The history of chronic airways disease/Chronic Obstructive Pulmonary Disease (COPD) dates back to late 17th century. It was first described by a medical researcher, Bonet who defined it as the “voluminous lung condition”. Further research by early scientists figured that human lungs in some patients had signs of turgidity as a result of air(Petty, 2006). Another scientist, Ruysh gave an elaborate description coupled with illustrations to indicate cases of enlarged airspaces in 1721. The disabling effect of chronic bronchitis was described in 1814 by Badham. An autopsy carried out in 1837 by a physician named Rene Laennecdetected lungs that could not collapse. He realized that these lungs were full of air. Mucus traces were also found in the airways. He gave the condition the name “emphysema” and gave a more detailed coverage of the condition in his book‘A Treatise on the Diseases of the Chest and of Mediate Auscultation’ (Petty, 2006). Efforts in the diagnosis of the disease got a boost with the invention in 1942 of a spirometer by Hutchinson. This initial spirometer however only measured lung volume capacity but not the airflow. Continued research in this area led to a description of the methodology to measure airflow by Gaensler in 1951. The use of the term Chronic Obstructive Pulmonary Disease (COPD) came into use in late 20th century as coined by William Briscoe in 1965 and is in use up to date(Fishman, 2005). The disease is today identified as occurring in two forms; chronic bronchitis characterized by persistent cough and emphysema entailing destruction of the lungs over time.
COPD prevalence is more pronounced among the elderly (65 years) and over. Out of every one thousand elderly people in England, at least thirty are diagnosed with COPD. This translates into approximately one person in every sixty in the population. In areas of low economic potential in the country, one in every thirty two is diagnosed with COPD compared to one in approximately one hundred in the more affluent areas(Torres, Moayedi, 2007). The prevalence in the United States is among the highest in the world with approximately one in every twenty being diagnosed with the condition(National Heart, Lung, and Blood Institute, 2009). In 1990, COPD was ranked sixth in the diseases causing death in patients and projections indicate that with its continued prevalence, then it would be the fourth leading killer disease by 2030. The projections are based on the current smoking trends and other demographic factors(Mathers, Loncar, 2006).
COPD is linked to more than one causative factor. The principal risk factor is prolonged tobacco smoking. Over 80% of COPD cases in the United States are linked to smoking. With increased cumulative smoking, the chance of developing COPD also increases. The cumulative smoking is determined by the number of cigarette packets used on a daily basis multiplied by the years under smoking(Rennard&Vestbo, 2006). Air pollution especially in the urban centers increases the chance of acquiring COPD with industrial waste gases from combustive industrial processes being major contributors to the menace. In many third world countries where biomass fuel is mainly used for cooking, the fire smoke has been found to be a leading cause of COPD mostly in women(Kennedy, Chambers, Du, Dimich-Ward, 2007).Exposure to dusts at the workplace as experienced by workers in coal and gold mines as well as in the textile and dangerous chemical industries such as those dealing with cadmium and isocyanates has had increased chance of COPD. Fumes generated by welding and other similar machines also cause blockage of airflows. This occupational exposure is however less lethal than smoking(Hnizdo,Vallyathan, 2003).
Genetic susceptibility has been identified as a contributing factor to the development of COPD in the population. Studies have shown that relatives of COPD patients who engage in heavy smoking are more likely to develop the condition as compared to unrelated smokers. The factors that increase genetic susceptibility to this condition is not clearly identified. However, it has been found that patients with Alpha1-antitrypsin gene defect are more prone to COPD. The gene is responsible for coding for the protein, alpha1-antitrypsin that protects lungs from degradative effects of protease enzymes such as trypsin and elastase. These enzymes are commonly released when smoke from tobacco triggers an inflammatory response(Silverman, et al. 1998). Recent research has indicated that the COPD is related to some immune responses. Patients with lifelong smoking history were found to have an active lung inflammation long after they had ceased smoking. The inflammation may actually persist for a very long durationgetting worse as time continues. Immunologists argue that this phenomenon is characteristic of an autoimmune response mediated by auto-immunoglobulin and auto reactive T cells(Feghali-Bostwick, et al., 2008). Like asthma, mainly triggered by allergens, COPD has also been shown to display characteristics such as sudden vasoconstriction in response to airborne inhalants. In severe cases, COPD may manifest through hyperrresponsiveness. Cases of continued infection of the lung have also been found to exacerbate the chances of getting a COPD attack. High cured meat products have also been linked with development of COPD probably due to the use of sodium nitrite as a preservative.
