Podcast
Questions and Answers
Which of the following is a primary goal in the treatment of hyperlipidemias?
Which of the following is a primary goal in the treatment of hyperlipidemias?
- Increase dietary fat intake
- Reduction of LDL cholesterol levels (correct)
- Elimination of triglycerides
- Increase HDL cholesterol levels
What is the relationship between LDL cholesterol levels and coronary heart disease risk?
What is the relationship between LDL cholesterol levels and coronary heart disease risk?
- Higher LDL levels decrease heart disease risk
- Lower LDL levels decrease heart disease risk (correct)
- Higher LDL levels have no effect on heart disease risk
- LDL levels only affect heart disease risk in older adults
Which of the following lipoproteins is often referred to as 'bad cholesterol'?
Which of the following lipoproteins is often referred to as 'bad cholesterol'?
- Chylomicrons
- High Density Lipoprotein (HDL)
- Very Low Density Lipoproteins (VLDL)
- Low Density Lipoprotein (LDL) (correct)
What is the effect of appropriate diet and medications on atherosclerosis-induced mortality?
What is the effect of appropriate diet and medications on atherosclerosis-induced mortality?
Which of the following factors contributes to elevated levels of cholesterol?
Which of the following factors contributes to elevated levels of cholesterol?
Which lipoproteins are considered to be major risk factors for atherosclerosis?
Which lipoproteins are considered to be major risk factors for atherosclerosis?
What process begins at the site of endothelial injury in a blood vessel?
What process begins at the site of endothelial injury in a blood vessel?
Which of the following is NOT a risk factor for coronary heart disease?
Which of the following is NOT a risk factor for coronary heart disease?
What is the normal range for HDL cholesterol levels in mg/dl?
What is the normal range for HDL cholesterol levels in mg/dl?
Which type of familial hyperlipoproteinemia is characterized by a deficient lipoprotein lipase?
Which type of familial hyperlipoproteinemia is characterized by a deficient lipoprotein lipase?
What is the main cause of Type IIa familial hypercholesterolemia?
What is the main cause of Type IIa familial hypercholesterolemia?
Which treatment option is suggested for patients with LDL levels greater than 160 mg/dL?
Which treatment option is suggested for patients with LDL levels greater than 160 mg/dL?
What is the aim of aggressive treatment in hyperlipidemia for patients with multiple risk factors?
What is the aim of aggressive treatment in hyperlipidemia for patients with multiple risk factors?
Which type of familial hyperlipoproteinemia is associated with overproduction of VLDL and triglycerides?
Which type of familial hyperlipoproteinemia is associated with overproduction of VLDL and triglycerides?
What treatment may be required for patients unwilling to make lifestyle changes to manage their hyperlipidemia?
What treatment may be required for patients unwilling to make lifestyle changes to manage their hyperlipidemia?
Which of the following conditions is NOT classified as a major risk factor for aggressive treatment of hypercholesterolemia?
Which of the following conditions is NOT classified as a major risk factor for aggressive treatment of hypercholesterolemia?
What is a potential adverse effect specifically associated with the use of clofibrate?
What is a potential adverse effect specifically associated with the use of clofibrate?
Which drug is indicated for lowering elevated triglycerides while having a potential risk of myopathy?
Which drug is indicated for lowering elevated triglycerides while having a potential risk of myopathy?
What happens to the levels of sulfonylureas when fibrates are used?
What happens to the levels of sulfonylureas when fibrates are used?
Which of the following statements about Niacin is correct?
Which of the following statements about Niacin is correct?
What is a significant risk of combining statins with fibrates?
What is a significant risk of combining statins with fibrates?
What is a primary effect of nicotinic acid on lipid metabolism shortly after administration?
What is a primary effect of nicotinic acid on lipid metabolism shortly after administration?
Which drug should not be used in patients with moderate to severe hepatic insufficiency?
Which drug should not be used in patients with moderate to severe hepatic insufficiency?
Which mechanism contributes to the increase of HDL cholesterol by fibric acid derivatives?
