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Chronic Obstructive Pulmonary Disease: Emphysema
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Cigarette smoke accounts for over 80% of all cases of chronic obstructive lung disease. It contains irritants that inflame the air passages, setting off a cascade of biochemical events that damage cells in the lung, increasing the risk both for COPD and lung cancer. Different effects of smoking can lead to emphysema or chronic bronchitis, but smokers generally have signs of both conditions. The specific diagnosis depends on which disease process predominates.
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Chronic bronchitis, emphysema or a combination of these conditions causes the airflow obstruction in COPD. Chronic bronchitis is defined in clinical terms as a productive cough present at least 3 months of the year for at least 2 consecutive years. Other etiologies must be ruled out for a diagnosis of bronchitis to be made. Emphysema has an anatomical definition based on physical changes in the lungs. It is characterized by abnormal and permanent enlargement of the air spaces distal to the terminal bronchiole with destruction of the alveolar wall.2
Because cigarette smoking contributes to both emphysema and chronic bronchitis, anyone who has COPD should stop smoking. Quitting smoking won't reverse the condition, but it might stop COPD from getting worse. Airborne irritants such as chemical fumes exacerbate symptoms and should ... be avoided. Standard treatment for COPD includes using bronchodilators, such as ipratropium and albuterol, to reduce muscle spasms, and corticosteroids to control inflammation in the airways. Acute flare-ups are treated with antibiotics. Severe COPD may require continuous oxygen therapy.
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Genetic factors are thought to make some individuals more susceptible to the pulmonary effects of tobacco smoke, but only one such factor has been identified. A deficiency in alpha1-antitrypsin is a common inherited state of partial or complete absence of the major serum protease inhibitor of human leukocyte elastase, an enzyme known to damage the lung parenchyma. Absence of alpha1-antitrypsin results in a susceptibility to protease injury. If persons with this deficiency smoke, they may develop a severe panlobular form of emphysema, often at an early age. Occurrences of familial clustering of COPD without an alpha1-antitrypsin deficiency (4,5) imply that other genetic factors are responsible for susceptibility to injury from tobacco smoke.
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Currently, researchers are attempting to get a better understanding of the disease to be able to more effectively treat COPD. There are several medications that are being researched. One such area of research is cytokine modulators. These substances are thought to work on certain chemicals in the body that may worsen COPD. Another option for some individuals may be surgery. There have been studies showing that emphysema patients may benefit from surgery to decrease their lung volume.
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COPD is defined as airflow obstruction resulting from chronic bronchitis or emphysema (2). This classification excludes a number of specific causes of chronic airflow limitation, including cystic fibrosis, asthma, bronchiectasis, and bronchiolitis obliterans. In the clinical setting... diagnosis of these alternative conditions, particularly asthma, is not always conclusive. For a list of features that can help in distinguishing COPD from asthma, see table 1.
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