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PHRM 844 > antihyperlipidemic > Flashcards

antihyperlipidemic Flashcards

1
Q

how are cholesterol and triglycerides transported in the blood?

A

in macromolecular aggregates known as lipoproteins

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2
Q

what are the major classes of lipoproteins based on?

A

density, composition, and electrophoretic mobility

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3
Q

Largest, has the most TG
a. chylomicrons
b. VLDL
c. IDL
d. LDL
e. HDL

A

a. chylomicrons

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4
Q

secreted by liver into blood, has lot of TG but less than chylomicrons,
a. chylomicrons
b. VLDL
c. IDL
d. LDL
e. HDL

A

b. VLDL

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5
Q

triglyceride-depleted VLDL’s
a. chylomicrons
b. VLDL
c. IDL
d. LDL
e. HDL

A

c. IDL

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6
Q

Main cholesterol form in blood.
a. chylomicrons
b. VLDL
c. IDL
d. LDL
e. HDL

A

d. LDL

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7
Q

secreted by liver and acquire cholesterol from peripheral tissues and atheromas (reverse cholesterol transport). most protein, low amounts of TG
a. chylomicrons
b. VLDL
c. IDL
d. LDL
e. HDL

A

e. HDL

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8
Q

structural in HDL; ligand of ABCA1 receptor, mediates reverse cholesterol transport
a. ApoA-1
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

a. ApoA-1

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9
Q

Produced in liver and intestine
a. ApoA-1
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

a. ApoA-1

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10
Q

structural in VLDL, IDL, LDL; LDL receptor ligand produced in liver
a. ApoA-1
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

b. ApoB-100

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11
Q

structural in chylomicrons
a. ApoA-1
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

c. ApoB-48

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12
Q

produced in intestine only (no other tissues)
a. ApoA-1
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

c. ApoB-48

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13
Q

Ligand for LDL remnant receptor. reverse cholesterol transport with HDL.
a. ApoA-1
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

d. ApoE

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14
Q

Found in chylomicrons, VLDL. binds to lipoprotein lipase to enhance TG hydrolysis
a. ApoA-1
b. ApoB-100
c. ApoB-48
d. ApoE
e. ApoCII

A

e. ApoCII

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15
Q

in capillaries of fat, cardiac, and skeletal muscle

A

lipoprotein lipase (LPL)

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16
Q

produced in liver, key in converting IDL to HDL

A

hepatic lipase (HL)

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17
Q

exogenous pathway= _____ __ + _____ _____

A

dietary fat + cholesterol intake

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18
Q

endogenous pathway=

A

liver can distribute fatty acids and carbs

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19
Q

what synthesis is the major source of cholesterol?

A

de novo

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20
Q

what is the key enzyme in the synthesis of cholesterol and what does it do?

A

HMG-CoA reductase, it forms mevalonate

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21
Q

what is considered high total cholesterol?

A

> 240

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22
Q

what is considered high LDL cholesterol?

A

> 160

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23
Q

what is considered high HDL cholesterol?

A

> 60

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24
Q

what is considered high TG?

A

> 200

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25
Q

ratio of total cholesterol to HDL is key in what

A

accessing risk of CVD

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26
Q

a ratio of __ is associated with increased risk of CVD

A

> 4.5

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27
Q

what are the two diseases associated with lipoprotein disorders?

A

hyperlipoproteinemia and hypertriglyceridemia

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28
Q

LDL receptors are present where?

A

oon endothelial cells

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29
Q

what role do macrophages have regarding cholesterol?

A

they take up a fuck ton of it

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30
Q

what is the uptake of cholesterol by macrophages initiated by?

A

LDL accumulation -> when there is too much LDL (the bad one) cholesterol gets taken up, leading to high cholesterol

31
Q

each _% reduction in cholesterol levels is associated with ~__-__% reduction in incidence of coronary heart disease?
a. 5, 5-10
b. 10, 5-10
c. 5, 10-30
d. 10, 10-30

A

d. 10, 10-30

32
Q

what 3 classes of drugs are mainly for high tg opposed to high chol?

A

fibrates, niacin, omega 3

33
Q

what do bile acid-binding resins lower?

A

serum cholesterol

34
Q

what is the MOA of bile acid-binding resins?

