NURS 6051 Knowledge Check: Cardiovascular and Respiratory

Walden University NURS 6051 Knowledge Check: Cardiovascular and Respiratory Disorders-Step-By-Step Guide

This guide will demonstrate how to complete the Walden University NURS 6051 Knowledge Check: Cardiovascular and Respiratory Disorders assignment 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 6051 Knowledge Check: Cardiovascular and Respiratory Disorders

Whether one passes or fails an academic assignment such as the Walden University NURS 6051 Knowledge Check: Cardiovascular and Respiratory Disorders 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 6051 Knowledge Check: Cardiovascular and Respiratory Disorders

The introduction for the Walden University NURS 6051 Knowledge Check: Cardiovascular and Respiratory Disorders 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 6051 Knowledge Check: Cardiovascular and Respiratory Disorders

After the introduction, move into the main part of the NURS 6051 Knowledge Check: Cardiovascular and Respiratory Disorders 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 6051 Knowledge Check: Cardiovascular and Respiratory Disorders

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 6051 Knowledge Check: Cardiovascular and Respiratory Disorders

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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NURS 6051 Knowledge Check: Cardiovascular and Respiratory Disorders

The chronic obstructive disease is a chronic respiratory disease characterized by persistent respiratory symptoms and airflow limitation attributed to airway and alveolar abnormalities (Pahal et al., 2022). Bronchitis and emphysema are types of chronic obstructive pulmonary disease (Pahal et al., 2022). Emphysema primarily affects airspaces distal to the terminal bronchioles and is characterized by abnormal permanent dilatation of airspaces, destruction of septal walls, and loss of lung elasticity (Pahal et al., 2022). The destruction of terminal airspaces is attributed to longstanding exposure to toxic particles and gases that trigger inflammation.

Various risk factors predispose to emphysema and COPD in general. These include smoking, male gender, air pollution, genetic predisposition, recurrent lung infections, allergies, advanced age, and occupational exposure to particles such as silica and coal dust (Sutradhar et al., 2019). Smoking is the strongest predisposing factor with the intensity of smoking and years of smoking being the predictors of disease progression (Pahal et al., 2022). The notable factors present in the patient in this scenario include advanced age and a positive 50-pack-per-year cigarette smoking history.

An imbalance between oxidative and antioxidative processes forms the basis for the pathogenesis of emphysema. Oxidative stress and hyperinflammation in response to noxious stmuli lead to the activation of proinflammatory transcription factors with a resultant heightened inflammatory response and destruction of elastic fibers by metalloproteinases (Rodrigues et al., 2021). The destruction of alveolar walls results in poor lung function due to a diminished gas exchange, permanent airspace enlargement, loss of lung elasticity, hyperinflation, and limitations of expiratory airflow (Rodrigues et al., 2021). Emphysema is thus a subtype of chronic obstructive pulmonary disease.

References

Pahal, P., Avula, A., & Sharma, S. (2022). Emphysema. In StatPearls. StatPearls Publishing.

Rodrigues, S. de, Cunha, C. M., Soares, G. M., Silva, P. L., Silva, A. R., & Gonçalves-de-Albuquerque, C. F. (2021). Mechanisms, pathophysiology, and currently proposed treatments of chronic obstructive pulmonary disease. Pharmaceuticals, 14(10), 979. https://doi.org/10.3390/ph14100979

Sutradhar, I., Das Gupta, R., Hasan, M., Wazib, A., & Sarker, M. (2019). Prevalence and risk factors of chronic obstructive pulmonary disease in Bangladesh: A systematic review. Cureus. https://doi.org/10.7759/cureus.3970

Question 1

Scenario 1: Peptic Ulcer

A 65-year-old female comes to the clinic with a complaint of abdominal pain in the epigastric area. The pain has been persistent for two weeks. The pain described as burning, non-radiating and worse after meals. Denies N&V, weight loss or obvious bleeding. She admits to frequent belching with bloating.

PMH: seasonal allergies with Chronic Sinusitis, positive for osteoarthritis,

Meds: Claritin 10 mg po daily, ibuprofen 400-600 mg po prn pain

Family Hx-non contributary

Social history: Separated recently pending divorce; stressful situation with trying to manage two homes. Works as a Legal Assistant at a local law firm. She has 35 PPY of smoking, drinks 1-2 glasses of wine a day, and 6-7 cups of coffee per day. She denies illicit drug use, vaping or unprotected sexual encounters.

Breath test in the office revealed + urease.

The healthcare provider suspects the client has peptic ulcer disease.

