Pharm Antihyperlipidemics

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Pharm Antihyperlipidemics - Quiz

In today’s quiz on drugs associated with particular medical conditions, we’ll be looking at antihyperlipidemic agents, which are used in the treatment of high levels of fats and cholesterol in the blood. What can you tell us about these drugs and what their specific uses are?


Questions and Answers
  • 1. 

    Directions: questions 1-4 Match each antihyperlipidemic drug with the appropriate description (each lettered option can be selected once, more than once, or not at all): This drug can sometimes cause hypertriglyceridemia

    • A.

      Cholestyramine

    • B.

      Ezetimibe

    • C.

      Gemfibrozil

    • D.

      Niacin

    • E.

      Lovastatin

    Correct Answer
    A. Cholestyramine
    Explanation
    Cholestyramine is a drug that is known to sometimes cause hypertriglyceridemia. Hypertriglyceridemia is a condition characterized by high levels of triglycerides in the blood. Cholestyramine works by binding to bile acids in the intestine, which helps to lower cholesterol levels. However, one of the potential side effects of cholestyramine is an increase in triglyceride levels. Therefore, it is important to monitor triglyceride levels when using this medication.

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  • 2. 

    Directions: questions 1-4 Match each antihyperlipidemic drug with the appropriate description (each lettered option can be selected once, more than once, or not at all): Facial flushing is the most common adverse effect of this drug

    • A.

      Cholestyramine

    • B.

      Ezetimibe

    • C.

      Gemfibrozil

    • D.

      Niacin

    • E.

      Lovastatin

    Correct Answer
    D. Niacin
    Explanation
    Niacin is associated with facial flushing as its most common adverse effect.

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  • 3. 

    Directions: questions 1-4 Match each antihyperlipidemic drug with the appropriate description (each lettered option can be selected once, more than once, or not at all): High doses of this drug can cause metabolic acidosis

    • A.

      Cholestyramine

    • B.

      Ezetimibe

    • C.

      Gemfibrozil

    • D.

      Niacin

    • E.

      Lovastatin

    Correct Answer
    A. Cholestyramine
    Explanation
    Cholestyramine is an antihyperlipidemic drug that can cause metabolic acidosis when taken in high doses.

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  • 4. 

    Directions: questions 1-4 Match each antihyperlipidemic drug with the appropriate description (each lettered option can be selected once, more than once, or not at all): This drug activates a nuclear transcription receptor

    • A.

      Cholestyramine

    • B.

      Ezetimibe

    • C.

      Gemfibrozil

    • D.

      Niacin

    • E.

      Lovastatin

    Correct Answer
    C. Gemfibrozil
    Explanation
    Gemfibrozil is the correct answer because it activates a nuclear transcription receptor. This drug is classified as a fibric acid derivative and works by activating the peroxisome proliferator-activated receptor-alpha (PPAR-alpha), which regulates the expression of genes involved in lipid metabolism. By activating this receptor, gemfibrozil helps to decrease triglyceride levels and increase HDL cholesterol levels in the blood.

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  • 5. 

    A 21-year-old woman recently diagnosed with familial combined hyperlipidemia, started a treatment with lovastatin. Which of the following molecular actions most likely mediated the therapeutic efficacy of the drug in the patient’s disease?

    • A.

      Down-regulation of hepatic LDL receptors

    • B.

      Increased synthesis of lipoprotein lipase

    • C.

      Decreased synthesis of mevalonic acid

    • D.

      Decreased storage of LDL in hepatic endosomes

    • E.

      Increased plasma levels of hepatic aminotransferases

    • F.