Pathophysiology and Pathology
Description of the Normal Function/Importance of the Relevant System
The respiratory system is the anatomical structure responsible for introduction of respiratory gases in living organisms. It is constituted of the lungs, muscles and the airways. Gases are exchanged within this system by passive diffusion between the external atmosphere and blood. The basic units in the lung facilitating this process are the alveoli also known as air sacs in mammals. Through this route, entry of oxygen results in oxygenation of blood accompanied by removal of carbon dioxide and other gaseous wastes from the circulation. Pressure difference is the underlying principle in the gaseous exchange process such that high internal lung pressure forces out air and vice versa.Infection in this system results in inhibited performance which may have adverse effect on the health of the individual(Meraz E, et al, 2011).
Pathophysiology/Pathology and Mechanisms Responsible
COPD is pathologically manifested by damage to the lung parenchyma, central airways, pulmonary vasculature and peripheral airways. The disorder is characterized by narrowing of the airways which reduces the rate of inflow and outflow of air into the alveoli. This in turn negatively affects the functioning of the lungs. Exhalation process is the most affected by COPD since there is a greater reduction of air flow as the pressure in the chest compresses instead of expanding the airways. Such a problem can be overcome by forcefully enhancing breathing process through increasing the pressure in the chest cavity during expiration, however withCOPD; the condition exerts a limit as to the level the air flow can be increased, described as expiratory flow limitation.Due to the low rate of airflow experienced by COPD patients, there is a likelihood of not breathing out completely before another breath is taken.This is mostly common when the patient has to take fast breaths as in exercise and other strenuous activities. A significant amount of air of the previous breath remains in the air sacs leading to accumulation of unnecessary air that results in high volume of air in the lungs described as dynamic hyperinflation. In such a situation, it becomes uncomfortable to breath since the effort required tobreath is enormous as the both the lungs and chest wall are already overstretched by hyperinflation(Calverley& Koulouris, 2005).
The shortness of breath is also exacerbated by the loss of surface area necessary for gaseous exchange especially in case of emphysema. The reduced surface area means that the rate of transfer of oxygen and carbon dioxide between the body and the atmosphere is greatly inhibited in turn causing low level ofoxygen and a high level of carbon dioxide in the patient’s body. The patient may therefore have to breathe deeply and faster to compensate for this deficiency; however this becomes difficult especially in case of emphysema where mucus blocks the air ways and the inherent possibility of hyperinflation(O’Donnell, 2006).An effort to breathe faster, especially in patients with advanced cases of the chronic airways disease, dyspnea may result. Furthermore, the accumulation of high levels of carbon dioxide in the body and the low oxygen levels renders the patient vulnerable to repeated headaches, drowsiness and in severe cases the patient may suffer a heart failure. Other complications associated with this condition include muscle wasting, weight loss, osteoporosis, and depression.COPD at times worsens as depicted by symptoms such as shortness of breath and increased amount of phlegm as well as darkening of its color. This is mainly as a result of bacterial or viral infection and other environmental pollutants. The deterioration of COPD may also arise from pulmonary emboli. This leads to increased airway inflammation that causes hyperinflation that is directly linked with irregular gas exchange. The condition may also cause hypoventilation that develops into hypoxia, inadequate muscle perfusion and eventually cell necrosis(Rabe, et al, 2007).
