Podcast
Questions and Answers
What is the primary defect in homozygous and heterozygous familial hypercholesterolemia?
What is the primary defect in homozygous and heterozygous familial hypercholesterolemia?
- Inability to synthesize cholesterol
- Inability to bind LDLC to LDLC receptors (correct)
- Elevated levels of triglycerides
- Increased biosynthesis of HDL
What is a consequence of hyperlipidemia?
What is a consequence of hyperlipidemia?
- Increased HDL levels
- Reduced risk of premature ASCVD
- Elevated blood levels of lipoproteins (correct)
- Decreased triglyceride levels
What is the goal of treating hyperlipidemia?
What is the goal of treating hyperlipidemia?
- To reduce mortality and CHD events by reducing TC and LDL, and increasing HDL (correct)
- To elevate triglyceride levels
- To increase LDL levels
- To decrease HDL levels
What type of dyslipidemia is caused by genetic defects?
What type of dyslipidemia is caused by genetic defects?
What is a characteristic of primary dyslipidemias?
What is a characteristic of primary dyslipidemias?
What is the initial management approach for secondary dyslipidemias?
What is the initial management approach for secondary dyslipidemias?
Which of the following can affect lipid levels?
Which of the following can affect lipid levels?
What is a type of medication that can affect lipid levels?
What is a type of medication that can affect lipid levels?
What is the effect of Thiazide diuretics on cholesterol levels?
What is the effect of Thiazide diuretics on cholesterol levels?
Which type of β-blockers have a greater effect on lipid profiles?
Which type of β-blockers have a greater effect on lipid profiles?
What is the effect of α-Agonists and antagonists on HDL-C levels?
What is the effect of α-Agonists and antagonists on HDL-C levels?
What is the effect of Oral contraceptives (α-Monophasics) on triglycerides?
What is the effect of Oral contraceptives (α-Monophasics) on triglycerides?
What is the effect of Ethanol on HDL-C levels?
What is the effect of Ethanol on HDL-C levels?
What is the effect of Isotretinoin on triglycerides?
What is the effect of Isotretinoin on triglycerides?
What is the effect of Cyclosporine on HDL-C levels?
What is the effect of Cyclosporine on HDL-C levels?
What is the typical presentation of patients with ASCVD?
What is the typical presentation of patients with ASCVD?
What is the central role of cholesterol in the body?
What is the central role of cholesterol in the body?
What is the primary function of lipoprotein particles in the body?
What is the primary function of lipoprotein particles in the body?
What is the outcome of the oxidation of LDL particles in vessel walls?
What is the outcome of the oxidation of LDL particles in vessel walls?
What is the collective term for coronary, cerebrovascular, and peripheral arterial disease?
What is the collective term for coronary, cerebrovascular, and peripheral arterial disease?
What is the primary risk factor associated with lipid abnormalities?
What is the primary risk factor associated with lipid abnormalities?
What is the process initiated by the migration of LDL particles into vessel walls?
What is the process initiated by the migration of LDL particles into vessel walls?
What is the result of macrophages taking up oxidized LDL particles?
What is the result of macrophages taking up oxidized LDL particles?
What is the term for the abnormal levels of lipids in the blood?
What is the term for the abnormal levels of lipids in the blood?
What is the age criterion for measuring fasting lipoprotein profile?
What is the age criterion for measuring fasting lipoprotein profile?
What is the recommended frequency for measuring fasting lipoprotein profile in adults?
What is the recommended frequency for measuring fasting lipoprotein profile in adults?
What is the unit of measurement for total cholesterol?
What is the unit of measurement for total cholesterol?
What is the purpose of calculating the 10-year ASCVD risk?
What is the purpose of calculating the 10-year ASCVD risk?
What is the effect of non-fasting on triglyceride levels?
What is the effect of non-fasting on triglyceride levels?
What is the purpose of measuring plasma cholesterol, triglyceride, and HDL levels after a 12-hour fast?
What is the purpose of measuring plasma cholesterol, triglyceride, and HDL levels after a 12-hour fast?
Cholesterol is a water-soluble molecule in the body.
Cholesterol is a water-soluble molecule in the body.
Atherosclerosis is a sudden process initiated by the migration of LDL particles into vessel walls.
Atherosclerosis is a sudden process initiated by the migration of LDL particles into vessel walls.
Lipid abnormalities decrease the risk of atherosclerotic cardiovascular disease.
