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Questions and Answers
What is the main source of lipid precursors in the body?
What is the main source of lipid precursors in the body?
- Intestine (correct)
- Liver
- Muscle tissue
- Adipose tissue
Which component gives lipoproteins their hydrophilic coat?
Which component gives lipoproteins their hydrophilic coat?
- Triglycerides
- Free fatty acids
- Cholesterol
- Phospholipids (correct)
What type of metabolic pathway involves the transport of absorbed cholesterol and triglycerides?
What type of metabolic pathway involves the transport of absorbed cholesterol and triglycerides?
- Exogenous pathway (correct)
- Lipid oxidation pathway
- Endogenous pathway
- Intracellular pathway
What is the primary function of lipoprotein lipase in lipid metabolism?
What is the primary function of lipoprotein lipase in lipid metabolism?
Which of the following is NOT a class of lipoproteins?
Which of the following is NOT a class of lipoproteins?
Which tissue is primarily responsible for the synthesis of lipoproteins?
Which tissue is primarily responsible for the synthesis of lipoproteins?
What is the primary storage form of lipids in adipose tissue?
What is the primary storage form of lipids in adipose tissue?
What component is found in the core of lipoproteins?
What component is found in the core of lipoproteins?
What type of hyperlipidemia is primarily characterized by an increase in chylomicrons?
What type of hyperlipidemia is primarily characterized by an increase in chylomicrons?
Which type of hyperlipidemia involves an increased level of both LDL and VLDL?
Which type of hyperlipidemia involves an increased level of both LDL and VLDL?
Familial dysbetalipoproteinemia is associated with an increase in which type of lipoprotein?
Familial dysbetalipoproteinemia is associated with an increase in which type of lipoprotein?
Which classification corresponds to Familial hypertriglyceridemia?
Which classification corresponds to Familial hypertriglyceridemia?
Which of the following is NOT a secondary cause of hyperlipidemia?
Which of the following is NOT a secondary cause of hyperlipidemia?
Type IV hyperlipidemia is characterized by an increase in which lipoprotein?
Type IV hyperlipidemia is characterized by an increase in which lipoprotein?
What type of hyperlipidemia is indicated by an increased level of chylomicrons and VLDL?
What type of hyperlipidemia is indicated by an increased level of chylomicrons and VLDL?
Which of the following lipoproteins is most significantly increased in Familial Combined Hyperlipidemia?
Which of the following lipoproteins is most significantly increased in Familial Combined Hyperlipidemia?
What is primarily stored and processed in the liver from the chylomicron remnants?
What is primarily stored and processed in the liver from the chylomicron remnants?
What happens to triglycerides in VLDL when delivered to the blood?
What happens to triglycerides in VLDL when delivered to the blood?
After being hydrolyzed, what term is used to describe the smaller VLDL particles that have more cholesterol?
After being hydrolyzed, what term is used to describe the smaller VLDL particles that have more cholesterol?
What are the three potential pathways for cholesterol in LDL?
What are the three potential pathways for cholesterol in LDL?
What role do HDL particles play in relation to cholesterol from dying cells?
What role do HDL particles play in relation to cholesterol from dying cells?
What does the endogenous pathway of cholesterol metabolism primarily involve?
What does the endogenous pathway of cholesterol metabolism primarily involve?
Which of the following is not a function of HDL particles?
Which of the following is not a function of HDL particles?
What can complications arise from the deposition of cholesterol in subintimal blood vessels?
What can complications arise from the deposition of cholesterol in subintimal blood vessels?
Cholesterol is primarily synthesized in the kidneys and then stored in the liver.
Cholesterol is primarily synthesized in the kidneys and then stored in the liver.
VLDL particles are larger and have more triglycerides compared to LDL particles.
VLDL particles are larger and have more triglycerides compared to LDL particles.
HDL particles facilitate the return of cholesterol from tissues back to the liver.
HDL particles facilitate the return of cholesterol from tissues back to the liver.
