Treatment of dyslipidemias Flashcards

1
Q

what are the 4 major statin benefit groups identified in whom CVD risk reduction clearly outweights risk of adverse events?

A
  1. secondary prevention - clinical ASCVD
  2. primary prevention - LDL-C over 190 mg/dL
  3. primary prevention - diabetics
  4. primary prevention - without diabetes high risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the most common adverse effect of statins?

A

muscle complaints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

statin triggered autoimmune myophaty is associated with what antibody?

A

anti-HMGCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

if statin-induced weakness does not resolve and CK remains elevated despite continuation what could be considered?

A

statin triggered autoimmune myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the non-statin lipid lowering therapies?

A

bile acid sequestrants
nicotinic acid (niacin)
fibric acids
ezetimibe (zetia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the MOA of bile acid sequestrants?

A

reduce reabsorption of bile acids / cholesterol in ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the outcomes of nicotinic acid (niacin)?

A

raises HDL-C

may reduce LP(a)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the primary therapeutic use of fibric acids?

A

hyperTG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the main side effect of fibric acids?

A

gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the MOA of ezetimibe?

A

impairs dietary and biliary cholesterol absorption without affecting TG or fat-soluble vitamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the indications for ezetimibe?

A

avoid high doses of statins (synergistic)

very high LDL not sufficiently controlled statin alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the effect of CETP deficiency in atherosclerosis?

A

marked increase in HDL-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the role of CETP activity in atherosclerosis?

A

inversely correlated with plasma HDL-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the two remaining CETP inhibitors?

A

evacetrapib

anacetrapib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the two options for homozygous FH?

A

mipomersen

lomitapide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the MOA of mipomersen?

A

crosses hepatocyte and nuclear membrane to target apoB mRNA

17
Q

what is the MOA of lomitapide?

A

decreases production of apoB containing lipoproteins such as VLDL and subsequently LDL-C

18
Q

what is the MOA of PCSK9?

A

regulates expression of LDLr - sequesters LDLr and internalizes them for degradation

19
Q

what are the LDLr and LDL clearance levels of gain of function PCSK9 mutations?

A

low LDLr

low LDL clearance (bad)

20
Q

what are the LDLr and LDL clearance levels of loss of function PCSK9 mutations?

A

high LDLr

high LDL clearance (good)

21
Q

outcome trials show that lowering LDL levels in primary prevention is efficacious for what populations?

A

very high LDL
average LDL
diabetics
elderly

22
Q

outcome trials show that lowering LDL levels in secondary prevention is efficacious for what populations?

A

estsablished CVD regardless of baseline cholesterol levels