Lipid abnormalities decrease the risk of atherosclerotic cardiovascular disease.
Triglycerides are one of the major lipids in the body.
Triglycerides are one of the major lipids in the body.
Lipoprotein particles are used to transport water-soluble molecules in the body.
Lipoprotein particles are used to transport water-soluble molecules in the body.
Endothelial cell dysfunction is a result of macrophages taking up oxidized LDL particles.
Endothelial cell dysfunction is a result of macrophages taking up oxidized LDL particles.
Cholesterol plays a minor role in the pathogenesis of atherosclerosis.
Cholesterol plays a minor role in the pathogenesis of atherosclerosis.
ASCVD is a collective term for coronary, cerebrovascular, and peripheral arterial disease.
ASCVD is a collective term for coronary, cerebrovascular, and peripheral arterial disease.
Elevated high-density lipoprotein (HDL) is a characteristic of hyperlipidemia.
Elevated high-density lipoprotein (HDL) is a characteristic of hyperlipidemia.
Primary dyslipidemias are caused by underlying abnormality, such as diabetes or hypothyroidism.
Primary dyslipidemias are caused by underlying abnormality, such as diabetes or hypothyroidism.
Reducing high-density lipoprotein (HDL) reduces mortality and CHD events.
Reducing high-density lipoprotein (HDL) reduces mortality and CHD events.
β-blockers are a type of medication that can decrease lipid levels.
β-blockers are a type of medication that can decrease lipid levels.
The primary goal of treating hyperlipidemia is to reduce triglycerides.
The primary goal of treating hyperlipidemia is to reduce triglycerides.
Familial hypercholesterolemia (FH) is a type of secondary dyslipidemia.
Familial hypercholesterolemia (FH) is a type of secondary dyslipidemia.
Glucocorticoids can decrease lipid levels.
Glucocorticoids can decrease lipid levels.
Primary dyslipidemias have a lower risk of premature ASCVD.
Primary dyslipidemias have a lower risk of premature ASCVD.
Thiazide diuretics initially decrease triglycerides by 30-50%
Thiazide diuretics initially decrease triglycerides by 30-50%
Selective β-blockers have a greater effect on lipid profiles than nonselective β-blockers
Selective β-blockers have a greater effect on lipid profiles than nonselective β-blockers
α-Agonists and antagonists increase cholesterol levels by 10-20%
α-Agonists and antagonists increase cholesterol levels by 10-20%
Oral contraceptives (α-Monophasics) decrease triglycerides by 10-20%
Oral contraceptives (α-Monophasics) decrease triglycerides by 10-20%
Ethanol consumption decreases HDL-C levels
Ethanol consumption decreases HDL-C levels
Isotretinoin decreases triglycerides by 10-20%
Isotretinoin decreases triglycerides by 10-20%
Cyclosporine decreases HDL-C levels
Cyclosporine decreases HDL-C levels
Most patients with ASCVD are symptomatic from an early stage
Most patients with ASCVD are symptomatic from an early stage
Chest pain is a symptom of anxiety.
Chest pain is a symptom of anxiety.
A total cholesterol level of 190 mg/dL is considered normal.
A total cholesterol level of 190 mg/dL is considered normal.
Elevated triglyceride levels are not affected by fasting.
Elevated triglyceride levels are not affected by fasting.
The 10-year ASCVD risk is calculated in primary prevention situations.
The 10-year ASCVD risk is calculated in primary prevention situations.
HDL-C levels are typically elevated in individuals with hyperlipidemia.
HDL-C levels are typically elevated in individuals with hyperlipidemia.
All adults 18 years of age or older should have their fasting lipoprotein profile measured at least once every 5 years.
All adults 18 years of age or older should have their fasting lipoprotein profile measured at least once every 5 years.
What is the central role of cholesterol in the pathogenesis of atherosclerosis?
What is the central role of cholesterol in the pathogenesis of atherosclerosis?
What is the purpose of lipoprotein particles in the body?
What is the purpose of lipoprotein particles in the body?
What is the outcome of the oxidation of LDL particles in vessel walls?
What is the outcome of the oxidation of LDL particles in vessel walls?
What is the collective term for coronary, cerebrovascular, and peripheral arterial disease?
What is the collective term for coronary, cerebrovascular, and peripheral arterial disease?
What is the primary risk factor associated with lipid abnormalities?
What is the primary risk factor associated with lipid abnormalities?
