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Pharmacology III > Block I: Dyslipidemia > Flashcards

Block I: Dyslipidemia Flashcards

1
Q

list lipids in order of their density

A 
LEAST DENSE
1. chylomicron
2. VLDL
3. LDL
4. HDL
MOST DENSE
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2
Q

[] is in the intestine and transports dietary TG

A

chylomicron

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3
Q

[] is in the liver and transports endogenous TG

A

VLDL

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4
Q

[] is formed in circulation and delivers cholesterol to periphery

A

LDL

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5
Q

[] takes systemic cholesterol to the liver for breakdown and excretion

A

HDL

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6
Q

what is the role of plasma lipids

A
  1. cell membrane
  2. hormone synthesis
  3. source of free fatty acids
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7
Q

what is the role of lipoprotines

A
  1. chylomicron and VLDL delivery tg to cells in body
  2. LDL delivers cholesterol to cells in body
  3. HDL involved in reverse cholesterol transport
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8
Q

when should individuals have their lipids measured?

A
  1. 20 + every 4-6 years

2. adults with ASCVD every 3-12 months

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9
Q

which lipoptorein is calculated, how?

A

LDL, friedewald formula

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10
Q

that is the goal of total cholesterol

A

= 150

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11
Q

what is the LDL goal

A

= 100

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12
Q

what is the goal triglycerides

A

= 150

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13
Q

what is the goal HDL

A

> /= 60

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14
Q

what is the most arthrogenetic cholesterol

A 
NON HDL (VLDL + LDL)
Apo B
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15
Q

what are arthrogenic cholesterols

A
  1. LDL

2. VLDL

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16
Q

what is uncertain if it is arthrogenic

A

chylomicrons

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17
Q

what is not arthrogenis

A

HDH

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18
Q

a 1% redux in LDL with reduce ASVD risk by []

A

1%

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19
Q

a 1% increase in HDL will reduce ASCVD risk by []%

A

2-3%

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20
Q

how does LDL lead to ASCVD

A

LDL accumulated in endothelial layer of BV, engulged by macrophage, foam cell made, arthersclerosis forms, cad

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21
Q

[] have an moa of: HMG-CoA reductase inhibitor. reduce cholesterol synthesis in liver by inhibiting enzyme that converts HMG-CoA to mevolonate.
rate-limiting step in cholesterol synthesis.`

A

Statins

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22
Q

what is the MOA of statin

A

HMG-CoA reductase inhibitor. inhibts rate limiting step in cholesterol synthesis.

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23
Q

what are some pleiotropic effects of statins?

A
  1. improve endothelial function
  2. inhibit platelet aggregation
  3. decrease LDL oxidation
  4. reduce vascular inflammation
  5. stabilize atherosclerotic plaque
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24
Q

what is the clinical use of statins

A

first line therapy for dislipiemia in primary and secondary prevention CAD

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25
Q

what is the first line therapy for dyslipidemia in primary and secondary prevention of CAD

A

statins

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26
Q

Statins lower LDL by []%

A

21-63

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27
Q

statins lower TG by []%

A

8-37%

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28
Q

statins [] HDL

A

raise

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29
Q

what are two high intensity statins

A
  1. rosuvastatin 20-40

2. atorvastatin 40–80

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30
Q

how much do high intensity statins affect LDL

A

50%

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31
Q

how much do moderate intensity statins affect LDL

A

30-49%

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32
Q

how much do low intensity statins affect LDL

A

< 30%

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33
Q

what intensity is atorvastatin 20

A

mod.

