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Chronic obstructive pulmonary disease (COPD)Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airway disease (COAD), is a group of diseases characterized by the pathological limitation of airflow in the airway that is not fully reversible. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other lung disorders. It is most often due to tobacco smoking,[1] but can be due to other airborne irritants such as coal dust, asbestos or solvents, as well as congenital conditions such as alpha-1-antitrypsin deficiency. Signs and symptomsThe main symptoms of COPD include dyspnea (shortness of breath) lasting for months or perhaps years, possibly accompanied by wheezing, and a persistent cough with sputum production.[2] It is possible the sputum may contain blood and become thicker (hemoptysis), usually due to damage of the blood vessels of the airways. Severe COPD could lead to cyanosis (bluish decolorization usually in the lips and fingers) caused by a lack of oxygen in the blood. In extreme cases it could lead to cor pulmonale due to the extra work required by the heart to get blood to flow through the lungs.[3] Causes:Cigarette smokingA primary risk factor of COPD is chronic tobacco smoking. In the United States, around 80 to 90% of cases of COPD are due to smoking.[6] Not all smokers will develop COPD, but continuous smokers have at least a 25% risk.[7] Occupational pollutantsSome occupational pollutants, such as cadmium and silica, have shown to be a contributing risk factor for COPD. The people at highest risk for these pollutants include coal workers. Air pollutionUrban air pollution may be a contributing factor for COPD as it is thought to impair the development of the lung function. In developing countries indoor air pollution, usually due to biomass fuel, has been linked to COPD, especially in women.[1] GeneticsVery rarely, there may be a deficiency in an enzyme known as alpha 1-antitrypsin which causes a form of COPD.[8] Other risk factorsIncreasing age, male gender, allergy, repeated airway infection and general impaired lung function are also related to the development of COPD. DiagnosisThe diagnosis of COPD is suggested by symptoms; it is a clinical diagnosis and no single test is definitive. A history is taken of smoking and occupation, and a physical examination is done. Measurement of lung function with a spirograph can reveal the loss of lung function.
Physical examinationA systematic review by the Rational Clinical Examination concluded that no single medical sign or symptom can adequately exclude the diagnosis of COPD.[12] One study found that the presence of either "a history of smoking more than 30 pack-years, diminished breath sounds, or peak flow less than 350 L/min" has a sensitivity of 98 percent.[13] ManagementAlthough COPD is not curable, it can be controlled in a variety of ways. Clinical practice guidelines by Global Initiative for Chronic Obstructive Lung Disease (GOLD), a collaboration including the American National Heart, Lung, and Blood Institute and the World Health Organization, are available.[11] Occupational changeWorkers may be able to transfer to a significantly less contaminated area of the company depending on circumstances. Often however, workers may need complete occupational change. PharmacotherapyBronchodilators There are several types of bronchodilators used clinically with varying efficacy: β2 agonists, M3 antimuscarinics, leukotriene antagonists, cromones and xanthines.[14] These drugs relax the smooth muscles of the airway allowing for improved airflow. The change in FEV1 may not be substantial, but changes in the vital capacity are significant. Many patients feel less breathless after taking bronchodilators. β2 agonists There are several highly specific β2 agonists available. Salbutamol (Ventolin) is the most widely used short acting β2 agonist to provide rapid relief and should be prescribed as a front line therapy for all classes of patients. Other β2 agonists are Bambuterol, Clenbuterol, Fenoterol, and Formoterol. Long acting β2 agonists (LABAs) such as Salmeterol act too slowly to be used as relief for dypsnea so these drugs should be used as maintenance therapy in the appropriate patient population. The TORCH study showed that LABA therapy reduced COPD exacerbation frequency over a 3 year period, compared to placebo [15].An increased risk is associated with long acting β2 agonists due to decreased sensitivity to inflammation so