Chronic Obstructive Pulmonary Disease, commonly known as COPD is the fourth leading cause of death in the world. This degenerative disease is causes gradual and progressive obstruction and destruction of the lungs and airways. Symptoms of COPD and its related lung conditions can include mild symptoms such as increased sputum, persistent cough and mild inflammation. The more severe symptoms are shortness of breath, severe inflammation, recurrent bacterial and viral infections and breathlessness. COPD includes several lung pathologies, specifically chronic bronchitis and emphysema. Chronic obstructive pulmonary disease is primarily caused by cigarette smoke. Other irritants and air pollutants can play a role as well, but the main culprit has proven to be cigarette smoke ("Clinical review: Copd," 2012).
Initially, cigarette smoke assaults the lining of the airways by paralyzing the cilia that line our airways. The function of the cilia is to help propel the mucus out of the airways. Over time and repeated exposure to smoke and other environmental irritants, the non-functioning cilia will degenerate and the surface of the airways will become bald. The airways now begin to fill with excess mucus that traps bacteria, but now there is no way to expel it. The mucus and bacteria begin to accumulate excessively. This results in frequent infections, air flow obstruction and inflammation leading to even more obstruction. Normally, the lining of the airways consist of columnar cells, however, once the cilia is lost, the columnar cells change into cuboidal cells that eventually change into simple squamous epithelium. This structural change in the airways is known as squamous cell metaplasia. Squamous cell metaplasia leads directly to chronic bronchitis and emphysema (Wojciechowski, 2010).
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Chronic bronchitis is an inflammation of the bronchial tubes due to recurrent infections. A clinical diagnosis of chronic bronchitis can be made after a patient suffers from bronchial congestion and infection for at least three months a year for two consecutive years. The inflammation and infection are triggered by the excess mucus and bacteria that cannot be expelled. Chronic bronchitis can result in air becoming trapped in the lungs and hyperinflation of the lungs. Hyperinflation is characterized by a "barrel-chested" appearance of the patient. Due to hyperinflation, the lung tissues lose their elasticity or their ability to recoil. As this chain of events continues, breathing becomes more and more difficult (Wojciechowski, 2011).
Emphysema is another condition directly involved with COPD. By definition, emphysema is the enlargement of the air spaces in the lungs. Symptoms include wheezing, shortness of breath, dyspnea (breathlessness), and difficulty exhaling due to the loss of elasticity of the lung tissues. This loss of elasticity also causes the walls of the alveolar air sacs to rupture upon inspiration. The alveoli normally consist of several tiny air sacs providing adequate surface area for gas exchanges. When the walls of these air sacs rupture, the alveoli is left with a few large air spaces and significantly less surface area for gas exchange, this results in blood pH imbalances and a lack of vital oxygen needed throughout the body. As the lungs struggle to take in oxygen and expel carbon dioxide through inflamed and obstructed airways, the gas exchange process is now hindered as well. The blood cannot be properly oxygenated and the carbon dioxide cannot be properly removed (Taraseviciene-Stewart & Voelkel, 2008).
The destruction continues as the inadequate gas exchange and supply causes a chain reaction of events that can lead directly to heart failure. The excess carbon dioxide in the blood will cause the blood pH to become acidic, this is a condition known as acidosis. The lack of oxygen in the blood causes oxygen deficiencies throughout the body tissues, including the heart. Now the heart muscle cannot accommodate the body's need for oxygenated blood as its pumping functions depreciate. The lungs and heart work closely together, therefore, the symptoms of heart failure are often the same as the symptoms of chronic obstructive pulmonary disease. When a patient complains of shortness of breath, fatigue or breathlessness, a physician should run tests for both heart failure as well as COPD ("Breathe easier--and reduce," 2012).
