Chronic obstructive pulmonary disease (COPD) is a heterogeneous lung disease state characterized by chronic respiratory symptoms and airflow limitation that is often progressive and not fully reversible.[1] Globally, there are about three million deaths from COPD each year.[2] Around 40% to 70% of cases of COPD are caused by cigarette smoking; other strong risk factors include advanced age (may be related to longer period of smoking), genetic factors (e.g., alpha-1 antitrypsin deficiency), and lung growth and development.[3] [4] In most patients with COPD, there is significant concomitant chronic disease, which has an impact on morbidity and mortality.[5]
Overview
Related Diseases & Conditions
Summary
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]Summary
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]Summary
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.Summary
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]Summary
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.Summary
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.
Citations
1. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for prevention, diagnosis and management of COPD: 2023 report. 2023 [internet publication].[Full Text]
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10. Spencer S, Jones PW; GLOBE Study Group. Time course of recovery of health status following an infective exacerbation of chronic bronchitis. Thorax. 2003;58:589-593.[Abstract][Full Text]
11. Xu W, Collet JP, Shapiro S, et al. Negative impacts of unreported COPD exacerbations on health-related quality of life at 1 year. Eur Respir J. 2010;35:1022-1030.[Abstract][Full Text]
12. Burge S, Wedzicha JA. COPD exacerbations: definitions and classifications. Eur Respir J Suppl. 2003;41:46s-53.[Abstract][Full Text]
13. Hurst JR, Vestbo J, Anzueto A, et al. Susceptibility to exacerbation in chronic obstructive pulmonary disease. N Engl J Med. 2010 Sep 16;363(12):1128-38.[Abstract][Full Text]
14. Donaldson GC, Seemungal TA, Bhowmik A, et al. Relationship between exacerbation frequency and lung function decline in chronic obstructive pulmonary disease. Thorax. 2002;57:847-852.[Abstract]
15. Laurell CB, Eriksson S. The electrophoretic alpha 1-globulin pattern of serum in alpha 1-antitrypsin deficiency. Scand J Clin Lab Invest. 1963;15:132-140.
16. Brantly M, Nukiwa T, Crystal RG. Molecular basis of alpha 1-antitrypsin deficiency. Am J Med. 1988;84:13-31.[Abstract]
17. Blanco I, Diego I, Bueno P, et al. Prevalence of alpha(1)-antitrypsin PiZZ genotypes in patients with COPD in Europe: a systematic review. Eur Respir Rev. 2020 Jul 21;29(157):200014.[Abstract][Full Text]
18. Alpha 1-antitrypsin deficiency: memorandum from a WHO meeting. Bull World Health Organ. 1997;75(5):397-415.[Abstract][Full Text]
