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Pharmacology Exam 4 > Antihyperlipidemics > Flashcards

Antihyperlipidemics Flashcards

(101 cards)

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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
statins PK
- oral, PM - extensive first pass metabolism - half life 3-20 hours - extorted by liver into bile
26
statins adverse effects
- GI irritation - HA - rash - hepatoxicity - myopathy
27
DDI statins
CYP3A3/2C9: vibrates, digoxin, warfarin, macrolides
28
What statin avoids P450 interactions?
pravastatin
29
CI statins
liver disease
30
MOA fabric acid derivatives
- agonist at peroxisome proliferation actcitvated receptor a
31
activation of PPAR-a
- increase proteins that oxidize FA - increase proteins that breakdown VLDL - reduce ApoCIII (enhance VLDL clearance) - stimulate ApoAI/II (increase HDL)
32
fibrates triglycerides
lower 40-55%
33
fibrates HDL
increase 10-25%
34
fibrates and LDL
variable effects
35
fibrates uses
- type III hyperlipoproteinemia - severe hypertriglyceridemia - hypertriglyceridemia with low HDL
36
PK of fibrates
- absorbed rapidly (>90%) - half life 1-20 hours - excreted as glucuronides
37
DDI fibrates
- oral anticoag enhanced | - with statins: myositis, myopathy
38
ADE fibrates
- GI disturbances (N/D,ab pain) - rash - urticaria - hair loss - myalgia - fatigue - HA
39
precaution and CI fibrates
renal and hepatic failure
40
Bile acid resin MOA
- bind bile acids and prevent reabsorption - increased breakdown of cholesterol - increase LDL receptors
41
Bile acid resin LDL
lower 10-20%
42
bile acid resin HDL
raise 5%
43
bile acid resins VLDL
no effect
44
bile acid resins uses
with statins for familial or primary hypercholesterolemia
45
PK bile acid resins
not absorbed from GI tract
46
DDI bile acid resins
bind many drugs and interfere with their absorption (take other meds 1 hour before or 3-4 hours after)
47
ADE bile acid resins
- bloating - dyspepsia - constipation - mild steatorrhea - compliance big issue
48
MOA niacin in adipose
- inhibit lipolysis of TGs by hormone sensitive lipase | - decrease hepatic TG synthesis
49
MOA niacin in liver
- reduce TG synthesis by inhibiting synthesis and esterification of FA
50
Niacin triglycerides
lower 355-50%
51
niacin LDL
lower 10-25%
52
niacin HDL
increase 15-30%
53
niacin uses
- hypertriglyeridemia with high LDL | - hypertriglyceridemia and low HDL
54
niacin MOA
readily absorbed from all parts of intestinal tract - half life 60 min - metabolized in liver or excreted unchanged
55
DDI niacin
myopathy with concomitant admin of statins
56
ADE niacin
- intense flush with pruritus - GI disturbances - hepatic toxicity - peptic ulcer - hyperglycemia - hyperuricemia
57
MOA ezetimibe
- inhibit cholesterol transport protein (NPC1L1)
58
Ezetimide LDL
reduce 18-25%
59
Ezetimide HDL
no significant change
60
ezetimide uses
adjective with statins
61
ezetimide PK
- absorbed well orally - excreted feces unchanged - rest conjugated in liver (glucouronidation) - half life 18-30 h
62
ADE ezetimide
- diarrhea | - many interactions with other anti-lipidemic drugs
63
Ezetimide and fibrates
increase ezetimide levels | increase risk of cholelithiasis
64
Ezetimide and niacin
increase ezetimide levels | increase risk of myotpathies
65
ezetimide and warfarin
increase prothrombin time
66
Omega3 FA MOA
small intestine absorbed EPA and DHA
67
Omega 3 FA VLDL
reduce
68
omega 3 FA uses
- OTC herbal, vitamin, nutritional supplement - Rx heart disease - Rx high triglyericde levels - adjunct to diet for severe hypertriglyceridemia
69
ADE omega 3FA
- arthralgia - nausea - fish burps - dyspepsia - increased LDL - may prolong bleeding time
70
PCSK9 inhibitors use
- alone or combo with statins | - lower hardest to treat elevated cholesterol levels who cannot tolerate high statins (SE)
71
PCSK9 inhibitors examples
evolocumab (repatha) | alirocumab (praluenut)
72
PCSK9 inhibitor MOA
- binds LDL receptor - enhance degradation of LDL receptor - mutations - effects on plasma lipids and lipoproteins - increase LDL receptors on surface
73
PCSK9 inhibitor LDL monotherapy
LDL-C reduce in dose dependent manner | 70%
74
PCSK9 inhibitor LDL with statin
lower 60%
75
what is recommended before use of PCSK9 inhibitors?
statins/ezetimibe
76
PK PCSK9 inhibitors
- SC injections Q2W or 1 monthly
77
ADE PCSK9 inhibitors
- small risk of neurocognitive effects - nasopharyngitis - UTI - URI - injection site reactions
78
T/F PCSK9 inhibitors increase risk of myopathies
FALSE! | Do NOT
79
Microsomal triglyeride transfer inhibitor (MTP) use
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
MTP MOA
- inhibit MTP (essential for formation of VLDL)
81
MTP drug
Lomitapide (small synthetic molecule)
82
Lomitapide LDL
reduces 50%
83
Lomitapide PK
- with water - without food - CYP3A4
84
ADE lomitapide
- GI: V/D/ab pain - hepatotoxicity - liver steatosis - increase hepatic fat - embryo toxic
85
Inhibitor of apoB B-100 synthesis drug
mipomersen
86
FH
autosomal dominant 300-500 heterozygous high levels of LDL
87
homozygous FH
1/1 million | - severe hypercholesterolemia with accelerated CHD in childhood
88
Mipomersen MOA
binds mRNA encoding ApoB (main component of LDL and VLDL) | - RNA degraded
89
Mipomersen LDL
lower 30-50%
90
mipomersen use
- as addition to lipid lowering meds and diet with hoFH
91
ADE mipomersen
makes not approved elsewhere, including Europe - injection site - flu like - fatigue - HA - hepatotoxicity
92
mipomersen PK
SC once a week half life 1-2 months - max LDL reduction after 6 months
93
CI mipomersen
liver disease
94
Statin main use
high LDL
95
fibrates main use
with statins
96
bile acid resin main use
with statins
97
niacin main use
patients with all types of lipoprotein disorders | often used in combo
98
ezetimibe main use
with statins
99
PCSK9 inhibitor main use
with statins
100
MTP inhibitor main use
adjunct to diet for lowering - LDL-C - total cholesterol - apoB - non HDL-C lipoproteins (hoFH)
101
inhibitor of apoB-100 synthesis main use
adjunct with lipid lowering meds and diet for hoFH

Pharmacology Exam 4 (7 decks)

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