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Chronic Obstructive Pulmonary Disease (COPD)Chronic Obstructive Pulmonary Disease is defined as chronic airflow obstruction and is characterized by an accelerated decline in lung function. COPD is used to describe a group of progressive lung diseases including emphysema, chronic bronchitis and refractory asthma (1). This disease or rather this group of diseases has currently no cure but with the right diagnosis and treatment there are many ways to manage and treat the symptoms in order to be able to have a better breathing cycle and live a normal life.
The disease mainly affects middle-aged and older adults, with an incline to smokers. Many of the patients have asymptomatic or even symptomatic disease that is not diagnosed and therefore not treated. The breathing problems tend to become gradually worse over time and can affect normal daily activities (2). Its rising rate of mortality is expected to make COPD the third most common cause of death by 2020(2). In order to have a better understanding of this, a short trip down the history of the COPD is the only wise thing to do before a look on modern time treatments and the feats of the medical society that made this disease, more, manageable.
One of the earliest descriptions of emphysema include Bonet’s description of voluminous lungs and it comes from as back as 1679. He assessed 19 cases where the lungs were described as turgid from air. The beginning of our clinical understanding of chronic bronchitis was not until 1814 by Badham who used the word catarrh to refer to chronic cough and mucus hypersecretion which are the main symptoms.
He described bronchiolitis and chronic bronchitis as disabling disorders. Laennec then described the component of emphysema as the disease in 1821 after completing careful dissections on patients that he was studying during their life. He managed to recognize emphysema lungs as hyperinflated and saw that they were unable to empty well. What was surprising for Laennec was that the disease was more common than he thought at first and this was due to the fact that emphysema was caused by exaggeration of the natural viscus condition. On the dissections he observed that the lungs did not collapse as he thought but filled the cavity completely on each side of the heart however a part of them was filled with mucous fluid. Today we realize that Laennec was actually describing a combination of emphysema and chronic bronchitis. Also, it is possible that emphysema could be associated with familial predisposition, however, it may be affected by other environmental factors since during that era smoking was very rare but such conditions were still present. Now fast forwarding through time, diagnosis was made possible in 1846 through the invention of the Spirometer which is still being used today, although it took more than 100 years for the Spirometer to be perfected as a diagnostic tool, however the main principles are still the same. In 1944 Ronald Christie suggested that diagnosis is certain when dyspnea on exertion of insidious onset is identified on a patient who has other physical signs of emphysema with chronic bronchitis and asthma which are not due to bronchospasm or left ventricular failure. (2)Charles Fletcher studied the natural history of COPD and was the first to recognize the risks of smoking and accelerated decline rate in FEV1 in susceptible smokers. On further research he and his colleagues also observed that stopping smoking would retard the rate of decline of FEV1 and established the scientific foundation for smoking cessation. Burrows and Earle described the course and prognosis of 200 patients with COPD in 1969 and later observed more patients with similar symptoms which led them to recognize that patients with a low FEV1/FVC percentage predicted the onset of rapid FEV1 decline over time. Patients with the most rapid decline rate had the worst prognosis. The discovery established the importance of early identification and intervention. Around that time over 50 years ago the only therapies for COPD were antibiotics for pneumonia, potassium iodide used as a mucus thinner and combination product containing ephedrine, theophylline and sedative (2). In the early 1960s inhaled isoproterenol began to be used, during that time oxygen was considered contraindicated and its use was prohibited to prevent right heart straining. It wasn’t until the late 1960s ” 70s when Noehren first described medical and surgical approaches to therapy that provided a new approach to the treatment and management of the disease. With this small and brief time-travel through the history of the disease a more in depth look into the disease and its treatment shall be easier to comprehend and interesting. (2)CausesExposure to tobacco smoke seems to be the most significant COPD risk factor and about 80-90% of all patients are smokers. Population-based studies have shown that smoking is associated with diminished lung