Carcinoma gallbladder is the third most common GI malignancy and the most common biliary tract malignancy in North India. Of all the known risk factors, gallstones are most commonly associated with GBC. Bile stasis and chronic inflammation along with occupational exposure to heavy metals, dietary carcinogens, and radiation exposure have been found to be responsible for the increased incidence of GB neoplasms. Infections with S. typhii and S. paratyphii along with Helicobacter sp. have also been associated with GBC. p 53 and ras gene mutations are strongly associated with GBC. Early diagnosis of GBC still remains a challenge and is often diagnosed as a part of investigations of any other disease. Most GBCs are at advanced stage at presentation. USG and CT scan are the common modes for the preliminary diagnosis of GBC. Surgery remains the key treatment modality and the only hope for long-term survival. A large number of patients present at the unresectable stage of the tumor, and palliation remains the only alternative to ensure better quality of life.
Carcinoma of the gallbladder is the most common cancers in North India which is very difficult to treat as well as manage as it is associated with many important issues. The current volume covers the topic right from its etiopathology to its palliation and gives an overview on the current knowledge of the disease. The international authorship of this book reflects the multidisciplinary nature of the book and of the field of gallbladder cancer care. The book promises to stimulate studies to provide specific answers to some unanswered questions. Above all it will destroy the myth that gallbladder carcinoma is incurable and will thus benefit a large number of patients. This edition focuses mainly on Etiopathogenesis of gallbladder cancer Management of gallbladder carcinoma Diagnosis and treatment outcomes Aggressive surgical management Molecular biology and pathogenesis of gallbladder cancer
The second edition of this book is intended as a definitive text on biliary tract and gallbladder cancers. Specifically, it will serve as a single-source reference on the current knowledge base for the multidisciplinary management of such cancers and thus covers epidemiological, surgical, radiotherapy, and chemotherapy approaches. A key feature is the demonstration of the impact of cutting-edge technical knowledge on treatment; for example, interventional radiology techniques, novel surgical approaches, and image-guided radiation therapy are all extensively discussed. Diagnosis is also considered in detail, with coverage of novel serum biomarkers, pathologic staging, molecular profiling, and the full range of current and emerging imaging strategies. This book will be an invaluable source of information on new techniques for experienced practitioners, yet is sufficiently concise to offer an introduction to the field for students and community practitioners.
Alcoholic liver disease involves an acute or chronic inflammation of liver occurring as a consequence of alcohol abuse. The pathological changes occur in 3 stages namely, fatty liver, alcoholic liver disease and cirrhosis, with the final stage traditionally considered to be irreversible. Alcoholic liver disease is responsible for a significant number of premature deaths per annum all around the globe. There is an urgent need to educate the masses about the hazards of alcohol abuse. An efficient system to encourage and prolong the period of alcohol abstinence is the need of the hour. The importance of lifestyle modifications like weight reduction and cessation of smoking in the progression of liver disease needs to be communicated to the patients and the medical community as well. Moreover, realization of the role of nutrition in the management and recovery of ALD would enhance the treatment strategies for this condition. This book has been designed to update the readers on the important aspects of ALD and is a step forward to enable the society in combating the social and economic losses that occur as a result of alcohol abuse. The book has stressed upon various aspects of ALD like the role of nutrition, epidemiology and pathogenesis, and the possible therapeutic strategies involved. Supportive case scenarios have also been incorporated with relevance to the topics covered under the book. Overall, the book presents to the readers an excellent compilation of clinically applicable literature sourced from the most acclaimed physicians in the country.
Hepatic encephalopathy is the clinical syndrome resulting from increased ammonia levels in blood. The most common cause of HE is chronic liver disease. However, acute liver failure, Reye’s syndrome, or metabolic defects are other causes. The true prevalence of overt HE is difficult to establish because of the considerable heterogeneity in etiology and disease severity. However, HE has been reported to be present in around 50% of patients with cirrhosis or with porto-caval shunts at some time during their illness. It is less common in patients with portosystemic shunts without liver disease. Thirty percent of patients dying of end-stage liver disease experience significant encephalopathy, approaching coma. After TIPS placement, approximately 1/3 of patients will experience overt HE. Minimal HE (MHE) is difficult to diagnose due to lack of standard diagnostic tests. Its clinical significance with regards to progression to overt encephalopathy has however, not been established. Conventional treatment of hepatic encephalopathy relies primarily on reducing the production and absorption of ammonia. Identification and correction of the precipitating factors and general supportive measures are important management steps. There are very few randomized controlled trials (RCT) of therapies and even these are bugged by lack of a control group and small sample sizes.
