Questions – Lipid Control

by Pravin Shukle, MD

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    00:01 Okay, let's move on to a question. The following will be effective in homozygous familial hypercholesterolemia except, colesevelam, mipomersen, ezetimibe, and rosuvastatin. Good for you, you chose rosuvastatin. Now this is a question that medical students are always getting wrong. They always get it wrong because they assume that rosuvastatin is really powerful. But remember statins, are definitely going to require aggresive normal LDL production. So let's move on to the second question. What is the mechanism of action of Ezetimibe? Is it A, a blockage of the enzyme that produces intracellular cholesterol. Is it B, increased synthesis of PCSK9. Is it C, increased uptake of luminal cholesterol in the blood stream or into the blood stream. Is it D, inhibition of intestinal cholesterol transport proteins. Or is it E, reduction of the calcium slow current. Good, you chose D. So D, inhibition of intestinal cholesterol transport proteins reduces the level LDL in the blood. A is incorrect because blockage of an enzyme that produces intracellular cholesterol, that's a statin. B. Increased synthesis of PCSK9, that's actually no drug. The PCSK9 inhibitors act as immune modulators or immunoglobulins that attach to PCSK9 and prevent it from doing it's job. C is wrong. Increase uptake of luminal cholesterol into the bloodstream. That almost does'nt even make any sense and E, reduction of the inward calcium slow current is wrong. They will do that to you because sometimes they will get you confused with a cardiac drug that sound similar.

    02:06 So pay attention to the drugs that you are using. Okay, let's go on to a question again. A 55-year old male has elevated LDL cholesterol. He was started on rosuvastatin 10mg daily. His current medications include perindopril for hypertension, aspirin, and fenofibrate for severe hypertriglyceridemia. What do you think the most appropriate strategy is going forward.

    02:34 So what should we do? Should we stop the fenofibrate as there is a very high likelihood of a fatal drug interaction.

    02:41 Should we reduce the fenofibrate dosage as there is a potential for a fatal drug reaction. Should we continue fenofibrate but monitor liver enzymes and follow closely. Or use a higher dose of rosuvastatin and continue the fenofibrate.

    02:59 I think that's reasonable. Continue fenofibrate but monitor liver enzymes and follow closely. Remember that a combination of fenofibrate and rosuvastatin has a very low risk of that really horrible fatal interaction, possibly in the 1 in 1000000 range. So to stop the medication of the severe hypertriglyceridemia in order to start a statin is not a rational choice. It might be what your patient wants to do, but it's not rational because there is not a real tangible risk other than that theoretical risk going forward. Monitoring and being careful is the best way to do this. Okay that's it. I hope you enjoyed the lecture and good luck on your exams.

    About the Lecture

    The lecture Questions – Lipid Control by Pravin Shukle, MD is from the course Cardiovascular Pharmacology. It contains the following chapters:

    • Question 1: Lipid Control
    • Question 2: Lipid Control
    • Case Study 1: Lipid Control

    Included Quiz Questions

    1. Ezetimibe Decreased absorption of cholesterol from the small intestine
    2. Statins Activation of lipoprotein lipase
    3. Fenofibrate PCSK 9 inhibition
    4. Alirocumab Inhibition of HMG-CoA reductase
    1. Fenofibrate can be used in combination with statins to treat severe hypertriglyceridemia.
    2. Fenofibrate can be used in combination with statins to treat high HDL.
    3. Fenofibrate is contraindicated in patients who are already treated with statins.
    4. Fenofibrate/statin combinations commonly cause renal failure.

    Author of lecture Questions – Lipid Control

     Pravin Shukle, MD

    Pravin Shukle, MD

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