      Increased plasma levels of creatine phosphokinase

    Correct Answer
    C. Decreased synthesis of mevalonic acid
    Explanation
    Learning objective: describe the mechanism of action of HMG-CoA reductase inhibitors
    Answer: C
    HMG-CoA reductase inhibitors inhibit the hydroxy-methylglutaryl-CoA reductase, which is the
    enzyme that catalyzes the synthesis of mevalonic acid from hydroxy-methylglutaryl-CoA. The
    formation of mevalonic acid is the rate-limiting step in cholesterol biosynthesis.
    A) The statin-induced inhibition of cholesterol synthesis in liver results in an up-regulation of
    hepatic high-affinity LDL receptors which in turn causes an increased removal of LDL from the
    blood
    B) Statins have no effect on lipoprotein lipase.
    D) The LDL removed from the blood fuse together in the liver, so forming larger vesicles called
    endosomes. Since removal of cholesterol from blood is increased by statins, also storage of
    LDL in hepatic endosomes will be increased, not decreased.
    E, F) Statins can increase the plasma levels of hepatic aminotransferase and creatine
    phosphokinase but this is a sign of potential toxicity, not of therapeutic efficacy of these drugs.

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  • 6. 

    A 28-year-old woman, recently diagnosed with familial combined hyperlipidemia, started a treatment with a low fat diet and cholestyramine. The therapy most likely caused the highest reduction of plasma levels of which of the following compounds?

    • A.

      VLDL

    • B.

      HDL

    • C.

      LDL

    • D.

      Chylomicrons

    • E.

      Triglycerides

    Correct Answer
    C. LDL
    Explanation
    Learning objective: describe the antihyperlipidemic effects of cholestyramine.
    Answer: C
    Type II hyperlipoproteinemia is characterized by an elevation of LDL which may be primary or
    secondary. Statins are currently used in this disease but the physician avoided them in this
    case because of the patient is a woman in fertile age. Bile acid binding resins increase the
    intestinal elimination of bile acids. This increased elimination causes an up-regulation of
    hepatic LDL receptors which in turn reduces the plasma level of LDL.
    A, B, D, E) These compounds are not consistently affected by bile acid binding resins.

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  • 7. 

    A 54-year-old obese man had a plasma LDL cholesterol of 270 mg/dL in spite of 4 month therapy with lovastatin. The physician decided to add cholestyramine to the patient’s regimen. Recently the patient was found to have a stage I hypertension and he was currently taking propranolol and hydrochlorothiazide. Which of the following changes in the pharmacokinetics of these two drugs most likely occurred because of cholestyramine administration?

    • A.

      Renal elimination of propranolol increased

    • B.

      Renal elimination of hydrochlorothiazide decreased

    • C.

      Oral bioavailability of propranolol increased

    • D.

      Oral bioavailability of hydrochlorothiazide decreased

    • E.

      Volume of distribution of propranolol increased

    • F.

      Volume of distribution of hydrochlorothiazide decreased

    Correct Answer
    D. Oral bioavailability of hydrochlorothiazide decreased
    Explanation
    Learning objective: describe the main drug interactions with cholestyramine.
    Answer: D
    Cholestyramine is an anion exchange resin which binds bile acids in the intestinal lumen so
    preventing their reabsorption. In fact the excretion of bile acid is increased up to tenfold when
    the resin is given. This in turn causes an enhanced conversion of cholesterol to bile acids in the
    liver, an increased uptake of LDL and IDL from plasma and an up-regulation of high-affinity
    LDL receptors on cell membranes. Resins can bind many drugs (including beta-blockers and
    thiazides) so reducing their intestinal absorption.
    A, B, E, F) Cholestyramine does not affect the distribution or the elimination of drugs given
    concomitantly.
    C) Intestinal absorption of propranolol is actually decreased and therefore the oral
    bioavailability is decreased, not increased.

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  • 8. 

    A 52-year-old man was found to have a total cholesterol of 380 mg/dL and triglycerides of 230 mg/dL in spite of three months of low saturated fat diet. The man had been suffering from hemophilia since birth and from external hemorrhoids for two years. An antihyperlipidemic therapy was prescribed. Which of the following drugs would be contraindicated in this patient?

    • A.

      Lovastatin

    • B.

      Cholestyramine

    • C.

      Ezetimibe

    • D.

      Niacin

    • E.

