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Chronic Obstructive Pulmonary Disorder - Essay Example

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As a chronic airway disease, Chronic Obstructive Pulmonary Disorder (COPD) is characterized by an irreversible airflow limitation that is progressive. It is a result of abnormal inflammatory lung response to inhaled substances and worsened by exacerbations and comorbidities in…
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Chronic Obstructive Pulmonary Disorder
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Literature Review Affiliation Literature Review Introduction As a chronic airway disease, Chronic Obstructive Pulmonary Disorder (COPD) is characterized by an irreversible airflow limitation that is progressive. It is a result of abnormal inflammatory lung response to inhaled substances and worsened by exacerbations and comorbidities in individual patients. Because of the adverse effects of COPD on the quality of life, this literature review explores the causes, risk factors, pathophysiology and its treatment in order to find better ways of preventing and managing the condition Background information Devereux (2010) acknowledged that the primary cause of COPD in most countries is tobacco smoking. Inhalational exposures due to indoor, outdoor and occupational activities release large amounts of smoke, dusts, and chemicals that are also predisposing factors. Similarly, the risk host factors are a hereditary deficiency of alpha -1 antitrypsin (AAT), impaired lung growth during pregnancy and early childhood and airway hyperresponsiveness. He further noted that the worldwide incidence of COPD is increasing due to the increase in tobacco smoking and increased use of biomass fuels especially in developing countries. It is estimated that the disease affects about 64 million people globally with the disease coming third in the causes of mortality with over 3 million deaths reported in 2005. In the U.S., a half of the 24 million people with airflow limitation have been diagnosed with COPD. Pathogenesis of COPD In an article by Tuder & Petrache (2012), the chronic airflow limitation in COPD is due to chronic inflammation. It leads to destructive changes in the airways, and if this destruction extends to the pulmonary vasculature and lung parenchyma, further exacerbations occur. Smoke and other airway irritants such as dust and chemicals get into the lungs and cause the release of inflammatory cells and other chemical mediators (Tuder & Petrache, 2012). The neutrophils, macrophages, B cells and CD8+ T-lymphocyte cells are released in large numbers. In turn, they trigger the release of the inflammatory mediators such as tissue necrosis factor alpha (TNF-α), leukotriene B4 (LTB4), and interleukins (IL-6 and IL-8) on activation. These molecules then move to the site of irritation to destroy and remove the offending agents. The inflammatory processes are useful in normal circumstances. However, repeated exposures perpetuate the ongoing inflammatory response leading to the development of COPD. Structural and physiological changes, which worsen with time, occur in the lungs. Tuder & Petrache (2012) noted that airway remodeling occurs with continued inflammation leading to constriction with excessive narrowing and swelling of the mucosa. The result is increased mucus production and mucociliary dysfunction causing failure to clear airway secretions, thus the hallmark of symptoms of COPD that include dyspnea, chronic cough, and chronic sputum production. In addition, non-clearance of mucus leads to build-up, and it attracts bacteria causing further inflammation and formation of pouch-like sacs in the bronchial tree. In a review by Stoller & Aboussouan (2012), they stated that COPD due to alpha-1 antitrypsin deficiency is caused when an imbalance occurs in the activity of proteases and antiproteases. The absence of antiprotease α1 –antitrypsin leads to a massive protease-mediated destruction of the lung tissues causing inflammation and excessive mucus secretion. In addition, inhibition of the antiproteases by the accumulation of free radicals and superoxide ions produced by active neutrophils and macrophages cause further damage. Apart from airflow limitation, a long-standing COPD can result in other complications such as pulmonary hypertension and right-sided heart failure (cor pulmonale) (Gooneratne, Patel & Corcoran, 2010). The pulmonary hypertension is due to increased pulmonary vascular tone and destruction of the pulmonary