LDL particles can directly deposit cholesterol into the brain to maintain neural function.
LDL particles can directly deposit cholesterol into the brain to maintain neural function.
Triglycerides in VLDL are hydrolyzed by lipoprotein lipase into fatty acids and glycerol.
Triglycerides in VLDL are hydrolyzed by lipoprotein lipase into fatty acids and glycerol.
Cholesterol returned to the liver from dying cells is carried exclusively by chylomicron remnants.
Cholesterol returned to the liver from dying cells is carried exclusively by chylomicron remnants.
Atherosclerosis is caused by cholesterol being deposited in subintimal blood vessels from HDL.
Atherosclerosis is caused by cholesterol being deposited in subintimal blood vessels from HDL.
The endogenous pathway involves the synthesis and assembly of chylomicrons in the intestines.
The endogenous pathway involves the synthesis and assembly of chylomicrons in the intestines.
Type III hyperlipidemia is characterized by an increase in IDL.
Type III hyperlipidemia is characterized by an increase in IDL.
Familial hypercholesterolemia correlates with elevated levels of triglycerides and VLDL.
Familial hypercholesterolemia correlates with elevated levels of triglycerides and VLDL.
Secondary hyperlipidemia can be caused by hypothyroidism.
Secondary hyperlipidemia can be caused by hypothyroidism.
Type IV hyperlipidemia is marked by increased levels of chylomicrons.
Type IV hyperlipidemia is marked by increased levels of chylomicrons.
Type IIb hyperlipidemia includes both LDL and VLDL elevation.
Type IIb hyperlipidemia includes both LDL and VLDL elevation.
Familial mixed hyperlipidemia is classified as Type V.
Familial mixed hyperlipidemia is classified as Type V.
Familial combined hyperlipidemia is solely linked to high levels of HDL.
Familial combined hyperlipidemia is solely linked to high levels of HDL.
Type I hyperlipidemia is known for elevated levels of LDL particles.
Type I hyperlipidemia is known for elevated levels of LDL particles.
Lipoproteins consist of a hydrophilic lipid core surrounded by a hydrophobic coat of phospholipids and proteins.
Lipoproteins consist of a hydrophilic lipid core surrounded by a hydrophobic coat of phospholipids and proteins.
The liver is the primary site for the synthesis of lipoproteins.
The liver is the primary site for the synthesis of lipoproteins.
Adipose tissue primarily synthesizes lipoproteins from triglycerides.
Adipose tissue primarily synthesizes lipoproteins from triglycerides.
Chylomicrons transport absorbed cholesterol and triglycerides via the endogenous pathway.
Chylomicrons transport absorbed cholesterol and triglycerides via the endogenous pathway.
Lipoprotein lipase hydrolyzes the core triglycerides into free fatty acids for tissue utilization.
Lipoprotein lipase hydrolyzes the core triglycerides into free fatty acids for tissue utilization.
There are four classes of lipoproteins based on their lipid composition and density.
There are four classes of lipoproteins based on their lipid composition and density.
The principal source of lipid precursors in the body is the liver.
The principal source of lipid precursors in the body is the liver.
Fat cells synthesize lipoproteins from the triglycerides they store.
Fat cells synthesize lipoproteins from the triglycerides they store.
What is the primary genetic cause of Type I hyperlipidemia?
What is the primary genetic cause of Type I hyperlipidemia?
Identifying the subtype, what characterizes Type IIb hyperlipidemia?
Identifying the subtype, what characterizes Type IIb hyperlipidemia?
Describe the lipoprotein elevation associated with Type IV hyperlipidemia.
Describe the lipoprotein elevation associated with Type IV hyperlipidemia.
What are the primary lipid abnormalities seen in Familial dysbetalipoproteinemia (Type III)?
What are the primary lipid abnormalities seen in Familial dysbetalipoproteinemia (Type III)?
Which acquired conditions are primarily associated with secondary hyperlipidemia?