What is the process initiated by the migration of LDL particles into vessel walls?
What is the process initiated by the migration of LDL particles into vessel walls?
What is the result of macrophages taking up oxidized LDL particles?
What is the result of macrophages taking up oxidized LDL particles?
What is the term for abnormal levels of lipids in the blood?
What is the term for abnormal levels of lipids in the blood?
What is the primary function of lipoprotein particles in the body, and how do they relate to hyperlipidemia?
What is the primary function of lipoprotein particles in the body, and how do they relate to hyperlipidemia?
How do primary dyslipidemias differ from secondary dyslipidemias, and what is the initial management approach for the latter?
How do primary dyslipidemias differ from secondary dyslipidemias, and what is the initial management approach for the latter?
What is the significance of LDL and HDL in the context of hyperlipidemia, and how do they relate to cardiovascular disease?
What is the significance of LDL and HDL in the context of hyperlipidemia, and how do they relate to cardiovascular disease?
What are some examples of medications that can affect lipid levels, and how do they impact cardiovascular disease risk?
What are some examples of medications that can affect lipid levels, and how do they impact cardiovascular disease risk?
What is the relationship between lipoprotein abnormalities and atherosclerosis, and how do these relate to cardiovascular disease?
What is the relationship between lipoprotein abnormalities and atherosclerosis, and how do these relate to cardiovascular disease?
What are the key differences between homozygous and heterozygous familial hypercholesterolemia, and how do they impact cardiovascular disease risk?
What are the key differences between homozygous and heterozygous familial hypercholesterolemia, and how do they impact cardiovascular disease risk?
How do lifestyle modifications, such as excessive alcohol use and weight gain, impact lipid levels and cardiovascular disease risk?
How do lifestyle modifications, such as excessive alcohol use and weight gain, impact lipid levels and cardiovascular disease risk?
What is the significance of ASCVD in the context of hyperlipidemia, and how is it related to lipoprotein abnormalities?
What is the significance of ASCVD in the context of hyperlipidemia, and how is it related to lipoprotein abnormalities?
What is the effect of loop diuretics on HDL-C levels?
What is the effect of loop diuretics on HDL-C levels?
What is the effect of nonselective β-blockers on triglycerides?
What is the effect of nonselective β-blockers on triglycerides?
What is the effect of α-Blocking β-blockers on lipid profiles?
What is the effect of α-Blocking β-blockers on lipid profiles?
What is the effect of α-Triphasics oral contraceptives on triglycerides?
What is the effect of α-Triphasics oral contraceptives on triglycerides?
What is the effect of glucocorticoids on triglycerides?
What is the effect of glucocorticoids on triglycerides?
What is the effect of ethanol on triglycerides?
What is the effect of ethanol on triglycerides?
What is the effect of isotretinoin on cholesterol levels?
What is the effect of isotretinoin on cholesterol levels?
What is the effect of cyclosporine on cholesterol levels?
What is the effect of cyclosporine on cholesterol levels?
What are the symptoms that may indicate acute coronary syndrome?
What are the symptoms that may indicate acute coronary syndrome?
What is the recommended frequency for measuring fasting lipoprotein profile in adults aged 20 years or older?
What is the recommended frequency for measuring fasting lipoprotein profile in adults aged 20 years or older?
What is elevated in laboratory tests for individuals with hyperlipidemia?
What is elevated in laboratory tests for individuals with hyperlipidemia?
What is the purpose of calculating the 10-year ASCVD risk?
What is the purpose of calculating the 10-year ASCVD risk?
Why is it important to measure plasma cholesterol, triglyceride, and HDL levels after a 12-hour fast?
Why is it important to measure plasma cholesterol, triglyceride, and HDL levels after a 12-hour fast?
What is the unit of measurement for total cholesterol?
What is the unit of measurement for total cholesterol?
Lipoprotein abnormalities (dyslipidemia) include > 1 of the following: Elevated total ______&(TC)
Lipoprotein abnormalities (dyslipidemia) include > 1 of the following: Elevated total ______&(TC)
In homozygous and heterozygous familial ______ (FH), the primary defect is the inability to bind LDLC to LDLC receptors.
In homozygous and heterozygous familial ______ (FH), the primary defect is the inability to bind LDLC to LDLC receptors.
Several drug classes and habits may affect lipid levels, including ______ alcohol use.
Several drug classes and habits may affect lipid levels, including ______ alcohol use.
