The Implications of Social Issues in Health and Social Care

This essay will discuss how society can impact health and wellbeing through the influence of socio-economic factors. These factors will be used to give a broader representation of reoccurring trends of health and illness in society to develop a depiction of inequality and poverty in society.

Health inequalities describe the differences in health status and in people accessing healthcare provisions, they arise between different populations in geographical areas, ethnic groups and social classes (Barry and Yuill, 2008). Focus will be given in this picture to understand the health experiences of women in poverty using a variety of theories recognise how groups and behaviours can become deviants in society and look at ways to reduce stigma around these experiences by raising awareness and education.

In 1980 The Black Report was commissioned; the purpose of the report was to investigate and determine the causes of inequalities in the UK. The lifestyles and health records of people from all backgrounds and social classes were analysed. The report’s discoveries were that health improvement between social classes had not been equal and that the gap was widening. It was uncovered that the problem was driven by social and economic factors such as income and poverty (Socialist Health Association, 2005).

In 2008, the Secretary of State of Health requested Sir Michael Marmot to chair an independent review to recommend effective approaches to decrease health inequalities in England. ‘Fair Society, Healthy Lives’ was the final report and  published in 2010, it determined for health inequalities to reduce in society six policy aims would need to be carried out;

‘to give every child the best start in life, enable all children, young people and adults to maximize their capabilities and have control over their lives, create fair employment and good work for all, ensure a healthy standard of living for all, create and develop healthy and sustainable places and communities and to strengthen the role and impact of ill health prevention’

(Marmot, 2010). It was established that the higher socio-economic position a person has in society, they have a better opportunity of life chances and more prospect to lead a prosperous life resulting in better health (Marmot, 2010). Throughout all the reports on health inequalities since The Black report in 1980 there is a devolution and a running theme that socio-economic background and health are linked; the more privileged people are socially and economically, the better their health and the higher life expectancy (Matthews, 2015).

Race and ethnicity are increasingly being used as variables in health research (Audit Commission, 2004). It has been recognised that ethnicity has an impact on the social distribution of health, this is a serious issue. It is suggested in research that on average persons from black and minority ethnic backgrounds show larger levels of poor health than the general population (Barry and Yuill, 2008). It has been suggested that this may be in relation to inequalities in life chances, such as housing, employment and education leading to poverty. For instance, as late as the 1970’s landlords could advertise property with one of the provisos of tenancy being ‘no blacks’, overt racism was a major factor before the Racial Discrimination Act in 1975 (Matthews, 2005).

Issues surrounding education leading to inequality can be linked with lower academic achievements, there is research to suggest that in particular women that are of ethnic minority graduates are less likely to be employed due to institutionalised racism and incomes are generally lower than those of white people (Larkin, 2011).  Income poverty is identified as one of the key determinants of health leading to lack of resources, lack of income can lead to destitution with an inability to afford essentials such as food, clothing, rent and fuel which are all essential for good health (Blenkinsopp et al., 2016). Those in destitution are said to use radical methods as coping strategies to economise such as skipping meals in order to afford other essentials, which often lead to malnutrition and cheap fast food cultures reducing life expectancy due to ill health. It is said that those in poverty have a reduced life expectancy of 25 years compared to the rich in society as a result of income (Pickett and Wilkinson, 2014).

Women in all ethnic groups have lower incomes than men in the same ethnic groups, Pakistani and Bangladeshi women have the largest gap and Chinese and Black Caribbean women the lowest. Poverty rates are higher for women in all ethnic groups compared to White British men, Pakistani and Bangladeshi women having the highest poverty rates at around 50 percent and a higher proportion of Black African and Black Caribbean women being lone parents at around 18 percent compared to 6 percent of all women in other groups (Nandi and Platt, 2010).

