Pathophysiology of COPD

Chronic obstructive pulmonary disease (COPD) encompasses a group of lung conditions that cause narrowing of the airways, leading to shortness of breath and difficulty in breathing. It is a progressive disease in which symptoms worsen with time.

Chronic bronchitis and emphysema are the most common forms of COPD. In chronic bronchitis, the lining of the airways is thickened as a result of constant irritation, which leads to excess secretion of mucus. In case of emphysema, the air sacs are gradually destructed, resulting in the obstruction of airflow.

Majority of the cases of chronic obstructive pulmonary disease are caused due to long-term smoking. Inhalation of lung irritants such as pollens, air pollutants, dust, smoke and other chemicals may also contribute to this disease. The early signs of this ailment are chronic cough and coughing up mucous secretions.

Other associated symptoms may include breathing difficulty, chest tightness or discomfort, wheezing and other respiratory symptoms. A patient with COPD is more susceptible to constant chest infections than a healthy person. Thus, COPD is one of the leading causes of medical complications and death in many countries.

The pathophysiology of this pulmonary disease is very complex and is not completely understood. A resistance to the airflow can be attributed to many factors such as mucociliary disorders, inflammatory responses and structural changes.

In short, the blockage or narrowing of the airways may be caused due to loss of elasticity of the airways, damage or inflammation in the walls of the airways, secretion of excess mucus in the airways and decrease in the surface area for exchange of air.

According to medical studies, chronic inflammatory responses of the airways are the major contributing factors for the development of COPD. It is stated that inflammatory responses resulting from COPD and those from asthma are different.

COPD associated inflammation induces the production of neutrophils, macrophages and lymphocytes. These cells along with reactive oxygen and protease enzymes are responsible for causing damage to the airways (alveoli). Smoking increases the number of neutrophils than the normal level.

Eventually, the airways are thickened and excess smooth muscles and connective tissues are produced by the body, leading to fibrosis in the airways. All these inflammatory responses are caused due to prolonged cigarette smoking and at times, frequent exposure to lung irritants.

The COPD pathophysiology thus includes -

• Narrowing of the airways
• Damage to the lungs and other supportive tissues
• Hyperactivity of the lungs
• Dysfunction of the cilia in the airways
• Constant damage of the alveolar walls

As the COPD condition progresses with time, patients manifest wheezing, productive cough, difficulty in clearing alveoli and shortness of breath (dyspnea). Since the pressure in the chest increases, the patient faces more difficulty during exhalation, rather than inhalation.

In medical science, there is no cure for COPD. To put in simple words, damage in the airways cannot be reversed back. However there are certain treatment options that can help manage the breathlessness symptoms.

The most effective treatment approach of COPD is to quit smoking; one can opt for nicotine replacement therapy to cope with the nicotine withdrawal symptoms.

Likewise, avoid exposure to chemicals and lung irritants as far as possible. Other treatment options for COPD include oxygen therapy (if necessary) and medication such as corticosteroids and antibiotics (for chest infection).