The mechanism behind lung damage in COPD is not clearly defined. However, oxidative stress arising from the high concentrations of free radicals emanating from smoke is supposedly the main cause. This results in destruction of the lung parenchymal layer adversely interfering with the normal structuring of the airways. The tobacco smoke’s free radicals interfere with the activity of the antiprotease enzymes, the main being the alpha1-antitrypsin. Inhibiting the activity of this enzyme results in the protease enzyme accessing and inflicting damage to the lungs.An immunological response in which the body releases cytokines against allergens such as dust and tobacco smoke particles has also been identified. The cytokines are usually released in response to inflammation, an initial reaction of body to irritants. With release of cytokines, other components of the immune systems such as neutrophils, lymphocytes and macrophages are recruited to the lung. Ongoing research has generated a significant breakthrough in understanding the mechanism of COPD proliferation. Studies on the immunologic components such as T cells and factors associated with cell apoptosis in tissues such as the lung are becoming clearer as well as the determination of the reasons behind the continued inflammation response long after ceasing smoking. Scientists have also tried to describe the mechanism of COPD development at the molecular level through study of blood samples and other tissues. Elements such as alpha2-antiplasmin, complement3, 1B-glycoprotein and apolipoprotein precursors have all been identified to take part in deterioration of the lung function. The research has however not comprehensively determined their role in cause and effect mechanisms(Rana, et al., 2010).
COPD is clinically manifested by several signs and symptoms. Shortness of breath is the most common feature of this condition and it is easily noticeable when performing a strenuous exercise. This phenomenon is called dyspnea. With continued deterioration of health due to COPD, dyspnea occurs even during mild daily chores such as walking and other house work. In extreme cases, the dyspnea is constantly present even during rest. The disease is also characterized by persistent or chronic cough with sputum and mucus production, chest tautness, general body fatigue and wheezing.SevereCOPD cases may develop complete respiratory failure. This manifests inform of a bluish discoloration of lips as a result of inadequate blood oxygen. The excessive availability of carbon dioxide and other metabolic gas wastes in the body may cause headaches and twitching. Owing to the poor performance of the lungs in advanced COPD, the heart tends to be overworked in an effort to pump blood through the inactive lungs. This is characterized at first by peripheral edema with dyspnea and swelling of limb parts such as the ankles being the signs. Eventually the heart may completely fail under the strain leading to death of the patient. Some of the patients with this disease may have rapid breathing rates, decreased intensity of breath, production of wheezing sounds as determined upon using the stethoscope, longer exhalation duration as compared to the inhalation duration, increased straining of neck muscles in an effort to breath, hyperaeration; a situation manifested by enlarged chest with reference to the front-to-back distance and barrel chest that is identified by comparing the ratio of the chest anteroposterior to the lateral chest frame(Mahler, 2006).
Diagnosis of chronic airways disease should be guided by signs such as dyspnea, chronic cough and patient history that indicate exposure to the commonly established causative factors. The diagnosis can not be based on any one symptom alone but rather a comprehensive diagnosis protocol. The most commonly used diagnostic test for COPD is spirometry. Using this method, a forced expiratory volume is measure per second. This measure gives the highest air volume breathable in the first second of a large breath. The test also measures the forced vital capacity;greatest air volume breathed out in one enormous breath. The ratio of these two measures should be at least 70%. If the ratio falls below 70%, the patient is diagnosed as having COPD. This test is usually carried out following a bronchodilator medication. This is termed as the GOLD criterion. Another criterion commonly used is the NICE model that is based on the highest air volume breathed out in the first second of a large breath. The other less commonly used criterion is the ERS which is based on the highest air volume breathed out in the first second of a large breathwith COPD diagnosed in women with less than 89% and in men with less than 88%. The value of these tests can be used to determine the level of severity of the chronic air disease as based on a ‘normal’ value scale which is categorized according to the age, weight, height and gender of the patient. The spirometry test is carried alongside other tests such as extent of dyspnea and exercise ability (Nathell, Nathell, Malmberg, Larsson, 2007).
