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Liver Cirrhosis
• RVS Chaitanya Koppala
Functions of liver
Causes of liver disease
Viral infections: HAV, HBV,
HCV, HDV, HEV
Alcohol
Non alcohol induced liver disease
(obesity , DM and other metabolic
disorders)
Immune disorders:
Autoimmune hepatitis (anti kidney,
anti smooth muscle antibodies)
Primary biliary cirrhosis (Anti
mitochondrial and granulomatous
destruction of lobular bile duct)
Primary sclerosing cholangitis( biliary
strictures, cholestatic and cirrhosis)
Vascular abnormalities
Metabolic and genetic
disorders:
 Hemochromatosis
 Wilson’s disease
 Alpha antitrypsin deficiency
 Glycogen deficiency
Drugs
Complications and symptoms
Investigations
Biochemical test:
simple, inexpensive and easy to perform
Aminotransferases (aspartate transaminases, alanine
transaminase): enzymes present in hepatocytes released
in blood only in case of liver damage (acute liver disease)
Alkaline phosphatase (present in cananicular and
sinusoidal membranes of liver and also in other sites like
bones, levels seen in chronic liver disease)
Gamma glutamyl transpeptidase (confirms the hepatic
origin of elevated levels of alkaline phosphatase enzyme)
Laboratory investigation of aetiology
• Derangement of liver functions should be investigation for Hepatitis
A, B and C
• Auto antibodies or immune globulins to screen for autoimmune
disease screening should be done
Serum ferratin
Ceruloplasmin
Alpha1 antitrypsin
Lipid profile
Imaging techniques
Ultrasound techniques for assessment of size, shape and texture , dilatation
of biliary duct
Patency of portal vein to check for portal hypertension (increased spleen ,
ascites) For checking Hepatocellular carcinoma, hepatobiliary malignancies
CT and MRI scan
Live biopsy:
Invasive procedure associated with mortality and morbidity
Remains the gold standard for diagnosis of liver damages and severity of
chronic liver disease
Recent advanced technique in liver biopsy is non invasive like
FIBROSCAN , effective in patients with HCV
In acute live dysfunction the liver biopsy is not necessary
Patient care
1. PRURITIS:
Prominent and distressing symptom in chronic liver disease and
tends to be most debilitating in cholestatic conditions.
Deposition of bile salts in the skin is primary contribution for pruritis.
Relief of biliary obstruction by endoscopy, radiology and surgical
means is indicated in patients with obstructed biliary systems
In some cases
Plasmapheresis (removing blood plasma from Blood)
Molecular Absorbants Recirculating Systems (MARS) (albumin
dialysis)
Liver transplantation recommended
Treatment
ANION EXCHANGE RESINS (Cholestyramine and Colestipol
4g/day/once or twice)
ANTIHISTAMINES (Cetirizine 10mg, Loratidine 10mg)
URSODEOXYCHOLIC ACID (10mg/kg daily in two doses)
RIFAMPICIN (↑Bile flow / 600mg/day/2-3wks)
OPIOID ANTAGONISTS (Naloxone , Naltrexone & Nalmefene)
TOPICAL PREPARATIONS (calamine lotion / menthol 2% in aq
cream)
Management of pruritis
2. Clotting abnormalities
• 70% patients with chronic liver disease and 100% of patients with
acute liver disease
• Majority of Clotting factors (except factor V) depends on the Vit-K
• Patients with liver disease receive Phytomenadione (vitamin k)
10mg/daily / 3days
• Doesn’t improve the prothrombin time, because liver cannot utilize
vitamin to synthesize the clotting factors
Clotting abnormalities : pathophysiology
Precautions
Aspirin, NSAIDS and anticoagulants should be avoided in all patients
risk of antiplatelet action, GIT bleeding and ulceration
NSAIDS also implicated in Renal dysfunction and Vericeal bleeding in
patients with chronic liver disease
COX-2 inhibitors causes less risk , but still they are prohibited in
patients with liver disease
3. Ascites
• The aim in treatment is to mobilise the
abnormal collection of third space fluid (intra
abdominal fluid)
• Achieved by ↓sodium intake (60-90mEq/day)
+ delayed reaccumulation of fluids (1-
1.5L/day)
• Aggressive fluid reduction in absence of
peripheral edema may leads to intravascular
fluid depletion and renal dysfuntion
• Potassium sparing diuretics, loop diuretics
and paracentasis (perforation in a cavity to
remove the fluids)/ colloid replacement
Approach in management of ascites
(chronic stage)
Management of ascites in patients
4. Hepatic encephalopathy
• Reversible neuropsychiatric complication that occurs with significant
liver function
• Main cause unknown , but there are three main factors which affect the
hepatic encephalopathy
Portosystemic shunting
Metabolic dysfuntion
Alteration of Blood brain barrier
• Agents which causes this conditions
Ammonia
Free fatty acids
GABA
Glutamate
Hepatic encephalopathy
Treatment of hepatic encephalopathy
Thank you

