Hyperlipidemias: pharmacological management MCQs With Answer

Hyperlipidemias: pharmacological management MCQs With Answer

Introduction: This quiz set is designed for M.Pharm students studying Pharmacotherapeutics I (MPP 102T) to deepen understanding of pharmacological strategies for managing hyperlipidemias. Questions emphasize mechanisms of action, clinical indications, pharmacokinetics, adverse effects, drug interactions and combination therapy principles. Cases include familial and secondary dyslipidemias, treatment targets, and appropriate laboratory monitoring. The MCQs probe detailed concepts such as HMG-CoA reductase inhibition, PPAR-α agonism, NPC1L1 inhibition, PCSK9 biology, bile acid sequestrants’ impact on enterohepatic circulation, and risks like statin-induced myopathy. Use these to assess and refine therapeutic reasoning and evidence-based drug selection in dyslipidemia management.

Q1. Which enzyme is directly inhibited by statins, leading to decreased cholesterol synthesis in the liver?

• Acetyl-CoA carboxylase
• HMG-CoA reductase
• Lanosterol synthase
• Squalene epoxidase

Correct Answer: HMG-CoA reductase

Q2. Which lipid parameter is reduced most substantially by fibrates and is the primary target when using these drugs?

• LDL cholesterol
• HDL cholesterol
• Triglycerides
• Total cholesterol

Correct Answer: Triglycerides

Q3. Which transporter is inhibited by ezetimibe to reduce intestinal cholesterol absorption?

• ABCG5/G8
• NPC1L1
• SR-BI
• OSTα-OSTβ

Correct Answer: NPC1L1

Q4. PCSK9 inhibitors lower LDL-C primarily by which mechanism?

• Blocking intestinal cholesterol absorption
• Increasing hepatic LDL receptor recycling and surface expression
• Directly inhibiting HMG-CoA reductase
• Enhancing CETP activity

Correct Answer: Increasing hepatic LDL receptor recycling and surface expression

Q5. Which adverse effect necessitates routine monitoring of creatine kinase (CK) in patients on high-intensity statin therapy?

• Hepatotoxicity
• Myopathy/rhabdomyolysis
• Hyperglycemia
• Neutropenia

Correct Answer: Myopathy/rhabdomyolysis

Q6. Which of the following lipid-lowering drugs is contraindicated in pregnancy due to teratogenic risk?

• Colesevelam
• Fenofibrate
• Statins (e.g., atorvastatin)
• Omega-3 fatty acids

Correct Answer: Statins (e.g., atorvastatin)

Q7. Bile acid sequestrants reduce LDL cholesterol mainly by which hepatic response?

• Inhibition of HMG-CoA reductase
• Upregulation of LDL receptors due to increased hepatic conversion of cholesterol to bile acids
• Activation of PPAR-α
• Enhanced VLDL synthesis

Correct Answer: Upregulation of LDL receptors due to increased hepatic conversion of cholesterol to bile acids

Q8. Which drug class works via activation of PPAR-α to increase lipoprotein lipase expression and reduce triglycerides?

• Bile acid sequestrants
• Fibrates
• Statins
• PCSK9 inhibitors

Correct Answer: Fibrates

Q9. Combining a statin with which agent requires caution due to increased risk of statin-associated myopathy through CYP3A4 inhibition?

• Ezetimibe
• Colestipol
• Gemfibrozil
• Omega-3 ethyl esters

Correct Answer: Gemfibrozil

Q10. Which parameter is the primary therapeutic target when treating patients with atherosclerotic cardiovascular disease according to guidelines?

• Reduction in triglycerides by ≥50%
• Absolute reduction in total cholesterol
• Lowering LDL-C to guideline-specific thresholds
• Raising HDL-C above 60 mg/dL

Correct Answer: Lowering LDL-C to guideline-specific thresholds

Q11. Niacin (vitamin B3) lowers LDL and triglycerides and raises HDL through which primary mechanism?