A

inhibit reabsorption of bile acids from the intestine by binding bile acids to form insoluble complexes excreted in feces

35
Q

T or F: Bile acid-binding resins down-regulate LDL receptors in the liver

A

F, they up-regulate

36
Q

Bile acid reabsorption inhibits further conversion of ______ to ________.

A

cholesterol, bile acids

37
Q

what does it mean if someone has primary hypercholesterolemia?

A

they have high LDL

38
Q

when are bile acid binding resins taken?

A

before meals

39
Q

T or F: Bile acid binding resins may decrease TG

A

F, may increase

40
Q

What are the two side effects of bile acid binding resins?

A

constipation and bloating

41
Q

what medication(s) fall under the cholesterol absorption inhibitor class?

A

ezetimibe (zetia)

42
Q

what are the 3 adverse effects of ezetimibe?

A

fatigue, diarrhea, GI upset

43
Q

what are 3 CI’s with ezetimibe?

A

pregnancy, breastfeeding, active hepatic disease or serum transaminase elevations

44
Q

what is the dosing of ezetimibe?

A

10 mg qd

45
Q

if you see NPC1L1 what med should you associate it with?

A

ezetimibe

46
Q

adverse effect(s) of ezetimibe

A

low incidence of liver/skeletal muscle damage

47
Q

which two statins are prodrugs?

A

lova and sim

48
Q

MOA of statins

A

competitively inhibit HMG-CoA reductase, the rate limiting enzyme in cholesterol biosynthesis

49
Q

statins up-regulate ___ receptors enabling more ___ delivered to liver, thus reducing plasma _______

A

LDL, LDL, cholesterol

50
Q

indication(s) of statins

A

hypercholesterolemia: elevated LDL; elevated LDL with slightly elevated TGs
also
standard practice to initiate after MI

51
Q

expected results from statins:
__-__% reduction in LDL
__-__% reduction in TG
__-__% increase in HDL

A

20-60
10-33
5-10

52
Q

when do you give short half-life statins?

A

in the evening (this was niche)

53
Q

which statins are metabolized by CYP3A4?

A

lova, sim, ator

54
Q

which statins are metabolized by CYP2C9?

A

flu, rosu

55
Q

which statin is metabolized by sulfation?

A

prava

56
Q

which statin is mainly excreted unchanged in the bile? also undergoes enterohepatic recirculation.

A

pita

57
Q

adverse effects of statins

A

skeletal muscle effects (rhabdo)
hepatotoxicity

58
Q

in cases of rhabdo, or for prevention of rhabdo, what do you want to monitor?

A

serum creatine phosphokinase (CPK)

59
Q

T or F: there is increased incidence of rhabdo with co-admin of cyp inhibitors

A

true

60
Q

in the case of hepatotoxicity, what should you monitor?

A

transaminase activity

61
Q

what medication belongs to the ATP-Citrate Lyase Inhibitor class?

A

bempedoic acid (nexletol)

62
Q

what is the dosing of bempedoic acid?

A

oral-qd -> adjunct to statins

63
Q

what is the significance of the ACL enzyme that bempedoic acid inhibits?

A

it is upstream of HMG-CoA reductase in the chol synth pathway

64
Q

T or F: Bempedoic acid reduces serum LDL and TG levels

A

F, reduces serum LDL and total cholesterol levels

65
Q

bempedoic acid is metabolized by ____________ and excreted via _______

A

glucuronidation, kidney

66
Q

bempedoic acid inhibits _____ in renal tubules and may cause ____

A

OAT2, gout

67
Q

PCSK9 is an enzyme that promotes degradation of what in where

A

LDL receptors in liver

68
Q

what two drugs are PCSK9 inhibitors?

A

Evolocumab (repatha) and Alirocumab (praluent)

69
Q

what is the dosing for evolocumab (repatha)

A

140 mg every 2 weeks
420 mg monthly

70
Q

what is the dosing for alirocumab (praluent)

A

75 mcg every two weeks, 150 mcg every 2 weeks post 4-8 weeks

71
Q

what are the adverse effects of PCSK9 inhibitors

A

GI upset, myalgia, increased LFTs, flu-like symptoms, injection site reactions

72
Q

what are the monitoring parameters for PCSK9 inhibitors?

A

LDL-C levels, LFTs, lipid profile before initiation

73
Q
A

PHRM 844 (12 decks)

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