Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2
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Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2
SECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2TanEpidemiology of liver diseaseIhe true epidemiology and incidence of liver disease is difficult to ascertain, as most liver diseases are insidious, with a latent period between disease occurrence and detection (Kim, 2002). Hence, population-based studies are often used as surrogates to estimate di Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2sease burden.The United StatesA population-based study by the CDC reported the incidence of newly diagnosed chronic liver disease in adults to be 63.9Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2
per 100.000 population as seen by gastrointestinal specialists, The most common aetiology of chronic liver disease was hepatitis c (hepatitis c virusSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2iver disease alone (8%). and hepatitis 8 (hepatitis 8 virus (IIBV)) (3%). Other aetiologies (primary sclerosing cholangitis, primary biliary cirrhosis, hereditary haemochromatosis. autoimmune hepatitis, al-antitrypsin deficiency, and hepatocellular carcinoma (HCC)) accounted for less than 3% of all Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2newly diagnosed cases of chronic liver disease (Bell, 2008).Ihe prevalence of antibodies against HCV (anti-HCV) was 1.8% in the third National HealthEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
and Nutrition Examination Survey (NHANES HI) study, which corresponds to approximately 3.9 million Americans infected with HCV. Of these, approximatelSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2 had superseded that of HIV in the US. With HCV and HBV deaths occurring disproportionately in middle-aged persons (Ly, 2012).Ihe prevalence of aminotransferase elevation In the general population in the NHANES 111 study was 7.9%—the majority of which could not be explained by alcohol consumption, V Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2iral hepatitis, or haemochromatosis. Aminotransferase elevation was more common in men compared to women (9.3% vs 6.6%), in Mexican Americans (14.9%),Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2
and In non-Htspanlc blacks compared to non-Hispanic whites (8.1% vs 7.1%). Unexplained aminotransferase elevation (69.0%) was strongly associated witSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2ulin, lower high-density lipoprotein (HDL); and type 2 diabetes and hypertension in women) and thus may represent NAFLD (Clark. 2003). Other studies based on histological sources (liver biopsy, autopsy, and postmortem series) Indicate that 10-40% (median ~ 20%) of the general population may have NAF Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2LD (including steatosis alone) and 2-5% have non-alcoholic steatohepatitis (NASH) (Falk-Ytter et al., 2001).Based on NHANES 111 data, the seroprevalenEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
ce of HBV surface antigen (HBsAg) or antibodies to HBV core antigen is 4.9% (McQuillan, 1999). HBV infection is more prevalent in non-whites than whitSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2underestimated (Kim, 2002). Approximately 240,000 new HBV infections occurred annually between 1988 and 1994 (Coleman, 1998), but in 1997 the estimated number of incident HBV cases was only 185,000.In both Europe and the US the Incidence of primary biliary cirrhosis (PBC) among adults (aged > 20 yea Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2rs) has been estimated to be between 2 and 3 per 100.000 persons per year, with a Strong female predominance. While the incidence has remained unchangEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
ed since 1995, the prevalence has risen, suggesting that the survival is longer, which may be due to early diagnosis (Kim. 2002).Ihe incidence of fulmSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2HAV), HBV, non-A non-8 hepatitis) was the most common aetiology of fulminant hepatic failure in the US. By the 1990s, drug-induced (especially acetaminophen) causes had become the most common cause of fulminant hepatic failure (Rakela, 1985; McCashland. 1996; Schlodt. 1999).Age-adjusted incidence ra Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2te of HCC increased from 1.4 per 100,000 during 1976-1980 to 4.7 per 100,000 during 1996-1997 (El-Serag and Mason, 1999). Asian-Americans have the higEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
hest incidence rates of HCC (up to 23 per 100,000 in Aslan men > 60 years of age), followed by African-Americans, whose Incidence is two to three timeSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2y 34,000 deaths annually (Kim, 2002; Kochanek, 2011).http //e-surg.com184 SÍCĨION6 LIVEREuropeIn the EƯ an estimated 29 million people have chronic liverdisease. Alcohol consumption, viral hepatitis B and c, and the metabolic syndrome are reported to be leading causes of liver cirrhosis and primary Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2liver tumours. Liver cirrhosis is responsible for around 170,000 deaths in Europe annually, with wide variations between countries—ranging from aboutEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
1 per 100.000 Greek women to 103 per 100,000 Hungarian men dying each year. The mortality rate from alcohol-related liver diseases is as high as 47 peSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 23). The mortality rate of primary liver cancer is very close to its incidence because of the lack of curative options for most patients (Blachier, 2013). The prevalence of NAFLD in the European population is 2-44% in the general population and 42.6-69.5% in patients with type 2 diabetes. The prevale Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2nce of chronic hepatitis c in the European population is 0.13-13.26%. whilst that of chronic hepatitis B is 0.5-0.7% (Anonymous, 2013; Blachier, 2013)Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2
.Liver anatomy and physiologyThe liver is the largest internal organ of the human body. It has a dual blood supply: the hepatic artery supplies oxygenSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2act, and also blood from the spleen and pancreas. Under normal circumstances the portal vein supplies approximately 70% of the liver’s blood supply and the hepatic artery is responsible for the remaining 30%. Blood from the hepatic artery and portal vein perfuse the liver sinusoids and is conducted Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2to the central vein of each liver lobule. Resistance to blood flow in the sinusoids Is low under normal circumstances. The central veins drain into heEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
patic veins that drain into the inferior vena cava. The endothelial lining of the hepatic sinusoids is fenestrated and discontinuous. Beneath this linSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2 found. The spaces of Disse connect with lymphatic vessels in the interlobular septa, allowing excess fluid to be removed.The liver plays a major role In metabolism, including plasma protein synthesis, carbohydrate homeostasis, lipid metabolism, and metabolism of toxins and drugs.Pathophysiology of Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2chronic liver diseaseLiver cirrhosisChronic liver injury results in fibrosis and, if unchecked, liver cirrhosis, defined as the histological developmeEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
nt of regenerative nodules, surrounded by fibrotic tissue that replaces normal hepatocytes. Fibrosis represents an excessive healing response to injurSECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2 secrete collagen. The collagen deposits (forming fibrotic tissue: liver fibrosis) separate isolated hepatocyte islands and portal vessels, resulting in impaired hepatocyte function. Liver fibrosis may progress to cirrhosis when the hepatic vasculature is significantly disrupted. The intrahepatic re Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2sistance to blood flow is Increased by fibrosis and regenerative nodules, andportal hypertension develops. Thus the portal pressure increases as a resEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
ult of an increased resistance to outflow through the liver (Gatta, 2008; Schuppan and Afdhal. 2008; Bosch, 2010; Thabut and Shah. 2010) (see Figures SECTION 6Liverhttp 7/e-surg comCHAPTER 19Liver disease: epidemiology, pathophysiology, and medical managementAndre De Wolf, Paul Marcin, and Hui'Hui T Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2c decrease in the production of NO and an increase in the production of vasoconstrictors, both a result of endothelial dysfunction (Iwaklri and Groszmann. 2007; Poordad, 2009; Bosch. 2010). This results In vasoconstriction of smooth muscle cells in the wall of hepatic and portal veins and venules an Ebook Oxford textbook of transplant anaesthesia and critical care: Part 2d of myofibroblasts located around the sinusoids and hepatic venules. Myofibroblasts are derived from stellate cells under cirrhotic conditions. It IsEbook Oxford textbook of transplant anaesthesia and critical care: Part 2
estimated that about 30% of the increased portal resistance is the result of hepatic vasoconstriction and impaired response to vasodilators. Finally,Gọi ngay
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