Clinical Medicine: Cirrhosis

Introduction

• Cirrhosis is irreversible fibrosis of the liver, leading to declined liver function and potentially portal hypertension.
• Support the channel by liking, commenting, subscribing, and visiting the website for additional resources like notes, illustrations, quizzes, and exam prep courses.

Pathophysiology

• Cirrhosis: Chronic liver damage & fibrosis, replacing normal tissue with fibrous tissue and nodular regeneration.
• Stellate cells lay down fibrous tissue when liver cells (hepatocytes) are repeatedly injured.
• Consequences: Decline in liver function (albumin synthesis, bilirubin conjugation, ammonia clearance, estrogen metabolism, coagulation protein synthesis) and portal hypertension.

Causes of Cirrhosis

Direct Parenchymal Damage

• Alcohol: Major cause due to chronic liver injury, leading to fatty liver (steatosis).
• Autoimmune Hepatitis: Involves antibodies like ANA, anti-smooth muscle antibodies, IgG, anti-LKM1; treatable with steroids.
• Viral Hepatitis: Hepatitis B & C; transmitted via unsafe sex, IV drug use, blood transfusions.

Metabolic Disorders

• Hemochromatosis: Iron buildup in liver; presents with diabetes, bronzed skin, cardiomyopathy.
• Wilson's Disease: Copper buildup; look for Kaiser-Fleischer rings, neurological symptoms.
• Alpha-1 Antitrypsin Deficiency: Causes liver and lung issues (e.g., youthful emphysema).
• Non-Alcoholic Fatty Liver Disease: Linked with obesity, hypertension, hyperlipidemia; leads to steatohepatitis and fibrosis.

Indirect Causes

• Right Heart Failure: Leads to hepatic congestion due to backpressure from heart.
• Budd-Chiari Syndrome: Clots in hepatic veins causing congestion; often due to malignancy or hypercoagulable states like polycythemia.
• Biliary Tract Diseases: Chronic inflammation causing bile backflow and hepatocyte injury, classified as primary biliary cholangitis (intracellular ducts) or primary sclerosing cholangitis (both intra and extrahepatic ducts).

Complications of Cirrhosis

Portal Hypertension

• Pathophysiology: Fibrous tissue compresses portal veins, raising portal blood pressure.
• Portosystemic Shunt: Causes hyperammonemia, leading to hepatic encephalopathy (confusion, asterixis, cerebral edema).
• Esophageal Varices: High portal pressure causes varices, risking fatal GI bleeding (hematemesis or melena).
• Ascites: Fluid buildup in the peritoneal cavity due to high hydrostatic pressure; risk of spontaneous bacterial peritonitis (SBP).

Liver Failure

• Albumin Deficiency: Causes ascites due to loss of osmotic pressure.
• Coagulopathy: Reduced synthesis of clotting factors leading to bleeding risks like epistaxis and GI bleeds.
• Hepatic Encephalopathy: Due to decreased ammonia clearance.
• Hyperestrogenemia: Causes gynecomastia, testicular atrophy, palmar erythema, spider angiomas.
• Jaundice: Due to failure in bilirubin conjugation and excretion.
• Hepatocellular Carcinoma: Increased risk due to chronic inflammation, necessitating regular ultrasounds and AFP monitoring for early detection.

Diagnosis

• Labs: CBC, liver function tests (AST, ALT), PT/INR, albumin, thrombopoietin (platelets).
• Imaging: Abdominal ultrasound with elastography for liver stiffness.
• Liver Biopsy: Definitive diagnosis showing areas of nodular fibrosis.
• Serum-Ascites Albumin Gradient (SAAG): Differentiates portal hypertension-related ascites (>1.1) from other causes.

Management

• Ascites: Sodium restriction, diuretics (spironolactone & furosemide), large-volume paracentesis with albumin replacement, TIPS procedure for refractory cases.
• SBP: Antibiotics like ceftriaxone, careful monitoring for reoccurrence.
• Hepatic Encephalopathy: Lactulose and rifaximin to reduce ammonia levels.
• Hepatorenal Syndrome: Medications like octreotide & midodrine, and albumin for volume management.
• Variceal Bleeds: Octreotide, antibiotics (ceftriaxone), emergency endoscopy for band ligation, possibly long-term beta-blockers like propranolol.
• Liver Transplantation: Considered for patients with decompensated cirrhosis:
  • Child-Pugh Score: Albumin, bilirubin, coagulopathy (INR), ascites, and hepatic encephalopathy.
  • MELD Sodium Score: Bilirubin, INR, sodium levels, dialysis history, creatinine.

Conclusion

• Early identification and management of cirrhosis complications can improve patient outcomes and quality of life.
• Regular monitoring, appropriate interventions, and consideration for transplantation are critical in managing advanced cirrhosis cases.