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BMS 615 Cardiovascular > Test 1: Wk2: 1 Antilipemics - Velentovic > Flashcards

Test 1: Wk2: 1 Antilipemics - Velentovic Flashcards

1
Q

Acceptable cholesterol level

A

<200

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2
Q

Acceptable LDL-C level

A

<100

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3
Q

Acceptable Triglyceride level

A

<150

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4
Q

Hyperlipidemia primary causes (2)

A

diet and genetics

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5
Q

Hyperlipidemia secondary causes (2)

A

drugs

certain diseases and conditions (diabetes and alcoholism)

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6
Q

1st Line of therapy

A

diet

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7
Q

decreasing total daily — intake will help cholesterol and triglyerides

A

fat

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8
Q

high triglycerides are caused by — reduce them by decreasing intake of — and —

A

high carb intake

carbs and alc

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9
Q

increasing exercise increases — levels

A

HDL

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10
Q

5 Drugs that lower Cholesterol

A 
resins
Statins
Nicotinic Acid
Ezetimibe
PCSK9 Inhibitors
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11
Q

what are the 3 resins

A

Cholestyramine
Colesevelam
Colestipol

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12
Q

the bioavailability of statins is — why?

A

0; not absorbed in GI

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13
Q

Normally bile acids undergo —

recirculation 6x/day blocked by —

A

Normally bile acids undergo enterohepatic

recirculation 6x/day blocked by resins

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14
Q

resins cause increased — excretion of —

A

fecal; bile acids

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15
Q

resins increase conversion of hepatic — to —

A

cholesterol to bile acids

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16
Q

bile acids have a negative feedback on — and — remove this negative feedback

A

7a hydroxylase

resins

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17
Q

resins increase number of — receptors

A

hepatic LDL

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18
Q

increased hepatic LDL receptors causes a compensation for — resulting in —

A

compensation for decreased intrahepatic
cholesterol

lower plasma LDL-C

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19
Q

resins are used to treat

A

hypercholesterolemia

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20
Q

how long for resins to have maximal effects

A

4 weeks

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21
Q

resins decrease LDL-C by — %

A

20

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22
Q

resins are often combine with (4 drugs)

A

HMG CoA reductase inhibitors

ezetimibe

fibrates

Nicotinic acid

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23
Q

can resins be used in pregnant women and children

A

yes

children older than 6

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24
Q

where do the major side effects of resins occur and what are they

A

GI

bloating and constipation

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25
Q

what is taken with resins to lessen side effects

A

Colesevelam

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26
Q

resins interfere with —

A

fat sol vit and drugs

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27
Q

how much should resin dosing be staggered

A

1 hr before

4 hrs after

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28
Q

HMG CoA Reductase Inhibitors are also known as

A

Statins

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29
Q

what are the 7 statins

A

Atorvastatin , Simvastatin , Lovastatin, Rosuvastatin Pravastatin, Fluvastatin &
Pitavastatin

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30
Q

Statin are a — inhibitor of — enzyme in — biosynthesis

A

competitive, HMG CoA reductase; cholesterol

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31
Q

Statin site of action is primarily in

A

the liver

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32
Q

Statins increase the number of — and increase the clearance of —

A

hepatic LDL receptors

plasma LDL

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33
Q

Statins are used to lower

A

cholesterol

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34
Q

what 2 statins are used to lower cholesterol and triglycerides

A

Atorvastatin and Rosuvastatin

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35
Q

Statins elevate — and —

A

plasma ALT/AST

CPK

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36
Q

Statins increase risk of — and —

A

hepatic and renal disease

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37
Q

the risks of statins — with — dose

A

increase with higher dose

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38
Q

increased CPK is associated with —

A

myalgia

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39
Q

what to statins have the least side effects

A

fluvastatin and pravastatin

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40
Q

3 Statin contraindications

A

Pregnancy X

Nursing mothers

Acute Liver Dz

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41
Q

max effect of statins takes

A

2 weeks

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42
Q

statins increase — levels

A

HDL

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43
Q

statins have — absorption and — bioavail

A

good, low

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44
Q

What statin can be used in pediatrics (8 yrs)

