NSG 533 – Advanced Pharmacology Exam 3
Wilkes University | 2026/2027 | Verified Study Guide with Correct
Coverage]
[ACADEMIC YEAR: 2026/2027 – Graduate Nursing Program]
[Alignment: NONPF Core Competencies, AANP/ANCC Certification
Standards, ACC/AHA 2026, GOLD 2026]
[UNIT 1: ISCHEMIC HEART DISEASE & ACUTE CORONARY SYNDROMES]
30 Items | Focus: Pathophysiology, Risk Stratification, Acute Management, Post-MI
Care
Q1: A 58-year-old male with hypertension and dyslipidemia presents for routine
follow-up. His LDL is 160 mg/dL, HDL is 38 mg/dL, and triglycerides are 180 mg/dL.
According to the response-to-injury hypothesis of atherosclerosis, which sequence
accurately describes plaque development?
A. Endothelial dysfunction → fatty streak → smooth muscle proliferation → fibrous
plaque → complicated lesion
B. Fatty streak → endothelial injury → macrophage infiltration → thrombus formation →
plaque rupture
C. Smooth muscle proliferation → LDL oxidation → endothelial dysfunction → fibrous
cap thinning → rupture
D. Monocyte adhesion → platelet aggregation → vasospasm → fatty streak →
calcification
Correct Answer: A
Rationale: [CORRECT] A: The response-to-injury hypothesis proposes that endothelial
injury/dysfunction initiates atherosclerosis. This leads to monocyte adhesion and
,migration, forming a fatty streak. Smooth muscle cells proliferate and migrate,
producing extracellular matrix and forming a fibrous plaque. Advanced complicated
lesions develop with thrombosis, hemorrhage, or calcification. B: Incorrect sequence –
endothelial injury precedes fatty streak. C: Incorrect – endothelial dysfunction is the
initial event. D: Incorrect – fatty streak develops before platelet aggregation.
Q2: A 45-year-old female with a family history of premature CAD asks about her
non-modifiable risk factors. Which of the following is NOT considered a non-modifiable
risk factor for coronary artery disease?
A. Postmenopausal status
B. African American ethnicity
C. History of preeclampsia
D. Elevated lipoprotein(a)
Correct Answer: C
Rationale: [CORRECT] C: History of preeclampsia is considered a novel/modifiable risk
factor that increases future cardiovascular risk but is not classified among traditional
non-modifiable factors. A: Postmenopausal status is non-modifiable
(age/gender-related). B: Ethnicity is non-modifiable. D: Lipoprotein(a) is genetically
determined and non-modifiable.
Q3: Which novel risk factor for CAD is characterized by elevated levels of acute-phase
reactants and reflects underlying vascular inflammation?
A. Elevated homocysteine
,B. Increased high-sensitivity C-reactive protein (hs-CRP)
C. Elevated lipoprotein(a)
D. Increased fibrinogen
Correct Answer: B
Rationale: [CORRECT] B: High-sensitivity CRP is an inflammatory marker and novel risk
factor indicating vascular inflammation. The JUPITER trial demonstrated that patients
with elevated hs-CRP benefited from statin therapy even with normal LDL levels. A, C, D:
While these are novel risk factors, they do not specifically indicate inflammation.
Q4: Regarding lipoprotein metabolism, which statement accurately describes the
function of HDL cholesterol?
A. HDL transports cholesterol from the liver to peripheral tissues
B. HDL delivers triglycerides to adipose tissue for storage
C. HDL transports cholesterol from peripheral tissues to the liver for excretion
D. HDL is the primary carrier of cholesterol to arterial walls
Correct Answer: C
Rationale: [CORRECT] C: HDL (high-density lipoprotein) is cardioprotective through
reverse cholesterol transport, moving cholesterol from peripheral tissues (including
arteries) to the liver for excretion. A, D: Describe LDL function (atherogenic). B:
Describes VLDL/chylomicron function.
, Q5: A 62-year-old female presents to the ED with substernal chest pain radiating to her
jaw, diaphoresis, and nausea. ECG reveals ST-segment elevations in leads V2-V4.
Cardiac troponin is elevated. Which of the following best describes the pathophysiology
underlying her presentation?
A. Stable atherosclerotic plaque with thick fibrous cap causing gradual lumen narrowing
B. Plaque rupture with thrombus formation causing acute coronary obstruction
C. Vasospasm of epicardial coronary arteries without underlying plaque
D. Myocardial oxygen demand exceeding supply in setting of fixed stenosis
Correct Answer: B
Rationale: [CORRECT] B: STEMI is an acute coronary syndrome caused by plaque
rupture with thrombus formation, leading to complete or near-complete coronary artery
occlusion. Unstable plaques have thin, macrophage-rich fibrous caps prone to rupture.
A: Describes stable angina pathophysiology. C: Describes Prinzmetal's vasospastic
angina. D: Describes demand ischemia, not acute plaque rupture.
Q6: A 55-year-old male with stable angina reports chest pain when walking uphill that
resolves with rest. Which pathophysiologic mechanism best explains his symptoms?
