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PMCOL 344 > Statins > Flashcards

Statins Flashcards

1
Q

what are 2 main approaches for treating dyslipidemia

A

diet/lifestyle

drugs

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2
Q

what are 3 lifestyle things to treat dyslipidemia

A
  • avoid high fat/cholesterol foods
  • consume agents that increase HDL
  • exercise
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3
Q

what are 3 main pharmacological lipid lowering approaches

A
  • prevent cholesterol synthesis
  • inhibit bile reabsorption from GI
  • inhibit cholesterol absorption from GI
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4
Q

what is a main way to prevent cholesterol synthesis

A

inhibit HMG-CoA reductase

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5
Q

how do you inhibit HMG-CoA reductase

A

statins

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6
Q

why does inhibiting HMG-CoA reductase help with cholesterol

A

low cholesterol stimulates increase in LDL receptors, the more LDL will be removed from blood

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7
Q

why does inhibiting bile reabsorption from GI help with cholesterol

A

because it increases bile synthesis which then decreases liver cholesterol levels

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8
Q

why does inhibiting cholesterol absorption from GI help with cholesterol

A

because less from diet so then less overall

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9
Q

what do statins do generally

A

inhibit cholesterol biosynthesis

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10
Q

what is an example of a statin

A

simvastatin

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11
Q

what do fibrates do generally

A

activate PPARalpha receptor (in many tissues) to alter expression of enzymes involved in lipid metabolism

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12
Q

what is an example of a fibrate

A

gemfibrozil

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13
Q

what do resins do generally

A

binda and sequester bile acids

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14
Q

what does nicotinic acid do generally

A

inhibit VLDL secretion

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15
Q

what is ezetimibe

A

inhibits cholesterol absorption

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16
Q

what are 5 risk factors for atherosclerosis

A

smoking, hypertension, diabetes, obesity, low HDL

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17
Q

what are the most effective and well tolerated drugs for dyslipidemia

A

statins

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18
Q

what is the mechanism of action of simvastatin

A

reversible competitive inhibitors of HMGCoA reductase

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19
Q

what is the role of HMGCoA reductase (general)

A

early rate limiting step in cholesterol synthesis in the liver

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20
Q

what % of cholesterol is made in liver

A

80%

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21
Q

what % of cholesterol is from your diet

A

20%

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22
Q

what is the top selling drug in the world

A

simvastatin

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23
Q

what is lovastatin

A

the first statin for human use

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24
Q

where did lovastatin come from

A

mould

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25
Q

what is the reaction that HMGCoA reductase catalysis

A

HMG-CoA –> mevalonate

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26
Q

how are statins able to inhibit HMGCoA reductase

A

they are structural analogues of HMG-CoA

27
Q

are statins reversible or irreversible inhibitors

A

reversible

28
Q

are statins competitive or non competitive inhibitors

A

competitive

29
Q

what is the affinity for statins compared to natural substrate

A

1000-10000X greater for statins!

30
Q

what are 2 main/important LDL effects when HMG-CoA reductase is inhibited

A

increased LDL receptor synthesis, increased LDL uptake

31
Q

how much can statins reduces plasma cholesterol

A

by up to 40%

32
Q

what do statins do to VLDL

A

reduce it

33
Q

what do statins do to plasma TGs

A

reduce

34
Q

what do statins do to LDL

A

reduce

35
Q

what do statins do to plasma cholesterol

A

reduce

36
Q

what do statins do to LDL receptor expression

A

increase

37
Q

what do statins do to LDL uptake

A

increae

38
Q

what are 2 main ways statins reduce plasma cholesterol

A
  • reduce VLDL: reduce TGs and LDL

- increase LDL receptor expression: increase LDL uptake

39
Q

how do statins decrease VLDL

A

decreased intracellular cholesterol (inhibit synthesis) decreases VLDL secretion

40
Q

why does the liver make more LDL receptors

A

because there is decreased delivery of cholesterol to tissues

41
Q

what 2 things contribute to decreased plasma LDL

A

increased LDL uptake and decreased plasma VLDL

42
Q

what do statins do to HDL levels

A

increase

43
Q

what do statins do to endothelial function

A

improve

44
Q

what do statins do to platelet aggregation

A

decrease

45
Q

what do statins do to ischemic tissue

A

increase neovascularization (new vessels in ischemic tissue)

46
Q

what do statins do to inflammation

A

anti

47
Q

what do statins do to plaque stability

A

increase

48
Q

what do statins do to LDL oxidation

A

inhibit

49
Q

what do statins do to endothelial progenitor cells

A

increase (so a healthier endothelial layer)

50
Q

what are 2 main patient groups that we give statins to

A 
primary prevention (risk factors but no CHD)
secondary prevention (people with CHD)
51
Q

what is the benefit of statins for people with risk factors and no CHD

A

reduces risk of CV event

52
Q

what is the benefit of statins for people with CHD

A

reduce cardiac events (MI), stroke and morality even if LDL is normal

53
Q

what did the ASTEOID trial in 2006 conclude

A

high dose of statin may cause CHD regression

54
Q

what are 2 side effect of statins

A

myositis and rhabdomyolysis

and type 2 diabetes

55
Q

what is myositis and rhabdomyolysis

A

breakdown of skeletal muscle

56
Q

how can myositis and rhabdomyolysis cause renal damage

A

accumulation of iron from myoglobin

57
Q

how can statins cause myositis and rhabdomyolysis

A

due to lack of cholesterol derived mediators required for muscle structure

58
Q

which kind of people taking statins get myositis and rhabdomyolysis

A

high doses or drugs that interfere with statin breakdown

59
Q

how many people die cause of myositis and rhabdomyolysis statins

A

1 per million

60
Q

besides myositis and rhabdomyolysis, what else can statins cause

A

increase risk of type 2 diabetes

61
Q

what is increase risk of type 2 diabetes with statins associated with

A

impaired insulin sensitivity and insulin secretion

62
Q

what increases risk for increase risk of type 2 diabetes in statins

A

dose dependent

63
Q

how can statins increase risk of type 2 diabetes

A

decrease both insulin production and insulin sensitivity of tissues (reduce glucose uptake)

PMCOL 344 (27 decks)

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