The Incidence Rate of Chronic Obstructive Pulmonary Disease - Essay Example

? Chronic Obstructive Pulmonary Disease - Chronic Obstructive Pulmonary Disease General Background What is Chronic Obstructive Pulmonary Disease? Chronic Obstructive Pulmonary Disease (COPD) is not a single entity but refers to a group of diseases that irreversibly limit the airflow to the lungs. To be more specific there is reduced maximal expiratory flow during a forceful expiration. COPD is a chronic disease and progressively reduces airflow over time. An important attribute of this obstruction is that it is not fully reversible. Therefore, the modifications induced by this chronic process have a long-lasting effect. Most of these modifications are at grossly structural as well as cellular levels. History and Epidemiology It is estimated that about 216 million people around the globe suffer from this condition (Fletcher et al 2011, p. 2). COPD affects more than 16 million people in the United States alone, where it is the fourth leading cause of death. Currently it is the sixth most common cause of death worldwide, but, according to estimations by the Global Initiative for Chronic Obstructive Lung Disease (GOLD), it is expected to rise to the third most common cause of death by 2020. (Kasper & Harrison 2005, p. 1547). According to a statistical study in the UK, about 81,500 patients aged above 65 years died of COPD during the period 1990-1992. (Yohannes & Connollyl 2001, p. 99). The incidence rate of this disease is on the rise due to increased exposure to the associated risk factors. Also, improved health care facilities in developed countries have elevated average life expectancies increasing the likelihood of elderly patients acquiring COPD. According to the World Health Organization (WHO) the annual loss of productivity due to COPD is about 27,700 years. COPD is considered to be among the diseases of old age, but about 50% of patients with COPD are under the age of 65. Therefore the disease can have a severe economic impact as it adds to the global disease burden. (Fletcher et al 2011, p. 2). Classification COPD as a group of disorders includes emphysema, chronic bronchitis and small airways disease. These pathologies add up to a common outcome; chronic airflow obstruction. If these disorders are present, but have not resulted in airflow obstruction, they cannot be considered as COPD. Understanding the associated diseases, however, can help in dissecting the complex pathophysiology of COPD. Emphysema and Chronic Bronchitis Emphysema is an anatomically defined disease condition in which the expanding abilities of lung alveoli are reduced leading to retention of air and decreased expiratory flow volume. Chronic bronchitis is characterised by mucus or phlegm production associated with severe cough. Unlike emphysema, chronic bronchitis leads to a mechanical obstruction of the airway. Small airways disease is a condition in which the lumens of small bronchioles are narrowed leading to mechanical obstruction similar to chronic bronchitis. (Kasper & Harrison 2005, p 1547). A patient suffering from COPD can show a range of these disease pathologies, and most of the time they overlap. The reduction in FEV1/FEV ratio, discussed later, is the most important indicator of COPD severity. Therefore, based on the percentage of predicted FEV1, COPD can be classified as mild, moderate, severe or very severe. However, there are two different sets of values given to each classification, depending on whether the British or American system is followed. (Wood, Tan & Stockley 2009, p. 2). Pathophysiology and Pathogenesis Risk Factors There are numerous risk factors that are very closely associated with the development of COPD. An overview of these is crucial to further understand the pathophysiology of this disease. Cigarette Smoking Cigarette smoking is a major risk factor in the development of COPD. Forced expiratory volume in the first second falls with progressive age at the rate of 20-30 ml in non smokers during their adult life. However, the rate of decline can accelerate up to 30-45 ml per year in smokers and up to 80-100 ml per year in smokers susceptible to COPD. (Lomas & Silverman 2001, p. 1). There is a dose-response relationship between smoking and respiratory diseases. This dose is mostly calculated as the number of cigarette packs smoked per year. The association of smoking intensity and reduction in the pulmonary function can partially explain why COPD has high prevalence with increasing age. Moreover, smoking can also be attributed to the fact that COPD is slightly more common in male as compared to female. But this difference is slowly reducing as more women become addict to cigarette smoking. (Kasper & Harrison 2005, p. 1547). Although, there is evidence of smoking being a major risk factor in the development of COPD, it alone is accountable for only 15% of cases. (Lomas & Silverman 2001, p. 1). This variability signifies that there are other risk factors apart from cigarette smoking that contribute to the establishment of COPD. Genetic Involvement Alpha 1 antitrypsin (alpha 1 AT) deficiency is the only genetic cause proven to be associated with the development of COPD. Alpha 1 AT is a protease inhibitor that protects the lung parenchyma, particularly the alveoli from excessive damage by enzymes. Its deficiency can bring about major destruction leading to loss of recoil ability of the lung’s alveoli. Therefore, it is one of the major pathological factors that can predispose an individual to develop emphysema. It has been seen that that homozygote