Lipoportein and lipid disorders

Question 1

healthy/risk factor limits
BMI
BP
FBS

Answer 1

BMI <28, >35

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

FBS <100, Diabetes

Question 2

LDL-C >____ = risk for ASCVD

HDL < ____ = risk for ASCVD

Trigs between ____ and ___ > Risk for CAD

(>1000 = pancreatitis)

Answer 2

LDL- C > 100

HDL <40

Trigs 200-499

Question 3

genetic lipid disorders

Answer 3

Type I

Type IIa

Question 4

lifestyle or disease driven lipid disorders

Answer 4

Type II B

Type III

Type IV

Type V

Question 5

Name and common presentation,

Type I

Answer 5

Severe hypertriglyceridemia

childhood with Trigs >2000

Question 6

Name and common presentation,

Type IIB

Answer 6

Familial Combinded Hyperlipedia

(or with metabolic syndrome)

LDL, VLDL high

(all numbers borderline)

Question 7

Name and common presentation, Type IIa

Answer 7

Familal Hypercholesterolemia

CAD Age<60,

LDL high

Question 8

Name and common presentation, Type III

Answer 8

Dysbetaliporoteineima

Premature CAD

excess VLDL, IDL

Question 9

Name and common presentation, type IV

Answer 9

hypertriglyceridemia

pancreatitis,

VLDL high, Trigs 500-1000

Question 10

Name and common presentation, type V

Answer 10

Hypertriglyceridemia

pancreatitis, usually diabetic

high VLDL+chylomicrons

Trigs>1000

Question 11

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

Answer 11

B-100

Question 12

LPL removes ___ from chylomicrons to mobilize fFA

Answer 12

TG

Question 13

LPL removes TG from ____, leading to fFA and IDL

Answer 13

VLDLs

Question 14

Pathogenesis of Type I (severe hyperchylomicronia)

Answer 14

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

Question 15

pathogenesis type IIA (FH)

Answer 15

LDL-R defective, LDL accumulates

Question 16

pathogenesis type IIB (Famial combined hyperlipidemia)

Answer 16

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

Question 17

role of Hepatic lipase

Answer 17

remove TG from HDL and LDL to form sdLDL and sdHDL

Question 18

pathogenesis type III (dysbetalipoproteinemia)

Answer 18

apoE2 on IDL is poorly recognized by LDL-R

Apo E2 overproduction

excess of VLDL and LDL

Question 19

pathogenesis type IV (Hypertriglyceridemia)

Answer 19

ApoC2 or apoC3 on VLDL do not work > VLDL accumulate

Question 20

Pathogenesis type V Familail hypertriglyceridemia

Answer 20

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

Question 21

ApoC2 impact on LPL

ApoC3 impact

Answer 21

ApoC2 - activates LPL > TG removal from VLDL/Chylo

ApoC3 - deactivates > particle can now mobilize

Question 22

inherited loss of LPL or defective apoC2/C3

chylomicrons fill with Trigs at enterocyte but cannot offload to periphery

Answer 22

Type I hyperchylomicronemia

Question 23

overproduction of VLDL,

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

TRigs 200-500

Answer 23

Type IIb FH

Question 24

Trigs 500-1000

Large VLDL (poor LPL function)

Answer 24

Type IV hypertriglyceridemia

Question 25

trigs\>1000 excess chylomicrons

Answer 25

Type I severe hypertriglyceridemia

Question 26

raise HDL via (besides diet)

Answer 26

Aerobic exercise Alcohol Estrogens

Question 27

PCSK9 catabolizes drug therapy aims:

Answer 27

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

Question 28

metabolic syndrome causes atherogenic dyslipediamia \> \_\_\_

Answer 28

increased LDL-P Increased VLDL remants (which are very atherogenic)

Question 29

Metabolic syndrome criteria, men

Answer 29

Waist \> 40in Trigs \>150 HDL\<40 BP 135/85 FPG \>100 (wait to have burgers, fatty)

Question 30

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

Answer 30

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

Question 31

metabolic syndrome "atherogenic dyslipidemia"

Answer 31

high trigs low HDL LDL particles \> LDL cholesterol