A. Acute plaque rupture with thrombus formation
B. Transient vasospasm of epicardial arteries
C. Fixed coronary stenosis with increased myocardial oxygen demand during exertion
D. Coronary artery dissection
Correct Answer: C
Wilkes University | 2026/2027 | Verified Study Guide with Correct
Coverage]
[ACADEMIC YEAR: 2026/2027 – Graduate Nursing Program]
[Alignment: NONPF Core Competencies, AANP/ANCC Certification
Standards, ACC/AHA 2026, GOLD 2026]
[UNIT 1: ISCHEMIC HEART DISEASE & ACUTE CORONARY SYNDROMES]
30 Items | Focus: Pathophysiology, Risk Stratification, Acute Management, Post-MI
Care
Q1: A 58-year-old male with hypertension and dyslipidemia presents for routine
follow-up. His LDL is 160 mg/dL, HDL is 38 mg/dL, and triglycerides are 180 mg/dL.
According to the response-to-injury hypothesis of atherosclerosis, which sequence
accurately describes plaque development?
A. Endothelial dysfunction → fatty streak → smooth muscle proliferation → fibrous
plaque → complicated lesion
B. Fatty streak → endothelial injury → macrophage infiltration → thrombus formation →
plaque rupture
C. Smooth muscle proliferation → LDL oxidation → endothelial dysfunction → fibrous
cap thinning → rupture
D. Monocyte adhesion → platelet aggregation → vasospasm → fatty streak →
calcification
Correct Answer: A
Rationale: [CORRECT] A: The response-to-injury hypothesis proposes that endothelial
injury/dysfunction initiates atherosclerosis. This leads to monocyte adhesion and
,migration, forming a fatty streak. Smooth muscle cells proliferate and migrate,
producing extracellular matrix and forming a fibrous plaque. Advanced complicated
lesions develop with thrombosis, hemorrhage, or calcification. B: Incorrect sequence –
endothelial injury precedes fatty streak. C: Incorrect – endothelial dysfunction is the
initial event. D: Incorrect – fatty streak develops before platelet aggregation.
Q2: A 45-year-old female with a family history of premature CAD asks about her
non-modifiable risk factors. Which of the following is NOT considered a non-modifiable
risk factor for coronary artery disease?
A. Postmenopausal status
B. African American ethnicity
C. History of preeclampsia
D. Elevated lipoprotein(a)
Correct Answer: C
Rationale: [CORRECT] C: History of preeclampsia is considered a novel/modifiable risk
factor that increases future cardiovascular risk but is not classified among traditional
non-modifiable factors. A: Postmenopausal status is non-modifiable
(age/gender-related). B: Ethnicity is non-modifiable. D: Lipoprotein(a) is genetically
determined and non-modifiable.
Q3: Which novel risk factor for CAD is characterized by elevated levels of acute-phase
reactants and reflects underlying vascular inflammation?
A. Elevated homocysteine
,B. Increased high-sensitivity C-reactive protein (hs-CRP)
C. Elevated lipoprotein(a)
D. Increased fibrinogen
Correct Answer: B
Rationale: [CORRECT] B: High-sensitivity CRP is an inflammatory marker and novel risk
factor indicating vascular inflammation. The JUPITER trial demonstrated that patients
with elevated hs-CRP benefited from statin therapy even with normal LDL levels. A, C, D:
While these are novel risk factors, they do not specifically indicate inflammation.
Q4: Regarding lipoprotein metabolism, which statement accurately describes the
function of HDL cholesterol?
A. HDL transports cholesterol from the liver to peripheral tissues
B. HDL delivers triglycerides to adipose tissue for storage
C. HDL transports cholesterol from peripheral tissues to the liver for excretion
D. HDL is the primary carrier of cholesterol to arterial walls
Correct Answer: C
Rationale: [CORRECT] C: HDL (high-density lipoprotein) is cardioprotective through
reverse cholesterol transport, moving cholesterol from peripheral tissues (including
arteries) to the liver for excretion. A, D: Describe LDL function (atherogenic). B:
Describes VLDL/chylomicron function.
, Q5: A 62-year-old female presents to the ED with substernal chest pain radiating to her
jaw, diaphoresis, and nausea. ECG reveals ST-segment elevations in leads V2-V4.
Cardiac troponin is elevated. Which of the following best describes the pathophysiology
underlying her presentation?
A. Stable atherosclerotic plaque with thick fibrous cap causing gradual lumen narrowing
B. Plaque rupture with thrombus formation causing acute coronary obstruction
C. Vasospasm of epicardial coronary arteries without underlying plaque
D. Myocardial oxygen demand exceeding supply in setting of fixed stenosis
Correct Answer: B
Rationale: [CORRECT] B: STEMI is an acute coronary syndrome caused by plaque
rupture with thrombus formation, leading to complete or near-complete coronary artery
occlusion. Unstable plaques have thin, macrophage-rich fibrous caps prone to rupture.
A: Describes stable angina pathophysiology. C: Describes Prinzmetal's vasospastic
angina. D: Describes demand ischemia, not acute plaque rupture.
Q6: A 55-year-old male with stable angina reports chest pain when walking uphill that
resolves with rest. Which pathophysiologic mechanism best explains his symptoms?
A. Acute plaque rupture with thrombus formation
B. Transient vasospasm of epicardial arteries
C. Fixed coronary stenosis with increased myocardial oxygen demand during exertion
D. Coronary artery dissection
Correct Answer: C