Diagnosis of COPD is based on several factors that may include patient history and genetic predispositions, spirometer readings, chest X-rays, complete blood count (CBC) tests, and oxygen saturation is also checked. A patient's history will include pre-existing conditions, whether or not the patient smokes and how much, the patient's work and home environments and family history giving clues as to any genetic susceptibilities. A spirometer is used to measure lung volume, particularly the forced vital capacity of the patient. Forced vital capacity refers to how much air the patient can forcefully expel from the lungs after taking the deepest breath possible. A chest X-ray is used to visually confirm or deny lung damage and conditions. A complete blood count blood test can confirm or eliminate anemia as a possible explanation for the symptoms such as breathlessness and fatigue. Oxygen saturation levels should be closely monitored. In the event that the patient has a SaO2 level that falls below ninety-two percent, the patient should be assessed for further oxygen therapy. Because the symptoms of COPD occur gradually over time, it can go undiagnosed for decades ("Clinical review: Copd," 2012).
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Another reason COPD goes undiagnosed for so long, is the social stigma that is attached to COPD patients. As we stated before, smoking is the number one cause of chronic obstructive pulmonary disease. Therefore, a smoker who chooses to self-induce obstructive lung disease is held responsible for their decisions. When a COPD patient has to carry around an oxygen tank, it limits the quality of social interaction. Along with social interaction, sympathy and opinions of others are also quite limited. That COPD patient chose to smoke, however, the tax payers and those who are forced to pay outrageous insurance premiums were not given a choice. These chronically ill patients become a burden on all of society and they have only themselves to blame (Barr, 2010).
A patient suffering from COPD may not seek diagnosis and treatment until exacerbation occurs. An exacerbation is when COPD symptoms radically change from mild and moderate to extremely severe. Exacerbations usually occur when a COPD patient gets a viral or bacterial infection. The most common viruses involved are rhinovirus, influenza and parainfluenza. Common bacteria can include Haemophilus influenzae, Streptococcus pneumoniae and Moxarella cattharalis. The pre-existing excessive bacteria make it difficult to pinpoint exactly which bacterium is causing the infection. Exacerbations recur often in COPD patients due to the constant overabundance of mucus and bacteria build-up ("Clinical review: Copd," 2012).
There are many medications and treatments that help alleviate the symptoms of COPD, however, there is no cure. Several medications, mostly inhalants are used such as bronchodilators to enlarge the airways, corticosteroids to reduce inflammation, antibiotics to fight infection, and expectorants to help loosen and expel mucus. Other treatments used are nebulizer treatments (often albuterol sulfate) which are used to help open the airways and concentrated oxygen therapy is used to compensate for the low oxygen levels. Smoking cessation aids and counseling are encouraged for every COPD patient. More invasive and drastic procedures that include lung volume reduction surgery and lung transplants have also been performed. New bronchoscopic procedures are also being developed by pulmonologists such as the insertion of one-way valves into the pockets of diseased lung tissue, biologic tissue destruction with induction of scarring, and stent placement to create decompression of hyperinflated lungs (Jancin, 2006).
Recently, scientists have discovered elevated levels of the EMAP11 cytokine in the lungs of patients with COPD. This cytokine is known for playing a role in the early development of the lungs, however, it is also known to cause cell death. A research team designed an antibody to specifically target the EMAP11 cytokine and inhibit the actions of it. These scientists performed tests on mice with smoke induced COPD, as they exhibited the identical EMAP11 cytokine present in their lungs. The mice that were treated with the antibody showed significantly less cell death than the mice that remained untreated. Currently, the research continues ("Protein could offer," 2011).
Both research and treatments of COPD are costly, totals have been estimated to be approximately fifty billion dollars each year and these annual costs continue to increase. All of this is predominantly caused by smoking cigarettes. The most cost-efficient choice one could make for everyone is to just stop smoking. This degenerative disease claims the lives of approximately 120,000 Americans each year (Reese, 2010). National awareness and education will hopefully deter future perspective smokers. In most cases, COPD could have been avoided had better choices been made. Even though, ninety percent of COPD cases involve smokers, not all smokers will develop COPD. Only twenty percent of smokers will develop some form of COPD (Wojciechowski, 2010). Genetics plays a key role in deciding who will develop COPD and who will not. Other environmental irritants and pollutants will also contribute to the deciding factors. COPD is a physically, emotionally and financially debilitating disease that is much too often, a path chosen by its patients. Prevention and early detection is vital, therefore, choose not to smoke and visit your physician regularly.