• Inhibition of intestinal cholesterol absorption
• Activation of hepatic PPAR-α receptors
• Inhibition of adipose tissue lipolysis decreasing free fatty acid flux to liver
• Direct inhibition of PCSK9 synthesis

Correct Answer: Inhibition of adipose tissue lipolysis decreasing free fatty acid flux to liver

Q12. Which lipid-modifying therapy has the greatest evidence for acute reduction of severe hypertriglyceridemia–induced pancreatitis risk?

• High-dose statin
• Fibrate therapy (e.g., fenofibrate)
• Bile acid sequestrant
• PCSK9 inhibitor

Correct Answer: Fibrate therapy (e.g., fenofibrate)

Q13. Which of the following is a common GI-related adverse effect and potential interaction of bile acid sequestrants?

• Pancreatitis
• Steatorrhea due to fat-soluble vitamin malabsorption and interference with absorption of co-administered drugs
• Nephrolithiasis
• Hyperkalemia

Correct Answer: Steatorrhea due to fat-soluble vitamin malabsorption and interference with absorption of co-administered drugs

Q14. Which statin characteristic reduces the risk of clinically significant CYP3A4-mediated drug interactions?

• High lipophilicity
• Extensive first-pass CYP3A4 metabolism (e.g., simvastatin)
• Hydrophilicity and renal elimination (e.g., pravastatin, rosuvastatin)
• Prodrug status

Correct Answer: Hydrophilicity and renal elimination (e.g., pravastatin, rosuvastatin)

Q15. Which biomarker elevation is most indicative of statin-induced hepatocellular injury and often monitored before and during therapy?

• Serum creatinine
• ALT/AST (transaminases)
• Alkaline phosphatase alone
• Serum amylase

Correct Answer: ALT/AST (transaminases)

Q16. In homozygous familial hypercholesterolemia with minimal LDL receptor function, which therapy directly lowers LDL-C independent of LDL receptor upregulation?

• High-dose statin alone
• PCSK9 inhibitor
• Lipoprotein apheresis or antisense oligonucleotide targeting ApoB or MTP inhibitor
• Ezetimibe monotherapy

Correct Answer: Lipoprotein apheresis or antisense oligonucleotide targeting ApoB or MTP inhibitor

Q17. Which omega-3 preparation has demonstrated triglyceride-lowering effects primarily by reducing hepatic VLDL production?

• Over-the-counter low-dose fish oil capsules only
• Prescription high-dose EPA and DHA ethyl esters (e.g., 4 g/day)
• Niacin combination products
• Bile acid sequestrants

Correct Answer: Prescription high-dose EPA and DHA ethyl esters (e.g., 4 g/day)

Q18. Which genetic defect is most commonly responsible for familial defective ApoB leading to impaired LDL receptor binding?

• Mutation in PCSK9 gene
• Mutation in LDLR gene
• Mutation in APOB gene (ApoB-100 defect)
• Mutation in LPL gene

Correct Answer: Mutation in APOB gene (ApoB-100 defect)

Q19. When combining ezetimibe with a statin, the complementary effect on LDL-C primarily arises because ezetimibe does which of the following?

• Further inhibits HMG-CoA reductase
• Reduces intestinal cholesterol absorption, decreasing hepatic cholesterol pool and enhancing statin-induced LDL receptor upregulation
• Activates PPAR-γ to increase LDL clearance
• Sequesters bile acids in the intestine

Correct Answer: Reduces intestinal cholesterol absorption, decreasing hepatic cholesterol pool and enhancing statin-induced LDL receptor upregulation

Q20. Which monitoring parameter is most appropriate to assess efficacy of lipid-lowering therapy and to guide dose adjustment?

• Fasting glucose
• Serial LDL-C measurements
• Serum potassium
• Hemoglobin concentration

Correct Answer: Serial LDL-C measurements

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