NURS 5434 CAD/Lipids Quiz (Family III, FNP 3) | UTA Study Guide |
Practice Questions, Answers & Rationales | Latest 2026 Edition
Prepare for the NURS 5434 CAD/Lipids Quiz (Family III, FNP 3) with this comprehensive study guide
designed to reinforce key concepts in cardiovascular disease prevention and lipid management. This
resource includes original practice questions, accurate answers, and detailed rationales covering
coronary artery disease, lipid disorders, cardiovascular risk assessment, cholesterol guidelines,
pharmacologic therapies, lifestyle interventions, and evidence-based clinical management. Organized in
a clear, easy-to-follow format, this study guide is ideal for self-assessment, focused review, and
strengthening your understanding before completing the quiz.
1. A 55-year-old male with a history of hypertension presents for
a routine wellness exam. According to the current ACC/AHA
guidelines, which of the following tools must be utilized to
estimate his 10-year risk of developing a primary atherosclerotic
cardiovascular disease (ASCVD) event?
A) Framingham Risk Score calculator
B) Pooled Cohort Equations (ASCVD Risk Estimator Plus)
C) CHADS2 scoring index matrix
D) TIMI risk stratification tool
Rationale: The ACC/AHA cholesterol guidelines recommend using the Pooled Cohort
Equations to estimate 10-year risk for atherosclerotic cardiovascular disease (ASCVD)
events in individuals aged 40–79 who do not have clinical ASCVD or diabetes.
2. A 48-year-old female patient with no clinical history of
cardiovascular disease undergoes a screening lipid panel. Her
results show an LDL-C level of 210 mg/dL. What is the
recommended management strategy according to national
cholesterol guidelines?
A) Initiate low-intensity statin therapy after a 6-month trial of lifestyle changes
B) Initiate high-intensity statin therapy immediately without requiring a 10-year
ASCVD risk calculation
C) Recheck the fasting lipid panel in 12 months before prescribing medication
D) Initiate fenofibrate monotherapy to target cellular lipid clearance pathways
,Rationale: An LDL-C level of ≥ 190 mg/dL is a primary indication for high-intensity statin
therapy due to the high likelihood of familial hypercholesterolemia, bypassing the need
for a 10-year ASCVD risk score calculation.
3. A clinician is prescribing high-intensity statin therapy for a 62-
year-old post-myocardial infarction patient. Which of the
following statin regimens is classified as high-intensity?
A) Simvastatin 40 mg daily
B) Pravastatin 40 mg daily
C) Atorvastatin 80 mg daily
D) Lovastatin 40 mg daily
Rationale: High-intensity statin therapy is defined as a regimen that lowers LDL-C by ≥
50%. The two standard high-intensity statin options are Atorvastatin 40–80 mg daily and
Rosuvastatin 20–40 mg daily.
4. A 64-year-old patient with established coronary artery disease
(CAD) has been taking Atorvastatin 80 mg daily for three months.
Her follow-up LDL-C remains elevated at 82 mg/dL. What is the
recommended next step in her pharmacological lipid
management?
A) Switch her medication to high-dose fenofibrate
B) Add Ezetimibe 10 mg daily to her high-intensity statin regimen
C) Double the daily dose of Atorvastatin to 160 mg daily
D) Add over-the-counter red yeast rice supplements
Rationale: For very high-risk ASCVD patients whose LDL-C remains ≥ 70 mg/dL despite
a maximally tolerated high-intensity statin, adding Ezetimibe is the recommended next
evidence-based step before considering a PCSK9 inhibitor.
5. Which of the following biological actions describes the precise
mechanism of action of Ezetimibe in the management of
hypercholesterolemia?
A) Inhibits HMG-CoA reductase to prevent hepatic cholesterol synthesis
B) Selectively inhibits cholesterol absorption at the brush border of the small
intestine via the NPC1L1 transporter
C) Binds bile acids in the intestinal lumen to increase fecal excretion
D) Upregulates peroxisome proliferator-activated receptor alpha (PPAR-alpha)
pathways
Rationale: Ezetimibe selectively inhibits cholesterol absorption at the brush border of
the small intestine by targeting the Niemann-Pick C1-Like 1 (NPC1L1) transporter
protein, which reduces hepatic cholesterol stores and upregulates LDL receptors.
