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Therapeutics 2 - Exam 5 > dyslipidemia > Flashcards

dyslipidemia Flashcards

chaudrey

1
Q

what are the risks of having high cholesterol?

A

heart disease
stroke

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2
Q

what is the pathogenesis of atherosclerosis?

A

endothelial injury –> inflammatory response –> macrophage infiltration –> platelet adhesion –> smooth muscle cell proliferation –> extracellular matrix accumulation

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3
Q

what are the symptoms of dyslipidemia?

A

mostly asymptomatic
chest pain
palpitations
sweating
anxiety
SOB
loss of consciousness
difficulty with speech or movement
abdominal pain
sudden death

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4
Q

what are the signs of dyslipidemia?

A

pancreatitis
eruptive xanthomas
peripheral polyneuropathy
increased BP
waist size
BMI > 30

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5
Q

what labs should be monitored for dyslipidemia?

A

increased non HDL-C, TC, LDL-C, TG, Apo-B, CRP, and LDL-P
decreased HDL

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6
Q

what is LDL-C?

A

the amount of cholesterol in LDL particles
primary lab ordered

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7
Q

what is LDL-P?

A

number of LDL particles

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8
Q

what is non-HDL-c?

A

amount of cholesterol in atherogenic particles

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9
Q

how would you solve for non-HDL-C?

A

TC - HDL

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10
Q

what is Apo-B?

A

number of atherogenic particles

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11
Q

when would a non-fasting lipid panel be appropriate to order?

A

measuring initial risk
patient is not on lipid-lowering therapy
patient does not have a family history of genetic hyperlipidemia
patient has low TGs

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12
Q

what is in a fasting lipid panel (FLP)?

A

TC
TG
HDL-C
LDL-C

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13
Q

how do you calculate LDL?

A

friedewald equation
= TC - HDL - (TG/5)

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14
Q

what is goal ration of TC to HDL?

A

under 5:1
optimal is 3-3.5:1

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15
Q

what are some lifetstyle modifications to make to manage dyslipidemia?

A

DASH diet
reduce percent of calories from saturated and trans fat (5-6%)
reduce sodium intake (under 1500 mg)
moderate to vigorous physical activity (90-150 minutes/week)
weight loss
smoking cessation

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16
Q

how many calories are in a single gram of fat?

A

9 calories

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17
Q

what is olestra?

A

non digestible, non absorbable, and noncaloric fat substitute to reduce intake of saturated fats and cholesterol

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18
Q

what soluble fibers lower LDL?

A

oat bran
pectins or gums
psyllium produc ts
plant stanols and sterols

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19
Q

what is MOA of psyllium?

A

bind to cholesterol in the gut to reduce hepatic production and clearance
reduce LDL and TC

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20
Q

what impact does fish oil have?

A

reduce TG
may increase LDL by 4-49%

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21
Q

what is vascepa?

A

icosapent ethyl
TG risk-based nonstatin therapy for ASCVD risk reduction
take 2g PO BID wf

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22
Q

what is Lavaza?

A

omega-3 fatty acid
2-4 g qd

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23
Q

what is the risk associated with omega-3 fatty acids?

A

atrial fibrillation

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24
Q

what affect on LDL does saturated fat consumption have?

A

having saturated fats under 7% of calories –> 8-10% reduction

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25
Q

what impact on LDL does cholesterol consumption have?

A

cholesterol consumption being under 200 mg/day –> 3-5% reduction

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26
Q

what impact on LDL does weight loss have?

A

10 pounds loss if overweight –> 5-8% reduction

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27
Q

what impact on LDL does adding soluble fiber have?

A

adding 5-10g of soluble fiber –> 3-5% reduction

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28
Q

what impact on LDL does adding plant sterols/stanols have?

A

adding 2g of plant sterols/stanols –> 5-15% reduction

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29
Q

how does statins impact LDL, HDL, and TG?

A

20-60% reduction in LDL
5-10% increase in HDL
10-33% reduction in TG

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30
Q

what impact does BARs have on cholesterol?

A

15-30% reduction LDL
minimal effects on HDL and TG

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31
Q

what impact does zetia have on cholesterol?