      Gemfibrozil

    Correct Answer
    B. Cholestyramine
    Explanation
    Learning objective: describe the main contraindications of cholestyramine
    Answer: B
    Cholestyramine can cause severe constipation and is therefore contraindicated in case of
    hemorrhoids. In addition the drug is also contraindicated in case of any coagulation defect,
    since it decreases the intestinal absorption of vit K.
    A, C, D, E) (see explanation above)

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  • 9. 

    A 24-year-old woman suffering from familial hypertriglyceridemia was screened with a blood profile during a follow-up visit. Relevant laboratory test results were: uric acid 15 mg/dL (normal 4-8.5), total cholesterol 170 mg/dL (normal < 200), triglycerides 1230 mg/dL (normal < 200). A lipid-lowering drug was prescribed. Which of the following was most likely the mechanism of action of that drug?

    • A.

      Decrease of lipid synthesis on adipose tissue

    • B.

      Down-regulation of LDL receptors in the liver

    • C.

      Inhibition HMG-CoA reductase activity in the liver

    • D.

      Stimulation of lipoprotein lipase synthesis

    • E.

      Decreased absorption of exogenous cholesterol

    Correct Answer
    D. Stimulation of lipoprotein lipase synthesis
    Explanation
    Learning objective: explain the mechanism of action of gemfibrozil.
    Answer: D
    The prescribed drug was most likely a fibrate. In fact fibrates are the drugs of first choice when
    there is a big, isolated increase in triglyceride level. Moreover in this patient niacin is
    contraindicated because of hyperuricemia, resins can cause an increase in triglyceride level
    and statins should be avoided in a woman in fertile age. The major mechanism of action
    recognized for fibrates is to increase the synthesis of lipoprotein lipase.
    A) Synthesis of lipids in adipose tissue is nearly undetectable in humans.
    B) The antihyperlipidemic agents tend to cause an up-regulation, not a down-regulation, of LDL
    receptors.
    C) Statins, not fibrates, inhibit HMG-CoA reductase activity in the liver.
    E) Fibrates have no effect on absorption of exogenous cholesterol.

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  • 10. 

    A 55-year-old obese woman was found to have a cholesterol level of 360 mg/dL despite many months of lovastatin treatment. The physician decided to add ezetimibe to the therapeutic regimen. Which of the following cells represents the main site of action of the added drug?

    • A.

      Adipocytes

    • B.

      Capillary endothelial cells

    • C.

      Platelets

    • D.

      Hepatocytes

    • E.

      Intestinal epithelial cells

    Correct Answer
    E. Intestinal epithelial cells
    Explanation
    Learning objective: describe the mechanism of action of ezetimibe.
    Answer: E
    Ezetimibe inhibits the absorption and of cholesterol by the small intestine, apparently by
    blocking a specific sterol transporter named Niemann-Pick C1-like 1 (NPC1L1) located on the
    epithelial cells of intestinal mucosa.
    A, B, C, D) (see explanation above)

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  • 11. 

    A 57-year-old man was found to have a LDL-cholesterol of 360 mg/dL in spite of 5 months of treatment with lovastatin. The physician decided to add ezetimibe to the therapeutic regimen. Which of the following statements best explain the rationale of adding this drug to lovastatin therapy?

    • A.

      The combination decreases the risk of lovastatin-induced myopathy

    • B.

      The combination results in synergistic cholesterol-lowering effects

    • C.

      Ezetimibe slows down the metabolism of lovastatin

    • D.

      Ezetimibe increases the intestinal absorption of lovastatin

    • E.

      The combination strongly increases HDL plasma levels

    Correct Answer
    B. The combination results in synergistic cholesterol-lowering effects
    Explanation
    Learning objective: describe the main drug interactions with ezetimibe
    Answer: B
    Ezetimibe lowers serum cholesterol concentration by selectively inhibiting the absorption of
    cholesterol from the small intestine. It has a modest cholesterol lowering effect when used
    alone, but the combination with HMG-reductase inhibitors can reduce LDL-cholesterol levels up
    to 70%.
    A) The risk of statins induced myopathy is not affected by the concomitant administration of
    ezetimibe (it is worth to note that the risk is increased by the concomitant administration of
    fibrates or niacin).
    C, D) Ezetimibe does not affect the pharmacokinetics of lovastatin.
    E) Ezetimibe does not increase appreciably the HDL-rising effect of lovastatin

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  • 12. 

