High concentrations of free radicals in tobacco smoke produce oxidative stress. Free radicals as well as tobacco smoke also impair the activity of anti-protease enzymes such as alpha 1-antitrypsin, allowing damage to the lung by protease enzymes. Cytokine release responds to irritant particles such as tobacco smoke in the airway due to the inflammation of the body.
The COPD phenotypes are of two kinds, emphysema and chronic bronchitis. In the past the two fold nature of the pathology has been studied. Each patient could be classified according to recent studies by many authors who find patients presenting a emphysematous phenotype, or a predominantly bronchial, by simply analyzing functional, radiological, and clinical findings or by studying interesting biomarkers. Also the specific predominant mechanism of airflow limitation is reflected by a statistical model for a specific patient. This has been trained and developed over a database obtained from hundreds of patients.
In chronic bronchitis there is inflammation and damage in the large airway that we called blue bloater. In clinical terms it is defined as a cough with the production of sputum on at least three months a year for two consecutive years. Sputum is produced on most days during this period. In the airways of the lungs hallmark of chronic bronchitis, there is increase in size of hypertrophy of the mucus glands and goblet cells of the airway as well as increase in the number of hyperplasia. Airways get narrowed as there is more mucus as compared to the usual mucus in the airways, and this causes coughing with sputum. The walls of the airways get infiltrated with the inflammatory cells if seen through a microscope.
Remodeling and scarring are the result of this inflammation which thickens the walls of the airways thus resulting in narrowing of airways. Abnormal changes take place in tissues lining the airways, which is called squamous metaplasia. Fibrosis is also caused which is the scarring and further thickening of the walls of the airways. Limitation of airflow is the consequence of these changes. As compared to emphysema patients with advanced COPD have chronic bronchitis primarily which were commonly referred to as ‘blue bloaters’. The term ‘blue bloaters’, is used because of the bluish color of the lips and the skin and hypoxia and fluid retention.
Lung surface in emphysema shows multiple cavities in the walls of the lungs lined by deposits of heavy black carbon that we called pink puffer. Inflammation of the air sacs called the alveoli and lung damage results in emphysema. Enlargement of the air spaces distal to the terminal bronchioles along with the walls of the airways being destructed is called emphysema. Less surface area is available for exchange of carbon dioxide and oxygen due to the destruction of air space walls during breathing. Airways embedded in the lung face loss of support as the elasticity of the lungs keep reducing . There is further limitation to airflow as these airways are more likely to collapse over a period of time. Patients have to put in more effort during exhalation causing a pink color in their faces. ‘Pink puffers’ is the commonly used term for such cases.
Effectiveness of the lungs gets limited with the narrowing of the airways which reduce the rate at which the air can flow from and to the air sacs which are called alveoli. It is during expiration or breathing out that the greatest reduction in air flow occurs in COPD. This happens because the pressure in the chest tends to compress rather than expanding the airways. By breathing more forcefully air flow could be increased thus increasing pressure in the chest during expiration. A situation known as expiratory flow limitation is caused and in COPD there is often a limit as to how much this can actually increase the air flow. While exercising breathing has to be faster, and if the airflow is very low people with COPD will not be able to finish breathing out completely before another breath has to be taken.
Before the next breath starts, some of the air of the previous breath remains within the lungs, which increases the volume of air in the lungs. Dynamic hyperinflation is the name of this process which is again closely linked to dyspnea which is also referred to as shortness of breath in COPD. With hyperinflation it is difficult to breathe, because more effort needs to be taken to move the chest wall and lungs when they have already been stretched due to hyperinflation. There is also loss of surface area available for exchange of carbon dioxide and oxygen with emphysema leading to high carbon dioxide levels and low oxygen levels in the body. To compensate the person with emphysema has to breathe faster which can be difficult to do if there is also hyperinflation or flow limitation. The condition calls for a well informed and researched take on medication and medical plan of action.