Acute pancreatitis is defined as an acute inflammatory process of the pancreas that may also involve peripancreatic tissues and/or remote organ systems. It typically presents with sudden deep, boring pain that starts in the epigastrium and radiates to the back, which usually worsens on intake of food. It may be of varying severity ranging from mild to severe. Mild disease, if managed promptly and adequately resolves with minimal or no sequelae and seldom leads to extended morbidity or mortality. However Severe Acute Pancreatitis has a longer course of resolution, usually requires hospitalization and has a greater propensity to lead to adverse outcomes. As a thumb rule, it has greater morbidity and mortality rates as compared to Mild Acute Pancreatitis. Understandably, the management protocol for the severe acute pancreatitis is more invasive and emergent, and may require intensive care management. Hence understanding and assessment of the condition in the first 48 hours is a critical step in deciding the outcome. The various assessment criteria that are used to prognosticate and plan the management for this disease have been discussed in this clinical update. Previously, the condition was thought to be caused by infection, but now it is an established fact that it is an acute inflammation of the pancreatic gland with activation of the pancreatic enzymes within the gland leading to its autodigestion. Previously, acute pancreatitis was considered to be mostly associated with chronic alcohol abuse or acute bouts of binge drinking. With the availability of data from recent studies in India and the Asian subcontinent, Biliary disease is emerging as the commonest etiological agent. Extensive genetic analysis and mapping have helped put a cause to the erstwhile "idiopathic" cases. Newer diagnostic modalities and minimal invasive procedures have made the conventional surgeries nearly obsolete now. The rationale and use of antimicrobial treatment in the medical management of the condition has also undergone a change. This clinical update has been designed to update the readers on the important aspects of Acute Pancreatitis. The book has stressed upon various aspects of the condition like the etiology, pathogenesis, diagnosis and evaluation along with an insight into the management approach of the patient including the supportive and nutritional management. Overall, the book presents to the readers an excellent compilation of clinically applicable literature sourced from the most acclaimed physicians in the country.
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.
The exocrine pancreatic function can be impaired by many different pancreatic disease as well as diseases that do not appear to be directly linked to the exocrine pancreas. Hormones stimulating exocrine function (e.g. CCK) might be reduced in diseases affecting the intestinal mucosa (IBD, celiac disease, AIDS) resulting in decreased exocrine secretion. The function of digestive enzymes might be affected by post-cibal asynchrony or by a decreased intraduodenal pH as in Zollinger-Ellison syndrome (ZE). An atrophy of pancreatic tissue might be caused by a lack of trophic factors, as may occur in IDDM, and pancreatic damage might occur due to drugs used for the treatment of other diseases. While some of these conditions appear to be rather rare and of minor clinical relevance, exocrine pancreatic involvement is very frequent in patients with diabetes mellitus. The diagnosis of the condition can be made by the exploration of the exocrine pancreatic secretion, which has been mainly used for the diagnosis of chronic pancreatitis and detection of pancreatic exocrine insufficiency of any etiology. Thus, diagnosis of the disease is classically based on the demonstration of either the morphological and/or the functional changes that typically develop over time in the course of the disease. Exocrine pancreatic function impairs progressively as chronic pancreatitis develops. Thus, exocrine pancreatic dysfunction refers to a mild, moderate or severe reduction of the exocrine pancreatic secretion. Finally, pancreatic function becomes insufficient to maintain a normal digestive process. Pancreatic exocrine insufficiency refers to the stage of maldigestion and malabsorption of nutrients as a consequence of a primarily and/or secondarily impaired exocrine pancreatic function. Pancreatic enzymes remain as the cornerstone for the effective treatment of various disease pathologies resulting in pancreatic exocrine insufficiency. The rigid criteria set forth by the FDA in the USA will ensure that effective pancreatic enzyme preparations will be available and allow the clinician to successfully treat maldigestion, malabsorption, vitamin deficiencies, protein-calorie malnutrition, and in selected patients, the abdominal pain associated with chronic pancreatitis and PEI. Pancreatic enzymes are particularly underused in chronic pancreatitis patients with PEI, post-gastric and intestinal surgery patients who develop an asynchrony of enzyme delivery to the intestine, and pancreatic cancer patients. Earlier use of potent pancreatic enzymes will enhance the quality of life for these patients. This clinical update has been designed to update the readers on the important aspects of the pancreatic exocrine insufficiency, resulting from different conditions and its impact on the patient. The book has stressed upon the various aspects of the condition like its etiology, diagnosis, evaluation, and management approach to the patient. Overall, the book presents to the readers an excellent compilation of clinically applicable literature sourced from the most acclaimed physicians across globe.
