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Drug Mech Final > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Macromolecule complexes that transport lipids of human plasma

A

Lipoproteins

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2
Q

Metabolic disorders that involve an increase in levels of any of the lipoprotein species

A

Hyperlipoproteinemias or Hyperlipidemias

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3
Q

Increased levels of triglycerides in plase

A

Hyperlipidemia

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4
Q

Marked hyperlipidemia causes life-threatening…

A

Acute pancreatitis

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5
Q

Spherical particles with hydrophobic core regions containing cholesteryl esters and triglycerides. Unesterified cholesterol, phospholipids, and apoproteins surround the core

A

Plasma lipoproteins

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6
Q

This lipoprotein contains very high molecular weight B-48 apoproteins (ApoB-48)

A

Chylomicrons

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7
Q

Where is ApoB-48 formed?

A

Intestines

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8
Q

Is VLDL a very low-density molecule, intermediate-density, or low-density?

A

Very low-density

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9
Q

Is IDL a low-density molecule, intermediate-density, or low-density?

A

Intermediate-density

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10
Q

Is LDL a low-density molecule, intermediate-density, or low-density?

A

Low density

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11
Q

What lipoproteins contain very high-molecular weight B-100 apoproteins (ApoB-100)?

A

VLDL, IDL, LDL

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12
Q

Where is ApoB-100 synthesized?

A

Liver

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13
Q

Proved structural stability to the lipoproteins

A

apoproteins

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14
Q

A number of apoproteins function as ________ in lipoprotein-receptor interactions or as ________ in enzymatic processes that regulate lipoprotein metabolism

A

ligands; cofactors

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15
Q

Formed in the intestine and carry triglyerides of dietary origin, cholesterol, and cholesteryl esters

A

Chylomicrons

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16
Q

The triglycerides are removed from the chylomicrons in _________ tissues

A

extrahepatic

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17
Q

Triglycerides in chylomicrons are hydrolyzed by what enzyme to free fatty acids?

A

lipoprotein lipase

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18
Q

Where is VLDL secreted from?

A

Liver

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19
Q

VLDL exports ________ to peripheral tissues

A

triglycerides

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20
Q

Where is IDL formed from?

A

VLDL

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21
Q

Some IDL are endocytosed directly by the ______; the rest are converted to ______ by further removal of triglycerides

A

liver; LDL

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22
Q

What mediates the removal of triglycerides in IDL?

A

LPL and hepatic lipase

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23
Q

How is LDL formed?

A

from VLDL (via IDL)

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24
Q

Which lipoprotein delivers cholesterol to hepatocytes and other cells?

A

LDL

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25
Q

Catabolism of LDL in hepatocytes and other cells involves ________________

A

receptor-mediated endocytosis

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26
Q

__________ from the LDL core are hydrolyzed, yielding free cholesterol which is used for the synthesis of cell membranes

A

Cholesteryl esters

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27
Q

High-density lipoproteins that exert antiatherogenic effects

A

HDL

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28
Q

They retrieve cholesterol from the artery wall and peripheral tissues that inhibit the oxidation of atherogenic liproteins

A

HDL

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29
Q

Where does much of the lipid in HDL come from during lipolysis?

A

Chylomicrons and VLDL

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30
Q

HDL can deliver cholesteryl esters directly to the liver via the ____________ which does not endocytose the lipoproteins

A

Scavenger Receptor (SR-BI)

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31
Q

Where is cholesterol synthesized?

A

Hepatocytes

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32
Q

How is cholesterol synthesized in the hepatocytes?

A

via the HMG-CoA reductase pathway

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33
Q

Cholesterol is exported from the hepatocytes to the general circulation via ________

A

VLDL

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34
Q

Hepatocytes are capable of eliminating cholesterol by secretion of cholesterol in the bile and by converting cholesterol to _______

A

bile acids

35
Q

Which class of drugs is the first choice and are the most effective in reducing LDL levels?

A

HMG-CoA reductase inhibitors (Statins)

36
Q

HMG-CoA reductase enzyme converts HMG-CoA to ______ (cholesterol biosynthesis)

A

mevalonate

37
Q

The statins are _______ inhibitors of HMG-CoA reductase enzyme and ______ of HMG-CoA intermediates

A

competitive, structural analogs

38
Q

Statins inhibit the ________ synthesis of cholesterol, leading to a decrease in cholesterol levels

A

de novo

39
Q

Niacin is also known as ______

A

Vitamin B3

40
Q

Modifies all plasma lipoproteins and lipids favorably

A

Niacin

41
Q

Niacin is promoted for the treatment of _______

A

hypertriglyceridemia

42
Q

Niacin inhibits ______ secretion from the hepatocytes, which leads to a decrease in the production of LDL

A

VLDL

43
Q

Niacin inhibits the intracellular lipase of adipose tissue via receptor-mediated signaling, which leads to (increase or decrease?) in the flux of free fatty acids to the liver

A

decrease

44
Q

The inhibition of intracellualr lipase reduces ______ production in the liver

A

VLDL

45
Q

Niacin ________ the clearance of VLDL via the LPL pathway, which leads to a decrease in triglyceride levels

A

induces

46
Q

Does Niacin increase or decrease the catabolic rate for HDL?

