Lipoprotein Disorders, Dyslipidemia & Metabolic Syndrome — Actual Notes
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51 Terms
Q: What are hyperlipoproteinemias?
A: Disorders with increased plasma lipoproteins.
Q: What causes Type I hyperlipoproteinemia?
A: LPL or ApoC-II deficiency.
Q: What does LPL normally do, and what activates it?
A: LPL hydrolyzes TGs in chylomicrons/VLDL; ApoC-II activates LPL.
Q: What accumulates in Type I hyperlipoproteinemia?
A: ↑ chylomicrons, ↑ VLDL, ↑ TGs, with ↓ LDL/HDL.
Q: Does Type I markedly increase coronary disease risk?
A: Usually no.
Q: What causes familial hypercholesterolemia (Type IIa)?
A: LDLR defect, ApoB-100 defect, or PCSK9 gain-of-function.
Q: What happens when LDL receptor function is impaired?
A: ↓ hepatic LDL uptake → ↑ plasma LDL/cholesterol → ↑ atherosclerosis/CAD.
Q: What does PCSK9 normally do?
A: Promotes lysosomal degradation of LDL receptors
Q: How do PCSK9 inhibitors lower LDL?
A: ↓ LDLR degradation → ↑ surface LDLR → ↑ hepatic LDL uptake → ↓ LDL.
Q: What are examples of PCSK9 inhibitors?
A: Alirocumab and evolocumab.
Q: What causes Type III familial dysbetalipoproteinemia?
A: ApoE defect.
Q: What does ApoE normally do?
A: Mediates hepatic uptake of chylomicron and VLDL remnants.
Q: What accumulates in Type III disease?
A: Chylomicron remnants and VLDL remnants, causing ↑ cholesterol/TG and xanthomas.
Q: What causes Type IV hyperlipoproteinemia?
A: Increased hepatic VLDL production.
Q: What is the major lipid abnormality in Type IV?
A: ↑ VLDL and ↑ triglycerides.
A: ↑ VLDL and ↑ triglycerides.
A: Obesity, insulin resistance, glucose intolerance, T2DM, and increased cardiovascular risk.
Q: What causes Tangier disease?
A: ABCA1 deficiency.
Q: What does ABCA1 do?
A: Transfers cellular cholesterol onto nascent HDL.
Q: What happens to HDL in Tangier disease?
A: Impaired cholesterol efflux and HDL maturation → very low HDL.
Q: What causes abetalipoproteinemia?
A: MTP deficiency.
Q: What does MTP do?
A: Loads lipids onto ApoB for lipoprotein assembly.
Q: What happens in MTP deficiency?
A: ↓ chylomicrons → ↓ VLDL → ↓ IDL → ↓ LDL.
Q: What causes hypoalphalipoproteinemia?
A: Accelerated degradation of ApoA-I/ApoA-II → ↓ HDL.
Q: What is ApoA-I's major function?
A: Major HDL apoprotein and activator of LCAT.
Q: What does LCAT do?
A: Converts free cholesterol into cholesteryl ester, allowing cholesterol to be stored in the HDL core.
Q: What is reverse cholesterol transport?
A: HDL-mediated movement of cholesterol from peripheral tissues toward the liver.
Q: What are the key steps in HDL maturation?
A: ABCA1 loads cholesterol onto HDL → ApoA-I activates LCAT → LCAT esterifies cholesterol → HDL transports cholesterol toward liver.
Q: What causes Wolman disease?
A: Lysosomal acid lipase deficiency.
Q: What accumulates in Wolman disease?
A: Triglycerides and cholesteryl esters within lysosomes/cells.
Q: What happens in LCAT deficiency?
A: ↓ cholesterol esterification → ↓/abnormal HDL → impaired reverse cholesterol transport; corneal opacification, anemia, renal disease can occur.
Q: Why can protein/amino-acid deficiency cause fatty liver?
A: ↓ Apo synthesis → ↓ VLDL assembly/export → TG remains in liver.
Q: Why can choline deficiency cause fatty liver?
A: ↓ phosphatidylcholine → impaired VLDL assembly/export → hepatic TG accumulation.
