Podcast
Questions and Answers
Which of the following pharmacologic classes of dyslipidemia medications primarily influences the absorption of cholesterol?
Which of the following pharmacologic classes of dyslipidemia medications primarily influences the absorption of cholesterol?
- Bile acid sequestrants (correct)
- HMG-CoA reductase inhibitors
- PCSK9 inhibitors
- Fibrates
A patient is prescribed a medication that inhibits the enzyme responsible for the first step in cholesterol biosynthesis. Which of the following medication classes is this likely to belong to?
A patient is prescribed a medication that inhibits the enzyme responsible for the first step in cholesterol biosynthesis. Which of the following medication classes is this likely to belong to?
- Fibrates
- PCSK9 inhibitors
- Bile acid sequestrants
- HMG-CoA reductase inhibitors (correct)
Which of the following statements accurately describes the action of fibrates on lipid levels?
Which of the following statements accurately describes the action of fibrates on lipid levels?
- Fibrates primarily increase HDL-C and increase TG.
- Fibrates primarily decrease LDL-C and increase HDL-C.
- Fibrates primarily decrease LDL-C and decrease TG.
- Fibrates primarily increase HDL-C and decrease TG. (correct)
Which of the following is a major drawback of using bile acid sequestrants for the long-term treatment of dyslipidemia?
Which of the following is a major drawback of using bile acid sequestrants for the long-term treatment of dyslipidemia?
A patient is taking a medication that inhibits the absorption of cholesterol in the small intestine. Which of the following adverse effects is most likely to occur?
A patient is taking a medication that inhibits the absorption of cholesterol in the small intestine. Which of the following adverse effects is most likely to occur?
Which of the following statements accurately describes the mechanism of action of PCSK9 inhibitors?
Which of the following statements accurately describes the mechanism of action of PCSK9 inhibitors?
A patient is taking a combination therapy for dyslipidemia, including a fibrate and a statin. Which of the following is a potential concern regarding this drug combination?
A patient is taking a combination therapy for dyslipidemia, including a fibrate and a statin. Which of the following is a potential concern regarding this drug combination?
Which of the following statements accurately describes the role of bile acids in cholesterol metabolism?
Which of the following statements accurately describes the role of bile acids in cholesterol metabolism?
What is the primary mechanism by which bile acids are reabsorbed from the intestines?
What is the primary mechanism by which bile acids are reabsorbed from the intestines?
How does the ionization state of bile acids influence their function as detergents?
How does the ionization state of bile acids influence their function as detergents?
Which of the following factors contributes to the decreased reabsorption of secondary bile acids?
Which of the following factors contributes to the decreased reabsorption of secondary bile acids?
Which of the following statements accurately describes the role of bacterial flora in bile acid metabolism?
Which of the following statements accurately describes the role of bacterial flora in bile acid metabolism?
What is the primary site of bile acid reabsorption in the gastrointestinal tract?
What is the primary site of bile acid reabsorption in the gastrointestinal tract?
How often are bile acids recycled in the body on average?
How often are bile acids recycled in the body on average?
Which of the following best describes the role of LDL-C in the development of dyslipidemia?
Which of the following best describes the role of LDL-C in the development of dyslipidemia?
Why is dyslipidemia considered a major health concern?
Why is dyslipidemia considered a major health concern?
What is the difference between primary and secondary dyslipidemia?
What is the difference between primary and secondary dyslipidemia?
What is the primary mechanism by which the ammonium cations function in bile acid sequestrants?
What is the primary mechanism by which the ammonium cations function in bile acid sequestrants?
What significant side effects are associated with the use of bile acid sequestrants?
What significant side effects are associated with the use of bile acid sequestrants?
Why was a new cholestyramine formulation developed?
Why was a new cholestyramine formulation developed?
What do anion-exchange resins contain that allows them to bind bile acids?
What do anion-exchange resins contain that allows them to bind bile acids?
What is the appropriate method to take the powder form of bile acid sequestrants?
What is the appropriate method to take the powder form of bile acid sequestrants?
What is the primary function of apolipoproteins in lipoproteins?
What is the primary function of apolipoproteins in lipoproteins?
Which characteristic distinguishes high density lipoproteins from low density lipoproteins?
Which characteristic distinguishes high density lipoproteins from low density lipoproteins?
How are lipoproteins structured to enable lipids to dissolve in blood?
How are lipoproteins structured to enable lipids to dissolve in blood?
What kind of structural feature do apolipoproteins possess?
What kind of structural feature do apolipoproteins possess?
What is the role of free cholesterol within the lipoprotein structure?
What is the role of free cholesterol within the lipoprotein structure?
In which location are apolipoproteins primarily produced?
In which location are apolipoproteins primarily produced?
What factor primarily determines the density class of a lipoprotein?
What factor primarily determines the density class of a lipoprotein?
How do lipid-soluble vitamins relate to lipoprotein transport?
