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Flashcards in 092914 lipid disorders Deck (32):
1

greatest risk factor for MI is

LDL:HDL ratio

2

Friedewald equation

LDL-C = Total cholesterol - (HDL-C + VLDL-C)

3

when is LDL-C at risk for ASCVD?

greater than 100

4

when is HDL at risk for ASCVD?

under 40

5

when are triglycerides at risk for CAD?

200-499

6

when are triglycerides at risk for pancreatitis?

greater than 1000

7

why does most heart disease happen in people with "normal" cholesterol?

if you look at average American, will have average American diet, but compare this to an urban Japanese population--Americans have a higher risk for CVD

"normal" does not mean optimal. only when you have optimal cholesterol levels, do you have a rare chance of having ASCVD

8

most cases of lipid disorders are the result of

genetic disorders that is unmasked or promoted by lifestyle or environment

9

which genetic hyperlipidemias are predominantly genetic with minimal lifestyle influence?

type I-severe hypertriglyceridemia
type IIa-familial hypercholesterolemia

10

least well recognized thing by LDL receptor in liver

LDL (because it only has B-100)--least well recognized by liver

11

you see elevated chylomicrons in what types of genetic hyperlipidemias

type I (in infants) and type V(in adults)

12

type I hyperlipidemia

severe hypertriglyeridemia
presents in childhood with trigly. greater than 2000

primary defect is LPL or apoC2, so chylomicrons are dysfuncation, so triglycerides are not removed from chylomicron

very rare

13

type IIa hyperlipidemia

familial hypercholesterolemia

primary defect is in LDL-R, so LDL accumulates

presents commonly with coronary artery disease under age 60

see slide

14

obese adults can have normal cholesterol but increased what?

small solid LDLs (they have increased small solid LDLs because their belly constantly releases free fatty acids to the liver, resulting in more VLDL production. CETP senses the fatty acids in VLDL and exchanges them with LDL. LDL now has more triglyceride than it used to have--, so hepatic lipase works on it to remove TGs. LDL becomes small dense LDLs)

15

effect of type IIb hyperlipidemia on HDL levels occurs how?

small dense HDLs easily get their apo A-I caps removed. Apo-A-I caps go to the kidney and get excreted, so HDL levels are lower.

16

what levels of lipids do you see with type II-B hyperlipidemia

high trigly.
low HDL
increased LDL-P

high triglycerides drive CETP which moves triglycerides to LDL and HDL prompting further LPL/HL activity

17

what is unique about apoE2

least well recognized apoE by LDL receptor

18

type III hyperlipidemia

dysbetalipoproteinemia
due to apo E2/E2 and environment
because apoE2/E2 on IDL is poorly recognized by LDL-R

see slide

19

type IV hyperlipidemia

hypertriglyceridemia-apoC2 or apoC3 on VLDL do not work, so accumulates

see slide

20

type II-B hyperlipidemia

familial combined hyperlipidemia or with metabolic syndrome

see slide

21

type V hyperlipidemia

familial hypertriglyceridemia-apoC2 or apoC3 on both VLDL and chylomicrons don't work, so accumulate

22

which particles are preodimnantely filled with triglycerides

chylomicrons, VLDL, IDL

23

which are the major triglyceride disorders?

type I, IIB, IV, V

24

cholesterol in intima can be removed by

HDL

25

which are the atherosclerogenic lipoproteins

LDL, IDL

90% of circulating cholesterol is in LDL

26

which are the lipid disorders that increase risk of ASCVD

type IIA, IIB, III

27

how do you raise HDL

exercise, alcohol, estrogens

28

what kind of genetic mutations are seen in type IIa familial hypercholesterolemia

LDL-R mutation (decreased number or fxn)--in 90% of cases. there are 1600 known mutations

apoB mutation (can't bind to LDL-R)

PCSK9 gain of fxn mutation (drugs that are PCSK9 inhibitors are in the pipeline)

29

metabolic syndrome requires 3 of 5. list them

see slide

waist diameter
trigerlycerides
HDL
BP
fasting blood glucose

30

in the case of type IIB hyperlipidemia, why are triglyceride rich VLDL bad?

CETP will try to balance ratio of TGs to cholesterol in lipoproteins. excess triglycerides promote ongoing LPL activity that reduces size of HDL and LDL-P. small LDL-P do not fit well into LDL-R and stay in circulation longer.

31

metabolic syndrome causes an atherogenic dyslipidemia--define

high trigs
low HDL
LDL-particles in ratio to LDL-cholesterol--the ratio is much larger than normal.

32

why can metabolic syndrome pts with normal LDL levels have a lot of disease?

b/c when HDL is abnormally low and triglycerides are abnormally high, the calculated LDL cholesterol levels do not correlate well with actual number of LDL particles. LDL particles are what build up in intima.