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53 Cards in this Set

  • Front
  • Back
what are ther major risk factors for coronary artery disease?
45+ man, 55+woman, family hx, DM, hypertension, smoking, abdominal obesity,lowl HDL (<40),high LDL
w/ CAD, what should be done to further evaluate plasma lipoproteins? (already have glc and cholesterol)
LDL panel after 10 hr fast
why identify risk factors for CAD?
1. reversible 2. determine LDL goal
LDL gaol for pts w/ known CAD or equivalent risk (DM, atherosclerotic diseases)
<100 mg/dl, maybe even 70
increased risk fo MI sudden death in 10 years in pts w/ known CAD or equivalent risk (DM, atherosclerotic diseases)
20%
LDL goal for pts w/ 2 or more CAD risk factors?
<130mg/dl
increased risk of MI or sudden death in 10 yrs in pts 2 or more CAD risk factors?
10-20%
LDL gaoal for pts w/ no or 1 risk factor for CAD?
<160mg/dl
risk of MI or death w/ in 10 years for pts w/ no or 1 risk factor for CAD?
<10%
in an LDL panel?
total cholesterol, triglycerides, HDL
how to calculated LDL?
total cholesterol-hdl-triglycerides/5
why is fasting important w/ LDL panel?
need to get rid of chylomicroms, which invalidates calculation in VLDL
role of LDL cholesterol
forward cholesterol transport (from liver to other cells)--> cholesterol is part of membranes, precursors for steroid hormones
why are elvetaed levels of ldl cholesterol
treatable risk factor for CAD (become foam cells when taken up by macrophages scavenger receptors in arterial walls)
role of hdl cholesterol
reverse cholesterol transport (removes cholesterol from tissues/arteries)--> returns to liver and excretes as bile acid
why are low levels of hdl important
indicate increased coronary risk
what is the major apoprotein in ldl
apob-100
what is the major apoprotein in hdl
apoa-1
genetic hyperlipoproteinemias?
familail combined hyperlipidemia (elevated VLDL/LDL, sometimes low HDL)
threshold cholesterol level for familail hypercholesterolemia?
300-400mg/dl
pathogenesis of familial combined hyperlipidemia?
production of apob-100 increased
effect of reducing cholesterol in someone who already has CAD
reduces risk of death or another MI, doesn't cahnge size of plaques/degree of stenosis, just makes them less likely to rupture
drugs to lower LDL-cholesterol (first priority in treatment)
HMGCo-A reductase inhibitors, bile acid sequestrants, niacin, cholesterol absorption inhibitors
mechanism of HMGCoA reductase inhibitors?
block RLS in choolesterol synthesis--> fall in cholesterol levels--> upregulate hepatic LDL receptors--> increased clearance of LDLfrom plasma + increased VLDL uptake
side fxs statins?
rare-myopathy, elevated transaminase, toxicity when given w/drugs that inhibit cyp3a4
first line drugs for lowering LDL cholesterol?
statins-HMGCoA-reductase inhibitors
mechanism of bile acid sequestrants
bile bile acids intestine + increase their fecal sequestrion--> more cholesterol oxidized to bile acids--> lower intracellular cholesterol levles--> upregulates LDL receptors--> increased LDLclearance
side fx of bile acid sequestrants?
constipation, flatulence, abdominal cramping, drug interference
mechanism of niacin?
decreases LDL & TG, increases LDL by activating receptor that inhibits lipolysis and realease of FFA--> decreased hepatic VLDL production--> decreased LDL production
side fx of niacin>
flushin, hepatitis, insulin resistance (hyperglucemia)
mechanism of action of ezetimibe?
inhibits cholesterol transport, blocking GI absorption of cholesterol
side fx of ezetimibe?
diarrhea, muscle aches
secondary (acquired) causes of hypercholesterolemia?
hypothyroidism, nephrotic syndrom, obstructive jaundice
secondary (acquired) causes of hypertiglycerlemia
hypothyroidism, nephrotic syndrome, DM, renal failure, alcohol abuse, oral estrogen therapy
defect in familail hypercholesteroemia?
deficient fxning ldl recepotrs: liver can't remove ldl --> low intracellular cholesterol--> increased hepatic cholesterol synthesis--> foam cells/atherosclerosis
levels of LDL in homozygotes of familail hypercholesterolemia? Heterozygotes?
homo- astronomic!, hetero- 1/2 receptors, 2x the cholesterol)
why do people w/ deficient fxning ldl receptors avoid atherosclerosis (familail hypercholesterolemia)>
SRA recpeots, not LDL receptors, are used to take cholesterol into arteries
what causes thick achilles' tendon in familail hypercholestrolemia?
tendon xatnomas- lipid filled macrophages in tendon (specific)
what is the corenal ring in familail hypercholesterolemia?
arcus conrea- accumulation of lipids (not specific)
how can you tell when chylomicrons are elevated?
plasma triglyceride >1000, (often elevated VLDL)
where do chylomicrons originate
synthesized by intestine from dietary fat
what is the major apoprotien of chylomicons?
apob-48
how are chylomicrons removed from plasma
lipoprotein lipase metabolism them by breakind down TGs in their core
what factors can elevate chylomicrons?
children- genetic deficiency of LPL or apo CII; adults- familail hyperlipidemia, familial hypertriglyceridemia, familial dysbetalipoproteinemia + diabetes, alcoholic, oral estrogens
difference between familail combined hyperlipidemia and familail hypertriglyceremia
in familial hyper TG- only VLDL and triglycerides (not cholesterol) are elevated= no increased risk of CAD
what is dysbetalipoproteinemia?
polymorphism of APO2= remant of VLDL can't be removed; TGs and cholesterol elevated
diabetes and lipoproteins?
poorly controled diabetes--> increased VLDL production and decreased LPL (clears chylomicorns) activity
cause of abdnominal pain in chyomicronemia?
pancreatitis
consequences of chylomicronemia?
pancreatitis, eruptive xantomas, lipemia retinalis, hepatosplenomagaly, dyspnea, neurologic dysfxn
mechanism of fibric acid derivatives?
treat hypertiglyceridemia- decreased hepaic VLDL secretion and lower plasma VLDL, activate PAPR (peroxisomes)
when to use fibric acid derivative?
only have elevated triglycerides
side fx fibric acid derivatives?
GI, hepaptitis, gall stones, myopathy
role of fish oil?
omega-3 fatty acids: inhibit TG synthesis, decrease vLDL production