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Quizzes > Health & Medicine > Human Anatomy & Medicine

How Well Do You Know Antihyperlipidemic Drugs? Take the Quiz!

Test your skills on lipid-lowering drugs and statins - start now!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art pills capsules charts for pharmacology quiz on antihyperlipidemics and lipid lowering drugs on teal background

Ready to master antihyperlipidemics? Dive into this free pharmacology quiz and test your understanding of lipid-lowering drugs, from the statins mechanism to apolipoproteins function. Whether you're a pharmacy student sharpening your skills or a healthcare professional brushing up on hyperlipidemia treatments, our antihyperlipidemic drugs quiz offers the perfect blend of challenge and insight. You'll learn best practices in prescribing, identify potential adverse effects, and deepen your grasp of novel therapies. Ready for a challenge? Start now, ace every question, see how you rank among peers, and elevate your clinical confidence!

Which of the following is a HMG-CoA reductase inhibitor?
Lovastatin
Cholestyramine
Gemfibrozil
Ezetimibe
Lovastatin is a statin that inhibits HMG-CoA reductase, reducing cholesterol synthesis. Bile acid sequestrants, fibrates, and cholesterol absorption inhibitors have different targets. Statins are first-line agents for lowering LDL cholesterol.
Which drug class works by inhibiting cholesterol absorption at the intestinal brush border?
Ezetimibe
Atorvastatin
Niacin
Colesevelam
Ezetimibe blocks NPC1L1 transporters in enterocytes, decreasing dietary cholesterol uptake. Statins inhibit hepatic cholesterol synthesis, and niacin and colesevelam have different mechanisms. This action lowers LDL levels effectively.
Niacin primarily lowers which lipoprotein fraction?
Triglycerides
LDL
HDL
VLDL
Niacin increases HDL cholesterol by reducing hepatic HDL clearance. It also modestly reduces LDL and VLDL but has the greatest effect on raising HDL. Flushing is a common side effect that can be mitigated by aspirin.
Which of the following agents is a fibrate?
Gemfibrozil
Ezetimibe
Rosuvastatin
Colestipol
Gemfibrozil is a fibrate that activates PPAR-alpha, increasing lipoprotein lipase activity to lower triglycerides. Ezetimibe, statins, and bile acid sequestrants act through other pathways. Fibrates are effective in patients with high TG levels.
Bile acid sequestrants lower LDL by what primary mechanism?
Increasing bile acid excretion
Blocking HMG-CoA reductase
Inhibiting NPC1L1
Activating PPAR-alpha
Bile acid sequestrants bind bile acids in the gut and increase their fecal excretion. The liver uses cholesterol to synthesize new bile acids, lowering LDL. They are often used when statins are contraindicated.
Which lipid-lowering drug is known to cause flushing as a common side effect?
Niacin
Atorvastatin
Ezetimibe
Fenofibrate
Niacin-induced flushing results from prostaglandin-mediated vasodilation. It can be reduced by taking aspirin before each dose. Statins, ezetimibe, and fibrates have different side effect profiles.
Statins upregulate which receptor on hepatocytes to clear LDL from circulation?
LDL receptor
HDL receptor
VLDL receptor
ABCA1 transporter
By inhibiting cholesterol synthesis, statins increase LDL receptor expression to uptake more LDL. This leads to reduced plasma LDL levels. Upregulation of HDL receptor and ABCA1 are not the primary mechanisms.
Which agent is a monoclonal antibody used to lower LDL cholesterol?
Alirocumab
Gemfibrozil
Niacin
Ezetimibe
Alirocumab is a PCSK9-inhibiting monoclonal antibody that increases LDL receptor recycling. Fibrates, niacin, and ezetimibe are small-molecule drugs with different mechanisms. PCSK9 inhibitors have shown significant LDL reductions.
Colesevelam belongs to which class of lipid-lowering drugs?
Bile acid sequestrant
Statin
Fibrate
Cholesterol absorption inhibitor
Colesevelam binds bile acids in the intestine to prevent their reabsorption. This class is called bile acid sequestrants. Statins, fibrates, and absorption inhibitors have different targets.
Which of the following is a common side effect associated with statin therapy?
Elevated liver enzymes
Hyperuricemia
Pancreatitis
Alopecia