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34
Q

what intensity is rosuvastatin 10

A

mod

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35
Q

what intensity is simvastatin 20-40

A

mod

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36
Q

what intensity if prevastatin 40

A

mod

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37
Q

what intensity is lovastatin 40

A

mod

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38
Q

what intensity is fluvastatin

A

mod

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39
Q

what intensity is atorvastatin 40-80

A

high

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40
Q

what intensity is rosuvastatin 20-40

A

high

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41
Q

what intensity is simvastatin 10

A

low

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42
Q

what intensity is pravastatin 20

A

low

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43
Q

what intensity is lovastatin 20

A

low

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44
Q

how would you monitor a patient on statins

A
  1. fasting lipids 4-12 weeks after initiation and every 3 months
    - 12 months once stable
  2. LFTS
    only if symptoms occur (fatigure, loss apetite, abdominal pain, jaundice)
  3. CPK
    baseline if pt. at risk for myopathy & in symptomatic pts.
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45
Q

contraindications statins

A
  1. liver disease

2. pregnancy

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46
Q

ADR statins

A
  1. myalgias
  2. rhabdo
  3. GI
  4. flu-like sx
  5. increase LFT
  6. increase rx DM in high dose
  7. confusion, cognitive impairment
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47
Q

what drug does this SE profile belong to?

  1. myalgias
  2. rhabdo
  3. GI
  4. flu-like sx
  5. increase LFT
  6. increase rx DM in high dose
  7. confusion, cognitive impairment
A

Statins

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48
Q

increased risk myopathy if statins are taken with []

A

other CYP3A4 drugs (except pravastatin, rosuvastatin)

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49
Q

what re some common drug interactiosn with statins

A
  1. CCB
  2. amiodarone
  3. ketoconazole
  4. fibric acid derivative
  5. rifampin

inhib. statin metabolism

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50
Q

what should you counsel your stain pateitns on about diet and statin

A

a ton of grapefruit juice will impair absorbtion

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51
Q

what are some statin cautions

A
  1. age > 75

2. decrease if LDL < 40 on 2 occaisons

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52
Q

MOA exetimibe

A

cholesterol absorbtion inhibitor, inhibits absorbtion in small intestine

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53
Q

[] is a cholesterol absorbtion inhibitor, inhibits absorbtion in small intestine

A

ezetimibe

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54
Q

ezetimibde can decrease LDL levels by []%

A

17

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55
Q

[] can be used second like if stain is not tolerated well, or LDL not controled on statin alone

A

ezetimibe, either second line or in combo with statin

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56
Q

what is the clinical use ezetimibde

A

2nd line if statin contI, not tolerated, or not meeting goal

can be added to statins well

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57
Q

[] can be useful in diabetic patients who cannot tolerate high dose statin therapy

A

ezetimibe

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58
Q

ezetimibe has a formulation mized with []

A

atorvastatin or simvastatin

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59
Q

what are contraindications ezetimibe

A
  1. acute liver disease

2. pregnancy (adverse effects in animals)

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60
Q

what are SE ezetimibe

A
  1. HA
  2. rash
    * usually well tolerated
61
Q

how would you monitor an ezetimibe patient

A
  1. fasting lipid panel and LFT at baseline

- +6-8 week after initiation and dose titration

62
Q

when should ezetimibe be d/c

A

if ALT > 3x

63
Q

[] bind bile acid and cholesterol, intestines, and decrease biliary cholesterol absorption

A

bile acid sequestrants

64
Q

what is the MOA BAS

A

bind bile acid and cholesterol in intestines, decrease biliary cholesterol absorption

65
Q

BAS decrease LDL by []%

66
Q

BAD increase HDL by []%

67
Q

what is the clinical use for BAS

A

LDL lowering after statin and niacin maxed or not tolerated

68
Q

[] is used when statin and niacin are maxed and pt. still not at goal

69
Q

cholestyramine is a []

70
Q

Colestipol is a []

71
Q

Colesevelam is a []

