Comprehensive Guide to Pathophysiology and Treatment of Hepatitis B

Abstract

Table of Contents Title page1 Introduction3 Pathophysiology of Hepatitis B4 Pharmacological treatments for Hepatitis B6 Patient education considerations 7 Conclusion 8 Reference List……………………………………………………………………………………..9 Hepatitis B Introduction Hepatitis B is a liver inflammation attributed to alcohol use, drugs/toxins, autoimmune or viral infections. World Health Organization (WHO) defines Hepatitis B as a life-threatening viral infection caused by the hepatitis B virus (HBV). It is an infection that affects the liver leading to acute and chronic disease like liver cancer and cirrhosis that claims many lives (WHO, 2021). Hepatitis B virus is spread through direct contact with the victim, like a mother to child during birth and delivery, blood or other body fluids contact, especially during sex with an infected partner. The virus is also transmitted through exposure to sharp instruments like razor blades, needles, and unsafe injections that have been in contact with an infected person. According to W.H.O. (2019), 230,154 people were living with chronic hepatitis B (C.H.B.), representing 0.9% of Australia's population, a rate that has increased from 0.74% in 2004. W.H.O. estimates 1.5 million infections of hepatitis B and over eight hundred thousand deaths attributed to cirrhosis and liver cancer globally each year. However, WHO (2019) confirms that C.H.B. claimed 427 Australian lives, with 316 and 111 deaths attributed to hepatocellular carcinoma (H.C.C.) and cirrhosis consecutively. Unfortunately, hepatitis B infects all people regardless of age or gender. Children are more prone to chronic hepatitis B. Aboriginals and Torres Strait Islanders contact HBV more than non-indigenous Australians. The essay will offer a thorough discussion of pathophysiology, pharmacological treatments, and patient education consideration of hepatitis B to understand better the origin, impact, and prevention of hepatitis B. Pathophysiology of Hepatitis B HBV introduces physical and biological abnormalities in the affected body, thus the need to analyze how the virus is contacted or transmitted and its effects on the body. HBV is a D.N.A. virus of the Hepadnaviridae family (Mehta, 2021). It is a very hardy virus that can survive on any surface for up to a month but only affects human beings (Peters, 2019). HBV is detected in semen, vaginal mucus, saliva, serum, and tears. It is a virus transmitted sexually and parenterally when victims contact the body fluids or mucous membranes of the infected persons through blood transfusions/blood products, shared needles while injecting drugs, needle sticks, and hemodialysis (Mehta, 2021). The virus is also transmitted perinatally, where 90% of infants of HBeAg-positive women are at a higher risk of contracting infection and chronic Hepatitis B virus in the long run. HBV causes innate and adaptive immune response dysfunction, which involves monocytes, dendritic cells, natural killer cells, and T cells (Li et al., 2019). Monocytes found in peripheral blood and organ tissues are natural immune cells that play a significant role in the innate and acquired immune responses (Li et al., 2019). According to Li et al. (2019), HBV induces suppressive function of the natural and adaptive immune cells, potentially contributing to the persistent HBV mechanism. It is imperative to note that HBV stimulates monocytes' secretion of transforming growth factors while inhibiting the secretion of tumor necrosis factor, thus playing a significant role in the immune parthenogenesis of chronic persistent infection (Li et al., 2019). The higher the level of monocytes in HBV victims, enhance the production of inflammatory cytokines and chemokines, causing liver damage. HBV also induces myeloid-derived suppressive cells differentiation, directly inhibiting T cell response through mechanisms like arginase and indirectly influencing immunomodulatory function by inducing regulatory T cells (Li et al., 2019). N.K. Cells limits liver fibrosis through cytotoxicity of activated H.S.C. thus, the presence of HBV induces suppressive N.K. Cells in liver fibrosis, hence the need for vaccination to limit the occurrence of such physical and biological abnormalities. According to (Mehta, 2021), the incubation period of an acute HBV infection is roughly 12 weeks. Infected persons experience mild illness during this period, with less than 1% experiencing fulminant hepatic failure. For instance, during the prodromal period that occurs immediately after the incubation period, the patient expresses some symptoms like fatigue, malaise, and anorexia' Further experiences may range from right upper quadrant pain due to hepatic inflammation while others experience fever, rash, or arthralgias (Mehat 2021). Mehta further confirms that during the icetric phase, HBV victims develop jaundice and painful hepatomegaly with dark-colored urine and pale-colored stool. Unfortunately, after this phase, the patients experience rapid improvements in symptoms leading to fulminant hepatic failure after some days or weeks, with developments of prolonged illnesses in the long run (Mehta, 2021). It is imperative to note that after the acute infection resolves, most HBV adult and infant victims develop antibodies that fight against H.B. surface antigen. It is after this fight that such a victim ends up recovering fully. However, the percentage of HBV cases develop chronic infection, with about 20% of cases developing cirrhosis and hepatic decomposition and a smaller percentage developing hepatocellular carcinoma (Mehta, 2021). Chronic hepatitis B infection patients can develop positive HBsAg for life, while all H.B. virus infection has the presence of anti-HBc. However, the HBV vaccine helps individuals develop...