module 10 lipid lowering meds Flashcards
pharm classes for lipid lowering drugs
HMG CoA reductase inhibitors bile acid sequestrants cholesterol absorption inhibitors fibrates niacin omega 3 fatty acids
HGM CoA reductase inhibitors mechanism of action
inhibit conversion of HGM-CoA to L-mevalonic acid and subsequently cholesterol. (inhibit synthesis of cholesterol)
- should be taken at night
HGM CoA affect on LDL/HDL/TG
LDL lowering
moderately effective at dec. TG
modestly raise HDL
- first line drug
HMG CoA reductase inhibitors AE
myopathy
myositis
rhabdomyolysis (monitor CK)
elevated transaminases (liver function)
HMG CoA drug interactions
metabolized by CYP 3A4
Bile acid sequestrants mechanism of action
highly charged molecules that bind to bile acids in small intestine -> resin-bile acid complex that is excreted in feces
-> causes compensatory conversion of hepatic cholesterol to bile, reducing stores of cholesterol -> up-regulation of LDL receptors -> dec. serum cholesterol
Need to be given after meals
Bile acid sequestrants
cholestyramine
colestipol
colesevelam
Bile acid sequestrants and LDL/HDL/TG
moderately lower LDL
not change to TG or slight inc.
modest increase in HDL
bile acid sequestrants AE
GI:
- bloating
- dyspepsia
Bile acid sequestrants drug interactions
bind of other drugs
dec. absorption of fat-soluable vitamins
HMG-CoA reductase inhibitors
STATINS atorvastastin fluvastatin lovastatin pitavastatin rosuvastatin simvastatin
Cholesterol absorption inhibitors
ezetimibe
ezetimibe MOA
blocks biliary and dietary cholesterol as well as phytosterol (plant) absorption in the small intestine
- > upregulation of LDL receptors and hepatic cholesterol biosynthesis
- often used in combo with statin to block biosynthesis
ezetimibe and LDL/HDL/TG
lowers LDL
lowers TG
modestly increases HDL
fibrates
gemfibrozil
fenofibrate
clofibrate
“fib”
fibrates MOA
activating PPARa -> reduction in TG-rich lipoproteins and inc. in HDL
- inc. fatty acid oxidation in hepatocytes
- dec. TG synthesis
Fibrates and LDL/HDL/TG
Dec. TG
dec. LDL, possible inc.
inc. HDL
- most effecting TG lowering drugs and used primarily in pt with elevated TG and low HDL
fibrate AE
GI discomfort
inc. transaminases
myopathy
arrhythmia
fibrate drug interaction
displace warfarin from albumin -> inc. fee warfarin
inc. cyclosporin clearance
Niacin
nicotinic acid
vitamin B3
niacin MOA
inhibits fatty acid release from adipose tissue and fatty acid/TG production in liver.
-> dec. LDL
Reduces uptake of HDL -> inc. HDL
niacin and LDL/HDL/TG
dec. LDL
inc. HDL
dec. TG
niacin AE
flushing (pretreat with aspirin) hepatotoxicity pruritis hyperuricemia myopathy impaired insulin sensitivity
omega 3 fatty acids
eicosapentaenoic acid
docosahexaenoic acid
fish oil
omega 3 fatty acid MOA
reduce TG biosynthesis
increase fatty acid oxidation in the liver
omega 3 fatty acid and LDL/HDL/TG
dec. TG
inc LDL
inc. HDL
PCSK9 inhibitors MOA
prvent the protein PCSK9 from biding and degrading LDL receptors in the liver
-> inc. LDL receptors -> dec. LDL serum levels
PCSK9 inhibitors
alirocumab
evolocumab
PCSK9 inhibitors and LDL/HDL/TG
dec. LDL
most potent statins
atorvastatin
rosuvastatin
