课件：临床表现.ppt

Jaundice seen in some cases Enlargement of liver and/or spleen Spider naevi, hepatic palms in cases with long history Abnormal LFTs: transaminase, bilirubin A/G Prognosis different: stable, breakthrough or flare, develop to Cir or Ca Liver failure (severe hepatitis) Bad prognosis Pathological basis: extensive necrosis of hepatic cells 4 subtypes: acute liver failure, subacute, acute-on-chronic, chronic Clinical syndrome including: jaundice deepen rapidly liver size become smaller bleeding, prolonged prothrombin time, PTA less than 40% cerebral edema, high intracranial pressure complicated infection: SBP hepatic encephalopathy toxic abdominal distension and ascites hepatic-renal syndrome Cholestatic viral hepatitis acute and chronic mild manifestation but deepen jaundice Hepatitis cirrhosis hepatic fibrosis compensated cirrhosis decompensated cirrhosis Asymptomatic HBV carrier HBV infection more than 6 months have no symptoms and signs normal LFTs 70%-80%have no pathologic change in liver biopsy Diagnosis Clinical Data Epidemiological evidences Laboratory investigations Ultrasound Biopsy Differential diagnosis Jaundice caused by other etiological agents Hepatitis caused by other etiological agents Treatment Basic principles of management guideline for daily living, physical activity , food and drink intake of the patients supportive and symptomatic treatment Hepatic function protective agents Anti-virus therapy most important treatment for chronic hepatitis B、acute and chronic hepatitis C hepatitis B indication: HBVDNA ≥105copies/ml for HBeAg~, HBVDNA ≥104copies/ml for HBeAg+; ALT ≥2ULN, or biopsy ≥G2S2 Drugs: interferon-