A

pravastatin

Age 10+ for other statins

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45
Q

peak cholesterol synthesis is from — to —

A

midnight to 2 am

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46
Q

what 3 statins are taken at night

A

Fluvastatin , Lovastatin, Simvastatin

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47
Q

what 3 statins can be taken any time of day

A

Atorvastatin, rosuvastatin and pravastatin taken

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48
Q

what 2 statins bioavail is lowered by food

A

Pravastatin & Pitavastatin

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49
Q

why do Atorvastatin and
Rosuvastin reduce
cholesterol and triglycerides
(3 reasons)

A

loner t1/2

higher increase in LDL receptors

increase clearance of IDL

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50
Q

— and — statins are prodrugs and are converted to active metabolites by — and —

A

Lovastatin and Simvastatin

intestinal carboxylesterase and CYP3A4

51
Q

— is the substrate for atorvastatin, lovastatin

and simvastatin

A

CYP3A4

52
Q

avoid grapefruit juice with

A

atorvastatin, lovastatin

and simvastatin

53
Q

— rosuvastatin and fluvastatin

A

CYP2C9 rosuvastatin and fluvastatin

54
Q

— simvastatin

A

CYP2D6 simvastatin

55
Q

simvastatin induced — is higher with — allele

A

muscle pain; CYP2D6*4

56
Q

— SNP lowers hepatic

uptake, higher plasma levels

A 
SCLO1B1 SNP (OATP1B1) lowers hepatic
uptake, higher plasma levels
57
Q

Ezetimibe inhibits — absorption at the —

A

cholesterol; brush border of SI

58
Q

Ezetimibe inhibits Inhibits cholesterol absorption at —

A

enterocytes

59
Q

Ezetimibe inhibits —transporter protein

A

NPC1L1

60
Q

Ezetimibe targets

A

dietary cholesterol

61
Q

Ezetimibe lowers LDL-C by max — %

A

20

62
Q

Ezetimibe works better when combined with – instead of doubling — dose

A

statin; statin

63
Q

Ezetimibe adverse effects and what is most common

A

minimal GI

diarrhea most common

64
Q

don’t use Ezetimibe with

A

hepatic dysfunction

65
Q

Ezetimibe increases risk of elevated — when combine with

A

transaminase; statins

66
Q

Ezetimibe not often combined with

A

resins

67
Q

2 PCSK9 Inhibitors

A

Alirocumab and Evolocumab

68
Q

PCSK9 inhibitors MOA

A

bind LDL receptor and degrades it
less LDL can be removed from blood

By inhibiting PCSK9, more LDL receptor can remove more LDL

69
Q

Alirocumab and Evolocumab are used with

A

statin or ezetimibe

70
Q

Alirocumab and Evolocumab dosig

A

every 2 wks sub Q

71
Q

Alirocumab and Evolocumab decrease — by —% when combined with —

A

LDL-C 50-70% Ezetimibe

72
Q

Alirocumab and Evolocumab side effects

A

allergy

73
Q

3 Drugs that lower triglycerides

A

Fibrates

Nicotinic Acid

Omega-3-Acid Ethyl Esters

74
Q

2 FIbrates

A

Gemfibrozil and Fenofibrate

75
Q

Fibrates bind — to stimulate —

A

PPARa; FA oxidation

76
Q

fibrates reduce — expression resulting in increased — activity

A

apoCIII

lipoprotein lipase

77
Q

Fibrates decrease hepatic production of — by increasing —

A

VLDL; clearance

78
Q

fibrates increase — by —%

A

HDL; 15%

79
Q

increased risk of gallstones is only associated with which fibrate

A

clofibrate

80
Q

fibrates have an increased risk of — when combined with —

A

myopathy; HMG CoA reductase inhibitors

81
Q

myopathy is worse with what fibrate

A

Gemfibrozil

82
Q

Gemfibrozil inhibits —

A

OATP2

83
Q

risk of myopathy is least with what fibrate

A

fenofibrate

84
Q

fibrate contraindications (3)

