NURS 6501 Cardiovascular and Respiratory Disorders Knowledge Check Essay

NURS 6501 Cardiovascular and Respiratory Disorders Knowledge Check Essay

NURS 6501 Cardiovascular and Respiratory Disorders Knowledge Check Sample Essay

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.

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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:

1. 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:

1. 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:

1. 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:

1. 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

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CARDIOVASCULAR AND RESPIRATORY DISORDERS

 

In this exercise, you will complete a 5-essay type question Knowledge Check to gauge your understanding of this module’s content.

Possible topics covered in this Knowledge Check include:

• myocardial infarction
• endocarditis
• myocarditis
• valvular disorders
• lipid panels
• coagulation
• clotting cascade
• deep vein thrombosis
• hypertension
• heart failure
• COPD
• asthma
• pneumonias

RESOURCES

Be sure to review the Learning Resources before completing this activity.
Click the weekly resources link to access the resources.

WEEKLY RESOURCES

BY DAY 7 OF WEEK 3

Complete the Knowledge Check by Day 7.

Flag question: Question 1

Question 14 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:

Which cholesterol is considered the “good” cholesterol and what does it do?

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pView keyboard shortcutsAccessibility Checker0 words</>Switch to the html editorFullscreen

Flag question: Question 2

Question 24 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?

View keyboard shortcuts

pView keyboard shortcutsAccessibility Checker0 words</>Switch to the html editorFullscreen

Flag question: Question 3

Question 34 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?

View keyboard shortcuts

pView keyboard shortcutsAccessibility Checker0 words</>Switch to the html editorFullscreen

Flag question: Question 4

Question 44 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)

View keyboard shortcuts

pView keyboard shortcutsAccessibility Checker0 words</>Switch to the html editorFullscreen

Flag question: Question 5

Question 54 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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