150 Questions
What is the primary defect in homozygous and heterozygous familial hypercholesterolemia?
Inability to bind LDLC to LDLC receptors
What is a consequence of hyperlipidemia?
Elevated blood levels of lipoproteins
What is the goal of treating hyperlipidemia?
To reduce mortality and CHD events by reducing TC and LDL, and increasing HDL
What type of dyslipidemia is caused by genetic defects?
Primary dyslipidemia
What is a characteristic of primary dyslipidemias?
They have an increased risk of premature ASCVD
What is the initial management approach for secondary dyslipidemias?
Correcting underlying abnormality when possible
Which of the following can affect lipid levels?
Excessive intake of carbohydrates or saturated fat
What is a type of medication that can affect lipid levels?
All of the above
What is the effect of Thiazide diuretics on cholesterol levels?
↑5–7%
Which type of β-blockers have a greater effect on lipid profiles?
Selective
What is the effect of α-Agonists and antagonists on HDL-C levels?
↑0–15%
What is the effect of Oral contraceptives (α-Monophasics) on triglycerides?
↑10–45%
What is the effect of Ethanol on HDL-C levels?
↑
What is the effect of Isotretinoin on triglycerides?
↑50–60%
What is the effect of Cyclosporine on HDL-C levels?
No change
What is the typical presentation of patients with ASCVD?
Most patients are asymptomatic for years
What is the central role of cholesterol in the body?
plays a central role in the pathogenesis of atherosclerosis
What is the primary function of lipoprotein particles in the body?
to transport lipids in the plasma
What is the outcome of the oxidation of LDL particles in vessel walls?
reduced ability of the endothelium to dilate the artery
What is the collective term for coronary, cerebrovascular, and peripheral arterial disease?
atherosclerotic cardiovascular disease (ASCVD)
What is the primary risk factor associated with lipid abnormalities?
increased risk of coronary, cerebrovascular, and peripheral arterial disease
What is the process initiated by the migration of LDL particles into vessel walls?
atherogenesis
What is the result of macrophages taking up oxidized LDL particles?
endothelial cell dysfunction
What is the term for the abnormal levels of lipids in the blood?
dyslipidemia
What is the age criterion for measuring fasting lipoprotein profile?
20 years of age or older
What is the recommended frequency for measuring fasting lipoprotein profile in adults?
Every 5 years
What is the unit of measurement for total cholesterol?
Milligrams per deciliter
What is the purpose of calculating the 10-year ASCVD risk?
To determine the risk of cardiovascular disease in primary prevention situations
What is the effect of non-fasting on triglyceride levels?
Triglyceride levels are increased
What is the purpose of measuring plasma cholesterol, triglyceride, and HDL levels after a 12-hour fast?
To get accurate measurements of triglyceride levels
Cholesterol is a water-soluble molecule in the body.
False
Atherosclerosis is a sudden process initiated by the migration of LDL particles into vessel walls.
False
Lipid abnormalities decrease the risk of atherosclerotic cardiovascular disease.
False
Triglycerides are one of the major lipids in the body.
True
Lipoprotein particles are used to transport water-soluble molecules in the body.
False
Endothelial cell dysfunction is a result of macrophages taking up oxidized LDL particles.
True
Cholesterol plays a minor role in the pathogenesis of atherosclerosis.
False
ASCVD is a collective term for coronary, cerebrovascular, and peripheral arterial disease.
True
Elevated high-density lipoprotein (HDL) is a characteristic of hyperlipidemia.
False
Primary dyslipidemias are caused by underlying abnormality, such as diabetes or hypothyroidism.
False
Reducing high-density lipoprotein (HDL) reduces mortality and CHD events.
False
β-blockers are a type of medication that can decrease lipid levels.
False
The primary goal of treating hyperlipidemia is to reduce triglycerides.
False
Familial hypercholesterolemia (FH) is a type of secondary dyslipidemia.
False
Glucocorticoids can decrease lipid levels.
False
Primary dyslipidemias have a lower risk of premature ASCVD.
