The NHS Blood and Transplant Authority are responsible for providing a reliable efficient supply of blood, organs and associated services to the NHS (NHSBT, 2009). Therefore, the screening and testing of donors for blood borne viruses which can be transmissible to the recipients of their blood and tissues has to be intrinsic to the service to prevent any foreseeable harm.
As the NHS becomes more cost efficient, the Senior Nurse Practitioner (SNP) role was introduced six months ago (June 2009) with aims to develop into what has traditionally been a medical role. The counselling of donors who have been found to be serologically positive for one of the routinely tested infectious blood borne diseases (Hepatitis B, C, HIV, Syphilis and HTLV) has been identified as an area for professional development, as it will be the SNP's role to identify the positive donor, and by appointment inform them of their positive blood results and refer on to the appropriate specialists accordingly.
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According to the Health Protection Agency (HPA, 2009), Hepatitis B is the most prevalent of the blood borne viruses found in most new and regular donors in England. It is due to this prevalence that the purpose of this study is to investigate Hepatitis B and the effect this has on normal physiological systems to form symptoms and disease. The identification of the disease will be explained, and current treatment options will also be explored and again, how these interplay with the physiological system in order to treat the person infected.
The professional benefits of gaining the most thorough insight into this disease is to inform when having to manage, counsel, and answer any questions posed by donors who are found to be positive when routinely screened for this infectious disease. The case scenario of Cheung (anonymised) will be used to explore this journey. Due to the many outcomes of Hepatitis B (see diagram one on page three), and the limited word count, it is only feasible to analyse Cheungs' case, that is one of chronic hepatitis B infection (CHB).
Hepatitis B, according to the Free Medical Dictionary (2009) "is a potentially serious form of liver inflammation due to infection by the hepatitis B virus (HBV). It occurs in both rapidly developing (acute) and long-lasting (chronic) forms, and is one of the most common chronic infectious diseases worldwide".
What determines the classification to chronic infection according to the texts is if the infection lasts more than six months (Mosby, 2009, Porth, 2009). Ninety-five percent of sufferers according to Mosby, (2009), recover three to four months after initial infection, but the rest go on to become carriers or remain ill. Kumar And Clark (2009) expand on this statement, claiming suggested outcomes such as death, non-progressive hepatitis, regressive hepatitis, liver cirrhosis, and hepatocellular carcinoma (see diagram one on page three).
The factors that determine clearance or chronic infection according to Kumar and Clark (2009) include the person's individual ability to fight the disease (immuno-competence), the age of the person, and the virulence of the virus. These authors also identify some genetic factors relating to the presence of a MHC class two genotype which affects the hosts' ability to defend against such disease (p337).
(Reference: Kumar and Clark, 2009, p337)
In terms of HBV transmission, there are many routes explained in the texts. Overall, it appears there has to be some form of blood or bodily fluid contact to allow the HBV virus to spread. Questions can often arise about how the donor became infected, so to understand HBV routes of transmission is important (see appendix one for example document).
Included in the HBV transmission routes is vertical transmission, which is from mother to child in utero, during the birthing process, or intimate post natal contact (Underwood, 1994, p398).
Transmission can be occupational, found in health care workers who have had accidental needle stick/sharps injuries, blood and body fluid splash incidents taken from those infected with the virus (Porth, 2009, p961).
HBV can be obtained through lifestyle choices, such as practising unsafe/promiscuous sexual activities with those infected, and recreational drug use whereby the practice of sharing needles has taken place (Porth, 2009, p961). This risk can also be applied to the acts of having tattoos where re-useable instruments have been insufficiently sterilized (Underwood, 1994, p398).
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Transfer by iatrogenic means, through blood transfusions and organ transplantation is well documented, even though decreasingly so due to increased HBV screening technology and screening practices adopted within blood and tissue services (Underwood, 1994, Porth, 2009, p961). HBV risk can occur when someone is tested for HBV during the pre-seroconversion period and therefore found to be negative for the disease (Kardon,2009). HBV spread could also have occurred therefore prior to the HBV test being developed (The National Academy of Sciences, 2009).
Extending the iatrogenic risk factor further, acupuncture therapy has also resulted in reported HBV cases, again, caused by re-usable instruments that have been insufficiently sterilized (Kent et al, 1988).
