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Questions and Answers
What role does lecithin: cholesterol acyltransferase (LCAT) play in the metabolism of cholesterol?
What role does lecithin: cholesterol acyltransferase (LCAT) play in the metabolism of cholesterol?
Which class of drugs is primarily used for reducing cholesterol synthesis in the liver?
Which class of drugs is primarily used for reducing cholesterol synthesis in the liver?
What classification do hyperlipoproteinaemias associated with diabetes and nephrotic syndrome fall under?
What classification do hyperlipoproteinaemias associated with diabetes and nephrotic syndrome fall under?
What is the primary consequence of excessive lipoprotein degradation in the body?
What is the primary consequence of excessive lipoprotein degradation in the body?
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Which type of hyperlipoproteinaemia can arise due to a single genetic defect?
Which type of hyperlipoproteinaemia can arise due to a single genetic defect?
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Which of the following drugs acts as a lipolysis and triglyceride synthesis inhibitor?
Which of the following drugs acts as a lipolysis and triglyceride synthesis inhibitor?
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Which lipoproteins are primarily associated with atherogenic risk when elevated?
Which lipoproteins are primarily associated with atherogenic risk when elevated?
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How does HDL contribute to cardiovascular health?
How does HDL contribute to cardiovascular health?
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What is the primary mechanism through which nicotinic acid reduces VLDL production in the liver?
What is the primary mechanism through which nicotinic acid reduces VLDL production in the liver?
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Which of the following is a known adverse effect of nicotinic acid when taken in large doses?
Which of the following is a known adverse effect of nicotinic acid when taken in large doses?
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Why is nicotinic acid contraindicated during pregnancy?
Why is nicotinic acid contraindicated during pregnancy?
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Which drug is most effective in reducing plasma triglyceride (TG) levels?
Which drug is most effective in reducing plasma triglyceride (TG) levels?
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What is the recommended starting dose of nicotinic acid?
What is the recommended starting dose of nicotinic acid?
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How does nicotinic acid primarily affect lipoprotein Lp (a)?
How does nicotinic acid primarily affect lipoprotein Lp (a)?
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Which patient condition presents a risk of postural hypotension when nicotinic acid is taken?
Which patient condition presents a risk of postural hypotension when nicotinic acid is taken?
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What is the effect of nicotinic acid on cholesterol levels?
What is the effect of nicotinic acid on cholesterol levels?
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What type of hyperlipoproteinaemia is characterized by a deficiency of lipoprotein lipase?
What type of hyperlipoproteinaemia is characterized by a deficiency of lipoprotein lipase?
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Which of the following types of hyperlipoproteinaemia is the most common?
Which of the following types of hyperlipoproteinaemia is the most common?
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In which disorder are IDL and chylomicron remnants elevated?
In which disorder are IDL and chylomicron remnants elevated?
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What is the main carrier of plasma cholesterol?
What is the main carrier of plasma cholesterol?
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What factor primarily causes Type IV hyperlipidaemia?
What factor primarily causes Type IV hyperlipidaemia?
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In familial hypercholesterolaemia, what is the primary issue affecting LDL uptake?
In familial hypercholesterolaemia, what is the primary issue affecting LDL uptake?
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Which of the following plasma lipid components does NOT have an elevated level in Type IIa hypercholesterolaemia?
Which of the following plasma lipid components does NOT have an elevated level in Type IIa hypercholesterolaemia?
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What is the most notable side effect of statins?
What is the most notable side effect of statins?
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What is the average half-life (t½) of atorvastatin compared to other statins?
What is the average half-life (t½) of atorvastatin compared to other statins?
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Which type of hyperlipoproteinaemia is classified as 'very rare'?
Which type of hyperlipoproteinaemia is classified as 'very rare'?
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Which statin is known to be hydrophilic?
Which statin is known to be hydrophilic?
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What is the maximum daily dose of atorvastatin?
What is the maximum daily dose of atorvastatin?
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Which condition is contraindicated for statin use?
Which condition is contraindicated for statin use?
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What concurrent medication is indicated to have the least interaction with statins?
What concurrent medication is indicated to have the least interaction with statins?
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What is the main mechanism that causes muscle-related adverse effects with statins?
What is the main mechanism that causes muscle-related adverse effects with statins?
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What is a notable characteristic of pravastatin at low doses?
What is a notable characteristic of pravastatin at low doses?
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What is the primary route of excretion for gemfibrozil?
What is the primary route of excretion for gemfibrozil?
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Which of the following is NOT a common side effect of gemfibrozil?