How do lipid-soluble vitamins relate to lipoprotein transport?
What is the primary structural difference between integral and peripheral apolipoproteins?
What is the primary structural difference between integral and peripheral apolipoproteins?
What is the primary function of VLDL in the body?
What is the primary function of VLDL in the body?
What percentage of triglycerides in VLDL is typically found in chylomicrons?
What percentage of triglycerides in VLDL is typically found in chylomicrons?
Which apolipoprotein is responsible for the activation of hepatic lipase and lipoprotein lipase?
Which apolipoprotein is responsible for the activation of hepatic lipase and lipoprotein lipase?
What stimulates the production of VLDL in the liver?
What stimulates the production of VLDL in the liver?
What role does ApoB play in the function of lipoproteins?
What role does ApoB play in the function of lipoproteins?
Which of the following describes the composition of VLDL compared to chylomicrons?
Which of the following describes the composition of VLDL compared to chylomicrons?
What is lipogenesis and how is it regulated?
What is lipogenesis and how is it regulated?
How are chylomicrons converted to chylomicron remnants?
How are chylomicrons converted to chylomicron remnants?
What is the main source of free fatty acids that stimulate VLDL production?
What is the main source of free fatty acids that stimulate VLDL production?
Which of the following receptors is NOT involved in the clearance of chylomicron remnants?
Which of the following receptors is NOT involved in the clearance of chylomicron remnants?
A patient presents with a 10-year ASCVD risk of 6%. Based on the 2018 AHA/ACC Cholesterol Guideline, which of these treatment options is MOST appropriate?
A patient presents with a 10-year ASCVD risk of 6%. Based on the 2018 AHA/ACC Cholesterol Guideline, which of these treatment options is MOST appropriate?
A patient is diagnosed with diabetes and has an LDL-C level of 160 mg/dL. They are 55 years old. What is the MOST appropriate statin therapy based on the 2018 AHA/ACC Cholesterol Guideline?
A patient is diagnosed with diabetes and has an LDL-C level of 160 mg/dL. They are 55 years old. What is the MOST appropriate statin therapy based on the 2018 AHA/ACC Cholesterol Guideline?
A patient with Clinical ASCVD has an LDL-C level of 100 mg/dL. Which type of statin therapy would be MOST appropriate for this patient?
A patient with Clinical ASCVD has an LDL-C level of 100 mg/dL. Which type of statin therapy would be MOST appropriate for this patient?
A patient with an LDL-C level of 200 mg/dL has no known history of ASCVD. Which of the following is MOST appropriate?
A patient with an LDL-C level of 200 mg/dL has no known history of ASCVD. Which of the following is MOST appropriate?
Which of the following lipid-lowering medications would be MOST effective in reducing LDL-C by 50% or more?
Which of the following lipid-lowering medications would be MOST effective in reducing LDL-C by 50% or more?
A patient is taking a moderate-intensity statin, and their LDL-C level has decreased to 110 mg/dL. Which of the following is the MOST appropriate next step in management?
A patient is taking a moderate-intensity statin, and their LDL-C level has decreased to 110 mg/dL. Which of the following is the MOST appropriate next step in management?
Which of the following is a PRIMARY reason for treating patients with dyslipidemia?
Which of the following is a PRIMARY reason for treating patients with dyslipidemia?
A patient is diagnosed with dyslipidemia and has an LDL-C level of 160 mg/dL. They are 35 years old and have no known history of ASCVD. Which of the following statements is MOST accurate?
A patient is diagnosed with dyslipidemia and has an LDL-C level of 160 mg/dL. They are 35 years old and have no known history of ASCVD. Which of the following statements is MOST accurate?
A patient has a family history of premature coronary heart disease. Which of the following is MOST appropriate for this patient?
A patient has a family history of premature coronary heart disease. Which of the following is MOST appropriate for this patient?
Which of these is NOT a common form of ASCVD?
Which of these is NOT a common form of ASCVD?
What is the primary mechanism by which bempedoic acid lowers LDL-C levels?
What is the primary mechanism by which bempedoic acid lowers LDL-C levels?
What is a major adverse effect associated with sustained-release niacin formulations?
What is a major adverse effect associated with sustained-release niacin formulations?
Which formulation of niacin is preferred for minimizing flushing while managing dyslipidemia?
Which formulation of niacin is preferred for minimizing flushing while managing dyslipidemia?
What differentiates phase II drug metabolism from phase I drug metabolism?
What differentiates phase II drug metabolism from phase I drug metabolism?
In patients with ASCVD, what is the primary goal of secondary prevention strategies?
In patients with ASCVD, what is the primary goal of secondary prevention strategies?
What is a key characteristic difference between PCSK9 monoclonal antibodies and siRNA therapy?
What is a key characteristic difference between PCSK9 monoclonal antibodies and siRNA therapy?
Which of the following is a contraindication for the use of fibrates in treatment?
Which of the following is a contraindication for the use of fibrates in treatment?