The ethnicity pay gap is a long-standing phenomenon, research suggests that people from ethnic minorities tend to earn less than white people this is often associated with social disadvantage and arguably caused by discrimination. New arrivals to the country may experience language barriers, possess qualifications that are not recognised and be unfamiliar with the countries culture, these factors all affecting pay. Immigrants entering the United Kingdom are often in low paid jobs and are over qualified for the job they do (Brynin and Longhi, 2017).  However, this is seen to be rectified by the more time immigrants spend in the country they gain the necessary knowledge, connections and skills to move into their desired occupation and earn higher salaries (Matthews, 2015).

Feminist theories would argue that women are disadvantaged due to structural oppression and inequality as a result of capitalism, patriarchy and racism. Women are significantly oppressed economically due to the gender wage gap which shows that men typically earn more than women for the same work. An intersectional view of this also reveals that women of colour are even further penalised relative to the earnings of white men.  Social feminists agree with Karl Marx and Marxist theories that the working class are exploited because of capitalism, but they extend on the theory by arguing that the exploitation is not just due to class but also gender. Although, they offer the insight that not all women suffer oppression in the same way and that the same forces that work to oppress women also oppress people of colour and other marginalised groups (Crossman, 2019). Karl Marx and his Marxism theory criticises capitalism as an economic system but also in terms of the social conditions associated with it. He identified that at the heart of capitalism there is a class struggle between the bourgeoise and the proletariat. The bourgeoise owning the means of production and the exploitation of their workers by paying them less than the value of their labour allowing them to extract surplus profits. His theory explains that the proletariat have no other choice than to accept the conditions through pressure and ideology, as a communist he believed that the proletariat should have a revolution and overthrow capitalism (Tutor2U, 2018).

As ethnic and racial identities and their social economic factors have implications on health it is important to have focus on drives for positive improvements for these diverse communities. Increased awareness and understanding can improve well-being and the delivery of health services through improved engagement and targeted resources (Cosford and Toleikyte, 2018). This can be addressed by means of empowering and advocating individuals to take charge of their health in ways of educating them through health promotion and preventative interventions working collaboratively with individuals to improve their health and access health services (Thompson, 2006).

It is well known that people with disabilities have poorer health than their non-disabled peers and die at a younger age, these differences are to an extent unavoidable and therefore are defined as health inequalities (Turner, 2017). People with disabilities often have unmet health needs partly due to difficulties in identifying and treating symptoms. On average the life expectancy of women with disabilities is eighteen years shorter than women in the general population (NHS Digital, 2017). Allerton and Emerson (2012) analysed data to investigate the premature deaths of adults with a chronic health condition or impairment and it was discovered that fourty percent of people with a disability reported difficulty in using health services compared to only eighteen percent of people without a chronic health condition or impairment. A number of factors are identified as causing barriers to disabled people accessing healthcare and creating health inequalities such as a lack of accessible transport links, anxiety or lack of confidence for people with a disability, lack of understanding from health care professionals and failure to make a correct diagnosis (Mencap, 2016).

It has been uncovered that the determinants of health inequalities in disabled people are caused by social influences, disabled people having a disproportionate risk of being poor with an income of below sixty percent below the national average. Additional living costs and benefit dependency being key reasons for this (Turner, 2017).  Disabled people are twice as likely to be unemployed as those without a disability or more likely to be in part-time, low status jobs with less security and regard for human rights (Allerton and Emerson, 2012). Disabled women are more likely to be in poverty than disabled men by twenty five percent. Women with disabilities make up only one and half percent of the populations work force, facing both stereotypes about people with disabilities and women in the workplace. Both are viewed as less capable in the workplace making them less likely to be employed, there are other barriers present such as work spaces not being accessible and policies that are against those with disabilities. Without employment in spaces that are accessible women with disabilities are forced into a benefit culture keeping them impoverished (World Health Organization, 2018) Many people with disabilities do not receive appropriate education, their education opportunities are limited due to others perceptions of their abilities rather than their actual abilities, this is especially prevalent in girls due to stereotyping and stigma which prevents them from accessing higher paid jobs later in life without education to prepare them for later in life girls with disabilities are less likely to obtain secure employment that pays well enough to lift them out of poverty (Edmonds, 2016).

