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148 Cards in this Set
- Front
- Back
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cholesterol from food is transported to the liver via
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chylomicrons
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chylomicrons is --- rich
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tg
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what adversely takes up ldl
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scavenger receptors: into macrophages
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from the liver what picks up the cholesterol
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vldl which is hydrolyzed to ldl
reuptake into liver or periphery |
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what picks up the ldl from the periphery and takes it back to the liver
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hdl
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what's on the membrane of the cholesterol
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apoprotein b100
apoprotein c apoprotein e |
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what's in the core of the cholesterol
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tg and cholesteryl esters
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which has more tg and less proteins
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vldl
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which has more proteins
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hdl
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what breaks down vldl
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lpl
hl (enzymes) |
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the more --- the more atherogenic
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TG
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hdl --- ---- rich: so antiatherogenic
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cholesterol ester rich
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which lipoprotein has the largest lipoprotein characteristic
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chylomicron
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which parts of the membrane are antiathrerogenic
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apo A-I
structural protein of HDL |
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which parts of the membrane are athergenic
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ApoB-100
ApoB-48 ApoE |
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the ldl receptor is recycled to be reused
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t
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vldl taken up into the ----- and is oxidized there
it enters a ------- and becomes a foam cell body |
subintima
macrophage |
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apo a1 secreted from liver and binds w/ the ---- receptor macrophage
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ABCA1
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abca1 is responsible for cholesterol ----
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efflux
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what modifies apo A1 to hdl
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LCAT
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hdl can go to the liver via
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SRB1
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hdl can also go to
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vldl and ldl
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BAS has a -- charge that binds to a --- charge on the bile acid
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positive
negative |
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bas bind to bile acids and prevents
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reabsorption
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w/ bas liver produces more bile acids and ldl -----
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receptors
this will pull cholesterol out of periphery |
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so what will be increased in bas
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ldl receptors ( to internalize ldl and vldl)
vldl and ldl removal |
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so bas not reabsorbed, so ldl receptors upregulated. . .
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the ldl receptors will pull more cholesterol in to make bile acids
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w/ bas there is a --- to --- reduction in ldl
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10-20 w/ high doses
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bas may increase ---- and has minimal effect on ----
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might increase TG
minimal effect on HDL |
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bas powders mixed w/ --- or ---- ---
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water
fruit juice |
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ok to mix bas w/ --- drink to mask taste
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pulpy
oj |
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when should you take bas
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w/in 1 hr of meal
when bile acids are secreted |
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why should you separate adminstration of other meds
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cuz bas has + charge and might bind
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t/f
bas absorpbed from gi tract |
f
not absorbed from gi tract |
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gi effects of bas
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bloating
fullness nausea flatulence constipation |
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how will tg be increased in bas
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due to an increse in vldl
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bas are --- exhange resins
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anionic
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what meds should not be taken w/ bas
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dig
levothyroxine warfarin bb thiazide |
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when should other meds be administered
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1 hr before meals
4 hrs after bas w/ any drug |
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ci of bas
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familial dysbetapoproteinemia (elevated TG)
tg > 400 mg/dl |
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relative ci w/ bas
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tg > 200 mg/dl
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t/f
bas has systemic se |
f
no systemic se |
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t/f
bas tolerated well |
f
poorly tolerated |
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primary use of bas is those needing -- reduction in ldl in conjunction w/ or failing a statin
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modest
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niemann-pick C1-Like 1 inhibitor
(NPC1L1) |
ezetimibe
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when ezetimibe inhibits NPC1L1 what's increased
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LDL receptors
so this internalzies LDL and reduced |
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ezetimibe --- inhibits intestinal cholesterol
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selectively
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ezetimibe ------ intestinal delivery of cholesterol to the liver
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decrease
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ezetimibe ---- expression of hepatic LDL receptors
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increase
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ezetimibe decrease cholesterol content of --- particles