Which mechanism contributes to the increase of HDL cholesterol by fibric acid derivatives?
What is the effect of niacin on VLDL and triglyceride (TG) levels after several hours of treatment?
What is the effect of niacin on VLDL and triglyceride (TG) levels after several hours of treatment?
What adverse effect is NOT commonly associated with niacin?
What adverse effect is NOT commonly associated with niacin?
Which of the following is true regarding the therapeutic use of fibric acid derivatives?
Which of the following is true regarding the therapeutic use of fibric acid derivatives?
Which class of drugs is the most potent for raising plasma HDL levels?
Which class of drugs is the most potent for raising plasma HDL levels?
Which of the following statements about the pharmacokinetics of ezetimibe is correct?
Which of the following statements about the pharmacokinetics of ezetimibe is correct?
Which drugs are considered efficacious in lowering triglycerides?
Which drugs are considered efficacious in lowering triglycerides?
What effect do HMG CoA reductase inhibitors have on LDL receptors?
What effect do HMG CoA reductase inhibitors have on LDL receptors?
Which of the following statins must be hydrolyzed to become active?
Which of the following statins must be hydrolyzed to become active?
Which statin is noted for having antioxidant effects?
Which statin is noted for having antioxidant effects?
What is the primary pharmacokinetic feature of atorvastatin and rosuvastatin?
What is the primary pharmacokinetic feature of atorvastatin and rosuvastatin?
What impact do HMG CoA reductase inhibitors have on HDL levels?
What impact do HMG CoA reductase inhibitors have on HDL levels?
Patients with which condition benefit the least from treatment with HMG CoA reductase inhibitors?
Patients with which condition benefit the least from treatment with HMG CoA reductase inhibitors?
Which statin is associated with the least risk of myopathy?
Which statin is associated with the least risk of myopathy?
What are common adverse effects of HMG CoA reductase inhibitors?
What are common adverse effects of HMG CoA reductase inhibitors?
Which of the following is a contraindication for the use of HMG CoA reductase inhibitors?
Which of the following is a contraindication for the use of HMG CoA reductase inhibitors?
What is a primary effect of bile acid-binding resins like cholestyramine?
What is a primary effect of bile acid-binding resins like cholestyramine?
What is a noted adverse effect of bile acid-binding resins?
What is a noted adverse effect of bile acid-binding resins?
How do bile acid resins affect cholesterol synthesis in the liver?
How do bile acid resins affect cholesterol synthesis in the liver?
Which drug is known to interfere with the intestinal absorption of multiple medications?
Which drug is known to interfere with the intestinal absorption of multiple medications?
What is the mechanism of action of Ezetimibe?
What is the mechanism of action of Ezetimibe?
Which bile acid-binding resin is noted for having fewer gastrointestinal side effects?
Which bile acid-binding resin is noted for having fewer gastrointestinal side effects?
Flashcards
Atherosclerosis
Atherosclerosis
A major cause of death in the US, responsible for heart attacks and strokes.
LDL (Low-density Lipoprotein)
LDL (Low-density Lipoprotein)
A type of lipoprotein that carries cholesterol from the liver to the tissues. It is often called 'bad cholesterol' due to its role in atherosclerosis.
HDL (High-density Lipoprotein)
HDL (High-density Lipoprotein)
A type of lipoprotein that collects cholesterol from tissues and transports it back to the liver. It is often called 'good cholesterol' due to its protective effect.
Role of lipoproteins in atherosclerosis
Role of lipoproteins in atherosclerosis
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Reduction of LDL levels
Reduction of LDL levels
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Causes of elevated cholesterol
Causes of elevated cholesterol
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Lifestyle modifications
Lifestyle modifications
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Drug therapy for hyperlipidemias
Drug therapy for hyperlipidemias
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Hyperlipidemia
Hyperlipidemia
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Hyperlipoproteinemia
Hyperlipoproteinemia
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Fredrickson Classification
Fredrickson Classification
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Lifestyle Modifications for Hypercholesterolemia
Lifestyle Modifications for Hypercholesterolemia
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Drug Therapy for Hypercholesterolemia
Drug Therapy for Hypercholesterolemia
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HMG CoA Reductase Inhibitors
HMG CoA Reductase Inhibitors
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How do HMG CoA Reductase Inhibitors work?