Statins can cause transaminase elevations due to hepatic metabolism. Monitoring liver function is recommended. They are not commonly associated with hyperuricemia, pancreatitis, or hair loss.
Which supplement is commonly recommended to reduce niacin-induced flushing?
Aspirin
Vitamin D
Omega-3 fatty acids
Coenzyme Q10
Low-dose aspirin inhibits prostaglandin synthesis and reduces niacin-induced flushing. Vitamin D, omega-3s, and CoQ10 do not mitigate flushing. Proper timing improves tolerance.
Fibrates lower triglycerides primarily by activating which nuclear receptor?
PPAR-alpha
LXR
FXR
PPAR-gamma
Fibrates activate PPAR-alpha, upregulating lipoprotein lipase and fatty acid oxidation. LXR, FXR, and PPAR-gamma are not the primary targets of fibrates. This reduces VLDL and triglyceride levels.
Ezetimibe specifically inhibits which protein?
NPC1L1
HMG-CoA reductase
PCSK9
CETP
Ezetimibe blocks the NPC1L1 transporter in the small intestine to reduce cholesterol absorption. It does not affect HMG-CoA reductase, PCSK9, or CETP. Combining with statins leads to additive LDL lowering.
PCSK9 inhibitors reduce LDL cholesterol by preventing degradation of what?
LDL receptors
LDL particles
PCSK9 enzyme
ApoB-100
PCSK9 binds LDL receptors and targets them for lysosomal degradation. Inhibiting PCSK9 increases receptor recycling, lowering LDL. They do not directly bind LDL particles or ApoB.
Which bile acid sequestrant is available as a powder for suspension?
Cholestyramine
Ezetimibe
Lovastatin
Fenofibrate
Cholestyramine is provided as a powder to mix with fluid and taken with meals. It binds bile acids and lowers LDL. The other agents are tablets or capsules.
Which statin undergoes extensive metabolism by CYP3A4?
Simvastatin
Pravastatin
Rosuvastatin
Pitavastatin
Simvastatin is metabolized by CYP3A4, making it susceptible to drug-drug interactions. Pravastatin and rosuvastatin have minimal CYP metabolism. Pitavastatin undergoes UGT-mediated glucuronidation.
Grapefruit juice increases plasma levels of which lipid-lowering drug?
Atorvastatin
Pravastatin
Colesevelam
Niacin
Grapefruit juice inhibits CYP3A4, raising atorvastatin levels. Pravastatin is not a CYP3A4 substrate. Bile acid sequestrants and niacin are not significantly affected.
Niacin reduces hepatic VLDL synthesis by inhibiting which process?
Diacylglycerol acyltransferase-2
HMG-CoA reductase
ACAT
Lipoprotein lipase
Niacin inhibits diacylglycerol acyltransferase-2, reducing triglyceride synthesis and VLDL secretion. It does not directly inhibit HMG-CoA reductase or ACAT, and it enhances rather than inhibits lipoprotein lipase.
Bile acid sequestrants can impair absorption of which vitamin?
Vitamin K
Vitamin B12
Vitamin D
Vitamin C
Sequestrants bind fat-soluble vitamins including A, D, E, and K, potentially causing deficiencies. Vitamin D absorption is particularly affected. Water-soluble vitamins like B12 and C are not significantly impacted.
Fibrates may increase the risk of gallstones by increasing which enzyme activity?
Cholesterol 7?-hydroxylase
HMG-CoA reductase
Lecithin–cholesterol acyltransferase
Squalene synthase
Fibrate-induced PPAR-alpha activation upregulates cholesterol 7?-hydroxylase, increasing bile acid synthesis and cholesterol saturation in bile. This predisposes to gallstone formation. Other enzymes listed are not directly involved.
Combination of ezetimibe with a statin is most beneficial for what reason?
Additive LDL lowering
Reduced flushing
Prevent gallstones
Increase HDL
Ezetimibe adds to statin therapy by blocking intestinal cholesterol absorption while statins inhibit synthesis. This synergy achieves greater LDL reduction. It does not affect flushing, gallstones, or HDL significantly.
A gain-of-function mutation in PCSK9 would result in which effect?
Higher LDL cholesterol
Lower HDL cholesterol
Increased triglycerides
Enhanced bile acid excretion
Gain-of-function PCSK9 mutations increase LDL receptor degradation, raising LDL levels. They do not directly affect HDL, triglycerides, or bile acid pathways. Loss-of-function mutations have the opposite effect.
Which pleiotropic effect is associated with statin therapy?
Improved endothelial function
Increased VLDL synthesis
Enhanced intestinal cholesterol absorption
Direct activation of PPAR-alpha