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Cirrhosis

  • 1. Liver Cirrhosis • RVS Chaitanya Koppala
  • 3. Causes of liver disease Viral infections: HAV, HBV, HCV, HDV, HEV Alcohol Non alcohol induced liver disease (obesity , DM and other metabolic disorders) Immune disorders: Autoimmune hepatitis (anti kidney, anti smooth muscle antibodies) Primary biliary cirrhosis (Anti mitochondrial and granulomatous destruction of lobular bile duct) Primary sclerosing cholangitis( biliary strictures, cholestatic and cirrhosis) Vascular abnormalities Metabolic and genetic disorders:  Hemochromatosis  Wilson’s disease  Alpha antitrypsin deficiency  Glycogen deficiency Drugs
  • 5. Investigations Biochemical test: simple, inexpensive and easy to perform Aminotransferases (aspartate transaminases, alanine transaminase): enzymes present in hepatocytes released in blood only in case of liver damage (acute liver disease) Alkaline phosphatase (present in cananicular and sinusoidal membranes of liver and also in other sites like bones, levels seen in chronic liver disease) Gamma glutamyl transpeptidase (confirms the hepatic origin of elevated levels of alkaline phosphatase enzyme)
  • 6. Laboratory investigation of aetiology • Derangement of liver functions should be investigation for Hepatitis A, B and C • Auto antibodies or immune globulins to screen for autoimmune disease screening should be done Serum ferratin Ceruloplasmin Alpha1 antitrypsin Lipid profile
  • 7. Imaging techniques Ultrasound techniques for assessment of size, shape and texture , dilatation of biliary duct Patency of portal vein to check for portal hypertension (increased spleen , ascites) For checking Hepatocellular carcinoma, hepatobiliary malignancies CT and MRI scan Live biopsy: Invasive procedure associated with mortality and morbidity Remains the gold standard for diagnosis of liver damages and severity of chronic liver disease Recent advanced technique in liver biopsy is non invasive like FIBROSCAN , effective in patients with HCV In acute live dysfunction the liver biopsy is not necessary
  • 8. Patient care 1. PRURITIS: Prominent and distressing symptom in chronic liver disease and tends to be most debilitating in cholestatic conditions. Deposition of bile salts in the skin is primary contribution for pruritis. Relief of biliary obstruction by endoscopy, radiology and surgical means is indicated in patients with obstructed biliary systems In some cases Plasmapheresis (removing blood plasma from Blood) Molecular Absorbants Recirculating Systems (MARS) (albumin dialysis) Liver transplantation recommended
  • 9. Treatment ANION EXCHANGE RESINS (Cholestyramine and Colestipol 4g/day/once or twice) ANTIHISTAMINES (Cetirizine 10mg, Loratidine 10mg) URSODEOXYCHOLIC ACID (10mg/kg daily in two doses) RIFAMPICIN (↑Bile flow / 600mg/day/2-3wks) OPIOID ANTAGONISTS (Naloxone , Naltrexone & Nalmefene) TOPICAL PREPARATIONS (calamine lotion / menthol 2% in aq cream)
  • 11. 2. Clotting abnormalities • 70% patients with chronic liver disease and 100% of patients with acute liver disease • Majority of Clotting factors (except factor V) depends on the Vit-K • Patients with liver disease receive Phytomenadione (vitamin k) 10mg/daily / 3days • Doesn’t improve the prothrombin time, because liver cannot utilize vitamin to synthesize the clotting factors
  • 12. Clotting abnormalities : pathophysiology
  • 13. Precautions Aspirin, NSAIDS and anticoagulants should be avoided in all patients risk of antiplatelet action, GIT bleeding and ulceration NSAIDS also implicated in Renal dysfunction and Vericeal bleeding in patients with chronic liver disease COX-2 inhibitors causes less risk , but still they are prohibited in patients with liver disease
  • 14. 3. Ascites • The aim in treatment is to mobilise the abnormal collection of third space fluid (intra abdominal fluid) • Achieved by ↓sodium intake (60-90mEq/day) + delayed reaccumulation of fluids (1- 1.5L/day) • Aggressive fluid reduction in absence of peripheral edema may leads to intravascular fluid depletion and renal dysfuntion • Potassium sparing diuretics, loop diuretics and paracentasis (perforation in a cavity to remove the fluids)/ colloid replacement
  • 15. Approach in management of ascites (chronic stage)
  • 16. Management of ascites in patients
  • 17. 4. Hepatic encephalopathy • Reversible neuropsychiatric complication that occurs with significant liver function • Main cause unknown , but there are three main factors which affect the hepatic encephalopathy Portosystemic shunting Metabolic dysfuntion Alteration of Blood brain barrier • Agents which causes this conditions Ammonia Free fatty acids GABA Glutamate
  • 19. Treatment of hepatic encephalopathy