How do HMG CoA Reductase Inhibitors work?
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Unique Characteristics of Lovastatin and Simvastatin
Unique Characteristics of Lovastatin and Simvastatin
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Atorvastatin and Rosuvastatin: Long-Acting Powerhouse
Atorvastatin and Rosuvastatin: Long-Acting Powerhouse
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Absorption of HMG CoA Reductase Inhibitors
Absorption of HMG CoA Reductase Inhibitors
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Metabolism and Elimination of HMG CoA Reductase Inhibitors
Metabolism and Elimination of HMG CoA Reductase Inhibitors
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Therapeutic Uses of HMG CoA Reductase Inhibitors
Therapeutic Uses of HMG CoA Reductase Inhibitors
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Statins: A Special Type of Drug
Statins: A Special Type of Drug
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Drugs for Hyperlipoproteinemia
Drugs for Hyperlipoproteinemia
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Myopathy
Myopathy
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Rhabdomyolysis
Rhabdomyolysis
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Flushing and Pruritus
Flushing and Pruritus
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What is the mechanism of action of statins?
What is the mechanism of action of statins?
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What is a major potential side effect of statins?
What is a major potential side effect of statins?
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How do bile acid-binding resins work?
How do bile acid-binding resins work?
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What are some common side effects of bile acid-binding resins?
What are some common side effects of bile acid-binding resins?
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How does ezetimibe work?
How does ezetimibe work?
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What is a potential consequence of bile acid-binding resin use?
What is a potential consequence of bile acid-binding resin use?
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Why is it important to take drugs at specific times when using bile acid-binding resins?
Why is it important to take drugs at specific times when using bile acid-binding resins?
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What is an additional use of cholestyramine?
What is an additional use of cholestyramine?
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How is Ezetimibe metabolized and excreted?
How is Ezetimibe metabolized and excreted?
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What are the immediate effects of Niacin on lipid levels?
What are the immediate effects of Niacin on lipid levels?
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What kind of conditions can Niacin be used to treat?
What kind of conditions can Niacin be used to treat?
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What is the main use of Niacin clinically?
What is the main use of Niacin clinically?
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What are the potential side effects of Niacin?
What are the potential side effects of Niacin?
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What are examples of fibrate medications and what do they do?
What are examples of fibrate medications and what do they do?
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How do fibrates work?
How do fibrates work?
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What conditions are fibrates used to treat?
What conditions are fibrates used to treat?
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Study Notes
Treatment of Hyperlipidemias
- Hyperlipidemia is the presence of high levels of fats (lipids) in the blood
- Risk factors for coronary heart disease (CHD) include high LDL cholesterol, low HDL cholesterol, cigarette smoking, hypertension, obesity, and diabetes
- Elevated cholesterol can be caused by multiple factors including lifestyle (lack of exercise and high saturated fat intake), single inherited gene defects in lipoprotein metabolism, or a combination of genetic and lifestyle factors
- The primary treatment goal is to reduce LDL cholesterol levels
- Higher heart disease risk necessitates more aggressive LDL-lowering therapies