generally the use of a concomitant corticosteroid is indicated[1][2][3] M3 muscarinic antagonists (anticholinergics) Derived from the deadly agaric Amanita muscaria, specific antimuscarinics were found to provide effective relief to COPD. Inhaled antimuscarinics have the advantage of avoiding endocrine and exocrine M3 receptors. The quaternary M3 muscarinic antagonist Ipratropium is widely prescribed with the β2 agonist salbutamol. [4]. Ipratropium is offered combined with salbutamol (Combivent) and with fenoterol (Duovent). Tiotropium provides improved specificity for M3 muscarinic receptors. It is a long acting muscarinic antagonist that has shown good efficacy in the reduction of exacerbations of COPD, especially when combined with a LABA and inhaled steroid[16]. Cromones Cromones are mast cell stabilizers that are thought to act on a chloride channel found on mast cells that help reduce the production of histamine and other inflammatory factors. Chromones are also thought to act on IgE-regulated calcium channels on mast cells. Cromoglicate and Nedocromil, which has a longer half-life, are two chromones available.[17] Leukotriene antagonists More recently leukotriene antagonists block the signalling molecules used by the immune system. Montelukast, Pranlukast, Zafirlukast are some of the leukotrienes antagonists.[18] Xanthines Theophylline is the prototype of the xanthine19] class of drug. Teas are natural sources of methylxanthines, xanthines and caffeine while chocolate is a source of theobromine. Caffeine is approximately 16% metabolized into theophylline. Nebulized theophylline is used in the EMR for treatment of dyspnea (Difficulty in breathing). Patients need continual monitoring as theophylline has a narrow therapeutic range. More aggressive EMR interventions include IV H1 antihistamines and IV dexamethasone. CorticosteroidsEnteral and parenteral corticosteroid therapy has long been the mainstay of treament of COPD, and is known to reduce hospital length of stay. Similarly, inhaled corticosteriods (specifically glucocorticoids) act in the inflammatory cascade and improve airway function considerably,[10] and have been shown in the ISOLDE trial to reduce the number of COPD exacerbations by 25%[21]. Corticosteroids are often combined with bronchodilators in a single inhaler. Some of the more common inhaled steroids in use are beclomethasone, mometasone, and fluticasone. Salmeterol and fluticasone are combined (Advair), however the reduction in death from all causes among patients with COPD in the combination therapy group did not reach the predetermined level of statistical significance.[22]23] TNF antagonistsTumor necrosis factor antagonists (TNF) are the most recent class of medications designed to deal with refractory cases. Tumor necrosis factor-alpha is a cachexin or cachectin and is considered a so-called biological drug. They are considerered immunosopressive with attendant risks. These rather expensive drugs include infliximab, adalimumab and etanercept.[24] Supplemental OxygenIn general, long-term administration of oxygen is usually reserved for individuals with COPD who have arterial hypoxemia (PaO2 less than 55 mm Hg), or a PaO2 between 55 and 60 mm Hg with evidence of pulmonary hypertension, cor pulmonale, or secondary erythrocytosis (hematocrit >55%). In these patients, continuous home oxygen therapy (for >15 h/d) sufficient to correct hypoxemia has been shown to improve survival. VaccinationPatients with COPD should be routinely vaccinated against influenza, pneumococcus and other diseases to prevent illness and the possibility of death.[14] Pulmonary rehabilitationPulmonary rehabilitation is a program of disease management, counseling and exercise coordinated to benefit the individual.[26] Pulmonary rehabilitation has been shown to relieve difficulties breathing and fatigue. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.[27] DietA recent French study conducted over 12 years with almost 43,000 men concluded that eating a Mediterranean diet "halves the risk of serious lung disease like emphysema and bronchitis". [5] PrognosisA good prognosis of COPD relies on an early diagnosis and prompt treatment. Most patients will have improvement in lung function once treatment is started, however eventually signs and symptoms will worsen as COPD progresses. The median survival is about 10 years if two-thirds of expected lung function was lost by diagnosis. References
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