20.9r Antihyperlipidemic Agents

low-density lipoproteins (LDLs)

Elevated levels of (?) have been clearly indicated as a causative factor in coronary artery disease.

Lipoproteins

(?) are essentially transport mechanisms for lipids (triglycerides and cholesterol).

plasma-soluble shell

Because lipids are insoluble in plasma, the body coats them in a (?) in order to transport them to their target destinations.

very low density (VLDL)

Lipoproteins are categorized as (?), low density (LDL), intermediate density (IDL), and high density (HDL).

cholesterol

LDLs contain most of the (?) in the blood and are required for transporting cholesterol from the liver to the peripheral tissues.

HDLs

Conversely, (?) carry cholesterol from the peripheral tissues to the liver, where it is broken down.

“good” cholesterol

HDLs have been described as (?) because they lower blood cholesterol levels and decrease the risk of coronary artery disease (CAD).

“bad” cholesterol

LDLs are known as (?) because they increase blood cholesterol levels and the risk of CAD.

fatty plaque

As blood cholesterol levels increase, (?) is deposited under the arteries’ endothelial tissues.

Atherosclerosis

(?) then develops, and coronary arteries decrease in diameter.

Coronary vasoconstriction

(?), in turn, reduces blood flow to the heart and, in times of increased myocardial oxygen demand, can lead to angina.

unstable

Also, newly deposited plaque is often (?).

endothelial tissues

Typically, the plaque is under the (?), which cap the plaque deposits.

cap

As the deposits age, the (?) usually becomes fairly stable.

breaks open

In some cases, however, the cap (?) and exposes the plaque to the blood.

platelet aggregation

When this happens, (?) and coagulation begin.

thrombus

If the developing clot breaks free of the vessel, it becomes a (?) and can completely occlude a coronary artery, leading to MI.

LDL levels

The goal in lowering (?) is to prevent atherosclerosis and subsequent CAD.

pharmaceutical means

While raising HDL levels would help accomplish this, no (?) of doing so currently exists.

dietary modification

By far, the best way to lower LDL levels remains (?).

antihyperlipidemic medications

If this is not sufficient, several classifications of (?) can be used.

hydroxymethylglutaryl coenzyme A (HMG CoA) reductase

The most common are medications that inhibit (?).

HMG CoA

The liver must have (?) to synthesize cholesterol.

LDL receptors

By inhibiting this enzyme, HMG CoA agents lower LDL levels; however, they also increase the number of (?) in the liver, causing a further uptake of LDL.

Five

Five HMG CoA reductase inhibitors are available.

statin

Because the names of all five end in (?), these agents are also known as statins.

lovastatin (Mevacor)

They include (?) and simvastatin (Zocor).

Lovastatin

(?) is the HMG CoA reductase inhibitors’ prototype.

well tolerated

Overall, these medications are (?).

headache

Their chief side effects are (?), rash, and flushing.

hepatotoxicity

In unusual cases, they can cause (?) and lead to liver failure.

Bile acid-binding resins

(?) can also reduce LDL levels.

Inert substances

(?), these agents pass straight through the GI system without being absorbed and are excreted in feces.

LDL receptors

They are useful, however, in that they indirectly increase the number of (?) in the liver by binding with bile acids, thus decreasing their availability.

cholesterol

Because the liver needs (?) to synthesize bile acids, it must have more cholesterol to compensate for the decrease in bile acids.

LDL receptors

The body therefore increases the (?) on the liver.

LDLs

As more (?) remain in the liver, their levels in the blood drop.

systemic effects

Because the body does not absorb bile acid-binding agents, LDL receptors have no (?).

constipation

Their chief untoward effect is (?).

Cholestyramine (Questran)

(?) is the prototype.