A

17% reduction in LDL
1% increase in HDL
7-8% reduction in TG

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32
Q

what impact does PCSK9 mAb have on cholesterol?

A

60-70% reduction in LDL
modest benefit on TG and HDL

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33
Q

what impact does inclisiran have on cholesterol?

A

48-52% reduction in LDL
5-6% increase in HDL
30-33% reduction in TG

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34
Q

what impact does bempedoic acid have on cholesterol?

A

18% reduction in LDL
minimal effect on HDL and TG

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35
Q

what impact does gemfibrozil have on cholesterol?

A

10-15% reduction in LDL
5-20% increase in HDL
35-50% reduction in TG

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36
Q

what impact does fenofibrate have on cholesterol?

A

6-20% reduction in LDL
5-20% increase in HDL
41-53% reduction in TG

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37
Q

what impact does lovaza have on cholesterol?

A

4-49% increase in LDL
5-9% increase in HDL
23-35% reduction in TG

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38
Q

what impact does niacin have on cholesterol?

A

10-25% reduction in LDL
15-25% increase in HDL
25-30% reduction in TG

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39
Q

what drugs are statins?

A

lovastatin
pravastatin
pitavastatin
simvastatin
fluvastatin
atorvastatin
rosuvastatin

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40
Q

what statins are preferred in renal impairment?

A

fluvastatin
atorvastatin
no dosage adjustments necessary

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41
Q

what are the low intensity statins?

A

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

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42
Q

what are the high intensity statins?

A

atorvastatin 40-80
rosuvastatin 20-40mg

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43
Q

what are hydrophilic statins?

A

pravastatin
rosuvastatin

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44
Q

what are lipophilic statins?

A

fluvastatin
pitavastatin
lovastatin
simvastatin
atorvastatin

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45
Q

what statins are metabolized by CYP3A4?

A

lovastatin
simvastatin
atorvastatin

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46
Q

what is unique about simvastatin?

A

needs to be taken in the evening due to short half-life

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47
Q

what risk is associated with simvastatin 80mg?

A

increased risk of myopathy and rhabdomyalgia
do not give to paitents

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48
Q

what SE are common in lipophilic statins?

A

muscle pain

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49
Q

what SE are common in hydrophilic statins?

A

increased risk of liver toxicity

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50
Q

what are SE of statins?

A

myopathy
rhabdomyolysis (unusual muscle pain/dark urine)

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51
Q

what are counseling points of statins?

A

obtain LFTs at baseline
avoid over 1qt of grapefruit juice
d/c if creatine kinase is over 10x ULN

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52
Q

at what LFT level should a statin be d/c?

A

if 3x ULN

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53
Q

what are characteristics that predispose patients to statin SE?

A

hepatic or renal dysfunction
prior statin intolerance
muscle disorders
unexplained ALT elevations over 3x ULN
other drugs that affect statin metabolism
over 75 years

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54
Q

what are the CI of statins?

A

acute liver disease
unexplained/persistent elevations of serum transaminases
pregnancy/breastfeeding

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55
Q

what is the preferred statin in patients taking a strong CYP3A4 inhibitor?

A

pravastatin
fluvastatin
rosuvastatin
pitavastatin

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56
Q

what is CoQ100?

A

an agent that can help prevent adverse muscle effects from statins
take 150-200mg

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57
Q

how should a muscle injury in statin be managed?

A

d/c statin
see if muscle pain resolves
switch to a hydrophilic statin
consider alternative dosing

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58
Q

how would you alternatively dose statin?

A

every other day –> dose needs to be double to achieve similar LDL lowering
once weekly dosing

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59
Q

what are the CI of simvastatin?

A

itraconazole
ketoconazole
posaconazole
erythromycin
clarithromycin
telithromycin
HIV protease inhibitors
nefazodone
gemfibrozil
cyclosporine
danazol

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60
Q

what is unique about simvastatin 10mg?

A

you cannot exceed this level when taking verapamil or diltiazem concurrently

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61
Q

what is unique about simvastatin 20mg?

A

you cannot exceed this level when taking amiodarone, amlodipine, or ranolazine concurrently

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62
Q

what classic disease state are statins associated with?

A

hyperglycemia

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63
Q

how would statins need to be monitored?

