CIRRHOSIS OF LIVER CIRRHOSIS OF LIVER Dr.Vemuri Chaitanya

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  • CIRRHOSIS OF LIVER CIRRHOSIS OF LIVER Dr.Vemuri Chaitanya
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  • Cirrhosis Chronic generalized liver disease Chronic generalized liver disease A condition that is defined histopathologically and has a variety of clinical manifestations and complications, some of which can be life threatening. A condition that is defined histopathologically and has a variety of clinical manifestations and complications, some of which can be life threatening. Pathologic features : development of fibrosis to the point that there is architectural distortion with formation of regenerative nodules ( micronodular / macronodular ) Pathologic features : development of fibrosis to the point that there is architectural distortion with formation of regenerative nodules ( micronodular / macronodular ) This results in decrease in hepatocellular mass, thus function. This results in decrease in hepatocellular mass, thus function.
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  • NORMAL
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  • Micronodular Cirrhosis
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  • Macronodular Cirrhosis
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  • Epidemiology 40% cases asymptomatic 40% cases asymptomatic It is the 12 th leading cause of death in United States. It is the 12 th leading cause of death in United States. Approximately 30,000 to 50,000 deaths per year Approximately 30,000 to 50,000 deaths per year Additional 10,000 deaths due to liver cancer secondary to cirrhosis Additional 10,000 deaths due to liver cancer secondary to cirrhosis
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  • This end stage of CLD is characterised by : Bridging Fibrous Septa Parenchymal nodules Disruption of the architecture of the entire liver
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  • pathogenesis Hepatocellular death Hepatocellular death Regeneration Regeneration Progressive fibrosis Progressive fibrosis The induction of fibrosis occurs with activation of hepatic stellate cells, resulting in formation of increased amounts of collagen & other components of extracellular matrix. The induction of fibrosis occurs with activation of hepatic stellate cells, resulting in formation of increased amounts of collagen & other components of extracellular matrix. Stimuli : 1.Chr.inflammation cytokines like TNF, Lymphotoxin, IL-1 Lymphotoxin, IL-1 2.Cytokine production by injured Kupffer cells, 2.Cytokine production by injured Kupffer cells, endothelial cells, hepatocytes, bile duct epithelial cells endothelial cells, hepatocytes, bile duct epithelial cells 3.Disruption of ECM 3.Disruption of ECM 4.Direct stimulation of stellate cells by toxins 4.Direct stimulation of stellate cells by toxins
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  • Etiology Alcoholism Alcoholism Chronic Viral Hepatitis Hepatitis B Chronic Viral Hepatitis Hepatitis B Hepatitis C Hepatitis C Autoimmune Hepatitis Autoimmune Hepatitis Nonalcoholic steatohepatitis Nonalcoholic steatohepatitis Biliary Cirrhosis Primary biliary cirrhosis Biliary Cirrhosis Primary biliary cirrhosis Primary sclerosing cholangitis Primary sclerosing cholangitis Autoimmune cholangiopathy Autoimmune cholangiopathy
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  • Etiology Cardiac Cirrhosis Cardiac Cirrhosis Budd Chiari Syndrome Budd Chiari Syndrome Inherited metabolic liver disease : Inherited metabolic liver disease : Hemochromatosis Hemochromatosis Wilsons Disease Wilsons Disease Alpha 1 Antitrypsin deficiency Alpha 1 Antitrypsin deficiency Cystic Fibrosis Cystic Fibrosis Cryptogenic Cirrhosis Cryptogenic Cirrhosis Others : Galactosemia, Tyrosinemia, Others : Galactosemia, Tyrosinemia, Drug induced : alpha methyldopa Drug induced : alpha methyldopa Syphilis Syphilis
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  • Clinical Features Asymptomatic for long periods. Asymptomatic for long periods. Onset of symptoms insidious, less often abrupt. Onset of symptoms insidious, less often abrupt. Non specific symptoms vague right upper quadrant pain, fever, nausea, vomiting,diarrhea,anorexia & malaise. Non specific symptoms vague right upper quadrant pain, fever, nausea, vomiting,diarrhea,anorexia & malaise. Or they may present with more specific complication of CLD ascites,upper GI bleed etc Or they may present with more specific complication of CLD ascites,upper GI bleed etc
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  • Signs Loss of hair ( alopecia ) Loss of hair ( alopecia ) Icterus Icterus Pallor Pallor KF Ring KF Ring Parotid enlargement Parotid enlargement Fetor hepaticus Fetor hepaticus Loss of axillary & pubic hair Loss of axillary & pubic hair Spider nevi Spider nevi Gynecomastia Gynecomastia Atrophy of breasts in females Atrophy of breasts in females Wasting of muscles Wasting of muscles
