Copd
COPD
COPD is characterized by airflow limitation that is poorly reversible. Cumulative, chronic exposure to cigarette smoking is the number one cause of the disease, but repeated exposure to secondhand smoke, air pollution and occupational exposure (to coal, cotton, grain) are also important risk factors.
Chronic inflammation plays a major role in COPD pathophysiology. Smoking and other airway irritants cause neutrophils, T-lymphocytes, and other inflammatory cells to accumulate in the airways. Once activated, they trigger an inflammatory response in which an influx of molecules, known as inflammatory mediators, navigate to the site in an attempt to destroy and remove inhaled foreign debris.
Under normal circumstances, the inflammatory response is useful and leads to healing. In fact, without it, the body would never recover from injury. In COPD, repeated exposure to airway irritants perpetuates an ongoing inflammatory response that never seems to shut itself off. Over time, this process causes structural and physiological lung changes that get progressively worse.
As inflammation continues, the airways constrict, becoming excessively narrow and swollen. This leads to excess mucus production and poorly functioning cilia, a combination that makes airway clearance especially difficult. When people with COPD can't clear their secretions, they develop the hallmark symptoms of COPD, including a chronic, productive cough, wheezing and dyspnea. Finally, the build-up of mucus attracts a host of bacteria that thrive and multiply in the warm, moist environment of the airway and lungs. The end result is further inflammation, the formation of diverticula (pouch-like sacs) in the bronchial tree, and bacterial lung infection, a common cause of COPD exacerbation.
Statistics
COPD is the third-leading cause of death in the United States, preceded by only heart disease and cancer. It kills over 126,000 Americans annually.
COPD is characterized by airflow limitation that is poorly reversible. Cumulative, chronic exposure to cigarette smoking is the number one cause of the disease, but repeated exposure to secondhand smoke, air pollution and occupational exposure (to coal, cotton, grain) are also important risk factors.
Chronic inflammation plays a major role in COPD pathophysiology. Smoking and other airway irritants cause neutrophils, T-lymphocytes, and other inflammatory cells to accumulate in the airways. Once activated, they trigger an inflammatory response in which an influx of molecules, known as inflammatory mediators, navigate to the site in an attempt to destroy and remove inhaled foreign debris.
Under normal circumstances, the inflammatory response is useful and leads to healing. In fact, without it, the body would never recover from injury. In COPD, repeated exposure to airway irritants perpetuates an ongoing inflammatory response that never seems to shut itself off. Over time, this process causes structural and physiological lung changes that get progressively worse.
As inflammation continues, the airways constrict, becoming excessively narrow and swollen. This leads to excess mucus production and poorly functioning cilia, a combination that makes airway clearance especially difficult. When people with COPD can't clear their secretions, they develop the hallmark symptoms of COPD, including a chronic, productive cough, wheezing and dyspnea. Finally, the build-up of mucus attracts a host of bacteria that thrive and multiply in the warm, moist environment of the airway and lungs. The end result is further inflammation, the formation of diverticula (pouch-like sacs) in the bronchial tree, and bacterial lung infection, a common cause of COPD exacerbation.
Statistics
COPD is the third-leading cause of death in the United States, preceded by only heart disease and cancer. It kills over 126,000 Americans annually.