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Cardio > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

statins are _____ inhibitors

A

HMG-CoA reductase

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2
Q

mechanism of statins

A

bind to HMG-CoA reductase so cholesterol cannot be formed from HMG-CoA. and up-regulation of LDL receptors

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3
Q

what are the high intensity statins?

A

Atorvastatin 40-80 mg and Rosuvastatin 20-40 mg

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4
Q

what are the classes of lipid-lowering agents

A

HMG-CoA reductase inhibitors, fibric acid derivatives, niacin, bile acid sequestrants, selective cholesterol absorption inhibitors, omega-3 fatty acids, PCSK9 inhibitors, siRNA, bempedoic acid, lomitapide, evinacumab

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5
Q

what are the lipophilic statins

A

atorvastatin, lovastatin, simvastatin

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6
Q

what are the pleiotropic effects of statins

A

reduce plaque inflammation, influence plaque stability

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7
Q

name the statins

A

atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin, pitavastatin

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8
Q

what is the rule of 7 with statins

A

doubling the dose of a statin reduces LDL by an additional 7%

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9
Q

what are the two main things that are adversely effected by statins

A

liver and muscle

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10
Q

how do statins effect the liver

A

increase AST/ALT

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11
Q

what are 3 muscle problems that can occur with statins

A

myalgias, myositis/myopathy, rhabdomyolysis

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12
Q

____ are muscle symptoms with normal creatine kinase

A

myalgias

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13
Q

______ are muscle symptoms with evidence of muscle injury (CK> normal)

A

myositis, myopathy

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14
Q

_____ is muscle symptoms with CK >10x normal and renal injury

A

rhabdomyolysis

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15
Q

which drugs have a dose cap with simvastatin and lovastatin

A

ticagrelor, amiodarone, amlodipine, conivaptan, diltiazem, ranolazine, verapamil

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16
Q

what is the role of statins in dyslipidemia

A

for types IIa, IIb, III they lower LDL up to 60%, lower triglycerides and increase HDL. they decrease total mortality, CHD mortality, major coronary events, and coronary interventions

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17
Q

what are the fibric acid derivatives

A

fenofibrate and gemfibrozil

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18
Q

what is the dosing for fenofibrate

A

145 mg qd

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19
Q

what is the dosing for gemfibrozil

A

600 mg bid ac

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20
Q

what are the adverse effects for fibric acid derivatives

A

GI, myopathy, transaminase elevations

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21
Q

what are the major interactions with statins

A

macrolide antibiotics, azole antifungals, HIV protease inhibitors, nefazodone, danazol, grapefruit juice, colchicine, cyclosporine, tacrolimus, gemfibrozil

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22
Q

what is the mechanism for fibric acid derivatives

A

PPAR alpha agonists, stimulate lipoprotein lipase, increase breakdown of VLDL, decrease VLDL synthesis from liver, increase HDL

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23
Q

fibric acid derivatives are preferred to lower ____

A

triglycerides

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24
Q

role of fibric acid derivatives in dyslipidemia

A

lower triglycerides, lower LDL a bit, increase HDL, reduce major coronary events

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25
Q

drug interactions with fibric acid derivatives

A

anticoagulants, cyclosporine, HMG-CoA reductase inhibitors, sulfonylureas

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26
Q

how do fibric acid derivatives interfere with anticoagulants

A

increase INR

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27
Q

how do fibric acid derivatives interfere with cyclosporine

A

increase or decrease effects

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28
Q

how do fibric acid derivates interfere with HMG-CoA reductase inhibitors

A

increase myopathy risk (GEMFIBROZIL)

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29
Q

how do fibric acid derivatives interfere with sulfonylureas

A

increase hypoglycemia (GEMFIBROZIL)

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30
Q

what are the forms of niacin

A

nicotinic acid, vitamin B3

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31
Q

how does niacin work

A

decrease production of VLDL in hepatocytes, increase HDL in circulation

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32
Q

adverse effects with niacin that make it unfavorable

A

GI exacerbation of peptic ulcer, skin flushing and itching, hepatotoxicity, myopathy, hyperglycemia, hyperuricemia

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33
Q

role of niacin in dyslipidemia

A

lower LDL and triglycerides, increase HDL, reduction in major coronary events

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34
Q

what are the PCSK9 inhibitors

A

alirocumab, evolocumab

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35
Q

what is the brand name of alirocumab

A

praluent

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36
Q

what is the brand name of evolocumab

A

repatha

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37
Q

what is PCSK9

A

it is an enzyme that takes LDL receptors out of commission and degrades them which is bad

38
Q

what is the mechanism of PCSK9 inhibitors

A

they bind to and inhibit PCSK9 so it can’t degrade the LDL receptors, now the LDL receptors can take LDL out of the blood like gang busters!

