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Year 2 CV > Exam 2 antihyperlipidemics- Kinder > Flashcards

Exam 2 antihyperlipidemics- Kinder Flashcards

1
Q

What are statins

A

HMG-CoA reductase inhibitors

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2
Q

what are the fibrate drugs

A

fenofibrate

gemfibrozil

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3
Q

what are the bile acid sequesterants

A

cholestyramine
colesevelam
colestipol

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4
Q

what are the cholesterol absorption inhibitors

A

ezetimibe

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5
Q

vytorin is a comination of what drugs

A

simvastatin and ezetimibe

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6
Q

what are the new Tx out for homozygous familial hypercholesterolemia

A

lomitapide

mipomersen

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7
Q

what are the major components of chylomicrons

A

dietary TGs and cholesterol

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8
Q

where are chylomicrons synthesized

A

intestine

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9
Q

what is the mechanism of catabolism of chylomicrons

A

TG hydrolysis by LPL and remant uptake by liver

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10
Q

What is LDL make up of

A

cholesteryl esters

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11
Q

what is HDL made up of

A

phospholipids, cholesteryl esters

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12
Q

what lipoproteins are made in the liver

A

VLDL and HDL

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13
Q

which lipoprotein has the most protein

A

HDL

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14
Q

which lipoprotein has the most lipid

A

chylomicrons

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15
Q

how do plaques form, general path sequence

A

LDL retention in subendothelial space leading to oxidation that increases plasminogen inhibitor and inhibits NO
massive accumulation of cholesterol with increased inflammatory response

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16
Q

What are the targe LDL choesterol levels and what is considered very high

A

want 190 very high

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17
Q

what is the target for total cholesterol and what is considered high

A

want 240 high

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18
Q

what are the normal ranges of HDL

A

60 is high

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19
Q

What is the LDL goal for CHD or CHD risk eqivalent?

at what LDL level do you intiate drug therapy

A

goal LDL 130

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20
Q

what is the LDL goal for patients with 0-1 risk factors? when do you start Tx

A

goal 190

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21
Q

What are the risk equivalents for CHD

A

symtomatic carotid artery disease
peripheral arterial disease
AAA
diabetes

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22
Q

what are the risk factors for hyperlipidemia

A 
age
family Hx of premature CHD
cigarette smoking
HTN
low HDL
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23
Q

what are non drug Tx options for HLD

A

lifestyle changes, diet, exercise, smokin cessation

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24
Q

what are the drug Tx options for HLD

A 
MHG-CoA Reductase Inhibitors (statins)
Niacin, Vit B3
Fibric Acid dervatives (fibrates)
bile acid sequestrants (resins)
cholesterol absorption inhibitors
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25
Q

non drug Tx for HLD should not be used alone in what scenarios

A

severe hypercholestermia
known CHD
CHD risk equivalents
PVD

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26
Q

what are the dietary recs for HLD

A

total fat 20-25% calories
saturated fat <200 mg
carbs 50-60% total calories
dietary fiber 20-30 g

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27
Q

What parts of diet increase TGs?

A

alcohol, total fat, excess caloric intae

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28
Q

what parts of diet increase LDL

A

cholesterol, saturated and trans fats

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29
Q

What is HMG-CoA reductase

A

the rate limiting enzyme in cholesterol synthesis

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30
Q

which statins have longer half lives

A

atorvastatin and rosuvastatin

31
Q

What statins use CYP3A4

A

lovastatin, simvastatin, atorvastatin

32
Q

what stains use CYP2C9

A

fluvastatin and rosuvastatin

33
Q

What are adverse reactions of statins

A

LFT elevation, CPK elevation, rhabdomyolysis, myopathy

34
Q

what are contraindications for statins

A

pregnancy

35
Q

What drugs cause bad interactions with statins

A

increase statin: CYP inhibitors, cyclosprine, ketoconozole fibrates
decrease statin: CYP inducers (phenytoin and rifampin)

