NURS 6501 Module 2: Knowledge Check Quiz

NURS 6501 Module 2: Knowledge Check Quiz

Scenario 1

This case study is about a 56-year-old patient that presents to Express Hospital Emergency Department with a chief complaint of chest pain radiating to his left arm. The pain started this morning and has been worsening, pointing to the mid-sternal area. The chest pain is rated at 9/10 and nitroglycerin tablet has decreased it to 7/10. A diagnosis of acute wall myocardial infarction has been made. Therefore, this essay examines the cholesterol that is considered good and its roles.

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Cholesterols exist in different types. They include low-density lipoproteins and high-density lipoproteins. Low density lipoproteins are the bad proteins while high density lipoproteins are the good proteins. High density lipoproteins are the good proteins because they absorb cholesterol from the contained in the blood and carries them to the liver for elimination. The benefit of high density lipoproteins is that it lowers the risk of an individual developing cardiovascular problems such as stroke, hypertension, arteriosclerosis, and heart failure (CDC, 2022). Low triglyceride levels in combination with high density lipoproteins are beneficial in lowering the risk of cardiovascular problems. High density lipoproteins also prevent the development of plaques in the arteries. This lowers the threshold of arteriosclerotic plaques in healthy individuals. High density lipoproteins are also not associated with inflammation due to oxidative processes (Brandts & Ray, 2020). As a result, they protect and preserve the health and survival or cells and artery walls.

In summary, high-density lipoproteins are the good proteins while low density lipoproteins are the bad ones. High density lipoproteins lower the individual risk of developing cardiovascular complications. Together with low triglyceride levels, high density lipoproteins protect the integrity of arterial walls by preventing development of plaques and oxidative processes that cause inflammation.

References

Brandts, J., & Ray, K. K. (2020). Low Density Lipoprotein Cholesterol–Lowering Strategies and Population Health. Circulation, 141(11), 873–876. https://doi.org/10.1161/CIRCULATIONAHA.119.043406

CDC. (2022, October 24). LDL and HDL Cholesterol and Triglycerides | cdc.gov. Centers for Disease Control and Prevention. https://www.cdc.gov/cholesterol/ldl_hdl.htm

Scenario 2

This scenario is a continuation from scenario 1. The patient has been diagnosed with acute inferior wall myocardial infection. This is after he presented with complaints that included chest pain radiating to his left arm worsening in nature and pain responsive to nitroglycerin. This paper examines the manner in which inflammation causes atherosclerosis.

Inflammatory processes contribute to the development of atherosclerosis. The first step in the process is the deposition of low density lipoproteins in the walls of the arteries. Elevated levels of triglycerides accelerate the deposition of low-density lipoproteins in the intima of the arteries. The deposition initiates a series of cascades that contribute to the development of atherosclerosis. First, there is the activation of the arteriole endothelium with the deposition. This promotes the sticking or adhesion of molecules in the walls of the arteries. There is also the recruitment of T cells and monocytes under the influence of chemokines. The released monocytes differentiate into macrophages, which are involved in the upregulation of pattern recognition receptors such as the scavenger receptors. The next step is the lipoprotein internalization under the influence of scavenger receptors, which lead to the formation of foam cells. Toll-like receptors stimulate the release of inflammatory cells such as proteases, vasoactive molecules and cytokines. These cells stimulate inflammation in the walls of the arteries and growth of the atherosclerotic plaques (Libby, 2021; Malekmohammad et al., 2021; Soehnlein & Libby, 2021). In severe inflammation, plaque rupture and proteolysis may occur leading to infarction, ischemia, and thrombus formation.

In summary, inflammatory processes contribute to atherosclerosis. The process begins with the deposition of low-density lipoproteins on the walls of the arteries. The deposition initiates a series of processes that lead to inflammation. Severe inflammation can cause plaque rupture, which leads to infarction, thrombus formation, and ischemia.