False
Thiazide diuretics initially decrease triglycerides by 30-50%
False
Selective β-blockers have a greater effect on lipid profiles than nonselective β-blockers
True
α-Agonists and antagonists increase cholesterol levels by 10-20%
False
Oral contraceptives (α-Monophasics) decrease triglycerides by 10-20%
False
Ethanol consumption decreases HDL-C levels
False
Isotretinoin decreases triglycerides by 10-20%
False
Cyclosporine decreases HDL-C levels
False
Most patients with ASCVD are symptomatic from an early stage
False
Chest pain is a symptom of anxiety.
False
A total cholesterol level of 190 mg/dL is considered normal.
False
Elevated triglyceride levels are not affected by fasting.
False
The 10-year ASCVD risk is calculated in primary prevention situations.
True
HDL-C levels are typically elevated in individuals with hyperlipidemia.
False
All adults 18 years of age or older should have their fasting lipoprotein profile measured at least once every 5 years.
False
What is the central role of cholesterol in the pathogenesis of atherosclerosis?
Cholesterol plays a central role in the pathogenesis of atherosclerosis.
What is the purpose of lipoprotein particles in the body?
Lipids are transported by lipoprotein particles.
What is the outcome of the oxidation of LDL particles in vessel walls?
Oxidized LDL particles are taken up by macrophages, inducing endothelial cell dysfunction.
What is the collective term for coronary, cerebrovascular, and peripheral arterial disease?
Atherosclerotic cardiovascular disease (ASCVD).
What is the primary risk factor associated with lipid abnormalities?
Increased risk of atherosclerotic cardiovascular disease.
What is the process initiated by the migration of LDL particles into vessel walls?
Atherogenesis.
What is the result of macrophages taking up oxidized LDL particles?
Induction of endothelial cell dysfunction.
What is the term for abnormal levels of lipids in the blood?
Dyslipidemia.
What is the primary function of lipoprotein particles in the body, and how do they relate to hyperlipidemia?
Lipoprotein particles transport lipids, including cholesterol and triglycerides, in the bloodstream. In hyperlipidemia, there are elevated blood levels of lipoproteins, leading to an increased risk of atherosclerosis.
How do primary dyslipidemias differ from secondary dyslipidemias, and what is the initial management approach for the latter?
Primary dyslipidemias are caused by genetic defects, whereas secondary dyslipidemias are caused by underlying conditions or medications. The initial management approach for secondary dyslipidemias is to correct the underlying abnormality when possible.
What is the significance of LDL and HDL in the context of hyperlipidemia, and how do they relate to cardiovascular disease?
LDL (bad cholesterol) is associated with increased cardiovascular disease risk, while HDL (good cholesterol) is associated with decreased risk. Elevated LDL and reduced HDL are characteristic of hyperlipidemia.
What are some examples of medications that can affect lipid levels, and how do they impact cardiovascular disease risk?
Examples include thiazide diuretics, progestins, glucocorticoids, β-blockers, isotretinoin, and cyclosporine. These medications can increase lipid levels, thereby increasing cardiovascular disease risk.
What is the relationship between lipoprotein abnormalities and atherosclerosis, and how do these relate to cardiovascular disease?
Lipoprotein abnormalities, such as elevated LDL and triglycerides, contribute to atherosclerosis, which is a major risk factor for cardiovascular disease.
What are the key differences between homozygous and heterozygous familial hypercholesterolemia, and how do they impact cardiovascular disease risk?
Both types are characterized by the inability to bind LDL to LDL receptors, leading to elevated cholesterol levels. Homozygous FH has a more severe phenotype, with earlier onset and higher cardiovascular disease risk.
How do lifestyle modifications, such as excessive alcohol use and weight gain, impact lipid levels and cardiovascular disease risk?
Excessive alcohol use and weight gain can elevate triglycerides and lower HDL, increasing cardiovascular disease risk.
What is the significance of ASCVD in the context of hyperlipidemia, and how is it related to lipoprotein abnormalities?
ASCVD (atherosclerotic cardiovascular disease) is a major consequence of hyperlipidemia, and lipoprotein abnormalities, such as elevated LDL and triglycerides, contribute to its development.
