Overview of chronic obstructive pulmonary disease (COPD)
This page compiles our content related to chronic obstructive pulmonary disease (COPD). For further information on diagnosis and treatment, follow the links below to our full BMJ Best Practice topics on the relevant conditions and symptoms.
Introduction
Afecciones relevantes
COPD | vaya a nuestro tema completo sobre COPD The hallmark of COPD is chronic inflammation that affects central and peripheral airways, lung parenchyma and alveoli, and pulmonary vasculature. 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. The pooled global prevalence of COPD is 15.7% in men and 9.93% in women.[6] |
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Acute COPD exacerbation | vaya a nuestro tema completo sobre Acute COPD exacerbation 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.[7][8][9][10][11] Acute exacerbations tend to become more frequent and more severe as COPD progresses, and may themselves accelerate the progression of COPD.[12][13][14] |
Smoking cessation | vaya a nuestro tema completo sobre Smoking cessation Avoidance of tobacco exposure (both active and passive measures) is an important part of COPD prevention and management. Among the different therapeutic modalities in COPD, smoking cessation is one of the only factors that improves survival. Healthcare professionals play a central role in motivating and assisting patients to quit. |
Alpha-1 antitrypsin deficiency | vaya a nuestro tema completo sobre Alpha-1 antitrypsin deficiency An autosomal codominant 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.[15][16] Pulmonary manifestations include emphysema, COPD, and bronchiectasis. One European study estimated that approximately 1 in every 850 patients with COPD has an alpha-1 antitrypsin protease inhibitor ZZ genotype, which is associated with severe disease.[17] The World Health Organization recommends that all patients with a diagnosis of COPD should be screened once, especially in areas with high prevalence of AAT deficiency.[18] |
Evaluation of dyspnea | vaya a nuestro tema completo sobre Evaluation of dyspnea The etiology of dyspnea covers a broad range of pathologies from mild, self-limited processes to life-threatening conditions. Diseases of the cardiovascular, pulmonary, and neuromuscular systems are the most common. Exacerbation of COPD is a common cause of subacute dyspnea. Chronic dyspnea is a feature of stable COPD. |
Evaluation of chronic cough | vaya a nuestro tema completo sobre Evaluation of chronic cough Subacute cough is most often self-limiting, but chronic cough may provide significant challenges for effective evaluation and management. Chronic bronchitis (one of the manifestations of COPD) is among the common causes. |
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This overview has been compiled using the information in existing sub-topics.
Referencias
Artículos de referencia
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