Author: Abhijit Chowdhury
Publisher: Elsevier Health Sciences
Published: 2009-07-15
Total Pages: 138
ISBN-13: 8131231860
DOWNLOAD EBOOKHepatitis means inflammation of the liver, which can be classified as acute or chronic depending upon the duration of the condition. Various etiological agents have been correlated with the occurrence of various forms of the disease. The developed countries have a majority of drug-induced and toxic liver injury, while the developing countries like India present with a majority of feco-oral and blood borne transmissions of the disease. Viral hepatitis virtually constitutes a separate etiological group. It causes a set of typical clinical, biochemical, and histological changes with or without icterus resulting from hepatic cell damage. It may be acute or chronic. The acute form causes considerable morbidity and mortality, and the chronic sequelae may prove to be fatal by resulting in liver cirrhosis and hepatocellular carcinoma (HCC). Hepatitis A and E are transmitted feco-orally, while B and C are transmitted only through blood/secretions. Hepatitis D occurs only in association with hepatitis B. Morphological pattern of liver injury in acute hepatitis varies with etiology and severity of insult. The typical lesion in all forms of acute viral hepatitis is panlobular infiltration with mononuclear cells, predominantly lymphocytes, hepatic cell necrosis, and variable degree of cholestasis, Kupffer cell hyperplasia. In fulminant hepatic failure, massive hepatic necrosis results in a soft shrunken liver. All forms of acute viral hepatitis run similar clinical course, which include incubation period after infection during which they are asymptomatic, followed by prodromal, icteric, and convalescent phases. Extrahepatic manifestations of viral hepatitis include renal, neurological, and hematological disorders. Most patients with acute viral hepatitis recover with supportive management. Hospitalization is required only in severe cases as evidenced by prolonged PT, altered sensorium, deep jaundice with ascites. Identification of etiology of acute hepatitis is of prime importance for the treatment of hepatitis. Definitive therapy is needed in drug-induced hepatitis. Most mild forms of viral hepatitis resolve with supportive treatment. Progressive liver failure mandates urgent liver transplantation. Prognostic models (Kings’ College criteria, Clichy’s criteria) have been developed for early identification of patients who would require liver transplant.
Book Synopsis Hepatitis - ECAB by : Abhijit Chowdhury
Download or read book Hepatitis - ECAB written by Abhijit Chowdhury and published by Elsevier Health Sciences. This book was released on 2009-07-15 with total page 138 pages. Available in PDF, EPUB and Kindle. Book excerpt: Hepatitis means inflammation of the liver, which can be classified as acute or chronic depending upon the duration of the condition. Various etiological agents have been correlated with the occurrence of various forms of the disease. The developed countries have a majority of drug-induced and toxic liver injury, while the developing countries like India present with a majority of feco-oral and blood borne transmissions of the disease. Viral hepatitis virtually constitutes a separate etiological group. It causes a set of typical clinical, biochemical, and histological changes with or without icterus resulting from hepatic cell damage. It may be acute or chronic. The acute form causes considerable morbidity and mortality, and the chronic sequelae may prove to be fatal by resulting in liver cirrhosis and hepatocellular carcinoma (HCC). Hepatitis A and E are transmitted feco-orally, while B and C are transmitted only through blood/secretions. Hepatitis D occurs only in association with hepatitis B. Morphological pattern of liver injury in acute hepatitis varies with etiology and severity of insult. The typical lesion in all forms of acute viral hepatitis is panlobular infiltration with mononuclear cells, predominantly lymphocytes, hepatic cell necrosis, and variable degree of cholestasis, Kupffer cell hyperplasia. In fulminant hepatic failure, massive hepatic necrosis results in a soft shrunken liver. All forms of acute viral hepatitis run similar clinical course, which include incubation period after infection during which they are asymptomatic, followed by prodromal, icteric, and convalescent phases. Extrahepatic manifestations of viral hepatitis include renal, neurological, and hematological disorders. Most patients with acute viral hepatitis recover with supportive management. Hospitalization is required only in severe cases as evidenced by prolonged PT, altered sensorium, deep jaundice with ascites. Identification of etiology of acute hepatitis is of prime importance for the treatment of hepatitis. Definitive therapy is needed in drug-induced hepatitis. Most mild forms of viral hepatitis resolve with supportive treatment. Progressive liver failure mandates urgent liver transplantation. Prognostic models (Kings’ College criteria, Clichy’s criteria) have been developed for early identification of patients who would require liver transplant.
