,NURS 6521 Week 3 Quiz | Advanced Pharmacology (2026)
Q&A | Walden University
1. Which of the following best describes the primary mechanism by which statins
lower low-density lipoprotein cholesterol?
A) Inhibiting HMG-CoA reductase to reduce hepatic cholesterol synthesis
B) Blocking intestinal cholesterol absorption
C) Increasing renal excretion of cholesterol
D) Activating lipoprotein lipase to break down triglycerides
Correct Answer: Inhibiting HMG-CoA reductase to reduce hepatic cholesterol
synthesis
Rationale: Statins competitively inhibit HMG-CoA reductase, the rate-limiting
enzyme in hepatic cholesterol synthesis. This inhibition leads to upregulation of low-
density lipoprotein receptors on hepatocytes and increased clearance of low-density
lipoprotein cholesterol from the bloodstream. They do not primarily block intestinal
absorption or increase renal excretion.
2. What is the primary mechanism of action of bile acid sequestrants such as
cholestyramine?
A) Inhibiting HMG-CoA reductase
B) Binding bile acids in the intestine and promoting their excretion
C) Blocking cholesterol absorption in the jejunum
D) Activating peroxisome proliferator-activated receptor alpha
,Correct Answer: Binding bile acids in the intestine and promoting their excretion
Rationale: Bile acid sequestrants bind bile acids in the intestinal lumen, preventing
their reabsorption and increasing fecal excretion. This depletes hepatic bile acid
pools, forcing the liver to convert cholesterol to bile acids, which upregulates low-
density lipoprotein receptors and lowers circulating low-density lipoprotein
cholesterol. They do not inhibit HMG-CoA reductase.
3. A nurse is reviewing the medication list of a patient with active liver disease. Which
lipid-lowering agent is contraindicated?
A) Cholestyramine
B) Ezetimibe
C) Atorvastatin
D) Niacin
Correct Answer: Atorvastatin
Rationale: Statins such as atorvastatin are contraindicated in patients with active
liver disease or unexplained persistent elevations of serum transaminases.
Cholestyramine, ezetimibe, and niacin are not absolutely contraindicated in liver
disease, although caution is advised. Baseline liver function tests should be obtained
before initiating statin therapy.
4. Which adverse effect is most commonly associated with niacin therapy?
A) Dry cough
B) Facial flushing and pruritus
C) Peripheral edema
, D) Bradycardia
Correct Answer: Facial flushing and pruritus
Rationale: Niacin commonly causes facial flushing and pruritus due to
prostaglandin-mediated vasodilation. Taking aspirin 30 minutes before the dose or
using extended-release formulations can minimize this effect. Dry cough is
associated with ACE inhibitors, and peripheral edema with calcium channel blockers.
5. What is the primary mechanism by which ezetimibe lowers low-density lipoprotein
cholesterol?
A) Inhibiting HMG-CoA reductase
B) Blocking intestinal cholesterol absorption at the NPC1L1 transporter
C) Increasing bile acid excretion
D) Activating lipoprotein lipase
Correct Answer: Blocking intestinal cholesterol absorption at the NPC1L1
transporter
Rationale: Ezetimibe inhibits the NPC1L1 transporter in the small intestine, reducing
intestinal cholesterol absorption. This leads to decreased delivery of cholesterol to
the liver and upregulation of low-density lipoprotein receptors. It is often used in
combination with statins for additional low-density lipoprotein reduction.
6. A patient taking a statin develops muscle pain and weakness. Which laboratory
test should be obtained immediately?
A) Serum potassium
Q&A | Walden University
1. Which of the following best describes the primary mechanism by which statins
lower low-density lipoprotein cholesterol?
A) Inhibiting HMG-CoA reductase to reduce hepatic cholesterol synthesis
B) Blocking intestinal cholesterol absorption
C) Increasing renal excretion of cholesterol
D) Activating lipoprotein lipase to break down triglycerides
Correct Answer: Inhibiting HMG-CoA reductase to reduce hepatic cholesterol
synthesis
Rationale: Statins competitively inhibit HMG-CoA reductase, the rate-limiting
enzyme in hepatic cholesterol synthesis. This inhibition leads to upregulation of low-
density lipoprotein receptors on hepatocytes and increased clearance of low-density
lipoprotein cholesterol from the bloodstream. They do not primarily block intestinal
absorption or increase renal excretion.
2. What is the primary mechanism of action of bile acid sequestrants such as
cholestyramine?
A) Inhibiting HMG-CoA reductase
B) Binding bile acids in the intestine and promoting their excretion
C) Blocking cholesterol absorption in the jejunum
D) Activating peroxisome proliferator-activated receptor alpha
,Correct Answer: Binding bile acids in the intestine and promoting their excretion
Rationale: Bile acid sequestrants bind bile acids in the intestinal lumen, preventing
their reabsorption and increasing fecal excretion. This depletes hepatic bile acid
pools, forcing the liver to convert cholesterol to bile acids, which upregulates low-
density lipoprotein receptors and lowers circulating low-density lipoprotein
cholesterol. They do not inhibit HMG-CoA reductase.
3. A nurse is reviewing the medication list of a patient with active liver disease. Which
lipid-lowering agent is contraindicated?
A) Cholestyramine
B) Ezetimibe
C) Atorvastatin
D) Niacin
Correct Answer: Atorvastatin
Rationale: Statins such as atorvastatin are contraindicated in patients with active
liver disease or unexplained persistent elevations of serum transaminases.
Cholestyramine, ezetimibe, and niacin are not absolutely contraindicated in liver
disease, although caution is advised. Baseline liver function tests should be obtained
before initiating statin therapy.
4. Which adverse effect is most commonly associated with niacin therapy?
A) Dry cough
B) Facial flushing and pruritus
C) Peripheral edema
, D) Bradycardia
Correct Answer: Facial flushing and pruritus
Rationale: Niacin commonly causes facial flushing and pruritus due to
prostaglandin-mediated vasodilation. Taking aspirin 30 minutes before the dose or
using extended-release formulations can minimize this effect. Dry cough is
associated with ACE inhibitors, and peripheral edema with calcium channel blockers.
5. What is the primary mechanism by which ezetimibe lowers low-density lipoprotein
cholesterol?
A) Inhibiting HMG-CoA reductase
B) Blocking intestinal cholesterol absorption at the NPC1L1 transporter
C) Increasing bile acid excretion
D) Activating lipoprotein lipase
Correct Answer: Blocking intestinal cholesterol absorption at the NPC1L1
transporter
Rationale: Ezetimibe inhibits the NPC1L1 transporter in the small intestine, reducing
intestinal cholesterol absorption. This leads to decreased delivery of cholesterol to
the liver and upregulation of low-density lipoprotein receptors. It is often used in
combination with statins for additional low-density lipoprotein reduction.
6. A patient taking a statin develops muscle pain and weakness. Which laboratory
test should be obtained immediately?
A) Serum potassium