The important finding of horizontal transmission is also listed in the texts. This is where through minor abrasions, sharing household articles (toothbrushes or children's toys) for prolonged periods has enabled transmission of HBV to occur (Underwood, 1994, Porth, 2009). HBV has been found to survive out of the body on surfaces for up to seven days (Centers for Disease Control and Prevention, 2009).
This latter means of infectivity is important as this rules out the traditional thought that Hepatitis B is spread through blood only, and therefore fortifies the argument that this disease should no longer be termed (confusingly) "serum hepatitis" which still appears prevalently in some older traditional texts and information sources (Anderson and Ness, 1994, Pamphilion, 1995).
Hepatitis B affects the liver's cells and therefore potentially its functions (Porth, 2009). According to the British Liver Trust (2009), the liver has over five hundred functions, ranging from fighting infections and diseases, destroying and dealing with poisons/drugs, filtering and cleaning blood, and producing bile and enzymes responsible for blood clotting. It can also store energy, sugars and vitamins including iron, and is involved in the production of cholesterol, and balancing hormones. It processes food once it has been digested, and because of it being made up of "stable cells" it can repair its own damage and renew itself (Lecture Notes, 2009).
By looking at Porth's (2009) diagram, it can be seen that if the liver starts to fail, what other physiological effects can occur (see diagram two). Approximately 80-90% of the liver has to be diseased before the liver begins to fail (Porth, 2009).
It is very important to know the liver' functions in its healthy state to help understand what happens when the organ becomes diseased, as some or all of these functions may be affected depending on the stage/severity of the disease, which would then cause the associated signs and symptoms (see diagram two).
Diagram Two: Reference (Porth, 2009, p971)
Initial symptoms of infection of HBV include fever, malaise, anorexia, nausea, vomiting, which then decline to leave jaundice, angiodema, urticarial skin lesions, and arthritis (Underwood, 1994).
When the virus enters the body, a series of inflammatory events take place. Fever, according to Bass et al, (2004) is caused by the release of "endogenous pyrogen" cytokines stimulated by the immune system in response to the virus. Examples of these cytokines, according to Bass et al (2004), include interluken-1 (IL-1) and 6 (IL-6), and Tumour Necrosis Factor (TNF). These act at the hypothalamus to increase body temperature. The rest of the systemic effects according to Bass et al (2004) are then probably mediated by cytokines (p86).
Cytokines are produced in immune response to inflammation, inflamed cells and injured cells (Bass et al, 2004), therefore pertinent to hepatitis and its subsequent cell injury. These circulating immuno-complexes can also explain the skin irritation/rashes associated with hepatitis B (Shomon, 2002). This is pertinent to Cheung, as during his "positive screen" interview, he presented with an unexplained skin rash.
Kent (2009) elaborates by stating that it is the release of lipo-polysaccharides from the cell wall of inflamed and damaged cells that triggers the immune system to produce the inflammatory cytokines (IL-1, IL-6, TNF). These released cytokines then act on the brain via the vagus nerves (Gohler, 2009).
A slow "transmission" pathway involving cytokines originating from the brain's choroid plexus and nearby circumventricular organs absorb into the brain via "volume transmission" (Gonsman, 2009). Peripheral cytokines may also enter the brain directly according to Banks, (2009). They may also induce the expression of other cytokines in the brain that cause malaise, fatigue, nausea and vomiting also known as sickness behaviour (Ban, 2009).
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Other than interleukins (which also mediate inflammation by communicating between white blood cells), there are other cytokines such as chemokines that promote chemotaxis, and interferons that have anti-viral effects (Martin and Leibovich, 2005). These are all important when recruiting help, mediating control, and eradicating foreign substances (Martin and Leibovich, 2005). This also explains why interferons are used as suitable treatment options for Hepatitis B (discussed further in the latter chapter), as they have been found to work by shutting down protein synthesis in host cells (Le Y, et al, 2004).
Further inflammatory responses include the production of eicosanoids, synthesised in the cell wall during times of cell trauma or by stimulus such as those from cytokenes and other growth factors (Wikipedia-Immune System, 2009). Eicosanoids include prostaglandins that have responsibilities for producing fever and the dilation of blood vessels associated with inflammation, and leukotrienes that attract white blood cells (leukocytes), which the cytokines then go on to mediate (Martin and Leibovich, 2005).
