Table of Contents
The chronic obstructive pulmonary disease (COPD) is defined as a chronic irreversible limitation of airflow characterized by inflammation of the lungs, especially in the peripheral airways and parenchyma. The diseases slowly progress leading to irreversible deterioration of the ability of the lungs to perform its functions. The primary risk factor is cigarette smoking that accounts for up to 90% of COPD cases in the developed world. The paper seeks to analyze the pathophysiology of the disease, clinical manifestations as well as therapeutic and nursing management.
Part A and B: Cellular Basis, Evolution, and Systemic Effects
The development of airflow limitation in patients with COPD emanates from two primary pathological processes. The processes are narrowing of the airways through bronchitis and lung parenchymal destruction (emphysema) including the alveolar. The conditions result from the exposure to majorly cigarette as well as other irritants that characterize polluted air. The inhalation of air containing cigarette smoke and other pollutants may activate surface macrophages and epithelial cells located in the airway. The activation of the cells leads to the release of chemokines and other mediators leading to the mobilization of neutrophils, lymphocytes, and neutrophils that initiate the inflammation and destruction of the cells of the lungs (Barnes, 2014). The inflammation that characterizes COPD is consequential of not only the activation of the innate and adaptive immune system but also the activation of structural epithelial cells of the airway and alveolar, fibroblasts and endothelial cells.
The activation of the epithelial cells through the inhalation of the cigarette smoke and other irritants induces the cells to produce tumor necrosis factor (TNF), interleukin 1, 6 and 8, and granulocyte-macrophage colony stimulating factor (GM-CSF) (Barnes et al., 2014). The local fibrosis witnessed in many cases of COPD result from the release of the Transforming growth factor (TGF) α. Further, the release of the mediators above by the epithelial cells block VEGF receptors leading to the apoptosis of the alveolar cells responsible for the reduced functionality of the lungs in patients with COPD.
Macrophages play a fundamental role in the pathophysiology of COPD. The cells tend to increase up to 10 fold in the airways, lungs, and sputum of the COPD patients. Typically, there is a direct relationship between the number of the macrophages and the degree of emphysema in COPD patients (Petrescu, Biciusca, & Fortofoiu, 2013). Activated by smoke and other irritants, macrophages release inflammatory mediators such as TNF-α, CXCL 1 & 8, reactive oxygen species (ROS) thus linking inflammation in COPD to smoking. The cells also release elastolytic enzymes that interfere with the elasticity of the lung tissues. In heavy smokers, the alveolar macrophages tend to have adverse elastolytic activity through the secretion of the enzyme MMP-9 and exhibit increased secretion of inflammatory proteins. In addition to the inflammatory proteins, the activated macrophages also release CXCL 9, 10 and 11 that are chemotactic for CD8+ and CD4+ T cells. Another feature of the COPD resulting from the activities of the macrophages the increased colonization of the lower airways by bacteria. Such is because the alveolar macrophages exhibit a reduction in the phagocytic functionality (Petrescu et al., 2013).
Neutrophils are also implicated in the pathophysiology of COPD. Like in the case of macrophages, the number of neutrophils correlate with the severity of COPD. Smoking directly stimulates the release of neutrophils from the bone marrow. The cells are recruited into the epithelial cells by E-selectin and migrate the airways by chemotaxis. The neutrophils secret multiple proteases such as elastase and matrix metalloproteinase (MMP) 8 and nine that significantly contribute to the destruction of alveolar (Barnes, 2014). Dendritic cells play a significant role in linking the innate and adaptive immunity in COPD pathophysiology. With an increased expression in COPD patients, dendritic cells are suspected to play a part in the activation of macrophages, neutrophils as well as the T and B lymphocytes.
Another group of cells that contributes to the pathophysiology of COPD is smoking patients are the T lymphocytes. Typically, in cases of COPD, there is a surge in the number of the T cells especially in the lung parenchyma and the airways. Of the T cells, CD8+ and CD4+ cells account for the increase in the figures. Compared to other smokers, COPD patients exhibit an increased number of T cells mainly CD8+ cells and a small increase in CD44 in the airways. CD8+ cells are implicated in the cytolysis and apoptosis of the epithelial cells if the alveolar (Petrescu et al., 2013). The cells release TNF-α, perforins, and granzyme B. The cells are also implicated in the apoptosis of the alveolar cells that characterize emphysema. The conjunction of the roles of the cells leads to the inflammation of the airways, destruction of the alveolar cells, decreased flexibility of the lungs and increased mucus secretion that limits the airflow.
