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Pharmacology Exam 4 > Antihyperlipidemics > Flashcards

Antihyperlipidemics Flashcards

1
Q

Dietary management of hyperlipidemia

A
  • decrease cholesterol and saturated fat
  • eat oily fish twice a week
  • foods rich in a-linolenic acid
  • increase soluble fiber intake
  • fish oil supplements
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2
Q

Optimal LDL

A

<100

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3
Q

High LDL

A

160-189

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4
Q

Near optimal LDL

A

100-129

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5
Q

Borderline high LDL

A

130-159

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6
Q

very high LDL

A

> 190

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7
Q

optimal cholesterol

A

<200

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8
Q

borderline high cholesterol

A

200-239

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9
Q

high cholesterol

A

> 240

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10
Q

Low HDL

A

<40

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11
Q

High HDL

A

> 60

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12
Q

Goal triglycerides

A

30 > LDL

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13
Q

HMG-CoA reductase inhbitors

A

statins

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14
Q

PPARa Activators

A

fibric acid derivatives

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15
Q

bile acid binding resins

A

colesevelam

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16
Q

nicotinic acid

A

niacin

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17
Q

cholesterol absorption inhibitor

A

Ezetimibe

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18
Q

Atorvastatin CYP

A

3A4

2C9

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19
Q

Rate limiting step for cholesterol synthesis

A

HMG CoA reductase

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20
Q

Statins MOA (3)

A
  • increase LDL receptors
  • enhance clearance o LDL precursors (VLDL, IDL)
  • decrease VLDL
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21
Q

Statins and LDL

A

lower 20-60% depending on dose

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22
Q

Statins and triglycerides

A

decreased 20%

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23
Q

Statins and HDL

A

increase 5-10%

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24
Q

first line therapy for hypercholesterolemia

A

statins

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25
Q

statins PK

A
  • oral, PM
  • extensive first pass metabolism
  • half life 3-20 hours
  • extorted by liver into bile
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26
Q

statins adverse effects

A
  • GI irritation
  • HA
  • rash
  • hepatoxicity
  • myopathy
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27
Q

DDI statins

A

CYP3A3/2C9: vibrates, digoxin, warfarin, macrolides

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28
Q

What statin avoids P450 interactions?

A

pravastatin

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29
Q

CI statins

A

liver disease

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30
Q

MOA fabric acid derivatives

A
  • agonist at peroxisome proliferation actcitvated receptor a
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31
Q

activation of PPAR-a

A
  • increase proteins that oxidize FA
  • increase proteins that breakdown VLDL
  • reduce ApoCIII (enhance VLDL clearance)
  • stimulate ApoAI/II (increase HDL)
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32
Q

fibrates triglycerides

A

lower 40-55%

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33
Q

fibrates HDL

A

increase 10-25%

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34
Q

fibrates and LDL

A

variable effects

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35
Q

fibrates uses

A
  • type III hyperlipoproteinemia
  • severe hypertriglyceridemia
  • hypertriglyceridemia with low HDL
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36
Q

PK of fibrates

A
  • absorbed rapidly (>90%)
  • half life 1-20 hours
  • excreted as glucuronides
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37
Q

DDI fibrates

A
  • oral anticoag enhanced

- with statins: myositis, myopathy

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38
Q

ADE fibrates

A
  • GI disturbances (N/D,ab pain)
  • rash
  • urticaria
  • hair loss
  • myalgia
  • fatigue
  • HA
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39
Q

precaution and CI fibrates

A

renal and hepatic failure

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40
Q

Bile acid resin MOA

A
  • bind bile acids and prevent reabsorption
  • increased breakdown of cholesterol
  • increase LDL receptors
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41
Q

Bile acid resin LDL

A

lower 10-20%

42
Q

bile acid resin HDL

A

raise 5%

43
Q

bile acid resins VLDL

A

no effect

44
Q

bile acid resins uses

A

with statins for familial or primary hypercholesterolemia

45
Q

PK bile acid resins

A

not absorbed from GI tract

46
Q

DDI bile acid resins

A

bind many drugs and interfere with their absorption (take other meds 1 hour before or 3-4 hours after)

47
Q

ADE bile acid resins

A
  • bloating
  • dyspepsia
  • constipation
  • mild steatorrhea
  • compliance big issue
48
Q

MOA niacin in adipose

A
  • inhibit lipolysis of TGs by hormone sensitive lipase

- decrease hepatic TG synthesis

49
Q

MOA niacin in liver

A
  • reduce TG synthesis by inhibiting synthesis and esterification of FA
50
Q

Niacin triglycerides

A

lower 355-50%

51
Q

niacin LDL

A

lower 10-25%

52
Q

niacin HDL

A

increase 15-30%

53
Q

niacin uses

A
  • hypertriglyeridemia with high LDL

- hypertriglyceridemia and low HDL

54
Q

niacin MOA

A

readily absorbed from all parts of intestinal tract

  • half life 60 min
  • metabolized in liver or excreted unchanged
55
Q

DDI niacin

A

myopathy with concomitant admin of statins

56
Q

ADE niacin

A
  • intense flush with pruritus
  • GI disturbances
  • hepatic toxicity
  • peptic ulcer
  • hyperglycemia
  • hyperuricemia
57
Q

