Practice Questions, Answers & Rationales | Latest 2026-2027
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 54-year-old male presents for a routine physical exam. He
has no history of clinical ASCVD or diabetes, is a non-smoker,
and has a blood pressure of 122/78 mmHg. His lipid panel reveals
a Total Cholesterol of 210 mg/dL, HDL-C of 45 mg/dL, and LDL-C
of 135 mg/dL. According to current ACC/AHA guidelines, what is
the next step to determine his eligibility for primary prevention
statin therapy?
A) Compute a Framingham Risk Score spreadsheet calculation
B) Calculate his 10-year risk using the Pooled Cohort Equations (ASCVD Risk
Estimator Plus)
C) Initiate low-intensity statin therapy immediately without further calculations
D) Order a 12-lead electrocardiogram (ECG) to screen for subclinical coronary ischemia
Rationale: For primary prevention in adults aged 40–79 with an LDL-C between 70–189
mg/dL and without diabetes, the ACC/AHA cholesterol guidelines recommend using the
Pooled Cohort Equations to evaluate 10-year risk for atherosclerotic cardiovascular
disease (ASCVD) before making treatment choices.
2. A 43-year-old female patient with a family history of premature
heart disease undergoes screening labs. Her lipid panel shows
an LDL-C level of 195 mg/dL. Her calculated 10-year ASCVD risk
score is 4.2%. What is the recommended management path for
this patient?
A) Implement dietary and lifestyle restrictions for 12 months before considering
medication
,B) Initiate a high-intensity statin immediately, bypassing the 10-year risk score
threshold
C) Initiate low-intensity statin therapy due to her young age and low risk score
D) Prescribe fenofibrate monotherapy to target cellular lipid clearance pathways
Rationale: An LDL-C level of 190 mg/dL or higher is a primary indication for high-
intensity statin therapy, often pointing to familial hypercholesterolemia. High-intensity
treatment is indicated regardless of the calculated 10-year risk score.
3. A clinician is selecting a high-intensity lipid-lowering
medication for a patient who recently underwent percutaneous
coronary intervention (PCI). Which of the following statin
prescriptions meets the definition of high-intensity therapy?
A) Pravastatin 40 mg daily
B) Simvastatin 40 mg daily
C) Atorvastatin 80 mg daily
D) Lovastatin 40 mg daily
Rationale: High-intensity statin therapy is defined as a daily dose that lowers baseline
LDL-C levels by an average of 50% or more. The two standard high-intensity statin
options are Atorvastatin 40–80 mg daily and Rosuvastatin 20–40 mg daily.
4. A 62-year-old patient with stable coronary artery disease (CAD)
has been taking Atorvastatin 80 mg daily for three months. A
repeat fasting lipid panel reveals that his LDL-C remains elevated
at 84 mg/dL. What is the recommended next step in his
pharmacological management?
A) Double his Atorvastatin dose to 160 mg daily
B) Switch his therapy from a statin to high-dose fenofibrate
C) Add Ezetimibe 10 mg daily to his current high-intensity statin regimen
D) Add a bile acid sequestrant like cholestyramine powder
Rationale: For very high-risk ASCVD patients whose LDL-C remains 70 mg/dL or higher
despite a maximally tolerated high-intensity statin, adding Ezetimibe is the
recommended next step before considering a PCSK9 inhibitor.
5. Which of the following descriptions accurately defines the
cellular mechanism of action of Ezetimibe?
A) Competitive inhibition of the HMG-CoA reductase enzyme in hepatocytes
B) Selective inhibition of cholesterol absorption at the small intestine brush
border via the NPC1L1 transporter
C) Binding to bile acids within the intestinal lumen to increase fecal excretion
) Upregulating peroxisome proliferator-activated receptor alpha (PPAR-alpha) to clear
lipids
,Rationale: Ezetimibe targets the Niemann-Pick C1-Like 1 (NPC1L1) transporter protein
on the brush border of enterocytes, reducing the absorption of dietary and biliary
cholesterol into the liver.
6. A 56-year-old male with a history of type 2 diabetes mellitus
presents for an annual wellness exam. His fasting lipid panel
shows an LDL-C of 110 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: Patients aged 40–75 with diabetes mellitus and an LDL-C between 70–189
mg/dL are candidates for at least moderate-intensity statin therapy for primary
prevention, regardless of their calculated 10-year risk score.
7. A patient who was started on Rosuvastatin 40 mg daily four
weeks ago returns to the clinic complaining of generalized,
symmetrical muscle aching and weakness in his thighs and
upper arms. He denies any dark urine or recent trauma. What is
the initial clinical step the nurse practitioner must take?
A) Advise the patient to push through the pain to maintain safety parameters
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: When a patient describes symmetrical proximal muscle pain or weakness on
a statin, the clinician should check a creatine kinase (CK) level to rule out
rhabdomyolysis and evaluate the severity of the muscle symptoms.
8. During a follow-up consultation 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 32-year-old female patient with a history of severe
heterozygous familial hypercholesterolemia informs her family
nurse practitioner that she is actively 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 lipid management?
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 developing fetus. Women of childbearing potential should stop statin therapy
before attempting to conceive.
10. Which class of lipid-lowering medications consists of
monoclonal antibodies that bind to proprotein convertase
subtilisin/kexin type 9, thereby preventing the degradation of
hepatic LDL receptors?
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 prevent the degradation of hepatic LDL receptors, leaving
more receptors on the liver surface to clear circulating low-density lipoprotein
cholesterol from the blood.
11. A 58-year-old male with chronic stable angina describes a
pattern of 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 driving this clinical presentation?
A) Sudden, complete thrombotic occlusion of a coronary artery
B) Focal coronary artery vasospasm without fixed plaque accumulation