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atherogenic
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ezetmibe and its active ----- metabolite circulate enterohepatically
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glucoronide
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ciruclating enterohepatically delivers agent back to the -- --- ---
and limits --- ----- |
site of action
systemic exposure this also prolongs its action |
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t/f
ok to give ezetimibe any time of day |
t
cuz of enterohepatic circulation there's a long period before it's eliminated |
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a fatty meal can increase cmax but doesn't affect the ---
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extent
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t/f
there's added benefit of plaque regression when a statin is added to tx w/ ezetimibe |
f
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how will tg be increased in bas
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due to an increse in vldl
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bas are --- exhange resins
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anionic
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what meds should not be taken w/ bas
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dig
levothyroxine warfarin bb thiazide |
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when should other meds be administered
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1 hr before meals
4 hrs after bas w/ any drug |
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ci of bas
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familial dysbetapoproteinemia (elevated TG)
tg > 400 mg/dl |
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---- drug interactions w/ eze
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minimal
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what can decrease absorption of eze
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bas
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when do you use eze
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adjunctive tx
failure of statins monotherapy for mildly elvated ldl in conjunction w/ a statin |
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rate limiting step of statins
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hmg-coA reductase
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statins prevent ---- ---- in the hepatocyte
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cholesterol synthesis
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w/ statins there's a decrease in
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cholesterol synthesis
ldl vldl idl intracellular cholesterol |
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what's increased w/ statins
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ldl receptors
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statins have ----- effectst that modulates the --- --- balance
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antiinflammatory
foam cell (cause inflammation) |
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t/f
statins have a low high pass effect that's why they're so effective |
f
high 1st pass, low bioavailability. . . this is good cuz it's needed in the liver |
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se of statins mainly due to --- ---
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drug interactions
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drugs w/ short t 1/2
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fluvastatin
lovastatin simvastatin pravastatin |
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drugs w/ long t 1/2
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atorvastatin
rosuvastatin pitavastatin ok not to take these drugs at night |
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more lipophilic drugs
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simvastatin
lovastatin atorvastatin |
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the more lipophilic the more --- --- and more 1st pass effect
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protein bound
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which aer more renally excreted
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ptiavastatin
pravastatin so avoid w/ renal dysfunction |
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doubling dose will decrease cholesterol by -- %
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6%
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which med shows a dose dependent increase in HDL at therapeutic doses
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rosuvastatin
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t/f
at high doses of atorvastatin there are increases in hdl |
f
decreases. . . not beneficial |
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w/ crp there are dose dependent ------
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decreases
cuz of antiimflammatory effects |
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crp or ldl
which do you decrease to see a better reduction in atheroma |
crp
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common se of statins
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ha
myalgia fatigue gi intolerance flu like symptoms elevated liver enzymes |
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how to manage liver enzymes
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reduce statins or d/c until leves back to norm
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breakdown of muscle
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myopathy
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pain w/ myopathy is usu unilateral/bilateral
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bilateral
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how do you reduce myopathy
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dose cautiously in pts w/ impaired renal fx
use the lowest effective dose cautiously combine w/ statins and fibrates avoid drug interactions monitor ck levels and symptoms |
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when would you stop statins w/ myopathy
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rhabdo
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ade statins
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overall well tolerated
hepatotoxicity peripheral neuropathy (mostly in elderly) |
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statins ci
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hepatic disease
pregnancy |
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relative ci in statins
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cylclosporin use
or other immunosuppresant gemfibrozil niacin erythomycin |
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most efficacious and best tolerated of all hyperlipidemia agents
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statins
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ok to give statins in post cardiac events even in absence in ldl
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yes
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fibrates possibly alters --- ---
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gene expression
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fibrates increase ---- ---- ----
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apo a1
apo a2 these elevate hdl |
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--- alters gene expression due to fibrartes
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PPAR-alpha agonism
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fibrates will decrease
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apo c3
apo e apo b these will decrease tg and increase ldl size |
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fibrates will incease lpl which will
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decrease tg
increase hdl |
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fibratels will incease hepatic ---- and ---- degradation and decrease ---- and --- production