Elevated ______ levels are a characteristic of hyperlipidemia.
Elevated ______ levels are a characteristic of hyperlipidemia.
Lipoprotein particles are used to transport ______ molecules in the body.
Lipoprotein particles are used to transport ______ molecules in the body.
The primary goal of treating hyperlipidemia is to reduce ______ and CHD events.
The primary goal of treating hyperlipidemia is to reduce ______ and CHD events.
Secondary dyslipidemias should be initially managed by correcting the underlying ______ when possible.
Secondary dyslipidemias should be initially managed by correcting the underlying ______ when possible.
Hyperlipidemia may lead to ______ blood levels of lipoproteins (cholesterol, triglycerides, phospholipids).
Hyperlipidemia may lead to ______ blood levels of lipoproteins (cholesterol, triglycerides, phospholipids).
Cholesterol, triglycerides, and phospholipids are the major ______ in the body
Cholesterol, triglycerides, and phospholipids are the major ______ in the body
Lipids are relatively ______ insoluble molecules in the body
Lipids are relatively ______ insoluble molecules in the body
Atherogenesis is a progressive process initiated by the migration of ______ lipoprotein into vessel walls
Atherogenesis is a progressive process initiated by the migration of ______ lipoprotein into vessel walls
Lipid abnormalities increase the risk of ______ cardiovascular disease
Lipid abnormalities increase the risk of ______ cardiovascular disease
Cholesterol plays the central role in the pathogenesis of ______
Cholesterol plays the central role in the pathogenesis of ______
Lipids are transported by ______ particles
Lipids are transported by ______ particles
The collective term for coronary, cerebrovascular, and peripheral arterial disease is ______
The collective term for coronary, cerebrovascular, and peripheral arterial disease is ______
Primary dyslipidemias are caused by ______ defects
Primary dyslipidemias are caused by ______ defects
Thiazide diuretics increase cholesterol levels by ______ initially
Thiazide diuretics increase cholesterol levels by ______ initially
Loop diuretics have no change in ______ levels
Loop diuretics have no change in ______ levels
Shortness of breath is a symptom of ______ in patients with cardiovascular disease.
Shortness of breath is a symptom of ______ in patients with cardiovascular disease.
Nonselective β-blockers increase ______ levels by 20-50%
Nonselective β-blockers increase ______ levels by 20-50%
Fasting lipoprotein profile should be measured in all adults ______ years of age or older at least once every 5 years.
Fasting lipoprotein profile should be measured in all adults ______ years of age or older at least once every 5 years.
α-Blocking effects have no change or ______ in cholesterol levels
α-Blocking effects have no change or ______ in cholesterol levels
Oral contraceptives (α-Monophasics) increase ______ levels by 10-45%
Oral contraceptives (α-Monophasics) increase ______ levels by 10-45%
If the total cholesterol is greater than ______ mg/dL (>5.17 mmol/L), a second determination is recommended.
If the total cholesterol is greater than ______ mg/dL (>5.17 mmol/L), a second determination is recommended.
Ethanol can increase ______ levels by up to 50%
Ethanol can increase ______ levels by up to 50%
Laboratory tests may show elevated ______ and high sensitivity C-reactive protein (hs-CRP).
Laboratory tests may show elevated ______ and high sensitivity C-reactive protein (hs-CRP).
Triglycerides may be elevated in ______ individuals.
Triglycerides may be elevated in ______ individuals.
Isotretinoin increases ______ levels by 50-60%
Isotretinoin increases ______ levels by 50-60%
Cyclosporine increases ______ levels by 15-20%
Cyclosporine increases ______ levels by 15-20%
The 10-year ______ risk is calculated in primary prevention situations.
The 10-year ______ risk is calculated in primary prevention situations.
