Dpoc
Prior to 1979, patients presenting with lung destruction and airflow obstruction were often classified by symptoms (Chronic asthma and Chronic bronchitis), or by pathological changes (Emphysema).
Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years.
Emphysema, on the other hand, is defined histopathologically as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.
Airflow limitation in emphysema is due to loss of elastic recoil and due to reduction of the surface area available for the exchange of gases during breathing, whereas in chronic bronchitis hyperplasia and hypertrophy of the goblet cells and mucous glands of the airway result in more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls further. As chronic bronchitis progresses, there is squamous metaplasia and fibrosis. All these changes lead to narrowing of airway caliber and increase in airway resistance. Although some patients predominantly display signs of one or the other, most fall somewhere in the middle of the spectrum. Recognition that these entities overlapped and often coexisted led to the term COPD.
Recent definition of COPD
‘COPD is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases’.
Pathophysiology
The pathogenic mechanisms are not clear but most likely involve diverse mechanisms. The increased number of activated polymorphonuclear