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58 Cards in this Set

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complexes of cholesterol, TGs, and protein used to transport cholesterol from the liver to peripheral cells and back.
lipoproteins
transports fatty acids and cholesterol derived from the diet or synthesized in the intestine from the gut to the liver
chylomicrons
- formed mainly in the liver
- transports endogenous TGs and cholesterol
- contains 15-20% of the total blood cholesterol and most of the TGs measured in the fasting pt
VLDLs
the cholesterol in VLDL is about ___ of total TG conc
1/5
- formed by VLDL catabolism
- transports (60-70%) of cholesterol to the cells
- greatest contribution to the development of artherosclerosis
- main target of cholesterol lowering drugs
LDLs
- formed in the liver and intestine
- transports cholesterol from peripheral cells to the liver
HDLs
a ___ hr fast is req'd to measure cholesterol
12
TG level must be < ___ to measure cholesterol
400 mg/dL
total cholesterol - (HDL + VLDL) = ___
LDL
what is not directly measured with a cholesterol measurement
VLDL (TG/5) and LDL (cholesterol - HDL and VLDL)
Type I hyperlipoproteinemia
elevated chylomicrons
Type IIa hyperlipoproteinemia
elevated LDL
Type IIb hyperlipoproteinemia
elevated LDL and VLDL
Type III hyperlipoproteinemia
elevated IDL
Type IV hyperlipoproteinemia
elevated VLDL
Type V hyperlipoproteinemia
elevated VLDL and chylomicrons
MC lipid abnormality
polygenic hypercholesterolemia
caused by a combination of environmental and genetic factors
according to ATP III classification, what are goals for LDL, HDL, TG, and total cholesterol levels?
LDL < 100 mg/dL
HDL 40-60 mg/dL
TG < 150 mg/dL
Total cholesterol <200
three categories of risk that modify LDL goals
(1) CHD and Diabetes < 100 mg/dL
(2) 2+ risk factors < 130 mg/dL
(3) <2 risk factors < 160 mg/dL
major risk factors
- cigarettes
- HTN (>140/90 mmHg)
- low HDLs (<40 mg/dL)
- FamHx of premature CHD
- men >45 y/o women >55 y/o
LDL level for considering drug therapy for (1) CHD (2) 2+ risk factors (3) <2 risk factors
(1) >130 mg/dL
(2) >130 mg/dL if 10 yr risk @ 10-20%; >160 mg/dL if 10 yr risk @ <10%
(3) >190 mg/dL
HMG CoA Reductase Inhibitors
"-statins"
contraindications for statins
absolute: liver dz
relative: drugs that inhibit P450 3A4 (macrolides, CCBs, and azole antifungals)
BCF statin
Simvastatin
most efficacious statins (2)
atorvastatin and rosuvastatin
statins that can be dosed anytime
atorvastatin and rosuvastatin
statins that can be used w/ renal insufficiency
atorvastatin and fluvastatin
statins that are not affected by C P450 drug interactions
pravastatin and fluvastatin
statin not highly protein bound
pravastatin
statin assoc w/ rhabdomyolysis or myopathy when combined w/ fibric acid
lovastatin
what must be monitored when administering statins?
CPK (myopathy and rhabdomyolysis)
LFTs (obtain baseline and repeat q 6 mos)
how long in between dosing changes w/ statins?
6 wks
which antihyperlipid drug class if liver dysfunction is present?
bile acid sequestrants (BAS)
what are SEs of BAS agents?
- GI distress/constipation
- decreased absorption of other drugs
MOA of BAS agents
more cholesterol gets converted into bile acids
how long between BAS agents and fat-soluble vits, folic and ascorbic acid?
6 hrs
colestipol (colestid) BCF
cholestyramine (questran)
colesevelam (welchol)
bile acid sequestrants
which antihyperlipid class is last line due to GI side effects?
BAS
which BAS agent reqs the smallest dose (best for pt compliance)?
colesevelam
which antihyperlipid class is DoC for pregnancy?
BAS
demonstrated therapeutic benefits of BAS incl:
- reduce major coronary events
- reduce CHD mortality
- only approved agent in pregnancy
MOA of nicotinic acid (niacin)
reduces VLDLs resulting in reduced LDLs
what is best antihyperlipid agent for increasing HDLs?
nicotinic acid (niacin)
what are SEs of Niacin?
- flushing and itching
- hyperglycemia
- hyperuricemia
- upper GI stress
- hepatotoxicity
how can flushing and itching assoc w/ niacin be minimized?
- ASA 30 min prior
- take w/ meals
- titrate up slowly
- use controlled release products
CIs for Niacin use:
- liver dz
- PUD
- hypersensitivity
- caution w/ statins (myopathy and rhabdomyolysis)
MOA of Fibric acids
stimulates lipoprotein lipase which removes chyolmicrons and VLDLs from plasma
what is best agents for decreasing TGs?
fibric acids
what happens to VLDLs when they are catabolized by lipases?
broken down into IDLs and LDLs
SEs of fibric acids:
- GI distress
- gallstones (Lithiasis)
- myopathy and muscle inflammation
CIs of Fibric Acids
- severe renal dz
- severe liver dz
- caution w/ statins (myopathy and rhabdomyolysis)
therapeutic benefits of fibric acids
- reduce progression of coronary lesions
- reduce major coronary events
Ezetimibe (Zetia)
Selective Cholesterol Absorption Inhibitor
lower doses of statins may be possible during combined therapy with:
Ezetimibe (Zetia)
antihyperlipidemic approved for children 10-18 y/o
Ezetimibe (Zetia)
tx for hypertriglyceridemia
niacin, fibrates, and atorvastatin
in txing hyper-TGs, avoid ___ in diabetics and ___ in high LDL pts
niacin; fibrates
stop HMG-CoA reductase inhibitor medication if LFT levels go to ___x the normal upper limit
3x