Cirrhosis of liver is the end result of the hepatocellular injury characterized by the presence of extensive fibrosis, regenerative nodules and loss of liver architecture.

1. LIVER CIRRHOSIS MEDICINE
By – Dr. ANMOL RAHEJA

2. Introduction
• chronic diffused liver disease.
• end result of the hepatocellular injury
• Characterised by:
• 1. Hepatic cell necrosis
• 2. Proliferation of connective tissue
• 3. Nodular regeneration

3. CAUSES
• Viral hepatitis (postnecrotic)
• Autoimmune hepatitis
• Alcohol (Laennec’s cirrhosis)
• Budd-chairi syndrome –hepatic vein obstruction
• Veno occlusive disease

4. CAUSES
• Drug induced
• Biliary cirrhosis
• Hemochromatosis-iron deposition/iron
overload in body
• Wilson’s disease –excess copper builds up in the
body
• Cardiac cirrhosis (prolonged CHF)
• Alpha-1 antitrypsin deficiency
• Cryptogenic (unknown etiology)

5. PATHOPHYSIOLOGY
• The activation of stellate cells (fat storing cells, Ito {presinusoidal} cells)
is the central event in the development of cirrhosis irrespective of the cause.
• The activated stellate cells transform into multifunctional cells upon
interaction with hepatocytes, Kupffer cells and cytokines
• The transformed cells form type I collagen leading to fibrosis.

6. CLINICAL FEATURES

7. CLINICAL FEATURES
• Features due to hepatocellular dysfunction
• • Jaundice
• • Ascites
• • Hepatomegaly (initial phase)
• • Spider nevi, palmar erythema
• • Gynecomastia, testicular atrophy
• • Menstrual abnormalities, breast atrophy
• • Bleeding tendency
• • Hepatic encephalopathy
• Features due to portal hypertension
• • Ascites
• • Splenomegaly
• • Variceal bleeding
• • Hepatic encephalopathy
• Others
• • Parotid and lacrimal gland enlargement
• • Clubbing
• • Opaque nails (leukonychia)
• • Dupuytren’s contracture
• • Skin pigmentation

8. INVESTIGATION
• a. Blood examination:
• • Aminotransferases (ALT, AST) are frequently elevated whereas a rise in the
serum bilirubin and ALP may occur later.
• • Serum albumin is low.
• • PT is frequently prolonged.
• • Anemia can occur due to bleeding, folate deficiency, marrow suppression or
hypersplenism.
• • Leukopenia and thrombocytopenia suggest hypersplenism.
• b. Imaging: Ultrasonography is helpful in the evaluation of liver size and
texture, ascites, portal hypertension and splenomegaly.
• c. Endoscopy: Upper gastrointestinal endoscopy is required
• to detect esophageal varices and to exclude other causes
• of upper gastrointestinal bleeding in the stomach and
• duodenum.
• d. Liver biopsy: Biopsy helps in the assessment of severity
• of the cirrhotic changes. Typical histological features
• may suggest the specific cause of the cirrhosis.

9. Management
• Management includes general management,
treatment of specific cause, management of the
complications and liver transplantation.

10. Management
• a. General management:
• • The diet should contain an adequate amount of
protein and calories.
• *However, protein intake should be reduced in case of hepatic encephalopathy.
• • Vitamin supplementation is helpful.
• • Salt restriction is required in case of ascites.
• • Medications which are hepatotoxic or metabolized
in liver should be given with caution.

11. Management
• b. Treatment of specific cause: Alcohol
abstinence is mandatory in alcoholic cirrhosis.
• Specific therapy in needed in hemochromatosis
and Wilson’s disease
• c. Management of complications: (discussed
later)
• d. Liver transplantation: The most common
indication for liver transplantation is
irreversible progressive chronic liver
failure due to cirrhosis

12. COMPLICATIONS
• Portal hypertension
• Upper GI bleed
• Ascites
• Spontaneous bacterial peritonitis (SBP)
• Hepatic encephalopathy
• Hepatorenal syndrome
• Hepatocellular carcinoma
• Coagulopathy

13. THANK
YOU