Match the following symptoms with their possible association with acute coronary syndrome:
Match the following symptoms with their possible association with acute coronary syndrome:
Match the following laboratory tests with their possible results in hyperlipidemia:
Match the following laboratory tests with their possible results in hyperlipidemia:
Match the following lipids with their measurement units:
Match the following lipids with their measurement units:
Match the following terms with their definitions:
Match the following terms with their definitions:
Match the following frequencies with their recommendations:
Match the following frequencies with their recommendations:
Match the following with their effects on lipid levels:
Match the following with their effects on lipid levels:
Match the following lipoprotein disorders with their characteristics:
Match the following lipoprotein disorders with their characteristics:
Match the following substances with their effects on lipid levels:
Match the following substances with their effects on lipid levels:
Match the following medications with their effects on lipid levels:
Match the following medications with their effects on lipid levels:
Match the following lipoprotein abnormalities with their characteristics:
Match the following lipoprotein abnormalities with their characteristics:
Match the following conditions with their effects on lipid levels:
Match the following conditions with their effects on lipid levels:
Match the following lipoprotein disorders with their risks:
Match the following lipoprotein disorders with their risks:
Match the following measures with their effects on CHD events:
Match the following measures with their effects on CHD events:
Match the following lipoprotein disorders with their management approaches:
Match the following lipoprotein disorders with their management approaches:
Match the lipids with their characteristic:
Match the lipids with their characteristic:
Match the disease with its cause:
Match the disease with its cause:
Match the term with its definition:
Match the term with its definition:
Match the process with its outcome:
Match the process with its outcome:
Match the type of dyslipidemia with its characteristic:
Match the type of dyslipidemia with its characteristic:
Match the medication with its effect on lipids:
Match the medication with its effect on lipids:
Match the term with its description:
Match the term with its description:
Match the process with its result:
Match the process with its result:
Match the following medications with their effect on cholesterol levels:
Match the following medications with their effect on cholesterol levels:
Match the following medications with their effect on triglycerides:
Match the following medications with their effect on triglycerides:
Match the following medications with their effect on HDL-C levels:
Match the following medications with their effect on HDL-C levels:
Match the following medications with their comments:
Match the following medications with their comments:
Match the following medications with their effects on triglycerides and HDL-C levels:
Match the following medications with their effects on triglycerides and HDL-C levels:
Match the following medications with their effects on cholesterol levels:
Match the following medications with their effects on cholesterol levels:
Match the following medications with their effects on triglycerides levels:
Match the following medications with their effects on triglycerides levels:
Match the following medications with their effects on HDL-C levels:
Match the following medications with their effects on HDL-C levels:
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Study Notes
Dyslipidemia and Hyperlipidemia
- Cholesterol, triglycerides, and phospholipids are the major lipids in the body, with cholesterol playing a central role in the pathogenesis of atherosclerosis.
- Lipids are relatively water-insoluble molecules, transported by lipoprotein particles in the plasma.
Atherogenesis
- Atherogenesis is a progressive process initiated by the migration of LDL+ lipoprotein into vessel walls, undergoing oxidation and being taken up by macrophages, inducing endothelial cell dysfunction and a prothrombotic state.
Lipid Abnormalities and Clinical Outcomes
- Lipid abnormalities increase the risk of coronary heart disease (CHD), cerebrovascular disease (CVA), peripheral arterial disease (PAD), and collectively, atherosclerotic cardiovascular disease (ASCVD).
- Lipoprotein abnormalities (dyslipidemia) include elevated total cholesterol, LDL, triglycerides, and reduced high-density lipoprotein (HDL).
Lipoprotein Disorders
- Primary dyslipidemia includes genetic defects resulting in hypercholesterolemia, hypertriglyceridemia, and disorders of HDL metabolism, leading to an increased risk of premature ASCVD.
- Secondary dyslipidemia should be initially managed by correcting underlying abnormalities, such as excessive alcohol use, weight gain, or certain medications.
Effects of Drugs on Lipids
- Various drugs, including diuretics, β-blockers, oral contraceptives, glucocorticoids, and isotretinoin, can affect lipid levels, with some causing increased cholesterol and triglycerides, while others may decrease HDL.
Clinical Presentation and Diagnosis
- Most patients with dyslipidemia are asymptomatic for years before developing ASCVD, which may produce symptoms such as chest pain, palpitations, and shortness of breath.
- Diagnosis involves measuring fasting lipoprotein profiles, including total cholesterol, LDL, HDL, and triglycerides, and calculating the 10-year ASCVD risk in primary prevention situations.
Laboratory Tests
- Laboratory tests may show elevated total cholesterol, LDL-C, triglycerides, apo-lipoprotein B, and high sensitivity C-reactive protein, and decreased HDL-C.
- Other baseline tests, such as AST/ALT, TSH, glucose, serum creatinine, BUN, and urinalysis, should be performed.
Dyslipidemia and Hyperlipidemia
- Cholesterol, triglycerides, and phospholipids are the major lipids in the body, with cholesterol playing a central role in the pathogenesis of atherosclerosis.
