Flashcards in Antihyperlipidemics Deck (35):
what is the lowest density lipoprotein?
what are the roles of the apolipoproteins?
2. ligands for receptors
3. structural stability
what is the role of NPC1L1?
which drug inhibits the NPC1L1 enzyme?
what is the role of acetyl CoA cholesterol acyltransferase?
converts cholesterol to cholesterol ester
what is the role of diglyceride acyltransferase?
converts monoglycerides to TGs
where are chylomicrons associated with the B28 apoprotein?
where do chylomicrons associate with apoC2 and apo3?
where are the chylomicrons broken down to TGs by lipoprotein lipase?
capillaries (via apoC2)
what is the importance of apoE?
allows chylomicron remnants to be taken back up by liver
what is the importance of apoB100 for VLDL particles?
ligand for LDL receptors (important for clearance of cholesterol from circulatory system)
what is reverse cholesterol transport?
1. HDL accepts excess cholesterol from peripheral tissues
2. HDL is transported to liver where it binds SRB1 via apoA1 and cholesterol esters are selectively delivered to hepatocytes
apoA1 is associated with which lipoproteins? what is its function?
1. HDL, chylomicrons
2. structural for HDL, activates LCAT, SRB1 ligand
apoA2 is associated with which lipoproteins? what is its function?
1. HDL, chylomicrons
2. structural for HDL
apoB48 is associated with which lipoproteins? what is its function?
1. chylomicrons, remnants
apoB100 is associated with which lipoproteins? what is its function?
1. VLDL, LDL, IDL
2. structural for above, ligand for LDL
apoC2 is associated with which lipoproteins? what is its function?
1. chylomicrons, VLDL, HDL
2. COFACTOR FOR LIPOPROTEIN LIPASE
apoE is associated with which lipoproteins? what is its function?
1. chylomicron, VLDL, IDL, HDL
2. ligand for LDL and remnant receptors
what is the cause of primary chylomicronemia? how does it manifest?
1. decrease in lipoprotein lipase activity
2. increased chylomicrons, VLDL
what is the cause of familial hypertriglyceridemia? how does it manifest?
1. impaired removal of VLDL and/or chylomicrons
2. increased VLDL (moderate), VLDL AND chylomicrons (severe)
what is the cause of familial combined hyperlipoproteinemia? how does it manifest?
1. increased VLDL production by liver
2. increased VLDL, LDL
what is the cause of familial dysbetalipoproteinemia? how does it manifest?
1. decreased clearance of VLDL, IDL, and chylomicrons due to dysfunction or absence of apoE
2. increased IDL chylomicrons
what is the cause of primary familial hypercholesterolemia? how does it manifest?
1. LDLr impairments, high fat diet, inactivity
2. increased LDL
what is the cause of familial ligand defective apoB? how does it manifest?
1. mutation in apoB100 - impaired endocytosis of LDL
2. increased LDL
what do the fibrates do? what is the MOA?
1. activate PPAR receptor
2. increase plasma HDL, lower TGs
3. increase oxidation of fatty acids
what are the fibrate drugs?
the fibrates are good for what condition?
what are the bile acid binding resins?
what do the bile acid binding resins do? what is the MOA?
1. soak up bile acids in intestine
2. liver makes more bile acids and uptakes cholesterol to do so
3. increases LDL receptors - decreases plasma LDL
what does niacin do? what is the MOA?
1. decreases VLDL and LDL
2. increases HDL, decreases plasma free fatty acids which decreases VLDL synthesis by liver
3. may also decrease plasma plasminogen (anti-thrombosis)
what are the side effects of niacin?
1. cutaneous flushing and itching
2. hyperuricemia (gout susceptible)
what is the main cholesterol uptake inhibitor drug? what is the MOA?
2. inhibits nieman pick C1 like protein
how do the statins work? what is the MOA?
1. inhibits cholesterol synthesis
2. competitive inhibitor of HMG CoA reductase
3. increases concentration of LDLr in blood, hepatocytes, and extrahepatic sites
what are the most potent statins?
atorvastatin and rosuvastatin