NURS 6501 Knowledge Check Cardiovascular and Respiratory Disorders
NURS 6501 Knowledge Check Cardiovascular and Respiratory Disorders
NURS 6501 Knowledge Check Cardiovascular and Respiratory Disorders
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.” 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. 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]
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]
NURS 6501 Knowledge Check Cardiovascular and Respiratory Disorders
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
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 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]