Which acquired conditions are primarily associated with secondary hyperlipidemia?
What is the significance of elevated LDL in Type IIa hyperlipidemia?
What is the significance of elevated LDL in Type IIa hyperlipidemia?
Explain the distinction between primary and secondary hyperlipidemia.
Explain the distinction between primary and secondary hyperlipidemia.
What are the three potential pathways for cholesterol in LDL particles?
What are the three potential pathways for cholesterol in LDL particles?
In familial mixed hyperlipidemia, what is the notable lipoprotein composition?
In familial mixed hyperlipidemia, what is the notable lipoprotein composition?
Describe the transformation of VLDL particles after triglycerides are hydrolyzed by lipoprotein lipase.
Describe the transformation of VLDL particles after triglycerides are hydrolyzed by lipoprotein lipase.
How do HDL particles function in relation to cholesterol from dying cells?
How do HDL particles function in relation to cholesterol from dying cells?
In the endogenous pathway, what key components are synthesized and assembled together?
In the endogenous pathway, what key components are synthesized and assembled together?
Explain the role of chylomicron remnants in cholesterol metabolism.
Explain the role of chylomicron remnants in cholesterol metabolism.
What complications can arise from the deposition of cholesterol in subintimal blood vessels?
What complications can arise from the deposition of cholesterol in subintimal blood vessels?
How is cholesterol transported and utilized by tissues after being released from VLDL?
How is cholesterol transported and utilized by tissues after being released from VLDL?
What happens to cholesterol in the body when cells die?
What happens to cholesterol in the body when cells die?
What is the primary factor that determines the classification of lipoproteins?
What is the primary factor that determines the classification of lipoproteins?
What is the role of the endothelial lipoprotein lipase in the metabolism of chylomicrons?
What is the role of the endothelial lipoprotein lipase in the metabolism of chylomicrons?
Explain the significance of adipose tissue in lipid metabolism.
Explain the significance of adipose tissue in lipid metabolism.
Identify the pathway associated with the transport of exogenous lipids and describe its process.
Identify the pathway associated with the transport of exogenous lipids and describe its process.
Discuss how lipoprotein composition influences its function in the body.
Discuss how lipoprotein composition influences its function in the body.
How does the liver contribute to lipoprotein metabolism?
How does the liver contribute to lipoprotein metabolism?
What type of lipoprotein is primarily formed from the hydrolysis of triglycerides in plasma?
What type of lipoprotein is primarily formed from the hydrolysis of triglycerides in plasma?
Define the main components of a lipoprotein and their significance in its structure.
Define the main components of a lipoprotein and their significance in its structure.
The chylomicron remnants mainly contain ______ which pass to the liver.
The chylomicron remnants mainly contain ______ which pass to the liver.
Cholesterol in LDL may be utilized by tissues or returned to the ______.
Cholesterol in LDL may be utilized by tissues or returned to the ______.
Lipoproteins consist of a hydrophobic lipid core surrounded by a hydrophilic coat of ______ and proteins.
Lipoproteins consist of a hydrophobic lipid core surrounded by a hydrophilic coat of ______ and proteins.
Smaller VLDL particles having less TGs and more cholesterol are termed ______.
Smaller VLDL particles having less TGs and more cholesterol are termed ______.
Atherosclerosis can be caused by cholesterol deposited in ______ blood vessels.
Atherosclerosis can be caused by cholesterol deposited in ______ blood vessels.
The liver is the main site of synthesis of ______.
The liver is the main site of synthesis of ______.
In the exogenous pathway, absorbed cholesterol and triglycerides are transported in plasma as ______.
In the exogenous pathway, absorbed cholesterol and triglycerides are transported in plasma as ______.
When cells die, cholesterol is returned to the liver as plasma ______ particles.
When cells die, cholesterol is returned to the liver as plasma ______ particles.
The endogenous pathway involves the assembly of ______ and delivery to the blood.
The endogenous pathway involves the assembly of ______ and delivery to the blood.