for the Z allele that codes for alpha 1 AT have a greater risk of developing COPD than the normal population. These individuals are referred to as Pl Z. However, there is considerable variability in developing COPD among these Pl Z genotypes. Only 1-2% of all COPD cases have associated severe alpha 1 AT deficiency. Therefore, there are other, yet to be identified, genetic factors that contribute to the development of this disease. (Lomas & Silverman 2001, p. 2). Occupational Exposure The considerable variability in the association of COPD and major risk factors highlights the need to identify other environmental factors that can lead to chronic airway obstruction. It has been observed that individuals exposed to smoke or dust in their occupation mostly present with respiratory symptoms of airway obstruction. It is estimated that 15% of all COPD is work related (Boschetto et al 2005). Workers mining at coal or gold mines are at a greater risk of developing COPD. Cadmium is a chemical gas that is believed to be responsible for significant forced vital capacity reduction in exposed individuals. But the ability of these risk factors to produce chronic airway obstruction alone is not certain. They are believed to be an adjunct to cigarette smoking and other major risk factors in contributing to COPD. (Kasper & Harrison 2005, p. 1547). Studies have shown that non smoker emphysema death rates are far greater in China compared to the USA. (Lomas & Silverman 2001, p. 2). This highlights the importance of environmental pollution as a valid risk factor. Airway Responsiveness Certain patients with COPD have shown an exaggerated airway response to exogenous stimuli. This is similar to the hyper response present in asthma patients, and led to the Dutch hypothesis that considers COPD and asthma to be buds of a similar underlying pathology. But the British hypothesis split asthma and COPD as different entities, whereby asthma is considered an allergic phenomenon and COPD is more an outcome of smoking related inflammation. (Kasper & Harrison 2005, p. 1547). Basic Physiology Lung alveoli are the smallest units composed of single cell compartments located at the terminal ends of the bronchioles where most of the gas exchange takes place. They are richly supplied by the blood vasculatures to facilitate this exchange. Breathing consists of inspiration and expiration, both equally important for effective gas exchange. During inspiration oxygen rich air is transported to the alveoli and expiration effectively removes the accumulated carbon dioxide from the lungs. This is required to create a concentration gradient that favours carbon dioxide excretion out of the blood and oxygen absorption by the red blood cells. Due to chronic obstruction of the airways, as in the case of COPD, expiration becomes ineffective. With the consequent decrease in forced expiratory volume. The expulsion of air from the alveoli depends on two major factors. The recoil ability of the alveoli and the resistance offered by the lung airway determine the force generated for expulsion. The airway consists of trachea, bronchi and bronchioles. Decrease in the cross sectional area of these airway passages increase the overall resistance. So the loss of elastic recoil of lung parenchyma as in the case of emphysema and decrease in cross sectional area of the airway as in the case of chronic bronchitis lowers the ability of lungs to effectively remove the inhaled air. Residual Volume and Hyperinflation In a normal lung, after a forced expiration, a certain volume of air remains within the lung parenchyma known as the residual volume. Patients suffering from COPD have increased retention of air known as air trapping. This can progressively develop into hyperinflation that is characterised by an increase in the total lung capacity. Although, this increase in the lung volume can partially compensate the airway obstruction by increasing the elastic recoil pressure and decreasing the airway resistance, there are certain adverse effects associated with this compensation. The flattened diaphragm as a result of hyperinflation can impair inspiration as inspiratory pressure drops below normal. (Kasper & Harrison 2005, p. 1549). Basis of Pathology To better understand the underlying pathology of COPD it is better to divide it into three distinct units. The three main structures of the lung that are distinctly involved are the large airway, small airway and the lung parenchyma. Large Airways The large airway includes trachea, bronchi and bigger bronchioles. Cigarette smoking predisposes these structures to several cellular modifications. Goblet cell hyperplasia is one of the most important changes induced by cigarette smoking along with impaired mucus clearance. This accumulation of mucus is responsible for the characteristic cough and sputum production in chronic bronchitis. Also, this mucus serves as a perfect medium for bacterial growth that explains upper respiratory infections in COPD patients. Smooth muscle hypertrophy and bronchial hypersensitivity further leads to airway obstruction. (Kasper & Harrison 2005, p. 1529). Small Airways Narrowing of the smaller bronchioles (< 2mm) provides the greatest resistance to airflow. This narrowing is caused by excessive mucus production due to goblet cell metaplasia induced by cigarette smoking. Moreover, the Clara cells that are responsible for surfactant production are replaced by mucus secreting cells. Surfactant is required to decrease the surface tension that prevents the airway from collapsing under negative pressure. This reduction in