36
Q

How does niacin work

A

inhibits lipolysis of TG in adipose and reduces circulatin FFA

37
Q

what are the affects of niacin on apoA1 and plasma HDL

A

decrease apoA1 clearance and increase plasma HDL

38
Q

what are the affects of niacin on clotting factors

A

decrease fibrinogen levels and increase tpa

39
Q

why do you have to dose constantly with nicotinic acid, niacin

A

extensive first pass. t1/2 is 60 minutes

40
Q

what are the adverse ractions with niacin

A

cutaneous flush (PG mediated), pruritis, acanthosis nigricans, hepatotoxicity

41
Q

what are the contraindications with niacin

A

hepatic disease, active PUD, caution DM

42
Q

how do fibrates work

A

PPARalpha agonists that regulate expression of proteins involved in lipoprotein structure and function, increased expression LPL

43
Q

what is the main result of fibrates

A

decreased TG levels

44
Q

what are the adverse reactions with fibrates

A

GI, lithiasis, myositis, myopathy

45
Q

what are the contraindications with fibrates

A

avoid in hepatic or renal dysfunction, pregnancy

46
Q

what main anticoagulant has a drug interaction with statins

A

warfarin, increased risk of rhabdomyolysis if used with statins

47
Q

how do bile acid sequestrants work

A

bind bile acids increasing excretion in stool. so ehnaced conversion of cholesterol to BA and increased LDL clearance

48
Q

what are the adverse reactions with bile acid sequestrants (resins)

A

GI constipation and nausea, impaired ADEK absorption

49
Q

what are the contraindications with resins

A

caution in diverticulitis, bowel disease and cholestasis

50
Q

what are the drug interactions with resins

A

impairs drug absorption- separate admin

51
Q

how does ezetimibe work

A

inhibits NPC1L1 inhibits absorption of cholesterol and plant sterols

52
Q

what is adverse reaction with ezetimibe

A

diarrhea

53
Q

what are the drug interactions with resins

A

have to separate time of administartion by at least 4 hours because resins will bind up drugs

54
Q

what is the overall effect of statins on lipoproteins

A

decrease LDL

55
Q

what is the overall effect of niacin on lipoproteins

A

increase HDL

56
Q

what is the overall effect of resins on lipoproteins

A

decrease LDL

57
Q

What is the main Tx course for atherosclerotic CV disease ASCVD

A

maximizing statin intesnsity reduces amount of events

58
Q

What are the 4 statin benefit groups

A

1) ASCVD
2) primary elevation of LDL-C >190 mg
3) age 40-75 with DM and LDL-C 70-189 mg
4) No clinical ASCVD or DM who are 40-75 y/o and LDL-C 70-189 mg with ASCVD risk >7.5%

59
Q

if patient is above 21 and has clinical ASCVD what Tx is first line

A

75 moderate intensity statin

60
Q

patient does not have ASCVD but has LDL-C >190 Tx?

A

high intesnsity statin

61
Q

patient does not have ASCVD or LDL-C >190 but has DM I or II and is 40-75. Tx?

A

moderate intensity

high if estimated 10 y risk is >7.5%

62
Q

what does high intesnsity statin mean

A

daily dose lowers LDL-C by approx 50%

63
Q

what does moderate intesnsity statin mean

A

daily dose lowers LDL-C by approx 30-<50%

64
Q

what are the high intesnsity statins available and doses

A

atorvastatin 40-80 mg

rosuvastatin 20 mg

65
Q

what cause homozygous familial hypercholesterolemia

A

defects in LDL R gene

66
Q

What are Tx options for homozygous familial hypercholesterolemi

A

Mipomersen injection

Lomitapide

67
Q

How does mipomersen lower cholesterol

A

inhibits apoB 100 synthesis by binding mRNA and reducing formation

68
Q

what are adverse reactions to mipomersen

A

injection site reactions, flue like symtoms, HA, elevated liver transaminases

69
Q

what are the contraindications for mipomersen

A

moderate or severe hepatic impairment, active liver disease

70
Q

what is administration method for lomitapide

A

once dialy oral dosew

71
Q

what is mechanism of lomitapide

A

binds and inhibits microsomal TG transfer protein, lcoated in lumen of ER. prevents assembly of apoB

72
Q

what are adverse reactions to lomitapide

A

GI diarrhea, nausea, increased liver transaminases, hepatic fat accumulation

73
Q

what are the contraindications of lomitapide

A

pregnancy

Year 2 CV (31 decks)

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