References

Libby, P. (2021). Inflammation in Atherosclerosis—No Longer a Theory. Clinical Chemistry, 67(1), 131–142. https://doi.org/10.1093/clinchem/hvaa275

Malekmohammad, K., Bezsonov, E. E., & Rafieian-Kopaei, M. (2021). Role of Lipid Accumulation and Inflammation in Atherosclerosis: Focus on Molecular and Cellular Mechanisms. Frontiers in Cardiovascular Medicine, 8. https://www.frontiersin.org/articles/10.3389/fcvm.2021.707529

Soehnlein, O., & Libby, P. (2021). Targeting inflammation in atherosclerosis—From experimental insights to the clinic. Nature Reviews Drug Discovery, 20(8), Article 8. https://doi.org/10.1038/s41573-021-00198-1

Scenario 3

This scenario is about a 35-year-old female patient that has been diagnosed with acute pericarditis. The patient has a positive history of systemic lupus erythematosus (SLE). She presents to the emergency room with complaints of sharp retrosternal chest pain that worsens with deep breathing or lying down. She reports a history low grade fever for the last five days. Therefore, this essay examines nurses’ inferences based on a history of pleural friction rub.

The advanced practice registered nurser recognizes that a pleural friction rub is among the adventitious sounds that indicate an underlying pathology. The rub results from inflammation and roughened pleural surfaces that rub against each other during breathing. The nurse would suspect causes such as serositis, pleuritis, or pleural effusion. The nurse would also infer that there is a reduced production of pleural fluid by the pleura, increasing the friction between pleural membranes. The accompanying symptoms would include pleuritic chest pain, which may be referred to the shoulder or the neck if it is near the diaphragm. Pain sensation the client reports is due to the somatic nerves that innervate the parietal pleural (Adderley & Sharma, 2022; Moriki et al., 2023). The nurse should anticipate prescribing analgesics and treating the cause.

In summary, the pleural friction rub is attributed to inflammatory process and reduced production of pleural fluid, causing friction. Patients experience sharp sternal pain during breathing or when lying down. The appropriate treatment will aim at relieving symptoms and treating the causative agent.

References

Adderley, N., & Sharma, S. (2022). Pleural Friction Rub. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK537118/

Moriki, D., Koumpagioti, D., Kalogiannis, M., Sardeli, O., Galani, A., Priftis, K. N., & Douros, K. (2023). Physicians’ ability to recognize adventitious lung sounds. Pediatric Pulmonology, 58(3), 866–870. https://doi.org/10.1002/ppul.26266

Scenario 4

This scenario is about an 81-year-old female patient that has been diagnosed with deep vein thrombosis. The patient is obese. She underwent left total hip replacement surgery 48 hours ago. She had severe nausea and vomiting, which has made it difficult for her to go for physical therapy. Her mucus membranes are dry. She report that her left leg is too tight, with physical examination revealing a swollen, red colored, and tense calf. Therefore, this essay examines the factors that contributed to the development of DVT.

Several factors are attributed to the development of DVT in the patient. One of them is immobility. Immobility increases the risk of DVT due to blood stasis. The patient in the case study has been bedridden because of severe nausea and vomiting. The other risk factor is surgery. Trauma in forms such as surgery increases the risk of blood clot formation within the blood vessels, leading to an increased risk of DVT. Surgeries of the legs and upper extremities have the highest risk of DVT. The patient is 48 hours post left total hip replacement surgery, hence, the risk. The other risk factor that increased the risk of patient developing DVT is dehydration. Dehydration increases blood viscosity. The implication is the sluggish blood flow from the extremities, which increase the risk of DVT. The patient in the case study has experienced severe nausea and vomiting. Her mucus membranes are also dry, which affects blood viscosity. The other risk factor is obesity. Obesity increases the risk of inflammation within the blood vessels due to the formation of plaques. The inflammation increases the risk of blood clotting (Wang et al., 2019; Yu et al., 2020; Zhang et al., 2019). Obesity is also a risk factor for other comorbidities such s diabetes, which are associated with the increased risk of DVT.