- Lipids are relatively water-insoluble molecules, transported by lipoprotein particles in the plasma.
Atherogenesis
- Atherogenesis is a progressive process initiated by the migration of LDL+ lipoprotein into vessel walls, undergoing oxidation and being taken up by macrophages, inducing endothelial cell dysfunction and a prothrombotic state.
Lipid Abnormalities and Clinical Outcomes
- Lipid abnormalities increase the risk of coronary heart disease (CHD), cerebrovascular disease (CVA), peripheral arterial disease (PAD), and collectively, atherosclerotic cardiovascular disease (ASCVD).
- Lipoprotein abnormalities (dyslipidemia) include elevated total cholesterol, LDL, triglycerides, and reduced high-density lipoprotein (HDL).
Lipoprotein Disorders
- Primary dyslipidemia includes genetic defects resulting in hypercholesterolemia, hypertriglyceridemia, and disorders of HDL metabolism, leading to an increased risk of premature ASCVD.
- Secondary dyslipidemia should be initially managed by correcting underlying abnormalities, such as excessive alcohol use, weight gain, or certain medications.
Effects of Drugs on Lipids
- Various drugs, including diuretics, β-blockers, oral contraceptives, glucocorticoids, and isotretinoin, can affect lipid levels, with some causing increased cholesterol and triglycerides, while others may decrease HDL.
Clinical Presentation and Diagnosis
- Most patients with dyslipidemia are asymptomatic for years before developing ASCVD, which may produce symptoms such as chest pain, palpitations, and shortness of breath.
- Diagnosis involves measuring fasting lipoprotein profiles, including total cholesterol, LDL, HDL, and triglycerides, and calculating the 10-year ASCVD risk in primary prevention situations.
Laboratory Tests
- Laboratory tests may show elevated total cholesterol, LDL-C, triglycerides, apo-lipoprotein B, and high sensitivity C-reactive protein, and decreased HDL-C.
- Other baseline tests, such as AST/ALT, TSH, glucose, serum creatinine, BUN, and urinalysis, should be performed.
Dyslipidemia and Hyperlipidemia
- Cholesterol, triglycerides, and phospholipids are the major lipids in the body, with cholesterol playing a central role in the pathogenesis of atherosclerosis.
- Lipids are relatively water-insoluble molecules, transported by lipoprotein particles in the plasma.
Atherogenesis
- Atherogenesis is a progressive process initiated by the migration of LDL+ lipoprotein into vessel walls, undergoing oxidation and being taken up by macrophages, inducing endothelial cell dysfunction and a prothrombotic state.
Lipid Abnormalities and Clinical Outcomes
- Lipid abnormalities increase the risk of coronary heart disease (CHD), cerebrovascular disease (CVA), peripheral arterial disease (PAD), and collectively, atherosclerotic cardiovascular disease (ASCVD).
- Lipoprotein abnormalities (dyslipidemia) include elevated total cholesterol, LDL, triglycerides, and reduced high-density lipoprotein (HDL).
Lipoprotein Disorders
- Primary dyslipidemia includes genetic defects resulting in hypercholesterolemia, hypertriglyceridemia, and disorders of HDL metabolism, leading to an increased risk of premature ASCVD.
- Secondary dyslipidemia should be initially managed by correcting underlying abnormalities, such as excessive alcohol use, weight gain, or certain medications.
Effects of Drugs on Lipids
- Various drugs, including diuretics, β-blockers, oral contraceptives, glucocorticoids, and isotretinoin, can affect lipid levels, with some causing increased cholesterol and triglycerides, while others may decrease HDL.
Clinical Presentation and Diagnosis
- Most patients with dyslipidemia are asymptomatic for years before developing ASCVD, which may produce symptoms such as chest pain, palpitations, and shortness of breath.
- Diagnosis involves measuring fasting lipoprotein profiles, including total cholesterol, LDL, HDL, and triglycerides, and calculating the 10-year ASCVD risk in primary prevention situations.
Laboratory Tests
- Laboratory tests may show elevated total cholesterol, LDL-C, triglycerides, apo-lipoprotein B, and high sensitivity C-reactive protein, and decreased HDL-C.
- Other baseline tests, such as AST/ALT, TSH, glucose, serum creatinine, BUN, and urinalysis, should be performed.
