Introduction - Disease overview
Asthma has emerged as the most chronic childhood disease, affecting one in every fifteen children (Shiel, 2010); though, it affects 5% of the North American adult population too and a considerable proportion of the UK adult population (Shiel, 2010). It is estimated that around 16 million people are asthmatics in the US and Canada (Shiel, 2010). In the UK over 5 million people are presently receiving treatment for asthma (asthma.org.uk). Over the past 20 years, hospitalisation rate due to asthma has increased by 30% (Shiel, 2010). This essay is based upon a case study of a forty six year old male called Derek Jones who has been suffering from Chronic asthma since 1997. The subject has agreed to participate in the case study with confidentiality ensured. The discourse will evaluate the condition, structure, function in addition to relating to its psychological impact.
Out of the various available definitions of asthma, the one propounded by the Global Strategy for Asthma Management and Prevention Report - "Asthma is a chronic inflammatory diseaseÂ of the airways in which many cell types play a role, in particularÂ mast cells, eosinophils and T lymphocytes" (Bousquet et al, 2000) appears closest to the pathological attributes of the disease. Asthma is characterised by inflammation and constriction of bronchial tubes or respiratory airwaves, tightening of the muscles of bronchial walls and production of excessive mucus (Bousquet et al, 2000).
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Asthma is incurable, but its progression can be checked and inhibited by avoiding asthma triggers and effective tracking of symptoms (Bousquet et al, 2000). Another characteristic of the disease is its changing profile which is systematic in the test subject, which makes it necessary to monitor it regularly in close consultation with the doctor (Bousquet et al, 2000). Out of the two types of asthma - allergic and irritant, the former is the most common, accounting for almost 90% of cases (Shiel, 2010). It is caused by nasal allergies and eczema (Shiel, 2010). The non-allergic variant is visible among the 30+ populace and its commonly known causative factor is respiratory tract infection (Shiel, 2010).
Causes of asthma are classified as allergens or irritants (Shiel, 2010). The first group constitutes airborne allergies like pollen, animal dander, mold, cockroaches, dust, etc. (Asthma Causes, 2010), and the second group consists of factors like viral infections of respiratory tract, cold climate, physical strain like exercise, air pollutants, sulphites, food preservatives, certain medicines like beta blockers and aspirin (Asthma Causes, 2010).
As can be derived from the test subject, asthma symptoms are typified by short breath, chest tightening or pain, wheezing and coughing (Asthma Symptoms, 2010). The patient's condition is aggravated by respiratory viral infections and is particularly troublesome during nights (Asthma Symptoms, 2010). An increase in intensity and recurrence rate of the disease is a sign of its aggravation, when the doctor should be consulted on a regular basis for deciding the treatment regime.
Treatment of asthma can be broadly divided into symptom-preventive and treating in-progress asthma. The former are prescriptive long-term treatment regimes which are case-variant. These regimes are aimed at keeping the airway inflammation under check (Asthma Treatment and Drugs, 2010). These inhibitive treatments are generally daily doses, foremost among which are inhaled corticosteroids (Asthma Treatment and Drugs, 2010). They carry a lesser risk of side effects and have good efficacy for long-term use (Asthma Treatment and Drugs, 2010). The test subject's use of Theophylline and Leukotriene modifiers solidify their impact in that they are both oral prescriptions that help in clearing of airway blockades, reducing inflammation and constriction, and relaxing airway muscles (Asthma Treatment and Drugs, 2010). Corticosteroids combined with long-acting beta agonists - LABAs, are also one of the mainstream treatments, but it may trigger acute attack in some cases (Asthma Treatment and Drugs, 2010).
Short-term treatments are aimed at emergency relief during attacks, and include inhaled doses like short-acting beta agonists and Ipratropium. A range of oral and IV formulations are also available, but they are known to be risk-prone in long term (Asthma Treatment and Drugs, 2010).
The 1992 publication of a research paper by Weiner et al (1992) opened a new direction in asthma treatment, that of muscle training. The group hypothesised that respiratory muscle strength was key to increasing their resistance to asthmatic hyperinflammation, and accordingly, devised an exercise regime Specific Inspiratory Muscle Training - SIMT (Weiner et al, 1992). They selected thirty moderate to acute asthmatic patients and divided them into two groups of 15 each. While the first group received SIMT for six months, the second group received sham training. The results showed marked post-training improvement in the first group as compared with baseline for asthma symptoms like night-time asthma, morning tightness, daytime asthma, cough, medical leave incidents, etc. (Weiner, 1992). Five patients from the first group were even able to stop taking inhaled corticosteroids during training tenure (Weiner, 1992).
