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PHM 521 > Week 1: Hyperlipidemia > Flashcards

Week 1: Hyperlipidemia Flashcards

1
Q

Atorvastatin

A

Lipitor

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2
Q

Fluvastatin

A

Lescol XL

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3
Q

Lovastatin

A

Mevacor

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4
Q

Pitavastatin

A

Livalo

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5
Q

Pravastatin

A

Pravachol

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6
Q

Rosuvastatin

A

Crestor

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7
Q

Simvastatin

A

Zocor

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8
Q

Atorvastatin

A

hyperlipidemia, atherosclerotic cv disease, familial hypercholesterolemia

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9
Q

Atorvastatin MOA

A

statins are hmg-coa reductase inhibitors, inhibit conversion of hmg-coa to mevalonate, increasing LDL receptors

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10
Q

atorvastatin contraindications

A

breastfeeding, active liver diseases

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11
Q

Atorvastatin ADR

A

myopathy, diarrhea, rhabdomyolysis, hepatotoxicity

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12
Q

atorvastatin key PK/PD

A

short half life (administer at night), most are lipophilic –> higher risk of muscle pain

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13
Q

which 2 statins have a much longer half life than others?

A

atorvastatin, rosuvastatin

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14
Q

hydrophilic statins

A

rosuvastatin, pravastatin

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15
Q

atorvastatin DDI

A

most statins are metabolized by CYP3A4- inhibitors such as azoles and amiodaron and inducers such as phenytoin and rifampin interact

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16
Q

atorvastatin cholesterol impacts

A

decreases: cholesterol synthesis, total cholesterol, LDL, TG, CRP
increases: LDL receptor expression, HDL

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17
Q

Atorvastatin pleiotropic effects

A

improved endothelial function, atherosclerotic stabilization, decreased inflammation, inhibition of thrombogenic response

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18
Q

high intensity statins

A

atorvastatin 40-80 mg
rosuvastatin 20-40 mg

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19
Q

low intensity statins

A

simvastatin 10mg
pravastatin 10-20 mg
lovastatin 20 mg
fluvastatin 20-40 mg
pitavastatin 1 mg

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19
Q

moderate intensity statins

A

atorvastatin 10-20 mg
rosuvastatin 5-10 mg
simvastatin 20-40 mg
pravastatin 40-80 mg
lovastatin 40 mg
fluvastatin 80 mg
pitavastatin 2-4 mg

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20
Q

statins metabolized by CYP2C9

A

fluvastatin, rosuvastatin

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20
Q

statins metabolized by CYP3A4

A

atorvastatin, fluvastatin, lovastatin, simvastatin

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21
Q

other statin metabolization

A

rosuvastatin: CYP2C19 and CYP2C9
pitavastatin: glucuronidation
pravastatin: sulfation

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22
Q

lipophilic statins

A

atorvastatin, fluvastatin, lovastatin, pitavastatin, simvastatin

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23
Q

fasting lipid panel

A

statin monitoring technique. monitor 4-12 weeks after initiation or therapy change. then monitor 3-12 months as needed

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24
Q

transaminases (ALT,AST)

A

statin monitoring technique
measures baseline, may measure in patients with symptoms that suggest hepatotoxicity

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25
Q

monitor for new-onset diabetes

A

to measure statin effects- especially in patients already with pre-diabetes risk

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26
Q

organic anion transporting polypeptide IBI (OATPIBI)

A

mediates uptake of statins for hepatic metabolism and biliary excretion

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27
Q

c.88G*5 and *15

A

low activity haplotype that increases statin plasma exposure and increases risk for myalgia

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28
Q

c88G*Ib

A

high activity haplotype that decreases statin plasma exposure- no clear effect

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29
Q

CPIC guidelines for low functioning haplotype

A

avoid simvastatin or use lower doses

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30
Q

ezetimibe

A

cholesterol inhibitor: Zetia

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31
Q

ezetimibe indication

A

hyperlipidemia, familial hypercholesterolemia

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32
Q

ezetimibe moa

A

inhibits absorption of cholesterol at brush border of small intestine via niemann-pick CI-like I

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33
Q

ezetimibe contraindications

A

gallbladder disease, severe hepatic dysfunction

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34
Q

ezetimibe ADR

A

urti, diarrhea, arthralgia (joint pain), sinusitis, pain in extremities, rhabdomyolysis, hepatotoxicity

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35
Q

ezetimibe key PK/PD

A

enterohepatic circulation, long half-life (almost a day)

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36
Q

ezetimibe DDI

A

plasma concentrations are much lower when administered with fibrates or cholestyramine

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37
Q

ezetimibe cholesterol impact

A

decreases: total cholesterol, LDL (more so with statin), ApoB, TG
increases: LDL

38
Q

aliocrumab

A

PCSK-9 inhibitor- praluent

39
Q

evolocumab

A

PCKS-9 inhibitor- repatha

40
Q

PCKS-9 inhibitor indications

A

hyperlipidemia, familial hypercholesterolemia

41
Q

PCKS-9 inhibitor MOA

A

human monoclonal antibody that binds to PCKS9 and increases available LDL receptors

