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Chronic Obstructive Pulmonary Disease Essay

Chronic Obstructive Pulmonary Disease (COPD), a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases (Global Initiative for Chronic Obstructive Lung Disease). COPD may include other airflow obstruction diseases such as, emphysema, asthma, and chronic bronchitis. Asthma is known as chronic reactive airway disease, it’s characterized by reversible inflammation and smooth muscle contraction of the bronchiole’s, hypersecretion of mucus, and edema.

Asthma is usually onset by cold weather, laboring activities, chemicals, medications, and viral infections. Chronic bronchitis is widespread inflammation of airways with narrowing or blocking of airways, increased production of sputum, and marked cyanosis. Emphysema is the most severe form of COPD, and is characterized by recurrent inflammation that damages and eventually destroys alveolar walls to create large blebs or bullae (air spaces) and collapsed bronchioles on expiration (air-trapping) (Nurses Lab). These diseases may share overlapping symptoms, however they are different disease processes (Med Surg).

The airway obstruction that occurs in COPD is progressive and associated with the lungs abnormal inflammatory response to inhalation of noxious particles or gas (med Surg). These inhaled particles can be indoor/outdoor air pollutants, chemicals, dust, but is most commonly tobacco smoke. These inhaled particles cause irritation and inflammation to the airway; prolonged exposure changes the epithelial cells, cilia, and goblet cells causing muco-ciliary impairment (Mech of Med). The inflammation can occur in the proximal (trachea and bronchi), peripheral airways (bronchioles), lung parenchyma, and pulmonary vascular.

Overtime the irritation and inflammation can cause small airway diseases and parenchymal destruction witch leads to bronchiole constriction and airflow limitation (Mech of Med). To compensate for the narrowing of the airways the submucosal glands and goblet cells may secrete an increased amount of mucus (Med Surg). Due to the limited air supply, and inflammation the alveoli’s structure is damaged and changes. The irritation and inflammation causes alveolar wall destruction with decreases the elastic recoil (Med Surg). The decrease in alveoli wall muscle results in the air sacs to get larger consequently trap air.

These changes make it difficult for the alveoli to supply oxygenated blood to the tissues of the body, difficult to get fresh air into the lungs, and difficult to breath (Mech of Med). Risk factors for COPD include environmental factors listed before, but the main risk factor is smoking. There is a direct correlation between duration of smoking and decline in pulmonary function; this is commonly measured in pack-years. Exposure to smoking accounts for an estimated 80%-90% of cases of chronic obstructive pulmonary disease (Med-Surg).

Other risks include secondhand smoke, occupational exposure, increased age, indoor/outdoor pollutants, and genetic abnormalities. Of patients with COPD 1%-2% have an alpha1-antitrypsin deficiency, which predisposes young people to rapid development of lobular emphysema, even in the absence of smoking. These patients are more susceptible to environmental, and eventually develop chronic symptoms (Med-surg). Manifestations of COPD are primarily: chronic cough, sputum production, and dyspnea (Gold, 2010). The cough may or may not produce sputum, the build up of mucus from submucosal glands.

As COPD progresses dyspnea will occur, becoming worse with activity and eventually even at rest. This constant work to breath is persistent and exhausting to people with severe COPD. The accessory muscles eventually are required in an attempt to breath; the hyperinflation of the lungs can cause a “barrel chest” thorax. The barrel chest is caused by the loss of lung elasticity and results in the ribs fixed in the inspiratory position. Some people with severe emphysema can be observed raising their shoulders upon inspiratory phase; during which the supraclavicular fossa can be seen retracting (Med-Surg).

Pulmonary function test is use to diagnose COPD, determine severity and monitor the progression of the disease. A spirometer is used to evaluate airflow limitation by a ratio between the forced expiratory volume (FEV) and forced vital capacity (FVC) (Med Surg). The results of the test are expressed in an absolute volume and as a percent of the predicted volume based normal values for the person’s age, gender and height. People with an obstruction will have a decreased FEV because it is difficult to forcibly exhale.

The test will determine the reversibility of an obstruction after the use of bronchiole dilators; measured by the pulmonary values (Med-Surg). The forced expiratory volume over 1 second (FEV1): Reduced FEV1 not only is the standard way of assessing the clinical course and degree of reversibility in response to therapy, but also is an important predictor of prognosis. Total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV): May be increased, indicating air trapping. In obstructive lung disease, the RV will make up the greater portion of the TLC (Nurse-Lab).

Arterial blood gases (ABGs) consist of the Pao2, Paco2, and the pH and are measured to establish a baseline oxygenation and gas exchange. Chest X-rays use used to rule out other diagnosis. Blood chemistry: alpha1-antitrypsin is measured to verify deficiency and diagnosis of primary emphysema (Nurses Lab). This screening is done on patients younger than 45, with a family history of COPD. Electrocardiogram (ECG) may be used to assess for dysrhythmias, which may be an indicator of COPD. COPD is classified into four grades based on the severity; the grades are determined by the pulmonary function tests.

