Tag: cholesterol

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Miscellanous Cholesterol Agents – Test Prep and Practice Pearls

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In this episode, we explore several important non-statin cholesterol-lowering therapies, focusing on their mechanisms, clinical uses, and practical considerations for patient care.

We start with bile acid sequestrants, also known as resins, including cholestyramine, colestipol, and colesevelam. These medications lower LDL cholesterol by binding bile acids in the gut, prompting the liver to use more cholesterol to make new bile acids. They are effective for LDL reduction but may cause gastrointestinal side effects and have drug interaction considerations.

Next, we cover niacin (vitamin B3), which can lower LDL and triglycerides while raising HDL cholesterol. While niacin was historically widely used, its role has declined due to flushing, gastrointestinal symptoms, and potential liver toxicity.

Omega-3 fatty acids, including icosapent ethyl (EPA), primarily lower triglycerides and are used in patients with severe hypertriglyceridemia to reduce the risk of pancreatitis. Icosapent ethyl is a purified EPA formulation with evidence of cardiovascular benefit in select high-risk patients.

Finally, we discuss bempedoic acid, a newer oral agent that inhibits ATP-citrate lyase in the liver. Because it is activated only in the liver, bempedoic acid may be useful for patients with statin-associated muscle symptoms. Common adverse effects include elevated uric acid and mild increases in liver enzymes.

This episode highlights how these non-statin agents can be strategically used alone or in combination with other therapies to help patients reach their lipid goals and reduce cardiovascular risk.

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Ezetimibe and PCSK-9 Inhibitors – Cholesterol Test Prep and Practice Pearls

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In this pharmacology podcast episode, we focus on two key non-statin cholesterol-lowering therapies: ezetimibe and PCSK9 inhibitors (Click here to listen to the statin podcast episode). These agents play a role in lipid management, particularly for patients who are unable to reach LDL cholesterol goals with statins alone or who have statin intolerance.

Ezetimibe works by inhibiting the absorption of dietary and biliary cholesterol at the brush border of the small intestine. By reducing the amount of cholesterol delivered to the liver, ezetimibe lowers circulating LDL cholesterol by approximately 15 to 25 percent. It is taken orally once daily and is commonly used as add-on therapy to statins in patients with established atherosclerotic cardiovascular disease or high baseline LDL levels. Ezetimibe is generally well tolerated, with a favorable safety profile and minimal systemic exposure, making it an attractive option in older adults and patients with multiple comorbidities.

PCSK9 inhibitors, including alirocumab and evolocumab, offer a much more potent LDL-lowering effect. These monoclonal antibodies work by blocking PCSK9, a protein that promotes degradation of LDL receptors in the liver. By preserving LDL receptors, PCSK9 inhibitors enhance clearance of LDL cholesterol from the bloodstream, often reducing LDL levels by 50 to 60 percent. They are administered via subcutaneous injection every two to four weeks and are most commonly used in patients with familial hypercholesterolemia, established cardiovascular disease, or persistently elevated LDL despite maximally tolerated statin and ezetimibe therapy.

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Fibrates – Test Prep and Practice Pearls

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Fibrate derivatives are lipid-lowering medications that primarily target triglycerides rather than LDL cholesterol. Common agents include gemfibrozil, fenofibrate, and fenofibric acid. While their use has declined with the widespread adoption of statins, fibrates remain an important option for patients with severe hypertriglyceridemia, particularly to reduce the risk of acute pancreatitis rather than for routine cardiovascular risk reduction.

Fibrates work by activating PPAR-alpha, which increases lipoprotein lipase activity and enhances the clearance of triglyceride-rich lipoproteins. This leads to significant reductions in triglycerides, modest increases in HDL cholesterol, and variable effects on LDL cholesterol. Because they are not strong LDL-lowering agents, fibrates should not replace statins in patients who require LDL reduction, but they can be effective in select clinical scenarios when triglycerides are the primary concern.

From a safety standpoint, fibrates are generally well tolerated but require careful monitoring. Common concerns include gastrointestinal side effects, liver enzyme elevations, gallstone risk, and muscle toxicity, especially when combined with statins. Gemfibrozil carries a higher risk of drug interactions, while fenofibrate is usually preferred if combination therapy is necessary. Appropriate patient selection, lab monitoring, and lifestyle counseling are essential to maximize benefit and minimize harm when using fibrate derivatives.

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Statin Test Prep and Practice Pearls

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On this podcast episode, I discuss important practice pearls and important test prep information about statins. Statins are cornerstone agents for ASCVD risk reduction, so test questions often focus on indication, intensity, and monitoring. Health care professionals should quickly identify statin intensity: high-intensity therapy (atorvastatin 40–80 mg, rosuvastatin 20–40 mg) lowers LDL by ~50% and is indicated for patients with clinical ASCVD, LDL ≥190 mg/dL, or high-risk diabetes patients age 40–75. Moderate-intensity statins (e.g., atorvastatin 10–20 mg, simvastatin 20–40 mg) are commonly tested for primary prevention.

