"Emphysema and How it Affects an Individual’ s Way of Life" is a worthy example of a paper on the respiratory system. During these modern times, more diseases affecting many people are being identified and studied in order to find a cure. While many diseases do restore the body’ s normal functions through medications, some illnesses do not have any full-recovery treatment, mainly because the organ afflicted with the disease was already partially or mostly damaged. Emphysema is one example of such diseases that could be halted but not totally cured. But what is emphysema? The term came from Greek words emphysan which means inflate (en=in + physa=breath). The disease arises from the destruction of the tissues that support the shape of the lungs due to a deficiency of an enzyme called alpha 1-antitrypsin. This is a result of habits and activities such as smoking, or the inability of the body to produce the enzyme. Symptoms include shortness of breath during exhalation and the characteristic expanded chest cavity. Being one of the leading causes of death in the United States today, it affects about 112.8 in 100,000 males and 55.4 in 100,000 females (Voelkel & MacNee, 2002, p.
41). Numbers continue to rise due to the prevalence of smoking in populations observed. Pathophysiologic Aspects of Emphysema Emphysema is a progressive and irreversible disease and is a part of chronic obstructive pulmonary disease syndrome (COPD) (Voelkel & MacNee, 2008, p. 63). Shortness of breath due to the collapse of the lung structure, mainly the alveoli prevents the expulsion of air, and that a buildup of carbon dioxide occurs, thus accounting for the shortness of breath. If the disease is not treated immediately, there is the deformation or expansion of the thoracic cavity to assist in the expulsion of air from the lungs. This deformation persists even if the individual afflicted has already been cured. COPD can either be congenital or acquired during adulthood. Also, the disease may be classified according to its location in the lungs: pan lobular emphysema, which is usually all around the lobes of the lung; and centrilobular, usually found around the central and upper portion (Stockley et al. , 2007, p.
3). Congenital COPD arises from the inability of the body to produce α 1-antitrypsin (A1AD), which negates the action of inflammatory response enzymes, such as neutrophil elastase (Voelkel & MacNee, 2008, p.
55). Such enzymes damage ciliated epithelium directly, as well as the structures called alveoli, which participate in the exchange of gases in the lungs. On the other hand, adult-onset emphysema arises mostly from the pollutants being collected in the lungs, which may be due to smoking, inhalation of second-hand smoke, exposure to highly contaminated air, etc. As the pollutants such as tar and other chemicals enter the lungs, inflammatory-response cells such as neutrophils and macrophages increase in number to engulf and destroy the pollutants (Stockley et al. , 2007, p.
6). However, chronic cigarette smoke accelerates the destruction of lung tissues due to the increase in the release of inflammatory-response cells that release digestive enzymes which ultimately destroy the maintenance of alveoli structure. Since emphysema is a gradually progressive disease (Pauwels et al. , 2005, p. 16), depending on how frequent contaminants are inhaled, an individual who has the illness would not be able to distinguish it from asthma due to the similarities in some of the symptoms. But as time passes, things that the person afflicted used to do quite easily become increasingly difficult, because of the collapse of the alveoli for gas exchange. Air that usually gets expelled easily becomes difficult to exhale, and this results in a buildup of carbon dioxide in the blood.
Also, because there is a faulty gas exchange in the alveoli, oxygen absorption is also affected. There would be a time that the affected individual would be working lesser hours due to breathing difficulties, and in turn, the person would be turning in lesser output at work or at home. Another effect of the disease in individuals would be a lesser quality of life. As most activities would require a lot of work and breathing, individuals with emphysema would enjoy their activities a lot lesser due to problems with breathing, as well as always catching their breath. Small things such as short, brisk walks and yard cleaning would become tedious tasks, moreover tiresome and energy-depleting (Pauwels et al. , 2005). Summary and Conclusion Emphysema is a disease of the lungs which is progressive in nature.
An individual having the disease may be cured but the effects of the disease may not fully be reversed. The destruction of the lung tissues may be attributed to an inborn α 1-antitrypsin deficiency (A1AD) which helps maintain the alveolar structure in the lungs. Constant exposure to air pollutants and/or excessive smoking may also trigger the disease either in persons with or without A1AD, though symptoms may be more pronounced in individuals with inborn A1AD. People may fail to seek treatment due to the similarities of the disease with asthma at early stages. It is commonly at its later stages that patients can feel the difference in symptoms due to the destruction of the alveoli, the structure responsible for gas exchange. This hinders the breathing process. Due to the incapacity of the lungs to expel air, structures such as the rib cage and muscles involved in breathing become deformed to be able to perform the function of removing air from the lungs. Due to such difficulties in process of breathing, an individual with emphysema then can have a hard time performing tasks which were initially quite easy to do. This would then decrease an individual’ s activities, which can affect work, family life and recreation. Early prognosis, as well as preventive measures, could slow down, if not stop the disease from taking over an individual and his or her life.
Pauwels, R.A., Postma, D.S. & Weiss, S.T. 2005. Long-term intervention in chronic obstructive lung disease. Monticello, NY: Marcel Dekker Inc.
Stockley, R., Rennard, S., Rabe, K. & Celli, B. 2007. Chronic obstructive pulmonary disease. Malden, MA: Blackwell Publishing Ltd.
Voelkel, N.F. & MacNee, W. 2002. Chronic obstructive lung diseases. Hamilton, Ontario: BC Decker Inc.
Voelkel, N.F. & MacNee, W. 2008. Chronic obstructive lung disease, Volume 2. Hamilton, Ontario: BC Decker Inc.