Antihyperlipidemic drugs

HDL cholesterol protects against heart disease so the higher the numbers the better. An HDL level less than 40 mg dL is low and considered a major risk factor for heart disease Triglyceride levels Hiat are borderline (150-190 mg dL) or high (above 190 mg dL) may need treatment in some individuals. 

An increase in serum lipids is believed to contribute to or cause atherosclerosis, a disease characterized by deposits of fatty plaques on the inner walls of arteries. These deposits result in a narrowing of the lumen (inside diameter) of the artery and a decrease in blood supply to the area served by the artery. When these fatty deposits occur in the coronary arteries, the patient experiences coronary artery disease. Lowering blood cholesterol levels can arrest or reverse atherosclerosis in the vessels and can significantly decrease the incidence of heart disease. 

Hyperlipidemia, particularly elevated serum cholesterol and LDL levels, is a risk factor in the development of atlierosclerotic heart disease. Other risk factors, besides cholesterol levels, play a role in the development of hyperlipidemia. Additional risk factors include  

In general, the higher the LDL level and the more risk factors involved, the greater the risk for heart disease. The main goal of treatment in patients with hyperlipidemia is to lower the LDL to a level that will reduce the risk of heart disease  

The primary care provider may initially seek to control the cholesterol level by encouraging therapeutic life changes (TLC). This includes a cholesterol-lowering diet (TLC diet), physical activity, quitting smoking (if applicable), and weight management. The TLC diet is a 

Tri ycerides and cholesterides are insoluble in water and must be bound to a lipid-containing protein (lipoprotein) for transportation throu out tlie body. AMiough several liix)proteins are found in tlie blood, tins cliapter will focus on tlie low-density liix)proteins (LDL), tlie Ih i-density liix)proteins (HDL), and cholesterol. Low-density lipoproteins (LDL) transport cholesterol to tlie peripheral cells. Wlien tlie cells liave all of the cholesterol tliey need, the excess cholesterol is discarded into tlie blood. Tins can result in an exc s of cholesterol, which can iien-etrate the walls of the arteries, resulting in atlierosclerotic 

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Discuss the general actions, uses, adverse reactions, contraindications, precautions, and interactions of antihyperlipidemic drugs. 

Discuss important preadministration and ongoing assessment activities the nurse should perform on the patient taking an antihyperlipidemic drug. 

Discuss ways to promote an optimal response to therapy, how to manage common adverse reactions, and important points to keep in mind when educating patients about the use of an antihyperlipidemic drug. 

Because hyperlipidemia is often treated on an outpatient basis, die nurse explains die drug regimen and possible adverse reactions. If printed dietary guidelines are given to die patient, die nurse emphasizes the importance of following these recommendations. Drug dierapy usually is discontinued if the antihyperlipidemic drug is not effective after 3 months of treatment. 

The antihyperlipidemic drugs, such as clofibrate, fenofibrate, bezafibrate, ciprofi-brate and gemfibrozil are associated with liver toxicity and hepatomegaly in some patients. Fenofibrate inhibits complex I and to lesser extent complex V, whereas clofibrate inhibits predominantly complex V. Gemfibrozil also inhibits complex I, even more potently than fenofibrate [52, 53]. 

Sec Ch. 21 in Lippincott s Illustrated Reviews Pharmacology (2nd and 3rd Eds) for a discussion of antihyperlipidemic drugs... 

Tacrolimus + sirolimus, tacrolimus + mycophenolate mofetil, and ciclosporin + sirolimus have been compared in recipients of their first kidney transplant (52). One-year patient and graft survival did not differ. Ciclosporin + sirolimus was associated with increased serum creatinine concentrations, reduced creatinine clearance, more frequent protocol discontinuation, more antihyperlipidemic drug therapy, and a higher incidence of post-transplant diabetes mellitus. 

Hyperlipidemia is a condition characterized by the presence of elevated lipoprotein levels in the blood. The term hyperlipidemia encompasses a number of different conditions, but it most often refers to high levels of cholesterol in the form of low-density lipoprotein (LDL). LDL cholesterol is often called bad cholesterol. High-density lipoprotein (HDL) is the good form of cholesterol. High LDL and/or low HDL levels are widely believed to be linked to increased heart disease risk. Because of the prevalence of hyperlipidemia in developed nations, antihyperlipidemic drugs are in high demand. 

One class of antihyperlipidemic drugs is the statins. Statins interfere with the biosynthesis of cholesterol (A.103) and specifically inhibit the enzyme 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase (Scheme A.l). The statins that have been approved by the FDA include lovastatin (Mevacor, A.104), simvastatin (Zocor, A.105), pravastatin (Prava-chol, A.106), atorvastatin (Lipitor, A.107), rosuvastatin (Crestor, A.108), and fluvastatin (Lescol, A.109) (Figure A.29). All six compounds are drawn here to highlight the similarities between HMG-CoA (A.99) and mevalonic acid (A.100), and the top portion of the various statins. As a class, the statins have been extremely successful in terms of sales and effective in decreasing LDL cholesterol levels in the blood. 

The fibrates are another class of antihyperlipidemic drug and are frequently coadministered with a statin. Fibrates act as agonists of the peroxisome proliferator-activated receptors (PPAR), particularly PPAR-a. PPARs are nuclear receptors that influence gene expression and lipid metabolism. Examples of fibrates include gemfibrozil (Lopid, A.110) and fenofibrate (Tricor, A.lll) (Figure A.30). Fenofibrate is hydrolyzed in the body to its active form, fenofibric acid (A.112). Fibrates do not decrease LDL levels as effectively as statins, but fibrates do elevate HDL cholesterol levels. 

Summary of antihyperlipidemic drugs.1 Described in Pharmacology update, p. 449. 

Which one of the following is the most common side effect of antihyperlipidemic drug therapy ... 

N. K. Tesla, M.A. Saperia, G.M. Platt, R. Discontinuta-lion of antihyperlipidemic drugs—do rates reported in clinical trials reflect rates in primary care settings N. Engl. J. Med. 1995, 332, 1125-1131. 

Answer B. Nicotinic acid inhibits the synthesis of the VLDL apoprotein and decreases VLDL production. Its use results in decreases of both cholesterol and triglycerides, so total choles- terol in the plasma decreases. The drug is not an inhibitor of HMG-CoA reductase, and it increases plasma HDL to a greater extent than any other available antihyperlipidemic drug. 

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