A

obtain baseline FLP
then 4-12 weeks after initiation
every 3-12 months thereafter
consider CK for patients with muscle symptoms or at increased risk

64
Q

what drugs are BARs?

A

cholestyramine (questran)
colestipol (colestid)
colesevelam (welchol)

65
Q

what is MOA of BARs?

A

trap bile in the intestine –> forces the body to make more bile via cholesterol –> decreases LDL and cholesterol levels

66
Q

what are the disadvantages of BARs?

A

may increase TG
take other medications 1 hour before or 4 hours after

67
Q

what are the SE of BARs?

A

constipation
bloating
N
flatulence
impaired absorption of fat soluble vitamines (ADEK)
hyerpnatremia
hyperchloremia
GI obstruction

68
Q

what are the CI of cholestyramine?

A

complete biliary obstruction

69
Q

what is the CI of colesevelam?

A

h/o of bowel obstruction
hypertriglyceridemia-induced pancreatitis
serum TG over 500

70
Q

what are the drug-drug interactions of BARs?

A

acetaminophen
TZDs
OCs
corticosteroids
zetia
fibrates
thiazide diuretics
warfarin
digoxin
decrease effects of these drugs

71
Q

what is niacin AE?

A

prostaglandin-mediated flushing and itching
increased LFTs
hyperuricemia
hyperglycemia
increased level of statins

72
Q

what are the brand names of niacin?

A

niacor
niaspan
slo-niacin

73
Q

what are the counseling points of niacin?

A

administer aspirin 325mg 30 minutes before taking niacin (to reduce flushing)
take close to meals
avoid alcohol and hot drinks (which worsens flushing)
start with lower dose and titrate up slowly

74
Q

what are the CI of niacin?

A

active hepatic disease
significant or unexplained persistent liver transaminase elevations
active peptic ulcer
arterial hemorrhage

75
Q

what is zetia?

A

a cholesterol absorption inhibitor that increases the clearance of cholesterol from blood
decreases LDL by 12-20% with statin

76
Q

what is vytorin?

A

zetia combination product with simvastatin

77
Q

what is the SE of zetia?

A

fatigue
diarrhea
GI upset

78
Q

what is the CI of zetia?

A

when used with a statin, all of its CI

79
Q

what are the SE of fibrates?

A

GI disturbances
rash
myalgia
dizziness

80
Q

what are the CI of fibrates?

A

history of gallbladder disease
ESRD or dialysis
peristent liver disease

81
Q

what drugs do fibrates increase the level of?

A

statins
zetia
sulfonylureas
warfarin

82
Q

what drugs are PCSK9 inhibitors?

A

alirocumab (praluent)
evolocumab (repatha)

83
Q

what is indication for PCSK9 inhibitors?

A

adjunct to diet and statin to reduce LDL in familial Heterozygous hypercholesterolemia or atherosclerotic CVD

84
Q

what is MOA of PCSK9i?

A

SQ injection
inhibits binding of PCSK9 to LDL receptors and up-regulates the recycling of LDL receptors
resulting in a drastic decrease in LDL-C (43-64%)

85
Q

what is SE of PCSK9 inhibitors?

A

GI upset
myalgia
increased LFTs
influenza
injection site reaction

86
Q

when should patients consider PCSK9i therapy?

A

ASCVD risk reduction for those on maximally-tolerated statin (with or without zetia) and an LDL >70 or non-HDL-C > 100
high-riisk patient with statin intolerance
further reduction of LDL-C if pretreatment LDL-C is > 190

87
Q

what is inclisiran?

A

leqvio
long-acting synthetic small interfering ribonucleic acid (siRNA)
inhibits the translation of PCSK9 protein thus inhibiting PCSK9 production –> prolongs the activity of LDL receptors –> reduces LDL and cholesterol

88
Q

when would inclisiran be used?

A

adjunct to diet and statin to reduce LDL in familial heterozygous hypercholesterolemia or ASCVD

89
Q

what are the SE of inclisiran?

A

injection site reactions
arthralgia
UTI
diarhhea
bronchitis
pain in extremities
dyspnea

90
Q

what is the dosing for inclisiran?