- Atherosclerosis is a major cause of death in the US, from heart attacks and strokes
- Risk factors for atherosclerosis include: hypertension, age, obesity, diabetes, high-fat diets, smoking, stress, low HDL, lack of exercise, and a family history
- Elevated plasma lipoproteins (VLDL, IDL, and LDL) are a significant risk factor in atherosclerosis
Lipoprotein Structure and Classification
- Lipoproteins are complex particles composed of a core of triacylglycerols and cholesteryl esters, surrounded by phospholipids and proteins (apolipoproteins)
- Lipoproteins are classified based on their density:
- Chylomicrons carry triacylglycerol from the intestines to the liver and adipose tissue
- Very-low-density lipoproteins (VLDL) carry triacylglycerol from the liver to adipose tissue
- Low-density lipoproteins (LDL) carry cholesterol from the liver to the tissues ("bad cholesterol")
- High-density lipoproteins (HDL) collect cholesterol from tissues and transport it back to the liver ("good cholesterol")
Composition of Lipoproteins
- Chylomicrons: Approximately 90% triacylglycerol
- Very-low-density lipoproteins (VLDL): Approximately 60% triacylglycerol
- Low-density lipoproteins (LDL): Approximately 50% cholesterol and cholesterol esters
- High-density lipoproteins (HDL): Approximately 20% protein and 30% cholesterol and cholesterol esters
Normal Lipoprotein Values
- Total Cholesterol: <200 mg/dL
- LDL Cholesterol: 100 mg/dL
- HDL Cholesterol: 40-50 mg/dL
- Triglycerides: 150 mg/dL
Treatment Options for Hyperlipidemia
- Moderate Hyperlipidemia
- Lifestyle modifications (diet, exercise, and weight loss)
- Drugs if lifestyle changes are insufficient
- High LDL cholesterol (>160 mg/dL): Drug Therapy
- Aggressive Treatment: Two or more risk factors requiring aggressive drug treatment to achieve LDL below 100 mg/dL (some cases as low as 70 mg/dL)
- Hypertriacylglycerolemia (Elevated TG): Drug Therapy
- Diet
- Exercise
- Drugs in lowering triglycerides include niacin and fibric acid derivatives
Lipid Lowering Drugs
-
HMG-CoA Reductase Inhibitors (Statins):
- Mechanism: Inhibit HMG-CoA reductase, reducing cholesterol synthesis
- Examples: lovastatin, simvastatin, atorvastatin, rosuvastatin, fluvastatin
- Indications: Lowering plasma cholesterol levels in all types of hyperlipidemia, except homozygous familial hypercholesterolemia (lack LDL receptors)
- Adverse Effects: Headache, sleep disturbances, hepatotoxicity, myopathy (muscle tenderness) and rhabdomyolysis, drug interactions
- Drug interactions: May increase Warfarin levels
-
Bile Acid-Binding Resins:
- Mechanism: Bind bile acids in the intestine, preventing their reabsorption, leading to increase in LDL receptors in the liver
- Examples: cholestyramine, colestipol, colesevelam
- Indications: Drugs of choice for Type IIA and Type IIB hyperlipidemia (often in combination with diet or niacin)
- Adverse Effects: Gastrointestinal (GI) disturbances (constipation, nausea, and flatulence), high doses may interfere with absorption of fat-soluble vitamins (A, D, E, and K)
- Drug interactions: Interferes with the intestinal absorption of drugs like tetracycline, phenobarbital, digoxin, warfarin, pravastatin, fuvastatin, aspirin, and thiazide diuretics
-
Ezetimibe (Cholesterol Uptake Inhibitor):
- Mechanism: Blocks cholesterol absorption in the small intestine
- Indications: Can be used in combination with statins
- Adverse Effects: Mild
- Drug interactions: None mentioned
-
Niacin (Nicotinic Acid):
- Mechanism: Reduces VLDL and TG production
- Indications: Most potent anti-hyperlipidemic agent for raising HDL levels, used in treating severe hypercholesterolemia, and familial hyperlipidemia
- Adverse Effects: Cutaneous vasodilation (flushing, itching), liver dysfunction, hyperglycemia, gout, peptic ulcers
- Drug interactions: None mentioned
-
Fibric Acid Derivatives:
- Mechanism: Increases lipoprotein lipase action and increases HDL Cholesterol
- Examples: Fenofibrate, Gemfibrozil, Clofibrate
- Indications: Treating hypertriacylglycerolemia, Type III hyperlipidemia, patients that do not respond to other measures.
- Adverse Effects: Myopathy (skeletal muscle inflammation, weakness, and tenderness), gallstones (especially with Clofibrate), drug interactions (with coumarin anticoagulants and sulfonylureas).
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