Fulminating Hepatitis B secondary to a lifetime use of IV drug abuse Research Paper

Fulminating Hepatitis B secondary to a lifetime use of IV medicine poke fun - Research Paper ExampleThis helps in identifying the initial treatment, as well as eliminating all contraindications to colorful-colored transplant. In addition, conducting proper prognosis helps in identifying patients who need a transplant and those who will survive without a liver transplant. Symptoms indueed by fulminant hepatitis B require immediate medical interventions to prevent further trauma on liver cells. However, in some patients, the condition is asymptomatic, which makes it difficult to detect. Patients of such nature may fiesta the condition to others unknowingly (Vandevante et al, 2011). Hepatitis B computer virus This paper looks into a case of a 51 yr old patient suffering from fulminating Hepatitis B as a result of prolonged intravenous drug abuse. The fulminant condition under consideration is as a result of hepatitis B virus. Currently, hepatitis B virus (HBV) is the leading cau se of fulminant hepatitis compared to other viral hepatitis. Hepatitis B virus attacks and replicates within hepatocytes. In harm of structure, hepatitis B virus has an outer shell and an inner core. The inner core bares the viral DNA, enzymes and proteins including hepatitis B virus core antigen (HBcAg) and HBVe antigen (HBeAg). The outer shell has the hepatitis B virus surface antigen (HbsAg), which is produced in excess by hepatocytes replicating the hepatitis B virus. ... In cases of acute HBV, a bigger number of viral DNA is cleared from liver cells by dint of a non-cytocidal process caused by inflammatory byproducts derived from CD8+ T lymphocytes. The release of inflammatory products occurs once CD+ T cells are stimulated by interferon-gamma and tumor necrosis factor-alfa, which are products of CD4+ T cells (Gish, 2009). The inflammatory byproducts lead to scratch off regulation of viral replication as well as triggering direct lysis of infected liver cells. The conclusio n of infected hepatocytes through lysis occurs due to action of HBV specific CD8+ cytotoxic T cells. Major destruction of hepatocytes in fulminant viral hepatitis is also as a result of host immune factors. HumoralAb response in fulminant hepatitis B is usually enhanced (Gish, 2009). This leads to an increased rate of HBsAG clearance from the liver. High level of anti-HBsAb is unvarnished in patients with fulminant hepatitis B on admission. Fulminating hepatitis B may either be hyperacute, acute, and subacute. In hyperacute, features present include encephalopathy within 7 days after the appearance of jaundice, and an increased rate of get intellectual oedema (Aspinal at al., 2011). Acute condition presents itself with jaundice to encephalopathy within8-28 days and a eminent risk of cerebral oedema. In subacutecondition, development of jaundice to encephalopathy may occur within 5-26 wks, and there is a minimal risk of cerebral oedema. Main clinical features in fulminating hepat itis B include encephalopathy, jaundice, and hepatocellular carcinoma. The liver may appear enlarged during the initial stages, but later reduces in size. Other conditions include cerebral oedema, renal failure, and