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  • Signs Glossitis, cheilitis Glossitis, cheilitis Palmar erythema Palmar erythema Clubbing Clubbing Leuconychia Leuconychia Dupuytrens contracture Dupuytrens contracture Ascites Ascites In 70 % cases liver is enlarged, firm if not hard and nodular In 70 % cases liver is enlarged, firm if not hard and nodular Splenomegaly Splenomegaly Caput medusae Caput medusae
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  • Signs Bleeding tendencies : deficiency of clotting factors check PT /INR Bleeding tendencies : deficiency of clotting factors check PT /INR Fever Fever Hyperpigmentation Hyperpigmentation Hyperdynamic circulatory state Hyperdynamic circulatory state Edema Edema Hernia Hernia Testicular atrophy Testicular atrophy Delirium Delirium Constructional apraxia Constructional apraxia Flapping tremors Flapping tremors Inversion of sleep rhythm Inversion of sleep rhythm
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  • Palmar erythema
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  • Alcoholic Cirrhosis Accurate history regarding amount & duration of alcohol consumption is required. Accurate history regarding amount & duration of alcohol consumption is required. Lab tests : Lab tests : Completely normal in early compensated alcoholic cirrhosis Completely normal in early compensated alcoholic cirrhosis Hb: Anemia + ( chr.GI loss, nutritional def, Hb: Anemia + ( chr.GI loss, nutritional def, hypersplenism ) hypersplenism ) Platelet count : reduced early in disease, Platelet count : reduced early in disease, portal htn with hypersplenism portal htn with hypersplenism
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  • Alcoholic Cirrhosis S.Bilirubin normal / elevated S.Bilirubin normal / elevated PT often prolonged PT often prolonged S. Transaminases elevated S. Transaminases elevated AST / ALT = > 2/1 AST / ALT = > 2/1 Liver biopsy Liver biopsy Treatment : Treatment : Abstinence is the cornerstone of therapy. Treatment of any complications Glucocorticoids if DF > 32 Oral Pentoxiphylline
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  • Cirrhosis d/t Chr.Hepatitis B & C Of patients exposed to HCV, approximately 80% develop Chronic hepatitis and of those, about 20 30 % will develop cirrhosis over 20-30 yrs. Of patients exposed to HCV, approximately 80% develop Chronic hepatitis and of those, about 20 30 % will develop cirrhosis over 20-30 yrs. Here, liver is small & shrunken with a characteristic features of mixed micro and macro nodular cirrhosis seen on biopsy. Here, liver is small & shrunken with a characteristic features of mixed micro and macro nodular cirrhosis seen on biopsy. Of patients exposed to HBV, about 5 % develop chronic hepatitis & about 20% of those patients go on to develop cirrhosis. Of patients exposed to HBV, about 5 % develop chronic hepatitis & about 20% of those patients go on to develop cirrhosis. Liver is small & shrunken and has mixed micro & macronodular cirrhotic pattern. Liver is small & shrunken and has mixed micro & macronodular cirrhotic pattern. Invg : Routine investigations + HCV RNA, HBsAg, anti HBs, HBeAg, anti HBe, HEV DNA. Invg : Routine investigations + HCV RNA, HBsAg, anti HBs, HBeAg, anti HBe, HEV DNA.
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  • Cirrhosis d/t Chr.Hepatitis B & C Specific Treatment : Specific Treatment : HBV : Lamivudine, Adefovir, Entecavir, Tenofovir HCV: Pegylated Interferon, Ribavirin
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  • Primary Biliary Cirrhosis Female preponderance Female preponderance Median age of around 50 yrs Median age of around 50 yrs Etiology : unknown Etiology : unknown Portal inflammation & necrosis of cholangiocytes in small and medium sized bile ducts. Portal inflammation & necrosis of cholangiocytes in small and medium sized bile ducts. Antimitochondrial antibodies in 90% of pts Antimitochondrial antibodies in 90% of pts Pathology : earliest lesion- Chronic Nonsuppurative Destructive Cholangitis Pathology : earliest lesion- Chronic Nonsuppurative Destructive Cholangitis
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  • Primary Biliary Cirrhosis Primary Biliary Cirrhosis Fatigue Fatigue Pruritis Pruritis On ex: hepatomegaly On ex: hepatomegaly splenomegaly splenomegaly ascites ascites edema edema Unique to PBC : Hyperpigmentation,Xanthelasma,Xanthomata
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  • Primary Biliary Cirrhosis LAB : Elevated GGT, ALP with mild elevations of AST & ALT Elevated GGT, ALP with mild elevations of AST & ALT Hyperbilirubinemia Hyperbilirubinemia Thrombocytopenia, leukopenia, anemia Thrombocytopenia, leukopenia, anemia TREATMENT : UDCA @ 13 15 mg/Kg per day Liver Transplantation Cholestyramine Bisphosphonates osteopenia/osteoporosis
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  • Primary Sclerosing Cholangitis Etiology : unknown Etiology : unknown Diffuse inflammation & fibrosis of entire biliary tree chronic cholestasis obliteration of intra & extrahepatic biliary tree biliary cirrhosis portal htn liver failure D