A

initial dose
another at 3 months
then every 6 months
needs to be administered by a health care professional

91
Q

when should bempedoic acid be used?

A

same indication as inclisiran
adjunct to diet and statin to reduce LDL in familial HeFH or ASCVD

92
Q

what is the brand name of bempedoic acid?

A

nexletol
nexlizet

93
Q

what is the SE of bempedoic acid?

A

URTI
muscle spasms
hyperuricemia
back pain
abdominal pain or discomfort
bronchitis
pain in extremity
anemia
elevated liver enzymes

94
Q

what are the warnings of bempedoic acid?

A

may increase blood uric acid levels (gout)
risk of tendon rupture
avoid concomitant use with simvastatin greater than 20 mg or pravastatin over 40 mg to avoid myopathy

95
Q

what is the MOA of bempedoic acid?

A

prodrug activated in the liver by ACSVL1 that inhibits ATP-citrate lyase and up-regulates LDL receptors (lowering LDL)

96
Q

what is red yeast rice?

A

medication that lowers TC, LDL-C, TG, CV events, and total mortality with the same AE as statins
OTC so not regulated

97
Q

what is lomitapide?

A

juxatpid
MTTPi indicated as an adjunct to a low-fat diet and other lipid-lowering treatments (including LDL aphaeresis)
reduces LDL-C, TC, apo B, and non-HDL-C in patients with HoFH

98
Q

what is the dosing of lomitapide?

A

5 to 60 mg po qd

99
Q

what is the boxed warning of lomitapide?

A

hepatotoxicity

100
Q

what is the MOA lomitapide?

A

directly binds and inhibits MTTP preventing the assembly of apo B containing lipoproteins (chylomicrons and VLDL) in enterocytes and hepatocytes

101
Q

what is evinacumab?

A

evkeeza
recombinant human mAb indicated as an adjunct to other lipid-lowering therapies to reduce LDL-C in adults and pediatric patients with HoFH

102
Q

what is the dose of evinacumab?

A

15mg/kg administered as IV infusion once monthly

103
Q

what is MOA of evinacumab?

A

binds and inhibits ANGPTL3 and rescues/allows LPL and EL to promote VLDL processing and clearance of LDL formation

104
Q

with primary prevention, how should you treat someone with DM?

A

moderate intensity statin (class I)
or risk assessment to consider high intensity statin (class IIa)

105
Q

in primary prevention, how would you treat a patient who is elderly?

A

clinical assessment and risk discussion

106
Q

in primary prevention, how would you treat a patient with primary hypercholesterolemia (an LDL-C over 190)?

A

no risk assessment
high intensity statin

107
Q

in primary prevention, what is the treatment for a patient aged 0-19?

A

lifestyle to prevent or reduce ASCVD risk
if diagnosis of FH, initiate a statin

108
Q

in primary prevention, how should a 20-39 be treated?

A

estimate lifetime risk to encourage lifestyle modifications
consider statin in family history of premature ASCVD and LDL-C >160

109
Q

in primary prevention, how should patients who 40-75 year, an LDL-C between 70-190, and no DM be treated?

A

preform a 10year ASCVD risk percent

110
Q

what does below 5% risk indicate?

A

lifestyle modifications to reduce risk factors

111
Q

what does a 5-7.49% risk indicate?

A

if risk enhancers are present, then have a discussion regarding moderate-intensity statin
if not, then just lifestyle modifications

112
Q

what does a 7.5% to 19.9% risk indicate?

A

if risk estimate and risk enhancers favor statin –> initiate a moderate intensity statin to reduce LDL-C by 30-49%
consider CAC if risk discussion is uncertain

113
Q

what does a greater than 20% risk indicate?

A

initiate statin tor reduce LCL-C by over 50%

114
Q

what are risk factor enhancers in primary prevention?

A

family h/o premature ASCVD
persistently elevated LDL-C > 160
CKD
pre-eclampsia
premature menopause
inflammatory disease
ethnicity
persistently elevated TG > 175
metabolic syndrome
other elevated labs (ApoB, Hs-CRP, Lpa)
decreased ankle-brachial index (ABI)

115
Q

in secondary prevention, how should patients under 75 and not at very high risk be treated?

