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Chronic obstructive pulmonary disease (COPD) is the umbrella term used to describe emphysema and chronic bronchitis. Along with asthma and cystic fibrosis, COPD is part of a larger class of lung diseases characterized by the obstruction of airflow through the respiratory system. While COPD pathophysiology is still not fully understood, the symptoms and progression of COPD seem to be closely tied to lung tissue inflammation. Long-term exposure to cigarette smoke or other irritants trigger the inflammatory response of the lungs, resulting in structural and cellular changes to the tissues of the respiratory system. COPD pathophysiology usually manifests as either emphysema, chronic bronchitis, or in many patients it is a combination of the two.
Cigarette smoking is usually cited as the most common risk factor for COPD. Other risk factors include workplace exposure to inhaled irritants such as coal dust or cadmium. Women, having proportionately smaller lungs and airways than men, are more likely to develop symptoms of COPD. There is also a genetic variant of the disease associated with a congenital absence of an important pulmonary enzyme; however, this form of COPD has a clearly defined pathophysiology that is distinct from irritant related COPD pathophysiology.
The common factor that causes emphysema and chronic bronchitis to be grouped together under the single diagnosis of COPD is airflow restriction. Since many patients exhibit symptoms of both diseases and the two share a common etiology and pathophysiology, it can make sense to refer to them as a single entity. Airflow restriction can occur as a result of loss of elasticity of the lung tissue due to emphysema, chronic mucus congestion associated with chronic bronchitis, or persistent narrowing of the airways due to inflammation. As a result, COPD patients are often prescribed medicine inhalers designed to open up the airways and make breathing easier.
Healthy lungs contain millions of tiny air sacs known as alveoli, through which oxygen is exchanged for carbon dioxide by way of a complex network of blood vessels. Emphysema causes these delicate sacs to rupture and blood vessels to be destroyed, leaving existing air sacs badly damaged. When this occurs, the lungs function less efficiently. It becomes increasingly difficult to get enough oxygen or to expel carbon dioxide, and the patient may suffer symptoms associated with a lack of oxygen.
While emphysema affects primarily the small air sacs and blood vessels of the lungs, chronic bronchitis targets the larger airways. When respiratory tissues are damaged, the body's inflammatory response causes the airways to become swollen and narrowed, and excess mucus is secreted in an effort to protect the lungs from inhaled irritants. Unfortunately, the airway inflammation and increased mucus lead to congestion and breathing difficulty. The combined COPD pathophysiology of emphysema and chronic bronchitis leads to shortness of breath, weakness, dizziness, fatigue, and a persistent, productive cough.
In the early stages of COPD, these symptoms may not be particularly noticeable or bothersome, and could easily be ignored or assumed to be just another part of aging. As the disease progresses, COPD is characterized by frequent exacerbations in which symptoms abruptly worsen following a period of illness. These exacerbations will often lead to the patient being hospitalized and treated with steroids and supplementary oxygen. Over time, COPD pathophysiology can come to include a barrel chest caused by hyperinflation of the lungs, bluing of the mouth and fingers from chronic lack of oxygen, and a persistent wheeze caused by narrowing and congestion of the airways.
If allowed to progress, COPD pathophysiology eventually will require constant oxygen supplementation and specialized nursing care. Complications of end-stage COPD include heart failure, collapsed lung, and sudden respiratory failure. COPD is an irreversible disease that results in a shortened overall lifespan and a drastically reduced quality of life. The most important step in a treatment plan is to quit smoking. Quitting smoking has been shown to slow the progression of the disease significantly, and if caught early, lung function can be retained and quality of life preserved well into the later years.