surfactant, therefore, increases the surface tension promoting further collapse and airway obstruction. Inflammation and infiltration of mononuclear inflammatory cells induce parenchymal destruction and fibrosis of the airway walls. Parenchymal tearing also cut the radial tractions that keep the walls in its definite shape. Therefore, airway distortion results in further narrowing of the small bronchioles leading to significant airway obstruction. (Kasper & Harrison 2005, p. 1549). Lung Parenchyma Emphysema is the destruction of the air spaces that results from chronic exposure to cigarette smoke. In this part of the airway, respiratory bronchiole, alveolar ducts and alveoli are affected. The normal smaller units of airspaces are obliterated transforming into larger and abnormal airspaces. Macrophage and neutrophil infiltrations are evident on bronchoalveolar lavage. Emphysema has various different pathological types, but centiacinar emphysema is most commonly associated with cigarette smoking. It is characterised by large air spaces mostly evident on the upper superior and middle part of the lungs. Alpha 1 AT deficiency can produce panacinar emphysema in which the lesions are more evenly distributed across acinar units and frequently affect the lower lobes. (Wood, Tan & Stockley 2009, p. 1). Pathogenesis Emphysema and narrowing of the small airways contribute significantly to the physiological changes in COPD. The exact pathogenesis of small airway obstruction apart from fibrosis is still under debate. Proteolytic activation of certain growth factors which promotes the release of profibrotic IGF is a proposed mechanism involved in small airway obstruction. However, much is known about emphysema and its pathogenesis. There are four distinct events that can merge to give the overall condition. Starting from the inflammation induced by smoking, the inflammatory cells further promote the release of proteinases that damage the extra cellular matrix. These two events are followed by apoptosis of the lung cells that are responsible for structural integrity. Lastly, this loss of structural integrity gives rise to larger but abnormal airspaces: the hallmark of emphysema. (Kasper & Harrison 2005, p. 1550). Diagnosis Key Symptoms Most patients with COPD present with a productive cough, wheeze and breathlessness. But these symptoms are evident after chronic exposure to cigarette smoke. Weather, dust and cold are factors that are associated with worsening of the symptoms. As the disease progress, the severity of the symptoms increases with more purulent sputum production as a result of some upper respiratory tract infection. Breathlessness becomes profound over time and can limit even mild physical activities such as dressing. Physical Findings The signs of COPD are very similar to most respiratory diseases. In milder form of COPD, patients only present with wheezes but in severe cases such as acute exacerbation air hunger, gasping and prolonged expiration are evident. Although, most patients present with difficulty breathing some may not be breathless but show signs of cyanosis which is due to CO2 insensitivity. (Kumar & Clark 2009, p. 902). Diagnostic Tests As discussed earlier, airway obstruction is the main characteristic feature of COPD. Therefore, reduction in the pulmonary function can be tested by spirometry. Calculating FEV1 and FEV1/FEV ratios are key steps in diagnosing the patients with COPD. Forced expiratory volume are decreased depending on the severity of the disease and thus used to determine the GOLD stage. This is the classification based on spirometry results of FEV1/FEV ratios and predicted FEV1. Spirometry is still the standard test to determine pulmonary function and diagnose COPD. Other tests can be done to support the diagnosis. Arterial blood gas is an important test that can reflect the alveolar ventilation status by providing information about arterial pH and PCO2. Radiological studies such as X-rays and CT scan can aid in identifying the underlying pathology such as emphysema and can reveal the extent of damage endured by the lungs. Complete blood count (CBC) can be helpful in determining chronic hypoxemia as it will be reflected as an increase in the hematocrit. Alpha 1 AT deficiency is a major risk factor for COPD. Therefore, calculating serum antitrypsin levels is an integral part of modern investigation protocols. If the deficiency is suspected it could be confirmed by PI type determination. (Kumar & Clark 2009, p. 903). Differential Diagnosis: Many other pathological conditions of respiratory tract can present with similar symptoms. Therefore, differential diagnosis of COPD includes Asthma, Bronchiectasis and TB. Other pathologies involving respiratory system can be present and can be included in the differential diagnosis based on the presenting signs and symptoms. Management Risk Factor Reduction The most important aspect in the management of COPD patients is to educate them about the associated risk factors such as cigarette smoking. Smoking cessation is essential to limit or control the damage already inflicted on the airways. According to the studies, the FEV1 increases significantly within one year of smoking cessation until it starts to decline again at a similar rate to a non smoker. (Ja 2003, p. 1). Avoiding other environmental factors such as occupational related pollutants can also be beneficial. Drug Therapies The aim of pharmacological management is to improve airway obstruction and decrease inflammation. Established drug treatment for COPD includes bronchodilators such as short and long acting