COPD is also diagnosed by use of chest x-ray. This is determined by flattened diaphragm, bullae, lung hyperinflation and increased retrospinal airspace. Use of scans such as the high-resolution computerized tomography detects emphysema characteristics in the lungs and this is useful in exclusion of other lung infections.Blood sample tests are used indiagnosis. Low oxygen and high carbon dioxide in arterial blood and high bloodcount in veinular blood samples could be an indication of COPD(Torres&Moayedi, 2007).
Historical Development of Therapeutics/Medical Treatments
The search for cure to COPD has been ongoing for the longest time; however it is now apparent that the disease has no cure. This may be attributed to the many years it takes to develop before it is externally manifested. Efforts have been ongoing in line with the Global Initiative for Chronic Obstructive Lung Disease to develop therapies with an aim to prevent the disease advancement, relieving symptoms, preventing and treating any complications and reducing mortality. Both medical and non-medical therapies have been attemptedbut evidently the most workable solution remains avoiding the causative factors.
Current Management Practices/Therapies – Benefits and Limitations
The current medical therapy in use is the bronchodilators. The drugs are classifiedinto three major categories as beta agonists, anticholinergics and methylxanthines. The drugs are used in different situations as they vary in effectiveness(Salpeter, Buckley, Salpeter, 2006). Due to their associated side effects, some patients are maintained by use of inhaled steroid medication. These are however used in low doses and have been shown to effectively contribute to patients’ life quality improvement(Gartlehner, Hansen , Carson, Lohr , 2006). In severe cases of COPD, more strong medical therapy is used such as the short-acting bronchodilators(Zhou, et al. 2006). Antibiotics are also commonly used if exacerbation is as a result of bacterial infection. Hospitalization with positive-pressure ventilation systems may also be used for patients who suffer adverse side effects from the strong medications.These medications have contributed to well being of millions of COPD patients all over the world. The main limitations are the side effects associated with this medication. Bronchodilators cause many side effects to patients such as chest pains, increased heart rate and blood pressure and blurred vision(Liesker, et al, 2002).
Development of New Therapies/Areas of Need
New therapeutic medications for COPD are currently under development. The newest of these is the phosphodiesterase-4 inhibitors, with its two makes, roflumilast and cilomilast being released in the market. The medication is aimed at enhancing relaxation of bronchial smooth muscles through inhibiting the mechanism that aids contraction.it is a modification of the bronchodilators but working with a more targeted mechanism and minimal side effects(Calverley, 2004).
Future perspectives in prediction, prevention and management of COPD
Research is ongoing to enhance early detection and management of COPD. Trials on retinoic acid is expected to be applied in restoration of damaged lung architecture and air sac function in man as has been demonstrated in mouse models. Human trials have indicated good response with the vitamin found to balance vital enzyme activity that prevent alveolar breakdown. Studies have also shown that flu vaccines can help reduce the COPD infection by up to 50%. Vaccines that protect against bacterial infection responsible for exacerbating the disease are also under review. Use of nutritional therapy is believed to be an effective booster in enhancing the performance of the medical therapy(Calverley, 2004).
The chronic airways disease/ Chronic Obstructive Pulmonary Disease (COPD) is a common lung disease which is among the leading killer diseases in the world. The disease existing in the forms of chronic bronchitis and emphysema or a combination of both is caused by among other factors tobacco smoking and exposure to dangerous fumes. It is also linked to genetic factors in some instances. The disease is clinically manifested by shortened breath, chronic cough and general body fatigue. The disease is easy to diagnose using several methods such as the use of spirometry test, chest x-ray and scanning. Once determined to be present, the disease is maintained using medical and nutritional therapies since it has no known cure.Behavioral tendencies such as smoking have to be avoided to enhance stable maintenance. Despite the lack of cure, research is still ongoing to develop medical therapies that could facilitate in prediction, prevention and management of the disease.
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