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Cardiovascular > Cholesterol and Lipoproteins > Flashcards

Cholesterol and Lipoproteins Flashcards

1
Q

LDL-R; mechanism

A

Receptor-mediated endocytosis; receptor recycled and apolipoprotein endosome fuses with lysosome

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1
Q

Metabolic syndrome symptoms

A

insulin resistance, hypertension, thrombosis, TAG:HDL ratio >4

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2
Q

Plants and sterols

A

Can’t synthesize cholesterol; only stigmasterol, ergosterol

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3
Q

Atherogenic lipoproteins

A

ApoB - VLDL, LDL-C/P, Chylomicrons, IDL

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4
Q

Apolipoproteins and associated apoprotein

A

ApoB-48 - chylomicrons; synthesized in intestines ApoB-100 - synthesized in liver -VLDLs - along with other apoproteins -IDLs -LDLs ApoA-I and ApoA-II - HDL

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4
Q

Type IIa

A

Familial Hypercholesteronemia Lipoprotein - LDL Mutation - AD; LDL-R, apoB, PCSK9 Lipid Effect - TC > 275, LDL > 190

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5
Q

Polycystic kidney disease effects which lipid

A

Increases LDL

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6
Q

Type IV symptoms

A

Autosomal dominant Pancreatitis

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8
Q

Cholesterol vs cholesteryl esters

A

Cholesteryl esters - more non-polar, hydrophobic; found in lipoproteins

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9
Q

Effect of hypothyroidism

A

Increased LDL, Increased TAGs

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10
Q

Apolipoprotein lipid profile

A

Chylomicrons - highest TAG:Cholesterol ratio VLDLs - high TAG:Cholesterol ratio HDLs - Lowest TAG:cholesterol ratio

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10
Q

PCSK9; mechanism

A

Serine protease: Binds to EGF-A region of LDL-R Induces endocytosis of complex Lysosomal degradation

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10
Q

Most Important Ischemic Heart Disease Risk Factor

A

LDL:HDL ratio Lifestyle

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10
Q

Optimal levels of lipids

A

TC 40/50 Non-HDL

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10
Q

Type I lipid disorder

A

Hyperchylomicronemia Lipoprotein - Chylomicron Mutation - LPL or apoC-II/III Lipid Effect - TAGs > 2000

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11
Q

LDL-R; regulation

A

Thyroxine/estrogen - induce LDL-R expression SREBP/Scap - regulation of LDL-R expression PCSK9 - inhibit LDL-R; stimulate it’s degradation

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12
Q

Apoproteins found in all apolipoproteins

A

ApoC-II = necessary for lipoprotein lipase activation ApoE = necessary for LDL-R/LRP interaction

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13
Q

Major TAG disorders

A

Type I, IIb, IV

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15
Q

ACAT; function

A

Esterification of cholesterol into cholesteryl esters

15
Q

PCSK9; mutations

A

Overexpression = decreased LDL-R = increased cholesterol levels = Increased CVD risk Underexpression = increased LDL-R = decreased cholesterol levels = decreased CVD risk AD - gain-of-function = increased CVD risk

16
Q

Type V

A

Hypertriglyceridemia Lipoprotein - VLDL, chylomicron Mutation - LPL or apoC-III Lipid Effect - TAGs > 1000

18
Q

LPL Deficiency

A

Severe hypertriglyceridemia

19
Q

LDL-R; ligand

A

ApoE

21
Q

LDL-R; mutations

A

AD - hypercholesterolemia; mutation of ligand binding region

22
Q

ACAT; types

A

ACAT-1 = sebaceous glands, macrophages, adrenocortical ACAT-2 = liver, intestines

23
Q

Ranges of Lipids

A

TC = 200-350 = ASCVD risk LDL >100 = ASCVD risk HDL 1000 = pancreatitis

24
Q

Type III

A

Dysbetalipoproteinemia Lipoprotein - VLDL, IDL Mutation - overexpression of ApoE-II Lipid Effect - TC/TAGs = 200-500

25
Q

Major ASCVD disorders

A

Type IIa, IIb, III

26
Q

Lipid panel includes?

A

TC, TAGs, HDL, LDL (calc), Non-HDL (calc) Can include - apoB, LDL-P

27
Q

Type I symptoms

A

Autosomal recessive Pancreatitis, hepatosplenmegaly, xanthomas. No increased ASCVD risk

29
Q

Regulation of LPL

A

High glycogen, fats = Induction of LPL for storage of lipids into adipose tissue Fasting = decreased LPL expression; prevents storage of lipids out of plasma

30
Q

Cholesterol is a precursor for what

A

Gonads -pregnenlone to progesterone to androgens to estrogens Adrenal -progesterone to mineralcorticoids (aldosterone and corticosterone) and glucocorticoids Vitamin D -7-dehydrocholesterol to cholecalciferol (Vitamin D) Liver -7-hydroxycholesterol to bile acid

31
Q

Type IV

A

Hypertriglyceridemia Lipoprotein - VLDL Mutation - LPL or apoC-III Lipid Effect - TAGs = 500-1000

32
Q

Cholesterol synthesis; important steps

A

HMG-CoA Synthase -Acetyl-CoA + Acetoacetyl-CoA = HMG-CoA HMG-CoA Reductase -HMG-CoA + 2NADPH = mevalonate *Rate-limiting step

34
Q

Cofactors of LPL

A

Heparin - anchors LPL to capillary endothelia IV heparin - used to displace LPL into plasma; for measuring LPL levels ApoC-II - obligatory cofactor

35
Q

Function of LPL

A

To hydrolyze phospholipids: TAG to DAG to MAG

36
Q

Location of LPL

A

Capillary endothelium; near adipose tissue, skeletal muscle, heart muscle, glands, etc.

36
Q

Factors lowering HDL

A

o Insulin resistance/metabolic syndrome o Anabolic steroids o Trans-fats o Progestins o Smoking

37
Q

Type IIa symptoms

A

Autosomal dominant Heterozygotes = TC = 300 mg/dL Homozygotes = TC = 700 mg/dL Accelerated atherosclerosis (MI before 20), xanthomas, corneal arcus

39
Q

Lipoprotein w/ longest half-life

A

LDL

40
Q

Type IIb

A

Familial Compound Hyperlipidemia Lipoprotein - VLDL, LDL Mutation - metabolic syndrome/insulin resistance; ApoB-100 Lipid Effect - TC = 100, TAGs = 200-500, HDL < 40/50 increased VLDL remnants and LDL-P

41
Q

Factors increasing HDL

A

o Aerobic exercise o Alcohol o Estrogens

43
Q

Metabolic Syndrome Criteria

A

add picture

44
Q

Obstructive kidney disease affects which lipid

A

Increases LDL

45
Q

What is the exogenous pathway of apolipoproteins

A

Dietary lipids in intestinal lumen (1) intestinal epithelial cell cytoplasm (2) esterification of cholesterol (3) efflux of plant sterols (4) chylomicron formation (5) transport of lipids to liver and tissues (6) chylomicron remnants 1 = NPC1L1 = influx of lipids into epithelial -ezetimibe targets NPC1L1 2 = ACAT-2 3 = ABCG5/8 = efflux of plant sterols out of cell -Mutation = sitosterolemia = xanthomas, increased CVD risk 4 = MTP = apoB-48 synthesized in intestine; MTP transports esters to apoB-48 5 = LDL-R/apoE 6 = processed by liver -apoB-48 degraded -other apoproteins recycled to HDL

Cardiovascular (12 decks)

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