Statin-associated muscle symptoms range from myalgias (most common, normal CK) to rare but serious rhabdomyolysis (marked CK elevation and AKI). Risk factors include high doses, advanced age, hypothyroidism, drug interactions, and renal impairment. If muscle symptoms occur, stopping the statin, ruling out secondary causes (like hypothyroidism), and rechallenging with a lower dose or different statin is often the correct clinical approach.

Drug interactions and statin selection frequently separate good from great test-takers. Lipophilic statins (simvastatin, atorvastatin, lovastatin) are more prone to muscle effects and CYP3A4 interactions, while hydrophilic statins (pravastatin, rosuvastatin) are preferred in patients with prior intolerance or complex drug regimens. Grapefruit juice, strong CYP3A4 inhibitors, and certain calcium channel blockers raise simvastatin levels—often prompting dose limits or avoidance on exams. If LDL goals aren’t met, adding ezetimibe or a PCSK9 inhibitor is the next evidence-based step.

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Fenofibrate Pharmacology Podcast Episode 310

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On this podcast episode, I discuss fenofibrate pharmacology, adverse effects, kinetics, drug interactions, and much more!

Fenofibrate is typically only used for hypertriglyceridemia. The primary risk of hypertriglyceridemia is pancreatitis so we treat these levels because of this risk.

LFTs elevation has been associated with fenofibrate use as well as myopathy. In the presence of myopathy, checking CPK may be considered.

Fenofibrate is a weak CYP2C9 inhibitor. Warfarin and phenytoin are two important medications that may be affected by the use of fenofibrate.

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Fluvastatin Pharmacolgy Podcast

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On this podcast episode, I discuss fluvastatin pharmacology, adverse effects, pharmacokinetics, and much more.

Fluvastatin is only a low to moderate-intensity statin which explains its limited use compared to rosuvastatin or atorvastatin.

I discuss drug interactions in the podcast but one important one to recognize is drugs that can inhibit CYP2C9.

Fluvastatin is considered a lipophilic statin. I have previously discussed this on the Meded101 blog which you can find here.

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Lovastatin Pharmacology Podcast

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On this episode of the Real Life Pharmacology Podcast, I discuss lovastatin pharmacology, adverse effect, drug interactions, and more!

Lovastatin is broken down by CYP3A4 so drugs like clarithromycin, diltiazem, and others may increase concentrations.

Lovastatin is a lipophilic statin and I discuss the importance of this on the podcast.

Lovastatin has a very short half-life which means that it is ideal to dose this medication at night for maximal efficacy.

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Niacin Pharmacology Podcast

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On this podcast episode, I discuss niacin pharmacology, adverse effects, drug interactions, and much more.

Niacin has historically been used to manage lipids but has fallen out of favor due to adverse effects, and newer, more effective therapies being developed.

Niacin can elevate uric acid. Be sure to use this medication cautiously in patients with gout.

Flushing is one of the most common adverse effects of niacin. High doses, immediate-release formulations, and the use of alcohol can increase the risk.

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Pravastatin Pharmacology

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On this episode, I breakdown pravastatin pharmacology, adverse effects, drug interactions and when you might see this drug used in practice.

Pravastatin is a statin and will lower LDL. Its use is a little limited in the fact that it is not as potent as other agents in its LDL lowering effects.

Pravastatin is hydrophilic which differentiates it from simvastatin, atorvastatin, and lovastatin.

I describe rhabdomyolysis in this podcast as it is a potential rare adverse effect of pravastatin.

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Atorvastatin Pharmacology

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On this episode, I discuss atorvastatin pharmacology, adverse effects, monitoring parameters, and drug interactions.

Atorvastatin (Lipitor) is an HMG-CoA reductase inhibitor, the rate-limiting step in the production of cholesterol. It is used to prevent atherosclerotic cardiovascular diseases by decreasing cholesterol.

Atorvastatin is more lipophilic in comparison to other statins such as rosuvastatin. If a patient does not tolerate a statin, switching from a lipophilic to a hydrophilic or vice versa may decrease the chances of those side effects reoccurring.

It can be a high-intensity statin depending on the dose. 10-20mg is considered moderate and 40-80mg is classified as high intensity. Not all statins can reach high-intensity doses, which is why atorvastatin is so commonly used.            

The FDA as of July 2021, has requested to remove the contraindication of pregnancy from the prescribing information. Here’s more information on that specific change and why it was requested. I’d encourage you to read it. 

Atorvastatin is commonly found to have adherence issues so it should be taken whenever it is going to be best remembered by the patient.

Common adverse effects include myopathy, muscle pain, and soreness. Many elderly patients can be overlooked when they experience aches and pains, so it is important to take their medications into consideration. There are rare risks of liver injury and rhabdomyolysis. CPK and LFTs do not need to be regularly monitored if no symptoms are present.  

Remind patients that their cholesterol will not be lowered right away. They will usually have their levels rechecked in 3-6 months.

Drugs that increase rhabdomyolysis risk when used concurrently include fibrates, red yeast rice, niacin, daptomycin. Monitor these patients closely for symptoms of muscle pain. Can also monitor CPK and decrease the dose of the statin in these patients. 3A4 interactions can increase the concentration of statins. These include clarithromycin, grapefruit juice, amiodarone, amantadine, and verapamil. 3A4 inducers can decrease the concentration of statins. These include St. John’s Wort and carbamazepine. 

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