What effect do PCSK9 inhibitors have on LDL receptors?
What effect do PCSK9 inhibitors have on LDL receptors?
Which dietary factor can increase the risk of statin-related adverse effects?
Which dietary factor can increase the risk of statin-related adverse effects?
A patient with hypertriglyceridemia is prescribed a statin. Which of the following statins would be the most appropriate choice based on its metabolism profile?
A patient with hypertriglyceridemia is prescribed a statin. Which of the following statins would be the most appropriate choice based on its metabolism profile?
A patient taking a statin experiences muscle pain and weakness. Which of the following factors could contribute to this side effect?
A patient taking a statin experiences muscle pain and weakness. Which of the following factors could contribute to this side effect?
A patient with familial hypercholesterolemia is prescribed a bile acid sequestrant. Which of the following mechanisms explains how this medication lowers LDL-C levels?
A patient with familial hypercholesterolemia is prescribed a bile acid sequestrant. Which of the following mechanisms explains how this medication lowers LDL-C levels?
A patient with severe hypertriglyceridemia is found to have triglycerides > 400 mg/dL. Which of the following statements is TRUE regarding the use of the Friedewald equation to estimate LDL-C in this patient?
A patient with severe hypertriglyceridemia is found to have triglycerides > 400 mg/dL. Which of the following statements is TRUE regarding the use of the Friedewald equation to estimate LDL-C in this patient?
A patient is prescribed lovastatin for hypercholesterolemia. What is the primary reason for the significant difference in bioavailability between lovastatin and rosuvastatin?
A patient is prescribed lovastatin for hypercholesterolemia. What is the primary reason for the significant difference in bioavailability between lovastatin and rosuvastatin?
Which of the following statements accurately describes the function of fenofibrate in the treatment of dyslipidemia?
Which of the following statements accurately describes the function of fenofibrate in the treatment of dyslipidemia?
Which of the following drugs is likely to increase plasma statin levels when co-administered with a statin medication?
Which of the following drugs is likely to increase plasma statin levels when co-administered with a statin medication?
A patient is taking a statin medication and reports experiencing muscle pain. Which of the following would be the most appropriate action for the healthcare provider?
A patient is taking a statin medication and reports experiencing muscle pain. Which of the following would be the most appropriate action for the healthcare provider?
Which of the following statements best explains why bile acid sequestrants are often used in combination with other lipid-lowering medications?
Which of the following statements best explains why bile acid sequestrants are often used in combination with other lipid-lowering medications?
A patient is prescribed a statin medication for primary prevention of cardiovascular disease. What is the primary rationale for this prescription?
A patient is prescribed a statin medication for primary prevention of cardiovascular disease. What is the primary rationale for this prescription?
What is the primary function of apoA1 in the context of HDL?
What is the primary function of apoA1 in the context of HDL?
Which process describes the removal of IDL particles from the blood?
Which process describes the removal of IDL particles from the blood?
What is the primary role of CETP in lipid metabolism?
What is the primary role of CETP in lipid metabolism?
Which lipoproteins are directly associated with apoB?
Which lipoproteins are directly associated with apoB?
What condition can lead to secondary dyslipidemia?
What condition can lead to secondary dyslipidemia?
What is the location for bile acid secretion in the gastrointestinal tract?
What is the location for bile acid secretion in the gastrointestinal tract?
What role does lipoprotein lipase play in lipid metabolism?
What role does lipoprotein lipase play in lipid metabolism?
What substance is directly formed from HMG-CoA as a result of HMG-CoA reductase activity?
What substance is directly formed from HMG-CoA as a result of HMG-CoA reductase activity?
How are fatty acids transported in the blood apart from being in lipoproteins?
How are fatty acids transported in the blood apart from being in lipoproteins?
What is the role of enterocytes in lipid absorption?
What is the role of enterocytes in lipid absorption?
A patient presents with elevated triglyceride levels and is at risk for pancreatitis. Which of the following conditions is MOST likely contributing to this risk?
A patient presents with elevated triglyceride levels and is at risk for pancreatitis. Which of the following conditions is MOST likely contributing to this risk?
A patient with a history of hyperlipidemia is prescribed a statin medication. What is the PRIMARY mechanism by which this medication reduces LDL cholesterol levels?
A patient with a history of hyperlipidemia is prescribed a statin medication. What is the PRIMARY mechanism by which this medication reduces LDL cholesterol levels?
A patient is diagnosed with corneal arcus. Which of the following lipid abnormalities is MOST likely associated with this condition?
A patient is diagnosed with corneal arcus. Which of the following lipid abnormalities is MOST likely associated with this condition?
A patient presents with symptoms of claudication and leg pain during exercise. Which of the following conditions is MOST likely associated with these symptoms?
A patient presents with symptoms of claudication and leg pain during exercise. Which of the following conditions is MOST likely associated with these symptoms?