Questions:

1. Explain what contributed to the development from this patient’s history of PUD?

Your Answer:

Helicobacter pylori infection: The presence of a positive urease test suggests the involvement of H. pylori, a common bacterium associated with PUD. H. pylori can disrupt the protective mucosal lining of the stomach and duodenum, leading to ulcers.
Medication use: The patient’s frequent use of ibuprofen (NSAID) for pain relief can irritate the stomach lining and increase the risk of developing ulcers. NSAIDs, including ibuprofen, are known to inhibit the production of prostaglandins, which help protect the stomach lining.
Lifestyle factors: The patient’s smoking habit, excessive alcohol consumption, and high coffee intake are known to increase the risk of developing peptic ulcers. Smoking and alcohol can impair the stomach’s protective mechanisms, while coffee stimulates acid production, which can contribute to ulcer formation.
Stressful situation: The patient’s recent separation, pending divorce, and the stress associated with managing two homes can lead to increased psychological stress. Stress itself does not cause ulcers, but it can exacerbate existing ulcers by affecting the body’s ability to heal and increasing acid production.
Other medical conditions: While not directly contributing to PUD, chronic sinusitis and osteoarthritis may have influenced the patient’s medication use and overall health, potentially affecting the susceptibility to ulcers.

Question 2

Scenario 1: Peptic Ulcer

NURS 6051 Knowledge Check Cardiovascular and Respiratory Disorders

PMH: seasonal allergies with Chronic Sinusitis, positive for osteoarthritis,

Meds: Claritin 10 mg po daily, ibuprofen 400-600 mg po prn pain

Family Hx-non contributary

Breath test in the office revealed + urease.

The healthcare provider suspects the client has peptic ulcer disease.

Question:

1. What is the pathophysiology of PUD/ formation of peptic ulcers?

Your Answer:

Peptic ulcer disease (PUD) occurs due to an imbalance between aggressive factors (such as H. pylori infection and excessive gastric acid secretion) and protective mechanisms (such as mucosal defense mechanisms). Factors like NSAID use and certain lifestyle habits (smoking, alcohol, caffeine) can contribute to ulcer formation.

Question 3

4 / 4 pts

Scenario 2: Gastroesophageal Reflux Disease (GERD)

A 44-year-old morbidly obese female comes to the clinic complaining of “burning in my chest and a funny taste in my mouth”. The symptoms have been present for years but patient states she had been treating the symptoms with antacid tablets which helped until the last 4 or 5 weeks. She never saw a healthcare provider for that. She says the symptoms get worse at night when she is lying down and has had to sleep with 2 pillows. She says she has started coughing at night which has been interfering with her sleep. She denies palpitations, shortness of breath, or nausea.

PMH-HTN, venous stasis ulcers, irritable bowel syndrome, osteoarthritis of knees, morbid obesity (BMI 48 kg/m²)

FH:non contributary

Medications: Lisinopril 10 mg po qd, Bentyl 10 mg po, ibuprofen 800 mg po q 6 hr prn

SH: 20 PPY of smoking, ETOH rarely, denies vaping

Diagnoses: Gastroesophageal reflux disease (GERD).

Question:

1. If the client asks what causes GERD how would you explain this as a provider?

Your Answer:

GERD is caused by a weakened or relaxed lower esophageal sphincter (LES), which allows stomach acid to flow back up into the esophagus. Factors such as obesity, hiatal hernia, certain foods/drinks, smoking, medications, and other medical conditions can contribute to GERD. Treatment aims to reduce symptoms and may include lifestyle changes and medication.

Question 4

Scenario 3: Upper GI Bleed

A 64-year-old male presents the clinic with complaints of passing dark, tarry, stools. He stated the first episode occurred last week, but it was only a small amount after he had eaten a dinner of beets and beef. The episode today was accompanied by nausea, sweating, and weakness. He states he has had some mid epigastric pain for several weeks and has been taking OTC antacids. The most likely diagnosis is upper GI bleed which won’t be confirmed until further endoscopic procedures are performed.

Question:

1. What are the variables here that contribute to an upper GI bleed?

Your Answer:

The variables that contribute to an upper gastrointestinal (GI) bleed in this scenario include peptic ulcer disease (PUD), diet (beets and beef), and the presence of symptoms such as nausea, sweating, weakness, and passing dark, tarry stools (melena). Medications and underlying conditions are also potential factors.

Question 5

Scenario 4: Diverticulitis

A 54-year-old schoolteacher is seeing your today for complaints of passing bright red blood when she had a bowel movement this morning. She stated the first episode occurred last week. The episode today was accompanied by nausea, sweating, and weakness. She states she has had some LLQ pain for several weeks but described it as “coming and going”. She says she has had a fever and abdominal cramps that have worsened this morning.

Diagnosis is lower GI bleed secondary to diverticulitis.

Question:

1. What can cause diverticulitis in the lower GI tract?

Your Answer:

Diverticulitis in the lower GI tract is caused by inflamed or infected diverticula, which are small pouches that form in the colon. Factors include the presence of diverticula, a low-fiber diet, age (typically over 50), lifestyle factors (obesity, sedentary lifestyle), and potential genetic factors. Prompt medical attention is crucial for evaluation and treatment.

