Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) is a chronic lung disease that encompasses a group of lung conditions that causes structural changes of the airways and alveoli, the dysfunction of cilia and an inflammatory response. It is a progressive disease that symptoms worsen over time and is characterized by an accelerated decline in lung function. Chronic bronchitis and emphysema are the most common forms of COPD and long- term smoking is the biggest contributing factor in the development and progression of the disease. COPD has become the 3rd leading cause of death worldwide and it affects nearly 32 million people in the U.S. alone. (Caress, Luker, & Chalmers, 2010) It is estimated that 90% of cases of COPD are caused by cigarette smoking but, interestingly, only 15-20% of smokers are diagnosed with COPD. (Wilson, Elborn, & Fitzsimmons, 2010) In addition to pulmonary abnormalities it has systemic affects as well including skeletal muscle dysfunctions, osteoporosis, cor pulmonale, body mass changes and mood disorders. (Garvey, 2011) The pathophysiology of COPD is not completely understood and is a mixed disorder that includes chronic bronchitis and/or emphysema. It is characterized by limited airflow associated with an abnormal inflammatory pulmonary response to noxious particles or gases, primarily from cigarette smoke. The blockages, or narrowing of the airways, may be caused due to loss of elasticity of the airways, damage or inflamation in the walls of the airways, secretion of excess musus and a decrease in the surface area of gas exchange or damage to the alveolar walls. COPD assoicated with inflamation induces the production of neutrophils, marcophages, and lymphocytes. These cells, along with reactive oxygen and protease enzymes are responsible for causing damage to the alveoli. Smoking cigarettes induces macrophages to release neutrophil chemotactic factors or elastases which leads to tissue destruction by causing the airways to become thickened and excess smooth muscle and connective tissue are then produced by the body leading to fibrosis in the lungs. Also, there is an increase of oxidative stress caused by free radicals in cigarette smoke and the oxidants released by phagocytes and polymorphonuclear leukocytes all may lead to necrosis of the exposed cells in the lungs.These inflammatory responses are due to prolonged cigarette smoking or frequent exposures to lung irritants or environmental pollents. ("COPD," n.d.) According to the research early diagnosis and treatment is essential in decreasing morbidity and mortality assoicated with COPD. The diagnostic tool of choice is spirometry or pulmonary function testing (PFT) along with symptom based questionnaires to provide an efficient and coordinated approach to identifing patients with COPD. Prevention is the key since COPD is predominantly caused by smoking. “There is no cure for COPD but refraining from smoking after diagnosis will slow the disease progression and is regarded as the primary intervention for COPD management.” (Wilson et al., 2010, p. 819) Once diagnosed with COPD, treatment will depend on the severity but there should be an ongoing management of symptom control, prevention and early management of exacerbations, and regular office follow-up. There are four stages of COPD ( I-IV) and medication therapy is determined by symptoms. Short acting beta-agnonists, such as albuterol, quickly improve acute dsypnea and are used in all stages of COPD but may be the only treatment needed in the early stages or mild COPD. Long acting brochodilators are the main pharmacotherapy with oral or inhaled steriods to improve pulmonary symptoms in stages II-IV with patients with moderate to severe COPD. Long acting beta-agonists and ICS combination drugs such as Advir are recommended or added for stage III-IV patients with severe COPD and...