    A 46-year-old man, suffering from familial hypercholesterolemia, was found to have a total cholesterol of 430 mg/dL in spite of many months of treatment with lovastatin. Triglyceride levels were normal. The physician decided to add niacin to the therapeutic regimen. Which of the following molecular action most likely mediated the therapeutic efficacy of the drug in the patient’s disease?

    • A.

      Inhibition of VLDL production by the hepatocyte

    • B.

      Inhibition of HDL synthesis by the liver

    • C.

      Increase of circulating fibrinogen

    • D.

      Stimulation of lipolysis in adipose tissue

    • E.

      Decreased absorption of exogenous cholesterol

    Correct Answer
    A. Inhibition of VLDL production by the hepatocyte
    Explanation
    Learning objective: explain the mechanism of action of niacin.
    Answer: A
    Niacin inhibits VLDL production by the hepatocyte, which in turn decreases production of LDL.
    The mechanism of this action is still uncertain but seems to involve:
    a) A decreased synthesis of triglycerides by the liver.
    b) An inhibition of lipolysis in adipose tissue that in turn causes a decreased delivery of free
    fatty acids to the liver.
    c) A stimulation of lipoprotein lipase activity which enhances hydrolysis of VLDL and enhanced
    delivery of triglycerides to adipose tissue.
    B) Niacin actually increases the synthesis of HDL by the liver.
    Niacin can cause hyperuricemia in about 20% of patients by an unknown mechanism.
    D) Niacin actually inhibits lipolysis of triglycerides by hormone sensitive lipase in adipose tissue.
    C) Niacin actually causes a substantial reduction of fibrinogen levels, which can be of value in
    case of of atherosclerosis or thrombosis.
    E) Niacin has negligible effects on exogenous cholesterol absorption.

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  • 13. 

    A 47-year-old man was brought by ambulance to the coronary unit with the admitting diagnosis of myocardial infarction. An emergency therapy was started which included alteplase, aspirin, heparin, and metoprolol. The next day lovastatin and ezetimibe were added to the therapeutic regimen. Which of the drugs received by the patient acts mainly on liver cell cytosol?

    • A.

      Alteplase

    • B.

      Aspirin

    • C.

      Lovastatin

    • D.

      Heparin

    • E.

      Ezetimibe

    • F.

      Metoprolol

    Correct Answer
    C. Lovastatin
    Explanation
    Learning objective: describe the site of action of HMG-CoA reductase inhibitors
    Answer: C
    All HMG-CoA reductase inhibitors, like lovastatin acts by inhibiting the enzyme which is located
    on the liver endoplasmic reticulum. Therefore liver cell cytosol is the main site of action of these
    drugs.
    A, D) These drugs act on plasma enzymes.
    B) Aspirin inhibits thromboxane synthesis on platelets.
    E) Ezetimibe acts on intestinal brush cell border.
    F) Metoprolol acts on receptors located on cell membranes.

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  • 14. 

    A 52-year-old obese man suffering from gout and hypertension was found to have LDL cholesterol of 360 mg/dL and a serum uric acid of 15.5 mg/dL during a follow-up visit. Other laboratory values were within normal limits. A lipid-lowering therapy is prescribed. Which of the following antihyperlipidemic drugs would be relatively contraindicated in this patient?

    • A.

      Cholestyramine

    • B.

      Niacin

    • C.

      Ezetimibe

    • D.

      Lovastatin

    • E.

      Gemfibrozil

    Correct Answer
    B. Niacin
    Explanation
    Learning objective: describe the main contraindications of niacin.
    Answer: B
    Niacin is contraindicated in patients suffering from gout and hyperuricemia because it tends to
    increase uric acid levels.
    A) Cholestyramine could be appropriated in this patient since he has an isolated increase of
    LDL.
    C, D) Statins are effective in all disorders involving elevated levels of LDL.
    E) Fibrates are useless (reduction of LDL is usually negligible) but not contraindicated in this
    patient.