Quiz Score: 20 out of 20

Question 1

3 / 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:

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

Your Answer:

High-density lipoprotein (HDL) cholesterol is considered the “good” cholesterol. HDL helps remove excess cholesterol from the bloodstream and carries it back to the liver, where it can be broken down and eliminated from the body. High levels of HDL cholesterol are associated with a lower risk of heart disease.

Question 2

3 / 4 pts

Scenario 1: Myocardial Infarction

His diagnosis is an acute inferior wall myocardial infarction.

Question:

How does inflammation contribute to the development of atherosclerosis?

Your Answer:

Chronic inflammation causes macrophages to build up. Inflammation is linked to disease severity and to the development of complicated lesions that are prone to spontaneous bleeding and other sudden medical crises. It’s a risk factor for atherosclerotic events and an active driver of atherosclerotic plaque development.

Question 3

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?

NURS 6051 Knowledge Check: Cardiovascular and Respiratory Disorders

Scenario 1: Myocardial Infarction

His diagnosis is an acute inferior wall myocardial infarction.

Question:

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

Your Answer:

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.

No reference listed to allow one to cross check for accuracy. Adding to the discussion. HDL functionality encompasses many other potentially beneficial functions, including antioxidant, anti-inflammatory, antithrombotic, anti-apoptotic, and vascular protective effects that may be critical protective pathways for various cells, including those in the kidney parenchyma

Scenario 1: Myocardial Infarction

His diagnosis is an acute inferior wall myocardial infarction.

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.

Your Answer:

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.

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Question 1

2 out of 2 points

CC: “I have been having terrible chest and arm pain for the past 2 hours and I think I am having a heart attack.”

HPI: Mr. Hammond is a 57-year-old African American male who presents to the Emergency Department with a chief complaint of chest pain that radiates down his left arm. He states that he started having pain several hours ago and says the pain “it feels like an elephant is sitting on my chest”. He rates the pain as 8/10. Nothing has made the pain better or worse. He denies any previous episode of chest pain. Denies nausea, dyspnea, or lightheadedness. He was given 0.4 mg nitroglycerine tablet sublingual x 1 which decreased, but not stopped the pain.

Lipid panel reveals Total Cholesterol 324 mg/dl, high density lipoprotein (HDL) 31 mg/dl, Low Density Lipoprotein (LDL) 122 mg/dl, Triglycerides 402 mg/dl, Very Low-Density Lipoprotein (VLDL) 54 mg/dl

His diagnosis is an acute inferior wall myocardial infarction.

1 of 2 Questions:

Why is HDL considered the “good” cholesterol?

Selected Answer:	HDL carries between 20-25% of the total cholesterol in plasma. It is a good cholesterol since it accumulates the excess cholesterol that exists in body cells for excretion in the liver.
Correct Answer:	HDL is considered the good cholesterol because it collects excess cholesterol in the body cells and transports it to the liver where it is excreted in the body cells and transports it to the liver where it is excreted in the body. HDL carries 20-25% of total plasma cholesterol.
Response Feedback:	[None Given]

Question 2

3 out of 3 points

CC: “I have been having terrible chest and arm pain for the past 2 hours and I think I am having a heart attack.”

His diagnosis is an acute inferior wall myocardial infarction.

2 of 2 Questions:

Explain the role inflammation has in the development of atherosclerosis.

Selected Answer:	Mitochondrial damage caused by chronic inflammatory processes cause inflammation in the heart muscles. These processes cause an increase in the production of free radicals that activate the continuous cycle of chronic inflammation.
Correct Answer:	Inflammation in the heart muscle caused by chronic inflammatory processes leads to mitochondrial damage that results in an increased free radical production that further activates the chronic inflammatory vicious cycle.
Response Feedback:	[None Given]

Question 3

1 out of 1 points

A 45-year-old woman with a 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 3-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:

What does the Advanced Practice Registered Nurse (APRN) recognize as the result of the pleural friction rub?

Selected Answer:	The pericardium tends to roughen following inflammation caused by a post-viral syndrome or an underlying autoimmune disease. The roughening is what produces a classic rub that an APRN can hear at the left sternal border and apex of the heart.
Correct Answer:	The inflammation of the pericardium, due to either the underlying autoimmune disease or a post viral syndrome, causes roughening of the pericardium. The roughening of the pericardium causes the classic “rub” which can best be heard at the apex of the heart and left sternal border.
Response Feedback:	[None Given]

Question 4

1 out of 1 points

A 15-year-old adolescent male comes to the clinic with his parents with a chief complaint of fever, nausea, vomiting, poorly localized abdominal pain, arthralgias, and “swollen lymph nodes”. States he has felt “lousy” for a couple weeks. The fevers have been as high as 102 F. His parents thought he had the flu and took him to an Urgent Care Center. He was given Tamiflu® and sent home. He says the Tamiflu didn’t seem to work. States had a slight sore throat a couple weeks ago and attributed it to the flu. Physical exam revealed thin young man who appears to be uncomfortable but not acutely ill. Posterior pharynx reddened and tonsils 3+ without exudate. + anterior and posterior cervical lymphadenopathy. Tachycardic and a new onset 2/6 high-pitched, crescendo-decrescendo systolic ejection murmur auscultated at the left sternal border. Rapid strep +. The patient was diagnosed with acute rheumatic heart disease (RHD).

