Anti Hyperlipidemic Flashcards
moa of statins
HMG-CoA reductase inhibitor
dec cholesterol synthisis resulting in::::::
- inc in LDL receptor
- dec VLDL production
SE of statins
hepatotoxicity
myopathy and rhabdomyolysis
inc effect of warfarin
c/i in pregnancy and lactation
moa of niacin
inhibits lipolysis in adipose tissue
dec f.a. release
dec liver synthisis of TGs since no f.a. available
dec VLDL and LDL formation
SE of niacin
inc cutaneous flush
pruritis
how to dec niacin induced SE
aspirin prior to niacin(flush is PG mediated)
slow titration of dose
sustained release
moa of fibrates
act via PPAR: dec TGs via
inc expression of lipoprotein lipase
dec apoCII
(inc HDL via apoAI and apoAII)
SE of fibrates
mc: git
INC BILIARY CHOLESTEROL EXCRETION: GALL STONES
myositis(like statins)
inc warfarin activity(like statins)
moa of bile acid binding resins
form complex with choleaterol which is excreted in feces.
THIS LEADS TO:
inc hepatocyte cholesterol conversion to bile
inc LDL uptake via receptors
SE of bile acid binding sequestrants
constipation, nausea , flatulance
dec absorption of fat soluble vitamins
interferance with drug absorption(digoxin, warfarin, thyroid)-so maintain gap
may raise TGs..C/I in significant hyperTGs(>400)
c/i of bile acid binding resins
hypertriglyceridemia
other use of cholestyramine
dec pruritis due to accumulation of bile acids due to biliary statsis
ezetimibe
cholesterol absorption inhibitor
redn in hrpatic stores and inc clearance from blood
omega 3 f.a.
ecosapentanoic acid EPA
decosahexanoic acif DHA
omega 3 f.a. lowers mainly
TGs
SE of omega 3 f.a.
git:abdominal pain, nausea , diarrhoea, fishy after taste
inc bleeding risk with anticoagulants/ antiplatelets
