NURS 6501 Mod 1-4 EXAM 2025 UPDATE Verified Questions And
NURS 6501 Mod 1-4
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1. Why is HDL considered good It's able to remove cholesterol from artery plaques and
cholesterol? recycle it back to the liver.
2. Why is HDL consider good cho- HDL is considered good cholesterol because it collects
lesterol excess cholesterol in the body cells and transports it to the
liver where it is excreted. HDL carries 20 to 25% of total
plasma cholesterol.
3. Explain the role inflammation Inflammation in the heart muscle caused by chronic in-
has in the development of ather- flammatory processes leads to mitochondrial damage that
osclerosis results in an increased free radical production that further
activates the chronic inflammatory vicious cycle
4. Explain the role inflammation Activated mast cells recruit inflammatory cells that provoke
has in the development of ather- plaque formation and lead to atherosclerosis. Chronic in-
osclerosis flammatory infiltrates occupy layers of arteries were stable
plaques are formed and associated with atherosclerosis.
5. Explain the role inflammation Additionally active inflammation involves a thinning at the
has in the development of ather- fibrous Of atherosclerotic plaque which predisposes vul-
osclerosis nerable plaque to rupture.
6. Why does the APRN recognize as The inflammation of the pericardium due to either the
the result of the pleural friction underlying autoimmune disease or a post viral syndrome
rub? causes roughening of the pericardium. This causes the
classic rug which can be best heard at the Apex of the heart
and left sternal border.
7. Explain how a positive strep test Rheumatic heart disease RHD only develops after a pha-
has caused the patient's symp- ryngeal infection with group a beta hemolytic strepto-
toms coccus. It is an abnormal response to humoral and cell
mediated response to M proteins. Inflammation causes
proliferative and exudative lesions in connective tissue.
, NURS 6501 Mod 1-4
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8. Explain how a positive strep test Inflammation causes scarring of the valve tissue. Inflam-
has caused the patient's symp- mation usually affects the endocardium which contains
toms the valves. Endocardial inflammation causes swelling of
leaflets in the valves.
9. Describe the factors that could Virchow's Triad caused damage to the walls of the ves-
have contributed to the develop- sels. Injury to the intimal layer of the vessel, antiplatelet
ment of a DVT in this patient and substances such as nitric oxide and prostacyclin, along
explain how each of the factors with the expression of collagen on the vessel wall, causes
could cause DVT adherence to the platelets to the vessel wall.
10. Describe the factors that could Platelets become activated, then aggregate, forming clots.
have contributed to the develop- Venous stasis is a result of obesity, patients advanced age,
ment of a DVT in this patient and and inability to perform physical therapy therapy.
explain how each of the factors
could cause DVT
11. Explain why large pulmonary The embolus lodges somewhere in the pulmonary circu-
embolus interferes with oxy- lation and causes a ventilation/perfusion mismatch V/Q.
genation Ventilation perfusion mismatch or V/Q defects are defects
in total long ventilation perfusion ratio.
12. Explain why large pulmonary It is a condition in which one or more areas of the lung
embolus interferes with oxy- receive oxygen but no blood flow, or they receive blood
genation flow but no oxygen due to obstruction somewhere in the
pulmonary circulation. This causes a decreased area for
oxygen exchange.
13. Explain why a large pulmonary The V/Q mismatch causes release of neurohumeral sub-
embolism causes right ventricu- stances and inflammatory mediators that cause vasocon-
lar strain striction of the pulmonary vasculature further impeding
oxygenation.
, NURS 6501 Mod 1-4
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14. Explain why a large pulmonary Hemodynamically this vasoconstriction results in pul-
embolism causes right ventricu- monary hypertension, making it difficult for the right ven-
lar strain tricle to pump blood.
15. Explain why a large pulmonary The V/Q mismatch also creates decreased production of
embolism causes right ventricu- surfactant causing atelectasis that further decreases sur-
lar strain face area available for oxygen exchange.
16. Explain early asthmatic respons- When there is an initial airway exposure to an antigen, an
es in the cells responsible for the innate and adaptive immune response is initiated.
responses
17. Explain early asthmatic respons- Cells that can initiate the inflammation of the bronchial
es in the cells responsible for the mucosa and hyperresonance of the airways include
responses Dedrick cells, T-helper 2 cells, lymphocytes, B lymphocytes,
mast cells, neutrophils, eosinophils, and basophils.
18. Explain early asthmatic respons- Early asthmatic response is a phase of bronchospasm that
es in the cells responsible for the peaks at about 30 minutes and usually resolves after about
responses 3 hours.
19. Explain late asthmatic responses Late asthmatic responses are mediated by earlier expo-
in the cells responsible for the sure in early phase that causes a latent release of in-
responses flammatory mediators. These mediators, leukotrienes and
prostaglandin D, cause bronchospasm, edema, and mu-
cus secretions that obstruct airflow.
20. Explain late asthmatic responses Airway obstruction creates resistance to airflow and causes
in the cells responsible for the air trapping. Continued air trapping increases intrapleural
responses and alveolar gas pressure, decreases ventilation and per-
fusion leading to uneven and variable ventilation/perfu-
sion in the lung.
NURS 6501 Mod 1-4
Answers | Guaranteed Success!!
