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40 Cards in this Set

  • Front
  • Back
mechanism of statins
HMG-CoA reductase inhibitors
this lowerrs the amount of cholesterol synthesized, also increases the amount of LDL receptors expressed by hepatocytes
degradation of LDL receptors also reduced
VLDL and IDL removal increased
HDL may increase
which drugs have the most decrease in TG?
nicotinic acid
fibric acids
which statin has the longest t1/2
which statins are metabolized by CYP3A4?
which statins are metabolized by CYP2C9?
which statin is not metabolized by CYP?
contraindications for statins
children, only if they have homozygous FH or some heterozygotes
when should statins be given?
in evening if single dose (increased cholesterol biosynthesis at 2am)
atorvastatin can be taken any time b/c of long t1/2
which statins are most efficacious for severe hypercholesterolemia?
(these drugs also have the greatest TG lowering capacity of the statins)
which statins level off at the high dose range?

which have linear dosings?
pravastatin, fluvastatin

lovastatin, simvastatin, atorvastatin
adverse effects of statins
hepatotoxicity (3x normal liver enzymes, esp if using EtOH)
which lipid lowering drug is recommended for cildren 11-20 yo
which drugs are resins
MOA of resins
resins are highly + charge, binding negatively charged bile acids
they are large, so not absorbed, bound bile acids are excreted in stool
hepatic cholesterol content declines, so LDL receptors are increased --> LDL clearance
BUT, then HMG-CoA reductase gets upregulated, so there is increased LDL synthesis, counteracting the LDL reduction
what will improve the action of resins?
what happens to TG levels in resin administration?
it increase TG synth, so contra-indicated in pts with severe hyper-TG
administration of resins
must be taken with food!
what is the interaction btwn resins and digitalis
removes dig from GI tract
adverse effects of resins
(both relieved by icreasing dietary fiber)
heartburn/diarrhea (occassional)
malabsorption of vitamin K and folate (rarely)
drug interactions with resins
only cholestyramine adn colestipol bind other drugs
take other drugs either 1 hr before or 3 hrs after resin
MOA of niacin
inhibits VLDL secreation
inhibits lipolysis of TG by lipase, reducing FFA transport to liver (decresaes TG synth)
enhanced LPL activatity, promoting clearance of chylomicrons and VLDL TGs
therapeutic uses of niacin
hyper-TG , hyper-LDL
esp useful in pts with high TG and low HDL
toxicity of niacin
cutaneous vasodilation adn feeling of warmth
acanthosis nigricans (associated with insulin resistance, so contraindicated)
nausea and abdominal discomfort
sustained release --> hepatotoxicity
contraindications of niacin
severe peptic disease
concurrent use wth statin --> myopathy
MOA of fibrates
activates PRAR-alpha (a transcription factor)
thos reduces TG by stimulating FA oxidation
this increases LPL
this reduces expression of apoC-III (which inhibits lipolytic processing) --> enhanced clearance of VLDL
this stimulates apoA-I and apoA-II expression (increase HDL levels)
only modest decrease in LDL, and can cause increases as TG levels are reduced
which fibrate is transported across placenta
contraindications for fibrates
pts with renal failure or hepatic dysfxn
therapeutic uses for fibrates
hyper-TG with predominance of VLDL
adverse effects of fibrates
GI sx
potentiates actions of oral anticoags
inhibitor of sterol absorption
primary effect of ezetimibe
reduction of LDL
minimal increase in HDL
mOA of ezetimibe
selective inhibition of intestinal absorption of cholesterol and phytosterols
effective in absence fo dietary cholesterol b/c inhibits reabsorption of cholesterol excreted in bile
adverse rxn of ezetimibe
reversible impaired hepatic fxn
do liver tests before starting drug, then again every 2-4 months
reasons for using drug combos
VLDL levels are significantly increased during resin tx
LDL and VLDL are elevated initially
LDL or VLDL not normalized with single agent
fibrate + resin
familial combined hyperlipidemia intolerant to niacin
statin + resin
may not control VLDL insome pts iwth familial combined hyperlipidemia
niacin + resin
controls VLDL in familial combined hyperlipidemia
controls VLDL in d/o involving increased VLDL and LDL
effective for heterozygous FH (reversal of CAD)
niacin + stsatin
more effective than either alone
most effective when treating familial combined hyperlipidemia
statin + ezetimibe
synergistic in combo
can treat homozygous FH
resin + niacin + statin
lower effective doses
treats severe d/o involving elevated LDL