Question:

Explain how a positive strep test has caused the patient’s symptoms.

Selected Answer:	A pharyngeal infection with GABHs (Group A Beta Hemolytic Streptococcus) often leads to the development of RHD, which is an abnormal response to cell-mediated responses. The inflammatory cascade associated with this process cause exudative and proliferative lesions, and scarring in the valve tissue. Since it is the endocardium which contains valves that is primarily affected, inflammation of the endocardium results to subsequent inflammation of valves.
Correct Answer:	Rheumatic Heart Disease (RHD) only develops after a pharyngeal infection with Group A beta hemolytic streptococcus. It is an abnormal response to humoral and cell-mediated response to M proteins on the microorganisms. The intense inflammation caused by these reactions cause proliferative and exudative lesions in connective tissue. This inflammation causes scarring of the valve tissue. The inflammation usually affects the endocardium which contains the valves. Endocardial inflammation causes swelling of leaflets in the valves.
Response Feedback:	[None Given]

Question 5

1 out of 1 points

The APRN sees a 74-year-old obese female patient who is 2 days post-op after undergoing left total hip replacement. The patient has had severe post op nausea and vomiting and has been unable to go to physical therapy. Her mucus membranes are dry. The patient says she feels like 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:

Describe the factors that could have contributed to the development of a DVT in this patient explain how each of the factors could cause DVT.

Selected Answer:	When there is injury to a blood vessel, there is platelet adherence to blood vessel walls influenced by antiplatelet substances. When platelets aggregate, they form clots. Therefore, virchow’s triad damaged the blood vessel walls. Since this patient is reportedly obese, inability to engage in physical therapy and an advanced age caused venous stasis,
Correct Answer:	Virchow’s Triad caused damage to the walls of the vessels. When there is injury to the intimal layer of the vessel, antiplatelet substances such as nitric oxide and prostacyclin, along with the expression of collagen on the vessel wall, causes adherence of the platelets to the vessel wall. The platelets become activated then aggregate forming clots. Venous stasis as a result of obesity, patient’s advanced age and inability to go to physical therapy.
Response Feedback:	[None Given]

Question 6

1 out of 1 points

A 45-year-old woman is 10 days status post partial small bowel resection for Crohn Disease and has been recuperating at home. She suddenly develops severe shortness of breath, becomes weak, and her blood pressure drops to 80/40 mmHg (previous readings ~130/80s mmHg). The pulse oximetry is 89% on room air. The APRN suspects the patient experienced a massive pulmonary embolus.

Question:

Explain why a large pulmonary embolus interferes with oxygenation.

Selected Answer:	The pulmonary embolus lodged itself strategically in pulmonary circulation resulting to a mismatch in ventilation/perfusion (V/Q) reducing the area for the exchange of oxygen.
Correct Answer:	The embolus lodges somewhere in the pulmonary circulation and causes a ventilation/perfusion mismatch (V/Q). Ventilation Perfusion mismatch or “V/Q defects” are defects in total lung ventilation perfusion ratio. It is a condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen due to obstruction somewhere in the pulmonary circulation. This causes a decreased area for oxygen exchange.
Response Feedback:	[None Given]

Question 7

1 out of 1 points

A 45-year-old woman is 10 days status post partial small bowel resection for Crohn Disease and has been recuperating at home. She suddenly develops severe shortness of breath, becomes weak, and her blood pressure drops to 80/40 mmHg (previous readings ~130/80s mmHg). The pulse oximetry is 89% on room air. While waiting for the Emergency Medical Service (EMS) to arrive, the APRN places EKG leads and the EKG demonstrates right ventricular strain.

Question:

Explain why a large pulmonary embolism causes right ventricular strain.

