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The Pathophysiology of Hepatitis B - Term Paper Example

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The Pathophysiology of Hepatitis B
Hepatitis B, an infectious disease caused by the Hepatitis B virus (HBV, a DNA virus), was formerly called serum hepatitis, inoculation hepatitis and post-transfusion hepatitis. …
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The Pathophysiology of Hepatitis B
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Download file to see previous pages Infection with HBV may result in acute, fulminant or chronic hepatitis, sometimes even resulting in a chronic asymptomatic carrier state, apart from hepatocellular carcinoma and liver cirrhosis (Davis 179). The disease is transmitted when an individual comes in contact with infected blood or objects. It may also be transferred from an infected mother to her infant either during or after birth (Harrison, Dusheiko and Zuckerman 211). Transmission may also occur by accidental inoculation from infected needles and hospital equipment, intravenous drug abuse, body piercing, tattooing, and mouth-mouth kissing (Harrison, Dusheiko and Zuckerman 210). The risk of Hepatitis B is particularly high in individuals with multiple sex partners, and in homosexuals. The HBV virus occurs in morphologically different forms in the serum of infected individuals. HBV infection has an incubation period of about 75 days. Systemic symptoms of the disease include fatigue, fever, dyspepsia, arthralgia, malaise, and rash, while local symptoms include hepatomegaly, jaundice, dark urine, and pale stools (Davis 179; Harrison, Dusheiko and Zuckerman 210). Anatomical/physiological/biochemical changes that lead to the disease Hepatitis B results from cellular injury to the liver, subsequently affecting its metabolic functions. However, the HBV is not cytopathic by itself. The pathogenesis of Hepatitis B occurs as a result of the interactions between the host’s immune system and the virus. The host immune system targets HBV in liver cells (hepatocytes), inadvertently causing damage to the liver. HBV derived proteins (nucleocapsid antigens – HBcAg and HBeAg) present on the surface of infected hepatocytes are recognized and targeted by activated CD4+ and CD8+ lymphocytes, resulting in an immunologic reaction that leads to hepatocellular damage (Pyrsopoulos & Reddy; Harrison, Dusheiko and Zuckerman 221). The immune response against hepatitis B is T-cell mediated. These immune responses against infected hepatocytes result in liver cirrhosis or hepatocellular carcinomas. Damage to hepatocytes also manifests as spotty acidophilic necrosis and lymphohistiocytic lobular inflammation in the liver (UPMC). Anatomical/physiological/biochemical changes the disease causes Hepatitis B disease pathology is mainly a result of impaired liver function due to hepatocellular damage. The anatomical and physiological changes that result from HBV infection are arthralgia, cholecystitis, cholangitis, bradycardia, irritability, lethargy, jaundice, fever, erythema, nausea, spider angiomas, splenomegaly and bile duct obstruction in some cases (Turkington and Ashby, 148; Davis 181). Patients experience extreme fatigue and malaise, and discharge dark urine and pale stools. In addition, there is significant weight loss. Chronic hepatitis may result in liver cancers (hepatocellular carcinomas). The incidence of hepatocellular carcinoma is highest in individuals with HBV infected cirrhotic liver (Harrison, Dusheiko and Zuckerman 234). These cancers develop due to integration of viral DNA in host genome, apart from a variety of other factors. Biochemical changes as a result of HBV infection include elevated aspartate aminotransferase (AST) levels due to liver damage. Jaundice, a common symptom in HBV infections, results from impaired bilirubin metabolism in the liver. Bilirubin is a yellow pigment that results from the breakdown of hemoglobin. Hemoglobin breakdown mainly occurs in the hepatocytes, where the resulting bilirubin is converted into a water-soluble compound and excreted through bile into the gut. Impairment of the hepatocytes due to HBV infection prevents the liver from carrying out this function effectively. Inability to excrete bilirubin results in its redistribution ...Download file to see next pagesRead More
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