The ______ tissue is the main site of storage of triglycerides.
The ______ tissue is the main site of storage of triglycerides.
On the vascular endothelium, the core triglycerides are hydrolyzed by a surface-bound lipoprotein ______.
On the vascular endothelium, the core triglycerides are hydrolyzed by a surface-bound lipoprotein ______.
Triglycerides in VLDL are hydrolyzed into free fatty acids by ______.
Triglycerides in VLDL are hydrolyzed into free fatty acids by ______.
There are ______ classes of lipoproteins depending on their relative proportion of core lipids.
There are ______ classes of lipoproteins depending on their relative proportion of core lipids.
Cholesterol in the liver undergoes oxidation to become ______ acids.
Cholesterol in the liver undergoes oxidation to become ______ acids.
Fat cells do not synthesize any ______.
Fat cells do not synthesize any ______.
The intestine is the main source of lipid ______.
The intestine is the main source of lipid ______.
Primary hyperlipidemia is ______ determined.
Primary hyperlipidemia is ______ determined.
Type I hyperlipidemia is characterized by an increase in ______.
Type I hyperlipidemia is characterized by an increase in ______.
Familial hypercholesterolemia correlates with elevated levels of ______.
Familial hypercholesterolemia correlates with elevated levels of ______.
Type IV hyperlipidemia is associated with high levels of ______.
Type IV hyperlipidemia is associated with high levels of ______.
Type III hyperlipidemia is characterized by an increase in ______.
Type III hyperlipidemia is characterized by an increase in ______.
Secondary hyperlipidemia can be caused by conditions such as ______.
Secondary hyperlipidemia can be caused by conditions such as ______.
Familial mixed hyperlipidemia is classified as Type ______.
Familial mixed hyperlipidemia is classified as Type ______.
Familial combined hyperlipidemia includes an increase in both ______ and VLDL.
Familial combined hyperlipidemia includes an increase in both ______ and VLDL.
Match the types of hyperlipidemia with their characteristics:
Match the types of hyperlipidemia with their characteristics:
Match the types of hyperlipidemia with their corresponding genetic conditions:
Match the types of hyperlipidemia with their corresponding genetic conditions:
Match the secondary causes of hyperlipidemia with their corresponding conditions:
Match the secondary causes of hyperlipidemia with their corresponding conditions:
Match the lipoprotein types with their primary increase in lipid class:
Match the lipoprotein types with their primary increase in lipid class:
Match the types of hyperlipidemia with their respective synonym:
Match the types of hyperlipidemia with their respective synonym:
Match each type of hyperlipidemia with its hallmark lipid elevation:
Match each type of hyperlipidemia with its hallmark lipid elevation:
Match the classification of hyperlipidemia with their genetic description:
Match the classification of hyperlipidemia with their genetic description:
Match the increase in lipoproteins with their respective type of hyperlipidemia:
Match the increase in lipoproteins with their respective type of hyperlipidemia:
Match the lipoproteins with their respective characteristics:
Match the lipoproteins with their respective characteristics:
Match the metabolic pathways with their functions:
Match the metabolic pathways with their functions:
Match the lipoprotein metabolism processes with their descriptions:
Match the lipoprotein metabolism processes with their descriptions:
Match the consequences of cholesterol deposition with their potential effects:
Match the consequences of cholesterol deposition with their potential effects:
Match the lipoprotein categories with their respective lipid compositions:
Match the lipoprotein categories with their respective lipid compositions:
Match the types of hyperlipidemia with their characteristics:
Match the types of hyperlipidemia with their characteristics:
Match the lipoprotein return processes with their outcomes:
Match the lipoprotein return processes with their outcomes:
Match the key players in lipid metabolism with their functions:
Match the key players in lipid metabolism with their functions:
Match the following types of hyperlipidemia with their characteristics:
Match the following types of hyperlipidemia with their characteristics:
Match the following lipoprotein properties with their respective classes:
Match the following lipoprotein properties with their respective classes:
Match the following metabolic pathways with their primary functions:
Match the following metabolic pathways with their primary functions:
Match the following components involved in lipoproteins with their features:
Match the following components involved in lipoproteins with their features:
Match the following conditions with their corresponding lipoprotein abnormalities:
Match the following conditions with their corresponding lipoprotein abnormalities:
Match the following lipoproteins with their primary role in lipid metabolism:
Match the following lipoproteins with their primary role in lipid metabolism:
Match the following characteristics with the corresponding lipoprotein metabolism site:
Match the following characteristics with the corresponding lipoprotein metabolism site:
Match the following pathways with their sequence of events in lipid absorption:
Match the following pathways with their sequence of events in lipid absorption:
Study Notes
Lipoproteins and Plasma Lipids
- Lipoproteins have a hydrophobic lipid core (triglycerides (TGs) or cholesterol) encased by a hydrophilic phospholipid and apoprotein coat, allowing miscibility in aqueous plasma.