In terms of the jaundice, oedema, urticarial skin lesions, and arthritis, some of these can be explained by looking at Porths, (2009) previous diagram (diagram two), which describes the consequence of liver disease, thus affecting protein synthesis (causing oedema). Cell necrosis reduces the liver's ability to metabolise and excrete bilirubin leading to a build up in the blood (causing jaundice). Unfiltered blood with circulating immune complexes such as immunoglobulins (G and M), as well as surface antigens and liver enzymes, are suggested in the cause of arthritis (Pease and Keat, 1985), and skin problems alike (Shomon, 2002).
At a cellular level, Hepatitis B is the only hepatitis virus that contains deoxyribonucleic acid (DNA), in that other hepatitis viruses contain RNA only (Underwood, 1994). The function of DNA is that of cell replication giving the virus the ability to control in this case, the liver cells own ability to live and reproduce (Porth, 2009).
Microscopically, the virus is made up of several antigen fragments that stimulate the body's immune system to produce the antibodies that destroy the virus (and thus the liver cell). It is this immune reaction, not the virus, which appears to cause the liver inflammation, or at least the carrier state if there is insufficient immune response (Underwood, 1994).
Diagram Three (Reference: http://upload.wikimedia.org/wikipedia/commons/8/8c/HBV )
In terms of pathogenesis, HBV virions (known as Dane particles) bind to the host hepatic cell and are then internalised by endocytosis (Kumar and Clark, 2009). After this penetration, the virus loses its outer coat and the virus core is transported the cell core without processing (p336). Once the virus infects the liver cell the viral replication occurs. This is when the HBV surface antigen can be detected as it expresses itself on the liver cell wall, and thus provokes the inflammatory response which destroys the cell (Underwood, 1994, Kumar and Clark, 2009). It is the adaptive immune system that responds, particularly virus-specific cytotoxic T lymphocytes (CTL's) (Porth, 2009)and this reaction causes most of the liver injury associated with HBV infection. These kill infected cells, producing the antiviral cytokines capable of purging HBV from viable hepatocytes. CTL's also eliminate the virus (Iannacone et al, 2007).
Hepatitis B is one of a few known non-retroviral viruses which use reverse transcription as a part of its replication process (Beck and Nassal, 2007). The virus gains entry into the cell by binding to an unknown receptor sited on the PreS1 and PreS2 surfaces of the HBV cell (see diagram three on page 9) (Kumar and Clark, 2009). Because the virus multiplies via RNA made by a host enzyme, the viral genomic DNA has to be transferred to the cell nucleus by host proteins called "chaperones" (Bruss, 2007).
The partially double stranded viral DNA is then made fully double stranded and transformed into closed circular DNA that serves as a template for transcription of further mRNAs (Bruss, 2007). The largest one is used to make the new copies of the genome and to make the "capsid" core protein and the viral DNA polymerase enzyme (Kumar and Clark, 2009).
According to Beck and Nassal (2007), these four viral transcripts undergo additional processing and go on to form progeny virions which are released from the cell or returned to the nucleus and re-cycled to produce even more copies. The long mRNA is then transported back to the cytoplasm where the virion P protein synthesizes DNA via its reverse transcriptase activity (Kumar and Clark, 2009, Beck and Nassal, 2007).
Translation into HBV proteins as well as replication of the genome takes place in the endoplasmic reticulum (Kumar and Clark, 2009). They are then packaged together and exported from the cell. There is an excess production of non-infective HbsAg particles which are expelled into the circulation. As the liver cell is destroyed the HBV cells components are then also expelled into the circulation (Kumar and Clark, 2009).
In terms of clearance of the virus, this is facilitated by the adaptive immune system CTL's which recognise the foreign HLA class 1 (surface antigen) on the hepatocytes. Responses involve further interlukens and gamma interferon (Kumar and Clark, 2009) which inhibit viral replication (Schoenborn and Wilson, 2007).
If the person is unable to clear the virus due to the reasons explained in page two, the following processes take place. Viral persistence with some but poor immune response causes healthy but inactive chronic HBV (Kumar and Clark, 2009). A better but not complete immune response unfortunately results in further hepatocellular damage resulting in chronic (unhealthy) hepatitis. This involves a disease process whereby the HBV remains actively replicating, with inflammation, and the person is highly infectious (Kumar and Clark, 2009).
Along with replication, Kumar and Clark (2009) also identify integration. This is where the HBV DNA becomes integrated into the hosts liver DNA and the viral genes are transcribed along with those of the hosts (p336). This can develop into cirrhosis, and Hepatocellular Carcinoma (HCC) in later stages. What is also proposed is that p53 induced apoptosis is affected leading to an increase of abnormal cells which then leads to the HCC (REVEAL study, cited in Kumar and Clark, 2009, p336).
