Chronic Obstructive Pulmonary Disease (COPD)
Introduction
Chronic Obstructive pulmonary disease also known as COPD is a group of diseases which make breathing difficult by obstructing airflow and causing other breathing related problems (Centers for Disease Control and Prevention [CDC], 2015). This disease which is described by the National Heart, Lung and Blood Institute (NHLBI) as progressive because it worsens over time includes chronic bronchitis, emphysema and asthma in some cases (CDC, 2013; NHLBI, 2013a). In developing countries, poor quality of indoor air is suspected to play a major role in the disease development and progression whereas in the Unites States, tobacco smoke is reported to be the major cause of COPD with the disease affecting mostly smokers or former smokers (CDC, 2005; CDC, 2013; NHLBI, 2013a). In addition to the above mentioned causes of the disease, respiratory infections, genetic factors and long term exposure to other lung irritants such as air pollutants (chemical fumes, dust) are also suspected to contribute to the disease development and progression (CDC, 2013; NHLBI, 2013a).
Pathophysiology of COPD
COPD is characterised by abnormal response to toxic agents’ inhalation such as abnormal lung inflammatory response which can result in clinical and physiological abnormalities such as mucous hypersecretion in the bronchioles (bronchitis) and cilia dysfunction (MacNee, 2006). Mucous hypersecretion is as a result of squamous metaplasia, elevated number of goblet cells and increase in the size of bronchial submucosal glands, resulting in chronic productive cough while cilia dysfunction occurs as a result of squamous metaplasia of epithelial cells and leads to abnormal mucociliary escalator and expectorating difficulty (MacNee, 2006). Other changes include airflow obstruction which occurs majorly in small conducting airways (diameters < 2mm) as a result of inflammation, presence of inflammatory exudates and consequent narrowing of these small airways (MacNee, 2006). Also contributing to airway inhibition is alveoli tissue destruction (emphysema) which causes air to be trapped during expiration and leads to hyperinflation which in turn inhibits respiratory capacity (MacNee, 2006). In addition to the above mentioned, gas exchange abnormalities, pulmonary hypertension and systemic effects have also been observed (MacNee, 2006; Rodriguez-Roisin and MacNee, 2006). Gas exchange abnormalities which occur in advanced stages of COPD is caused by an abnormal ventilation distribution: perfusion ratio as a result of anatomical changes accompanying COPD and is characterised by hypoxaemia which may be accompanied by hypercapnia (MacNee, 2006). Pulmonary hypertension is reported to develop late in COPD when gas exchange abnormality becomes severe and pulmonary arterioles structural changes lead to persistent pulmonary hypertension as well as right ventricular hypertrophy and factors which contribute to this include hypoxia which leads to pulmonary arterial constriction, endothelial dysfunction, pulmonary arteries remodelling and pulmonary capillary bed destruction (MacNee, 2006). Systemic effects include systemic inflammation and wasting of skeletal muscle, both of which contribute to limit the patient’s exercise capacity and worsen the likely course of the disease regardless of the extent of airflow obstruction (MacNee, 2016).
Signs and symptoms of COPD
In the early stages of the disease, there may be mild or a complete absence of symptoms, however, as the disease progresses, symptoms tend to become more severe and common symptoms include; an ongoing cough which produces a lot of mucous (“smokers cough”), shortness of breath often during physical activity, noisy breathing (production of whistling/squeaky sound during breathing), tightness of the chest, while changes in skin colour (skin turns yellow or grey), changes in lips and nails colour (development of a bluish colour), increased heart rate, loss of breath while talking, insufficiency of recommended symptom treatment, swelling of ankles, weight loss and decreased muscle endurance occur in severe cases(NHLBI, 2013b; WebMD, 2015). Furthermore, infection, ambient temperature changes and air pollution can exacerbate this condition (MacNee, 2006 and WebMD, 2015). It is however worthy of note that COPD may manifest symptoms different from the above mentioned with some of its symptoms similar to that of other conditions, also presentation of the above mentioned symptoms may not be indicative of COPD hence the need for proper diagnosis which is based on signs and symptoms manifested, medical and family history and test results (NHLBI, 2013b; NHLBI, 2013c). Tests commonly used include spirometry; a lung function test and chest x ray/chest CT scan while arterial blood gas test is used to evaluate the severity of the disease (Mannino et al., 2000 NHLBI, 2013c).
COPD treatment
Although COPD currently has no cure, treatments are available which slow the progress of the disease, reduce symptom manifestations, decrease the severity and frequency of exacerbations and improve exercise tolerance (CDC, 2013; National Health Service [NHS], 2004). Cessation of smoking for those who smoke is the most important treatment measure, in addition to this, elimination of tobacco smoke and other air pollutants is also necessary (CDC, 2013). Medication can also be administered to treat symptoms such as cough and noisy breathing while educating the patient on COPD management strategies which include breathing strategies, nutritional counselling and energy conserving techniques can also be done to increase quality of life (CDC, 2013; NHS, 2004). Furthermore, vaccination during flu season and the treatment of respiratory infections with antibiotics (if appropriate) is also recommended (CDC, 2013). Preventive measures against this disease includes avoiding the inhalation of tobacco smoke, air pollutants as well as respiratory infection (CDC, 2013).
References
American Lung Association (2016). Lung Health & Diseases; COPD. Retrieved online from http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/copd/ on the 12th of August, 2016.
Centers for Disease Control and Prevention (2013). Chronic Obstructive Pulmonary Disease (COPD). Retrieved online from http://www.cdc.gov/copd/index.html on the 12th of August, 2016.
Centers for Disease Control and Prevention. (2005). Annual smoking-attributable mortality, years of potential life lost, and productivity losses—United States, 1997–2001. CDC’s Morbidity and Mortality Week Report, 54(250):625-628.
MacNee, W. (2006). Pathology, pathogenesis, and pathophysiology. British Medical Journal, 332(7551), 1202–1204.
Mannino, D.M., Gagnon, R.C., Petty, T.L. and Lydick, E. (2000). Obstructive lung disease and low lung function in adults in the United States: data from the National Health and Nutrition Examination Survey 1988-1994. Archives of Internal Medicine, 160:1683-1689.
National Health Service. (2004). Treating COPD. Retrieved online from http://www.nhs.uk/Conditions/Chronic-obstructive-pulmonary-disease/Pages/treatment. aspx on the 13th of August, 2016.
National Heart, Lung and Blood Institute (2013a). What is COPD? Retrieved online from http://www.nhlbi.nih.gov/health/health-topics/topics/copd on the 12th of August, 2016.
National Heart, Lung and Blood Institute (2013b). What are the signs and symptoms of COPD? Retrieved online from https://www.nhlbi.nih.gov/health/health-topics/topics/copd/signs on the 13th of August, 2016.
National Heart, Lung and Blood Institute (2013c). How is COPD Diagnosed? Retrieved online from https://www.nhlbi.nih.gov/health/health-topics/topics/copd/diagnosis on the 13th of August, 2016.
Rodriguez-Roisin, R. and MacNee, W. (2006). Pathophysiology of chronic obstructive pulmonary disease. European Respiratory Society Monograph, 38: 177.