,6. A 52-year-old male with type 2 diabetes mellitus presents for
an annual check-up. His lipid panel reveals an LDL-C of 115
mg/dL. He has no other cardiovascular risk factors. What is the
recommended statin intensity for this patient?
A) Low-intensity statin therapy
B) Moderate-intensity statin therapy
C) Statin therapy is completely contraindicated in diabetic patients
D) PCSK9 inhibitor monotherapy immediately
Rationale: Individuals aged 40–75 with diabetes mellitus and an LDL-C between 70–
189 mg/dL are indicated for at least moderate-intensity statin therapy, regardless of
their calculated 10-year ASCVD risk score.
7. A patient who recently started Rosuvastatin 40 mg daily
returns to the clinic complaining of diffuse, symmetrical muscle
aching and weakness in his thighs, without any dark urine or
trauma. What is the initial clinical step the nurse practitioner
must take?
A) Advise the patient to push through the pain to maintain cardiovascular safety
B) Obtain a serum creatine kinase (CK) level and evaluate for statin-associated
muscle symptoms
C) Order an immediate bilateral lower extremity venous duplex ultrasound
D) Discontinue the statin and switch the patient to high-dose niacin therapy
Rationale: Symmetrical proximal muscle pain or weakness is a known side effect of
statin therapy. Clinicians should evaluate symptoms, check a baseline creatine kinase
(CK) level to rule out rhabdomyolysis, and consider a statin holiday or dose reduction.
8. During a follow-up visit for a patient on lipid-lowering therapy,
the clinician reviews a lab panel. Which of the following
elevations represents an absolute clinical threshold to
temporarily hold or stop a statin due to potential hepatotoxicity?
A) Serum alanine aminotransferase (ALT) level exactly 1.5 times the upper limit of
normal
B) Serum aspartate aminotransferase (AST) level exactly 2 times the upper limit of
normal
C) Serum transaminase levels (ALT or AST) greater than 3 times the upper limit of
normal
D) Total bilirubin level exactly 1.1 times the upper limit of normal
Rationale: Routine monitoring of liver enzymes is no longer required unless
symptomatic, but an elevation of transaminases (ALT or AST) > 3 times the upper limit
of normal warrants holding or discontinuing statin therapy.
, 9. A 38-year-old female patient with a history of familial
hypercholesterolemia is planning to become pregnant over the
next few months. She is currently taking Atorvastatin 40 mg
daily. What is the correct clinical directive regarding her statin
therapy?
A) Continue the statin at the same dose throughout pregnancy
B) Double the statin dose during the third trimester to counter metabolic shifts
C) Discontinue the statin immediately prior to attempting conception due to
potential teratogenic risks
D) Switch her therapy to oral fenofibrate throughout the gestational period
Rationale: Statins are contraindicated during pregnancy due to potential teratogenic
risks to the fetus. Women of childbearing potential should stop statin therapy before
attempting to conceive.
10. Which class of lipid-lowering medications works by binding
to proprotein convertase subtilisin/kexin type 9, thereby
preventing the degradation of hepatic LDL receptors and
dramatically increasing LDL-C clearance from the blood?
A) Bile acid sequestrants
B) Fibric acid derivatives
C) PCSK9 inhibitors (e.g., Alirocumab, Evolocumab)
D) Adenosine triphosphate-citrate lyase (ACL) inhibitors
Rationale: PCSK9 inhibitors are monoclonal antibodies that bind to PCSK9 proteins,
preventing them from degrading LDL receptors. This leaves more receptors on the liver
surface to clear LDL-C from the bloodstream.
11. A 58-year-old male with chronic stable angina presents with
substernal chest discomfort that predictably occurs when
walking up two flights of stairs and resolves completely within 5
minutes of rest. What is the primary underlying pathophysiology
of this condition?
A) Sudden, complete thrombotic occlusion of a coronary artery
B) Focal coronary artery vasospasm without fixed plaque accumulation
C) Fixed atherosclerotic plaque causing a predictable imbalance between
myocardial oxygen supply and demand
D) Acute inflammatory pericardial friction and fluid buildup
Rationale: Chronic stable angina is driven by fixed atherosclerotic narrowing of the
coronary arteries. Physical exertion uregulates myocardial oxygen demand, creating a
predictable supply-demand mismatch that resolves with rest.
