1-Statins and Fibrates Flashcards
LDL vs HDL
LDL is seen as bad
HDL seen as good
what is atherosclerosis/plaque
fatty deposits /cholesterol that occlude blood vessels
where does cholesterol accumulate ?
in macrophages (foam cells) that have invaded in the endothelial wall
LDL and HDL flow in macrophages
LDL taken up via receptors
cholesterol is often transported out which is mediated by HDL
what causes vessel occlusion
when the plaque cap ruptures from macrophages dyinh
how do statins work (broad)
reduce circulating LDL and total cholesterol
two ways that cholesterol become packages
dietary/extrinsic (taken up by LDL receptor)
OR synthesized in liver hepatosite
where do statins effect
hint: enzyme
HMG-CoA reductase
what kind of enzyme is HMG-CoA reductase and where is it located
transmembrane protein in ER membrane
how do statins effect HMG-CoA reductase
competitive inhibition
what happens when HMG-CoA reductase gets inhibited
less cholesterol is made in hepatocytes, leading to an increase of LDL receptors, therefore reducing circulating LDL
how do statins reduce circulating LDL
less cholesterol is made in hepatocytes, leading to an increase of LDL receptors, therefore reducing circulating LDL
example of statin
atorvastatin
extraction rate/ratio of statins
high! meaning rapidly processed by first pass metabolism
fibrate example
fenofibrate
what do fibrates target
PPAR receptors
what do PPAR receptors do
increase expression of lipoprotein lipase
what does lipoprotein lipase do
breaksdown triacylglycerides in LDLs and increases uptake of acids as fuel
increase LDL uptake in liver
reduced VLDL production in liver
what kind of receptors are PPARs
intracellular receptors, act as transcription factors
what kind of drugs are fibrates
agonists
what does HMG-CoA reductase do
help synthesize cholesterol
what is a lipoprotein
a complex of cholesterol, triglycerides, and apolipoproteins involved in lipid transport
