Hepatitis Year 4 Paediatrics Notes OmpathStudy

Hepatitis Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / PAEDS 4.2 / MUNGE / GIT -- Slide 1 Viral Hepatitis Dr Rose Munge Slide 2 Viral hepatitis continues to be a major health problem in both developing and developed countries; there has been significant progress in efforts to recognize and to treat infected subjects.\nThis disorder is caused by the 5 pathogenic hepatotropic viruses recognized to date: hepatitis A (HAV), B (HBV), C (HCV), D (HDV), and E (HEV) viruses.\nMany other viruses (and diseases) can cause hepatitis, usually as a component of a multisystem disease. These include herpes simplex virus, cytomegalovirus, Epstein-Barr virus, varicella-zoster virus, HIV, rubella, adenoviruses, enteroviruses, parvovirus B19, and arboviruses. Slide 4 The hepatotropic viruses are a heterogeneous group of infectious agents that cause similar acute clinical illness.\nIn most pediatric patients, the acute phase causes no or mild clinical disease.\nMorbidity is related to rare cases of acute liver failure (ALF) in susceptible patients, or to the development of a chronic disease state and attendant complications that several of these viruses (hepatitides B, C, and D) commonly cause. Slide 5 Issues Common to All Forms of Viral Hepatitis Differential Diagnosis Often what brings the patient with hepatitis to medical attention is clinical icterus, with yellow skin and/or mucous membranes.\nThe liver is usually enlarged and tender to palpation and percussion.\nSplenomegaly and lymphadenopathy may be present.\nExtrahepatic symptoms (rashes, arthritis) are more commonly seen in HBV and HCV infections.\nClinical signs of bleeding, altered sensorium, or hyperreflexia should be carefully sought, because they mark the onset of encephalopathy and ALF. Slide 6 The differential diagnosis varies with age of presentation.\n In the newborn period, infection is a common cause of conjugated hyperbilirubinemia; the infectious cause is either a bacterial agent (e.g., Escherichia coli, Listeria, syphilis) or a nonhepatotropic virus (e.g., enteroviruses, cytomegalovirus, and herpes simplex virus, which may also cause a nonicteric severe hepatitis). Metabolic diseases (α1 -antitrypsin deficiency, cystic fibrosis, tyrosinemia), anatomic causes (biliary atresia, choledochal cysts), and inherited forms of intrahepatic cholestasis should always be excluded. Slide 7 In later childhood, extrahepatic obstruction (gallstones, primary sclerosing cholangitis, pancreatic pathology), inflammatory conditions (autoimmune hepatitis, juvenile inflammatory arthritis, Kawasaki disease), immune dysregulation (hemophagocyti lymphohistiocytosis), infiltrative disorders (malignancies), toxins and medications, metabolic disorders (Wilson disease, cystic fibrosis), and infection (Epstein-Barr virus, varicella, malaria, leptospirosis, syphilis) should be ruled out. Slide 8 Pathogenesis The acute response of the liver to hepatotropic viruses involves a direct cytopathic and/or an immune-mediated injury.\nThe entire liver is involved. Necrosis is usually most marked in the centrilobular areas.\nAn acute mixed inflammatory infiltrate predominates in the portal areas but also affects the lobules. The lobular architecture remains intact, although balloon degeneration and necrosis of single or groups of parenchymal cells commonly occur.\nFatty change is rare except with HCV infection.\nBile duct proliferation, but not bile duct damage, is common. Diffuse Kupffer cell hyperplasia is noticeable in the sinusoids.\nNeonates often respond to hepatic injury by forming giant cells.\nIn fulminant hepatitis, parenchymal collapse occurs on the described background. Slide 9 With recovery, the liver morphology returns to normal within 3 mo of the acute infection.\n If chronic hepatitis develops, the inflammatory infiltrate settles in the periportal areas and often leads to progressive scarring.\n Both of these hallmarks of chronic hepatitis are seen in cases of HBV and HCV Slide 10 Common Biochemical Profiles in the Acute Infectious Phase Acute liver injury caused by these viruses manifests in 3 main functional liver biochemical profiles.\nThese serve as an important guide to diagnosis, supportive care, and monitoring in the acute phase of the infection for all viruses.\nAs a reflection of cytopathic injury to the hepatocytes, there is a rise in serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST).\nThe magnitude of enzyme elevation does not correlate with the extent of hepatocellular necrosis and has little prognostic value.\nThere is usually slow improvement over several weeks, but AST and ALT levels lag the serum bilirubin level, which tends to normalize first. Slide 11 Rapidly falling aminotransferase levels can predict a poor outcome, particularly if their decline occurs in conjunction with a rising bilirubin level and a prolonged prothrombin time (PT); this combination of findings usually indicates that massive hepatic injury ha