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Pharmacology > module 10 lipid lowering meds > Flashcards

module 10 lipid lowering meds Flashcards

1
Q

pharm classes for lipid lowering drugs

A 
HMG CoA reductase inhibitors
bile acid sequestrants
cholesterol absorption inhibitors 
fibrates
niacin 
omega 3 fatty acids
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2
Q

HGM CoA reductase inhibitors mechanism of action

A

inhibit conversion of HGM-CoA to L-mevalonic acid and subsequently cholesterol. (inhibit synthesis of cholesterol)
- should be taken at night

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3
Q

HGM CoA affect on LDL/HDL/TG

A

LDL lowering
moderately effective at dec. TG
modestly raise HDL
- first line drug

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4
Q

HMG CoA reductase inhibitors AE

A

myopathy
myositis
rhabdomyolysis (monitor CK)
elevated transaminases (liver function)

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5
Q

HMG CoA drug interactions

A

metabolized by CYP 3A4

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6
Q

Bile acid sequestrants mechanism of action

A

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

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7
Q

Bile acid sequestrants

A

cholestyramine
colestipol
colesevelam

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8
Q

Bile acid sequestrants and LDL/HDL/TG

A

moderately lower LDL
not change to TG or slight inc.
modest increase in HDL

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9
Q

bile acid sequestrants AE

A

GI:

  • bloating
  • dyspepsia
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10
Q

Bile acid sequestrants drug interactions

A

bind of other drugs

dec. absorption of fat-soluable vitamins

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11
Q

HMG-CoA reductase inhibitors

A 
STATINS
atorvastastin 
fluvastatin
lovastatin
pitavastatin 
rosuvastatin
simvastatin
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12
Q

Cholesterol absorption inhibitors

A

ezetimibe

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13
Q

ezetimibe MOA

A

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
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14
Q

ezetimibe and LDL/HDL/TG

A

lowers LDL
lowers TG
modestly increases HDL

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15
Q

fibrates

A

gemfibrozil
fenofibrate
clofibrate
“fib”

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16
Q

fibrates MOA

A

activating PPARa -> reduction in TG-rich lipoproteins and inc. in HDL

  • inc. fatty acid oxidation in hepatocytes
  • dec. TG synthesis
17
Q

Fibrates and LDL/HDL/TG

A

Dec. TG

dec. LDL, possible inc.
inc. HDL
- most effecting TG lowering drugs and used primarily in pt with elevated TG and low HDL

18
Q

fibrate AE

A

GI discomfort
inc. transaminases
myopathy
arrhythmia

19
Q

fibrate drug interaction

A

displace warfarin from albumin -> inc. fee warfarin

inc. cyclosporin clearance

20
Q

Niacin

A

nicotinic acid

vitamin B3

21
Q

niacin MOA

A

inhibits fatty acid release from adipose tissue and fatty acid/TG production in liver.
-> dec. LDL
Reduces uptake of HDL -> inc. HDL

22
Q

niacin and LDL/HDL/TG

A

dec. LDL
inc. HDL
dec. TG

23
Q

niacin AE

A 
flushing (pretreat with aspirin)
hepatotoxicity
pruritis 
hyperuricemia
myopathy
impaired insulin sensitivity
24
Q

omega 3 fatty acids

A

eicosapentaenoic acid
docosahexaenoic acid
fish oil

25
Q

omega 3 fatty acid MOA

A

reduce TG biosynthesis

increase fatty acid oxidation in the liver

26
Q

omega 3 fatty acid and LDL/HDL/TG

A

dec. TG
inc LDL
inc. HDL

27
Q

PCSK9 inhibitors MOA

A

prvent the protein PCSK9 from biding and degrading LDL receptors in the liver
-> inc. LDL receptors -> dec. LDL serum levels

28
Q

PCSK9 inhibitors

A

alirocumab

evolocumab

29
Q

PCSK9 inhibitors and LDL/HDL/TG

A

dec. LDL

30
Q

most potent statins

A

atorvastatin

rosuvastatin

Pharmacology (78 decks)

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