A

high-intensity statin (to reduce LDL-C by 50%)

116
Q

in secondary prevention, how should patients who are intolerant to their statin, under 75, and not at very high risk be treated?

A

switch to a moderate intensity statin

117
Q

when should zetia be added in secondary prevention?

A

when the LDL-C is still greater than 70 and the patient is already at maximal statin therapy

118
Q

in secondary prevention, how should patients who are older than 75 and not at very high-risk be treated?

A

initiate moderate to high intensity statin OR continue high intensity statin

119
Q

in secondary prevention, how should patients who are at very high risk be treated

A

high intensity statin or maximal statin

120
Q

in secondary prevention, when should a PCSK9i be added?

A

if a patient is on maximal LDL-C lowering therapy and LDL-C >70 or non HDL-C >100
and already at very high risk

121
Q

what are the risk groups?

A

clinical ASCVD
DM and age 40-75y
LDL > 190
age > 75y
ASCVD risk

122
Q

what populations would benefit from statin use?

A

clinical ASCVD at any age
FH
primary hypercholesterolemia (LDL-C > 190)
patients aged 45-70 with or without diabetes

123
Q

what is the f/u and monitoring recommendations for statins?

A

initiate statin
follow up with FLP in 4-12 weeks until dose is stable
then f/u every 3-12 months

124
Q

what is the CAC test?

A

coronary artery calcium
CT of the chest to measure calcium buildup
determine the initiation of statin if risk decision is uncertain

125
Q

what does a CAC score of 0 mean?

A

assess other risk factors to determine the need

126
Q

what does a CAC score of 1-99 mean?

A

favors statin therapy especially over the age of 55

127
Q

what does a CAC score of >100 mean?

A

initiate at least a moderate-intensity statin

128
Q

after the maximally tolerated statin, what drugs should be considered?

A
  1. zetia
  2. PCSK9i
  3. BARs
129
Q

what is the role of zetia in treatment after maximally tolerated statin?

A

if LDL is not at goal or patient with diabetes have an ASCVD risk over greater than 20%

130
Q

what is the role of a PCSK9i in treatment after maximally tolerated statin?

A

consider if LDL or non-HDL-C not at goal or patients cannot tolerate statin and/or zetia

131
Q

what is the role of BARs in treatment after maximally tolerated statin?

A

if 50% reduction in LDL-C on maximally tolerated statin and zetia with TG over 300

132
Q

what are the goal LDL levels to target?

A

primary –> under 100
secondary –> under 70

133
Q

what is persistent hypertriglyceridemia?

A

fasting TG > 150 mg/dL following at least 4-12 weeks of lifestyle interventions
stable dose of maximally tolerated statin
secondary cause evaluation

134
Q

how is moderate hypertriglyceridemia classified?

A

150-499 mg/dL
excess TGs are carried in VLDLs

135
Q

how is severe hypertriglyceridemia?

A

> 500 mg/dL
excess TGs are carried in VLDL and chylomcirons
increased risk of acute pancreatitis

136
Q

what are secondary lifestyle factors that in those >20 with moderate hypertriglyceridemia?

A

obesity
metabolic syndrome
excessive alcohol use

137
Q

what are secondary disorder factors that in those >20 with moderate hypertriglyceridemia?

A

diabetes
hypothyroidism
chronic liver disease
CKD
nephrotic syndrome

138
Q

what medications are secondary to moderate hypertriglyceridemia?

A

hormone related
immune-related
beta blockers
thiazides
atypical antipsychotics
rosiglitazone
BARs
L-asparaginase

139
Q

what are some lifestyle modifications to make to reduce TGs?

A

5-10% weight loss (20% decrease in TGs)
very low fat diet
restrict alcohol, sugar, and refined carbs
moderate to high intensity exercise

140
Q

what is the pharmacological treatment of hypertriglyceridemia?

A
  1. statin therapy in adults 40-75 with moderate or severe hypertriglyceridemia with ASCVD risk > 7.5%
  2. statin and fibrate or omega-3 FA in patients 40-75 year with severe hypertriglyceridemia
141
Q

what treatment of adults with ASCVD and fasting TG >150 or non-fasting TG >175 and TG <500?