Statins increase nitric oxide bioavailability, improving endothelial function. They do not increase VLDL synthesis or absorption, nor do they directly activate PPAR-alpha. Pleiotropic benefits include anti-inflammatory effects.
Which lab value is most important to monitor in patients on fibrate therapy?
CK (creatine kinase)
INR
TSH
Glucose
Fibrates can rarely cause myopathy or rhabdomyolysis, so CK monitoring is recommended. INR, TSH, and glucose are not specifically affected by fibrates.
In patients with triglycerides >500 mg/dL, the first-line therapy is usually:
Fibrate
Bile acid sequestrant
Ezetimibe
Ezitimibe
Fibrates effectively reduce high triglyceride levels and lower pancreatitis risk. Bile acid sequestrants and ezetimibe primarily lower LDL, not TG. High TG requires fibrate or fish oil therapy.
Which agent increases lipoprotein lipase activity to clear triglyceride-rich lipoproteins?
Fenofibrate
Ezetimibe
Colestipol
Alirocumab
Fenofibrate activates PPAR-alpha, increasing lipoprotein lipase activity to catabolize VLDL. Ezetimibe, colestipol, and alirocumab have different mechanisms.
Which lipid-lowering agent is contraindicated in severe hepatic impairment?
Statins
Bile acid sequestrants
Niacin
Fibrates
Statins are metabolized by the liver and contraindicated in active hepatic disease. Sequestrants act in the gut, niacin and fibrates have different hepatic risk profiles.
Which antihyperlipidemic is contraindicated in pregnancy due to teratogenic risk?
Statins
Bile acid sequestrants
Colesevelam
Ezetimibe
Statins are contraindicated in pregnancy due to potential teratogenicity. Bile acid sequestrants and ezetimibe are category B and may be used if clearly needed.
For rapid LDL reduction in acute coronary syndrome, which drug is preferred?
High-intensity statin
Niacin
Cholestyramine
Fenofibrate
High-intensity statins lower LDL quickly and stabilize plaques post-ACS. Niacin, bile sequestrants, and fibrates work more slowly and are not first-line in ACS.
What is considered a high-intensity atorvastatin dose?
80 mg daily
10 mg daily
5 mg daily
20 mg daily
Atorvastatin 40–80 mg daily is classified as high-intensity, lowering LDL by ?50%. Lower doses yield moderate LDL reductions.
Niacin can exacerbate gout because it affects which pathway?
Uric acid excretion
Purine synthesis
Pyrimidine degradation
Adenosine uptake
Niacin decreases renal excretion of uric acid, raising serum levels and precipitating gout. It does not directly affect purine synthesis or pyrimidine pathways.
Which effect do bile acid sequestrants have on plasma triglyceride levels?
Increase triglycerides
Decrease triglycerides
No effect
Increase HDL
By interrupting bile acid reabsorption, these agents can cause compensatory VLDL production, raising triglycerides. They primarily target LDL reduction. HDL changes are minimal.
A patient on simvastatin develops muscle pain and CK elevation. The most likely interaction is with:
Itraconazole
Metformin
Lisinopril
Metoprolol
Itraconazole is a potent CYP3A4 inhibitor, raising simvastatin levels and risk of myopathy. Metformin, lisinopril, and metoprolol do not inhibit CYP3A4 significantly.
Which combination therapy carries the highest risk of hepatotoxicity?
Statin plus niacin
Ezetimibe plus bile acid sequestrant
Fibrate plus bile acid sequestrant
PCSK9 inhibitor plus statin
Niacin and statin coadministration increases risk of liver enzyme elevations. Other combinations lack significant overlapping hepatotoxicity. PCSK9 inhibitors have minimal hepatic metabolism.
Which lipid parameter does PCSK9 inhibition NOT directly affect?
Lp(a)
HDL cholesterol
LDL cholesterol
ApoB
PCSK9 inhibitors mainly lower LDL and ApoB and also reduce Lp(a) modestly. They do not significantly raise HDL levels.
Which genetic polymorphism most affects statin-induced myopathy risk?
SLCO1B1 c.521T>C
HMGCR rs3846662
CETP TaqIB
APOE ?4
The SLCO1B1 c.521T>C variant reduces hepatic statin uptake, elevating plasma levels and myopathy risk. Other polymorphisms influence cholesterol metabolism but not myopathy directly.
In severe hypertriglyceridemia, what is the role of icosapent ethyl?
Reduces TG by EPA-mediated effects
Inhibits HMG-CoA reductase
Binds bile acids
Monoclonal antibody against PCSK9