A patient with a history of hyperlipidemia is found to have a genetic predisposition to the condition. Which of the following factors is MOST likely responsible for this predisposition?
A patient with a history of hyperlipidemia is found to have a genetic predisposition to the condition. Which of the following factors is MOST likely responsible for this predisposition?
A physician is evaluating a patient with hyperlipidemia and is considering treatment options. Which of the following statin medications would be considered a HIGH-INTENSITY statin?
A physician is evaluating a patient with hyperlipidemia and is considering treatment options. Which of the following statin medications would be considered a HIGH-INTENSITY statin?
A patient with dyslipidemia is prescribed a medication that inhibits the absorption of cholesterol in the small intestine. Which of the following medication classes is this medication likely to belong to?
A patient with dyslipidemia is prescribed a medication that inhibits the absorption of cholesterol in the small intestine. Which of the following medication classes is this medication likely to belong to?
A patient is diagnosed with hyperlipidemia and is prescribed a combination therapy of a statin and a fibrate. Which of the following is a POTENTIAL CONCERN associated with this combination?
A patient is diagnosed with hyperlipidemia and is prescribed a combination therapy of a statin and a fibrate. Which of the following is a POTENTIAL CONCERN associated with this combination?
A patient with hyperlipidemia is experiencing abdominal pain and discomfort. Which of the following conditions, associated with hyperlipidemia, is MOST likely contributing to these symptoms?
A patient with hyperlipidemia is experiencing abdominal pain and discomfort. Which of the following conditions, associated with hyperlipidemia, is MOST likely contributing to these symptoms?
A patient with a history of hyperlipidemia is being monitored for the development of atherosclerotic cardiovascular disease (ASCVD). Which of the following conditions is a MAJOR risk factor for ASCVD?
A patient with a history of hyperlipidemia is being monitored for the development of atherosclerotic cardiovascular disease (ASCVD). Which of the following conditions is a MAJOR risk factor for ASCVD?
What is the primary function of lipoprotein lipase (LPL) in lipoprotein metabolism?
What is the primary function of lipoprotein lipase (LPL) in lipoprotein metabolism?
Which of the following statements accurately describes the role of chylomicron remnants in lipoprotein metabolism?
Which of the following statements accurately describes the role of chylomicron remnants in lipoprotein metabolism?
What is the primary mechanism by which high-density lipoproteins (HDL) contribute to reducing the risk of atherosclerosis?
What is the primary mechanism by which high-density lipoproteins (HDL) contribute to reducing the risk of atherosclerosis?
Which of the following lipoprotein classes is primarily responsible for transporting triglycerides from the liver to peripheral tissues?
Which of the following lipoprotein classes is primarily responsible for transporting triglycerides from the liver to peripheral tissues?
Which of the following statements accurately describes the relationship between LDL cholesterol and atherosclerosis?
Which of the following statements accurately describes the relationship between LDL cholesterol and atherosclerosis?
Which of the following is a key difference between chylomicrons and very-low-density lipoproteins (VLDLs)?
Which of the following is a key difference between chylomicrons and very-low-density lipoproteins (VLDLs)?
What is the primary mechanism by which the liver regulates cholesterol levels in the blood?
What is the primary mechanism by which the liver regulates cholesterol levels in the blood?
Which of the following accurately describes the process of foam cell formation in atherosclerosis?
Which of the following accurately describes the process of foam cell formation in atherosclerosis?
Which of the following lipoprotein classes is most closely associated with high triglyceride levels in the blood?
Which of the following lipoprotein classes is most closely associated with high triglyceride levels in the blood?
What is the primary function of HMG-CoA Reductase in cholesterol metabolism?
What is the primary function of HMG-CoA Reductase in cholesterol metabolism?
Which enzyme is inhibited by PCSK9, leading to reduced LDL receptor availability?
Which enzyme is inhibited by PCSK9, leading to reduced LDL receptor availability?
What role does Lecithin-Cholesterol Acyltransferase (LCAT) play in lipid metabolism?
What role does Lecithin-Cholesterol Acyltransferase (LCAT) play in lipid metabolism?
Which of the following best describes the role of ATP-Binding Cassette Transporter A1 (ABCA1)?
Which of the following best describes the role of ATP-Binding Cassette Transporter A1 (ABCA1)?
How does lipoprotein lipase (LPL) function in lipid metabolism?
How does lipoprotein lipase (LPL) function in lipid metabolism?
In which scenario would high-intensity statins be recommended according to ASCVD guidelines?
In which scenario would high-intensity statins be recommended according to ASCVD guidelines?
What is the effect of activating ApoC-II on lipoprotein metabolism?
What is the effect of activating ApoC-II on lipoprotein metabolism?
What describes the action of Cholesteryl Ester Transfer Protein (CETP)?
What describes the action of Cholesteryl Ester Transfer Protein (CETP)?
Which enzyme plays a crucial role in the hydrolysis of triglycerides in VLDL?
Which enzyme plays a crucial role in the hydrolysis of triglycerides in VLDL?