What is the effect of loop diuretics on HDL-C levels?
↓ to 15%
What is the effect of nonselective β-blockers on triglycerides?
↑20-50%
What is the effect of α-Blocking β-blockers on lipid profiles?
No change or ↓
What is the effect of α-Triphasics oral contraceptives on triglycerides?
↑10-15%
What is the effect of glucocorticoids on triglycerides?
↑15-20%
What is the effect of ethanol on triglycerides?
↑up to 50%
What is the effect of isotretinoin on cholesterol levels?
↑5-20%
What is the effect of cyclosporine on cholesterol levels?
↑15-20%
What are the symptoms that may indicate acute coronary syndrome?
Chest pain, palpitations, sweating, anxiety, shortness of breath, loss of consciousness, difficulty with speech or movement, or abdominal pain.
What is the recommended frequency for measuring fasting lipoprotein profile in adults aged 20 years or older?
At least once every 5 years.
What is elevated in laboratory tests for individuals with hyperlipidemia?
Total cholesterol, LDL-C, triglycerides, apo-lipoprotein B, and high sensitivity C-reactive protein (hs-CRP).
What is the purpose of calculating the 10-year ASCVD risk?
To assess the risk of atherosclerotic cardiovascular disease.
Why is it important to measure plasma cholesterol, triglyceride, and HDL levels after a 12-hour fast?
Because triglycerides may be elevated in non-fasting individuals.
What is the unit of measurement for total cholesterol?
Milligrams per deciliter (mg/dL).
Lipoprotein abnormalities (dyslipidemia) include > 1 of the following: Elevated total ______&(TC)
cholesterol
In homozygous and heterozygous familial ______ (FH), the primary defect is the inability to bind LDLC to LDLC receptors.
hypercholesterolemia
Several drug classes and habits may affect lipid levels, including ______ alcohol use.
excessive
Elevated ______ levels are a characteristic of hyperlipidemia.
blood
Lipoprotein particles are used to transport ______ molecules in the body.
lipid
The primary goal of treating hyperlipidemia is to reduce ______ and CHD events.
mortality
Secondary dyslipidemias should be initially managed by correcting the underlying ______ when possible.
abnormality
Hyperlipidemia may lead to ______ blood levels of lipoproteins (cholesterol, triglycerides, phospholipids).
elevated
Cholesterol, triglycerides, and phospholipids are the major ______ in the body
lipids
Lipids are relatively ______ insoluble molecules in the body
water
Atherogenesis is a progressive process initiated by the migration of ______ lipoprotein into vessel walls
LDL
Lipid abnormalities increase the risk of ______ cardiovascular disease
atherosclerotic
Cholesterol plays the central role in the pathogenesis of ______
atherosclerosis
Lipids are transported by ______ particles
lipoprotein
The collective term for coronary, cerebrovascular, and peripheral arterial disease is ______
ASCVD
Primary dyslipidemias are caused by ______ defects
genetic
Thiazide diuretics increase cholesterol levels by ______ initially
5-7%
Loop diuretics have no change in ______ levels
triglycerides
Shortness of breath is a symptom of ______ in patients with cardiovascular disease.
anxiety
Nonselective β-blockers increase ______ levels by 20-50%
triglycerides
Fasting lipoprotein profile should be measured in all adults ______ years of age or older at least once every 5 years.
20
α-Blocking effects have no change or ______ in cholesterol levels
decrease
Oral contraceptives (α-Monophasics) increase ______ levels by 10-45%
triglycerides
If the total cholesterol is greater than ______ mg/dL (>5.17 mmol/L), a second determination is recommended.
200
Ethanol can increase ______ levels by up to 50%
triglycerides
Laboratory tests may show elevated ______ and high sensitivity C-reactive protein (hs-CRP).
TC
Triglycerides may be elevated in ______ individuals.
non-fasting
Isotretinoin increases ______ levels by 50-60%
triglycerides
Cyclosporine increases ______ levels by 15-20%
cholesterol
The 10-year ______ risk is calculated in primary prevention situations.
