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