39
Q

what are the adverse effects of PCSK9 inhibitors

A

injection site reactions, hypersensitivity, neurocognitive events (not really tho)

40
Q

role of PCSK9 inhibitors in dyslipidemia

A

types IIa, IIb lowers LDL by 40-70% which makes it good for statin intolerant patients or adjunct to maximally tolerated statins, lowers CHD mortality/events

41
Q

what is the alirocumab dose for primary dyslipidemia

A

75 or 150 mg SC q 2 weeks; or 300 mg SC q 4 weeks

42
Q

what is the alirocumab dose for HoFH

A

150 mg SC q 2 weeks

43
Q

what is the evolocumab dose for primary dyslipidemia

A

140 mg SC q 2 weeks or 420 mg q monthly

44
Q

what is the evolocumab dose for HoFH

A

420 mg SC q monthly, may increase to q 2 weeks if needed

45
Q

what is the siRNA drug for dyslipidemia

A

Inclisiran

46
Q

what is the brand name for inclisiran

47
Q

what is a downfall of inclisiran

A

requires administration by a clinician

48
Q

what is inclisiran indicated for

A

HeFH, clinical ASCVD

49
Q

adverse events of inclisiran

A

injection-site reactions, arthralgia, antibody development

50
Q

what is arthralgia

A

joint pain/aches

51
Q

what is the role of inclisiran in dyslipidemia

A

types IIa, IIb, ASCVD and FH, lowers LDL 50%, adjunct to maximally tolerated statins

52
Q

inclisiran is attached to a molecule called _____ that allows rapid and targeted uptake of inclisiran by the liver through interactions with ASGPRs expressed exclusively on hepatocytes

53
Q

inclisiran binds to ____

54
Q

what happens after inclisiran binds to risc

A

the sense and antisense strands separate, the antisense strand directs RISC to find complementary RNA which it cleaves, inhibiting PCSK9 protein synthesis

55
Q

what are the bile acid sequestrants

A

cholestyramine, colesevelam, colestipol

56
Q

how do the bile acid sequestrants work

A

they cause the liver to produce more bile acids, lowering LDL secondary to LDL receptor upregulation

57
Q

what are the adverse effects of bile acid sequestrants

A

GI nausea, bloating, constipation, decrease absorption of other drugs, hypertriglyceridemia

58
Q

role of bile acid sequestrants in dyslipidemia

A

lower LDL, increase HDL, increase triglycerides (BAD), reduction in major coronary events, reduction in CHD mortality

59
Q

what is the selective cholesterol absorption inhibitor

60
Q

how does ezetimibe work

A

it inhibits cholesterol absorption by the intestinal mucosal wall (niemann-pick C1-like 1, NPC1L1 protein). decreases cholesterol delivery to the liver and increases blood clearance of cholesterol

61
Q

ezetimibe works on which fat pathway

62
Q

what does ezetimibe upregulate

A

LDL receptors

63
Q

ezetimibe drug interactions

A

bile acid sequestrants, cyclosporine, amiodarone, verapamil

64
Q

ezetimibe adverse effects

65
Q

ezetimibe by itself lowers LDL by __%

66
Q

ezetimibe with a statin adds an additional __% reduction in LDL

67
Q

ezetimibe dosing

68
Q

role of ezetimibe in dyslipidemia

A

type IIa, lowers LDL, synergistic with statins

69
Q

what are the omega 3 fatty acids

A

omega-3 ethyl esters, icosapent ethyl, non-prescription fish oil (no effect)

70
Q

mechanism of omega 3 fatty acids

A

inhibit acyltransferase, increase peroxisomal beta-oxidation in liver, decrease triglyceride synthesis from liver

71
Q

what is the brand name of omega 3 acid ethyl esters

72
Q

what is the brand name of icosapent ethyl

73
Q

what is the indication for lovaza

A

adjunct to diet in patients with TRG >500

74
Q

what are the indications for vascepa

A

adjunct to diet in patients with triglycerides > 500. reduce the risk of MI/stroke//revascularization/unstable angina requiring hospitalization in patients on maximally tolerated statins w/ TRG > 150 and ASCVD or DM and 2 risk factors

75
Q

role of omega 3 fatty acids in dyslipidemia

A

lower triglycerides, no change or slight increase in LDL and HDL, reduction in CV events (vascepa)

76
Q

dosing of omega 3 fatty acids

77
Q

adverse effects for omega 3 fatty acids

A

GI: belching, dyspepsia, altered taste; rash; arthralgia

78
Q

drug interactions with omega 3 fatty acids

A

anticoagulants- potential for increased bleeding

79
Q

what drug class is bempedoic acid

A

ACL inhibitor (adenosine triphosphate-citrate lyase)

80
Q

what is the mechanism for bempedoic acid

A

prevents pyruvate—> acetyl CoA (a step ahead of statins)

81
Q

what is the role of bempedoic acid in dyslipidemia

A

lower LDL, adjunct to maximally tolerated statins, ASCVD and FH

82
Q

what are the adverse effects for bempedoic acid

A

hyperuricemia, tendon rupture/injury

83
Q

what are the drug interactions for bempedoic acid

A

simvastatin dose cap 20 mg, pravastatin dose cap 40 mg

84
Q

what is lomitapide indicated for

85
Q

why is lomitapide in the REMS program

A

hepatotoxicity

86
Q

role of lomitapide in dyslipidemia

A

lowers ldl around 40%

87
Q

drug interactions with lomitapide

A

moderate to strong inhibitors of CYP3A4

88
Q

adverse reactions for lomitapide

A

GI (nausea, diarrhea, vomiting, hepatic steatosis, transaminitis), change in liver fat content (fat soluble nutrient deficiency)

89
Q

what is evinacumab

A

a recombinant human monoclonal antibody that inhibits angiopoietin-like protein 3

90
Q

what is the mechanism of evinacumab

A

inhibits lipoprotein lipase and endothelial lipase, leading to decreased LDL, HDL, and TRG

91
Q

what is evinacumab for

92
Q

adverse reactions with evinacumab

A

nasopharyngitis, dizziness, flu-like symptoms, infusion-related reactions, teratogenicity

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