function, other respiratory symptoms and high COPD-related deaths. However, not everyone who smokes gets COPD, and only one in five smokers actually get severely affected by the disease. Harmful chemicals present in smoke can damage the lining of the lungs and airways therefore quitting smoking seems to prevent COPD exacerbation and better response to treatment is also seen. Research is ongoing in order to figure out why some smokers get COPD while others do not. Pipe and cigar smoking are also associated with increased COPD risk but at a lower rate than cigarette smoking. Furthermore, some research suggests that even being exposed to second hand smoke may increase risk of COPD.COPD may also be related to genetics as the second most significant cause is a1-antitrypsin deficiency, since alpha-1-antitrypsin is a substance that protects our lungs and without it they are more vulnerable to damage. Alpha-1 Antitrypsin is a protein produced in liver and secreted into bloodstream to help protect our lungs. Without this protein white blood cells begin harming the lungs causing lung deterioration and this can even affect children. It has been noted that COPD can develop in people who have never smoked before but have a1-antitrypsin deficiency. However only 1% of all cases is attributed to a1-antitrypsin deficiency. People with this deficiency seem to develop COPD at a younger age usually before 35, especially if they are smokers. It is also believed that there might be other genetic factors related to the disease.Other factors that seem to increase risk of COPD are exposure to certain types of dust and chemicals or burning fumes for a long period of time, which may cause damage to the lungs. These include cadmium dust and fumes, grain and flour dust, silica dust, welding fumes, isocyanates and coal dust. Age is another risk factor as COPD develops slowly over a long period of time so most people do not start to experience symptoms before the age of 40.PathogenesisNormally air travels down the trachea, into the bronchi and then into the bronchioles which end into alveoli. The alveoli have very thin walls full of capillaries where gas exchange occurs. Our lungs rely on bronchial tubes and alveoli’s natural elasticity to force air out, COPD causes loss of elasticity and overexpansion which causes some air to remain trapped in the lungs after exhalation, as the bronchioles or the alveoli are blocked due to an obstruction. The two main forms of airway obstruction are chronic bronchitis and emphysema.In chronic bronchitis the bronchioles become inflamed and narrowed and the lungs produce more mucus which further blocks and narrows the tubes, leading to a chronic cough as the patient is trying to empty his airways. Chronic Bronchitis is defined by cough and sputum production caused by an innate immune response to inhaled toxic particles from cigarette smoke. Also an inflammation of central airways epithelium and mucous-producing glands, related to increased mucous production, reduced mucociliary clearance and increased permeability of airspace epithelial barrier is observed. Mucous hypersecretion does not seem to contribute to airflow limitations in early stages of COPD as mucus production in smokers with normal lung function does not appear to predict later COPD development. However, chronic mucus hypersecretion may contribute to later stages due to an increased risk of exacerbations that might increase FEV1 loss. Chronic mucus hypersecretion may be caused by submucosal, glands inflammatory response to inflammatory cells releasing serine proteases potent to mucal secretagogues. Oxidants from cigarette smoke or from inflammatory leucocytes may also affect mucin overproduction by MUC5AC gene induction.In emphysema the alveolar walls and elastic fibers are destructed, causing small airways to collapse on exhalation impairing airflow out of the lungs. Emphysema is the enlargement of distal airspaces, beyond the terminal bronchioles due to the airway walls destruction. Emphysematous lung destruction leads to reduced maximal expiratory airflow as the elastic recoil force driving air out of the lungs is decreased. Centriacinar emphysema is caused by respiratory bronchioles’ dilation or destruction and is the emphysema type most closely associated with tobacco smoking. Panacinar emphysema on the other hand is usually associated with a1-antitrypsin (a1-AT) deficiency and results in a more even dilation and destruction of the entire acinus. It is suggested that either of these types prevail in severe disease and that centriacinar emphysema is highly associated with severe small-airway obstruction. Also a relationship between emphysema degree and pack of smoking per year is seen, but is not a strong one. Only around 40%There are no sources in the current document.of heavy smokers develop significant lung destruction from emphysema and emphysema may also be seen in individuals with normal lung function.
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