The process of being informed of a positive donor within the NHSBT's is by the National Testing Centre (NTRML) (see appendix two for Cheung's blood report). The process of testing within the NHSBT is complex, but can be simplified as following.
Donors give blood samples with their donation. There has to be negative results in all samples before the donated tissue/component will be released. If there is a positive result the same test is undertaken three more times (locally). If it flags up as negative, the donation is released. If it flags up as a further positive, it is treated as positive. The samples are then sent to NTRML (in Colindale, the NHSBT's National Testing Centre) whereby two further tests are carried out using different testing kits. If they are negative - the donor is classed as being falsely positive, and is informed and re-tested in a further three months. If the donor is positive, NTRML carry out further testing again using several testing kits, and several tests to gain an insight into the status of the disease.
The most commonly used tests used to detect HBV within the NHSBT are the Enzyme-Linked Immuno-Sorbent Assay (or ELISA or EIA), developed for use in 1971 (BloodBook.com), and the NAT (nucleic-acid amplification test), developed for use in 1999 (BloodBook.com).
It can be seen by the report (see appendix two), NHSBT tests for HBV include, HbsAg (an ELISA test), HBV DNA (a NAT test), HbeAg (ELISA), antiHBe (ELISA), AntiHBc (ELISA), antiHBs (ELISA). These shall be explained in the following chapters.
The ELISA can be performed to evaluate either the presence of antigen or the presence of antibody in a sample, and is a biochemical technique used mainly in immunology (Lequin, 2005). The NAT test employs a form of testing technology that directly detects the genetic material of viruses (Strong, 1999).
The NAT test has been questioned as costly and time consuming (Strong, 1999). It proves its worth because NAT testing according to Sowadsky, (1999), detects the genetic material of a virus, instead of having to wait for the human body's response to a virus the formation of antibodies against it. It therefore offers the potential advantage over the current tests of reducing the window period, thus further improving blood safety. In comparison, NAT testing shortens the average window periods by weeks, making NAT testing for HBV a higher priority in screening the blood supply (Sowadsky, 1999). This can obviously have a positive effect on the frequency of blood donation, and its subsequent release of products (Strong, 1999).
Because NAT testing is very complicated and difficult to do, individual testing of donor's blood is not efficient (Strong, 1999). It is made efficient by pooling together multiple samples of blood, and then performing a NAT test on the pooled samples. If the pooled sample is found to be positive, further tests are done to try to determine which individual sample (in that pooled sample) is the potentially infected sample.
In terms of testing, it is beneficial to know the serological events of the HBV disease process, as to understand this is important when having to analyse blood reports against the norm.
Diagram Four (Reference: http://en.wikipedia.org/wiki/File:HBV_serum_markers.png)
The above diagram denotes the time course of serological changes that can be seen following acute infection with hepatitis B virus and healthy clearance.
The "time course" of the serological changes seen following infection with hepatitis B virus and healthy clearance starts with acute infection, where the antigen HBsAg appears in the blood (from about 6 weeks to 3 months) and then disappears. (Kumar and Clark, 2009).
It can be seen that HBeAg rises early and usually declines rapidly in a similar time period. Anti-HBc is the first antibody to appear and high titres of IgM anti-HBc suggest an acute and continuing viral replication (Kumar and Clark, 2009). Antibodies (Anti-HBs) appear late indicating immunity. These can persist for many months (ibid).
IgM anti-HBc may be the only serological indicator of recent HBV infection in a period when HBsAg has disappeared and anti-HBs is not detectable in the serum (Kumar and Clark, 2009). Anti-HBe appears after the anti-HBc and its appearance relates to a decreased infectivity (ibid).
With chronic hepatitis, the HBsAg persists and therefore indicates a chronic continuing infectivity (Kumar and Clark, 2009). HBeAg persists and correlates with increased severity and infectivity and the development of chronic liver disease. When anti-HBe develops (defined as the point of HBV seroconversion) the HBeAg disappears and there is a rise in ALT (altered liver enzymes) indicative of liver disease. HBV DNA presence would suggest continual viral replication (Kumar and Clark, 2009). For a summary of the clinical status for HBV, see table one below.