A

liver dysfunction
renal dz
gallbladder dz

85
Q

Nicotinic Acid decreases production of —

A

hepatic VLDL

86
Q

Nicotinic acid inhibits — decreasing delivery of — to the —

A

lipolysis
FFAs
liver

87
Q

Nicotinic acid inhibits — in -fat cells decreasing circulation of —

A

hormone sensitive lipase

FFAs

88
Q

increased — increases — clearance

A

lipoprotein lipase; VLDL

89
Q

Nicotinic acid does not interact with

A

PPARa

90
Q

Nicotinic acid lowers

A

TG and Cholesterol

91
Q

Nicotinic acid adverse effects (3)

A

itching, flushing

increased ALT/AST

92
Q

what needs to be monitored when Nicotinic acid is combined with satins

A

creatine kinase

93
Q

Nicotinic acid should not be used in pts with

A

peptic ulcer

94
Q

Nicotinic acid may cause — and —

A

hyperuricemia and glucose intolerance

95
Q

Nicotinic acid contraindications

A

bleeding disorder
liver dz
peptic ulcer

96
Q

Icosapent Ethyl lowers — in individuals with —

A

TGs, high >500 mg/dl TG

97
Q

Icosapent Ethyl inhibits

A

DGAT

98
Q

Icosapent Ethyl decreases — synthesis

A

VLDL

99
Q

Icosapent Ethyl increases —

A

lipoprotein lipase eicosapentatonic acid

100
Q

Icosapent Ethyl adverse effects

A

arthralgia

101
Q

Icosapent Ethyl contraindications

A

hypersensativity

102
Q

Familial hyperchylomicronemia Type 1 has elevated — and —

A

chylomicrons and TGs

103
Q

Familial hyperchylomicronemia Type 1 has defect in

A

lipoprotein lipase or Apo CII

104
Q

Familial hyperchylomicronemia Type 1 control

A

diet therapy

fibrates and nicotinic acid

105
Q

Familial hypercholesterolemia IIa elevated — and —

A

cholesterol and LDL

106
Q

Familial hypercholesterolemia IIa increased risk for

A

CVD

107
Q

Familial hypercholesterolemia IIa decreased clearance of

A

LDL

108
Q

Familial hypercholesterolemia IIa tx

A

resins

statins, ezetimibe combined with PCSK9

109
Q

Familial hypercholesterolemia IIb elevated — and —

A

VLDL and LDL

110
Q

Familial hypercholesterolemia IIb tx

A

Statins and Nicotinic acid

111
Q

Familial dysbetalipoproteinemia III elevated — and —

A

TGs and Cholesterol

112
Q

Familial dysbetalipoproteinemia III — and — remnants

A

IDL and chylomicron

113
Q

Familial dysbetalipoproteinemia III presence of abnormal

A

Apo E - E2

114
Q

Familial dysbetalipoproteinemia III increased — production

A

VLDL

115
Q

Familial dysbetalipoproteinemia III most sensitive to

A

fibrates

50% TG redcution

116
Q

Familial hypertriglyceridemia IV elevated — and —

A

TG and VLDL

117
Q

Familial hypertriglyceridemia IV associated with — and or —

A

hyperuricemia and glucose intolerance

118
Q

Familial hypertriglyceridemia IV tx

A

fibrates

nicotinic acid

119
Q

Diseases cholesterol elevated in

A

biliary dz
renal dz
hypothyroidism
diabetes

120
Q

Diseases Triglycerides elevated in

A

alcoholism
renal dz
diabetes

121
Q

thiazide diuretics elevated — and — by —%

A

cholesterol and TGs by 10-15%

122
Q

Beta Blockers elevate — and decrease —

A

TG and HDL

123
Q

oral contraceptives elevate

A

TGs

BMS 615 Cardiovascular (49 decks)

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