Flashcards in 092914 lipid disorders Deck (32):
greatest risk factor for MI is
LDL-C = Total cholesterol - (HDL-C + VLDL-C)
when is LDL-C at risk for ASCVD?
greater than 100
when is HDL at risk for ASCVD?
when are triglycerides at risk for CAD?
when are triglycerides at risk for pancreatitis?
greater than 1000
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
most cases of lipid disorders are the result of
genetic disorders that is unmasked or promoted by lifestyle or environment
which genetic hyperlipidemias are predominantly genetic with minimal lifestyle influence?
type I-severe hypertriglyceridemia
type IIa-familial hypercholesterolemia
least well recognized thing by LDL receptor in liver
LDL (because it only has B-100)--least well recognized by liver
you see elevated chylomicrons in what types of genetic hyperlipidemias
type I (in infants) and type V(in adults)
type I hyperlipidemia
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
type IIa hyperlipidemia
primary defect is in LDL-R, so LDL accumulates
presents commonly with coronary artery disease under age 60
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)
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.
what levels of lipids do you see with type II-B hyperlipidemia
high triglycerides drive CETP which moves triglycerides to LDL and HDL prompting further LPL/HL activity
what is unique about apoE2
least well recognized apoE by LDL receptor
type III hyperlipidemia
due to apo E2/E2 and environment
because apoE2/E2 on IDL is poorly recognized by LDL-R
type IV hyperlipidemia
hypertriglyceridemia-apoC2 or apoC3 on VLDL do not work, so accumulates
type II-B hyperlipidemia
familial combined hyperlipidemia or with metabolic syndrome
type V hyperlipidemia
familial hypertriglyceridemia-apoC2 or apoC3 on both VLDL and chylomicrons don't work, so accumulate
which particles are preodimnantely filled with triglycerides
chylomicrons, VLDL, IDL
which are the major triglyceride disorders?
type I, IIB, IV, V
cholesterol in intima can be removed by
which are the atherosclerogenic lipoproteins
90% of circulating cholesterol is in LDL
which are the lipid disorders that increase risk of ASCVD
type IIA, IIB, III
how do you raise HDL
exercise, alcohol, estrogens
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)
metabolic syndrome requires 3 of 5. list them
fasting blood glucose
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.
metabolic syndrome causes an atherogenic dyslipidemia--define
LDL-particles in ratio to LDL-cholesterol--the ratio is much larger than normal.