The social model of disability identifies that social exclusion from society, negative attitudes and systematic barriers are the cause of disability rather than a health condition or impairment, meaning society is the main contributing factor in disabling people. It looks at ways of removing barriers that restrict life choices for disabled people (Disability Nottinghamshire, 2019). Health research about disability and impairment is dominated by positivist theories, focusing on ways to reduce impairments it examines environments as well as the individual. However, functionalists theories emphasise on the role of medicine to cure and to maintain normal functioning within society. Within this theory there is focus on the ‘sick role’ involving compliance and wanting to get well, this can make people with disabilities seem to be deviant. The link between disability and social deviance that functionalists make influences health care and supports dominance of professionally controlled health and welfare services for people with disabilities devaluing individuals (Oliver, 1998).

There is evidence to suggest that a proportionate amount of people with disabilities do not access health checks due to barriers, studies have shown that health care professionals can vastly improve this through empowering and encouraging individuals to attend appointments by reminding them and facilitating follow up phone calls (Mencap, 2016). Service delivery can be improved by making a range of modifications and adjustments, to facilitate access to health care services by means of changing the layout of services making them accessible to people with mobility issues or communicating information in formats that are accessible such as braille. People with disabilities can be empowered to maximize their health by providing peer support, information and training (World Health Organisation, 2018).

In conclusion, it has been highlighted that health inequalities across social classes are hugely impacted by socio-economic factors in society, reducing access to health services and therefore having an impact on health, poverty particularly having an adverse effect. Race and ethnic minorities have been discussed and how institutionalised racism and discrimination play a huge part in influencing health.

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Stroke is a global problem of the increasing elderly population. According to the Department of Health (2007a), stroke is the third leading cause of death in the UK, with more than 110,000 individuals falling victim to a stroke each year at a cost to the National Health Services exceeding £2.8 billion. The Stroke Association (2007) places this number at 130,000 with a mortality rate at 67,000 per year, including indirect costs of £1.8 billion and costs for informal healthcare following stroke at £2.4 billion. Incidence of stroke is equally as prevalent elsewhere, such as in the United States where, as the third leading cause of US deaths (Becker & Wira 2006; Nolan & Naylor 2003) stroke is the leading cause of disability (Becker & Wira 2006; Stroke Association as cited by Amber 2003, p. 316; Stroke Association 2007). Becker and Wira (2006) state the incidence of stroke within the United States is 400,000 individuals per year with an anticipated growth to over 1 million yearly stroke victims by 2050. The American Stroke Association (as cited by Amber 2003, p. 316) states “every 45 seconds, someone in America has a stroke. Every 3.1 minutes, someone dies of one.”

Nolan and Naylor (2003) state an average of 35,000 individuals suffer strokes when hospitalized for other unrelated illnesses. Such was the case for Ms. C., who suffered an ischemic stroke while hospitalized for a pacemaker implant.

As the unit nurse assigned to care for Ms. C., subtle signs of her stroke were noticed and reported to the Code Gray


^[1]

team for immediate response. The many roles of a unit nurse in the presence of a crisis are vital in providing adequate care to her patient, including the need to maintain a calm demeanour in the face of chaos. A number of rapid physical assessments must be performed including the use of the FAST criteria


^[2]

(Mathiesen et al, 2006), response teams must be alerted and the nurse must keep the patient calm and oriented throughout the flurry of activity that can easily upset an elderly individual. While all emergencies call for rapid response, it is even more critical in the case of stroke when, if the patient is eligible for recombinant tissue plasminogen activator (t-PA)


^[3]

a detailed physical history and examination, a neurological assessment, computed tomography (CT) scan and additional blood work must be performed before irreparable damage from the stroke occurs.

With a focus on patient impact and nursing interventions, this paper will present the case study of Ms. C.