Which of the following is NOT a common side effect of gemfibrozil?
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Which of the following statements about fenofibrate is correct?
Which of the following statements about fenofibrate is correct?
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What dosage of gemfibrozil is recommended for patients with markedly raised triglyceride levels?
What dosage of gemfibrozil is recommended for patients with markedly raised triglyceride levels?
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Gemfibrozil is contraindicated in which of the following conditions?
Gemfibrozil is contraindicated in which of the following conditions?
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What effect does the combination of gemfibrozil with a statin have?
What effect does the combination of gemfibrozil with a statin have?
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Which of the following side effects is least associated with fenofibrate?
Which of the following side effects is least associated with fenofibrate?
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What is the elimination half-life of fenofibrate?
What is the elimination half-life of fenofibrate?
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What was the primary reason for the discontinuation of torcetrapib development?
What was the primary reason for the discontinuation of torcetrapib development?
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How is ezetimibe mainly excreted from the body?
How is ezetimibe mainly excreted from the body?
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What is the calculated plasma half-life of ezetimibe?
What is the calculated plasma half-life of ezetimibe?
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What is the maximum LDL cholesterol lowering effect that can be achieved with ezetimibe when used alone?
What is the maximum LDL cholesterol lowering effect that can be achieved with ezetimibe when used alone?
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What is the main therapeutic role of ezetimibe in treating hypercholesterolemia?
What is the main therapeutic role of ezetimibe in treating hypercholesterolemia?
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What effect do statins have on cardiovascular mortality and morbidity?
What effect do statins have on cardiovascular mortality and morbidity?
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Which of the following studies indicated the prophylactic use of statins in CAD patients?
Which of the following studies indicated the prophylactic use of statins in CAD patients?
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What is a significant risk factor for coronary artery disease (CAD)?
What is a significant risk factor for coronary artery disease (CAD)?
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Study Notes
Hyperlipoproteinaemias
- Types of primary hyperlipoproteinaemias are categorized (I, IIa, IIb, III, IV, V) based on elevated plasma lipoproteins and lipids.
- Genetic (G) or Multifactorial (MF) causes are noted for each type, with varying degrees of prevalence.
- Elevated plasma lipoproteins (LDL, VLDL, IDL, Chylomicron remnants) are linked to specific disorders.
- Cholesterol (CH) and triglycerides (TG) levels are affected differently across the types.
Classification of Hypolipidaemic Drugs
- HMG-CoA reductase inhibitors (statins) lower cholesterol synthesis, including lovastatin, simvastatin, atorvastatin, rosuvastatin, and pitavastatin.
- Bile acid sequestrants (resins), such as cholestyramine and colestipol, reduce bile acid absorption.
- Lipoprotein lipase activators (fibrates), like clofibrate, gemfibrozil, bezafibrate, and fenofibrate, activate lipoprotein lipase to lower triglycerides.
- Nicotinic acid inhibits sterol absorption and reduces triglycerides.
- Ezetimibe, inhibits cholesterol absorption.
Mechanism of Action and Lipid-Lowering Effects
- Statins reduce cholesterol synthesis by inhibiting HMG-CoA reductase, leading to increased LDL uptake and decreased LDL cholesterol (LDL-C).
- Statins also show effects on HDL and triglycerides (TG).
- Bile acid sequestrants reduce cholesterol by increasing its excretion.
- Fibrates enhance lipoprotein lipase activity, decreasing triglycerides.
- Nicotinic acid reduces VLDL production and increases HDL cholesterol.
- Ezetimibe directly lowers cholesterol absorption.
Adverse Effects
- Statins can cause muscle aches, liver abnormalities, and rarely rhabdomyolysis.
- Fibrates can cause gastrointestinal discomfort.
- Bile acid sequestrants may cause gastrointestinal issues.
- Nicotinic acid is associated with flushing and other effects.
Treatment Considerations
- Statins are often the first-line treatment for hyperlipidemia.
- Treatment decisions consider genetic factors, type of hyperlipidemia, and individual patient's needs.
- Treatment may continue indefinitely depending on patient profile.
- Combination therapies may be considered.
- Monitoring is important during treatment and adjustments to the treatment regimen may be made based on individual responses.
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Description
This quiz covers the classification of hyperlipoproteinaemias, detailing the different types based on elevated plasma lipoproteins and their genetic and multifactorial causes. Additionally, it explores various hypolipidaemic drugs, including statins and fibrates, and their mechanisms in lowering cholesterol and triglyceride levels.