Icosapent ethyl is a purified EPA that lowers triglycerides via several mechanisms including reduced VLDL synthesis. It does not inhibit HMG-CoA reductase or affect bile acids or PCSK9.
Which agent is most appropriate for homozygous familial hypercholesterolemia?
Lomitapide
Cholestyramine
Ezetimibe
Niacin
Lomitapide inhibits microsomal triglyceride transfer protein, reducing VLDL secretion, and is indicated in homozygous familial hypercholesterolemia. Sequestrants and ezetimibe are less effective in receptor-negative patients.
Which medication reduces Lp(a) levels most effectively?
PCSK9 inhibitors
Statins
Fibrates
Bile acid sequestrants
PCSK9 inhibitors lower Lp(a) by up to 30%, partly via increased receptor clearance. Statins have minimal effect on Lp(a). Fibrates and sequestrants do not significantly change Lp(a).
Which therapy is titrated based on apolipoprotein B levels rather than LDL cholesterol?
PCSK9 inhibitors
Niacin
Bile acid sequestrants
Fibrates
PCSK9 inhibitors show better correlation with ApoB lowering as they reduce particle number. Other agents are typically dosed by LDL reduction. Monitoring ApoB can guide PCSK9 dosing.
Which lipid-lowering strategy is recommended for patients with refractory hypercholesterolemia on maximal oral therapy?
LDL apheresis
Increase niacin dose
Add bile acid sequestrant
Swap to fluvastatin
LDL apheresis mechanically removes LDL particles and is reserved for refractory cases. Increasing niacin or adding sequestrants may help but are often insufficient. Statin switch has limited impact if already maximized.
Which enzyme pathway is directly inhibited by lomitapide in lipid metabolism?
Microsomal triglyceride transfer protein
HMG-CoA reductase
Lipoprotein lipase
CETP
Lomitapide blocks microsomal triglyceride transfer protein, preventing assembly of VLDL and chylomicrons. It does not inhibit HMG-CoA reductase, lipoprotein lipase, or CETP.
Which agent is used to treat dyslipidemia in patients with chronic kidney disease due to minimal hepatic metabolism?
Pravastatin
Simvastatin
Fenofibrate
Ezetimibe
Pravastatin undergoes non-CYP metabolism and is safer in CKD. Simvastatin is CYP3A4-metabolized. Fibrates can accumulate in renal impairment. Ezetimibe is not specifically preferred in CKD.
What is the effect of CETP inhibitors like anacetrapib on lipid profiles?
Increase HDL and lower LDL
Lower HDL and increase LDL
No change in HDL
Increase TG
CETP inhibitors block transfer of cholesteryl esters to VLDL, raising HDL and lowering LDL. They do not reduce HDL or raise TG. Clinical benefit was under investigation.
Which novel RNA-based therapy targets ApoC-III to lower triglycerides?
Volanesorsen
Inclisiran
Mipomersen
Lomitapide
Volanesorsen is an antisense oligonucleotide that inhibits ApoC-III synthesis, reducing triglyceride levels. Inclisiran targets PCSK9 mRNA, mipomersen targets ApoB, and lomitapide inhibits MTP.
Inclisiran lowers LDL cholesterol by silencing which gene?
PCSK9
HMGCR
NPC1L1
APOB
Inclisiran is an siRNA that degrades PCSK9 mRNA, increasing LDL receptor recycling. It does not target HMGCR, NPC1L1, or APOB. Dosing is twice yearly after initial loading.
In patients with mixed dyslipidemia and diabetes, which combination is preferred to reduce cardiovascular risk?
Statin plus icosapent ethyl
Niacin plus fibrate
Ezetimibe plus bile acid sequestrant
PCSK9 inhibitor plus niacin
Icosapent ethyl added to statin therapy reduces cardiovascular events in diabetic patients with elevated TG. Niacin-fibrate combos increase adverse effects without proven benefit. Other combos have less outcome data.
Which imaging modality can assess plaque stabilization after statin therapy?
Intravascular ultrasound
CT angiography
Carotid duplex ultrasound
MRI
Intravascular ultrasound (IVUS) quantifies plaque volume and composition changes post-statin therapy. CT angiography and carotid duplex assess luminal stenosis but not plaque stabilization. MRI has limited coronary use.
Which pathway is targeted by evinacumab for refractory hypercholesterolemia?
ANGPTL3
PCSK9
HMG-CoA reductase
CETP
Evinacumab is a monoclonal antibody against ANGPTL3, lowering LDL and TG in homozygous familial hypercholesterolemia independent of LDL receptors. It does not target PCSK9, HMG-CoA reductase, or CETP.
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Study Outcomes