Case presentation

Ms. C., a 78-year-old, ambulatory, Caucasian female was admitted to the hospital for the replacement of a cardiac pacemaker. Ms. C. was widowed 5 years prior to her current hospitalization and lived alone having two married children living in Scotland and Wales. Prior to admission Ms. C. was diagnosed with high blood pressure (HBP), high cholesterol, was diabetic, and was on pharmaceutical medication for all three conditions. In spring 1995, Ms. C. had recurrent bouts of tachycardia alternating with bradycardia. Following an attempt to control the situation through pharmaceutical intervention, her cardiologist recommended she receive a cardiac pacemaker; which was implanted without complication the same year. She reports remaining in good health since that time; although additional medical notes indicate the onset of dementia, as she appears confused at times.

Upon admission, vitals were normal, with the exception of her blood pressure (BP) which was 175/95. Her physician ordered Ms. C. be started on Losartan


^[4]

. Subsequent vitals indicated a fluctuation in BP ranging from a low of 170/90 at 1AM to a high of 195/110 at 10AM. As Ms. C. was not responding to medication or fluid balancing recommended by her physician and her BP continued to climb, her cardiologist postponed surgery until her BP was brought under control. At 11:48am, when taking Ms. C.’s vitals, she appeared confused, her speech was slurred, there was slight facial droop and she could not extend her arm for the blood pressure cuff. At 11:50am a Code Gray alert was sounded.

Impact on the patient

When assessing the impact to the patient when a stroke occurs, the nurse must be aware of the implications on a variety of levels, including biological, psychological and sociological. In the case of Ms. C., there were additional implications for each of these due to the combination of her low-level, yet progressive dementia.

Biological changes in an ischemic stroke (confirmed by the CT scan as opposed to hemorrhagic) were the result of a thrombolytic occlusion at the cerebral artery branch point due to atherosclerosis. On the cellular level, neuronal damage occurs when neurons become depolarized and allow for inordinate amounts of calcium to cross the cellular membrane that ultimately leads to a destruction of said cellular membrane and other structures within the neuron (Becker & Wira 2006). Becker and Wira (2006) also comment on the neuronal damage caused by free radical, arachidonic acid and nitric acid generation that takes place during the ischemic cascade


^[5]

. Genetic activation also takes place and leads to the production of cytokines in response to and as a cause of inflammation that can “consume” the ischemic penumbra (Becker & Wira 2006). If one can limit the degree of injury to the ischemic penumbra located within the origami, the degree of permanent damage due to the ischemic episode is limited and is the goal of immediate stroke response (Becker & Wira 2006).

A combination of diagnostic laboratory tests


^[6]

and rapid nursing assessments would be required to assess the level of damage. Although the Code Gray approach is geared towards rapid response to allow for administering t-PA within the three-hour window, Ms. C. was not eligible for t-PA treatment due to her uncontrolled hypertension (Bonnono et al. 2000, p. 300).

The psychological impact on Ms. C was the most dramatic as her post-stroke status left her more confused and fearful than one might find in a strike victim due to the comorbid dementia. In addition to being frightened of the unknown and feeling very alone as a widow and without her children present, Ms. C. felt betrayed by her body and didn’t understand what was happening to her or why. Psychologically Ms. C. had to be kept calm and be reminded of what was occurring and why, with such orienting comments as “You are going to be examined by Dr. X” or “You are going to have a test done that won’t hurt you. There is no need to be afraid; I’ll be with you to assure you’re safe.” With the unknown of any comprehension deficits caused by the stroke it was also important to remind other team members that Ms. C. had problems with confusion and that it was important “for patients with dementia in particular to understand what is about to happen to them” (Cunningham & McWilliam 2006, p. 14). Cunningham and McWilliam (2006, p. 14) suggest that nursing staff must compensate in their communication with dementia patients and that this often requires nurses to re-prioritize their tasks and sense of immediacy in order to offer the patient the greatest level of psychological and/or emotional support. Lipley (2005) states one of the most important nursing tasks is offering support to a stroke patient.

