NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2
Walden University NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2– Step-By-Step Guide
This guide will demonstrate how to complete the Walden University NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2
Whether one passes or fails an academic assignment such as the Walden University NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2 depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2
The introduction for the Walden University NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2 is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
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How to Write the Body for NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2
After the introduction, move into the main part of the NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2 assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Sample Answer for NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2
The case study for NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2 portrays a 45-year-old female presenting with complaints of dyspnea, fevers, and a productive cough having thick green sputum for three days. She is a known COPD patient and has a chronic cough that has worsened and disrupted her sleep. She states that the sputum has become too thick and hard, and she is unable to expectorate. Chest auscultation findings include hyperresonance, rhonchi, and coarse rales in all lung fields. Chest X-ray shows an increased AP diameter and a flattened diaphragm. The purpose of the NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2 paper is to discuss the pathophysiologic processes in the cardiovascular and pulmonary systems causing the symptoms and racial/ethnic factors that may affect physiological functioning.
Cardiovascular and Cardiopulmonary Pathophysiologic Processes Causing the Symptoms
The patient’s symptoms can be attributed to inflammation of the bronchi and bronchioles due to exposure to irritants, such as cigarette smoke. The irritants elicit inflammation of the airways, vasodilation, mucosal edema, congestion, and bronchospasm (Brandsma et al., 2020). The patient has had chronic inflammation due to a long history of COPD. The inflammation increased the number and size of mucous glands, resulting in the production of copious amounts of thick mucus, which explains the patient’s symptoms of thick mucus and chronic cough (Choi & Rhee, 2020). Besides, the bronchial walls thicken, obstructing airflow.
The bronchial wall thickening and excessive mucus obstruct some smaller airways and constrict larger ones. This explains the patient’s dyspnea. The excessive mucus becomes a breeding ground for microbes resulting in chronic low-grade infection. The most common infections are caused by Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae (Choi & Rhee, 2020). The patient’s fevers and green sputum are due to the low-grade infection, which could be caused by one of these bacteria.
Racial/Ethnic Variables Impacting Physiological Functioning
Cigarette smoking is considered the greatest risk factor for COPD. The prevalence of tobacco smoking is highest among Alaskan Natives and Northern Plains American Indians. It is also higher among African Americans (Hikichi et al., 2019). Therefore, individuals from these ethnic/racial groups with a history of smoking or exposure to second-hand smoke have a high risk of developing inflammation of the airways resulting in COPD.
How These Processes Interact To Affect the Patient
The pathophysiologic processes in COPD significantly affect the patient due to limitation in airflow caused by constriction of airways and obstruction of airflow. Consequently, oxygenation of all body tissues is affected. Reduced oxygenation can cause tissue anoxia and necrosis (Brandsma et al., 2020). The patient develops major complications due to reduced gas exchange and oxygenation levels, including hypoxemia, acidosis, respiratory infection, dysrhythmias, and cardiac failure.
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Conclusion
The patient’s symptoms can be attributed to inflammation of the airways by irritants. The inflammation causes increased mucus production, which clogs the airways limiting airflow and gas exchange, resulting in cough, dyspnea, and production of thick mucus. Cigarette smoke is a major irritant, and therefore ethnic groups with a high smoking rate such as African Americans, American Indians, and Alaskan Natives have a higher prevalence of COPD.
References
Brandsma, C. A., Van den Berge, M., Hackett, T. L., Brusselle, G., & Timens, W. (2020). Recent advances in chronic obstructive pulmonary disease pathogenesis: from disease mechanisms to precision medicine. The Journal of pathology, 250(5), 624–635. https://doi.org/10.1002/path.5364
Choi, J. Y., & Rhee, C. K. (2020). Diagnosis and Treatment of Early Chronic Obstructive Lung Disease (COPD). Journal of clinical medicine, 9(11), 3426. https://doi.org/10.3390/jcm9113426
Hikichi, M., Mizumura, K., Maruoka, S., & Gon, Y. (2019). Pathogenesis of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke. Journal of thoracic disease, 11(Suppl 17), S2129–S2140. https://doi.org/10.21037/jtd.2019.10.43
Sample Answer 2 for NURS 6501 CARDIOVASCULAR AND RESPIRATORY DISORDERS MODULE 2
Scenario 1: Myocardial Infarction
CC: “I woke up this morning at 6 a.m. with numbness in my left arm and pain in my chest. It feels tight right here (mid-sternal).” “My dad had a heart attack when he was 56-years-old and I am scared because I am 56-years-old.”