The table below is from the Global Initiative for Chronic Obstructive Pulmonary Disease website, www. goldcopd. org and show’s the four grades and the interpretation of the grade. Medications for COPD do not improve lung functioning; rather they help manage the symptoms and limit the frequency and severity of exacerbations. Bronchodilators help reduce bronchospasms and reduce airway obstruction to allow more air to fill the lungs and increase alveolar ventilation. Bronchodilators are delivered through inhalation using metered-dose-inhalers, nebulization, oral pill or liquid (Med-Surg).

Bronchodilator medications are available in both short and long acting depending on the severity of the COPD and the patient’s response to the medication. Other medications include inhaled and oral corticosteroids. Inhaled Corticosteroids: In COPD patients with FEV1< 60% predicted, regular treatment with inhaled corticosteroids improves symptoms, lung function, and quality of life, and reduces the frequency of exacerbations (Gold). Corticosteroids may be used in combination with bronchodilators in moderate to severe patients, however there is an increase risk of pneumonia.

It’s also not advised to use oral corticosteroids for long-term treatment (Gold). Other medication’s used are Phosphodiesterase-4 inhibitors and Methylxanthines which are less effective then the corticosteroids and bronchodilators alone but are sometimes used in combination to reduce exacerbations. Pneumococcal polysaccharide and Influenza vaccination is extremely important in COPD patients and can reduce the risk of illness and death (Gold). Medical treatment is primarily based on the patients’ status and usually involves the management of exacerbations.

Dependent on the situation this usually involves corticosteroids, antibiotics, oxygen therapy and possibly intensive respiratory intervention (Med-Surg 626). Oxygen therapy is administered to prevent acute dyspnea and during exacerbation. Depending on the severity of the COPD the patient may be on oxygen short or long-term (more than 15hrs per day) (Med-Surg 627). The goal of supplemental oxygen is to increase the baseline resting partial pressure of the arteriole oxygen saturation to at least 60mm Hg. Administering too much oxygen or if the patient is sensitive to oxygen can cause retention of C02.

It’s important to monitor the patient’s oxygen saturation and during administration of supplemental oxygen (Med-Surg 627). Surgical treatments include Bullectomy, Lung Volume Reduction Surgery and Lung Transplantation. The advantage of lung volume reduction surgery (LVRS) over medical therapy is more significant among patients with upper-lobe predominant emphysema and low exercise capacity prior to treatment, although LVRS is costly relative to health-care programs not including surgery In appropriately selected patients with very severe COPD, lung transplantation has been shown to improve quality of life and functional capacity (Gold).

A multidisciplinary team can be beneficial in the care of the COPD patient. COPD. com recommends a healthcare team involving a Primary Care Physician, Pulmonologist, Pharmacist, and Respiratory Therapist (COPD. com). Depending on the severity Palliative Care, Hospice Care, and End-of-Life Care may be necessary. Smoking cessation can begin in a variety of healthcare settings-out patient clinics, community hospitals, and in the home.

Regardless of the setting, nurses have the opportunity to teach the patient about the benefits of smoking cessation (Med-Surg 624). COPD often coexists with other diseases (comorbidities) that may have a significant impact on prognosis (Gold). Heart disease, the two most common cardiovascular diseases in COPD are pulmonary hypertension (high blood pressure in the lungs) and cor pulmonale (heart failure that results from lung disease) (Lung Chicago). Smokers are at a greater risk of Osteoporosis due to low Vitamin D levels secondary to steroid treatment.

Lung infections such as pneumonia can occur much easier because the damaged lungs decreased ability to rid its self of foreign particles. Lung cancer is the most frequent cause of death in patients with mild COPD (Gold). COPD patients are also at risk for other comorbidities such as anemia, anxiety, cognitive decline, GERD, glaucoma, sleep disorders, diabetes and others (Chicago). Pulmonary function testing classified patients as having Global Initiative on Obstructive Lung Disease (GOLD) stage 0, 1, 2, 3 or 4 COPD or restriction.

COPD is associated with only a modest reduction in life expectancy for never smokers, but with a very large reduction for current and former smokers. At age 65, the reductions in male life expectancy for stage 1, stage 2, and stages 3 or 4 disease in current smokers are 0. 3 years, 2. 2 years, and 5. 8 years. These are in addition to the 3. 5 years lost due to smoking. In former smokers the reductions are 1. 4 years and 5. 6 years for stage 2 and stages 3 or 4 disease, and in never smokers they are 0. 7 and 1. 3 years

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