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Med Chem 7 > Antilipidemics (4) > Flashcards

Antilipidemics (4) Flashcards

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1
Q

t/f thyroid hormones can have hypocholesterimic effects

A

true

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2
Q

what does dextrothyroxine require?

A

99% + pure optical isomer

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3
Q

dextrothyroxine overall effect

A

increase LDL receptors (enhance removal of LDL)

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4
Q

Dextrothyroxine stimulates the ______ of cholesterol in liver through increase of _______

A

oxidative catabolism

7a-cholesterol-hydroxylase

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5
Q

Adverse effects of dextrothyroxine

A
  • increase frequency and severity of anginal attacks
  • cause cardiac arrhythmias
  • potentiates action of anticoagulants
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6
Q

Diabetics and dextrothyroxine

A

requires increased dose of insulin or hypoglycemic agents

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7
Q

What is a vitamin used as hypocholesteremic?

A

niacin

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8
Q

Niacin is effective for all types of hyperlipidemica except _____ at doses given as vitamin supplement

A

type I

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9
Q

niacin overall effect

A
  • decrease VLDL synthesis (decrease IDL, LDL)
  • inhibit lipolysis
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10
Q

What is the drug of choice for all type II hyperlipoproteinemias?

A

Niacin

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11
Q

Why is niacin have limited use?

A

vasodilation side effects

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12
Q

What is an extended release preparation of niacin?

A

Nispan

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13
Q

Probucol overall effect

A

decrease level of cholesterol by increasing rate of LDL catabolism

  • may also inhibit cholesterol synthesis and delay cholesterol absorption
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14
Q

How does probucol decrease levels of cholesterol?

A

increasing rate of LDL catabolism

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15
Q

What is probucol believed to act on?

A

ABCA1

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16
Q

Why was probucol withdrawn from market?

A

cause QTc prolongation

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17
Q

Cholestyramine is a ______ that binds _____ in GI tract and prevents reabsorption

A

bile acid sequestrant

bile

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18
Q

Cholestyramine is a ____ resion with what type of group?

A

strong ion exchange resin

quaternary ammonium group

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19
Q

With cholestyramine, due to loss of bile acids, more ____ is converted to bild acids in liver to normalize levels

A

plasma cholesterol

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20
Q

cholestyramine overall effect

A

decrease plasma cholesterol levels

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21
Q

What does ACAT do?

A

catalyze cholesterol esterification and cholesterol absorption

maintain cholesterol homeostasis in blood

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22
Q

What is a new attractive target for hyperlipidemia?

A

ACAT inhibitors

23
Q

ACAT1 regulates cholesterol homeostasis where?

A

brain

macrophages

adrenal glands

24
Q

ACAT2 ____ cholesterol where?

A

esterfies

intestine and liver

25
Q

What regulates cholesterol homeostasis in brain, macrophages and adrenal glands?

A

ACAT1

26
Q

What esterfies cholesterol in small intestine and liver?

A

ACAT2

27
Q

what is CIMT?

A

carotid intima media thickness

28
Q

What does CETP do?

A

facilitates transport of cholesteryl esters and TGs between lipoproteins

29
Q

What are CETP designed to do?

A

raise HDL (thought to be protective)

30
Q

What can reverse transport of cholesterol out of macrophages?

A

CETP: so cholesterol can be metabolized

31
Q

How does CETP work?

A

collects TGs from VLDL or LDL and exchange for cholesteryl esters from HDL

32
Q

What CETP inhibitor does not have cardiovascular problems?

A

dalcetrapib

33
Q

What CETP inhibitor is on the market?

A

NONE!

34
Q

CETP inhibitors may produce a form of ____ that does not enhance reverse cholesterol transport

A

HDL

35
Q

What is an adipose tissue derived adipokine?

A

resistein

36
Q

resistin AKA

A
  • ADSF or XCP1
37
Q

resistin is a small, _____ protein secreted from ____

A

cysteine rich

macrophages and adipose tissue

38
Q

resistin overall effect

A

increase LDL in human liver cells

degrae LDL receptors in liver

39
Q

What is thought to be an important link between obesity and insulin resistance and diabetes?

A

resistin

40
Q

serum levels of ____ are increased in human obesity and + correlated with ____

A

resistin

atherosclerotic CVD

41
Q

At physiological levels observed in human obesity, resistin reduces human hepatocyte expression of ____

A

LDLRs

42
Q

Statins are ineffective in 40% of patients due to ____ secretion in adipose tissue

A

resistin

43
Q

____ may be new therapeutic target because statins may be ineffective in some

A

resistin

44
Q

What is a key regulator of LDL-C metabolism?

A

PCSK9

45
Q

PCSK9 has been shown to be stimulated by ____ and leads to what?

A

resistin

downregulation of LDLR

46
Q

Resistin and PCSK9 have notable structural similarity where?

A

cysteine rich C terminal domain

47
Q

Atherosclerosis is buildup of what lipoproteins?

A

LDL-C

48
Q

PCSK9 inhibitors in transgenic mice lower ____

A

LDL

49
Q

ODYSSEY long term study

A

65 weeks

alirocumab reduced risk of major events compared to those with placebo and max tolerated statin

50
Q

ODYSSEY results

A

decrease LDL 61%

79% achieved target LDL <70 after treatment with alirocumab

51
Q

Why were CETP inhibitor trials stopped?

A

lack of clinically meaningful efficacy

52
Q

What are CETP inhibitors thought to do?

A

Increase HDL

53
Q

What do PCSK9 inhibitors supposed to do?

A

decrease LDL

Med Chem 7 (9 decks)

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