Reference The Cleveland Clinic (2009):
In Cheung's report (see appendix two) it can be seen that there is a positive (reactive) result for NTMRL EIA's 1 and 2 (surface antigen tests by two testing kits) indicating HBV infection. The total anti-HBc (anti-HBc (T) EIA) result is also positive, but the IgM antibody (anti-HBc (M) EIA) is negative, this absence according to Martin (2009) indicates chronic infection. The anti-HBe result is positive but HbeAg is negative (indicating that seroconversion has taken place). The HBV DNA test is positive, indicating current infection. The outcome using the above literature information to interpret is therefore that of a positive chronic carrier state.
Chronicity of Hepatitis B can be active or inactive (Kumar and Clark, 2009). In terms of Cheung, because he has a negative HBeAg result, implies he has chronic "inactive" HBV infection, but due to him being positive for the HBV DNA implies a state called "e" antigen chronic HBV (Martin, 2009). This can be explained as following.
According to Martin (2009), the term "healthy carrier" has fallen out of favour because chronic HBV infection, even in the absence of clinically overt liver disease, conveys an increased risk of hepatocellular carcinoma. This author elaborates to discuss how reactivation of HBV replication, either spontaneously (or iatrogenically induced by chemotherapy or immuno-suppression), can lead to severe liver disease (ibid).
Another important issue is to consider according to Martin (2009) is whether the patient has detectable HBV DNA in serum, as in Cheung's case. Although "e" antigen was for many years the serum marker of HBV replication, it has become apparent that although many chronically infected patients shed "e" antigen in response to host immune pressure (Kumar and Clark, 2009), and they may have persistence of replication. This form of HBV, called "e" antigen chronic HBV typically occurs after many years of infection (Martin, 2009).
Martin (2009) proposes that recent literature has also drawn attention to the insensitivity of serum amino-transferases (liver function tests) in excluding hepatic inflammatory activity. A number of reports have described substantial inflammatory changes and fibrosis in patients with chronic HBV infection and normal liver chemistries but persistent serum markers of replication, including HBV DNA (ibid).
Therefore, an important additional diagnostic test in this patient is a serum HBV DNA, again justifying this previously mentioned costly practice. If serum HBV DNA is absent, the patient is in the inactive carrier state and requires monitoring. If serum HBV DNA is present, the patient has "e" antigen chronic HBV infection. Irrespective of the presence or absence of detectable HBV DNA, these patients require regular follow-ups and monitoring for hepatocellular carcinoma and reactivation of HBV replication (Martin, 2009).
In terms of treatment options, this does not form part of the SNP's role, as NHSBT does not become involved with treatment for HBV, but in case of questioning by the donor, it is important to have some understanding in order to alleviate anxiety.
The decision of whether to start treatment should be based on careful patient evaluation, blood tests, and sometimes a liver biopsy (Kumar and Clark, 2009). Studies show that the current treatments appear to be of greatest benefit to those who show signs of "active liver disease". These would include those with elevated liver enzymes (ALT), Positive blood tests for Hepatitis B virus (HBsAg) and Hepatitis B e-antigen (HBeAg), and elevated levels of hepatitis B DNA (Kumar and Clark, 2009, Martin, 2009). Ordering a liver biopsy to help decide whether treatment is needed can be undertaken, but this practice is not as common as it used to be (Hepatitis B foundation, 2009).
Table2: Suggested follow-up for patients not considered for treatment:
â€¢ HBeAg-positive Chronic HBV (CHB) with HBV DNA â‰¥20,000 IU/mL and normal ALT
o ALT every 3-6 month
o Consider liver biopsy examination and/or treatment when ALT levels become
â€¢ HBeAg-negative CHB with HBV DNA â‰¥2,000 IU/mL and normal ALT
o ALT every 3-6 months
o Consider liver biopsy examination and/or treatment when ALT levels become
â€¢ Inactive carrier state
o ALT every 6-12 month
o If ALT levels become increased, check serum HBV DNA and exclude other
causes of disease
Reference : Hep B Treatment Algorithm: http://www.hepb.org/pdf/treatmentalgorithm08.pdf (p95)
Treatments for chronic Hepatitis B are dependent on whether the condition is active or inactive, thus determined by continued further testing and monitoring of liver disease.