A

decrease

47
Q

Name the fibric acid derivatives

A

Gemfibrozil
Fenofibrate
Fenofibric Acid

48
Q

Do fibric acid derivatives decrease or increase the levels of VLDL in plasma?

A

decrease

49
Q

Fibric acid derivatives lower ____________ by 30-50% and may increase _______ cholesterol

A

triglycerides; HDL

50
Q

When fibric acid derivatives decrease elevated triglycerides, LDL cholesterol may increase or decrease?

A

increase

51
Q

Which fibric acid derivative is the only fibrate with demonstrated beneficial effects on CV outcomes

A

Gemfibrozil

52
Q

Fibrates are useful in hypertriglyceridemias in which ________ predominate

A

VLDL

53
Q

Which drugs bind to PPAR-alpha and induce lipolysis of VLDL triglycerides via LPL, which results in a decrease in VLDL levels?

A

Fibric Acid Derivatives

54
Q

What is cholesterol metabolized in the liver to?

A

Bile acids

55
Q

Where are bile acids excreted to via the bile?

A

intestine

56
Q

Where are bile acids efficiently reabsorbed?

A

jejunum and ileum

57
Q

Are bile acid sequestrants soluble or insoluble in water?

A

insoluble

58
Q

Name the bile acid sequestrants

A

Colestipol
Cholestyramine
Colsevelam

59
Q

Name the selective inhibitor of intestinal absorption of both dietary and biliary cholesterol and phytosterols

A

Ezetimibe

60
Q

What is the target for Ezetimibe?

A

a transport protein (NPC1L1) for cholesterol and phytosterols (plant sterols)

61
Q

What is Ezetimibe’s primary clinical effect?

A

reduction of LDL levels in plasma

62
Q

Which class of drugs is Ezetimibe synergistic with in reducing LDL-cholesterol levels?

A

statins

63
Q

Name the Omega-3 polyunsaturated fatty acids (PUFA) (fish oil)

A

Lovaza

Vascepa

64
Q

What are the two most important omega-3 PUFAs?

A 
Eicosapentaenoic Acid (EPA)
Docoshaexanoic Acid (DHA)
65
Q

Which omega-3 PUFA contains the ethyl esters of both EPA and DHA?

A

Lovaza

66
Q

Which omega-3 PUFA contains only EPA as the ethyl ester?

A

Vascepa

67
Q

What is the MOA of omega-3 PUFAs?

A

They decrease triglyceride levels by reducing hepatic triglyceride production and increasing triglyceride clearance

68
Q

Name the antisense oligonucleotide

A

Mipomersen

69
Q

Mipomersen is an antisense oligonucleotide inhibitor of?

A

ApoB-100 synthesis

70
Q

What is the principal apoprotein in LDL and VLDL lipoproteins?

A

ApoB-100

71
Q

__________ is a synthetic strand of nucleic acid, binds to mRNA that encodes ApoB resulting in degradation or disruption of the mRNA. This leads to a decrease in the synthesis of ApoB and a decrease in the synthesis of VLDL and LDL

A

Mipomersen

72
Q

Decreased synthesis of VLDL and LDL leads to a (increase or decrease?) in plasma levels of LDL-cholesterol

A

decrease

73
Q

Name the Microsomal Triglyceride Transfer Protein (MTP) Inhibitor

A

Lomitapide

74
Q

What drug is both a substrate and an inhibitor of CYP3A4? It is also an inhibitor of the active-efflux transporter P-glycoprotein (P-gp)

A

Lomitapide

75
Q

Lomitapide is contraindicated for use with other inhibitors of _________

A

CYP3A4

76
Q

Where is microsomal triglyceride transfer protein (MTP) located?

A

in the lumen of the ER of hepatocytes and enterocytes

77
Q

What is the function of MTP?

A

the assembly/formation of ApoB-containing lipoproteins in the liver and intestine

78
Q

What binds to and inhibits MTP?

A

Lomitapide

79
Q

Since Lomitapide inhibits MTP and the synthesis of chylomicrons and VLDL, what is the result?

A

LDL will not be synthesized from VLDL, leading to a significant reduction in plasma levels of LDL-cholesterol.

80
Q

What is transcriptionally regulated by the content of cholesterol on the cell?

A

Production of LDL receptors and HMG-CoA reductase enzyme

81
Q

Increased plasma levels of LDL can result from?

A

Increased secretion of VLDL, increased levels of IDL, decreased LDL catabolism and decreased LDL receptors

82
Q

Cholesterol is delivered to the liver by

A

LDL, HDL, remnants of VLDL and chylomicrons

83
Q

Fibric acid derivatives are ____ for ____

A

ligands, PPAR-alpha

84
Q

Which omega-3 PUFAs are poor substrates responsible for triglyceride synthesis and inhibit esterification of other fatty acids?

A

EPA and DHA

Drug Mech Final (7 decks)

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