- Five classes of lipoproteins are defined by core lipid composition, apoprotein type, size, and density.
Sources and Metabolism of Lipoproteins
- The intestine is the primary source of lipid precursors, while the liver synthesizes lipoproteins.
- Adipose tissue serves as the main storage site for triglycerides; fat cells do not synthesize lipoproteins.
Exogenous Pathway
- Chylomicrons transport absorbed cholesterol and TGs in plasma.
- Lipoprotein lipase hydrolyzes core TGs on vascular endothelium, releasing free fatty acids (FFAs) for tissue utilization.
- Chylomicron remnants, primarily cholesterol, are taken up by the liver for storage, bile acid synthesis, or VLDL production.
Endogenous Pathway
- VLDL, assembled from cholesterol and newly synthesized TGs, circulates in the blood and undergoes hydrolysis to release FFAs.
- Smaller VLDL particles, with reduced TGs and increased cholesterol, are classified as LDL.
- LDL cholesterol can be used by tissues, returned to the liver, or deposited in subintimal regions, potentially causing atherosclerosis.
- HDL particles return cholesterol from dead cell membranes to the liver, functioning as scavenger lipoproteins.
Classification of Hyperlipidemia
-
Primary (Familial; Hereditary) Hyperlipidemia: Genetically determined.
- Type I: Increased chylomicrons (Familial chylomicronemia).
- Type IIa: Increased LDL (Familial hypercholesterolemia).
- Type IIb: Increased LDL and VLDL (Familial combined hyperlipidemia).
- Type III: Increased IDL (Familial dysbetalipoproteinemia).
- Type IV: Increased VLDL (Familial hypertriglyceridemia).
- Type V: Increased VLDL and chylomicrons (Familial mixed hyperlipidemia).
-
Secondary (Acquired) Hyperlipidemia: Associated with factors such as:
- Hypercholesterolemia linked to hypothyroidism, nephrotic syndrome, and certain drugs.
Lipoproteins and Plasma Lipids
- Lipoproteins have a hydrophobic lipid core (triglycerides (TGs) or cholesterol) encased by a hydrophilic phospholipid and apoprotein coat, allowing miscibility in aqueous plasma.
- Five classes of lipoproteins are defined by core lipid composition, apoprotein type, size, and density.
Sources and Metabolism of Lipoproteins
- The intestine is the primary source of lipid precursors, while the liver synthesizes lipoproteins.
- Adipose tissue serves as the main storage site for triglycerides; fat cells do not synthesize lipoproteins.
Exogenous Pathway
- Chylomicrons transport absorbed cholesterol and TGs in plasma.
- Lipoprotein lipase hydrolyzes core TGs on vascular endothelium, releasing free fatty acids (FFAs) for tissue utilization.
- Chylomicron remnants, primarily cholesterol, are taken up by the liver for storage, bile acid synthesis, or VLDL production.
Endogenous Pathway
- VLDL, assembled from cholesterol and newly synthesized TGs, circulates in the blood and undergoes hydrolysis to release FFAs.
