dyslipidemia Flashcards
(29 cards)
statins MOA and when to take
inhibition of HMG-CoA reductase -> no conversion of HMG-CoA to mevalonate (RLS in cholesterol biosynthesis)
take in the evening; cholesterol synthesis is max from 12 - 2 AM
statin metabolism
metabolized by CYP3A4
AE’s increased with concomitant use of CYP3A4 inhibitors, macrolides, azole antifungles, amiodarone, HN protease inhibitors, and gemfibrozil
statin AE
increase in serum transaminases, myalgia, weakness, rhabdomyolysis
statin contraindications
acute liver disease, persistent unexplained increased serum transaminases, pregnancy
statin monitoring
LFTs (baselines and as clinically indicated thereafter); discontinue if >3x ULN CK levels (baseline and if sxs appear); discontinue if >10x ULN
statin avoiders
grapefruit juice (interferes with CYP3A4) red yeast rice (contains statin active ingredient)
bile acid-binding resins agents
holesyramine, colestipol, colesevelam
BARs MOA
increase LDL catabolism and decrease cholesterol absorption
bind bile acids to prevent reabsorption -> increase cholesterol-using bile synthesis -> increase LDL uptake and clearance
BARs ADME
powder form mixed with water
not systemically absorbed
BARs AE’s
GI (dyspepsia, bloating, abdominal discomfort)
hepatic (hypertriglyceridemia, increased serum transaminases)
pancreatitis
BAR absorption interactions
levothyroxine, warfarin, verapamil, phenytoin (administer 1 hr before or 3-4 after BAR)
fibric acid derivatives agents
gemfibrozil, fenofibrate, fenofibric acid
fibric acid derivatives MOA
increase VLDL clearance and decrease synthesis
activate nuclear transcription factor perioxisome proliferator activated receptor alpha (PPAR-alpha) on hepatocytes -> regulate lipid and glucose metabolism genes -> inhibit lipolysis and decrease hepatic fatty acid uptake
fibric acid derivatives AE’s
increased serum transaminases, myalgia / weakness
fibric acid derivatives contraindications
significant hepatic or renal dysfunction, primary biliary cirrhosis, pre-existing gall bladder disease
fibric acid derivatives intreactions
gemfibrozil > fenofibrate due to hepatic metabolism
fibric acid derivatives monitoring
LFT’s - discontinue if > 3 x ULN
Niacin (nicotinic acid) MOA
decrease LDL and VLDL synthesis
inhibition of triglyceride synthesis, inhibition of lipolysis, enhance LPL activity -> increase VLDL clearance
enhance HDL synthesis by blocking apoA breakdown
Niacin (nicotinic acid) AE’s
flushing (prostaglandin mediated)
dyspepsia, peptic ulcer disease, nausea, hyperuricemia, decreased glucose tolerance, hepatotoxicity
Niacin (nicotinic acid) contraindications
acute liver disease, pregnancy, gout
cholesterol absorption inhibitor agent and MOA
ezetimibe
decrease cholesterol and LDL
inhibit cholesterol absorption at small intestine brush border -> decreased cholesterol delivery -> increased LDLR and clearance
not used much
cholesterol absorption inhibitor AE’s
well tolerated; increases incidence of myopathy and increased transaminases when given with statin
Fish oil MOA
reduce hepatic triglyceride synthesis and increase clearance
fish oil AE’s
dyspepsia, taste aversion, prolonged bleeding time