Practice Questions, Answers & Rationales | Latest 2026 Edition
Prepare for the NURS 5434 CAD/Lipids Quiz (Family III, FNP 3) with this comprehensive study guide
designed to reinforce key concepts in cardiovascular disease prevention and lipid management. This
resource includes original practice questions, accurate answers, and detailed rationales covering
coronary artery disease, lipid disorders, cardiovascular risk assessment, cholesterol guidelines,
pharmacologic therapies, lifestyle interventions, and evidence-based clinical management. Organized in
a clear, easy-to-follow format, this study guide is ideal for self-assessment, focused review, and
strengthening your understanding before completing the quiz.
1. A 55-year-old male with a history of hypertension presents for
a routine wellness exam. According to the current ACC/AHA
guidelines, which of the following tools must be utilized to
estimate his 10-year risk of developing a primary atherosclerotic
cardiovascular disease (ASCVD) event?
A) Framingham Risk Score calculator
B) Pooled Cohort Equations (ASCVD Risk Estimator Plus)
C) CHADS2 scoring index matrix
D) TIMI risk stratification tool
Rationale: The ACC/AHA cholesterol guidelines recommend using the Pooled Cohort
Equations to estimate 10-year risk for atherosclerotic cardiovascular disease (ASCVD)
events in individuals aged 40–79 who do not have clinical ASCVD or diabetes.
2. A 48-year-old female patient with no clinical history of
cardiovascular disease undergoes a screening lipid panel. Her
results show an LDL-C level of 210 mg/dL. What is the
recommended management strategy according to national
cholesterol guidelines?
A) Initiate low-intensity statin therapy after a 6-month trial of lifestyle changes
B) Initiate high-intensity statin therapy immediately without requiring a 10-year
ASCVD risk calculation
C) Recheck the fasting lipid panel in 12 months before prescribing medication
D) Initiate fenofibrate monotherapy to target cellular lipid clearance pathways
,Rationale: An LDL-C level of ≥ 190 mg/dL is a primary indication for high-intensity statin
therapy due to the high likelihood of familial hypercholesterolemia, bypassing the need
for a 10-year ASCVD risk score calculation.
3. A clinician is prescribing high-intensity statin therapy for a 62-
year-old post-myocardial infarction patient. Which of the
following statin regimens is classified as high-intensity?
A) Simvastatin 40 mg daily
B) Pravastatin 40 mg daily
C) Atorvastatin 80 mg daily
D) Lovastatin 40 mg daily
Rationale: High-intensity statin therapy is defined as a regimen that lowers LDL-C by ≥
50%. The two standard high-intensity statin options are Atorvastatin 40–80 mg daily and
Rosuvastatin 20–40 mg daily.
4. A 64-year-old patient with established coronary artery disease
(CAD) has been taking Atorvastatin 80 mg daily for three months.
Her follow-up LDL-C remains elevated at 82 mg/dL. What is the
recommended next step in her pharmacological lipid
management?
A) Switch her medication to high-dose fenofibrate
B) Add Ezetimibe 10 mg daily to her high-intensity statin regimen
C) Double the daily dose of Atorvastatin to 160 mg daily
D) Add over-the-counter red yeast rice supplements
Rationale: For very high-risk ASCVD patients whose LDL-C remains ≥ 70 mg/dL despite
a maximally tolerated high-intensity statin, adding Ezetimibe is the recommended next
evidence-based step before considering a PCSK9 inhibitor.
5. Which of the following biological actions describes the precise
mechanism of action of Ezetimibe in the management of
hypercholesterolemia?
A) Inhibits HMG-CoA reductase to prevent hepatic cholesterol synthesis
B) Selectively inhibits cholesterol absorption at the brush border of the small
intestine via the NPC1L1 transporter
C) Binds bile acids in the intestinal lumen to increase fecal excretion
D) Upregulates peroxisome proliferator-activated receptor alpha (PPAR-alpha)
pathways
Rationale: Ezetimibe selectively inhibits cholesterol absorption at the brush border of
the small intestine by targeting the Niemann-Pick C1-Like 1 (NPC1L1) transporter
protein, which reduces hepatic cholesterol stores and upregulates LDL receptors.
