Lipoportein and lipid disorders Flashcards

1
Q

healthy/risk factor limits
BMI
BP
FBS

A

BMI <28, >35

BP 120/90, 135/85 (or Rx)

FBS <100, Diabetes

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2
Q

LDL-C >____ = risk for ASCVD

HDL < ____ = risk for ASCVD

Trigs between ____ and ___ > Risk for CAD

(>1000 = pancreatitis)

A

LDL- C > 100

HDL <40

Trigs 200-499

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3
Q

genetic lipid disorders

A

Type I

Type IIa

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4
Q

lifestyle or disease driven lipid disorders

A

Type II B

Type III

Type IV

Type V

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5
Q

Name and common presentation,

Type I

A

Severe hypertriglyceridemia

childhood with Trigs >2000

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6
Q

Name and common presentation,

Type IIB

A

Familial Combinded Hyperlipedia

(or with metabolic syndrome)

LDL, VLDL high

(all numbers borderline)

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7
Q

Name and common presentation, Type IIa

A

Familal Hypercholesterolemia

CAD Age<60,

LDL high

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8
Q

Name and common presentation, Type III

A

Dysbetaliporoteineima

Premature CAD

excess VLDL, IDL

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9
Q

Name and common presentation, type IV

A

hypertriglyceridemia

pancreatitis,

VLDL high, Trigs 500-1000

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10
Q

Name and common presentation, type V

A

Hypertriglyceridemia

pancreatitis, usually diabetic

high VLDL+chylomicrons

Trigs>1000

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11
Q

least well-recognized by LDL receptor in liver, leading to long half life in plasma

A

B-100

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12
Q

LPL removes ___ from chylomicrons to mobilize fFA

A

TG

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13
Q

LPL removes TG from ____, leading to fFA and IDL

A

VLDLs

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14
Q

Pathogenesis of Type I (severe hyperchylomicronia)

A

LPL, ApoC2, or APO-C3 on chylo dysfunctional so TGs not removed from chylo

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15
Q

pathogenesis type IIA (FH)

A

LDL-R defective, LDL accumulates

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16
Q

pathogenesis type IIB (Famial combined hyperlipidemia)

A

Central adipositiy and insulin resistance

(High Trigs, low HDL, increased LDLP)

Trigs drives CETP > moves trigs to LDL and HDL promoting further LPL+HL activitiy

17
Q

role of Hepatic lipase

A

remove TG from HDL and LDL to form sdLDL and sdHDL

18
Q

pathogenesis type III (dysbetalipoproteinemia)

A

apoE2 on IDL is poorly recognized by LDL-R

Apo E2 overproduction

excess of VLDL and LDL

19
Q

pathogenesis type IV (Hypertriglyceridemia)

A

ApoC2 or apoC3 on VLDL do not work > VLDL accumulate

20
Q

Pathogenesis type V Familail hypertriglyceridemia

A

ApoC2 or ApoC3 on both VLDL **AND **Chylomicrons don’t work > accumualte

21
Q

ApoC2 impact on LPL

ApoC3 impact

A

ApoC2 - activates LPL > TG removal from VLDL/Chylo

ApoC3 - deactivates > particle can now mobilize

22
Q

inherited loss of LPL or defective apoC2/C3

chylomicrons fill with Trigs at enterocyte but cannot offload to periphery

A

Type I hyperchylomicronemia

23
Q

overproduction of VLDL,

commonly seen with insulin resistance, metabolic syndrome, inflammation of visceral adiposity

TRigs 200-500

A

Type IIb FH

24
Q

Trigs 500-1000

Large VLDL (poor LPL function)

A

Type IV hypertriglyceridemia

25
Q

trigs>1000

excess chylomicrons

A

Type I severe hypertriglyceridemia

26
Q

raise HDL via (besides diet)

A

Aerobic exercise

Alcohol

Estrogens

27
Q

PCSK9 catabolizes

drug therapy aims:

A

LDL - receptor

drug targets to increase LDL receptor more often to increase pull from blood

28
Q

metabolic syndrome causes atherogenic dyslipediamia > ___

A

increased LDL-P

Increased VLDL remants (which are very atherogenic)

29
Q

Metabolic syndrome criteria, men

A

Waist > 40in

Trigs >150

HDL<40

BP 135/85

FPG >100

(wait to have burgers, fatty)

30
Q

in metabolic syndrome+ type IIb, visceral adiposity and insulin resistance drive ______ leading to ___ push into circulation

the excess ___ promote ongoing LOL activity that reduce HDL and LDL-P, which stay in circulation longer

A

in metabolic syndrome+ type IIb, visceral adiposity and insulin resistance drive FFA to liver leading to trig-rich VLDL push into circulation

the excess Trigs promote ongoing LOL activity that reduce HDL and LDL-P, which stay in circulation longer

31
Q

metabolic syndrome “atherogenic dyslipidemia”

A

high trigs

low HDL

LDL particles > LDL cholesterol