Last Updated: 2015-01-28
Chronic obstructive pulmonary disease (COPD) is a disorder that is usually progressive, characterized by airflow limitation that is not fully reversible.   It encompasses both emphysema and chronic bronchitis. Around 90% of cases of COPD are caused by cigarette smoking; other strong risk factors include more advanced age (may be related to longer period of smoking) and genetic factors (e.g., alpha-1 antitrypsin deficiency).
Suspected in patients with a history of smoking, occupational/environmental risk factors, or a personal or family history of chronic lung disease. Presents with progressive shortness of breath, wheeze, cough, and sputum production. Treatment includes smoking cessation, bronchodilators, and corticosteroids. Long-term oxygen therapy improves survival in severe COPD.1[B] Evidence Evidence
Acute exacerbations of COPD range from very mild to severe and life-threatening, and are commonly triggered by bacterial or viral pathogens, pollutants, or changes in temperature and humidity. They present with an acute-onset, sustained worsening of the patient's respiratory symptoms, lung function, functional status, and quality of life.      Acute exacerbations tend to become more frequent and more severe as COPD progresses,   and may themselves accelerate the progression of COPD.   In addition to the usual therapies used for COPD, antibiotics have been found to be beneficial for the treatment of acute exacerbations,   and are recommended in patients suspected of having a bacterial trigger. 
Diagnostic tests such as spirometry, PFTs, CXR, ABG analysis, and chest CT scan help to confirm COPD and to exclude alternate diagnoses.
Cough is the usual initial symptom of COPD: frequently, a morning cough that may become constant as the disease progresses. Usually productive, and sputum quality may change with exacerbations or superimposed infection.
A genetic disorder in which affected individuals lack effective activity of a specific protease inhibitor, alpha-1 antitrypsin (AAT). This enzyme is responsible for neutralizing neutrophil elastase and thus preventing inflammatory tissue damage in the lungs.   AAT deficiency usually manifests as early onset emphysema in smokers. However, nonsmokers may also be affected, while some smokers may never exhibit disease.
Often presents with recurrent pulmonary infections, including a chronic daily productive cough with copious mucopurulent sputum. Identification and treatment of comorbid diseases and the underlying condition are important to treatment success.