What is the role of Cholesterol 7α-Hydroxylase (CYP7A1) in lipid metabolism?
What is the role of Cholesterol 7α-Hydroxylase (CYP7A1) in lipid metabolism?
How does Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) affect LDL receptors?
How does Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) affect LDL receptors?
What is the activation mechanism of Lipoprotein Lipase (LPL)?
What is the activation mechanism of Lipoprotein Lipase (LPL)?
Which receptor facilitates the hepatic uptake of apoE-containing lipoproteins?
Which receptor facilitates the hepatic uptake of apoE-containing lipoproteins?
In the context of managing dyslipidemia, what is the goal for LDL-C reduction in primary prevention?
In the context of managing dyslipidemia, what is the goal for LDL-C reduction in primary prevention?
What is one of the key clinical targets of statins in dyslipidemia management?
What is one of the key clinical targets of statins in dyslipidemia management?
What does the ATP-Binding Cassette Transporter A1 (ABCA1) do in lipid metabolism?
What does the ATP-Binding Cassette Transporter A1 (ABCA1) do in lipid metabolism?
Which enzyme is involved in the transfer of cholesteryl esters between lipoproteins?
Which enzyme is involved in the transfer of cholesteryl esters between lipoproteins?
What is the primary function of HMG-CoA reductase in cholesterol biosynthesis?
What is the primary function of HMG-CoA reductase in cholesterol biosynthesis?
Which of the following enzymes is primarily activated by apoC-II?
Which of the following enzymes is primarily activated by apoC-II?
What is the role of Scavenger Receptor Class B Type I (SR-B1) in lipid metabolism?
What is the role of Scavenger Receptor Class B Type I (SR-B1) in lipid metabolism?
Which enzyme is involved in the synthesis of bile acids from cholesterol in the liver?
Which enzyme is involved in the synthesis of bile acids from cholesterol in the liver?
According to ASCVD guidelines for primary prevention, which statin regimen is recommended for patients with high risk?
According to ASCVD guidelines for primary prevention, which statin regimen is recommended for patients with high risk?
What is the primary action of Lecithin-Cholesterol Acyltransferase (LCAT)?
What is the primary action of Lecithin-Cholesterol Acyltransferase (LCAT)?
What clinical target has been associated with the enzyme HMG-CoA reductase?
What clinical target has been associated with the enzyme HMG-CoA reductase?
Which receptor primarily mediates the cellular uptake of LDL particles?
Which receptor primarily mediates the cellular uptake of LDL particles?
What is the function of Acyl Coenzyme A: Cholesterol Acyltransferase (ACAT)?
What is the function of Acyl Coenzyme A: Cholesterol Acyltransferase (ACAT)?
Which lipid-altering medication is least likely to affect triglyceride levels significantly?
Which lipid-altering medication is least likely to affect triglyceride levels significantly?
A patient experiences a moderate reduction in LDL, a slight increase in HDL, and a significant reduction in triglycerides. Which agent is most likely responsible for these changes?
A patient experiences a moderate reduction in LDL, a slight increase in HDL, and a significant reduction in triglycerides. Which agent is most likely responsible for these changes?
Which dyslipidemia treatment option primarily reduces LDL by enhancing LDL receptor recycling?
Which dyslipidemia treatment option primarily reduces LDL by enhancing LDL receptor recycling?
Which lipid profile change is most indicative of Niacin treatment?
Which lipid profile change is most indicative of Niacin treatment?
Which drug class is associated with the most substantial reduction in triglycerides?
Which drug class is associated with the most substantial reduction in triglycerides?
How do omega-3 fatty acids primarily affect lipid levels?
How do omega-3 fatty acids primarily affect lipid levels?
Which medication has a mechanism of action that directly affects cholesterol absorption in the intestines?
Which medication has a mechanism of action that directly affects cholesterol absorption in the intestines?
A patient taking a lipid-lowering medication experiences a 17% reduction in LDL, a 6% reduction in HDL, and no change in triglycerides. Which medication are they most likely taking?
A patient taking a lipid-lowering medication experiences a 17% reduction in LDL, a 6% reduction in HDL, and no change in triglycerides. Which medication are they most likely taking?
Which drug class inhibits cholesterol synthesis in the liver, consequently upregulating LDL receptors?
Which drug class inhibits cholesterol synthesis in the liver, consequently upregulating LDL receptors?
A patient's lipid panel shows a 50% reduction in LDL, a 10% increase in HDL, and a 20% reduction in triglycerides. Which agent is most likely responsible for this profile?
A patient's lipid panel shows a 50% reduction in LDL, a 10% increase in HDL, and a 20% reduction in triglycerides. Which agent is most likely responsible for this profile?
Flashcards
Dyslipidemia
Dyslipidemia
A condition where lipid levels in the blood are abnormal, leading to an increased risk of heart disease. It can be primary, meaning it's caused by genetics, or secondary, meaning it's caused by other factors like medications, diet, or health conditions.