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vldl
apo b vldl apo b |
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fibrates 2ndary moa
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decrease PAI-1 and CRP
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which do you watch for renal cl
gem or feno |
gemfibrozil
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which has a short t1/2 and requires more frequent dosing
gem or feno |
gemfibrozil
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which has better bioavailability
gem or feno |
fenofibrate cuz micronized
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when to take gem
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30 min before meals and dinner
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when to take feno
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w/ meals
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fibrates decrease:
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tg by 20-50%
ldl-c by 5-20% tc by 15% |
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fibrates increase
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hdl by 10-35%
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ae of fibrates
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n/d
abd pain cholellithiasis myopathy increase risk of ca? |
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ezetimibe might have an increase risk of ---
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ca
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if pt has a hx of gallstones ok to give fibrates
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f
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ci w/ fibrates
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pregnancy
severe hepatic and renal dysfunction existing gall disease |
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di w/ fibrates:
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increase anticoagulatn effects of warfarin
hmg co a reducatase inhibitors bas |
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di w/ fib and statins mainly due to?
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hepatotoxicity
myopathies |
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primary indication of fibrates
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tg > 1000 mg/dl
remant removal disease low HDL |
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niacin is a --- complex vitamin
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B
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nicotinic acid is used as an ------
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antilipemic
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amide form of nicotinic acid:
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niacinamide
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t/f
niacinamide is effectve as antilipemic |
f
(doesn't cause flushing) |
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ir niacin
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niacin
niacor |
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long acting niacin
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niacin
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er niacin
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niaspan
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t/f
inositol hexaniacinate does not cause flushing ,but ineffective against cholesterol |
t
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otc has to be the --- dose and pt needs ----
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appropriate
f/u |
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niacin decrease release of ---- from ---
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ffa
adipocytes so no ingredients to make tg |
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niacin primary role in lipids
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decreases HDL
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dose of niacin depends on:
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t 1/2
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ir should be given during what time of day
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during day to get benefits
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er should be given
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at hs
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which is better ir or er
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ir
better reduction in tg and increase in hdl |
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arachidonic leads to ---- which leads to ---
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prostaglandins
vasodilation |
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when will flushing toleracne develop
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w/in 1-2 weeks
although missing a dose can cause loss of tolerance |
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gi ae
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nausea
abd discomfort (give niacin after meals or snack) |
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w/ larger doses of niacin what possible
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elevated lft's
glucose uric acid decreased glucose tolerance |
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absolute ci
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chronic liver disease
arterial bleeding peptic ulcer disease |
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how is aterial bleeding and peptic ulcer caused
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due prostaglandin release w/ vasodilation
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relative ci
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hx of symptomatic gout
significant hyperuricemia dm |
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don't give niacin to a ---dm cuz might
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predm
cuz might push over to dm |
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niacins and statins increase risk of
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rhabdo
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bas w/ niacin interaction
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decrease absoption
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etoh and niacin interaction
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exacerbate vasodilation
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antiHTN and niacin
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exacerbate vasodilatory effects
(take asa) |
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niacin useful for pt w/ elevated --- and low ----
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elevated tg
low hdl |
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niacin useful as combo tx for pt w/ ----- dyslipidemia and elevated ldl
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atherogenic
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fish oils lower
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tg
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fish oil composed of omega 3 acids
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EPA
DHA |
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fish oil might increase
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ldl
total cholesterol |
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cholesteryl ester transfer of ---- form hdl to ldl and vldl
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ce
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inhibition of cetp raises ----- greater than 50%
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HDL
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pcsk9 facilitates ldlr --- and is inducded by ---
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degradation
statins |
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what binds to ldl receptor and lead to degradation
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pcsk9
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