092914 lipid disorders

Question 1

greatest risk factor for MI is

Answer 1

LDL:HDL ratio

Question 2

Friedewald equation

Answer 2

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

Question 3

when is LDL-C at risk for ASCVD?

Answer 3

greater than 100

Question 4

when is HDL at risk for ASCVD?

Answer 4

under 40

Question 5

when are triglycerides at risk for CAD?

Answer 5

200-499

Question 6

when are triglycerides at risk for pancreatitis?

Answer 6

greater than 1000

Question 7

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

Answer 7

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

Question 8

most cases of lipid disorders are the result of

Answer 8

genetic disorders that is unmasked or promoted by lifestyle or environment

Question 9

which genetic hyperlipidemias are predominantly genetic with minimal lifestyle influence?

Answer 9

type I-severe hypertriglyceridemia

type IIa-familial hypercholesterolemia

Question 10

least well recognized thing by LDL receptor in liver

Answer 10

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

Question 11

you see elevated chylomicrons in what types of genetic hyperlipidemias

Answer 11

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

Question 12

type I hyperlipidemia

Answer 12

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

Question 13

type IIa hyperlipidemia

Answer 13

familial hypercholesterolemia

primary defect is in LDL-R, so LDL accumulates

presents commonly with coronary artery disease under age 60

see slide

Question 14

obese adults can have normal cholesterol but increased what?

Answer 14

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)

Question 15

effect of type IIb hyperlipidemia on HDL levels occurs how?

Answer 15

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.

Question 16

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

Answer 16

high trigly.
low HDL
increased LDL-P

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

Question 17

what is unique about apoE2

Answer 17

least well recognized apoE by LDL receptor

Question 18

type III hyperlipidemia

Answer 18

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

see slide

Question 19

type IV hyperlipidemia

Answer 19

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

see slide

Question 20

type II-B hyperlipidemia

Answer 20

familial combined hyperlipidemia or with metabolic syndrome

see slide

Question 21

type V hyperlipidemia

Answer 21

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

Question 22

which particles are preodimnantely filled with triglycerides

Answer 22

chylomicrons, VLDL, IDL

Question 23

which are the major triglyceride disorders?

Answer 23

type I, IIB, IV, V

Question 24

cholesterol in intima can be removed by

Answer 24

HDL

Question 25

which are the atherosclerogenic lipoproteins

Answer 25

LDL, IDL

90% of circulating cholesterol is in LDL

Question 26

which are the lipid disorders that increase risk of ASCVD

Answer 26

type IIA, IIB, III

Question 27

how do you raise HDL

Answer 27

exercise, alcohol, estrogens

Question 28

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

Answer 28

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)

Question 29

metabolic syndrome requires 3 of 5. list them

Answer 29

see slide

waist diameter
trigerlycerides
HDL
BP
fasting blood glucose

Question 30

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

Answer 30

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.

Question 31

metabolic syndrome causes an atherogenic dyslipidemia–define

Answer 31

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

Question 32

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

Answer 32

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.