HPI: Patient is a 56-year-old Caucasian male who presents to Express Hospital Emergency Department with a chief complaint of chest pain that radiates down his left arm. He states this started this morning and has been getting worse, pointing to the mid-sternal area, “it feels like an elephant is sitting on my chest and having a hard time breathing”. He rates the pain as 9/10. Nothing has made the pain better or worse. He denies any previous episode of chest pain. Denies nausea, or lightheadedness. Nitroglycerin 0.4 mg tablet sublingual x 1 which decreased pain to 7/10.
Lipid panel reveals Total Cholesterol 424 mg/dl, high density lipoprotein (HDL) 26 mg/dl, Low Density Lipoprotein (LDL) 166 mg/dl, Triglycerides 702 mg/dl, Very Low-Density Lipoprotein (VLDL) 64 mg/dl
His diagnosis is an acute inferior wall myocardial infarction.
Question:
Which cholesterol is considered the “good” cholesterol and what does it do?
High-density lipoprotein (HDL) is also called the “good” cholesterol, while low-density lipoprotein (LDL) is called “bad” cholesterol. HDL absorbs cholesterol in the blood and transports it back to the liver. The liver then flushes the cholesterol from the body. High levels of HDL cholesterol lower the risk of heart disease and stroke. HDL has a diverse protein and lipid composition, contributing to its atheroprotective function (Jomard & Osto, 2020). In the vessel wall, HDL undergoes transcytosis through endothelial cells into the sub-endothelial space, where it efflux cholesterol from foam cells, preventing plaque formation. In addition, HDLs have other beneficial properties, like nitric oxide production stimulation, anti-oxidant capacity, anti-inflammatory, and anti-apoptotic actions.
Scenario 1: Myocardial Infarction
CC: “I woke up this morning at 6 a.m. with numbness in my left arm and pain in my chest. It feels tight right here (mid-sternal).” “My dad had a heart attack when he was 56-years-old and I am scared because I am 56-years-old.”
HPI: Patient is a 56-year-old Caucasian male who presents to Express Hospital Emergency Department with a chief complaint of chest pain that radiates down his left arm. He states this started this morning and has been getting worse, pointing to the mid-sternal area, “it feels like an elephant is sitting on my chest and having a hard time breathing”. He rates the pain as 9/10. Nothing has made the pain better or worse. He denies any previous episode of chest pain. Denies nausea, or lightheadedness. Nitroglycerin 0.4 mg tablet sublingual x 1 which decreased pain to 7/10.
Lipid panel reveals Total Cholesterol 424 mg/dl, high density lipoprotein (HDL) 26 mg/dl, Low Density Lipoprotein (LDL) 166 mg/dl, Triglycerides 702 mg/dl, Very Low-Density Lipoprotein (VLDL) 64 mg/dl
His diagnosis is an acute inferior wall myocardial infarction.
Question:
- How does inflammation contribute to the development of atherosclerosis?
Atherosclerosis is a chronic inflammatory condition with an autoimmune component. It is accompanied by a chronic, low-grade inflammatory response that attracts cells of the innate and adaptive immune systems into the atherosclerotic plaque (Wolf & Ley, 2019). The autoimmune response is clinically best documented by antibodies against LDL and other atherosclerosis antigens. The continued development of atherosclerosis involves an inflammatory response, which begins with injury to the vascular endothelium. Inflammation has multiple effects on the arterial wall, including attracting inflammatory cells like macrophages (Jebari-Benslaiman et al., 2022). The macrophages infiltrate the injured vascular endothelium and ingest lipids, making them foam cells. Activated macrophages release biochemical substances that can further damage the endothelium, attracting platelets and initiating clotting.
Scenario 2: Pleural Friction Rub
A 35-year-old female with a positive history of systemic lupus erythematosus (SLE) presents to the Emergency Room (ER) with complaints of sharp retrosternal chest pain that worsens with deep breathing or lying down. She reports a 5-day history of low-grade fever, listlessness and says she feels like she had the flu. Physical exam reveals tachycardia and a pleural friction rub. She was diagnosed with acute pericarditis.
Question:
- Because of the result of a pleural friction rub, what does the APRN recognize?
