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ORGANIZATION OF CLASS

Drugs used in the treatment of elevated serum lipids (hyperlipidemias) are targeted to decrease production of lipoprotein or cholesterol, increase degradation of a lipoprotein, or increase removal of cholesterol from the body.

The lipoproteins are large assemblies of lipids and proteins that bind and transport fats, such as lipids and triglycerides, in the blood. The lipids include free esterified cholesterol, triglycerides, and phospholipids. The proteins are known as apolipoproteins or apoproteins. They are classified according to lipid and protein content, transport function, and mechanism of lipid delivery. The high-density lipoproteins (HDL) are often referred to as the “good cholesterol” in contrast to the low- and very-low-density lipoproteins (LDL and VLDL), the “bad cholesterol.” Now would be a good time to review the physiology and biochemistry of fats, lipoproteins, and lipoprotein receptors.

The most important facts about the relatively few drugs in this class are the mechanisms of action. Practically speaking, taste, dose, and cost are also important considerations.

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Drugs Mechanism

ATORVASTIN

cerivastatin

fluvastatin

lovastatin

pitavastatin

PRAVASTATIN

ROSUVASTATIN

SIMVASTATIN

Inhibit HMG-CoA reductase

CHOLESTYRAMINE

colesevelam

colestipol

EZETIMIBE

alirocumab

evolocumab

niacin

fenofibrate

gemfibrozil

bempedoic acid

Bile acid–binding resins

 

 

Inhibits absorption of cholesterol

PCSK9 inhibitors

 

?

Activate nuclear transcription factor peroxisome proliferator-activated receptor-alpha (PPAR-alpha)

ACL inhibitor

First, compare the list of drugs in the preceding box with that in your textbook or class handouts and add or delete drugs as needed. Next, compare the mechanisms of action noted here to those in your textbook or handouts. Some of these mechanisms are not entirely worked out so there may be discrepancies. Don’t let that throw you off.

Basically, this box summarizes the most important things to know. If there is too much information here for you to absorb at one sitting, start by learning the two bile-binding resins and the drugs that inhibit HMG-CoA reductase (identified by their common ending of “-statin”). The rest of the drugs alter metabolism of lipoproteins. If you already have a good grasp of this content, you can skip the rest of this chapter.

ADDITIONAL EXPLANATION OF MECHANISMS

The HMG-CoA reductase inhibitors are the first-choice drugs for the treatment of patients who require lipid-lowering therapy.

These drugs, referred to generally as “-statins,” contain structural analogues of 3-hydroxy-3-methylglutarate (HMG), which is a precursor of cholesterol. They inhibit HMG-CoA reductase, the enzyme that controls the rate-limiting step in cholesterol synthesis. This depletes intracellular cholesterol. The cell then looks to the extracellular space for the cholesterol it needs. Since cholesterol is a required component of VLDLs, reduction in the synthesis of cholesterol by statins will also reduce hepatic VLDL production. Statins also improve endothelial function, decrease platelet aggregation, and reduce inflammation. The first side effect to know is myalgia, which is fairly common ...

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