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Pharm > Antihyperlipidemics > Flashcards

Antihyperlipidemics Flashcards

1
Q

What are the lowest density lipoproteins?

A

Chylomicrons

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2
Q

What are the apolipoproteins on chylomicrons?

A

B48
C
E
A

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3
Q

What are the apolipoproteins on VLDL?

A

C

B-100 E

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4
Q

What are the apolipoproteins on LDL?

A

B100

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5
Q

What are the apolipoproteins on HDL?

A 
AI
AII
C
E
D
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6
Q

What type of lipoprotein has the highest ratio of TG;cholesterol?

A

Chylomicrons

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7
Q

Where are chylomicrons synthesized?

A

Intestines

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8
Q

Where aer VLDLs synthesized?

A

liver

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9
Q

Where are HDL particles synthesized?

A

intestines, liver

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10
Q

Cholesterol enters enterocytes through what protein?

A

Niemann-Pick C1-like protein (NPC1L1)

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11
Q

Once inside the enterocytes cholesterol is reesterified by what enzyme?

A

acetyl-CoA: cholesterol acyltransferase (ACAT)

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12
Q

What are the apolipoproteins that chylomicrons receive from HDL?

A

E

C-II

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13
Q

What is the MOA of ezetimibe?

A

Inhibits NPC1L1

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14
Q

What percent of bile is lost through the feces normally?

A

5%

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15
Q

What is the function of apolipoprotein CII?

A

Binds to lipoprotein lipase, causing breakdown of the chylomicron

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16
Q

Where does HDL get its apolipoprotein CII from?

A

From the reminants of LDL

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17
Q

What is the function of apolipoprotein E on HDL?

A

Binds to receptor on liver for breakdown

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18
Q

What is lipoprotein lipase, and where is it found?

A

Enzyme that breaks down chylomicron TGs,

found on cell surface of tissues

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19
Q

What is the consequence of a decrease in apo CII expression?

A

Hypertriglyceridemia

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20
Q

What are the receptors on the liver that apo E binds to?

A

remnant receptors

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21
Q

What are the two fates of IDL?

A

Conversion to LDL

Broken down by liver

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22
Q

What is the apolipoprotein that forms the structural component and is the messenger tag for LDL degradtion by the live ?

A

B100

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23
Q

What happens to the apolipoproteins on IDLs as they are converted to LDL?

A

apo E and CII are transferred to HDL

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24
Q

What is the receptor on LDL that serves as the receptor for degradation in the liver?

A

B100

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25
Q

What is the function of apolipoprotein AI on HDLs?

A

Facilitates the exchange of cholesterol from macrophages/other cells

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26
Q

What are the tissues in the body that can synthesize cholesterol de novo?

A

Liver
Gonads
Adrenal cortex

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27
Q

What are the substrates for cholesterol synthesis de novo?

A

Acetyl-coa and acetoacetyl coa

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28
Q

What is the enzyme that converted HMG CoA to mevalonate, a precursor to cholesterol?

A

HMG CoA reductase

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29
Q

What is the enzyamtic target of statins?

A

HMG CoA reducatase

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30
Q

What is the function of LCAT?

A

Convertes cholesterol into cholesterol esters in HDL particles for storage in HDLs

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31
Q

What is the receptor on the liver that binds to Apo A1 on HDL particles for uptake?

A

SRBI

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32
Q

What lipoprotein has the apolipoprotein AI on it? What is its function?

A

HDL, chylomicrons

Activates LCAT

Ligand for SRB1 receptor

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33
Q

What lipoprotein has the apolipoprotein A-II on it? What is its function?

A

HDL, chylomicrons

Structural protein for HDL

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34
Q

What lipoprotein has the apolipoprotein B-48 on it? What is its function?

A

Chylomicrons

Structural protein

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35
Q

What lipoprotein has the apolipoprotein B100 on it? What is its function?

A

VLDL, IDL, LDL

Structural protein that binds to LDL receptor

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36
Q

What lipoprotein has the apolipoprotein C-II on it? What is its function?

A

Chylomicrons, VLDL, HDL

Cofactor for lipoprotein lipase

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37
Q

What lipoprotein has the apolipoprotein E on it? What is its function?

A

Chylomicrons, VLDL, IDL, HDL

Ligand for binding to LDL receptor and remnant

38
Q

What are the major goals of treating dyslipidemias?

A

Prevent acute pancreatitis

Prevent CVD

39
Q

How does endothelial dysfunction lead to the development of CVD?

A

altered NO biosynthesis

40
Q

How does injury of dysfunction endothelium lead to the development of CVD?

A

Expression of adhesion molecules, encouraging monocyte attachment

41
Q

How does LDL transport into vessel walls lead to CVD?

A

production of ROS

42
Q

What are the components of fatty streaks on vessels?

A

Foam cells

T cells

43
Q

What is the protective effect of HDL?

A

Uptake of lipids from arterial walls

44
Q

What is the inflammatory fibroproliferative response seen in atherosclerosis?

A

cytokine activation of immune cells leading to deposition of CT

45
Q

Why are plaque ruptures bad?

A

Provide a substrate for thrombosis

46
Q

What are mixed hyperlipidemias?