,6. A 52-year-old male with type 2 diabetes mellitus presents for
an annual check-up. His lipid panel reveals an LDL-C of 115
mg/dL. He has no other cardiovascular risk factors. What is the
recommended statin intensity for this patient?
A) Low-intensity statin therapy
B) Moderate-intensity statin therapy
C) Statin therapy is completely contraindicated in diabetic patients
D) PCSK9 inhibitor monotherapy immediately
Rationale: Individuals aged 40–75 with diabetes mellitus and an LDL-C between 70–
189 mg/dL are indicated for at least moderate-intensity statin therapy, regardless of
their calculated 10-year ASCVD risk score.
7. A patient who recently started Rosuvastatin 40 mg daily
returns to the clinic complaining of diffuse, symmetrical muscle
aching and weakness in his thighs, without any dark urine or
trauma. What is the initial clinical step the nurse practitioner
must take?
A) Advise the patient to push through the pain to maintain cardiovascular safety
B) Obtain a serum creatine kinase (CK) level and evaluate for statin-associated
muscle symptoms
C) Order an immediate bilateral lower extremity venous duplex ultrasound
D) Discontinue the statin and switch the patient to high-dose niacin therapy
Rationale: Symmetrical proximal muscle pain or weakness is a known side effect of
statin therapy. Clinicians should evaluate symptoms, check a baseline creatine kinase
(CK) level to rule out rhabdomyolysis, and consider a statin holiday or dose reduction.
8. During a follow-up visit for a patient on lipid-lowering therapy,
the clinician reviews a lab panel. Which of the following
elevations represents an absolute clinical threshold to
temporarily hold or stop a statin due to potential hepatotoxicity?
A) Serum alanine aminotransferase (ALT) level exactly 1.5 times the upper limit of
normal
B) Serum aspartate aminotransferase (AST) level exactly 2 times the upper limit of
normal
C) Serum transaminase levels (ALT or AST) greater than 3 times the upper limit of
normal
D) Total bilirubin level exactly 1.1 times the upper limit of normal
Rationale: Routine monitoring of liver enzymes is no longer required unless
symptomatic, but an elevation of transaminases (ALT or AST) > 3 times the upper limit
of normal warrants holding or discontinuing statin therapy.
, 9. A 38-year-old female patient with a history of familial
hypercholesterolemia is planning to become pregnant over the
next few months. She is currently taking Atorvastatin 40 mg
daily. What is the correct clinical directive regarding her statin
therapy?
A) Continue the statin at the same dose throughout pregnancy
B) Double the statin dose during the third trimester to counter metabolic shifts
C) Discontinue the statin immediately prior to attempting conception due to
potential teratogenic risks
D) Switch her therapy to oral fenofibrate throughout the gestational period
Rationale: Statins are contraindicated during pregnancy due to potential teratogenic
risks to the fetus. Women of childbearing potential should stop statin therapy before
attempting to conceive.
10. Which class of lipid-lowering medications works by binding
to proprotein convertase subtilisin/kexin type 9, thereby
preventing the degradation of hepatic LDL receptors and
dramatically increasing LDL-C clearance from the blood?
A) Bile acid sequestrants
B) Fibric acid derivatives
C) PCSK9 inhibitors (e.g., Alirocumab, Evolocumab)
D) Adenosine triphosphate-citrate lyase (ACL) inhibitors
Rationale: PCSK9 inhibitors are monoclonal antibodies that bind to PCSK9 proteins,
preventing them from degrading LDL receptors. This leaves more receptors on the liver
surface to clear LDL-C from the bloodstream.
11. A 58-year-old male with chronic stable angina presents with
substernal chest discomfort that predictably occurs when
walking up two flights of stairs and resolves completely within 5
minutes of rest. What is the primary underlying pathophysiology
of this condition?
A) Sudden, complete thrombotic occlusion of a coronary artery
B) Focal coronary artery vasospasm without fixed plaque accumulation
C) Fixed atherosclerotic plaque causing a predictable imbalance between
myocardial oxygen supply and demand
D) Acute inflammatory pericardial friction and fluid buildup
Rationale: Chronic stable angina is driven by fixed atherosclerotic narrowing of the
coronary arteries. Physical exertion uregulates myocardial oxygen demand, creating a
predictable supply-demand mismatch that resolves with rest.