Secondary Dyslipidemia
Secondary Dyslipidemia
Caused by factors outside the body, such as medications, diseases like diabetes, and certain lifestyle choices.
Atherosclerosis
Atherosclerosis
A process that involves the buildup of plaque within the arteries. It starts with damage to the artery wall, leading to inflammation and the accumulation of LDL cholesterol, immune cells, and other substances. This plaque hardens and narrows the arteries, disrupting blood flow and increasing the risk of heart attack or stroke.
HMG-CoA Reductase Inhibitors (Statins)
HMG-CoA Reductase Inhibitors (Statins)
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Fibrates
Fibrates
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Bile Acid Sequestrants
Bile Acid Sequestrants
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Cholesterol Absorption Inhibitors
Cholesterol Absorption Inhibitors
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Lipoproteins
Lipoproteins
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Lipoprotein structure
Lipoprotein structure
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Apolipoproteins (apo)
Apolipoproteins (apo)
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Cholesteryl ester synthesis
Cholesteryl ester synthesis
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Chylomicron
Chylomicron
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TG into chylomicron
TG into chylomicron
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Lipoprotein density
Lipoprotein density
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Low-density lipoprotein (LDL)
Low-density lipoprotein (LDL)
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High-density lipoprotein (HDL)
High-density lipoprotein (HDL)
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Bile acids: Synthesis and Storage
Bile acids: Synthesis and Storage
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Bile Acids: Ionization
Bile Acids: Ionization
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Cholesterol Secretion and Excretion
Cholesterol Secretion and Excretion
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Bile Acid Reabsorption
Bile Acid Reabsorption
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Bile Acid Recycling
Bile Acid Recycling
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Bile Acid Recycling Rate
Bile Acid Recycling Rate
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Secondary Bile Acid Formation
Secondary Bile Acid Formation
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Secondary Bile Acid Solubility
Secondary Bile Acid Solubility
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Dyslipidemia: Definition
Dyslipidemia: Definition
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Dyslipidemia: Types
Dyslipidemia: Types
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What are VLDLs?
What are VLDLs?
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How do chylomicrons differ from VLDLs?
How do chylomicrons differ from VLDLs?
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What is the role of LPL?
What is the role of LPL?
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What happens to chylomicrons after LPL action?
What happens to chylomicrons after LPL action?
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What type of triglycerides do VLDLs transport?
What type of triglycerides do VLDLs transport?
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What happens to the free fatty acids released from VLDL?
What happens to the free fatty acids released from VLDL?
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What stimulates VLDL production?
What stimulates VLDL production?
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What apolipoproteins are found in VLDL?
What apolipoproteins are found in VLDL?
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How does VLDL cholesterol content differ from chylomicrons?
How does VLDL cholesterol content differ from chylomicrons?
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What is the role of hepatic lipase in VLDL metabolism?
What is the role of hepatic lipase in VLDL metabolism?
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What are bile acid sequestrants (BASs)?
What are bile acid sequestrants (BASs)?
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How do BASs work as anion-exchange resins?
How do BASs work as anion-exchange resins?
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What is the mechanism of action for BASs in lowering cholesterol?
What is the mechanism of action for BASs in lowering cholesterol?
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What are some challenges and solutions for using BASs?
What are some challenges and solutions for using BASs?
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How are BASs typically administered?
How are BASs typically administered?
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Atherosclerotic Cardiovascular Disease (ASCVD)
Atherosclerotic Cardiovascular Disease (ASCVD)
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Statins
Statins
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High-intensity statin therapy
High-intensity statin therapy
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Moderate-intensity statin therapy
Moderate-intensity statin therapy
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Patients with Clinical ASCVD
Patients with Clinical ASCVD
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Patients with LDL-C ≥ 190 mg/dL
Patients with LDL-C ≥ 190 mg/dL
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Patients aged 40-75 with diabetes
Patients aged 40-75 with diabetes
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Patients aged 40-75 with elevated LDL-C and high ASCVD risk
Patients aged 40-75 with elevated LDL-C and high ASCVD risk
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Primary goal of treating dyslipidemia
Primary goal of treating dyslipidemia
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What is the Friedewald Equation used for?
What is the Friedewald Equation used for?
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What is first-pass metabolism?
What is first-pass metabolism?
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How are statins broken down?
How are statins broken down?
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How do statins leave the body?
How do statins leave the body?
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What's special about lovastatin and simvastatin?
What's special about lovastatin and simvastatin?
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How do bile acid sequestrants work?
How do bile acid sequestrants work?
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What is the mechanism of action for bile acid sequestrants?
What is the mechanism of action for bile acid sequestrants?
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What challenges do bile acid sequestrants face?
What challenges do bile acid sequestrants face?
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How are bile acid sequestrants typically administered?
How are bile acid sequestrants typically administered?
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What is the difference between nicotinic acid and nicotinamide?
