Reply separately to two of your classmates posts (See attached classmates posts, post#1 and post#2). INSTRUCTIONS: "In your reply to each of your peers, discuss content that you learned while explorin

POST # 2 KEEGAN

Note: For your reply, consider elaborating on the statement --- If inflammation is severe enough, bile in the blood will build-up from biliary stasis (Hubert & VanMeter, 2018).

The purpose of this discussion post is to discuss Case Study Three on hepatitis B and cirrhosis. This writer will describe the pathophysiology of acute hepatitis B, what serum markers remain high when chronic hepatitis B is present, and explain how cirrhosis develops from chronic hepatitis B. Hepatitis B used to be called serum hepatitis and is caused by HBV (the hepatitis B virus) (Hubert & VanMeter, 2018). A person can be contagious for HBV but remain asymptomatic: this is called a carrier state (Hubert & VanMeter, 2018). Hepatitis B typically has an incubation period of approximately two months, making this disease more complicated to track contacts and sources of the infection (Hubert & VanMeter, 2018). There can be a long while before either symptoms or elevated serum markers can be detected, however, HBV can still be transmitted during this time to others (Hubert & VanMeter, 2018). 

HBV infections are mainly transmitted through infected blood, nevertheless, it can be identified in various bodily secretions (Hubert & VanMeter, 2018). Intravenous drug use, hemodialysis, sexual transmission, tattooing, and body piercing have all been identified as means of transmission (Hubert & VanMeter, 2018). Healthcare workers can be at increased risk from exposure to body fluids and blood when proper precautions are not utilized (Hubert & VanMeter, 2018). Also, fetuses can contract HBV through pregnancy (Hubert & VanMeter, 2018). Today, there is an HBV vaccine used in healthcare professionals and routinely in children, which provides long-term protection (Hubert & VanMeter, 2018). For infected individuals, there is a temporary measure used, known as HBV immune globulin (Hubert & VanMeter, 2018).

HBV is a partly double-stranded DNA virus (Hubert & VanMeter, 2018). The Dane particle is what the complete and infective form of the virus (virion) is often referred to as (Hubert & VanMeter, 2018). The virion is a “42-nm spherical, double-shelled particle composed of small spheres and rods and with an average width of 22 nm” (Pyrsopoulos, 2018). HBV is highly resistant to extreme humidity and temperatures and works by invading the hepatocytes (Pyrsopoulos, 2018). 

HPV is comprised of three different antigens that stimulate the production of antibodies in the body (Hubert & VanMeter, 2018). These antigens are HBcAg (core antigen), HBeAg (core antigen), and HBsAg (surface antigen) (Hubert & VanMeter, 2018). These serum antibodies and antigens are valuable in both the diagnostic and monitoring process of acute and chronic hepatitis (Hubert & VanMeter, 2018). In early hepatitis B, high levels of HBsAg are produced by infected liver cells: when these levels remain high in the serum, the patient is at increased risk of “continued active infection and damage to the liver (chronic disease),” (Hubert & VanMeter, 2018, p.459).

The cell-mediated immune response to HBV damages the liver cells, which results in liver tissue and hepatocyte inflammation and diffuse necrosis (Hubert & VanMeter, 2018). If inflammation is severe enough, bile in the blood will build-up from biliary stasis (Hubert & VanMeter, 2018). Depending on the degree of inflammation, hepatic cells will either regenerate (if inflammation is minor) or the liver will form fibrous scar tissue (if inflammation is severe) (Hubert & VanMeter, 2018). Eventually, ischemia can occur if the scar tissue inhibits the liver lobule organization (Hubert & VanMeter, 2018). The early formation of scar tissue is called fibrosis, while severe damage is referred to as cirrhosis (Hep, 2019). Approximately 25 percent of infants and children infected with HBV, and approximately 15 percent of adults infected, will eventually die from either liver cancer or cirrhosis (Hep, 2019). 

Unfortunately, most individuals will not manifest symptoms until end-stage liver disease or cirrhosis onset (Hep, 2019). Cirrhosis can either be compensated or decompensated. If the liver continues to function relatively well, this is compensated cirrhosis (Hep, 2019). Symptoms include decreased appetite, dark urine, fatigue, peripheral edema, confusion, pruritis, jaundice, nausea, muscle cramping, clay-colored or pale stool, spider veins, weight loss, and erythema on the palms of the hands (Hep, 2019). Once cirrhosis moves into decompensation, the patient will be much more symptomatic with ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, variceal hemorrhage (Hep, 2019). It is essential to identify high risk groups and screen appropriately for HBV. Prevention and early intervention for this disease is of utmost importance.

References

Hep. (2019)., Cirrhosis and hepatitis B. https://www.hepmag.com/basics/hepatitis-b-basics/cirrhosis-hepatitis-b

Hubert, R. J., & VanMeter, K. C. (2018). Gould's pathophysiology for the health professions. St. Louis, MO: Elsevier Saunders.

Pyrsopoulos, N. (2018). Hepatitis B. https://emedicine.medscape.com/article/177632-overview#a3