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  • 15. 

    A 56-year-old woman, suffering from familial hypercholesterolemia, was found to have a total cholesterol of 470 mg/dL in spite of many months of treatment with lovastatin. Triglyceride levels were normal. The physician decided to add niacin to the therapeutic regimen. Which of the following drugs should be given during the first days of therapy, to avoid niacin induced hot flushes?

    • A.

      Warfarin

    • B.

      Atropine

    • C.

      Aspirin

    • D.

      Prazosin

    • E.

      Gemfibrozil

    Correct Answer
    C. Aspirin
    Explanation
    Learning objective: describe the clinically relevant drug interactions with niacin.
    Answer: C
    The cutaneous vasodilation and uncomfortable flushes are adverse effects that most persons
    experience after each dose of niacin. They seem mainly prostaglandin-mediated and therefore
    an aspirin (or another NSAID) can alleviate the flushing in many patients. Since these effects
    undergo rapid tolerance aspirin is needed only during the first days of therapy.
    A) There is no rationale for the use of warfarin. In fact niacin can cause a substantial reduction
    of circulating fibrinogen levels, which actually reduces the risk of thrombosis.
    B) There is no rationale for the use of atropine. Moreover the drug would worsen the
    cholestyramine induced constipation.
    D) Prazosin would increase the niacin induced vasodilation.
    E) Gemfibrozil is used only in case of hypertriglyceridemia. In this patient triglyceride levels are
    normal.

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  • 16. 

    A 45-year-old obese man suffering from type I diabetes mellitus and hyperlipidemia was admitted to the hospital because of vomiting and circulatory collapse. The patient had started an antihyperlipidemic therapy one month ago. Pertinent plasma data on admission were: pH 7.32, HCO3 12 mEq/L (normal 22-26), PaCO2 16 mm Hg (normal 25- 45), Cl 125 mEq/L (normal 90-105). Which of the following drugs could have contributed to the syndrome the patient was suffering from?

    • A.

      Lovastatin

    • B.

      Insulin

    • C.

      Niacin

    • D.

      Gemfibrozil

    • E.

      Cholestyramine

    Correct Answer
    E. Cholestyramine
    Explanation
    Learning objective:: describe the adverse effects of cholestyramine.
    Answer: E
    The symptoms and signs of the patient indicate that he is suffering from metabolic acidosis
    most likely due to cholestyramine overdose. A very high dose of cholestyramine can cause
    metabolic acidosis mainly in patients at risk as in the present one, who is prone to metabolic
    acidosis because of diabetes.
    Cholestyramine is an anion exchange resin that binds negatively charged bile acids. Chloride is
    released from binding sites in exchange from bile acids, so chloride anions can be absorbed.
    When an anion other than bicarbonate is increased in plasma, HCO3- must decrease in order
    to maintain electroneutrality. A reduced plasma bicarbonate concentration is defined acidosis.
    Since in this case acidosis is due to an increase in chloride anion, it is named hyperchloremic.
    B) Insulin protects diabetic patients from ketoacidosis so, in this case, one can suspect that an
    insufficient insulin dosage or an inappropriate diet were likely contributing factors.
    A, C, D) These drugs do not cause or trigger metabolic acidosis.

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  • 17. 

    A 57-year-old woman was found to have triglyceride levels of 630 mg/dL during a follow-up visit.. A therapy with gemfibrozil was prescribed. Which of the following cellular structures most likely represents the site of action of this drug?

    • A.

      Smooth endoplasmic reticulum

    • B.

      Nucleus

    • C.

      Cell membrane

    • D.

      Cytoplasm

    • E.

      Rough endoplasmic reticulum

    • F.