In summary, the patient in the case study has several risk factors for DVT. They include her being obese, surgery, immobility, and dehydration. Therefore, prophylactic interventions should be adopted to prevent complications.

References

Wang, P., Kandemir, U., Zhang, B., Wang, B., Li, J., Zhuang, Y., Wang, H., Zhang, H., Liu, P., & Zhang, K. (2019). Incidence and Risk Factors of Deep Vein Thrombosis in Patients With Pelvic and Acetabular Fractures. Clinical and Applied Thrombosis/Hemostasis, 25, 1076029619845066. https://doi.org/10.1177/1076029619845066

Yu, Y., Tu, J., Lei, B., Shu, H., Zou, X., Li, R., Huang, C., Qu, Y., & Shang, Y. (2020). Incidence and Risk Factors of Deep Vein Thrombosis in Hospitalized COVID-19 Patients. Clinical and Applied Thrombosis/Hemostasis, 26, 1076029620953217. https://doi.org/10.1177/1076029620953217

Zhang, W., Huai, Y., Wang, W., Xue, K., Chen, L., Chen, C., & Qian, A. (2019). A Retrospective cohort study on the risk factors of deep vein thrombosis (DVT) for patients with traumatic fracture at Honghui Hospital. BMJ Open, 9(3), e024247. https://doi.org/10.1136/bmjopen-2018-02424

 

 

Scenario 5

This essay is about scenario 5. The essay focuses on a 66-year-old female patient with a 50 pack/year history of cigarette smoking. She had a CT scan and was diagnosed with emphysema. The patient asks is it means that she has chronic obstructive pulmonary disease. Therefore, the paper examines the pathophysiology of emphysema and its relationship to COPD.

Emphysema is a respiratory condition characterized by the reduction in pulmonary elasticity recoil. The reduction results in air trapping within the lungs and increase in the lung volume beyond the normal level. These changes alter the physiological process of air exchange in the pleura and alveoli, leading to the compression of the airways. In addition, there is the reduction in airflow during the tidal and forced expiration. Consequently, there is the destruction in the matching of the required ventilation by the body with the alveolar pressure, leading to respiratory collapse. A relationship between emphysema and COPD exists. Emphysema is a type of COPD. However, patients may be diagnosed with COPD and not have emphysema (Amariei et al., 2019; Leap et al., 2021). Emphysema precipitates symptoms of COPD due to the damage to the alveoli, which makes them lose elasticity, hence, air trapping.

In summary, emphysema develops from the damage to the alveoli. The damage results in the loss of lung elasticity. Emphysema is related to COPD. The mechanisms in emphysema produce symptoms related to those of COPD.

References

Amariei, D. E., Dodia, N., Deepak, J., Hines, S. E., Galvin, J. R., Atamas, S. P., & Todd, N. W. (2019). Combined Pulmonary Fibrosis and Emphysema: Pulmonary Function Testing and a Pathophysiology Perspective. Medicina, 55(9), Article 9. https://doi.org/10.3390/medicina55090580

Leap, J., Arshad, O., Cheema, T., & Balaan, M. (2021). Pathophysiology of COPD. Critical Care Nursing Quarterly, 44(1), 2. https://doi.org/10.1097/CNQ.0000000000000334

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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?

Question 2 4 pts

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:

1. How does inflammation contribute to the development of atherosclerosis?

 

Question 3 4 pts

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:

1. Because of the result of a pleural friction rub, what does the APRN recognize?

 

Question 4 4 pts

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:

1. Given the history of the patient explain what contributed to the development of a deep venous thrombosis (DVT)

 

Question 5 4 pts

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:

1. There is a clear relationship between emphysema and COPD, explain the pathophysiology of emphysema and the relationship to COPD.

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