Flashcards in Anti-hyperlipidemia/dyslipidemia drugs Deck (19)
atorvastatin & rosuvastatin
moderate intensity statins?
atorvastatin, rosuvastatin, simvastatin, pravastatin, lovastatin, fluvastatin, pitavastatin
low intensity statins?
simvastatin, pravastatin, lovastatin, fluvastatin, pitavastatin
MOA of statin?
inhibit HMG-CoA reductase, inhibits cholesterol production, increases cholesterol uptake from blood stream by increasing LDL receptors, PCSK9 upregulation
distinguishing characteristics: variable onset, peaks effectively typically in a few weeks, duration variable, metabolism variable & typically involves a CYP
statins that don't utilize CYP3A4?
predicted action for statins? uses?
first line therapy for primary & secondary prevention of ASCVD and familial hypercholesterolemia
uses: ASCVD, hypercholesterolemia
C/I in active liver dz, PG & breast feeding; can cause myopathy, increase in liver enzymes, nausea, H/A
natural products that interact w/statin therapy?
red yeast rice will propagate
niacin might increase response
alcohol induces toxicity
grapefruit inhibits CYP3A4
BAS used as tx for hyperlipidemia?
MOA: resins that bind bile acids in the intestines, reduces enterohepatic recycling, increases hepatic conversion of cholesterol to bile acid, upregulates LDL receptors on the liver
distinguishing characteristics: not metabolized
uses: hypercholesterolemia for high risk pt who is intolerant to other main tx or are on maximal dose of other tx
MOA: prevents absorption of dietary biliary cholesterol, upregulates LDL receptors in liver, lowers plasma LDL
distinguishing characteristics: 30% undergoes glucoronide conjugation in the small intestine and liver; about 80% excreted in the feces
uses: adjunctive tx in homozygous familial hypercholeseterolemia and primary hyperlipidemia, typically used when intolerant to other main tx
C/I in PG and breast feeding, increase in liver enzymes when administered w/other main tx
inhibits sterol absorption in the gut and would lower effectiveness of green tea, omega-3 FAs, sitostanol and b-sitosterol
MOA: lowers production & increased clearance of VLDL, increases HDL production, lowers TG & increases HDL but has variable effect on LDL
distinguishing characteristics: metabolized through glucuronidation in the liver or KD, excretion is ~60% in the urine
fibrates: fenofibrate and gemifibrozil
uses: hypercholesterolemia or mixed dyslipidemia as adjunct therapy or monotherapy in pts who can't tolerate other main tx; hypertriglyceridemia (first line tx)
C/I in liver dz, severe renal impairment, ESRD, pre-existing GB dz, break feeding
SEs: dyspepsia, gallstones, myopathy
interaction w/red rice yeast may increase myopathy risk, niacin might increase hepatotoxicity of this tx, alcohol might increase hepatotoxicity
fibrates: fenofibrate & gemifibrozil
2 supplements that might help w/dyslipidemia?
niacin & omega 3 FAs
MOA: unclear, may increase lipoprotein lipase activity, enhance TG removal from plasma, reduce TG synthesis, increase HDL-C levels
distinguishing characteristics: metabolized into NAD+ in liver, but pathways become saturated at doses used to tx hyperlipidemia, ~70% excreted in urine
uses: hypercholesterolemia or mixed dyslipidemia as adjunct therapy for pts who do not tolerate fibrates or omega 3 FAs or monotherapy for pts who don't tolerate statins, BAS or fibrates
C/I in active liver dz, gout, PUD
SEs: hepatotoxicity, hyperglycemia, hyperuricemia, upper GI distress, flushing, itching