NR 507 Week 3 Case Study

Sample Answer

Pathophysiology and Clinical Findings

Question One

The patient’s spirometry results are consistent with obstructive pulmonary disease, as evidenced by the low forced expiratory volume in 1 second that ranges typically above 80%. The COPD diagnosis was considered since patient A.C. has presented with complaints of dry cough in the morning, dyspnea, sputum production, and history of exposure to tobacco smoke.

However, the forced spirometry will demonstrate the presence of non-fully reversible airflow limitation using post-bronchodilator FEV1/FVC < 0.70 is compulsory to confirm the COPD diagnosis. A.C most likely pulmonary diagnosis is COPD based on the spirometry findings. The predicted results revealed that the Absolute FEV1/FVC ratio was 81%. Following the test, the pre-bronchodilator and post-bronchodilator predictions were 69% and 64%, which are less than 70% of the predicted value.

Question Two

Chronic obstructive pulmonary disease is a heterogeneous condition characterized by a wide range of chronic respiratory symptoms, which can be linked to airway abnormalities and alveoli that can cause persistent and airflow obstruction (Venkatesan, 2023). Emphysema can be characterized by the destruction of alveoli walls owing to the imbalance of proteinase–antiproteinase enzymatic activities (Leap et al., 2021). In healthy lung tissues, the protective antiproteinase counteracts the protein-degrading enzymes secreted by white blood cells.

Under rare circumstances, a genetic condition, alpha-1 antitrypsin deficiency, could play a function in causing COPD. Persons living with the condition tend to have low alpha-1 antitrypsin, a protein produced in the liver. Chronic inflammation can be caused by chronic exposure to lung irritants, or long-term cigarette smoking recurrently recruits white blood cells into the alveoli (Dunphy et al., 2023). The burning of cigarettes produces a mixture of gases and chemicals that reach the alveoli and peripheral airways, where particles can easily collide with the surfaces and cause damage (Higham, et al., 2019).

Counter to the atopic asthma processes, the COPD lymphocytic infiltration constitutes mainly of CD8+ T cells instead of CD4+ T-helper cells. Neutrophils and monocyte-/macrophage-derived proteins progressively destroy the alveolar walls and overcomes anti-proteinase defenses resulting in overdistended, hyperinflated, and weak elastic alveoli. As a result, there is air trapping, an increase in residual lung volume, low expiratory flow, and carbon dioxide retention.

Persons may experience hypercapnia but maintain adequate oxygenation in the early stages of the disease process. The desensitization of the central respiratory receptors to PCO2 occurs with long-term hypercapnia leading to the loss of normal respiratory stimulus to breathe independently and reliance on low oxygen levels to activate breathing. Chronic bronchitis is the more common pathological mechanism involved in COPD. Airflow obstruction is caused by bronchiole edema, mucus-producing goblet cell hyperplasia, and bronchiole smooth muscle hypertrophy (Dunphy et al., 2023).

Chronic bronchitis is presented as long-term coughing or recurrent sputum production. Persons with cyanosis and hypoxia develop problems with ventilatory obstruction and suboptimal blood oxygen. Whereas, in chronic bronchitis, long-term hypoxia can lead to pulmonary vasoconstriction and pulmonary hypertension. The increased pulmonary resistance against the right ventricle leads to pulmonale or right ventricular failure. Chronic hypoxia stimulates renal erythropoietin that triggers and prolongs red blood cell synthesis in the bone marrow, increasing hemoglobin concentration and hematocrit. Acute exacerbations of chronic bronchitis are characteristic of COPD evidenced by Increased purulent sputum and worsened shortness of breath.

Question Three

The patient has presented with chief complaints of fatigue and increasing dyspnea on exertion for the last three months, but he did not seek medical help. In addition, he has been experiencing Dry, nonproductive cough in the morning. The patient has smoking history of 35 years. However, he has considerably reduced to one cigarette daily after the initiation of cardiac intervention.

Question Four

The chest ray exam has indicated signs of hyperinflation as both lungs are hyper-inflated and flattening of the diaphragm. The second objective finding is the presence of bilateral wheezing where there is forced exhalation and prolonging of expiratory phase. The vital signs reveal that respiratory rate and oxygen saturation is 22 and 93%. The patient has a history of cardiology consultation, rehabilitation, and successful angioplasty. Finally, the spirometry results reveal pre-bronchodilator and post-bronchodilator predictions for the FEV1/FVC ratio were 69% and 64%, which are less than 70% of the predicted value.

