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Pharm Unit 8 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

cholesterol is synthesized by ___

A

liver

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2
Q

additional cholesterol comes from __

A

diet

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3
Q

cholesterol has a ___ structure

A

membrane

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4
Q

cholesterol is a precursor to ___

A

steroid hormones

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5
Q

lipid categories

A

endogenous and dietary cholesterol

triglycerides

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6
Q

total - c =

A

LDL-c + HDL-c + VLDL - c

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7
Q

LDL

A

low density lipoproteins – bad

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8
Q

HDL

A

high density lipoproteins – good

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9
Q

triglyceride categories:

A

vldl-c

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10
Q

optimal LDL

A

<100

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11
Q

high LDL

A

160-189

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12
Q

causes of secondary dyslipidemia

A 
diabetes
hypothyroid
obstructive liver disease
chronic renal failure
drugs
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13
Q

TLC diet to lower LDL

A

reduced intake of cholesterol raising nutrients

LDL lowering therapeutic options

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14
Q

major features of TLC that lower LDL

A

TLC diet
weight reduction
increased physical activity

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15
Q

most commonly prescribed drugs from high cholesterol

A

HmG CoA reductase inhibitors (statins)

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16
Q

major side effects of statins

A

myopathy (increased CK)

increased liver enzymes (increased AST/ALT)

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17
Q

absolute contraindications to statins

A

liver disease

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18
Q

relative contraindication to statins

A

use with certain drugs

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19
Q

statins demonstrated ___

A 
therapeutic benefits: 
reduce coronary events
reduce CHD
reduce coronary procedures
reduce stroke
reduce mortality
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20
Q

MOA of statins

A

block rate - limiting step in cholesterol synthesis

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21
Q

statin induced myopathy

A

serum CK >10x ULN with unexplained muscle weakness

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22
Q

statin induced rhabdomyalsis

A

serum CK >40x ULN w/ unexplained muscle pain or wekness

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23
Q

patients tend to present with statin induced myopathy within the first ___

A

12 mo

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24
Q

highest risk of statin induced myopathy

A

high dose simvastatin (zocor)

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25
Q

statin induced myopathy is due to ___

A

metabolism by cyp3a4

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26
Q

if patient’s experience SEs w/ statin, try ___

A

a different statin

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27
Q

HMG CoA Reductase Inhibitors

A

atorvastatin

rosuvastatin

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28
Q

cost of pitavastatin

A

295 – not available generically anymore

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29
Q

rosuvastatin (Crestor) lowers LDL by

A

63%

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30
Q

atorvastatin decreases LDL by ___

A

57%

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31
Q

simvastatin decreases LDL by ___

A

46%

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32
Q

high dose simvastatin

A

80mg

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33
Q

low dose simvastatin

34
Q

high dose simvastatin users are at risk for

A

myopathy and rhabdo

35
Q

low dose simvastatin users are at risk for

A

myopathy but not rhabdo

36
Q

restricting dosing fo simvastatin:

37
Q

use of 80mg dose of simvastatin should be restricted to patients who:

A

have bene taking it for >12mo without s/s of toxic effect son muscles

38
Q

patients on 80mg dose without AE but need to take a c/I drug should ___

A

switch to a noter statin

39
Q

patents who’s LDL-C cannot be reached on 40mg dose should be switched to statin with ___

A

less risk of myopathy

40
Q

gemfibrozil is c/I w/ ___

A

simvastatin

41
Q

when taking amiodarone, verapamil or diltiazem, do not ___

A

exceed 10mg simvastatin daily

42
Q

if taking amlodipine, ranolazine, do not ___

A

exceed 20mg simvastatin daily

43
Q

if drinking grapefruit juice, do not

A

ingest > 1 quart daily if taking simvastatin

44
Q

____ on statins is not a reason to sotp

A

elevated transaminases

45
Q

statin side effects are often ___

A

agent specific, not always class specific

46
Q

if unexplained myalgia on statin w/o CK elevation, ___

A

try a different statin

47
Q

await follow up of ___

A

simvastatin relabeling

48
Q

very few patients receive ___

A

new scripts for simvastatin

49
Q

MOA of bile acid sequestrates (BAS)

A

bind dietary cholesterol

50
Q

major actions of BAS

A

reduces LDL by 20-25%
raises HDL by 3-5%
may increase TG

51
Q

side effects w/ BAS

A

GI distress/constipation, diarrhea, bloating

decreased absorption of other drugs

52
Q

contraindications to BAS

A 
severe hepatic impairment
raised TG (especially >400mg/dl)
53
Q

BAS

A

cholestyramine
cholestipol
coleseyelam

54
Q

generic cost of 30 day supply of coleseyelam

55
Q

BAS is typically add on therapy to ___

A

max dose statin

56
Q

major actions of niacin

A

lowers LDL 5-25%
raises HDL 15-35%
lowers TG 10-50%

57
Q

s/e of niacin

58
Q

flushing with niacin is minimized by:

A

pretreatment with aspirin or NSAIDS 30-60 minutes prior to ingestion

59
Q

niacin is currently used as ___

A

add on therapy (not monotherapy) if used at all

60
Q

niacin did not reduce incidence of ___

A

primary composite endpoint

61
Q

unexpected increase in ___ in niacin patients

62
Q

use niacin for ____

A

statin intolerant patients

63
Q

niacin did not reduce risk of ___ but did increase risk of ___

A

major CV cents / serious adverse effects

64
Q

niacin is ___

A

little used

65
Q

fibric acids decrease TG and VLDL C by

66
Q

fibric acids may lower LDL by ___ w/ normal TG

67
Q

fibric acids may raise LDL with ___

68
Q

fibric acids may raise HDLC by

69
Q

fibric acids

A

gemfibrozil

fenofibrate

70
Q

cholesterol absorption inhibitor

A

ezetimibe (zetia)

71
Q

new class of cholesterol absorption inhibitor inhibits ___

A

intestinal absorption of cholesterol

72
Q

ezetimibe lowers LDL by ___

73
Q

ezetimibe combined with a statin:

A

increases effect of statin by 10-15% w/o s/e

74
Q

Vytorin =

A

ezetimibe + simvastatin

75
Q

MOA of monoclonal antibodies

A

bind to pro protein converts subtilizing/kexin (PCSK9) receptors

76
Q

addition to statins, monoclonal antibodies reduce LDL by

77
Q

monoclonal antibodies are given by ____

A

SC injetion q 2-4 wks

78
Q

when should you give monoclonal AB?

A

add on to max dose statin

79
Q

bempedoic acid is not ___

A

FDA approved yet

80
Q

MOA of bemepdoic acid

A

inhibits ATP citrate lyase (key enzymes cholesterol synth)

81
Q

dosing of bempedoic acid

A

180 mg PO DAILY

82
Q

BPDA results:

A 
LDL decrease
Non-HDL decrease
TC decrease
apolipoprotein B decrease
high sensitivity CRP decrease

Pharm Unit 8 (3 decks)

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