- Smaller VLDL particles, with reduced TGs and increased cholesterol, are classified as LDL.
- LDL cholesterol can be used by tissues, returned to the liver, or deposited in subintimal regions, potentially causing atherosclerosis.
- HDL particles return cholesterol from dead cell membranes to the liver, functioning as scavenger lipoproteins.
Classification of Hyperlipidemia
-
Primary (Familial; Hereditary) Hyperlipidemia: Genetically determined.
- Type I: Increased chylomicrons (Familial chylomicronemia).
- Type IIa: Increased LDL (Familial hypercholesterolemia).
- Type IIb: Increased LDL and VLDL (Familial combined hyperlipidemia).
- Type III: Increased IDL (Familial dysbetalipoproteinemia).
- Type IV: Increased VLDL (Familial hypertriglyceridemia).
- Type V: Increased VLDL and chylomicrons (Familial mixed hyperlipidemia).
-
Secondary (Acquired) Hyperlipidemia: Associated with factors such as:
- Hypercholesterolemia linked to hypothyroidism, nephrotic syndrome, and certain drugs.
Lipoproteins and Plasma Lipids
- Lipoproteins have a hydrophobic lipid core (triglycerides (TGs) or cholesterol) encased by a hydrophilic phospholipid and apoprotein coat, allowing miscibility in aqueous plasma.
- Five classes of lipoproteins are defined by core lipid composition, apoprotein type, size, and density.
Sources and Metabolism of Lipoproteins
- The intestine is the primary source of lipid precursors, while the liver synthesizes lipoproteins.
- Adipose tissue serves as the main storage site for triglycerides; fat cells do not synthesize lipoproteins.
Exogenous Pathway
- Chylomicrons transport absorbed cholesterol and TGs in plasma.
- Lipoprotein lipase hydrolyzes core TGs on vascular endothelium, releasing free fatty acids (FFAs) for tissue utilization.
- Chylomicron remnants, primarily cholesterol, are taken up by the liver for storage, bile acid synthesis, or VLDL production.
Endogenous Pathway
- VLDL, assembled from cholesterol and newly synthesized TGs, circulates in the blood and undergoes hydrolysis to release FFAs.
- Smaller VLDL particles, with reduced TGs and increased cholesterol, are classified as LDL.
- LDL cholesterol can be used by tissues, returned to the liver, or deposited in subintimal regions, potentially causing atherosclerosis.
- HDL particles return cholesterol from dead cell membranes to the liver, functioning as scavenger lipoproteins.
Classification of Hyperlipidemia
-
Primary (Familial; Hereditary) Hyperlipidemia: Genetically determined.
- Type I: Increased chylomicrons (Familial chylomicronemia).
- Type IIa: Increased LDL (Familial hypercholesterolemia).
- Type IIb: Increased LDL and VLDL (Familial combined hyperlipidemia).
- Type III: Increased IDL (Familial dysbetalipoproteinemia).
- Type IV: Increased VLDL (Familial hypertriglyceridemia).
- Type V: Increased VLDL and chylomicrons (Familial mixed hyperlipidemia).
-
Secondary (Acquired) Hyperlipidemia: Associated with factors such as:
- Hypercholesterolemia linked to hypothyroidism, nephrotic syndrome, and certain drugs.
Lipoproteins and Plasma Lipids
- Lipoproteins have a hydrophobic lipid core (triglycerides (TGs) or cholesterol) encased by a hydrophilic phospholipid and apoprotein coat, allowing miscibility in aqueous plasma.
- Five classes of lipoproteins are defined by core lipid composition, apoprotein type, size, and density.
Sources and Metabolism of Lipoproteins
- The intestine is the primary source of lipid precursors, while the liver synthesizes lipoproteins.
- Adipose tissue serves as the main storage site for triglycerides; fat cells do not synthesize lipoproteins.
Exogenous Pathway
- Chylomicrons transport absorbed cholesterol and TGs in plasma.