  1. Understand Antihyperlipidemic Drug Classes -

    Gain clarity on major classes of antihyperlipidemics, including statins, fibrates, bile acid sequestrants, and PCSK9 inhibitors, by examining their primary targets and mechanisms.

  2. Describe Statins Mechanism of Action -

    Detail how statins inhibit HMG-CoA reductase to reduce cholesterol synthesis and upregulate LDL receptors, reinforcing your grasp of the statins mechanism.

  3. Explain Apolipoproteins Function in Lipid Metabolism -

    Clarify the roles of key apolipoproteins such as ApoA-I and ApoB in lipid transport and clearance, enhancing your understanding of apolipoproteins function.

  4. Analyze Clinical Use of Lipid-Lowering Drugs -

    Assess patient scenarios to select appropriate lipid-lowering drugs based on efficacy, tolerability, and comorbidities, reinforcing decision-making skills.

  5. Evaluate Adverse Effects and Safety Profiles -

    Identify common and serious side effects associated with antihyperlipidemics and outline monitoring strategies to ensure patient safety.

  6. Differentiate Hyperlipidemia Treatment Strategies -

    Compare and contrast hyperlipidemia treatments, considering factors like intensity of LDL reduction, combination therapy, and patient-specific goals.

Cheat Sheet

  1. Statins Mechanism (HMG-CoA Reductase Inhibition) -

    Statins are cornerstone antihyperlipidemics that competitively block HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, lowering LDL-C by 20 - 60%. Upregulated LDL receptors then enhance hepatic uptake of circulating cholesterol. Use the mnemonic "SLOW" (Statins Lower Our Way) to recall their action.

  2. Apolipoproteins Function in Lipid Transport -

    Apolipoproteins are protein components of lipoproteins that direct lipid-lowering drugs to their targets and help stabilize lipoprotein particles. For example, ApoB-100 on VLDL/LDL mediates LDL receptor binding, while ApoA-I on HDL activates LCAT to esterify cholesterol. Remember "B for Bad, A for Ally" to distinguish ApoB and ApoA roles.

  3. Fibrates and PPARĪ± Activation -

    Fibrates (e.g., gemfibrozil, fenofibrate) activate PPARĪ± nuclear receptors to increase lipoprotein lipase expression, enhancing triglyceride clearance by up to 50%. They also modestly raise HDL levels by upregulating ApoA-I and ApoA-II synthesis. Think "FATS down" to link fibrates with fat (TG) reduction.

  4. PCSK9 Inhibitors in Modern Hyperlipidemia Treatments -

    PCSK9 inhibitors are monoclonal antibodies that prevent PCSK9 from degrading LDL receptors, allowing more receptors to clear LDL-C and reducing levels by another 50 - 60% when added to statins. This novel hyperlipidemia treatment is backed by large-scale trials like FOURIER. Their brand-name endings ( - cumab) signal a monoclonal antibody agent.

  5. Bile Acid Sequestrants and the "Cholesterol Chaser" Trick -

    Bile acid sequestrants (e.g., cholestyramine, colesevelam) bind intestinal bile acids, forcing the liver to convert more cholesterol into bile and lowering LDL by 15 - 30%. Since they aren't absorbed, GI upset is the main side effect - take other drugs at least 4 hours apart. Use "CHYA" (Cholesterol Holds Your Attention) to recall their action.

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