Table 3: Recommendations for Treatment: HBeAg-Negative Chronic HBV (CHB):
HBV DNA ALT Treatment Strategy
<2,000 Normal â€¢ No treatment; majority are inactive
â€¢ Monitor every 6-12 months
â€¢ Consider therapy in patients with
known significant histologic disease,
even if low-level replication
â‰¥2,000 Normal â€¢ Consider biopsy; treat if disease
present. In the absence of biopsy,
observe for rise in serum ALT levels.
â€¢ If treated, entecavir, tenofovir, or
peginterferon alfa-2a preferred
â‰¥2,000 Elevated â€¢ Entecavir, tenofovir, or
peginterferon alfa-2 preferred
â€¢ Long-term treatment required for oral agents
Reference: Hep B Treatment Algorithm: http://www.hepb.org/pdf/treatmentalgorithm08.pdf (p101)
Entecavir and Tenovir are oral treatments which belong to a category known as reverse transcriptase inhibitors (Kumar and Clark, 2009). These work by inhibiting the reverse transcriptase activity, the viral DNA polymerase enzyme that retroviruses need to reproduce (previously mentioned in page 10), and is a long term oral treatment (Kumar and Clark, 2009).
Peginterferon alfa-2 is a subcutaneous treatment (also known as pegasys) and is the current drug of choice according to the Hepatitis B Foundation (2009, see table three). This has a dual action, both antiviral and on the immune system. Two large international trials included more than 1500 people with chronic hepatitis B who were treated with pegasys (including people with the HBeAg-positive and the HBeAg-negative variations of chronic hepatitis B). Hepatitis B patients treated with pegasys had higher rates of response than with oral treatment in these common tests of hepatitis B infection (Assy et al, 2004).
Effects included a reduction in viral load (therefore a suppressed HBV DNA response) the measure of how much virus there is in the blood and therefore how active the infection is in the liver. Normality of ALTs, bringing liver enzymes back to normal and therefore a good indication of the liver's health (Assy et al, 2004).
In terms of prognosis, the outcome of HBV is variable, but treatments have improved survival (Kumar and Clark, 2009). Cirrhosis is associated with a poor prognosis, so for chronic sufferers as referenced in table's two and three (page 19), it is evident that monitoring for this needs to be part of the treatment aim. Because HCC is also associated with chronic cases, the plan should again depend upon keen monitoring, treatment when necessary (if in a state of reactivation), and promoting a good healthy lifestyle to the sufferer, as a poor lifestyle could contribute to an even less favourable prognosis (Kennard, 2006).
With all "positive screen" interviews (see appendix one for example profile) there is an element of risk assessment, which aims to detail anyone else who could be at risk, including partners, children, siblings, or significant others, to enable efficient information giving and inclusion of others as a part of the referral information. Occupational risks are also assessed, in case the donor has had close contact or invasive contact with other people. A look back into their medical history is undertaken with an attempt to ascertain the origin of the infection, and possible transmission routes so information can be provided. In the case of HBV, there is also a chance to note alcohol intake.
Overall, this is an important and accountable act, as it does lead on to the referral of others who have been in some sort of contact, and is a chance to notify, offer immediate advice such as health promotion, as well as track any previous donations and begin a "look back" exercise if deemed necessary.
Cheung, a twenty-two year old male, enrolled as a blood donor in June 2009, and was found to be HBV positive on his first donation so no "look back" was required. From his positive donor screen, he was from China, a country endemic with HBV (Porth, 2009), but emigrated to this country with his parents when he was twelve years old. Cheung could remember having childhood jaundice but was a little vague. He was newly married, and he and his partner were trying for a child and were immediately advised to stop and begin the use of contraception. The referral therefore needed to include this information to help in the next stage.
The end point for the SNP role is that of referral to the relevant liver specialist, and notifying the donor's GP. Although it is difficult to comprehend this end point as a nurse, who is used to treatment and caring, it is never the less imperitive that within this service, a safe supply of blood and tissues is maintained, and that referred donors receive the best possible "within limitation" care.
In conclusion, this essay has enabled me to take an in-depth look at Hepatitis B, to be able to be informed to effectively counsel such a case, answer any questions, and hopefully reassure. Not included within this essay are such essential factors as effective communication, as it is hoped that to be able to work at such a senior level would imply that these skills are already in place. During such scenarios, the use of Heron (2001) is employed, especially the cathartic intervention, as well as Egans (1998) SOLER skills which enable the conveying of information, listening, and help release emotion and build trust. What was lacking was the in-depth patho-physiology that underpins such information, which this essay (and module) has definitely helped to achieve.