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Chronic_Liver_Disease.pptx
- 1. Approach to ChronicLiver Disease Nu’man AS Daud Gatroentero Hepatology Division Departement of Internal Medicine Hasanuddin University November 12, 2016
- 2. History • Usually nonspecific •Constitutional-malaise, listless, weight loss, nausea • Alcohol ingestion • Drugs-all of them, including IVDU • Herbals • Family history • Transfusion
- 3. Physical exam • HEAD:parotid, enlargement, JVP elevation • HANDS: muscular wasting, palmarerythema, dupuytren’s • CHEST: Spider nevi, gynecomastia, R pleural effusion • Abdomen / pelvis : caput medusae, testicular atropy, lymphadenopathy, ascites, splenomegaly, liver size, texture and tenderness, mass
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- 7. Abnormal Liver Chemistry •ALT (alanineaminotransferase) • AST (asparateaminotransferase) • SAP / ALP (serum alkaline phosphatase) • GGTP (gamma glutamyltranspeptidase) • Bilirubin (conjugated or not) • Albumin (produced) • INR
- 8. Liver injury /Hepatocellular • AST and ALT released • High levels with acute injury • AST also from heart and skeletal muscle
- 9. Cholestatic injury • Anythingthat impairs bile flow • SAP, GGTP raised when chronic, • Transaminas eselevated with acute obstruction, e.g., passing a stone • Bilirubinrises with biliary obstruction. • Mixed conjugated and unconjugated. • Nearly pure unconjugated with hemolysis or Gilbert’s syndrome
- 10. Liver function • Albumindecreased with advanced liver failure. Remember losses of albumin from kidney and gut and malnutrition also decrease • INR/prothrombintime. Also correlates with liver function
- 11. Liver function • Albumindecreased with advanced liver failure. • Remember losses of albumin from kidney and gut and malnutrition also decrease • INR / prothrombin time. • Also correlates with liver function.
- 12. Approach to Liverdisease • Start with pattern, degree and duration of enzyme changes. • Hepatocellular vs. cholestatic
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- 15. Source of virus feces blood/ blood-derived bodyfluids blood/ blood-derived body fluids blood/ blood-derived body fluids feces Route of transmission fecal-oral percutaneous permucosal percutaneous permucosal percutaneous permucosal fecal-oral Chronic infection no yes yes yes no Prevention pre/post- exposure immunization pre/post- exposure immunization blood donor screening; risk behavior modification pre/post- exposure immunization; risk behavior modification ensure safe drinking water Type of Hepatitis A B C D E
- 16. Hepatitis A • Neverchronic • IgM HAV positive (IgG positive = previous infection) • AST>ALT
- 17. Fecal HAV Symptoms 0 1 23 4 5 6 1 2 2 4 Total anti-HAV Titre ALT IgM anti-HAV Months after exposure Typical Serological Course
- 18. Hepatitis B • Contactwith blood/body fluids • Incubation 1-4 months • 90% acute only, and 10 % chronic • Chronic (IT, IC,LR dan Reactvasion)
- 19. Symptoms HBeAg anti-HBe Total anti-HBc IgManti-HBc anti-HBs HBsAg 0 4 8 12 16 20 24 28 32 36 52 100 Acute Hepatitis B Virus Infection with Recovery Typical Serologic Course Weeks after Exposure Titre
- 20. IgM anti-HBc Total anti-HBc HBsAg Acute (6months) HBeAg Chronic (Years) anti-HBe 0 4 8 12 16 20 24 28 32 36 52 Years Weeks after Exposure Titre Progression to Chronic Hepatitis B Virus Infection Typical Serologic Course
- 21. Symptomatic Infection Chronic Infection Ageat Infection Symptomatic Infection (%) Birth 1-6 months 7-12 months 1-4 years Older Children and Adults 0 20 40 60 80 100 100 80 60 40 20 0 Outcome of Hepatitis B Virus Infection by Age at Infection Chronic Infection (%)
- 22. Clinical Characteristics ofHBV chronic
- 23. Serologic test ofHBV HBsAg appears before symptoms; used to screen blood donor; negative = viral clearence Anti HBeAg HBeAg IgM Anti- HBcAg HBcAg Anti HBsAg HBV DNA resolution of acute disease & immunity (sole marker after vaccination) not found in blood test 1st AB to appear; acute infection previous (HBsAg-) or chronic (HBsAg +) HBV infection IgG Anti- HBcAg by product (evidance) of viral replication (↑ infectivity/acute infection) waning viral replication, infectivity active viral replication
- 24. Natural history ofchronic hepatitis B.
- 25. Hepatitis C • Rarelysee acute infection • 80% become chronic and of these only 20% develop end stage liver disease and/or HCC • Screen with HCVAb • HCV RNA to confirm active infection
- 26. Symptoms anti- HCV ALT Normal 0 1 23 4 5 6 1 2 3 4 Typical Serologic Course Titre Month s Years Time after Exposure
- 27. Serologic test ofHCV Anti-HCV acute infection/ resolving infection/false positive (confirm HCV qualitative) quantitative HCV RNA qualitative in serum, livertissue, peripheral blood lymphocytes (+) 2 weeks, marker active infection (< 50IU/ml), order with HIV & hemodyalisis viral load ( high >800.000 IU/ml), along with genotyping determination to define treatment schedule & evaluate response therapy
- 28. Clinical Course HBV& HCV HC V HB V Chronic Infection Portal hypertension Hepatic syntetic failure HBV 10-39 x increase risk even without cirrhosis (highest: perinatal acquired and HBeAg+/↑viral load) neonatus approaching 100%, children 70%, healthy adult 1%; 70-85% HCV 20-30% 2-5% of HCV cirrhotics/year (usually after 20-30 years)
- 29. Alcoholic Liver Disease •Starts with fatty liver and progresses to cirrhosis • Need 60 gms/day in males and 30 gms/day in females. One drinks is 10 gms. • Not everyone is susceptible • Acute alcoholic hepatitis-AST>ALT. • If severe consider corticosteroids for 1 month in consult with IM/Hepatology.
- 30. Drug /Toxic Hepatitis •Acetaminophen (esp. with ethanol) • INH, rifampin • Minocycline, trimethaprim, clavulinicacid • Diclofenac, phenytoin, valproic acid, DDI, tamoxifen, methotrexate, amiodarone • MANY herbals
- 31. Autoimmune Hepatitis • Mostlyfemale and middle aged • High gammaglobulins (IgG increase for Girls) • Raised AST/ALT • Low SAP/ALP • Positive ANA and ASM (smooth muscle) • Treatable
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- 33. Metabolic Liver Disease •NASH/NAFLD • 20% of obese, 2-3% cirrhosis • assoc. with metabolic syndrome • biopsy is AST/ALT>2ULN • Statins • treatment is weight loss • similar biopsy to alcoholic liver disease
- 34. Metabolic Liver Disease •Alpha 1 antitrypsin deficiency • Protein electrophoresis • Hemachromatosis sceenwith Fe /TIBC • If >45% consider genetic testing and liver biopsy
- 35. Metabolic Liver Disease •Metabolic: Wilson’s Disease • acute or chronic, • < 40 years • association neurological disease and KF rings. • Abnormal Cu excretion in bile • Screen with ceruloplasmin
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- 37. Cholestatic Liver Disease •SAP/ALP elevates with age-esp in females • GGTP/5’NT as elevated with liver disease • Rule out extrahepatic obstruction/infiltrative with US, MRCP, or ERCP • Primary BiliaryCirrhosis (PBC) • AMA (mitochrondrial) • Improved with Ursodiol.
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