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PHM 521 > Week 1: Hyperlipidemia > Flashcards

Week 1: Hyperlipidemia Flashcards

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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
fasting lipid panel
statin monitoring technique. monitor 4-12 weeks after initiation or therapy change. then monitor 3-12 months as needed
24
transaminases (ALT,AST)
statin monitoring technique measures baseline, may measure in patients with symptoms that suggest hepatotoxicity
25
monitor for new-onset diabetes
to measure statin effects- especially in patients already with pre-diabetes risk
26
organic anion transporting polypeptide IBI (OATPIBI)
mediates uptake of statins for hepatic metabolism and biliary excretion
27
c.88G*5 and *15
low activity haplotype that increases statin plasma exposure and increases risk for myalgia
28
c88G*Ib
high activity haplotype that decreases statin plasma exposure- no clear effect
29
CPIC guidelines for low functioning haplotype
avoid simvastatin or use lower doses
30
ezetimibe
cholesterol inhibitor: Zetia
31
ezetimibe indication
hyperlipidemia, familial hypercholesterolemia
32
ezetimibe moa
inhibits absorption of cholesterol at brush border of small intestine via niemann-pick CI-like I
33
ezetimibe contraindications
gallbladder disease, severe hepatic dysfunction
34
ezetimibe ADR
urti, diarrhea, arthralgia (joint pain), sinusitis, pain in extremities, rhabdomyolysis, hepatotoxicity
35
ezetimibe key PK/PD
enterohepatic circulation, long half-life (almost a day)
36
ezetimibe DDI
plasma concentrations are much lower when administered with fibrates or cholestyramine
37
ezetimibe cholesterol impact
decreases: total cholesterol, LDL (more so with statin), ApoB, TG increases: LDL
38
aliocrumab
PCSK-9 inhibitor- praluent
39
evolocumab
PCKS-9 inhibitor- repatha
40
PCKS-9 inhibitor indications
hyperlipidemia, familial hypercholesterolemia
41
PCKS-9 inhibitor MOA
human monoclonal antibody that binds to PCKS9 and increases available LDL receptors
42
PCKS-9 inhibitor ADR
nasopharyngitis, influenza, urti, injection site rxns, back pain
43
PCKS-9 inhibitor key PK/PD
subcutaneous injections every 2-4 weeks
44
PCKS-9 inhibitor impact on cholesterol
decreases: total cholesterol, LDL, ApoB, TG, Lp(a) increases: HDL
45
Inclisiran
RNAI inhibitor of PCKS-9- Leqvio
46
Inclisiran indications
prevention of atherosclerotic cv disease, familial hypercholesterolemia
47
Inclisiran MOA
small-interfering rna (sirna) LDL-C lowering therapy, blocks PCKS-9 synthesis
48
Inclisiran contraindications
pregnancy
49
Inclisiran ADR
injection site rxns, arthralgia
50
Inclisiran key points
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
Inclisiran impact on cholesterol
decreases: LDL
52
Bempedoic acid
ATP citrate lysase inhibitor- nexletol
53
bempedoic acid indication
prevention of atherosclerotic cv disease, familial hypercholesterolemia
54
bempedoic acid MOA
ACL inhibitor- decreases cholesterol synthesis and lowers LDL in blood via upregulation of ldl receptors
55
bempedoic acid contraindications
pregnancy
56
bempedoic acid ADR
hyperuricemia --> gout flares with prior history, tendon rupture
57
bempedoic acid DDI
increases concentrations of pravastatin (max dose=40mg) and simvastatin (max dose = 20mg)
58
bempedoic acid impact on cholesterol
decreases: LDL (more so with statin)
59
colesevelam
bile acid sequestrant- welchol
60
colestipol
bile acid sequestrant- colestid
61
cholestyramine
bile acid sequestrant- prevalite, questran
62
colesevelam indications
hyperlipidemia
63
colesevelam moa
binds with bile acids in the intestine to form insoluble complex eliminated in the feces
64
colesevelam contraindications
history of bowel obstruction, triglycerides>500mg/dL, hypertriglyceridemia induced pancreatitis
65
coleselevam ADR
constipation, dyspepsia (indigestion), nausea, pancreatitis, bowel obstruction
66
coleselevam key PK/PD
drugs do not absorb, excreted in feces
67
coleselevam DDI
impacts drug absorption for most medications- take 1 hour before or 2 hours after BAS
68
coleselevam key points
take with food- mix packet in water or swallow tablets with liquid, most need to be started on a low dose and increased
69
coleselevam impact on cholesterol
decreases: LDL increases: VLDL (may increase TG)
70
omega-3 ethyl esters
lovaza
71
icosapent ethyl
vascepa (omega 3)
72
omega 3 impact on cholesterol
decreases: TG increases: HDL, may increase LDL
73
Fenofibrate
fibric acid- antara, fenoglide
74
gemfibrozil
lopid
75
fenofibrate MOA
activate PPARa (peroxisome proliferator activated receptor alpha)- decreases TG, increases LDL particle size which are catabolized rapidly
76
fenofibrate contraindications
gallbladder disease
77
fenofibrate ADR
abdominal pain, diarrhea, increased transaminases, hepatotoxicity, rhabdomyolysis (increased risk with statin use)
78
fenofibrate key PK/PD
gemfibrozil has a much shorter half life than fenofibrate
79
fenofibrate DDI
increase risk of myopathy with statin use (worse in gemfibrozil)
80
fenofibrate impact on cholesterol
decreases: TG, LDL (or increases) increases: HDL, LDL (potentially)
81
Niacin
antilipemic- niaspan
82
niacin MOA
`not well defined- decreases synthesis of VLDL and LDL
83
niacin contraindications
severe hepatic dysfunction, peptic ulcer disease
84
niacin ADR
flushing, headache, hepatotoxicity, rhabdomyolysis
85
niacin key points
start at low dose and slowly increase over time to decrease side effects (flushing), avoid alcohol and spicy foods, this is vitamin B3
86
87
Niacin impact on cholesterol
decreases: LDL, TG increases: HDL
88
those who may not benefit from lipid lowering therapy for primary prevention
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
groups who benefit from lipid lowering therapy for primary prevention
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
high risk ASCVD patients
LDL levels above 190, ASCVD risk score above 7.5%
91
high risk therapy goals
lower LDL 50% or greater, LDL < 100 mg/dL, non-HDL <103mg/dL
92
high risk treatment
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
moderate risk patients
patients 40-75 years with diabetes, with LDL 70< and <190, can be high risk based on ASCVD risk
94
moderate risk treatment goals
LDL lowered 30-49%, LDL <100mg/dL, non HDL < 130
95
moderate risk treatment plan
1) moderate intensity statin 2)high intensity statin 3) ezetimibe

PHM 521 (11 decks)

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