The sociological impact relating to Ms. C.’s crisis was limited for the immediate future while hospitalized, although she indicated that she wanted her children contacted and requested they come to the hospital. The biggest sociological change and challenges facing Ms. C. would be following her discharge from the hospital. Depending on the amount of total damage suffered from her stroke and the subsequent progress with therapy to regain lost functionality, it was probable that Ms. C. would relocate to either live with one of her children and/or settle in a home for the aged. This required the nurse to contact a social worker to help Ms. C. with her adjustment.

Implications for the organization

One of the six strategic goals established by the Department of Health’s National Stroke Strategy (2007b) is to “accelerate the emergency response to stroke and improve coordination between different agencies and professionals involved including through improved access to CT scanning.” Fortunately, the hospital where Ms. C. suffered her stroke complied with this goal and had a Code Gray team assembled. National Health Services (2007) approximates 90 percent of hospitals in England as prepared to administer specialized stroke services.

The number of stroke victims is increasing every year. The nurses must be aware of required interventions. This paper has highlighted the ischemic stroke and patient impacts, as well as those on the organization and nurse. The charts below presents required nursing interventions in response to an inpatient stroke.

Reference

Amber, R., & Watkins, W., 2003. The community impact of Code Gray.

Critical Care Nursing Quarterly

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1

Footnotes

^[1]
The term generally accepted in the medical community for multidisciplinary stroke response teams. The typical composition of a Code Gray team includes a primary care RN, charge RN from the Stroke/cardio care unit, an ICU RN, ICU resident, a neurologist, CT technologist and an individual responsible for telecommunications (Nolan & Naylor 2003, p. 297). The Department of Health (2007c) reports that other Code Gray teams also include occupational therapists, physiotherapists, speech and language therapists, dieticians, pharmacists, a clinical psychologist and social worker.

^[2]
FAST criteria is the acronym also known as the Cincinnati Pre-hospital Stroke Scale, such that F = Facial Droop, A = Arm drift, S = Speech and T = Time (Mathiesen et al. 2006; Lipley 2005).

^[3]
t-PA must be administered within three hours of the first onset of symptoms (Amber 2003).

^[4]
Losartan is an angiotensin receptor blocker. The choice was made to use this type of intervention based on the muscle relaxing nature of the medication rather than incorporating those that lowered BP through a modification of electrical activity within the nervous or cardiac system due to the reliance on her pacemaker and the potential other such forms of medication might have on recurrent tachycardia or bradycardia.

^[5]
Ischemic cascade is the term referring to the chain of events that takes place following an ischemic stroke.

^[6]
Although a variety of diagnostic blood work was already performed on Ms. C, a CBC, chemistry panel and cardiac biomarkers were ordered following the stroke for comparison against pre-stroke values along with coagulation studies (Becker & Wira 2006).

The causative agent for Acquired immunodeficiency syndrome AIDS is the Human Immunodeficiency virus HIV. These are diploid and enveloped, single-stranded, positive-sense RNA viruses, which have the ability to integrate viral genome that persists within the host-cell DNA through viral intermediate copy DNA (cDNA)[1].

They are retroviruses with 2 structurally related forms HIV-1 and HIV-2.

The diploid positive single-stranded

RNA

codes for the nine

genes

enclosed by a conical

capsid

. The nine genes are used to code for the proteins and enzymes used for replication. The three main genes are the gag, the pol, and env. It is known that the gag gene is responsible for coding the core proteins in the viral particle whilst the pol gene encodes the enzymes protease, reverse transcriptase, and integrase. The env gene holds the codes with which the HIV structural glycoproteins are manufactured. The rest of the genes—rev, nef, vif, vpu, vpr, and tat—are important for viral replication and mostly responsible for HIV’s penetrance and infectivity rate[1].