A

High cholesterol and TG levels

47
Q

What is the cause of, and manifestation of: primary chylomicronemia?

A

Decrease in LPL activity

Increased chylomicron VLDL

48
Q

What is the cause of, and manifestation of: familial hypertriglyceridemia?

A

Impaired removeal of VLDL and/or chylomicrons

Increased VLDL/chylomicrons

49
Q

What is the cause of, and manifestation of: Familiaal combined hyperlipoproteinemia

A

Increased VLDL production

Increased VLDL

50
Q

What is the cause of, and manifestation of: familial dysbetalipoproteinemia?

A

Decreased clearance of VLDL, IDL and chylomicrons

Increased above

51
Q

What is the cause of, and manifestation of: familial hyper-cholesterolemia?

A

LDLR impairments

Increased LDL

52
Q

What is the cause of, and manifestation of: familial ligand-defective apoB?

A

Mutation in apoB, resulting in impaired endocytosis of LDL

Increased LDL

53
Q

Major or minor risk factor for atherosclerosis: low HDL

A

Major

54
Q

Major or minor risk factor for atherosclerosis: elevated LDL

A

Major

55
Q

Major or minor risk factor for atherosclerosis: high triglycerides

A

Minor

56
Q

Major or minor risk factor for atherosclerosis: VLDL and IDL remnatns

A

minor

57
Q

What is the general MOA of fibric acid derivatives?

A

PPAR activators

58
Q

What happens to plasma triglyceridea when using fibric acid derivatives? HDL?

A

Decreased triglycerides

Increased HDL

59
Q

What are the two fibric acid derivatives?

A

Gemfibrozil and fenofibrate

60
Q

What is the MOA of gemfibrozil?

A

PPAR activators

61
Q

What is the MOA of fenofibrate?

A

PPAR activator

62
Q

What is PPAR alpha and how do fibratesuse this to treat hyperlipidemia?

A

transcription factor that increases the expression of lipoprotein lipase, Apo AI, AII, and decreases inhibitor apoprotein C-III

63
Q

What is the effect of the upregulation of apoA-I and apoA-II proteins by fibrate activation of PPARs?

A

Increase HDL

64
Q

What is the effect of the downregulation of apoC-III proteins by fibrate activation of PPARs?

A

Increase FA uptake

65
Q

What is the effect of the upregulation of LPL proteins by fibrate activation of PPARs?

A

Increase FA uptake and breakdown

66
Q

What is the major adverse effec of combining fibrates with statins?

A

Myopathy

67
Q

What is the MOA of chloestyramine?

A

Bind to bile acids in the intestines, causing increased synthesis of bile acids

68
Q

What is the MOA of colesevelam?

A

Bind to bile acids in the intestines, causing increased synthesis of bile acids

69
Q

What is the MOA of colestipol?

A

Bind to bile acids in the intestines, causing increased synthesis of bile acids

70
Q

What happens to the liver when bile acid-binding resins are used?

A

Increased LDL receptor to increase the uptake of LDL by the liver for bile acid synthesis

71
Q

What is the major adverse efect of bile-acid binding resins?

A

Tend to increase plasma triglycerides

72
Q

What is the drug of choice for pregnant women for treating hypercholesterolemias? Why?

A

Cholesterol binding resins since they are not absorbed

73
Q

What is the MOA of niacin for treating dyslipidemias?

A

Binds to GPCR on adipocytes, decreasing hormone sensitive lipase activity

74
Q

What is the function of hormone sensitie lipase?

A

Incrase lipolysis during fasting states when activation by epi, or other hormones

75
Q

What are the adverse symptoms of Niacin?

A

Hyperuricemia

Hepatotoxicity

76
Q

How does niacin increase HDL levels?

A

Increaseing levels of apo AI

77
Q

What is the MOA of ezetimibe?

A

Blocks intestinal absorption of cholesterol by inhibiting NPC1 protein

78
Q

What is the effect on the liver of ezetimibe use?

A

Increases LDL receptors

79
Q

What are the adverse effects of ezetimibe?

A

Few, if any

80
Q

What is the MOA of all of the statins?

A

Competitive inhibitor of HMG-CoA reductase

81
Q

What is the least potent statin?

A

Fluvastatin

82
Q

What are the two most potent statins?

A

Rosuvastatin

Atorvastatin

83
Q

What is the effect of statins on the liver? Why?

A

Increases LDL receptor

Attempt to obtain more cholesterol from the plasma

84
Q

What are the pleotropic effects of statins?

A

Whole bunch of good things

85
Q

What are the adverse effects of statins?

A

Myopathy
Rhabdo
Hepatotoxicity

86
Q

What are the labs that are commonly elevated with statin use? When are these concerning?

A

LFTs

Concerning if bili rises as well

87
Q

True or false: statins are contraindicated in pregnancy

A

True

88
Q

What is niacin used in the treatment of?

A

All triglycerideemias and hypercholesterolemias

89
Q

What are resins used to treat?

A

Familiar hypercholesterolemias

90
Q

What is the drug of choice for treating familial dysbetalipoproteinemia?

A

Fibrates

91
Q

What is the drug of choice for treating primary chylomicronemia?

A

Fibrates

Pharm (73 decks)

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