Chronic Obstructive Pulmonary Disease (COPD)
Understanding The Causes Of COPD
Chronic Obstructive Pulmonary Disease (COPD) is a slowly progressing disease that often develops over decades as a result of chronic exposure to inhaled irritants, which trigger an inflammatory response in the lungs (Rabe 2007). In a typical case, a patient will experience declining lung function for many years before being diagnosed with COPD and receiving therapy. During this time, the lungs are undergoing several changes characteristic of COPD (Crawford 2008).
Three pathologic processes play a significant role in COPD-related lung damage: (1) oxidative stress, (2) inflammation, and (3) an imbalance in enzymes (e.g., proteases ) involved in cell injury and repair (Fischer 2011).
The bulk of lung tissue is composed of alveoli - tiny air sacs where the exchange of oxygen and carbon dioxide takes place. Having a large surface area and blood supply makes the lungs susceptible to oxidative injury caused by reactive oxygen species (ROS) and free radicals either in air pollutants or released through metabolic processes. Cigarette smoke itself contains numerous oxidizing agents (Loukides 2011).
As a first line of defense, the lungs produce antioxidants such as glutathione, catalases, and peroxidases to detoxify the reactive species. However, in COPD, increased oxidant burden and/or decreased antioxidant defense causes an imbalance (oxidative stress) between the amount of ROS and the body's ability to neutralize them (Stanojkovic 2011). Oxidative stress can cause the air sacs to become less elastic, and the extracellular matrix of the lungs to become damaged (Loukides 2011; Fischer 2011).
The underlying cause of COPD damage is an inflammatory response mounted by the immune system. Chronic exposure to an irritant (e.g., cigarette smoke) causes inflammatory cells (e.g., neutrophils, macrophages, eosinophils) to gather in the airspaces of the lung. In response to the toxins, macrophages release inflammatory chemicals and begin to recruit more immune-system cells, which in turn release more inflammatory chemicals as well as protease enzymes that degrade the extracellular matrix (Fischer 2011; GOLD 2011; Mosenifar 2011).
The two main disease types encompassing COPD are emphysema and chronic bronchitis (Fischer 2011).
- Emphysema occurs when alveoli enlarge and cluster. This process destroys the air sacs where gas exchange occurs. As tissue walls become damaged and disintegrate, the alveoli expand and coalesce into larger, thinner-walled air sacs (i.e., blebs or bullae). As the walls lose their elasticity, the lung tissues become less efficient gas chambers. Gas exchange for oxygen and carbon dioxide worsens as the disease progresses. With weakened air sacs, the airway collapses during expiration (breathing out) causing airway obstruction (Crawford 2008; GOLD 2011).
- As inflammatory cells migrate to the midsize airways, mucus glands in the lungs become enlarged, causing more mucus production and cough. Over time, the bronchial walls thicken, airways narrow (becoming deformed), and airflow becomes more limited (Crawford 2008; GOLD 2011). A number of airway changes occur, including hypertrophy (increase in size) of smooth muscle cells, fibrosis (formation of scar tissue) in the airway walls, and infiltration of inflammatory cells. The term for the lung damage and inflammation of the mucus membrane in the airways is chronic bronchitis. Chronic bronchitis is diagnosed by the presence of cough and sputum production for at least 3 months in each of two consecutive years (GOLD 2011).
Because changes in the lungs develop incrementally, symptoms appear gradually and may be present for many years before medical treatment is initiated. Progressive and chronic coughing, sputum production, and shortness of breath (dyspnea) are the characteristic symptoms of COPD.
A majority of people with COPD also suffer from other medical conditions (e.g., heart disease, osteoporosis, anemia, metabolic syndrome, diabetes, depression, respiratory infections, wasting of the skeletal muscles, and lung cancer) that can affect prognosis (GOLD 2011; Divo 2012). Poor lung function and poor nutrition may also exacerbate muscle weakness, abnormalities in fluid and electrolyte balance, and depression (GOLD 2011; Decramer 2012).