DISCUSS THE PATHOPHYSIOLOGY, ASSESSMENT AND DIAGNOSIS, AND MANAGEMENT OF ASTHMA IN THE ADULT PATIENT.Asthma is the most frequently diagnosed respiratory disease in adults, affecting approximately 8% of the working adult population (Cartier and Sastre, 2011).
DISCUSS THE PATHOPHYSIOLOGY, ASSESSMENT AND DIAGNOSIS, AND MANAGEMENT OF ASTHMA IN THE ADULT PATIENT.Asthma is the most frequently diagnosed respiratory disease in adults, affecting approximately 8% of the working adult population (Cartier and Sastre, 2011).
Introduction
Asthma is the most frequently diagnosed respiratory disease in adults, affecting approximately 8% of the working adult population (Cartier and Sastre, 2011). In the United Kingdom (UK), an estimated 4.3 million adults are being treated for asthma alone (Kaufman, 2012). Asthma has a considerable impact on the quality of life of those affected by it, as well as their families; chronic asthma symptoms cause substantial morbidity, with poor control resulting in an increased rate of admissions to hospital (Rees, 2010). Whilst the morbidity associated with asthma in significant, mortality rates from asthma have reduced in recent decades; despite this, more than a thousand individuals still died from severe asthma in 2012 (British Lung Foundation, 2016). Unfortunately, the number of deaths from asthma reported in the UK is amid the highest in Europe: comparisons of international death rates for 5- to 34-year-olds during 2001-2010 reveal that asthma mortality in the UK is one of the highest in Europe, and is akin to those in the USA, Australia and New Zealand (Royal College of Physicians, 2015).

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Pathophysiology of asthma
It is widely noted within the literature that there is no conclusive ‘gold standard’ definition of asthma (Kaufman, 2011). The World Health Organization (WHO) (2010) proposes that asthma is an inflammatory condition which is characterised by repeated episodes of breathlessness and wheezing: these episodes vary on a day-to-day basis, and in seriousness. Killeen and Skora (2013, p.11), however, define asthma as ‘a chronic inflammatory disorder that is characterized by 3 distinct responses: pulmonary inflammation, airway hyperresponsiveness, and airway remodeling in response to a host of triggers that affect only those who are predisposed to the disease’. Linzer (2007) suggests that asthma can simply be defined as recurrent reversible bronchospasm due to a trigger. Busse et al. (2006), however, assert that asthma is a complicated disease that can involve possible permanent airway obstruction, airway hyperresponsiveness, and multicellular inflammation. Recruitment and activation of immune cells, such as mast cells, macrophages, dendritic cells, neutrophils, eosinophils, and T lymphocytes, results in an inflammatory and cellular infiltration into the airways. In particular, Type 2 T-helper cells (Th2) appear to play a significant role in the activation of the immune cascade which results in the underlying inflammation, and can lead to the late asthmatic response; this can be seen in Figure 1 below (Durham et al., 2000). This leads to the release of several pre-formed and generated mediators, resulting in airway remodeling with deposition of extracellular proteins, smooth muscle hypertrophy, and increased goblet cell production (Holgate et al., 2000). As a result of these mechanisms, the airway epithelium becomes fragile and denuded, and the epithelial sub-basement membranes thicken, with increased mucus production and consistency and endothelial leakage leading to mucosal oedema (Linzer, 2007). In addition, mediator-induced abnormalities in the parasympathetic and non-adrenergic non-cholinergic nervous systems can result in increased bronchial hyperresponsiveness.
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