      Mitochondria

    Correct Answer
    B. Nucleus
    Explanation
    Learning objective: describe the site of action of gemfibrozil.
    Answer: B
    Fibrates bind to and activate a nuclear receptor (the peroxisome proliferator-activated receptor
    alpha) in hepatocytes, skeletal muscle and the heart. Activation of this receptor in turn activates
    transcription of genes which modulate protein expression. The main consequence is the
    increased expression of lipoprotein lipase.
    A, C, D, E, F) (see explanation above)

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  • 18. 

    A 45-year-old man complained to his physician of muscle aches, soreness and weakness. The patient had been suffering from duodenal ulcer for 2 years, from familial hypercholesterolemia for 5 years and from open angle glaucoma for one year. Present therapy included famotidine and sucralfate for ulcer, lovastatin for hyperlipidemia and timolol and latanoprost for glaucoma. An urinalysis showed myoglobinuria. Which of the following drugs most likely caused this finding?

    • A.

      Latanoprost

    • B.

      Famotidine

    • C.

      Timolol

    • D.

      Sucralfate

    • E.

      Lovastatin

    Correct Answer
    E. Lovastatin
    Explanation
    Learning objective: describe the adverse effects of HMG-CoA reductase inhibitors.
    Answer: E
    The patient was most likely affected by myopathy, a rare but serious adverse effects of statins.
    The disorder occurs in >0.1% of patients when statins are given alone, but can occur more
    often when they are given together with niacin or fibrates (up to 5%, when given with
    gemfibrozil). Myopathy can cause rhabdomyolysis with myoglobinuria, like in the present case.
    A, B, C, D) These drugs do not cause myopathy.

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  • 19. 

    A 49-year-old man was found to have the following lipid profile during a routine visit: LDL cholesterol 180 mg/dL (normal < 200), HDL cholesterol 14 mg/dL (normal > 35), triglycerides 150 mg/dL (normal < 200). The man weighted 134 Kg and was a heavy cigarette-smoker. Which of the following antihyperlipidemic drugs would be most appropriate for this patient?

    • A.

      Gemfibrozil

    • B.

      Lovastatin

    • C.

      Cholestyramine

    • D.

      Niacin

    • E.

      Ezetimibe

    Correct Answer
    D. Niacin
    Explanation
    Learning objective: describe the antihyperlipidemic effects of niacin
    Answer: D
    Low HDL level is a predictor of increased coronary artery disease (CAD), independent of all
    other risk factors. Therefore it is important to raise HDL, even if the other lipid fractions are
    normal, especially if the patient has other risk factors for (CAD), like in the present case.
    Main factors that are correlated with low HDL include cigarette smoking, obesity, androgenic or
    related steroids, hypertriglyceridemia and genetic factors. Some lipid-lowering drugs can raise
    HDL even if other lipid parameters are in the normal range, as in the present case. Niacin (by
    an unknown mechanism) has the greatest ability to raise HDL, up to 30% and is therefore the
    drug of choice in disorders associated with extremely low serum levels of HDL (these patients
    ten to have premature atherosclerosis and the low HDL level may be the only identified risk
    factor)
    A) Gemfibrozil can raise HDL up to 10%.
    B) Statins can raise HDL up to 10%
    C, E) Resins and Ezetimibe have little effect on HDL.

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  • 20. 

    A 26-year-old obese woman, who was found to have a LDL-cholesterol level of 270 mg/mL despite four months of diet, started a lipid-lowering therapy with cholestyramine. Which of the following is the main site of action of action of this drug?

    • A.

      Liver

    • B.

      Small intestine

    • C.

      Colon

    • D.

      Plasma

    • E.

      Adipose tissue

    • F.

      Gall bladder

    Correct Answer
    B. Small intestine
    Explanation
    Learning objective: describe the main site of action of cholestiramine.
    Answer: B
    Cholestyramine is an acid-binding resins. These drugs act by binding bile acids and similar
    steroids in the small intestine so preventing reabsorption of bile acid secreted by the liver. In
    this way they increase the need of cholesterol by the liver which in turn induces an up
    regulation of liver LDL receptors.
    A, C, D, E) (see explanation above)

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