Explain the pathophysiology behind the signs and symptoms of COPD

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    Explain the pathophysiology behind the signs and symptoms of COPD

    Explain the pathophysiology behind the signs and symptoms of COPD Chronic Obstructive Pulmonary Disease (COPD) is just as it sounds, a chronic obstruction in the pulmonary function that causes disease. This disease is comprised of two major phenotypes, of which are bronchitis (hypersecretion of mucus and chronic productive cough that occurs consecutively for at least two years with at least a consecutive three-month period each year) (McCance & Huether, 2019) and emphysema (an abnormal permanent enlargement of gas-exchange airways or acini, accompanied by destruction of the alveolar walls without obvious fibrosis (McCance & Huether, 2019). The leading cause of COPD is that of smoking. However, there is another factor that contributes to COPD and that is an inherited mutation in the a1-antitrypsin gene. The development of COPD results from this gene, even in those who do not participate in the consumption of smoke inhalation4. Both emphysema and chronic bronchitis affect ventilation-perfusion mismatch with hypoxemia; however, in chronic bronchitis, bronchial edema is caused by the

    Explain the pathophysiology behind the signs and symptoms of COPD

    Chronic Obstructive Pulmonary Disease (COPD) is just as it sounds, a chronic obstruction in the pulmonary function that causes disease. This disease is comprised of two major phenotypes, of which are bronchitis (hypersecretion of mucus and chronic productive cough that occurs consecutively for at least two years with at least a consecutive three-month period each year) (McCance & Huether, 2019) and emphysema (an abnormal permanent enlargement of gas-exchange airways or acini, accompanied by destruction of the alveolar walls without obvious fibrosis (McCance & Huether, 2019). The leading cause of COPD is that of smoking. However, there is another factor that contributes to COPD and that is an inherited mutation in the a1-antitrypsin gene. The development of COPD results from this gene, even in those who do not participate in the consumption of smoke inhalation4. Both emphysema and chronic bronchitis affect ventilation-perfusion mismatch with hypoxemia; however, in chronic bronchitis, bronchial edema is caused by the inspiration of irritants that increases the number and size of mucus glands and goblet cells of the airway (McCance & Huether, 2019). This produces an environment in which mucus cannot be cleared of the airway due to narrowing. Eventually, the continuous production of copious amounts of secretions and narrowed airways lead to an obstruction. In Emphysema, the increases in neutrophils of the airway release protease and elastase that cleave structural collagen and promote tissue breakdown (McCance & Huether, 2019). The introduction of macrophages is also present, which contribute to reduction of surface area regarding gas exchange and loss of cellular apoptosis. When it comes to COPD, the difficulty of expiration is due to the accumulation of copious mucus membranes, loss of elastic recoil (from expansion), and epithelial edema. According to the Centers for Disease Control (CDC), as of 2014, COPD has accounted for 39.1 percent of 100,000 deaths in the United States (CDC, 2018). The CDC also states that, the prevalence of COPD varied amongst states, with Colorado, Hawaii, and Utah exhibiting <4% of cases; Tennesse, West Virginia, Alabama, and Kentucky exhibiting >9%, and states along the lower Mississippi rivers and Ohio exhibit the highest prevalence of COPD (CDC, 2018).

    What relationship do you see with Mr. Brown’s vital signs – 26 RR, 91% oxygen saturation, temp: 37.8, HR: 93 BP: 150/70 

    When observing Mr. Brown’s vital signs, his respiration rates are increased at 26. Eupnea (normal breathing) is 8 to 16 beats per minute according to our text (McCance & Huether, 2019). Due to this patients’ history of COPD for 10 years, it is safe to say that this patient is breathing heavier due to lack of perfused oxygen. His lungs are working harder at this point to keep him oxygenized. HIs oxygen saturation of 91% exhibits hypoxemia and possibly ‘air trapping’, which can be correlated to the reduction of oxygenation of tissue cells. You must be careful when increasing oxygenation to these patients by nasal cannula, as these patients tend to not be receptive of oxygen outside of airways in increased amounts and may develop hypercapnia. The patient is also running a fever of 100.04 degrees Fahrenheit. This could be a resultant of an infection. The patients’ blood pressure is also elevated. From our last discussion, we discussed risks of constriction due to narrowing of vessels when dealing with increased blood pressures or hypertension.

    Describe the goals of care for Mr. Brown. Make sure to use the COPD gold standards of care( https://goldcopd.org/wp-content/uploads/2018/02/WMS-GOLD-2018-Feb-Final-to-print-v2.pdf (Links to an external site.) (Links to an external site.)) for your plan.

    As Mr. Brown has not been noted to be an unstable patient of COPD, I will assume for this lesson that he is stable. In saying this, I will address the stable COPD patients’ goals according to the COPD gold standards of care. Smoking cessation is highly encouraged if the patient is a smoker. As there is no cure, maintenance of the disease is highly profitable to the patient in regards of symptoms and exacerbation risks in the future. These patients are asked to identify and reduce irritant exposure. Continuation of prescribed medications such as bronchodilators, corticosteroids, oxygen therapy, and macrolides, to reduce the symptoms experienced by this patient is also reinforced.

    How would you follow up on your proposed plan of care? 

    Routine follow-up visits are required of this individual, as well as, blood gases, chest x-rays, and pulmonary function test. If not definitive, the introduction of high-resolution CT scanning may be indicated. As COPD is not a curative disease, it is however, a manageable one. Maintaining a functional oxygenation level and exhibiting the abilities to continue to perform activities of daily living (ADL’s) is the end goal of these types of patients.

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