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PHRM 844 > Anti-hyperlipidemics > Flashcards

Anti-hyperlipidemics Flashcards

1
Q

Structure of cholesterol?

A
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2
Q

What do lipoproteins do?

A

Transport TG and cholesterol in blood

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3
Q

What are lipoprotein’s surface made of?

A

Phospholipids, proteins, and cholesterol

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4
Q

What are lipoprotein’s core made of?

A

Cholesterol esters and TGs

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5
Q

What is the lipoprotein lipase system?

A

Release of free FAs from the lipoprotein

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6
Q

Chylomicron function

A

Involved in transport of dietary lipids from from gut to liver and intestine

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7
Q

What is VLDL

A

It is the main source of TGs that is secreted in the blood from liver

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8
Q

What is IDL

A

TG-free LDL

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9
Q

What is LDL

A

Main source of cholesterol in blood

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10
Q

HDL function

A

Secreted from liver and acquires free cholesterol from peripheral tissues and atheromas

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11
Q

ApoA-1 info

A

Found in HDL and forms its structure
ABCA1 receptor ligand
Mediates reverse cholesterol transport
Produced in liver and intestine

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12
Q

ApoB-100 info

A

Found in VLDL, IDL, LDL and forms their structure
LDL receptor ligand
Produced in liver

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13
Q

ApoB-48 info

A

Forms chylomicron structure
Produced in intestine

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14
Q

ApoE info

A

Found in HDL
LDL remnant receptor ligand
Produced in liver and other tissues

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15
Q

ApoCII info

A

Found in chylomicron, LDL
Binds to LPL and enhances TG hydrolysis

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16
Q

Lipid absorption and transport diagram

A
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17
Q

Liver synthesis of cholesterol pathway

A

De novo synthesis is major source of cholesterol

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18
Q

Lipoprotein disorders ratios

A

> 4.5 is associated with increased risk of CVD
<=3.5 desirable
<3 optimal

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19
Q

cholesterol levels

A

<200 desirable
200-239 borderline high
>240 high

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20
Q

LDL levels

A

<140 desirable
140-159 borderline high
>160 high

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21
Q

TG levels

A

<150 desirable
150-199 borderline high
>200 high

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22
Q

HDL levels

A

> 40 in men desirable
50 in women desirable

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23
Q

Goals of therapy for hyperlipidemia

A

Decrease reabsorption of excreted bile acids
Decrease liver secretion of VLDL
Decrease synthesis of cholesterol
Increase hydrolysis of lipoprotein TGs

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24
Q

Bile acid binding resins MOA

A

Inhibits reabsorption of bile acids by binding bile acids from intestine to form insoluble complex excreted in feces; upregulate LDL receptors in liver

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25
Q

bile acid binding resins drugs

A

Cholestyramine (Queastran)
Colestipol (Cholestipid)

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26
Q

bile acid binding resins therapeutic use

A

tx of primary hypercholesterolemia

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27
Q

bile acid binding resins effects

A

produces 20% decrease in LDL in 2-4 weeks
may cause 5% increase in HDL
may increase TG

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28
Q

bile acid binding resins SEs

A

constipation
bloating

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29
Q

bile acid binding resins drug interactions

A

acetaminophen, thiazides, digoxin, warfarin, fibrates, zetia, oral contraceptives, corticosteroids, thiazolindineiones

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30
Q

cholesterol absorption inhibitor MOA

A

inhibits absorption of cholesterol from dietary lipids and reabsorption of cholesterol excreted in bile
AKA inhibits NPC1-L1

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31
Q

cholesterol absorption inhibitor drug

A

Ezetimibe (Zetia)

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32
Q

zetia effects

A

reduction of LDL levels by 17%
adjunct with statins (enhances LDL reduction to 20%)

33
Q

zetia AEs

A

low incidence of myopathy/rhabdomylosis

34
Q

HMG-CoA reductase inhibitor drugs

35
Q

which statins are prodrugs

A

Lovastatin (Alteprav)
Simvastatin (Zocor)

36
Q

what are statins derived from

A

mevalonic acid

37
Q

which statins do not get metabolized by CYPs

A

pravastatin (pravachol) - sulfation
pitavastatin (livalo) - excreted unchanged

38
Q

which statins get metabolized by CYP3A4

A

lovastatin (alteprev)
simvastatin (zocor)
atorvastatin (lipitor)