What is the difference between nicotinic acid and nicotinamide?
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Explain the different formulations of niacin and their clinical impact.
Explain the different formulations of niacin and their clinical impact.
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What are the main adverse events associated with Niacin, and how do different formulations affect them?
What are the main adverse events associated with Niacin, and how do different formulations affect them?
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What are the active components of fish oil and their effects on lipid profiles?
What are the active components of fish oil and their effects on lipid profiles?
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What are the FDA-approved indications for PCSK9 inhibitors?
What are the FDA-approved indications for PCSK9 inhibitors?
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Compare and contrast the mechanisms of action and clinical impact between PCSK9 mAbs and siRNA therapy.
Compare and contrast the mechanisms of action and clinical impact between PCSK9 mAbs and siRNA therapy.
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Compare the mechanisms of action of bempedoic acid and statins.
Compare the mechanisms of action of bempedoic acid and statins.
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Compare and contrast the clinical impact of bempedoic acid and statins.
Compare and contrast the clinical impact of bempedoic acid and statins.
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Explain the differences between phase I and phase II drug metabolism pathways.
Explain the differences between phase I and phase II drug metabolism pathways.
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Describe the drug metabolism profiles of common dyslipidemia medications.
Describe the drug metabolism profiles of common dyslipidemia medications.
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What is a chylomicron?
What is a chylomicron?
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What is apoE-mediated receptor endocytosis?
What is apoE-mediated receptor endocytosis?
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What are the enzymes involved in intracellular vesicle processing?
What are the enzymes involved in intracellular vesicle processing?
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What is apoA1?
What is apoA1?
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What is apoB-mediated receptor endocytosis?
What is apoB-mediated receptor endocytosis?
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What is IDL?
What is IDL?
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What is HDL?
What is HDL?
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What is apoCII?
What is apoCII?
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What is apoCIII?
What is apoCIII?
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What is CETP?
What is CETP?
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Xanthomas
Xanthomas
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Xanthelasma
Xanthelasma
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Corneal Arcus
Corneal Arcus
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Hepatic Steatosis
Hepatic Steatosis
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Pancreatitis
Pancreatitis
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What is cholesterol?
What is cholesterol?
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What are lipoproteins?
What are lipoproteins?
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What is LDL (low-density lipoprotein)?
What is LDL (low-density lipoprotein)?
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What is HDL (high-density lipoprotein)?
What is HDL (high-density lipoprotein)?
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What is hyperlipidemia?
What is hyperlipidemia?
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What is lipoprotein lipase (LPL)?
What is lipoprotein lipase (LPL)?
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What is VLDL (very-low-density lipoprotein)?
What is VLDL (very-low-density lipoprotein)?
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What is atherosclerosis?
What is atherosclerosis?
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What are chylomicrons?
What are chylomicrons?
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What are statins?
What are statins?
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What is the function of HMG-CoA reductase?
What is the function of HMG-CoA reductase?
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What does lipoprotein lipase (LPL) do?
What does lipoprotein lipase (LPL) do?
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What is the function of cholesterol 7α-hydroxylase (CYP7A1)?
What is the function of cholesterol 7α-hydroxylase (CYP7A1)?
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How does the LDL receptor work?
How does the LDL receptor work?
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What is the role of the Scavenger Receptor Class B Type I (SR-B1)?
What is the role of the Scavenger Receptor Class B Type I (SR-B1)?
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How to assess ASCVD risk in primary prevention?
How to assess ASCVD risk in primary prevention?
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What is the recommendation for secondary ASCVD prevention?
What is the recommendation for secondary ASCVD prevention?
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Study Notes
Dyslipidemia Part 1 Learning Objectives
- Describe the incidence and impact of CVD in the US, including current trends in event and death rates.
- Detail the steps in triglyceride and cholesterol digestion and absorption.
- Define the differences between cholesterol and cholesteryl esters.
- Define a lipoprotein, describing the role of each component in a lipoprotein particle.
- Differentiate between the major lipoprotein groups—chylomicrons, chylomicron remnants, VLDL, IDL, LDL, and HDL.
- Identify the major apolipoproteins and lipids associated with each lipoprotein, their biological role, and metabolic fates.
- Detail the liver's role in lipid transport and metabolism, including apoE- and apoB-mediated receptor endocytosis.
- Describe the reverse cholesterol transport pathway and the role of cholesteryl ester transfer protein in cholesterol transport from HDL.
- Explain cholesterol acquisition by the body.
- Summarize the biochemical steps for cholesterol synthesis, highlighting HMG-CoA reductase's role.
- Define the roles of apoAl, apoB, apoCII, apoCIII, and apoE in lipoproteins.
- Describe cholesterol transport in the blood and excretion from the body.
- Outline bile acid synthesis, structure, and function.
- Differentiate between hypercholesterolemia, hypertriglyceridemia, and combined hypercholesterolemia and hypertriglyceridemia.