MOA ezetimibe

A
  • inhibit cholesterol transport protein (NPC1L1)
58
Q

Ezetimide LDL

A

reduce 18-25%

59
Q

Ezetimide HDL

A

no significant change

60
Q

ezetimide uses

A

adjective with statins

61
Q

ezetimide PK

A
  • absorbed well orally
  • excreted feces unchanged
  • rest conjugated in liver (glucouronidation)
  • half life 18-30 h
62
Q

ADE ezetimide

A
  • diarrhea

- many interactions with other anti-lipidemic drugs

63
Q

Ezetimide and fibrates

A

increase ezetimide levels

increase risk of cholelithiasis

64
Q

Ezetimide and niacin

A

increase ezetimide levels

increase risk of myotpathies

65
Q

ezetimide and warfarin

A

increase prothrombin time

66
Q

Omega3 FA MOA

A

small intestine absorbed EPA and DHA

67
Q

Omega 3 FA VLDL

A

reduce

68
Q

omega 3 FA uses

A
  • OTC herbal, vitamin, nutritional supplement
  • Rx heart disease
  • Rx high triglyericde levels
  • adjunct to diet for severe hypertriglyceridemia
69
Q

ADE omega 3FA

A
  • arthralgia
  • nausea
  • fish burps
  • dyspepsia
  • increased LDL
  • may prolong bleeding time
70
Q

PCSK9 inhibitors use

A
  • alone or combo with statins

- lower hardest to treat elevated cholesterol levels who cannot tolerate high statins (SE)

71
Q

PCSK9 inhibitors examples

A

evolocumab (repatha)

alirocumab (praluenut)

72
Q

PCSK9 inhibitor MOA

A
  • binds LDL receptor
  • enhance degradation of LDL receptor
  • mutations
  • effects on plasma lipids and lipoproteins
  • increase LDL receptors on surface
73
Q

PCSK9 inhibitor LDL monotherapy

A

LDL-C reduce in dose dependent manner

70%

74
Q

PCSK9 inhibitor LDL with statin

A

lower 60%

75
Q

what is recommended before use of PCSK9 inhibitors?

A

statins/ezetimibe

76
Q

PK PCSK9 inhibitors

A
  • SC injections Q2W or 1 monthly
77
Q

ADE PCSK9 inhibitors

A
  • small risk of neurocognitive effects
  • nasopharyngitis
  • UTI
  • URI
  • injection site reactions
78
Q

T/F PCSK9 inhibitors increase risk of myopathies

A

FALSE!

Do NOT

79
Q

Microsomal triglyeride transfer inhibitor (MTP) use

A

alternative way to lower LDL

  • use in combo with max tolerated statin
  • adjunct for lowering LDL-C, total cholesterol, apoB and non-HDL-C lipoproteins (hoFH)
80
Q

MTP MOA

A
  • inhibit MTP (essential for formation of VLDL)
81
Q

MTP drug

A

Lomitapide (small synthetic molecule)

82
Q

Lomitapide LDL

A

reduces 50%

83
Q

Lomitapide PK

A
  • with water
  • without food
  • CYP3A4
84
Q

ADE lomitapide

A
  • GI: V/D/ab pain
  • hepatotoxicity
  • liver steatosis
  • increase hepatic fat
  • embryo toxic
85
Q

Inhibitor of apoB B-100 synthesis drug

A

mipomersen

86
Q

FH

A

autosomal dominant
300-500 heterozygous
high levels of LDL

87
Q

homozygous FH

A

1/1 million

- severe hypercholesterolemia with accelerated CHD in childhood

88
Q

Mipomersen MOA

A

binds mRNA encoding ApoB (main component of LDL and VLDL)

- RNA degraded

89
Q

Mipomersen LDL

A

lower 30-50%

90
Q

mipomersen use

A
  • as addition to lipid lowering meds and diet with hoFH
91
Q

ADE mipomersen

A

makes not approved elsewhere, including Europe

  • injection site
  • flu like
  • fatigue
  • HA
  • hepatotoxicity
92
Q

mipomersen PK

A

SC once a week
half life 1-2 months
- max LDL reduction after 6 months

93
Q

CI mipomersen

A

liver disease

94
Q

Statin main use

A

high LDL

95
Q

fibrates main use

A

with statins

96
Q

bile acid resin main use

A

with statins

97
Q

niacin main use

A

patients with all types of lipoprotein disorders

often used in combo

98
Q

ezetimibe main use

A

with statins

99
Q

PCSK9 inhibitor main use

A

with statins

100
Q

MTP inhibitor main use

A

adjunct to diet for lowering

  • LDL-C
  • total cholesterol
  • apoB
  • non HDL-C lipoproteins (hoFH)
101
Q

inhibitor of apoB-100 synthesis main use

A

adjunct with lipid lowering meds and diet for hoFH

Pharmacology Exam 4 (7 decks)

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