The destruction of the lung tissues and the inflammation of the airways that characterize COPD leads to multiple systemic effects. Markers of inflammation such as the C – reactive protein, reactive oxygen species, cytokines, interleukins, TNF-α, neutrophils among others have been found in other parts of the body in patients with stable COPD (Mohan, Sen & Ranganatha, 2012). The systemic inflammation arises from the impacts of the COPD on the respiratory system. The systemic inflammation leads to a myriad of health complications that may result in fatalities from the disease. COPD and diseases of the heart are correlated (Mohan et al., 2012). The reduction in the functionality of the lungs that is consequential of inflammation reduced elasticity and tissue destruction leads overworking of the heart to ensure an adequate supply of oxygen. Therefore, heart-related conditions arise. COPD also lead to weight loss through the wasting of the skeletal muscles. As a result of increased prevalence of TNF-α, interleukin-1 in circulation, osteoporosis may arise (Gaur & Goel, 2012). The two factors stem from the systemic inflammation.
Part C: Symptoms
During the early stages of COPD, the signs and symptoms may not be apparent. However, the initial symptom of the disease is chronic coughing that increases with time. At the advent of a cough, the disease is mild. Following the coughing is shortness of breath as the inflammation of the airways and destruction of the lung tissues takes the course. The shortness of breath is prevalent during physical activities. As the disease becomes severe, there is wheezing, which result from the constriction of the airways as a consequence of the inflammation affecting the airways (NIHa, 2014). The fourth symptom of COPD is the tightness of the chest. The tightening indicates that the diseases has reached severe levels and is life threatening. The tightening of the chest is characterized by the blockage of the airways from the inflammation and widespread damage to the lungs.
Part D: Medical Treatments
The most commonly administered medication for the COPD patients is bronchodilators. Depending on the severity of the disease, a patient may be put on long acting or short acting bronchodilators which last for up to 12 and 6 hours respectively (NIHb, 2014). Both the short and long acting bronchodilators can be Beta-2-agonists or anticholinergics. The second type of treatment that can be given to COPD is anti-inflammatory. Considering that the airflow limitation in COPD partly emanates from inflammation of the airways, the use of the drugs would ease the patient of the difficulties in breathing. Antibiotics can also be administered to patients with COPD especially during exacerbations. In most instances, the exacerbations result from bacterial infections that increase the inflammation of the airways and the lung compartments.
Part E: Other Therapeutic Interventions
Besides pharmacologic interventions, COPD may also be subjected to undergo other forms of therapy aimed at easing their conditions. One such therapy entails exercise training. Physical activities have the impact of maximizing skeletal muscle. Improving breathing, optimize the functioning of the heart and general fitness. Cumulatively, such will lead to improved health status as far as COPD is concerned. In severe cases of COPD, oxygen therapy may be employed in the advanced stages of COPD (NIHb, 2014). Oxygen therapy makes it easier for the patients to breath leading to the healthy functioning of the body especially the vital organs such as brain that require considerable amounts of oxygen. Patients with COPD may also need psychological therapy as they go about the treatment process (Pumar et al., 2014). The therapy goes a long way to assist in the healing process considering that the patient may become easily depressed tend to worsen their conditions.
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Part F: Nursing Management
The usual nursing care for the condition is to manage symptoms and maximize functions in the patients. The management dictates the kind of care given to the patient based on the severity of the condition. To effectively assist the patients, nurses are obliged to inform the patients on how to cope with the conditions while minimizing the symptoms. The care given to the patient should be those that are unique to the status of the patient so that a tailored care is administered. The effect of such is the consideration of the patient on as an individual.
The three considerations of nursing for COPD is to manage symptoms, optimize the functioning of the body and teach self-care skills (Bauldoff, 2014). Each of the consideration plays a crucial role towards the healing of the patient. Managing symptoms is the most important steps and is indicative of progress in the healing process. The functioning of the body has to be maximized to enable the patients to return to their initial status. Teaching self-care skills is important for the patient especially after discharge. The skills will help the patients take care of themselves and avoid readmission as a result of acute exacerbations.
The priority nursing goal in the management of COPD is to ease dyspnea among the patients. The goal can be achieved through three different techniques. First, the patients should be informed about the breathing techniques. A COPD patient should adopt a pursed-lip breathing that improves the expiratory pace while reducing respirations. Slowing the expiration rate is helpful in postponing small-airway (Bauldoff et al., 2014). Secondly, the patients should be informed about how to sit or stand. Tripod position that entails leaning forward stabilizes the chest and minimize the energy utilized in breathing. A third technique is how to conserve energy. COPD patients are informed about pacing activities, breaking activities into bits, using assistive devices to limit the amount of energy utilized by the body.
If not controlled, COPD may lead to a collapse of the respiratory system and death. Besides a breakdown of the respiratory system, COPD may also result in fatalities through the systemic effects such as CVDs. COPD has continued to raise interest in the public health sector due to its adverse effects on the patients, those charged with giving care and health systems. As at 2008, COPD was implicated in 5.8% of the deaths globally (Garvey, Hanania & Altman, 2014). In the same year, the disease was declared as the third cause of mortalities in the United States overtaking the heart-related conditions. Further, the disease accounted for over 700,000 admission cases in hospitals across the US as well as up to 15.4 million physician visits. The statistics point to the serious need for education as well as the implementation of mechanisms that will ensure early detection of the disease.
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