39
Q

statins MOA

A

competitively inhibit HMG-coa reductase, the rate limiting step in cholesterol synthesis

40
Q

statins indications

A

hypercholesteremia

41
Q

statins efficacy

A

20-60% decrease in LDL
10-33% decrease in TG
5-10% increase in HDL

42
Q

which statins are metabolized by CYP2C9

A

fluvastatin (lescol)
rosuvastatin (crestor)

43
Q

statins AEs

A

skeletal muscle effects - rhabdomyolysis with renal dynsfunction; monitor serum creatine phosphokinase
hepatotoxicity

44
Q

ATP citrate lyase inhibitor drug

A

bempedoic acid (nexletol)

45
Q

what is bempedoic acid used adjunct to

A

used as adjunct to statins

46
Q

nexletol indication and effects

A

reduces serum LDL and cholesterol in pts with HeFH or ASCVD

47
Q

nexletol metabolism

A

metabolized by glucoronidation via kidneys

48
Q

PCSK9 inhibitor drugs

A

alirocumab (praluent)
evolocumab (repatha)
inclisiran (leqvio)

49
Q

PCSK9 inhib effects

A

increases LDL receptor # and reduce serum LDL levels

50
Q

what are PCSK9 inhibs used as

A

adjunct to statins for patients with HeFH, HoFH, and ASCVD

51
Q

leqvio moa

A

a siRNA that inhibits PSCK9 protein translation and directs degradation against hepatacytes

52
Q

ApoB lipoprotein synthesis inhibitor drug

A

Juxtapid (Lomitapide)
Mipomersen (Kynamro)

53
Q

what is juxtapid

A

small molecule microsomal TG transfer protein inhibitor

54
Q

juxtapid moa

A

disrupts chylomicron and LDL processes
inhibits assembly of apob containing lipoproteins

55
Q

which drugs have high risk of liver damage

A

juxtapid (lomitapide)
Mipomersen (Kynamro)

56
Q

what is kynamro

A

phosphorothioate anti-sense oligonucleotide inhibitor of apob100

57
Q

kynamro moa

A

hybridizes apob100 mrna in liver and promotes degradation

58
Q

kynamro indication

A

as adjunct to other tx for pts with HoFH

59
Q

angiopoietin-like protein 3 inhibitor

A

evinacumab-dgnb (evkeeza)

60
Q

evkeeza indication

A

tx of HoFH

61
Q

what does evinacumab do

A

increases LPL and endothelial lipase activity by preventing ANGPTL3 mediated inhibition
lowers LDL cholesterol

62
Q

types of fibrates

63
Q

fibrates moa

A

fibrates bind to PPAR alpha and regulate gene transcription along with retinoic acid receptor

64
Q

fibrates efficacy

A

reduce serum LDL by 6-20%
reduce serum TGs by 35-52%
elevate HDL by 15-30%

65
Q

fibrates indication

A

hypertriglyceridemia

66
Q

fibrates SEs

A

gallstones
rhabdomyolysis

67
Q

niacin structure

68
Q

niacin effects

A

reduces serum TGs
increases lipase activity to increase clearance of VLDL
decreases hepatic VLDL production
may significantly reduce serum LDL and TG
usually increases HDL levels

69
Q

niacin in adipose tissue effect

A

inhibits TG lipolysis by hormone sensitive lipase, decreasing FA transport to liver via activation of GPR109A

70
Q

niacin in liver effect

A

inhibits FA synthesis and esterification reducing TG export via VLDL
reduces clearance of ApoA1

71
Q

niacin in macrophages effect

A

increases expression of CD36 and ABCA1

72
Q

niacin indications

A

mixed hyperlipidemias
hypertriglyceridemia with high risk of pancreatitis

73
Q

niacin AEs

A

marked vasodilation - flushing, itching, tingling (treat with prostaglandins)
hepatotoxicity

74
Q

omega-3 FA drugs

A

Lovaza
Omtryg (EPA + DHA)
Vascepa (EPA only)

75
Q

O3FA moa

A

reduce synthesis of TGs in liver
inhibit esterification of other FAs

76
Q

O3FA indications

A

severe hypertriglyceridemia >500 mg/dl
combined with statins to reduce LDL levels

77
Q

what is done before initiating lovaza

A

start lipid lowering diet

78
Q

O3FA AE

A

can increase LDL levels; Vascepa cannot alone

PHRM 844 (13 decks)

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