beta 2 agonists. But the degree of airway obstruction reversibility is variable among different patients. This variable response has been attributed to polymorphism in the beta 2 adreno-ceptor gene, but no conclusive studies exist to confirm this association. Long acting beta 2 agonists have also shown some anti-inflammatory properties but such effect is not evident in all patients. Oral or inhaled steroids are other major line drugs that are used in patients with COPD to decrease inflammation by suppressing immunity. Mostly these drugs are reserved for the exacerbation of COPD, but sometimes when the autoimmune component is more dominant in the disease they can be used as front line drugs. (Wood, Tan & Stockley 2009, p. 5). Theophylline has also shown improvements in pulmonary function of COPD patients. Supplemental Oxygen Treatment with supplemental oxygen is very beneficial in patients with resting hypoxemia (O2 saturation less than 90%). It is the only pharmacological therapy that is associated with decreasing mortality in COPD patients. (Kasper & Harrison 2005, p. 1552). Non-Pharmacological Treatment Non pharmacological treatment for COPD patients includes pulmonary rehabilitation and surgery. Pulmonary Rehabilitation Pulmonary rehabilitation includes education and physical exercises that aim to decrease the sense of breathlessness and increase general well being. These practices can only improve quality of life and do not contribute to decreasing the mortality associated with COPD. Surgery The surgery that is performed on COPD patients is known as Lung Volume Reduction Surgery (LVRS). It is reserved for mild to moderate stages of COPD, as in severe cases it is associated with high mortality and is avoided in patients with FEV1 less than 20% predicted. (Kasper & Harrison 2005, p. 1552-1553). This surgery can help patients by increasing the lung’s recoil capacity and decreasing airflow obstruction the main contributing factors to COPD. Lung transplantation can be performed in some cases where end stage emphysema is confirmed. The patient has a 75% chance of surviving 3 years post transplantation, but finding a donor is a major limiting factor in this management. (Kumar & Clark 2009, p. 906). Prevention and Prognosis Early Intervention As discussed earlier, there are various risk factors that are inevitably associated with COPD. An awareness campaign about cigarette smoking and its association with COPD can discourage smokers. Moreover, building rehabilitation centres for those willing to give up cigarette smoking should be an integral part of the campaign. It is important to remember that COPD is a chronic process that takes years to unfold. Avoiding risk factors such as cigarette smoking anywhere during disease progression can significantly decrease the mortality associated with COPD. Early intervention can be helpful in reducing the complications associated with COPD. Prognosis COPD prognosis depends upon the severity of the disease and the extent of lung function decline. However, patients with severe COPD have 50% chance of surviving more than 5 years. But even in the severe cases, smoking cessation is associated with improved prognosis signifying the importance of early prevention and control of the associated risk factors in the development of COPD. (Kumar & Clark 2009, p. 906). Summary and Conclusion COPD is a chronic condition characterised by airway obstruction that is not fully reversible. There are significant impacts of this disease globally and incidences are on the rise. Certain risk factors both environmental and genetic are believed to play a major role in the pathogenesis of COPD. Therefore, management of the disease mostly focuses on reducing exposure to these risk factors. From this, we can conclude that COPD is a fatal but preventable disease and its recent progression indicates a need for awareness among individuals to avoid cigarette smoking. Preventing the incidences of COPD significantly contributes to decreasing the global disease burden. Reference: Boschetto P, Quintavalle S, Miotto D, Lo Cascio N, Zeni E, & Mapp Ce. 2006. Chronic obstructive pulmonary disease (COPD) and occupational exposures. Journal of Occupational Medicine and Toxicology (London, England). Fletcher,M J, Upton, J, Fishwick, J T, Buist, S A, Jenkins, C, Hutton, J, Barnes, N, Molen, T V D, Walsh, J W, Jones, P & Walker, S. 2011. COPD uncovered: an international survey on the impact of chronic obstructive pulmonary disease [COPD] on a working age population. BioMed Central Ltd. http://www.biomedcentral.com/1471-2458/11/612. Ja, K. 2003. ‘Chronic Obstructive Pulmonary Disease’ in South African Family Practice; vol 45, No 2. http://ajol.info/index.php/safp/article/view/50575. Kasper, D. L., & HARRISON, T. R. 2005. Harrison's principles of internal medicine. McGraw-Hill, Medical Pub. Division, New York. Kumar, P. J., & CLARK, M. L. 2009. Kumar & Clark's clinical medicine. Saunders Elsevier, Edinburgh. Lomas, David A, & Silverman, E K. 2001. The genetics of chronic obstructive pulmonary disease. BioMed Central Ltd. BioMed Central Ltd. http://respiratory-research.com/content/2/1/20. Wood, A M, Tan, S, & Stockley, R A. 2009. Chronic obstructive pulmonary disease: towards pharmacogenetics. BioMed Central Ltd. BioMed Central Ltd. http://genomemedicine.com/content/1/11/112. Yohannes, A M., & Connolly, M J. 2001. Predictors of hospital admission and mortality in patients with chronic obstructive pulmonary disease in Clinical Gerontology, vol. 11, No. 1, p. 99-106. Cambridge University Press. http://hdl.handle.net/2173/3011. Read More