- Explain the difference between primary and secondary dyslipidemia.
- Identify common causes of secondary dyslipidemia.
- Summarize the steps involved in atherosclerosis formation, identifying the role of LDL-C in the process.
- Describe how dyslipidemia medications affect TG and cholesterol synthesis or absorption by various mechanisms.
- Describe how dyslipidemia medications change LDL-C, HDL-C and TG levels.
- Identify the pharmacologic classification of various dyslipidemia medications.
- Describe the general effects of various dyslipidemia medications on LDL-C, HDL-C, and TG.
Dyslipidemia Rat 2 Learning Objectives
- Calculate LDL-C using the Friedewald equation, and when the equation is not valid.
- Describe first-pass metabolism, its impact on oral bioavailability of HMG-CoA reductase inhibitors, and their metabolism/excretion pathways.
- Detail the bioactivation of lovastatin, simvastatin, and fenofibrate.
- Describe the anion-exchange process in bile acid sequestrants and bile acids.
- Differentiate between nicotinic acid and nicotinamide.
- Describe the metabolism of various formulations of niacin.
- Identify two active components of fish oil for dyslipidemia management (EPA and DHA).
- Summarize FDA-approved indications for PCSK9 inhibitors (reducing cardiovascular events in patients with established CVD or DM with additional CVD risk factors, and as adjunctive therapy for primary hyperlipidemia, including heterozygous familial hypercholesterolemia).
- Discuss similarities/differences in mechanisms and effects of PCSK9 mAbs and PCSK9 siRNA therapy (siRNA targets and degrades mRNA for PCSK9, while monoclonal antibodies bind and inhibit PCSK9 activity).
- Compare/contrast the mechanisms and effects of bempedoic acid and statins (bempedoic acid inhibits ATP-citrate lyase, thus reducing cholesterol synthesis).
- Describe drug metabolism profiles of dyslipidemia drugs (including CYP450 interactions, and potential for drug-drug interactions).
- Identify contraindications for dyslipidemia medications (include liver and kidney disease, pregnancy).
- Identify drug-drug/food/disease interactions involving dyslipidemia medications.
- Differentiate between primary and secondary prevention of ASCVD (primary prevention focuses on patients who have never had a cardiovascular event, while secondary prevention focuses on those who have already).
- Identify and describe clinical forms of ASCVD (coronary artery disease, angina, myocardial infarction, acute coronary syndrome, cerebrovascular disease, transient ischemic attack, peripheral artery disease, and abdominal aortic aneurysm).
- Identify the primary goal for treating patients with dyslipidemia (prevent ASCVD, and modify lipoprotein concentrations based on individual risk).
- Describe the relationship between LDL-C and ASCVD (higher LDL-C increases risk).
- Describe 4 patient management groups that benefit from lipid-altering therapy (secondary ASCVD prevention, severe hypercholesterolemia, diabetes mellitus, and primary prevention).
- Describe low-, moderate-, and high-intensity statin therapy (LDL-C reduction ≥50% [high], 30-49% [moderate], <30% [low]).
- Classify a given statin/dosage according to intensity.
- Describe the system utilized to grade recommendations based on strength & evidence (ACC/AHA Cholesterol Guideline).
- Describe recommended treatment/intensity for secondary prevention and additional therapies to reduce ASCVD outcomes.
- Explain the evidence-based approach to treat severe hypercholesterolemia .
- Explain the recommended treatment for patients with diabetes and personalization of therapy based on age, 10-year ASCVD risk, and diabetes risk enhancers (consider 10-year risk and risk-enhancing factors, and use either moderate or high-intensity statins).
- List risk factors used in the Pooled Cohort Equations to estimate 10-year ASCVD risk.
- Calculate 10-year ASCVD risk.
- Classify patients into appropriate risk categories based on 10-year ASCVD risk in primary prevention (low, borderline, intermediate, high).
- Explain limitations of the Pooled Cohort Equations for ASCVD risk assessment (age is a strong population risk factor, but does not necessarily reflect every individual patient's risk).
- Analyze why statins are first-line therapy for dyslipidemia, identifying other medications with evidence to reduce ASCVD risk, and
- Recommend treatment for patients with varying severities of hypertriglyceridemia (consider lifestyle modifications first, statins as primary, fibrates or omega-3s for very high TG levels).
- Create a plan to monitor effectiveness and adverse effects of lipid-lowering medications (regular lipid panels, liver function tests, creatine kinase monitoring for muscle effects, blood glucose for diabetes risks).
- Include specific considerations for specific populations regarding dyslipidemia management (e.g., children, pregnant women, older adults, those with kidney or liver disease, or those with other comorbidities, and ethnic groups).
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Description
This quiz explores various pharmacologic classes of dyslipidemia medications, focusing on their mechanisms, actions, and potential drawbacks. Test your knowledge on cholesterol absorption inhibitors, fibrates, statins, and combination therapies for effective dyslipidemia management.
