Pathogenesis of COPD

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized and defined by limitation of expiratory airflow. This can result from several types of anatomical lesions, including loss of lung elastic recoil and fibrosis and narrowing of small airways. Inflammation, edema, and secretions also contribute variably to airflow limitation. Smoking can cause COPD through several mechanisms. First, smoke is a powerful inducer of an inflammatory response. Inflammatory mediators, including oxidants and proteases, are believed to play a major role in causing lung damage. Smoke can also alter lung repair responses in several ways. Inhibition of repair may lead to tissue destruction that characterizes emphysema, whereas abnormal repair can lead to the peribronchiolar fibrosis that causes airflow limitation in small airways. Genetic factors likely play a major role and probably account for much of the heterogeneity susceptibility to smoke and other factors. Many factors may play a role, but to date, only alpha-1 protease inhibitor deficiency has been unambiguously identified. Exposures other than cigarette smoke can contribute to the development of COPD. Inflammation of the lower respiratory tract that results from asthma or other chronic disorders may also contribute to the development of fixed airway obstruction. COPD is not only a disease of the lungs but is also a systemic inflammatory disorder. Muscular weakness, increased risk for atherosclerotic vascular disease, depression, osteoporosis, and abnormalities in fluids and electrolyte balance may all be consequences of COPD. Advances in understanding the pathogenesis of COPD have the potential for identifying new therapeutic targets that could alter the natural history of this devastating disorder.

Mechanisms to dyspnoea and dynamic hyperinflation related exercise intolerance in COPD

“…Elastic recoil of the lungs can reduce because of destruction in the alveolar attachment and as a consequence static hyperinflation can develop (2,21,41). Airway resistance is increased in COPD, and as a consequence, flow limitation can develop (2,21,41). Flow limitation is progressive; it has association with chronic inflammation of the airways in response to noxious particles and gases (2).…”

“…As a basic feature of emphysema, the alveolar wall can be destroyed and the surface of gas exchange can reduce. Elastic recoil of the lungs can reduce because of destruction in the alveolar attachment and as a consequence static hyperinflation can develop (2,21,41). Airway resistance is increased in COPD, and as a consequence, flow limitation can develop (2,21,41).…”

“…COPD is a structural and functional disorder of the lungs, which has an effect on lung parenchyma and lung mechanics (2,5,21,41). As a basic feature of emphysema, the alveolar wall can be destroyed and the surface of gas exchange can reduce.…”

Circulating Endothelial Microparticles as a Measure of Early Lung Destruction in Cigarette Smokers

“…When put under the chronic stress of cigarette smoking, alveoli may be destroyed, resulting in emphysema (2)(3)(4)(5)(6). The pathogenesis of emphysema is complex and includes the balance of proteases and antiproteases in the lung, tilted toward an excess of unopposed proteases that destroy the connective tissue backbone of the lung parenchyma (2-7).…”

C-reactive protein levels, airflow obstruction, and chronic kidney disease

“…Increasing evidence suggests that COPD is associated with systemic inflammation, cardiovascular diseases, diabetes, and hypertension [2,[6][7][8], which leads to the possibility that COPD is not only a disease of the lungs but also a systemic inflammatory disorder. However, the underlying mechanisms of COPD are still poorly understood [2,9,10].…”