Ecab Clinical Hepatology

ECAB Clinical Hepatology - E-Book

ECAB Recent Advances in Hepatology - E-Book

ECAB Non-alcoholic Fatty Liver Disease - E-Book

Non-alcoholic fatty liver disease is a common cause of chronic liver disease, and its incidence is rising worldwide. Understanding its pathogenesis, biochemical parameters, histological grading and staging, and its management is a vital issue in today’s clinical practice. It appears to be linked directly to the growing epidemic of obesity in adults as well as in children. Thus, in a sense, NAFLD is a self-inflicted liver disease, much like alcoholic liver disease. The exact causes responsible for the development of NAFLD have not been established yet. However, some researchers consider that cluster of disorders that increases the risk of developing heart disease, diabetes, and stroke may be the factor behind development of NAFLD. Most patients with NAFLD have no symptoms or signs of liver disease at the time of diagnosis. In these patients, abnormal liver function tests are often discovered incidentally. Non-alcoholic steatohepatitis (NASH) is that stage of the spectrum that involves fat accumulation (steatosis), inflammation (hepatitis), and scarring (fibrosis) in the liver. Those who have fatty liver or hepatic steatosis with non-specific inflammation as fatty liver with non-specific inflammation generally have a benign longterm prognosis, whereas those who have NASH can progress to cirrhosis. NASH-related cirrhosis may have similar prognosis as cirrhosis from other causes. Hepatocellular carcinoma (HCC) is part of the spectrum of NAFLD, and screening for HCC seems reasonable in patients who have NASH-related cirrhosis. No established treatment is available for NAFLD. Some empiric treatment strategies have been suggested. Presumably, weight loss through exercise and diet modification along with insulinsensitizing agents will help reverse fatty infiltration of the liver. Its incidence is reportedly on the rise the world over as well as in India. Realizing its significance, there is now greater understanding of its etiology, pathogenesis, and management. The efforts of Elsevier have been directed toward addressing these aspects. Elsevier has thus pooled its existing resources with those of the internationally acclaimed Gastroenterologists of India who have chosen to share their rich clinical knowledge, experience, and expertize to serve the practitioners and patient community.

ECAB Clinical Update – Pancreatic Tumors - E-Book

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.