72
Q

what is the ROA BAS

A
  1. tablet
  2. powder
  3. oral suspension
73
Q

contraindications BAS

A
  1. complete biliary obstruction
  2. TG > 300
  3. hyperlipoproteinemia
74
Q

what drug has these AE

  1. GI distress
  2. constipation
  3. hypernatremia
  4. hyperchloremia
  5. impaired fat soluble vitamin absorbtion
75
Q

what are some AE BAS

A
  1. GI distress
  2. constipation
  3. hypernatremia
  4. hyperchloremia
  5. impaired fat soluble vitamin absorbtion
76
Q

what caution is assoc. with BAS

A

other meds that can cause constipation

-TAC, fiber sup, narcotics

77
Q

what drug interactions with BAS

A

can bind other drugs and excrete them,

should take other meds 2-4 hours apart

78
Q

how should you monitor a patient on BAS

A
  1. fasting lipid panel baseline and 6-8 weeks after initiation
    - every 6-12 months therefter
  2. d/c if TG exceeds 400 mg/dL while on thereapy
79
Q

what is the MOA of PCSK9 inhib

A

binds PCSK9 to prevent degradation of LDL-c receptors,

  • maintain functionality of LDL-c receptors that take in LDL from bloodstream into cell
  • decrease LDL from circulation
80
Q

what is the clinical use of PCSK 9 inhib

A
  1. heterozygous familial hypercholesteroleemia

2. clnical ASCVD

81
Q

PCSK9 inhib decrease LDL by [] %

82
Q

PCSK9 inhib decrease TC by []%

83
Q

PCSK9 inhib decrease lipoprotein []%

84
Q

PCSK9 inhib increase HDL by []%

85
Q

how should you monitor a patient on PCSK9 inhib

A
  1. fasting lipid panel
    - reassess 4-8 weeks after initiation/titration
  2. assess for hypersensitivity reactions
86
Q

alirocumad belongs to what class

A

PCSK9 inhibitor

87
Q

Evolocumab belongs to what class

A

PCSK9 inhibitor

88
Q

contraindication PCSK9 inhib

A

hypersensitivity

89
Q
  1. nasopharyngitis
  2. flu sx
  3. increased LFT
  4. injection site reaction
  5. myalgia
  6. cough

side effect profile fo []

A

PCSK9 inhib.

90
Q

what is the MOA of bempepoidic acid

A

ATP citrate lyase inhibitor (ACL)

halts LDL synthesis by inhibiting ACL (higher up on cholesterol synthesis than statin)

91
Q

what are some indications for bempedoidic acid/ACL inhib.

A

ASVCD, HeFH

usually in combo with max tolerated statin

92
Q

bempedoidic acid decreases LDL by [] %

93
Q

[] is a prodrug

A

bempedoidic acid/ACL inhib

94
Q

drug interactions with bempedoici acid

A
  1. antivrials
  2. max dose simvastatin 20, pravastatin 40
    - due to inhibitor OATP…
95
Q

what drug has the following SE profile

  1. gout
  2. tendon rupture
  3. a fib
  4. GI distress
  5. anemia
  6. leukopenia
  7. increased BUN/Scr
A

bempedoidic acid/ACL inh

96
Q

what drug may cause gout

A

ACL in /bempedoic acid

97
Q

what drug may cause tendon rupture

A

ACL/bempedoic acid

98
Q

what drug may increase BUN/Scr

A

ACL in /bempedoic acid

99
Q

how would you monitor a patient on ACL inhib

A
  1. lipid levels 8-12 wk
  2. uric acid levels
  3. s/sx tendon rupture
100
Q

if a pt TG are 174-499 how would you treat?

A

lifestyle mod

101
Q

if pt TG are > 500 what do you rec

A

statin init.

