treatment of dyslipidemias Flashcards
Statins aka
HMG coA reductase inhibitors
(HMG Coa –> mevalonate –> *–> cholesterol
indication for statin therapy
- secondary prevention ASCVD
- LDLC>190
- age >21
- primary prevention diabetes
(LDL 70-189) - primary prevention no diabetes
(LDL 70-189, >7.5% 10yr ASCVD risk)
Max benefit high intensity statin therapy should be used when?
In secondary prevention and
In primary prevention when LDLC >190 or diabetes is present
(atorvastatin or
Rosuvastatin)
Moderate intensity statin should be used when?
When the 10 year ASCVD risk >7.5%
(atorvastatin, rosuvastatin, simvastatin, pravastatin, lovastatin, fluvastatin)
Main mech of statins is the inhibition of HMG CoA reductase, but what is actually the primary means that they lower LDLC?
they increase the number of intrahepatic LDL receptors
and
Increasing the subsequent uptake and catabolism of circulating LDL
Adverse effects of statins
rare but: myopathy myalgias elevation in CPK new onset T2D
When should you use the weaker sauce Bile acid sequestrants?
add on therapy only when monotherapy statins are not tolerated, or during pregnancy
How do bile acid sequestrants work?
reduce enterohepatic circulation of bile acids by increasing intrahepatic LDL receptors
- reduce LDLC by 10-30%
Ezetimibe
lowers cholesterol by selectively inhibiting cholesterol absorption
- great as add on to statins to reduce CVD risk
PCSK9 inhibitors
lowers LDLC up to 60%!
adjuncts to diet + statins for pts with hetero familial hypercholesterolemia or atherosclerotic CVD
Combination therapy for very high LDLC
homo familial hypercholesterolemia, hetero FH + statin intolerance
Statin +
Ezetimibe/
bile acid sequestrants +
Fibrate/niacin
maybe: LDL apheresis
Niacin/nicotinic acid
- lowers LDLC and TG
- raises HDLC