Asthma and the respiratory system
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Contrary to the general function of inflammation which is repair and restoration of damaged tissues, asthmatic inflammation caused in the airways walls generates a healing process which does not repair and restore but alters the basic structure of the walls (Bousquet et al, 2000). This change occurs due to two aspects: 1) Increased thickness involving an increase in muscle mass in mucous glands, and 2) Thickening of airway walls and considerable permanent reduction in airways' functioning capacity and competency (Bousquet et al, 2000). The restructured airways architecture, combined with enhanced mucous secretion and increased surface tension due to lesser elasticity of airways leads to acute and chronic asthma and even attacks.
Given this background of asthmatic pathogenesis, it is noted that the respiratory tract undergoes permanent structural alteration in chronic asthmatic condition. Various studies on the subject have demonstrated differing conclusions. While the Finney, Karlsson and Persson (1985) examination on the effects of bronchoconstrictors and bronchodilators on small airways concludes that a considerable degree of resistance to flow is localised to small airways (Finney, Karlsson & Persson, 1985), the Bousquet et al (2000) study says that airflow obstruction due to increased smooth muscle mass is spread evenly across both small and large airways (Bousquet et al, 2000).
Contractility of human small airways; source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1916766/?page=3
Asthma and breathing muscles
The breathing muscles, more particularly the soft muscle mass of airways, increases considerably in asthma, which is responsible for wall-thickening of airways and air obstruction - "There is a 3-to-4-fold increase in muscle volume in asthmatic patients, the muscles may occupy up to 20% of the bronchial wall" (Bousquet et al, 2000). This muscle accumulation occurs in both central and peripheral airways (Bousquet et al, 2000), thus affecting airflow in totem. Accumulation of muscle mass is attributed to factor like smooth muscle induction by inflammatory mediators, cytokines, repeated episodes of bronchospasms, myogenic activity and hypertrophy (Bousquet et al, 2000). Studies have shown that smooth muscle in asthmatic airways needs to shorten by just 40% of its restive length to cause complete closure of airway lumen (Bousquet et al, 2000). The below-depicted graphic demonstrates the shut down of airway tubes during asthma attack:
Apart from the above pathological attributes of muscle mass change that aggravate symptoms, chemical attributes with similar effect are also noted. Muscle cells have synthetic and secretory potency with the release of RANTES, a chemokine (Altman et al, 1997). Chronic inflammation is aggravated when RANTES react with Th1 and Th2-derived cytokines to trigger activities of eosinophils, T lymphocytes and monocytes/macrophages (Bousquet et al, 2000). Muscle cells are also potent facilitators of extracellular matrix, ECM environment alteration, thus generating key events in the process of chronic airway remodelling (Bousquet et al, 2000).
During attacks, soft muscle mass accumulation can lead to severe bronchial obstruction. Additionally, occasional enlargement of mucous glands resulting in excessive mucus secretion aggravates the attack. Apart from the naturally increasing muscle mass, its inflammation that occurs during ongoing attacks causes extra air blockage and results in exacerbations and bronchial hyper responsiveness (Weiner, 1992). Thus, the natural thickening of airway walls due to increased muscle mass, as also the topical inflammation during attacks cause acute bronchial constriction.
A body of literature on asthma research is found to be supporting the thesis that permanent restructuring of airway architecture of bronchioles, in particular the thickening of airway walls, for which the increased soft muscle mass is the main reason, have considerable impact on asthmatic condition. The Wheatley et al (1990) experiment used nine subjects and concluded that during induced asthma spontaneous hyperinflation minimises the total respiratory muscle work and may constitute a mechanism for minimising energy expenditure (Wheatley et al, 1990). The Martin et al (1980) experiment examined lung and chest wall mechanics in seven subjects during hyperinflation in asthma; it indicated persistent inspiratory muscle contraction throughout expiration and concluded that the increase in functional residual capacity - FRC in induced asthma is substantially influenced by persistent inspiratory intercostal and accessory muscle activity during expiration (Martin et al, 1980).
Psychological impact of asthma
Asthma as a disease with symptoms like wheezing, coughing, short breath, etc. has considerable impact on the public profile of the patient. Also, the symptoms aggravate during night time (Asthma Symptoms, 2010) in several cases, causing emotions like embarrassment and inhibition which is a persistent occurrence with the patient. Several factors such as age and occupation of the patient, and also the severity of disease put the patient at a psychological disadvantage. The resulting behavioural and psycho-physiological alteration is wide-ranging and case-dependant; fear and anxiety, hypervigilance, loss of control, denial mode of behaviour, guilt, anger, embarrassment and confusion are some of the fallouts (All About Asthma, 2007). Several alternate therapies like yoga and meditation are found to be helpful in tackling the disease's psychological impact, as also in developing acceptance and caring for one's self (All About Asthma, 2007).
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The discourse has related to chronic asthma as prevalent in the test subject and thus in conclusion, it can be stated that the permanent restructuring of airway architecture and the behaviour of breathing muscles, the soft muscle mass are major factors facilitating acute and chronic asthmatic conditions. Future research and treatment regimes should be directed at inhibiting these causal factors. Furthermore, a larger case/empirical study may lead to better diagnosis and treatments.