Study online at https://quizlet.com/_hhagk4
1. Why is HDL considered good It's able to remove cholesterol from artery plaques and
cholesterol? recycle it back to the liver.
2. Why is HDL consider good cho- HDL is considered good cholesterol because it collects
lesterol excess cholesterol in the body cells and transports it to the
liver where it is excreted. HDL carries 20 to 25% of total
plasma cholesterol.
3. Explain the role inflammation Inflammation in the heart muscle caused by chronic in-
has in the development of ather- flammatory processes leads to mitochondrial damage that
osclerosis results in an increased free radical production that further
activates the chronic inflammatory vicious cycle
4. Explain the role inflammation Activated mast cells recruit inflammatory cells that provoke
has in the development of ather- plaque formation and lead to atherosclerosis. Chronic in-
osclerosis flammatory infiltrates occupy layers of arteries were stable
plaques are formed and associated with atherosclerosis.
5. Explain the role inflammation Additionally active inflammation involves a thinning at the
has in the development of ather- fibrous Of atherosclerotic plaque which predisposes vul-
osclerosis nerable plaque to rupture.
6. Why does the APRN recognize as The inflammation of the pericardium due to either the
the result of the pleural friction underlying autoimmune disease or a post viral syndrome
rub? causes roughening of the pericardium. This causes the
classic rug which can be best heard at the Apex of the heart
and left sternal border.
7. Explain how a positive strep test Rheumatic heart disease RHD only develops after a pha-
has caused the patient's symp- ryngeal infection with group a beta hemolytic strepto-
toms coccus. It is an abnormal response to humoral and cell
mediated response to M proteins. Inflammation causes
proliferative and exudative lesions in connective tissue.
, NURS 6501 Mod 1-4
Study online at https://quizlet.com/_hhagk4
8. Explain how a positive strep test Inflammation causes scarring of the valve tissue. Inflam-
has caused the patient's symp- mation usually affects the endocardium which contains
toms the valves. Endocardial inflammation causes swelling of
leaflets in the valves.
9. Describe the factors that could Virchow's Triad caused damage to the walls of the ves-
have contributed to the develop- sels. Injury to the intimal layer of the vessel, antiplatelet
ment of a DVT in this patient and substances such as nitric oxide and prostacyclin, along
explain how each of the factors with the expression of collagen on the vessel wall, causes
could cause DVT adherence to the platelets to the vessel wall.
10. Describe the factors that could Platelets become activated, then aggregate, forming clots.
have contributed to the develop- Venous stasis is a result of obesity, patients advanced age,
ment of a DVT in this patient and and inability to perform physical therapy therapy.
explain how each of the factors
could cause DVT
11. Explain why large pulmonary The embolus lodges somewhere in the pulmonary circu-
embolus interferes with oxy- lation and causes a ventilation/perfusion mismatch V/Q.
genation Ventilation perfusion mismatch or V/Q defects are defects
in total long ventilation perfusion ratio.
12. Explain why large pulmonary It is a condition in which one or more areas of the lung
embolus interferes with oxy- receive oxygen but no blood flow, or they receive blood
genation flow but no oxygen due to obstruction somewhere in the
pulmonary circulation. This causes a decreased area for
oxygen exchange.
13. Explain why a large pulmonary The V/Q mismatch causes release of neurohumeral sub-
embolism causes right ventricu- stances and inflammatory mediators that cause vasocon-
lar strain striction of the pulmonary vasculature further impeding
oxygenation.
, NURS 6501 Mod 1-4
Study online at https://quizlet.com/_hhagk4
14. Explain why a large pulmonary Hemodynamically this vasoconstriction results in pul-
embolism causes right ventricu- monary hypertension, making it difficult for the right ven-
lar strain tricle to pump blood.
15. Explain why a large pulmonary The V/Q mismatch also creates decreased production of
embolism causes right ventricu- surfactant causing atelectasis that further decreases sur-
lar strain face area available for oxygen exchange.
16. Explain early asthmatic respons- When there is an initial airway exposure to an antigen, an
es in the cells responsible for the innate and adaptive immune response is initiated.
responses
17. Explain early asthmatic respons- Cells that can initiate the inflammation of the bronchial
es in the cells responsible for the mucosa and hyperresonance of the airways include
responses Dedrick cells, T-helper 2 cells, lymphocytes, B lymphocytes,
mast cells, neutrophils, eosinophils, and basophils.
18. Explain early asthmatic respons- Early asthmatic response is a phase of bronchospasm that
es in the cells responsible for the peaks at about 30 minutes and usually resolves after about
responses 3 hours.
19. Explain late asthmatic responses Late asthmatic responses are mediated by earlier expo-
in the cells responsible for the sure in early phase that causes a latent release of in-
responses flammatory mediators. These mediators, leukotrienes and
prostaglandin D, cause bronchospasm, edema, and mu-
cus secretions that obstruct airflow.
20. Explain late asthmatic responses Airway obstruction creates resistance to airflow and causes
in the cells responsible for the air trapping. Continued air trapping increases intrapleural
responses and alveolar gas pressure, decreases ventilation and per-
fusion leading to uneven and variable ventilation/perfu-
sion in the lung.