Selected Answer:	The ventilation/perfusion mismatch caused the release of inflammatory mediators resulting to vasoconstriction of the pulmonary system obstructing oxygenation and subsequent hypertension. This causes atelectasis and makes pumping of blood by the right ventricle difficult
Correct Answer:	The V/Q mismatch causes release of neurohumeral substances and inflammatory mediators that cause vasoconstriction of the pulmonary vasculature further impeding oxygenation. Hemodynamically, this vasoconstriction results in pulmonary hypertension, making it difficult for the right ventricle to pump blood. The V/Q mismatch also causes decreased production of surfactant causing atelectasis that further decreases surface area available for oxygen exchange.
Response Feedback:	[None Given]

Question 8

2 out of 2 points

A 12-year-old girl is brought to the Emergency Room (ER) by her mother with complaints of shortness of breath, wheezing, tachypnea, tachycardia, and a non-productive cough. The mother states they had just come from a fall festival where the entire family enjoyed a hayride. The symptoms began shortly after they left the festival but got better a couple hours after they returned home. The symptoms began again about 6 hours later and seem to be worse. The mother states there is no history of allergies or frequent respiratory infections. The child is up to date on all vaccinations. The child was diagnosed with asthma. The nurse practitioner explained to the mother that her child was exhibiting symptoms of asthma, and probably had an early asthmatic response and a late asthmatic response.

Question 1 of 2:

Explain early asthmatic responses and the cells responsible for the responses.

Selected Answer:	There is an adaptive and innate immune response following an initial airway exposure to an antigen. Basophils, T helper cells, eosinophils, dendritic cells, and mast cells can initiate the inflammatory process. This process can peak at thirty minutes and resolve after three hours.
Correct Answer:	When there is an initial airway exposure to an antigen, an innate and adaptive immune response is initiated. Cells that can initiate the inflammation of the bronchial mucosa and hyperresonance of the airways include dendritic cells, T helper 2 lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, and basophils. Early asthmatic response is a phase of bronchospasm that peaks at about 30 minutes and usually resolves after about 3 hours.
Response Feedback:	[None Given]

Question 9

1.8 out of 2 points

Question 2 of 2:

Explain late asthmatic responses and the cells responsible for the responses.

Selected Answer:	Early exposure in the initial phase mediate late asthma responses resulting to the release of inflammatory mediators such as prostaglandins D and leukotrienes with subsequent edema, bronchospasms, and secretion of mucus that obstruct the flow of air. With continuous obstruction, resistance sets in and air is trapped hence reduced lung perfusion and ventilation.
Correct Answer:	Late asthmatic responses are mediated by earlier exposure in early phase that causes a latent release of inflammatory mediators. These mediators, leukotrienes and prostaglandin D, cause bronchospasm, edema, and mucus secretions that obstruct airflow. Airway obstruction creates resistance to airflow and causes air trapping. Continued air trapping increases intrapleural and alveolar gas pressure, decreases ventilation and perfusion leading to uneven and variable ventilation/perfusion in the lung
Response Feedback:	timing of phase

Question 10

2 out of 2 points

A 64-year-old man with a 40 pack/year history of cigarette smoking has been diagnosed with emphysema. He asks the APRN if this means he has COPD.

Question 1 of 2:

Explain the pathophysiology of emphysema and how it relates to COPD.

Selected Answer:	Emphysema causes the permanent airway enlargement characterized by damage to alveolar walls. With continuous exposure to irritants, there is an inflammatory oxidative stress involving lymphocytes, neutrophils, and macrophages causing more alveoli damage. This process reduces the surface area required for the exchange of gases with a significant ventilation/perfusion mismatch.
Correct Answer:	Emphysema is a disease of the airways that causes permanent enlargement of the gasexchange airways. It is accompanied by destruction of the alveolar walls do not appear to be fibrotic. Chronic exposure to irritants recruit neutrophils, macrophages, and lymphocytes to the lung resulting in progressive damage from inflammatory oxidative stress. Emphysema is characterized by destruction of alveoli leading to decreased surface area for gas exchange that causes significant ventilation/perfusion mismatch.
Response Feedback:	[None Given]

Question 11

2 out of 2 points

A 64-year-old man with a 40 pack/year history of cigarette smoking has been diagnosed with emphysema. He asks the APRN if this means he has COPD.

Question 2 of 2:

Explain the pathophysiology of chronic bronchitis and how it relates to COPD.

Selected Answer:	The bronchi becomes inflamed when an individual inhales irritants. Inflammation increases the number and size of goblet cells and mucus glands, causes edema of the bronchial, and hypertrophy of the smooth muscles. Over time, the airway undergoes fibrosis and narrows. Since the functioning of the ciliary is also impaired, continuous mucus production hinders the patient’s ability to cough. In the advanced stages, both the large and small airways get involved, with an obstructed airflow during expiration that can result to a VQ mismatch.
Correct Answer:	Chronic bronchitis is caused by inhalation of irritants that promote bronchial inflammation. This inflammation causes bronchial edema, increase in the size and number of mucus glands and goblet cells, smooth muscle hypertrophy with fibrosis and narrowing of the airway. Increased secretions of thick mucus happen, and the patient cannot cough it up due to impairment of ciliary function. As the disease, progresses, the smaller airways are involved as well as the large airways. These airways, due to hypertrophy, cause narrowing of the smooth muscle and obstruct airflow, especially during expiration. The obstruction can lead to VQ mismatches.
Response Feedback:	[None Given]

Question 12

1 out of 1 points

Mr. Jones is a 78-year-old gentleman who presents to the clinic with a chief complaint of fever, chills and cough. He also reports some dyspnea. He has a history of right sided CVA, COPD, dyslipidemia, and HTN. Current medications include atorvastatin 40 mg po qhs, lisinopril, and fluticasone/salmeterol. He reports more use of his albuterol rescue inhaler.

