD = 3.8 × ln(bilirubin) + 11.2 × ln(INR) + 9.6 × ln(creatinine) + 6.4
  • MELD ≥15: Indicates need for liver transplant.

6. Complications

ComplicationKey FeaturesManagement
Variceal BleedingHematemesis, shockBand ligation, IV octreotide, NSBB (propranolol).
AscitesShifting dullness, abdominal distensionSalt restriction, spironolactone + furosemide.
SBP (Spontaneous Bacterial Peritonitis)Ascitic fluid PMN >250IV cefotaxime.
Hepatic EncephalopathyConfusion, asterixisLactulose, rifaximin.
Hepatorenal SyndromeOliguria, ↑CrAlbumin + vasoconstrictors (terlipressin).
HCC↑AFP, liver massSurveillance (US every 6 months).

7. Management & Treatment

General Approach

  1. Treat underlying cause:
  • HCV: Direct-acting antivirals (sofosbuvir/velpatasvir).
  • Alcohol: Abstinence.
  • Autoimmune: Steroids (AIH), ursodeoxycholic acid (PBC).
  1. Monitor for complications (ascites, varices, HCC).
  2. Liver transplant for decompensated cirrhosis (MELD ≥15).

Symptomatic Management

  • Ascites: Salt restriction + diuretics (spironolactone + furosemide).
  • Varices: Non-selective beta-blockers (propranolol) + endoscopic banding.
  • Encephalopathy: Lactulose (reduces ammonia), rifaximin.

8. Prognosis

  • Compensated cirrhosis: 10-year survival ~50%.
  • Decompensated cirrhosis: 2-year survival ~50%.
  • Hepatorenal syndrome: Poor prognosis without transplant.

9. Key Takeaways & Mnemonics

Mnemonics

  • Causes of Cirrhosis: “VW HAPPENS” (Viral, Wilson’s, Hemochromatosis, Alcohol, PBC/PSC, NASH, Storage diseases).
  • AST:ALT Ratio >2:1 → Alcoholic hepatitis.
  • SAAG ≥1.1 g/dL → Portal HTN-related ascites.

High-Yield Exam Points

  • Kayser-Fleischer ringsWilson’s disease.
  • AMA+Primary Biliary Cholangitis (PBC).
  • Spider angiomas + palmar erythemaHyperestrogenism in cirrhosis.
  • First-line for SBPCefotaxime.

Final Notes

  • Cirrhosis is irreversible, but early intervention can slow progression.
  • Screen for HCC (ultrasound + AFP every 6 months).
  • Refer for transplant if decompensated (Child-Pugh C or MELD ≥15).

This guide covers everything a medical student needs for exams and clinical practice.

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