The difference between HIV 1 and 2 is the absence of vpu in HIV 2

The three major enzymes produced by the virus are important for functioning at different times during the replicative cycle. Therefore theses enzymes are the target of pharmacologic blockade as antiviral therapy. The RNA-dependent DNA-polymerase (with its RNase H function) acts mostly in the initial phases of viral replication to form a double-stranded DNA or copy DNA of the virus RNA. The integrase then act within the cell nucleus to integrate the viral cDNA into the host chromosomal DNA.

The Protease enzyme functions by processing the Gag and Gag-Pol polyproteins during maturation of the viral particle either at the cell surface or at the budding viron[1].

Despite considerable progress in research into the virology of HIV as elucidated above, some of the specific details of the pathologic process that leads to AIDS have not been fully understood especially the reactive immune response of the human host, which is the driving force for the quest to a much better understanding of the AIDS.

What is noted is that there is a noticeable decline in the CD4

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helper T cells, which results in the reversal of the CD4/CD8 T-cell ratio which affects adversely the regulation and production of B-cell antibody. This result in a reduction of both cellular and humoral immune responses to certain antigens and inadequate response of the host to opportunistic infections and otherwise normally harmless commensal organisms. However, the defect overwhelmingly affects cellular immunity more, the infections tend to be mycobacterial, fungal, or viral [2].

Despite the above understanding and targeted blockade of the understood processes of viral replication, there has not been adequate control of viral load commensurate with intervention. Direct blood injection and inoculation and genital/anal exposure are the main portal of entry for HIV infection, the GI tract which is laden with a vast amount of lymphoid tissue, has been noted to be an ideal site for HIV replication. It is now believed that most of the initial processes of HIV infection are derived [3].

Therefore, Gut Associated Lymphoid Tissue or GALT, is an important site of early viral concentration and replication leading to a significant pro-viral reservoir. It is strongly believed that this reservoir is mostly responsible for the difficulty in efforts to reduce the levels of HIV provirus through sustained treatment with antiretroviral drugs[4]

The GALT is compartmentalized, and this provides an additional feature of HIV replication and reservoir even among different segments of the gastrointestinal tract. Measurements of CD4

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T cells in GALT has shown lower effect of antiretroviral therapy than that noted in corresponding peripheral blood [4].

One hypothesis explaining the above discrepancy is that there is continous viral replication in the gut lymphoid tissue, and the ensuing trigger of an immune response involved, may actually adversely affect efficient CD4

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T-cell replenishment [5].

Right from the onset, after HIV was identified in 1985, Cooper and colleagues described the clinical features of acute HIV infection . A virus-like illness by recently infected individual can present within 1 to 3 weeks. Symptoms consist of headache, sore throat, muscle aches, retro orbital pain, with low-grade or high-grade fever, and swollen lymph nodes, and most times a non pruritic macular erythematous rash involving the trunk and, later, the extremities [6].

In some cases, oral candidiasis and ulcerations in the esophagus or anal canal occur, and central nervous system disorders can be seen (e.g., encephalitis.

Children will most often with the common bacterial infections of childhood like pneumonia, otitis media and sinusitis. These can be more severe and occur more frequently than similar infections in immunologically competent children.

In children infected by mothers through pregnancy (vertical transmission) with HIV become symptomatic from the neonatal period up to age 8 years and that 57% of this group have associated disease within the first year [7].

A panel on Antiretroviral Therapy and Medical Management of HIV-Infected Children in 2010 made recommendations for diagnosis of HIV in infants as follows [8]:

• Due to the fact that maternal HIV antibody persists up to 18 months, infants younger than 18 months require direct virologic assays that detect HIV to make a diagnosis of HIV infection
• The recommended virologic assays include the HIV bDNA Polymerase Chain Reaction and HIV RNA assays
• Additional testing is recommended in infants with exposure to HIV in the perinatal period, at 14 days, at 1 month, and at 4 months.
• After age 18 months, regular HIV antibody assays can be used for diagnosis

Continous monitoring of the CD4

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levels or percentages in patients newly diagnosed with HIV.