Vital signs Temp 101.8 F, pulse 108, respirations 21. PaO₂ on room air 86% and on O₂ 4 L nasal canula 94%. CMP WNL, WBC 18.4. Physical exam reveals thin, anxious gentleman with mild hemiparesis on left side due to CVA. HEENT WNL except for diminished gag reflex and uneven elevation of the uvula, CV-HR 108 RRR without murmurs, rubs, or click, no bruits. Resp-coarse rhonchi throughout lung fields. CXR reveals consolidation in right lower lobe. He was diagnosed with community acquired pneumonia (CAP).

Question:

Patient was hypoxic as evidenced by the low PaO₂. Explain the pathologic processes that caused this patient’s hypoxemia.

Selected Answer:	Continuous flow of blood in the pulmonary artery results to lung consolidation with a subsequent V/Q mismatch. This process influences the release of mediators with an inflamed bronchi-alveolar membrane. However, when the surfactant becomes inactivated, the alveoli collapses, and gets filled with exudates which decreases the surface area for the exchange of gases.
Correct Answer:	Arterial hypoxemia early in acute pneumococcal pneumonia is principally caused by persistence of pulmonary artery blood flow to be consolidated lung resulting in an intrapulmonary shunt, and by ventilation-perfusion mismatch later. Release of mediators cause widespread inflammation of the bronchial structures, especially the alveolarcapillary membrane. The alveoli collapse due to inactivation of surfactant and the alveoli fill with exudate, decreasing surface area for gas exchange.
Response Feedback:	[None Given]

Question 13

1 out of 1 points

A 64-year-old woman with moderately severe COPD comes to the pulmonary clinic for her quarterly checkup. The APRN reviewing the chart notes that the patient has lost 5% of her body weight since her last visit. The APRN questions the patient and patient admits to not having much of an appetite and she also admits to missing some meals because it “takes too much work” to cook and consume dinner.

Question:

The APRN recognizes that COPD has a deleterious effect on patients. Explain why patients with COPD are at risk for malnutrition.

Selected Answer:	Most patients diagnosed with COPD are malnourished since they require a diet that is low in carbohydrates to prevent hypercapnia that may occur from the metabolism of CHO.
Correct Answer:	Many of the patients with severe COPD are lean, and frequently in a malnourished or undernourished state, which is characterized by loss of fat-free body mass causing muscle wasting. The muscle wasting in COPD not only leads to decreased skeletal muscle function associated with reduced exercise capacity but is also a major determinant of mortality in COPD. Patients with COPD require a low carbohydrate diet as increased CHO can lead to hypercapnia as the end products of CHO metabolism are CO2 and H2O.
Response Feedback:	[None Given]

Review Test Submission: Module 2 Knowledge Check

The circulatory system and the respiratory system are powerful partners in health. While they work closely together in good health, a disease or disorder that manifests in one can have a significant impact on both, hampering the pair’s ability to collaborate.

Cardiovascular and respiratory disease and disorders are among the most common reasons for hospital visits, and among the leading causes of fatality. Heart disease and pneumonias are among the most familiar, but a wide variety of issues can impact physiological functioning of one or both systems.

This week, you examine fundamental concepts of cardiovascular and respiratory disorders. You explore common diseases and disorders that impact these systems, and you apply the key terms and concepts that help communicate the pathophysiological nature of these issues to patients.

Click here to ORDER NOW FOR AN ORIGINAL PAPER ASSIGNMENT ON NURS 6051 Knowledge Check: Cardiovascular and Respiratory Disorders

Learning Objectives

Students will:

Analyze concepts and principles of pathophysiology across the lifespan

Learning Resources

Required Readings (click to expand/reduce)

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.

Chapter 32: Structure and Function of the Cardiovascular and Lymphatic Systems; Summary Review

Chapter 33: Alterations of Cardiovascular Function (stop at Dysrhythmias); Summary Review

Chapter 35: Structure and Function of the Pulmonary System; Summary Review

Chapter 36: Alterations of Pulmonary Function (stop at Disorders of the chest wall and pleura); (obstructive pulmonary diseases) (stop at Pulmonary artery hypertension); Summary Review

Inamdar, A. A. & Inamdar, A. C. (2016). Heart failure: Diagnosis, management, and utilization, 5(7). doi:10.3390/jcm5070062

Cardiovascular Respiratory Disorders – Week 3 (16m)

Pneumonia

MedCram. (2015, September 14). Pneumonia explained clearly by MedCram.com [Video file]. Retrieved from https://www.youtube.com/watch?v=nqyPECmkSeo

Note: The approximate length of the media program is 13 minutes.

