NURS215 Week 5 Disease Research Paper

Overview

You will write an 8-10-page paper examining the pathophysiology of a disease of interest covered in Modules 1 — 8: Weeks 1 — 8 of this course. You are encouraged to choose a topic that will impact your current practice. The Research Paper will be completed and submitted in 2 separate parts.

Include a thorough examination at the cellular level. This must include clinical manifestations associated with cellular-level change, diagnostics and numerical lab data correlation, and nursing interventions and evidence-based implications for nursing practice. Integrate the Christian worldview of disease and its effects on population outcomes into your examination of the disease process.
Instructions

Create a title page and a reference page citing 5–7 peer-reviewed sources (published within the last 5 years), including the textbook, for instructor feedback. Current APA formatting must be used. Refer to the Writing Style Guide for APA formatting requirements.

To allow for early feedback, correction, and professional completion of this paper, refer to the due dates for the first and final research paper assignments.

Solution: NURS215 Week 5 Disease Research Paper

Disease Research Paper

Among the major global and national health concerns is cardiovascular disease (CVD), a leading cause of economic burden, morbidity, and mortality cause (Bulto & Hendriks, 2024). About 17.9 million deaths across the globe are caused by CVDs which include coronary artery disease (CAD), cerebrovascular disease, heart failure, and rheumatic heart disease, among others (National Heart, Lung and Blood Institute, 2023). In the United States (U.S), CVD causes one death every 33 seconds, was responsible for approximately 695,000 deaths (1 in 5 deaths) in 2021, and its annual costs (including direct and indirect) amount to approximately $239.9 billion (Centers for Disease Control and Prevention [CDC], 2024). Despite medical advancements for CVDs, there is still a need for nursing interventions to help improve CVD control and management (Bulto & Hendriks, 2024). For nurses to develop appropriate interventions for CVD, they must understand it, how it develops, diagnostic approaches, treatments, and complications. The focus of this paper is CAD, including a discussion of cellular changes and associated clinical manifestations, diagnostics and numerical laboratory data, nursing interventions, evidence-based implications and nursing, and the Christian worldview and how it impacts population outcomes.

Cellular Level Changes and Clinical Manifestations

According to the CDC (2024), CAD is the most prevalent CVD, affecting 1 in 20 adults (5%), and the leading mortality cause in the U.S, accounting for 375,476 deaths in 2021, with 2 in 10 of the deaths affecting persons aged below 65 years (CDC, 2024). CAD is characterized by insufficient flow of blood and oxygen to the heart muscle (myocardium) caused by blockage of the coronary artery following the formation of atherosclerotic plaque in the vessel’s lumen, leading to myocardium failure (Shahjehan & Bhutta, 2023). The cellular-level changes in CAD involve multiple cell types including endothelial cells, smooth muscle cells, macrophages, and platelets (Raman & Khanal, 2021). Endothelial dysfunction occurs due to damage caused by high blood pressure (BP), smoking, inflammation, high cholesterol, and other factors (Lawton et al., 2022). This results in reduced production of nitric oxide (NO), a molecule essential in maintaining vessel dilation and preventing the aggregation of platelets, leading to reduced vasodilation and increased susceptibility to clotting (Raman & Khanal, 2021). The clinical manifestations of endothelial dysfunction include chest pain and/or discomfort especially during stress or physical exertion (angina pectoris) due to reduced vasodilation and blood clot formation and associated acute coronary syndromes.  Following endothelial dysfunction, low-density lipoproteins (LDL) infiltrate the endothelial layer and accumulate in the artery wall’s innermost layer, resulting in oxidative modification. Macrophages then ingest the oxidized LDL, changing into foam cells, lipid-laden cells that contribute to the formation of “fatty atherosclerotic plaque formation (Raman & Khanal, 2021). These processes result in clinical manifestations of stable angina (chronic, predictable chest pain that results from gradual narrowing of the coronary arteries due to plaque buildup), and unstable angina (sudden, unpredictable chest pain due to dynamic alterations in plaque structure or sudden formation of thrombus) (Shahjehan & Bhutta,…..Click the paypal icon to purchase full solution for $10

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