42
Q

PCKS-9 inhibitor ADR

A

nasopharyngitis, influenza, urti, injection site rxns, back pain

43
Q

PCKS-9 inhibitor key PK/PD

A

subcutaneous injections every 2-4 weeks

44
Q

PCKS-9 inhibitor impact on cholesterol

A

decreases: total cholesterol, LDL, ApoB, TG, Lp(a)
increases: HDL

45
Q

Inclisiran

A

RNAI inhibitor of PCKS-9- Leqvio

46
Q

Inclisiran indications

A

prevention of atherosclerotic cv disease, familial hypercholesterolemia

47
Q

Inclisiran MOA

A

small-interfering rna (sirna) LDL-C lowering therapy, blocks PCKS-9 synthesis

48
Q

Inclisiran contraindications

49
Q

Inclisiran ADR

A

injection site rxns, arthralgia

50
Q

Inclisiran key points

A

subcutaneous injection into abdomen, upper arm, or thigh once then in 3 months, then q6mo after
cannot be self administered or administered at pharmacy

51
Q

Inclisiran impact on cholesterol

A

decreases: LDL

52
Q

Bempedoic acid

A

ATP citrate lysase inhibitor- nexletol

53
Q

bempedoic acid indication

A

prevention of atherosclerotic cv disease, familial hypercholesterolemia

54
Q

bempedoic acid MOA

A

ACL inhibitor- decreases cholesterol synthesis and lowers LDL in blood via upregulation of ldl receptors

55
Q

bempedoic acid contraindications

56
Q

bempedoic acid ADR

A

hyperuricemia –> gout flares with prior history, tendon rupture

57
Q

bempedoic acid DDI

A

increases concentrations of pravastatin (max dose=40mg) and simvastatin (max dose = 20mg)

58
Q

bempedoic acid impact on cholesterol

A

decreases: LDL (more so with statin)

59
Q

colesevelam

A

bile acid sequestrant- welchol

60
Q

colestipol

A

bile acid sequestrant- colestid

61
Q

cholestyramine

A

bile acid sequestrant- prevalite, questran

62
Q

colesevelam indications

A

hyperlipidemia

63
Q

colesevelam moa

A

binds with bile acids in the intestine to form insoluble complex eliminated in the feces

64
Q

colesevelam contraindications

A

history of bowel obstruction, triglycerides>500mg/dL, hypertriglyceridemia induced pancreatitis

65
Q

coleselevam ADR

A

constipation, dyspepsia (indigestion), nausea, pancreatitis, bowel obstruction

66
Q

coleselevam key PK/PD

A

drugs do not absorb, excreted in feces

67
Q

coleselevam DDI

A

impacts drug absorption for most medications- take 1 hour before or 2 hours after BAS

68
Q

coleselevam key points

A

take with food- mix packet in water or swallow tablets with liquid, most need to be started on a low dose and increased

69
Q

coleselevam impact on cholesterol

A

decreases: LDL
increases: VLDL (may increase TG)

70
Q

omega-3 ethyl esters

71
Q

icosapent ethyl

A

vascepa (omega 3)

72
Q

omega 3 impact on cholesterol

A

decreases: TG
increases: HDL, may increase LDL

73
Q

Fenofibrate

A

fibric acid- antara, fenoglide

74
Q

gemfibrozil

75
Q

fenofibrate MOA

A

activate PPARa (peroxisome proliferator activated receptor alpha)- decreases TG, increases LDL particle size which are catabolized rapidly

76
Q

fenofibrate contraindications

A

gallbladder disease

77
Q

fenofibrate ADR

A

abdominal pain, diarrhea, increased transaminases, hepatotoxicity, rhabdomyolysis (increased risk with statin use)

78
Q

fenofibrate key PK/PD

A

gemfibrozil has a much shorter half life than fenofibrate

79
Q

fenofibrate DDI

A

increase risk of myopathy with statin use (worse in gemfibrozil)

80
Q

fenofibrate impact on cholesterol

A

decreases: TG, LDL (or increases)
increases: HDL, LDL (potentially)

81
Q

Niacin

A

antilipemic- niaspan

82
Q

niacin MOA

A

`not well defined- decreases synthesis of VLDL and LDL

83
Q

niacin contraindications

A

severe hepatic dysfunction, peptic ulcer disease

84
Q

niacin ADR

A

flushing, headache, hepatotoxicity, rhabdomyolysis

85
Q

niacin key points

A

start at low dose and slowly increase over time to decrease side effects (flushing), avoid alcohol and spicy foods, this is vitamin B3

87
Q

Niacin impact on cholesterol

A

decreases: LDL, TG
increases: HDL

88
Q

those who may not benefit from lipid lowering therapy for primary prevention

A

1) anyone under the age of 39- unless they have a history of ASCVD, hypercholesterolemia, or LDL levels above 160 mg/dL
2) patients over the age of 75

89
Q

groups who benefit from lipid lowering therapy for primary prevention

A

1) all patients with LDL levels greater than or equal to 190 mg/dL
2) patients 40-75 years of age with diabetes
3) patients 40-75 years with LDL levels above 70, but less than 190- without diabetes

90
Q

high risk ASCVD patients

A

LDL levels above 190, ASCVD risk score above 7.5%

91
Q

high risk therapy goals

A

lower LDL 50% or greater, LDL < 100 mg/dL, non-HDL <103mg/dL

92
Q

high risk treatment

A

1) high intensity statin (atorvastatin 40-80. rosuvastatin 20-40)
2) ezetimibe (if less than 25% additional reduction needed) and/or PCSK9 (>25% additional reduction)
3) bempedoic (addition 17% needed) acid or inclisiran (>17% needed- should not be used with PCSK9)

93
Q

moderate risk patients

A

patients 40-75 years with diabetes, with LDL 70< and <190, can be high risk based on ASCVD risk

94
Q

moderate risk treatment goals

A

LDL lowered 30-49%, LDL <100mg/dL, non HDL < 130

95
Q

moderate risk treatment plan

A

1) moderate intensity statin
2)high intensity statin
3) ezetimibe

PHM 521 (11 decks)

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