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Questions and Answers
What can be done to minimize the undesirable effects of niacin therapy?
Premedication with a small dose of aspirin or a nonsteroidal antiinflammatory drug 30 minutes before taking the niacin, as well as taking the niacin with meals.
What is the primary effect of fibric acid derivatives on lipid levels?
Lowering triglyceride levels, and may also lower total cholesterol and LDL levels and raise HDL levels.
What is the mechanism of action of fibric acid derivatives?
Activating lipase, suppressing the release of free fatty acid from adipose tissue, inhibiting synthesis of triglycerides in the liver, and increasing secretion of cholesterol in the bile.
What is the indication for fibric acid derivatives in the treatment of hyperlipidemia?
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What are some contraindications for the use of fibric acid derivatives?
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What are some common adverse effects of fibric acid derivatives?
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What is the risk of combining fibric acid derivatives with statins?
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What is the effect of fibric acid derivatives on HDL cholesterol levels?
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What is the primary indication for the use of omega-3 fatty acids in the treatment of hyperlipidemia?
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What is a potential interaction to be aware of when administering omega-3 fatty acids?
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What is an important nursing implication to consider before beginning therapy for hyperlipidemia?
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Why would a patient who has already been taking simvastatin for 12 months with no evidence of myopathy benefit from administration of simvastatin 80 mg?
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What is a potential adverse effect of niacin therapy?
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What is a potential interaction to be aware of when administering antilipidemic drugs?
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What is a potential adverse effect of bile acid sequestrants?
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What is an important consideration when prescribing simvastatin in patients taking verapamil?
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What is the primary mechanism of action of bile acid sequestrants in reducing lipid levels?
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According to the National Cholesterol Education Program Adult Treatment Panel III, what is the minimum duration of nondrug means of controlling blood cholesterol levels before considering drug therapy?
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What is the primary mechanism of action of Bile Acid Sequestrants in treating hyperlipidemia?
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What is the primary lipid-lowering mechanism of niacin therapy?
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What is the indication for using Bile Acid Sequestrants in relief of pruritus associated with partial biliary obstruction?
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What is the most serious potential adverse effect of HMG-CoA reductase inhibitors, and how can it be prevented?
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What is the primary mechanism of action of HMG-CoA reductase inhibitors in reducing lipid levels?
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What are the common adverse effects of Bile Acid Sequestrants, which tend to disappear over time?
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What is the primary indication for the use of fibrates in hyperlipidemia treatment?
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What is the difference between the dosing schedule of Atorvastatin (Lipitor) and Simvastatin (Zocor)?
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What is the mechanism of action of Atorvastatin (Lipitor) in lowering total and LDL cholesterol levels?
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What is the role of mipomersen in the treatment of hyperlipidemia?
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What is the primary indication for using Bile Acid Sequestrants in hyperlipidemia treatment?
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What is the primary mechanism of action of PCSK9 inhibitors in reducing lipid levels?
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What is the difference between the forms of Colestipol (Colestid) and Colesevelam (Welchol)?
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What is the advantage of using Simvastatin (Zocor) over Atorvastatin (Lipitor)?
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What is the key to understanding the use of antilipemic drugs?
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What are the two primary forms of lipids in the blood?
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What is the function of high-density lipoprotein (HDL)?
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What is the precursor lesion of atherosclerosis?
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What is the risk of coronary heart disease in patients with elevated cholesterol levels?
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What is the role of low-density lipoprotein (LDL)?
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What is the function of very-low-density lipoprotein (VLDL)?
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What is the consequence of elevated serum cholesterol levels?
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Study Notes
Hyperlipidemias and Treatment Guidelines
- National Cholesterol Education Program Adult Treatment Panel III of the National Institutes of Health provides guidelines for hyperlipidemias treatment.
- Antilipemic drugs are used to lower lipid levels as an adjunct to diet therapy.
- Drug choice is based on the specific lipid profile of the patient (phenotyping).
Antilipemics
- ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults (2018) recommends:
- Hydroxymethylglutaryl–coenzyme A (HMG–CoA) reductase inhibitors (statins)
- Bile acid sequestrants
- B vitamin niacin (vitamin B3, nicotinic acid)
- Fibric acid derivatives (fibrates)
- Cholesterol absorption inhibitor (Zetia)
- Combination drugs (Vytorin)
Newer Drugs
- Mipomersen: a weekly subcutaneous injection
- Microsomal triglyceride transfer protein inhibitor (Lomitapide, Juxtapid)
- Proprotein convertase subtilisin kexin 9 (PCSK9) inhibitors (Alirocumab, Praluent; Evolocumab, Repatha)
- ATP-citrate lyase inhibitor (Bempedoic acid, Nexletol)
Antilipemics: HMG-CoA Reductase Inhibitors (Statins)
- Indications:
- Patients with clinical atherosclerotic cardiovascular disease (CVD)
- Patients with LDL cholesterol levels >190 mg/dL
- Patients with diabetes age 40 to 75 years with LDL levels of 70 to 189 mg/dL and without evidence of CVD
- Patients without evidence of CVD or diabetes but who have LDL levels between 70 and 189 mg/dL and a 10-year risk of CVD > 7.5%
- Examples:
- Lovastatin (Mevacor)
- Pravastatin (Pravachol)
- Simvastatin (Zocor)
- Atorvastatin (Lipitor)
- Fluvastatin (Lescol)
- Rosuvastatin (Crestor)
- Pitavastatin (Livalo)
HMG-CoA Reductase Inhibitors: Mechanism of Action
- Inhibit HMG-CoA reductase, which is used by the liver to produce cholesterol
- Lower the rate of cholesterol production
HMG-CoA Reductase Inhibitors: Indications
- First-line drug therapy for hypercholesterolemia
- Treatment of types IIa and IIb hyperlipidemias
- Reduces LDL levels by up to 50%
- Increases HDL levels by 2% to 15%
- Reduces triglycerides by 10% to 30%
HMG-CoA Reductase Inhibitors: Adverse Effects
- Mild, transient gastrointestinal (GI) disturbances
- Rash
- Headache
- Myopathy (muscle pain), possibly leading to rhabdomyolysis
- Elevations in liver enzymes or liver disease
Rhabdomyolysis
- Breakdown of muscle protein
- Myoglobinuria: urinary elimination of the muscle protein myoglobin
- Can lead to acute renal failure and even death
- When recognized reasonably early, rhabdomyolysis is usually reversible with discontinuation of the statin drug.
Fibric Acid Derivatives
- Primarily affect triglyceride levels but may also lower total cholesterol and LDL levels and raise HDL levels
- Examples:
- Gemfibrozil (Lopid)
- Fenofibrate (Tricor)
Fibric Acid Derivatives: Mechanism of Action
- Believed to work by activating lipase, which breaks down cholesterol
- Suppress the release of free fatty acid from adipose tissue, inhibit synthesis of triglycerides in the liver, and increase secretion of cholesterol in the bile
Fibric Acid Derivatives: Indications
- Treatment of type III, IV, and V hyperlipidemias
- Decrease triglyceride levels and increase HDL cholesterol levels by up to 25%
Fibric Acid Derivatives: Contraindications
- Known drug allergy
- Severe liver or kidney disease
- Cirrhosis
- Gallbladder disease
Fibric Acid Derivatives: Adverse Effects
- Abdominal discomfort, diarrhea, nausea
- Blurred vision, headache
- Increased risk of gallstones
- Prolonged prothrombin time
- Liver studies may show increased enzyme levels
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