Nursing CEU Continuing Education Credit Online
Take nursing courses visit: nursing continuing education online
The following is an excerpt from an online continuing education course for Nursing Continuing CEU credit:
1.9 Therapeutic Options:
Drug Treatment
Four major classes of medications are used to treat dyslipidemia:
• HMG-CoA reductase inhibitors (statins)
• Bile acid sequestrants
• Nicotinic acid
• Fibric acids
Statins (rosuvastatin, atorvastatin, simvastatin, pravastatin, fluvastatin, and lovastatin) can lower LDL levels 18% to 55%, and triglyceride levels 7% to 30%. They can also raise HDL levels by 5% to 15%. Major side effects include myopathy and elevation of liver enzyme levels.
Many clinical trials have shown that statins reduce incidence of major coronary events, CHD death, and stroke, and they may also reduce the need for coronary procedures, and lower total mortality. However, there is controversy.
Statins work by inhibiting the enzyme HMG-CoA reductase and are therefore also known as HMG-CoA reductase inhibitors. The process begins with acetyl-CoA. Three acetyl-CoA molecules combine to form hydroxymethyl glutaric acid (HMG). The step from HMG to mevalonate requires HMG-CoA reductase. Statin drugs work by inhibiting this enzyme, and herein lies the potential for numerous side effects because statin drugs inhibit not just the production of cholesterol, but a whole family of intermediary substances, many if not all of which have important biochemical functions.
Cholesterol is one of three end products in the mevalonate chain. The two others are ubiquinone and dilochol. Ubiquinone, also known as Co-Enzyme Q10, is a critical cellular nutrient biosynthesized in the mitochondria. It plays a role in ATP production in the cells and functions as an electron carrier to cytochrome oxidase, a major respiratory enzyme. The heart also requires high levels of Co-Q10. Ubiquinone is found in all cell membranes, where it plays a role in maintaining membrane integrity critical to nerve conduction and muscle integrity. Co-Q10 is also vital to the formation of elastin and collagen. Side effects of Co-Q10 deficiency include muscle-wasting leading to weakness and severe back pain, heart failure (the heart is a muscle), neuropathy, and inflammation of the tendons and ligaments often leading to rupture.
Finally, there is controversy regarding the mechanism by which statins reduce CHD risk. While statins significantly reduce serum cholesterol levels, this may not be the cause of reduction of cardiac events. The fact that some studies have shown that statins can prevent heart disease, at least in the short term, is most likely explained not by the inhibition of cholesterol production but because they block the creation of mevalonate. Reduced amounts of mevalonate seem to make smooth muscle cells less active, and platelets less able to produce thromboxane. Atherosclerosis begins with the growth of smooth muscle cells in side artery walls, and thromboxane is necessary for blood clotting.
Bile acid sequestrants (cholestyramine, and colestipol) can reduce LDL levels 15% to 30% and raise HDL levels 3% to 5%. They have no effect on triglyceride levels. Major side effects include gastrointestinal distress, constipation, and a decrease in the absorption of other drugs. Clinical trials have shown that these agents reduce the incidence of major coronary events and CHD death.
Nicotinic acid (niacin/vitamin B3) can reduce LDL levels 5% to 25% and triglyceride levels 20% to 50%. Nicotinic acid also raises HDL levels 15% to 35%. Major side effects of nicotinic acid include flushing, hyperglycemia, hyperuricemia, gastrointestinal distress, and hepatotoxicity. Clinical trials have shown it can prevent major coronary events.
Fibric acids (fenofibrate, and gemfibrozil) can reduce LDL levels 5% to 20% and triglyceride levels 20% to 50%, as well as raise HDL levels 10% to 20%. Major side effects include dyspepsia, gallstones, myopathy, and unexplained noncardiac death. Clinical trials have shown that they lower the risk of major coronary events.