102
Q

if pt TG > 1,000 what do you rec

A

very low fat diet

avoid ref carb

avoid alcohol

initiate fibrates/omega-3

103
Q

[] has an MOA of activating PAR-alpha, the gene that regulates/controls lipid metabolism, reduces hepatic production VLDL and increases lipoprotein lipate-mediated clearance

104
Q

clinical use fibrates

A

reserved for pt with TG > 500

105
Q

fibrates decrease tg []%

106
Q

fibrates increase HDL [] %

107
Q

gemfibrozil is a [] drug

108
Q

fenofibrate is a [] drug

109
Q

fenofibritic acid is a [] drug

110
Q

what is the MOA gemfibrozil

A

activate PPAR-alpha to reduce TG

111
Q

contraindications fibrates

A
  1. hepatic disease

2. statins, may increase rhabdo

112
Q

what drug should NOT be mixed with a statin

A

gemfibrozil

113
Q

what drug has this side effect profile

  1. GI upset
  2. dyspepsia
  3. rash
  4. gallstones
  5. myopathy
  6. LFT and Scr elevatoin
114
Q

what drug may cause gall stones

115
Q

how would you monitor fibrates

A
  1. fastin lipid
  2. ALT
  3. CPK if muscle pain
116
Q

MOA omega 3

A

inhibit hepatic secretion of TG and promote metabolism TG

117
Q

omega 3 decreases Tg by [] %

118
Q

what is the clinical use of omega 3

A
  1. dietary aduvant for very high TG levels
119
Q

what is a safe dose omega 3

A

< 3 G

2-4 may be needed

120
Q

AE omega 3

A
  1. GI disturbance
  2. fishy aftertate
  3. increased bleeding risk
  4. worsening glycemic control
  5. increased LDL
  6. abnormal LFT
121
Q
  1. increased bleeding risk
  2. worsening glycemic control
  3. increased LDL
  4. increased LFT

SE profile of what

122
Q

what drug comes with an increased risk bleeding

123
Q

DI omega 3

A
  1. antiplatelets and anticoagulants

* bleeding risk

124
Q

how to monitor omega 3

A
  1. TG baseline
  2. ALT
  3. eval GI dis. skin change, bleeding
125
Q

lovaza belongs to what class

126
Q

omtyg belongs to what glass

127
Q

epanova belongs to what class

128
Q

vascepa belongs to what class

129
Q

MOA inhibit mobilization free fatty acids from peripheral adipose tissue to liver and reduce VLDL synthesis

130
Q

what is MOA niacin

A

inhibit mobilization free fatty acids from peripheral adipose tissue to liver and reduce VLDL synth

131
Q

niacin decreased tg by [] %

132
Q

niacin decreased LDL by [] %

133
Q

niacin increased HDL by [] %

134
Q

what is the clnical use of niacin

A

if TG > 500

135
Q

can is niacin sometimes combined with?

A
  1. lovostatin

2. simvastatin

136
Q

how are you monitoring your niacin pt

A
  1. CPK if statin
  2. fasting lipid
  3. blodo glucose
  4. uric acid
  5. lft
137
Q

niacin with [] increasing myopathy risk

A

statin or gemfibrozil

138
Q

interactions with niacin

A
  1. statin/gemfibrozil (increased myopathy risk)
  2. alcohol
  3. antidiabetic
139
Q

CI niacin

A

liver disease
sever gout
peptic ulcer disease
AST/ALT > 2-3x

140
Q

[] can cause persistent hyperlgycemia, cutaneous symptoms, acute gout

141
Q

what drug causes facial flushing

142
Q

ADR niacin

A
  1. flushing
  2. hyerglycemia
  3. hyperuricemia
  4. upper gi distress
  5. hepatotox
  6. myopathy
143
Q

[] is contraindicated in pregnancy (category x)

144
Q

[] is category C, no harm in animal studies

A

niacin
d/c if hyperlipidemia
d/c if hypertriglyceridemia

145
Q

B/C not systemically absorbed, may interfere with vitamin absorbtion

146
Q

[] C harm shown in animal studies, other agents pref.

A

cholesterol absorbtion inhbit

147
Q

[] C adverse events observed in animal studies, maternal toxicity rare

148
Q

in a ASCVD pt. less than 75 yoa what is the treatment and what is the goal

A

high intesnity stain

LDL 50% lowering

149
Q

clinical ASVCD on max tolerated dose statin, next step

A

ezetimibde

or PCKS9 if severe risk

Pharmacology III (6 decks)

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