Chronic Obstructive Pulmonary Disease (COPD) Pathophysiology: A Case Study Analysis, Cheat Sheet of Nursing

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Advanced Pathophysiology Week 4 Assignment Walden University NURS-6501N- Mary Smith, PhD(c), DNP, FNP-BC, FAANP

Case Study: A 50-year-old white female presents to the emergency room with complaints of increased chest congestion with purulent sputum production for the last 3 days. The patient reports she has had some increased dyspnea and is using her albuterol inhaler which isn’t helping her symptoms. The patient reports a history of tobacco use for last 10 years and a history of COPD which was diagnosed last year. The patient reports that her primary care provider ordered another medication for the COPD but she couldn’t afford it. The patient denies fever. The patient’s vital signs: BP 148/90, pulse 108, respirations 22, O2 sat 92%, and temp 98.1F. Chest x-ray reveals hyperinflation with flattened diaphragm but is without effusions or infiltrates. Pulmonary Pathophysiologic Processes The patient's symptoms and history suggest an exacerbation of Chronic Obstructive Pulmonary Disease (COPD). COPD is characterized by persistent respiratory symptoms and airflow limitation due to airway and alveolar abnormalities, often caused by significant exposure to noxious particles or gases, such as tobacco smoke in this patient's case. Mucus hypersecretion, airway inflammation, airway remodeling, oxidative stress, and loss of elastic recoil are pulmonary pathophysiologic processes seen in COPD (McCance et al., 2019). Mucus hypersecretion is chronic inflammation that stimulates goblet cells in the airway epithelium to produce excessive mucus. This thick, sticky mucus contributes to airway obstruction by narrowing the airways and trapping particulate matter and pathogens (Lange et al., 2021). Mucus hypersecretion also predisposes individuals to recurrent respiratory infections and exacerbations of COPD. Airway inflammation is the inhalation of noxious particles and gases, primarily from cigarette smoke but also from environmental pollutants, triggers an inflammatory response in the airways. This

racial and ethnic groups may have a higher susceptibility to COPD due to genetic factors or differences in lung development. Smoking is the primary risk factor for COPD in all racial and ethnic groups. However, there may be differences in smoking patterns and exposure levels among different populations. For example, African American smokers tend to have lower levels of cigarette consumption compared to non-Hispanic whites but may still have a higher risk of developing COPD due to other factors such as genetic predisposition or environmental exposures (Lange et al., 2021). In addition to smoking, exposure to indoor and outdoor air pollution, occupational hazards, and biomass fuels can contribute to the development and exacerbation of COPD. Racial and ethnic minorities may be disproportionately exposed to these environmental pollutants due to factors such as socioeconomic status, residential segregation, and occupational disparities. Disparities in healthcare access and quality can affect the diagnosis, treatment, and management of COPD among different racial and ethnic groups. Minority populations may face barriers to accessing healthcare services, including lack of insurance coverage, limited availability of healthcare facilities in underserved areas, language barriers, cultural differences, and mistrust of the healthcare system (Silverman, 2020). These disparities can lead to delays in diagnosis, suboptimal management of symptoms, and poorer outcomes for COPD patients from minority backgrounds. How These Processes Interact to Affect the Patient The patient's history of tobacco use, and COPD predispose her to chronic airflow limitation and airway inflammation. The exacerbation may have been triggered by a respiratory infection, leading to increased mucus production and worsening airway obstruction (Silverman, 2020). The patient's inability to afford prescribed medication for COPD may have also contributed to the exacerbation by inadequately controlling her symptoms and inflammation (McCance et al., 2019). Overall, the patient's presentation

underscores the complex interplay between genetic, environmental, and socioeconomic factors in the pathophysiology and management of COPD, with potential racial and ethnic disparities influencing disease outcomes (Lange et al., 2021). By addressing these factors, healthcare providers and policymakers can work towards achieving health equity and improving outcomes for all individuals affected by COPD, regardless of race or ethnicity.