- Lipoprotein lipase hydrolyzes core TGs on vascular endothelium, releasing free fatty acids (FFAs) for tissue utilization.
- Chylomicron remnants, primarily cholesterol, are taken up by the liver for storage, bile acid synthesis, or VLDL production.
Endogenous Pathway
- VLDL, assembled from cholesterol and newly synthesized TGs, circulates in the blood and undergoes hydrolysis to release FFAs.
- Smaller VLDL particles, with reduced TGs and increased cholesterol, are classified as LDL.
- LDL cholesterol can be used by tissues, returned to the liver, or deposited in subintimal regions, potentially causing atherosclerosis.
- HDL particles return cholesterol from dead cell membranes to the liver, functioning as scavenger lipoproteins.
Classification of Hyperlipidemia
-
Primary (Familial; Hereditary) Hyperlipidemia: Genetically determined.
- Type I: Increased chylomicrons (Familial chylomicronemia).
- Type IIa: Increased LDL (Familial hypercholesterolemia).
- Type IIb: Increased LDL and VLDL (Familial combined hyperlipidemia).
- Type III: Increased IDL (Familial dysbetalipoproteinemia).
- Type IV: Increased VLDL (Familial hypertriglyceridemia).
- Type V: Increased VLDL and chylomicrons (Familial mixed hyperlipidemia).
-
Secondary (Acquired) Hyperlipidemia: Associated with factors such as:
- Hypercholesterolemia linked to hypothyroidism, nephrotic syndrome, and certain drugs.
Lipoproteins and Plasma Lipids
- Lipoproteins have a hydrophobic lipid core (triglycerides (TGs) or cholesterol) encased by a hydrophilic phospholipid and apoprotein coat, allowing miscibility in aqueous plasma.
- Five classes of lipoproteins are defined by core lipid composition, apoprotein type, size, and density.
Sources and Metabolism of Lipoproteins
- The intestine is the primary source of lipid precursors, while the liver synthesizes lipoproteins.
- Adipose tissue serves as the main storage site for triglycerides; fat cells do not synthesize lipoproteins.
Exogenous Pathway
- Chylomicrons transport absorbed cholesterol and TGs in plasma.
- Lipoprotein lipase hydrolyzes core TGs on vascular endothelium, releasing free fatty acids (FFAs) for tissue utilization.
- Chylomicron remnants, primarily cholesterol, are taken up by the liver for storage, bile acid synthesis, or VLDL production.
Endogenous Pathway
- VLDL, assembled from cholesterol and newly synthesized TGs, circulates in the blood and undergoes hydrolysis to release FFAs.
- Smaller VLDL particles, with reduced TGs and increased cholesterol, are classified as LDL.
- LDL cholesterol can be used by tissues, returned to the liver, or deposited in subintimal regions, potentially causing atherosclerosis.
- HDL particles return cholesterol from dead cell membranes to the liver, functioning as scavenger lipoproteins.
Classification of Hyperlipidemia
-
Primary (Familial; Hereditary) Hyperlipidemia: Genetically determined.
- Type I: Increased chylomicrons (Familial chylomicronemia).
- Type IIa: Increased LDL (Familial hypercholesterolemia).
- Type IIb: Increased LDL and VLDL (Familial combined hyperlipidemia).
- Type III: Increased IDL (Familial dysbetalipoproteinemia).
- Type IV: Increased VLDL (Familial hypertriglyceridemia).
- Type V: Increased VLDL and chylomicrons (Familial mixed hyperlipidemia).
-
Secondary (Acquired) Hyperlipidemia: Associated with factors such as:
- Hypercholesterolemia linked to hypothyroidism, nephrotic syndrome, and certain drugs.
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Description
This quiz covers essential concepts related to hyperlipidemia, including the types of drugs used to lower plasma lipids. It is designed to enhance understanding of lipoproteins and their role in lipid management. Ideal for students studying pharmacology or related health sciences.