Management of COPD

Question One

The spirometric cut points have been proposed for simplicity in Table 2.5 of the GOLD standards. The spirometry results reveal that pre-bronchodilator and post-bronchodilator predictions for the FEV1 were 64% and 64%. The current classification is stage 2 moderate as stated in the GOLD criteria, where the FEV1 values are greater than 50 percent and lower than 80 percent (Global Initiative for Chronic Obstructive Lung Disease, 2023). After analyzing the patient CA’s well-managed symptoms, spirometry results, and assessment that reveals pulmonary decline is minimized, he can be considered stable.

Question Two

Pharmacological therapy is used to lessen symptoms, severity, and frequency of exacerbations and improve health status. The medication classes used to treat COPD are shown in Table 3.3. The choice in each medication class depends on the availability, cost, and clinical responses balanced against side effects. The clinician should individualize the treatment regimen since the relationship between symptom severity, airflow obstruction, and exacerbations differ between patients. The recommended medication classes are bronchodilators and antimuscarinic drugs. Examples of short-acting beta-agonists are Albuterol and long-acting beta-agonists are Formoterol. Examples of short-acting antimuscarinics, ipratropium and long-acting muscarinic antagonists are tiotropium and aclidinium.

Question Three

The available empirical data suggests that numerous pharmacological treatment options can reduce the mortality. The inhaled bronchodilators will be used to increase the FEV1 values and alter the other variables in the spirometric tests. The mechanism of action is alteration of the airway’s smooth muscle tone as well as improvements in expiratory flows, which can be reflected in the airways widening as opposed to changes in lungs elastic recoil. In addition, the bronchodilators can also lessen dynamic hyperinflation presented during resting periods and exercise and improvement in performance (Global Initiative for Chronic Obstructive Lung Disease, 2023).

Specifically, the principal mechanism action of the beta2-agonist drugs is the relaxation of airways’ smooth muscles by the stimulation of beta2-adrenergic receptors to boost cyclic AMP and generate functional antagonism and bronchoconstriction. The short-acting beta2-agonists improve FEV1, and symptoms and effects usually wear off within four to six hours, while long-acting beta2-agonists improve FEV1, lung volumes, dyspnea, exacerbation rates, no hospitalizations, and health status.

Secondly, the antimuscarinic medication class aids in blocking the bronchoconstrictor acetylcholine effect on the M3 muscarinic receptors within the airway smooth muscles. The short-acting antimuscarinic drugs block the inhibitory neuronal receptors M2 that trigger vagal- induced bronchoconstriction. At the same time, the long-acting muscarinic antagonists bind to M3 muscarinic receptors, which has faster dissociation from M2 muscarinic receptors, which prolongs the duration of bronchodilator effects.

Question Four

The available empirical data suggests that numerous non-pharmacological treatment options can reduce the mortality. The recommended non-pharmacological therapies for patient AC is smoking cessation and pulmonary rehabilitation. First, smoking cessation is considered the single most effective non-pharmacological treatment option to reduce the progression of COPD. The Lung Health Study conducted a randomized clinical trial including asymptomatic or mildly symptomatic COPD patients who were treated with a ten-week smoking cessation program and followed up for 14.50 years, where there was a reduction in overall mortality rate in the smoking cessation intervention group than regular care group (Global Initiative for Chronic Obstructive Lung Disease, 2023).

Hence, the patient should be asked about the progress in all visits. Secondly, pulmonary rehabilitation is comprehensive intervention, which is based on thorough assessment followed by the delivery of patient-tailored therapies including exercise training, patient education, self-management interventions aiming at behavior changes. The program is designed to improve the psychological and physical condition of people and promote the long-term adherence to health-enhancing behaviors. The core components of the pulmonary rehabilitation will improve exercise capacity, prevent symptoms, and increase quality of life. Finally, participation in an outpatient pulmonary rehabilitation program will assist in improving the shortness of breath and overall health status.

References

• Dunphy L. M. H. Winland-Brown J. E. Porter B. O. & Thomas D. J. (2023). Primary care The art and science of advanced practice nursing – an interprofessional approach. F.A. Davis Company.
• Global Initiative for Chronic Obstructive Lung Disease, Inc. (2023). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. https //goldcopd.org/wp-content/uploads/2023/01/GOLD-2023-ver-1.2-7Jan2023_WMV.pdf
• Higham, A., Quinn, A. M., Cançado, J. E. D., & Singh, D. (2019). The pathology of small airways disease in COPD historical aspects and future directions. Respiratory research, 20(1), 1-11. https //doi.org/10.1186/s12931-019-1017-y
• Leap, J., Arshad, O., Cheema, T., & Balaan, M. (2021). Pathophysiology of COPD. Critical Care Nursing Quarterly, 44(1), 2-8. https //doi.org/10.1097/CNQ.0000000000000334
• Venkatesan, P. (2023). GOLD COPD report 2023 update. The Lancet Respiratory Medicine, 11(1), 18 https //doi.org/10.1016/S2213-2600(22)00494-5