Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterised by airflow limitation that is not fully reversible.

The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.

Although COPD affects the lungs, it also produces significant systemic consequences.

Chronic bronchitis is defined clinically as chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of productive chronic cough have been excluded [1].

Emphysema is defined pathologically as the presence of permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis [2].

In patients with COPD either of those conditions may be present. However, the relative contribution of each to the disease process is often difficult to discern.

Asthma differs from COPD in its pathogenic and therapeutic response, and should therefore be considered a different clinical entity [3]. However, some patients with asthma develop poorly reversible airflow limitation. These patients are indistinguishable from patients with COPD but for practical purposes are treated as asthma.

The high prevalence of asthma and COPD in the general population results in the co-existence of both disease entities in many individuals. This is characterised by significant airflow limitation and a large response to bronchodilators. In these patients, the forced expiratory volume in one second (FEV1) does not return to normal and frequently worsens over time. There is a great need to design studies aimed at determining the prevalence, natural history, clinical course and therapeutic response in these patients.

Other conditions: poorly reversible airflow limitation associated with bronchiectasis, cystic fibrosis and fibrosis due to tuberculosis are not included in the definition of COPD and should be considered in its differential diagnosis.

All patients with a family history of respiratory illnesses, patients presenting with airflow limitation at a relatively early age (4th or 5th decade) should be tested for ?1-antyripsin deficiency.