Q: How does LDL contribute to atherosclerosis?
A: LDL enters arterial wall → oxidation → macrophage uptake → foam cells → plaque.
Q: Why is HDL generally considered protective?
A: It promotes reverse cholesterol transport and has additional protective effects.
Q: What enzyme do statins inhibit?
A: HMG-CoA reductase.
Q: How do statins lower plasma LDL?
A: ↓ hepatic cholesterol synthesis → ↑ hepatic LDL receptors → ↑ LDL uptake → ↓ plasma LDL.
Q: Name three statins.
A: Atorvastatin, simvastatin, rosuvastatin.
Q: How do bile acid sequestrants lower LDL?
A: Bind intestinal bile acids → ↑ fecal loss → liver uses cholesterol to make bile acids → ↑ LDL receptors → ↓ LDL.
Q: Name two bile acid sequestrants.
A: Cholestyramine and colestipol.
Q: What does ezetimibe do?
A: Blocks intestinal cholesterol absorption, lowering hepatic cholesterol and increasing LDL receptors.
Q: What is the primary lipid association of fibrates?
A: ↓ triglycerides/VLDL through increased LPL-mediated clearance.
Q: Name a fibrate.
A: Gemfibrozil.
Q: What are the major lipid effects of niacin?
A: ↓ TG, ↓ LDL, ↑ HDL, and ↓ Lp(a).
Q: What is metabolic syndrome?
A: A cluster of abnormalities associated with insulin resistance and increased cardiovascular/T2DM risk.
Q: What are the five major features of metabolic syndrome?
A: Central obesity, ↑ TG, ↓ HDL, ↑ BP, ↑ fasting glucose/T2DM.
Q: What TG and glucose values are used in the lecture's metabolic syndrome criteria?
A: TG ≥150 mg/dL and fasting glucose ≥100 mg/dL or established T2DM.
Q: What HDL values count as low in metabolic syndrome?
A: <40 mg/dL in men; <50 mg/dL in women.
Q: What BP threshold is used in the lecture's metabolic syndrome criteria?
A: ≥130 systolic or ≥85 diastolic.
Q: What is the characteristic lipid pattern of metabolic syndrome?
A: ↑ TG + ↓ HDL, often with more atherogenic LDL particles.
Q: Match the major proteins to their functions: LPL, ApoC-II, ApoB-100, ApoE, ABCA1, ApoA-I, LCAT, MTP, PCSK9.
A: LPL: breaks down TG; ApoC-II: activates LPL; ApoB-100: LDLR binding; ApoE: remnant uptake; ABCA1: cholesterol efflux to HDL; ApoA-I: activates LCAT; LCAT: cholesterol esterification; MTP: lipid loading onto ApoB; PCSK9: LDLR degradation.
🔥 12 Cards to Know Cold
Type I = LPL/ApoC-II deficiency → ↑ chylomicrons → ↑ TG
Type IIa = LDLR/ApoB/PCSK9 → ↑ LDL → ↑ cholesterol/CAD
Type III = ApoE → ↓ remnant clearance → ↑ remnants
Type IV = ↑ VLDL production → ↑ TG
ABCA1 = cellular cholesterol → HDL
ApoA-I = activates LCAT
LCAT = free cholesterol → cholesteryl ester
MTP = loads lipid onto ApoB
PCSK9 = LDL receptor degradation
Statins = inhibit HMG-CoA reductase → ↑ hepatic LDL receptors → ↓ LDL
Fibrates = ↓ TG/VLDL
Metabolic syndrome = central obesity + ↑ TG + ↓ HDL + ↑ BP + ↑ glucose
One final mental map
LPL → TG breakdown
ApoC-II → LPL activation
ApoB-100 → LDL receptor binding
ApoE → remnant clearance
ABCA1 → cholesterol onto HDL
ApoA-I → LCAT activation
LCAT → cholesterol esterification
MTP → ApoB lipoprotein assembly
PCSK9 → LDLR degradation
Statins → HMG-CoA reductase inhibition → ↑ LDLR → ↓ LDL