capillary bed. The presence of other comorbidities such as lung cancer, osteoporosis or coronary artery disease (CAD) adversely affects the patients quality of life. Diagnosis, Management, and Prevention According to Vestbo, Hurd, Agusti, Jones, Vogelmeier, Anzueto, & Rodriguez-Roisin (2013), COPD presents with the symptoms of emphysema, chronic bronchitis, and reactive airways. Thus, spirometry is required for diagnosis in addition to the symptoms and history of exposure to the risk factors as well as family history. The physical examination can also reveal cyanosis, decreased breath sounds, wheezing, respiratory crackles and use of accessory respiratory muscles during breathing. While using spirometry, a reduction in FEV1/FVC to less than 70% is a confirmation of persistent airflow limitation. Both pharmacological and nonpharmacological approaches can be used in the management of COPD. The goal of pharmacotherapy is to reduce symptoms, frequency, severity of exacerbations, and to improve health status (Morjaria, Malerba & Polosa, 2010). The effective medications in the treatment of COPD include bronchodilators, phosphodiesterase-4 inhibitors, inhaled and oral corticosteroids or a combination therapy depending on how well the disease is controlled in an individual patient. Other pharmacologic treatments include vaccines, antibiotics, mucolytic agents, and alpha-1 antitrypsin augmentation therapy in patients with alpha-1 antitrypsin deficiency. On the other hand, some of the non-pharmacological methods include smoking cessation, elimination or reduction of exposures of the exposures at home and workplace and regular exercise. Healthy People 2020 Indicator-Environmental quality Because of the direct impacts environment has on health, People & US Department of Health and Human Services (2011) identified environmental quality as one of the leading health indicators. It influences the quality of life with about 25% of total global deaths and diseases resulting from environmental factors. Thus, good environmental quality can help in the prevention of some of the environmentally related diseases such as cancers, asthma and other respiratory and cardiovascular disorders. Environmental quality includes safe air, water, and land. Individuals who are at risk are the ones mostly affected by poor environmental quality. According to People & US Department of Health and Human Services (2011), air pollution, and second-hand tobacco smoke has been found to cause, trigger and exacerbate asthma in children and adults. The primary risk factor in both smokers and nonsmokers in COPD is tobacco smoke and other predisposing factors such as dusts and chemicals resulting from air pollution. Conclusions The sources used in this literature review reveal that the development of COPD is directly related to the air pollutants especially the tobacco smoke. Therefore, achieving the aims of a Healthy People indicator of environmental quality would help in keeping the environment clean and safe, and prevent the COPD risk factors such as tobacco smoke and other air pollutants. Though an accurate diagnosis is paramount for appropriate treatment can be instituted, prevention of risk factors related to the environment is the most effective method of management of the disease. Therefore, more efforts should focus on environmental conservation and reduce pollution. References Devereux, G. S. (2010). Definition, Epidemiology and Risk Factors. ABC of COPD Gooneratne, N. S., Patel, N. P., & Corcoran, A. (2010). Chronic obstructive pulmonary disease diagnosis and management in older adults.Journal of the American Geriatrics Society, 58(6), 1153-1162 Morjaria, J. B., Malerba, M., & Polosa, R. (2010). Biologic and pharmacologic therapies in clinical development for the inflammatory response in COPD. Drug discovery today, 15(9), 396-405 People, H., & US Department of Health and Human Services. (2011). Healthy People 2020 Stoller, J. K., & Aboussouan, L. S. (2012). A Review of?? 1-Antitrypsin Deficiency. American journal of respiratory and critical care medicine, 185(3), 246-259 Tuder, R. M., & Petrache, I. (2012). Pathogenesis of chronic obstructive pulmonary disease. The Journal of clinical investigation, 122(8), 2749 Vestbo, J. R., Hurd, S. S., Agust, A. G., Jones, P. W., Vogelmeier, C., Anzueto, A., ... & Rodriguez-Roisin, R. (2013). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary.American journal of respiratory and critical care medicine, 187(4), 347-365 Read More
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