A
  1. Rule out secondary causes
  2. Optimize diet and lifestyle
  3. Optimize glycemic control
  4. Maximize statin therapy, preferably high-intensity statin and optimize statin adherence
142
Q

what is the treatment of persistent fasting hypertriglyceridemia (150-499) in patients with LDL-C <70 + ASCVD?

A
  1. Rule out secondary causes
  2. Further optimize lifestyle
  3. TG risk-based approach (icosapent ethyl)
143
Q

what is the treatment of persistent fasting hypertriglyceridemia (150-499) in patients with LDL-C 70-99 + ASCVD

A
  1. Shared decision-making, patient preference
  2. Combined TG (icosapent ethyl)/ LDL-C (ezetimibe, PCSK9i, bempedoic acid) risk-based approach, or just TG or LDL-C alone
144
Q

what is the tTreatment of persistent fasting hypertriglyceridemia (150-499) in patients with LDL-C >100 + ASCVD?

A
  1. Maximize statin therapy and optimize adherence
  2. Consider LDL-C-guided non-statin therapy (LDL-C risk-based approach)
  3. TG risk-based approach
145
Q

what is the drug for TG risk-based approached?

A

icosapent ethyl

146
Q

what is the drug for LDL-C risk-based approach?

A

Ezetimibe, PCSK9i, or bempedoic acid

147
Q

what is the treatment of moderate hypertriglyceridemia (fasting TG >150, non-fasting TG>175, TG<500) for adults >40 with diabetes + no ASCVD?

A
  1. Rule out secondary causes
  2. Optimize glycemia control
  3. Optimize diet and lifestyle
  4. Maximize statin therapy (LDL-C risk-based approach)

*If 50+ with 1 or more ASCVD high-risk feature, consider icosapent ethyl

148
Q

what is the treatment of moderate hypertriglyceridemia of patients 20+ with no ASCVD or diabetes?

A
  1. Rule out secondary causes
  2. Optimize diet and lifestyle
  3. If persistent, determine 10-year ASCVD risk and consider risk-enhancing factors
149
Q

what is the treatment of moderate hypertriglyceridemia with no diabetes or ASCVD based on risk assessment?

A

<5%: Optimize diet and lifestyle, perform a periodic 10-year ASCVD risk assessment

5-19.9%: Shared decision-making, patient preference, consider initiation or intensification of statin therapy

> 20%: Shared decision-making, patient preference, initiate or intensify to high-intensity statin therapy

150
Q

what is the treatment of adults >20 with TG 500-900?

A
  1. Rule out secondary causes
  2. Optimize diet and lifestyle
  3. Optimize glycemic control
151
Q

what is the treatment of adults 20-39 or those 40-75 with TG 500-999 and 10-year ASCVD risk <5% without ASCVD or diabetes?

A
  1. Emphasize a low-fat diet; consider a very low-fat diet in select patients
  2. Consider fibrate or prescription omega-3 acids (icosapent ethyl or omega-3 ethyl esters) to reduce risk of pancreatitis
152
Q

what is the treatment of adults aged 40-75 with TG 500-999 and 10-year ASCVD risk >5%, ASCVD, or diabetes?

A
  1. Emphasize low-fat diet; consider very low-fat diet in select patients
  2. Initiate or increase intensity of statin therapy and optimize statin adherence
  3. Consider fibrate or prescription omega-3 acids (icosapent ethyl or omega-3 ethyl esters) to reduce risk of pancreatitis
153
Q

what is the treatment of adults aged 20+ with TG>1000

A
  1. Rule out secondary causes
  2. Implement very low-fat diet and optimize lifestyle
  3. Optimize glycemic control
  4. Consider fibrate or prescription omega-3 acids (icosapent ethyl or omega-3 ethyl esters) to reduce risk of pancreatitis
  5. Consider statin initiation or intensification in appropriate management groups
154
Q

can statins alone prevent acute pancreatitis?

A

no, not in the setting of secondary causes

155
Q

what is the treatment to reduce the risk of acute pancreatitis in severe hypertriglyceridemia?

A

fibrates or omega-3 fatty acids

Therapeutics 2 - Exam 5 (14 decks)

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