Physical findings in a pleural friction rub include an adventitious breath sound on chest auscultation, which is heard as a harsh, grunting sound during systole and diastole. When examining the patient with a friction rub, the APRN will identify that SLE caused an inflammation of the pericardium resulting in pericarditis (Dein et al., 2019). When the patient was in active lupus, antigen-antibody complexes formed and mediated inflammation of the pericardium. Therefore, the APRN will recognize that the client’s symptoms are caused by pericarditis, which is characterized by fever, dyspnea, tachycardia, and faint heart sounds. Pericardial rub is a common finding on physical exam.
Scenario 4: Deep Venous Thrombosis (DVT)
A 81-year-old obese female patient who 48 hours post-op left total hip replacement. The patient has had severe nausea and vomiting and has been unable to go to physical therapy. Her mucus membranes are dry. The patient says the skin on her left leg is too tight. Exam reveals a swollen, tense, and red colored calf. The patient has a duplex ultrasound which reveals the presence of a deep venous thrombosis (DVT).
Question:
- Given the history of the patient explain what contributed to the development of a deep venous thrombosis (DVT)
The patient’s DVT was caused by venous stasis, activation of the coagulation pathway, and vein damage. The patient was at risk of developing a thrombus due to being obese. The patient likely developed Venous stasis following vein damage during the total hip replacement. Immobility of the left leg following surgery and failure to attend physical therapy caused venous stasis contributing to DVT (Chindamo & Marques, 2019). The venous stasis caused an increased viscosity resulting in the formation of microthrombi, which are not cleared by fluid movement when there is high blood viscosity. This resulted in the formation of a blood clot from the microthrombi, which interrupted blood flow in the vein.
Scenario 5: COPD
A 66-year-old female with a 50 pack/year history of cigarette smoking had a CT scan and was diagnosed with emphysema. He asks if this means he has chronic obstructive pulmonary disease (COPD).
Question:
- There is a clear relationship between emphysema and COPD, explain the pathophysiology of emphysema and the relationship to COPD.
Emphysema is characterized by two significant changes: loss of lung elasticity and hyperinflation of the lung. It occurs when protein-degrading enzymes called proteases are at higher-than-normal levels. They damage the alveoli and the small airways by breaking down elastin (Rodrigues et al., 2021). High protease levels make the alveolar sacs lose their elasticity, and the small airways collapse or narrow. Some alveoli get destroyed, and others become large and flaccid with reduced area for effective gas exchange. An increased amount of air is trapped in the lungs due to loss of elastic recoil in the alveolar walls, overstretching and enlargement of the alveoli into air-filled spaces, and collapse of small airways (Rodrigues et al., 2021). Emphysema is linked to COPD since oxygenation is affected by the loss of alveolar tissue and the increased work of breathing. Usually, inhalation begins before exhalation is completed, causing an uncoordinated breathing pattern.
References
Chindamo, M. C., & Marques, M. A. (2019). Role of ambulation to prevent venous thromboembolism in medical patients: where do we stand?. Jornal Vascular Brasileiro, 18. https://doi.org/10.1590/1677-5449.180107
Dein, E., Douglas, H., Petri, M., Law, G., & Timlin, H. (2019). Pericarditis in Lupus. Cureus, 11(3), e4166. https://doi.org/10.7759/cureus.4166
Jebari-Benslaiman, S., Galicia-García, U., Larrea-Sebal, A., Olaetxea, J. R., Alloza, I., Vandenbroeck, K., Benito-Vicente, A., & Martín, C. (2022). Pathophysiology of Atherosclerosis. International journal of molecular sciences, 23(6), 3346. https://doi.org/10.3390/ijms23063346
Jomard, A., & Osto, E. (2020). High density lipoproteins: metabolism, function, and therapeutic potential. Front Cardiovasc Med. 2020; 7: 39. https://doi.org/10.3389/fcvm.2020.00039
Rodrigues, S. O., Cunha, C. M. C. D., Soares, G. M. V., Silva, P. L., Silva, A. R., & Gonçalves-de-Albuquerque, C. F. (2021). Mechanisms, Pathophysiology and Currently Proposed Treatments of Chronic Obstructive Pulmonary Disease. Pharmaceuticals (Basel, Switzerland), 14(10), 979. https://doi.org/10.3390/ph14100979
Wolf, D., & Ley, K. (2019). Immunity and inflammation in atherosclerosis. Circulation research, 124(2), 315-327.https://doi.org/10.1161/CIRCRESAHA.118.313591