Chronic obstructive pulmonary disease (COPD): Clinical

Chronic obstructive pulmonary disease, or COPD is characterized by obstruction of airflow due to either inflammation of the airways, or chronic bronchitis, and destruction of the alveolar wall with dilation of the airspaces, or emphysema.

These events are due to inflammation that’s often triggered by inhalation of toxic substances, like tobacco smoke, as well as occupational pollutants like dust and silica.

Most people have elements of both chronic bronchitis and emphysema, so they’re often clumped together under the term COPD.

Alright, now chronic bronchitis is characterized by an inflammatory process that leads to increased mucus production, which obstructs the airways and leads to air trapping behind those mucus plugs.

Chronic bronchitis is clinically defined as having a productive cough for more than 3 months each year for 2 or more consecutive years.

Now, zooming in for a moment, the body maintains a balance between elastases, which destroy elastin in the alveolar wall and respiratory bronchioles, and anti-elastases, which stop elastase from doing just that.

In emphysema an inflammatory response to tobacco smoke tips the balance towards elastases, causing excessive destruction of the alveolar wall.

Without elastin, the elastic recoil that normally maintains the patency of the alveoli and respiratory bronchioles during exhalation is lost, and so these small airways collapse when the person tries to breathe out.

If air can’t get out, it becomes trapped in the alveoli, causing the airspaces to “puff up”.

Also, by destroying the alveolar-pulmonary capillary interface, gas exchange is impaired, resulting in hypoxemia and retention of carbon dioxide or CO2.

But not all cases of COPD are directly related to smoking.

In people under 45 years of age with COPD, it’s important to consider alpha-1 antitrypsin deficiency which is an autosomal dominant disorder.