Online Media from Pathophysiology: The Biologic Basis for Disease in Adults and Children

In addition to this week’s media, it is highly recommended that you access and view the resources included with the course text, Pathophysiology: The Biologic Basis for Disease in Adults and Children. Focus on the videos and animations in Chapters 32, 33, 35, and 36 that relate to cardiorespiratory systems and alteration in cardiorespiratory systems. Refer to the Learning Resources in Week 1 for registration instructions. If you have already registered, you may access the resources at https://evolve.elsevier.com/

Knowledge Check: Cardiovascular and Respiratory Disorders

In this exercise, you will complete a 10- to 20-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

Photo Credit: Getty Images/Science Photo Library RF

Complete the Knowledge Check by Day 7 of Week 3

To complete this Knowledge Check:

Module 2 Knowledge Check

What’s Coming Up in Week 4?

Photo Credit: [BrianAJackson]/[iStock / Getty Images Plus]/Getty Images

Next week, you will examine the alterations in the cardiovascular and respiratory systems and the resultant disease processes through case study analysis. You will also consider patient characteristics, including racial and ethnic variables, which may impact altered physiology.

Next Week

To go to the next week:

Week 4

Question 1

1 out of 1 points

Correct

Sympathetic stimulation causes airways to:
Selected Answer:
Correct

dilate
Answers:
Correct

dilate

constrict

collapse

trap air

Question 2

1 out of 1 points

Correct

Sympathetic nerves to the heart releases what the neurotransmitter?
Selected Answer:
Correct

norepinephrine
Answers:

serotonin

epinephrine

Correct

norepinephrine

1 out of 1 points

Correct

Inflammatory mediators released during an acute asthma episode cause:
Selected Answer:
Correct

inflammation, hypersecretion of mucous, and bronchial smooth muscle constriction
Answers:
Correct

inflammation, hypersecretion of mucous, and bronchial smooth muscle constriction

inflammation, bleeding, and bronchial smooth muscle constriction

bronchial smooth muscle dilation, alveolar collapse, and retained PaCO2

bronchial smooth muscle dilation, inflammation, and thick mucous

1 out of 1 points

Correct

Binding of ATP to myosin that enables myocardial contraction requires which electrolyte?
Selected Answer:
Correct

calcium
Answers:
Correct

calcium

magnesium

sodium

potassium

Question 16

1 out of 1 points

Correct

How much oxygen does the myocardium extract from the coronary arteries?
Selected Answer:
Correct

70%
Answers:

40%

50%

60%

Correct

70%

Question 17

1 out of 1 points

Correct

The right side of the heart is a high-pressure system
Selected Answer:
Correct

False
Answers:

True

Correct

False

Question 18

1 out of 1 points

Correct

Collapse of alveoli is a(n):
Selected Answer:
Correct

Atelectasis
Answers:

Empyema

Aspiration

Correct

Atelectasis

Hemoptysis

Question 19

1 out of 1 points

Correct

The tunica media is the middle layer of blood vessels and is composed of what type of tissue?

Selected Answer:
Correct

smooth muscle and elastic fibers
Answers:

endothelium and elastic fibers

endothelium and connective tissue

Correct

smooth muscle and elastic fibers

smooth muscle and connective tissue

Question 20

1 out of 1 points

Correct

Prinzmetal angina is caused by:
Selected Answer:
Correct

vasospasm of the coronary artery
Answers:

obstruction of a coronary artery

Correct

vasospasm of the coronary artery

thrombus within the coronary artery

dissection of the coronary artery

Question 13

1 out of 1 points

Question:

The APRN recognizes that COPD has a deleterious effect on patients. Explain why patients with COPD are at risk for malnutrition.

Selected Answer:	Most patients diagnosed with COPD are malnourished since they require a diet that is low in carbohydrates to prevent hypercapnia that may occur from the metabolism of CHO.
Correct Answer:	Many of the patients with severe COPD are lean, and frequently in a malnourished or undernourished state, which is characterized by loss of fat-free body mass causing muscle wasting. The muscle wasting in COPD not only leads to decreased skeletal muscle function associated with reduced exercise capacity but is also a major determinant of mortality in COPD. Patients with COPD require a low carbohydrate diet as increased CHO can lead to hypercapnia as the end products of CHO metabolism are CO2 and H2O.
Response Feedback:	[None Given]

Week 3: Concepts of Cardiovascular and Respiratory Disorders

Learning Objectives

Students will:

Analyze concepts and principles of pathophysiology across the lifespan

Learning Resources

Required Readings (click to expand/reduce)

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.