ASCVD
Match the following symptoms with their possible association with acute coronary syndrome:
Chest pain = Typical symptom Palpitations = Possible symptom Sweating = Common symptom Difficulty with speech or movement = Atypical symptom
Match the following laboratory tests with their possible results in hyperlipidemia:
Total cholesterol = Elevated HDL-C = Low Triglycerides = Elevated hs-CRP = High
Match the following lipids with their measurement units:
Total cholesterol = Milligrams per deciliter (mg/dL) LDL-C = Milligrams per deciliter (mg/dL) Triglycerides = Milligrams per deciliter (mg/dL) HDL-C = Milligrams per deciliter (mg/dL)
Match the following terms with their definitions:
ASCVD = Atherosclerotic cardiovascular disease Dyslipidemia = Abnormal levels of lipids in the blood Hyperlipidemia = Elevated levels of lipids in the blood Hypothyroidism = Underlying abnormality causing dyslipidemia
Match the following frequencies with their recommendations:
Fasting lipoprotein profile measurement = At least once every 5 years Triglyceride level measurement = After a 12-hour fast Cholesterol level measurement = After a 12-hour fast HDL-C level measurement = After a 12-hour fast
Match the following with their effects on lipid levels:
Fasting = Does not significantly affect total cholesterol levels Non-fasting = Elevates triglyceride levels Thiazide diuretics = Increases triglyceride levels Ethanol = Increases HDL-C levels
Match the following lipoprotein disorders with their characteristics:
Primary dyslipidemia = Genetic defects resulting in hypercholesterolemia, hypertriglyceridemia, and disorders of HDL metabolism Secondary dyslipidemia = Initially managed by correcting underlying abnormality when possible Familial hypercholesterolemia (FH) = Inability to bind LDL-C to LDL-C receptors Homozygous familial hypercholesterolemia = Lack of LDL-C degradation by cells and unregulated biosynthesis of cholesterol
Match the following substances with their effects on lipid levels:
Excessive alcohol use = Increases triglycerides Thiazide diuretics = Increases cholesterol levels Glucocorticoids = Increases triglycerides Progestins = Increases cholesterol levels
Match the following medications with their effects on lipid levels:
β-blockers = Increases triglycerides Isotretinoin = Increases triglycerides Cyclosporine = Increases triglycerides Sirolimus = Increases triglycerides
Match the following lipoprotein abnormalities with their characteristics:
Elevated total cholesterol = Increases risk of premature ASCVD Elevated low-density lipoprotein (LDL) = Increases risk of premature ASCVD Elevated triglycerides = Increases risk of premature ASCVD Reduced high-density lipoprotein (HDL) = Increases risk of premature ASCVD
Match the following conditions with their effects on lipid levels:
Weight gain = Increases triglycerides Excessive intake of carbohydrates = Increases triglycerides Excessive intake of saturated fat = Increases cholesterol levels Diabetes = Increases triglycerides and cholesterol levels
Match the following lipoprotein disorders with their risks:
Primary dyslipidemia = Increased risk of premature ASCVD Secondary dyslipidemia = Lower risk of premature ASCVD Familial hypercholesterolemia (FH) = Increased risk of premature ASCVD Homozygous familial hypercholesterolemia = Increased risk of premature ASCVD
Match the following measures with their effects on CHD events:
↓ TC (total cholesterol) = Reduces mortality and CHD events ↓ LDL (low-density lipoprotein) = Reduces mortality and CHD events ↑ HDL (high-density lipoprotein) = Reduces mortality and CHD events ↓ TG (triglycerides) = No effect on mortality and CHD events
Match the following lipoprotein disorders with their management approaches:
Primary dyslipidemia = Lifestyle modifications and medications Secondary dyslipidemia = Correcting underlying abnormality when possible Familial hypercholesterolemia (FH) = Lifestyle modifications and medications Homozygous familial hypercholesterolemia = Lifestyle modifications and medications
Match the lipids with their characteristic:
Cholesterol = Plays a central role in the pathogenesis of atherosclerosis Triglycerides = One of the major lipids in the body Phospholipids = Major lipids in the body Lipoprotein = Transport lipids in the body
Match the disease with its cause:
ASCVD = Lipid abnormalities Atherosclerosis = Migration of LDL into vessel walls Hyperlipidemia = Imbalance of lipids in the blood Hypothyroidism = Secondary dyslipidemia
Match the term with its definition:
Atherosclerosis = Progressive process initiated by LDL particles in vessel walls ASCVD = Collective term for coronary, cerebrovascular, and peripheral arterial disease Hyperlipidemia = Abnormal levels of lipids in the blood Dyslipidemia = Imbalance of lipids in the blood
Match the process with its outcome:
Oxidation of LDL particles = Endothelial cell dysfunction Migration of LDL particles = Atherosclerosis Macrophages taking up oxidized LDL particles = Inflammation Lipid abnormalities = ASCVD
Match the type of dyslipidemia with its characteristic:
Primary dyslipidemia = Caused by genetic defects Secondary dyslipidemia = Caused by underlying abnormality, such as diabetes Familial hypercholesterolemia = Caused by genetic defects Hypothyroidism = Caused by underlying abnormality, such as diabetes
Match the medication with its effect on lipids:
Thiazide diuretics = Increase triglycerides β-blockers = Increase triglycerides and decrease HDL-C Glucocorticoids = Increase triglycerides and decrease HDL-C Oral contraceptives (α-Monophasics) = Decrease triglycerides and HDL-C
Match the term with its description:
Lipoprotein particles = Transport cholesterol, triglycerides, and phospholipids in the body LDL particles = Low-density lipoprotein particles HDL particles = High-density lipoprotein particles ASCVD risk = 10-year risk of cardiovascular disease
Match the process with its result:
Atherogenesis = Endothelial cell dysfunction and inflammation Lipid abnormalities = ASCVD Macrophages taking up oxidized LDL particles = Inflammation and foam cell formation Oxidation of LDL particles = Inflammation and foam cell formation
Match the following medications with their effect on cholesterol levels:
Thiazides = ↑5–7% initially, ↑0–3% later β-blockers (Nonselective) = No change α-Blocking = No change or ↓ Glucocorticoids = ↑5–10
Match the following medications with their effect on triglycerides:
Diuretics (Loop) = No change β-blockers (Selective) = ↑15–30 Ethanol = ↑up to 50 Isotretinoin = ↑50–60
Match the following medications with their effect on HDL-C levels:
Thiazides = ↑1 β-blockers (Nonselective) = ↓10–15 α-Agonists and antagonists = ↑0–15 Cyclosporine = No change
Match the following medications with their comments:
Diuretics (Thiazides) = Effects transient; monitor for long-term effects β-blockers = Selective β-blockers have greater effects than nonselective α-Blocking = Lipid neutral Oral contraceptives (α-Monophasics) = Effects caused by reduced lipolytic activity and/or ↑VLDL synthesis
Match the following medications with their effects on triglycerides and HDL-C levels:
Oral contraceptives (α-Triphasics) = ↑10–15 and ↑5–10 Glucocorticoids = ↑15–20 and No change Isotretinoin = ↑50–60 and ↓10–15 Ethanol = ↑up to 50 and ↑
Match the following medications with their effects on cholesterol levels:
Cyclosporine = ↑15–20 Isotretinoin = ↑5–20 Glucocorticoids = ↑5–10 α-Blocking = No change or ↓
Match the following medications with their effects on triglycerides levels:
Oral contraceptives (α-Monophasics) = ↑10–45 Oral contraceptives (α-Triphasics) = ↑10–15 β-blockers (Selective) = ↑15–30 Ethanol = ↑up to 50
Match the following medications with their effects on HDL-C levels:
Oral contraceptives (α-Monophasics) = ↑15 to ↓15 Oral contraceptives (α-Triphasics) = ↑5–10 Isotretinoin = ↓10–15 Ethanol = ↑
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.
This quiz covers the background, diagnosis, treatment, and management of dyslipidemia, including pharmacological and non-pharmacological approaches. It also touches on hyperlipidemia, low HDL, and core treatments.
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