Dyslipidemia and Hyperlipidemia
- Cholesterol, triglycerides, and phospholipids are the major lipids in the body, with cholesterol playing a central role in the pathogenesis of atherosclerosis.
- Lipids are relatively water-insoluble molecules, transported by lipoprotein particles in the plasma.
Atherogenesis
- Atherogenesis is a progressive process initiated by the migration of LDL+ lipoprotein into vessel walls, undergoing oxidation and being taken up by macrophages, inducing endothelial cell dysfunction and a prothrombotic state.
Lipid Abnormalities and Clinical Outcomes
- Lipid abnormalities increase the risk of coronary heart disease (CHD), cerebrovascular disease (CVA), peripheral arterial disease (PAD), and collectively, atherosclerotic cardiovascular disease (ASCVD).
- Lipoprotein abnormalities (dyslipidemia) include elevated total cholesterol, LDL, triglycerides, and reduced high-density lipoprotein (HDL).
Lipoprotein Disorders
- Primary dyslipidemia includes genetic defects resulting in hypercholesterolemia, hypertriglyceridemia, and disorders of HDL metabolism, leading to an increased risk of premature ASCVD.
- Secondary dyslipidemia should be initially managed by correcting underlying abnormalities, such as excessive alcohol use, weight gain, or certain medications.
Effects of Drugs on Lipids
- Various drugs, including diuretics, β-blockers, oral contraceptives, glucocorticoids, and isotretinoin, can affect lipid levels, with some causing increased cholesterol and triglycerides, while others may decrease HDL.
Clinical Presentation and Diagnosis
- Most patients with dyslipidemia are asymptomatic for years before developing ASCVD, which may produce symptoms such as chest pain, palpitations, and shortness of breath.
- Diagnosis involves measuring fasting lipoprotein profiles, including total cholesterol, LDL, HDL, and triglycerides, and calculating the 10-year ASCVD risk in primary prevention situations.
Laboratory Tests
- Laboratory tests may show elevated total cholesterol, LDL-C, triglycerides, apo-lipoprotein B, and high sensitivity C-reactive protein, and decreased HDL-C.
- Other baseline tests, such as AST/ALT, TSH, glucose, serum creatinine, BUN, and urinalysis, should be performed.
Dyslipidemia and Hyperlipidemia
- Cholesterol, triglycerides, and phospholipids are the major lipids in the body, with cholesterol playing a central role in the pathogenesis of atherosclerosis.
- Lipids are relatively water-insoluble molecules, transported by lipoprotein particles in the plasma.
Atherogenesis
- Atherogenesis is a progressive process initiated by the migration of LDL+ lipoprotein into vessel walls, undergoing oxidation and being taken up by macrophages, inducing endothelial cell dysfunction and a prothrombotic state.
Lipid Abnormalities and Clinical Outcomes
- Lipid abnormalities increase the risk of coronary heart disease (CHD), cerebrovascular disease (CVA), peripheral arterial disease (PAD), and collectively, atherosclerotic cardiovascular disease (ASCVD).
- Lipoprotein abnormalities (dyslipidemia) include elevated total cholesterol, LDL, triglycerides, and reduced high-density lipoprotein (HDL).
Lipoprotein Disorders
- Primary dyslipidemia includes genetic defects resulting in hypercholesterolemia, hypertriglyceridemia, and disorders of HDL metabolism, leading to an increased risk of premature ASCVD.
- Secondary dyslipidemia should be initially managed by correcting underlying abnormalities, such as excessive alcohol use, weight gain, or certain medications.
Effects of Drugs on Lipids
- Various drugs, including diuretics, β-blockers, oral contraceptives, glucocorticoids, and isotretinoin, can affect lipid levels, with some causing increased cholesterol and triglycerides, while others may decrease HDL.
Clinical Presentation and Diagnosis
- Most patients with dyslipidemia are asymptomatic for years before developing ASCVD, which may produce symptoms such as chest pain, palpitations, and shortness of breath.
- Diagnosis involves measuring fasting lipoprotein profiles, including total cholesterol, LDL, HDL, and triglycerides, and calculating the 10-year ASCVD risk in primary prevention situations.
Laboratory Tests
- Laboratory tests may show elevated total cholesterol, LDL-C, triglycerides, apo-lipoprotein B, and high sensitivity C-reactive protein, and decreased HDL-C.
- Other baseline tests, such as AST/ALT, TSH, glucose, serum creatinine, BUN, and urinalysis, should be performed.
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