Chapter 32: Structure and Function of the Cardiovascular and Lymphatic Systems; Summary Review
Chapter 33: Alterations of Cardiovascular Function (stop at Dysrhythmias); Summary Review
Chapter 35: Structure and Function of the Pulmonary System; Summary Review
Chapter 36: Alterations of Pulmonary Function (stop at Disorders of the chest wall and pleura); (obstructive pulmonary diseases) (stop at Pulmonary artery hypertension); Summary Review

Inamdar, A. A. & Inamdar, A. C. (2016). Heart failure: Diagnosis, management, and utilization, 5(7). doi:10.3390/jcm5070062

Required Media (click to expand/reduce)

Module 2 Overview with Dr. Tara Harris

Dr. Tara Harris reviews the structure of Module 2 as well as the expectations for the module. Consider how you will manage your time as you review your media and Learning Resources throughout the module to prepare for your Knowledge Check and Assignment. (4m)

Cardiovascular Respiratory Disorders – Week 3 (16m)

Pneumonia

MedCram. (2015, September 14). Pneumonia explained clearly by MedCram.com [Video file]. Retrieved from https://www.youtube.com/watch?v=nqyPECmkSeo

Note: The approximate length of the media program is 13 minutes.

Online Media from Pathophysiology: The Biologic Basis for Disease in Adults and Children

Knowledge Check: 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

Photo Credit: Getty Images/Science Photo Library RF

Complete the Knowledge Check by Day 7 of Week 3

To complete this Knowledge Check:

Module 2 Knowledge Check

What’s Coming Up in Week 4?

Photo Credit: [BrianAJackson]/[iStock / Getty Images Plus]/Getty Images

Next Week

To go to the next week:

Week 4

An elderly 81-year-old obese lady developed deep venous thrombosis confirmed by a duplex ultrasound 48 hours after a left total hip replacement operation. She presented with severe nausea and vomiting that resulted in dry mucous membranes. She presented with typical features of deep venous thrombosis such as leg swelling, calf tenderness, and redness on the operated leg (Mazzolai et al., 2018). The development of deep venous thrombosis is a common complication following total hip replacement surgery (Yu et al., 2021). The consequences include prolonged hospital stay, adverse patient outcomes, predisposition to pulmonary embolism, and high economic implications.

Various mechanisms lead to the development of deep venous thrombosis. These include factors that lead to venous stasis, endothelial injury, and hypercoagulability described as Virchow’s triad (McLendon et al., 2022). Identified risk factors include immobilization, surgery, and trauma (Othieno et al., 2018). Obesity, advanced age, dehydration, thrombocytosis, and a previous history also predispose to deep venous thrombosis (Waheed et al., 2022). The patient in this scenario was elderly, obese, and had just undergone surgery. Surgery activates inflammatory response with the release of cytokines which activates the coagulation system (Yu et al., 2021). The surgery also contributed to immobility due to the resultant bed rest and immobility under anesthesia during the long operation. There is a history of severe nausea and vomiting. This may have led to dehydration evidenced by dry mucous membranes with resultant hypercoagulability. There is no mention of postoperative prophylactic anticoagulant therapy which would have minimized the development of deep venous thrombosis.

References

Mazzolai, L., Aboyans, V., Ageno, W., Agnelli, G., Alatri, A., Bauersachs, R., Brekelmans, M. P., Büller, H. R., Elias, A., Farge, D., Konstantinides, S., Palareti, G., Prandoni, P., Righini, M., Torbicki, A., Vlachopoulos, C., & Brodmann, M. (2018). Diagnosis and management of acute deep vein thrombosis: A joint consensus document from the European Society of cardiology working groups of the aorta and peripheral vascular diseases and pulmonary circulation and right ventricular function. European Heart Journal, 39(47), 4208–4218. https://doi.org/10.1093/eurheartj/ehx003

McLendon, K., Goyal, A., & Attia, M. (2022). Deep Venous Thrombosis Risk Factors. In StatPearls. StatPearls Publishing.

Othieno, R., Okpo, E., & Forster, R. (2018). Home versus in-patient treatment for deep vein thrombosis. Cochrane Database of Systematic Reviews, 2018(1). https://doi.org/10.1002/14651858.cd003076.pub3

Waheed, S. M., Kudaravalli, P., & Hotwagner, D. T. (2022). Deep Vein Thrombosis. In StatPearls. StatPearls Publishing.

Yu, X., Wu, Y. & Ning, R. The deep vein thrombosis of the lower limb after total hip arthroplasty: what should we care. BMC Musculoskelet Disord 22, 547 (2021). https://doi.org/10.1186/s12891-021-04417-z