The 2010 Panel recommends that in children younger than 5 years, using CD4 percentages every 3- to 4-months to monitor patients’ immune status and disease progression due to the fact that absolute CD4 counts tends to vary with age [8].

CBC count with differential and a urinalysis is done every 1-3 months in infants

If the mother is HIV positive, the recommendation is to use appropriate serologic screening tests to check for hepatitis C, hepatitis B, toxoplasmosis, and syphilis.

Features of HIV that affect the anti-retroviral treatment modalities[8];

• Integrated virus can be latent and can remain unaffected by the immune response
• Virus can spread by cell-to-cell transfer
• Infected cells are a major source of HIV transmission and pathogenesis
• Infected T cells, B cells, and macrophages can be circulating reservoirs for HIV; tissue macrophages and GALT cells can be resident reservoirs that persistently release virus
• Virus can infect brain cells (astrocytes and oligodendrocytes);therapy must pass the blood-brain barrier
• Virus can escape neutralizing antibodies; in some cases, virus infection is sensitive to enhancement by antibodies
• Antigenic variations occur widely among HIV-1 and HIV-2 strains
• Sequence mutations can occur early in the regions coding for the HIV envelope and regulatory genes
• Opportunistic infections, such as candidiasis, herpes and varicella-zoster virus infection, should elicit high index of suspicion, and appropriate prophylactic treatment strategies deviced.

Anti Retroviral Therapeutic agents or ARTs has been and remains the most important aspect of human immunodeficiency virus (HIV) treatment.

In 1987 the first drug, the nucleoside reverse transcriptase inhibitor (NRTI) zidovudine (AZT), was approved for use in patients infected with HIV. Seven other drugs in this class followed and other classes were introduced.

There are six broad groups of ARTs [9].

• Nucleoside or nucleotide reverse transcriptase inhibitors (NRTIs)
• Protease inhibitors (PIs)
• Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
• Fusion inhibitors
• CCR5 co-receptor antagonists (entry inhibitors)
• HIV integrase strand transfer inhibitors

The current general recommendation for an initial ART regimen includes two NRTIs and a third drug from a different class [8. 9].

For of infected infants, children, and adolescents, combination ART (cARTs) with at least 3 drugs from at least 2 classes of drugs is recommended for initial treatment because it provides the best opportunity to inhibit viral transcription, yet preserve immune function by delay in disease progression.

NRTIs stop HIV replication by terminating the transcription of viral RNA to DNA via a viral encoded protein reverse transcriptase

RTIs (NRTIs & NNRTIs) also inhibit human DNA polymerase including mitochondrial DNA (mtDNA) which results in depletion of mtDNA and drug-related toxicities. These toxicities can be life-changing and include diabetes mellitus, peripheral neuropathy, lipodystrophy, pancreatitis, myopathies, renal tubular acidosis, and steatohepatitis, [8, 9].

Protease Inhibitors block the formation of the core structural proteins of the virus in the late stages of viral replication.

Children with HIV Early Antiretroviral Therapy trial or CHEAT trial, showed that early intervention and treatment with ART led to a 75% reduction in HIV progression and moreso a 76% reduction in infant mortality [10].

• It is recommended that treatment be initiated in children aged 12 months or older who have mild symptoms or asymptomatic or and have a CD4 of 25% or more.
• Also children who are 1-4 years of age with more than 350 cells/μL
• And in children aged 5 years or older who have plasma HIV RNA of 100,000 copies/mL or more.

The biggest challenge in the management of children with HIV infection is the compliance to the regimen. Hence some regimen and/or dosing frequency may clearly constitute a burden for younger children..

So studies looking into the use of a simple once daily cART regimen may therefore be a powerful solution to optimize treatment adherence and the patient’s quality of life [11].

The only preferred regimens for children younger than 3 years are co formulated lopinavir/ritonavir-based therapy and nevirapine-based therapy

Another viable solution to the issue of compliance is a fast and efficient reduction of the viral load using medications known as highly active ART (HAART) which will significantly slow viral replication and prevent resistant mutations from developing [8].