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FPC2 Exam 8 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What is the risk of high lipids?

A

Cardiovascular risk

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2
Q

Lipproteins particles include:

A

HDL, IDL, LDL, VLDL, chylomicrons, triglycerides.

Used for ell membranes.

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3
Q

Chylomicrons carry ____

A

dietary lipid

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4
Q

VLDL carry ___ and to a less degree ____

A

endogenous triglycerides

cholesterol

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5
Q

IDL carry ___ and ___

A

cholesterol esters and triglycerides

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6
Q

LDL particles carry ____

A

Cholesterol esters . ApoB100 and C3

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7
Q

HDL particles carry ___

A

cholesterol esters

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8
Q

What is the path from dietary fat to lipoprotein?

A

dietary fat-> chylomicrons-> travel in blood + synthesized in cells-> cholesterol-> lipoprotein packaged with protein, phospholipids, and apolipoprotein

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9
Q

___ is the major transporter of cholesterol (⅔ of all body cholesterol)

A

LDL

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10
Q

___ takes excess cholesterol back to liver for excretion

A

HDL

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11
Q

Cholesterol is involved in the formation of ____

A

VitD, hormones from adrenal glands, bile salts

cell membrane

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12
Q

Pathophysiology of cholesterol affecting CV risk

A

Elevated LDL-> atherosclerotic plaques-> endothelial damage-> LDL permeate-> cholesterol in intima->macrophages -> -> fibrous plaque formed

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13
Q

Apoprotein ___ is associated with increased CVD risk

A

CIII.

Triglycerides + CV is unclear but does increase APO C=III (pancreatitis)

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14
Q

Screening for diagnosis of dyslipidemia

A

FH of lipid disorders, FH of CVD, pancreatitis

50% of people have abnormal lipid

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15
Q

NMR lipid profile is used to ______

A

adjudicate response to treatment + guide adjustment in therapy

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16
Q

Physical exam findings in someone with high cholesterol?

A

tuberoeruptive xanthomata, palmar xanthomata, eruptive xanthomata

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17
Q

LDL > ____ should be treated. HDL < ____ should be treated

A

160

40

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18
Q

Triglyceride level >___ is elevated. Why are high triglycerides bad

A

150

high trigly-> decreased chylomicron clearance-> pancreatitis

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19
Q

LDL goal for someone who has T2DM?

A

<100

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20
Q

_______ is the most common AD genetic disease.

A

Familial hypercholesterolemia.

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21
Q

Clinical syndrome of familial hypercholesterolemia is____

A

extremely elevated LDL-> early onset atherosclerotic CVD

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22
Q

Familial hypercholesterolemia is a mutation in ____

A

one of the genes critical for LDL catabolism (>190mg or first degree relative for clinical dx)

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23
Q

______ are associated with dyslipidemia

A

HIV and antiviral therapy

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24
Q

What are ASCVD? (atherosclerotic coronary vascular disease)

A

Hx of ACS, MI, angina, coronary or arterial revascularization, stroke, TIA, peripheral artery dz

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25
Q

What are the recommendations for screening with lipid panel

A

adults >20 years old

significant FH- earlier

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26
Q

Do you need to fast for a lipid panel?

A

no

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27
Q

What does the pooled cohort equation (PCE) look at?

A

ASCVD ridk- 10 year risk of non fatal MI, CV death, or stroke (low borderline intermediate high risk)

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28
Q

What does SCORE look at for ASCVD

A

10 year risk of first fatal event of a CVD

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29
Q

When should you not use PCE for determine risk for ASCVD

A

PCE is used to assess primary prevention. If there is already clinical ASCVD or LDL-C>190mg/dL do not use it

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30
Q

What does PCE not include?

A

all races/ethnicities (over/underestimation)

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31
Q

First line treatment for ASCVD primary and secondary prevention are

A

statins!!!!

32
Q

What is the MOA of statins?

A

acts at HMG-CoA reductase. blocks HMG-CoA -> mevalonic acid (which later turns into cholesterol)

33
Q

What are the statin categories

A 
low intensity (30% reduction in LDL-C)
Moderate (30-50%)
High Intensity (>50%)
34
Q

What are the two statins that are offered at high intensity

A

atorvastatin 40-80mg

rosuvastatin 20-40mg

35
Q

What are the monitoring procedure for statins? what are the baseline labs?

A

lipid panel 4-12 weeks after initiation then 3-12 months

transaminases + lipi panel

36
Q

What is the point of a low intensity statin?

A

some patients that is the max dose they can tolerate

37
Q

What are the statin-

associated muscle symptoms

A

myalgia (muscle weak w/o CK elevation), myopathy (muscle weak with CK elevation), myositis (muscle inflammation), rhabdomyolysis (up CK ULN w myoglobinuria acute renal failure)

38
Q

What are risk factors for statin associated muscle symptoms

A

higher intensity, older, frequent exerciser, small body, female, CKD, drug drug (EtOH), hypothyroid, VitD deficiency

39
Q

Only __ in ___ patients who qualify for a high intensity statin are actually prescribed one

A

1 in 5

40
Q

In patients at a very high risk, reduction of LDL-C to ____ with the addition of non statin therapies

A

<70mg/dL

41
Q

The lower achieved LDL-C, the lower the risk of ____ with no _____

A

CV events

lower limit for LDL values

42
Q

What is not actually helpful for statin associated muscle symptoms

A

CoQ10 supplement

routine CK monitoring

43
Q

Who is in the clinical ASCVD bucket and what should they be prescribed

A

Age <75 = high intensity statin

Age >75: moderate or high intensity

44
Q

Who are “very high risk patients” for ASCVD? What is the treatment goal?

A

multiple major ascend events or 1 major and multiple high risk conditions.
want LDL to be <70mg

45
Q

What are non statin therapies for ASCVD

A

ezetimibe 1st line

PSCK9 inhibitor if want LDL to be even lower (this is expensive though)

46
Q

What is the MOA of ezetimibe?

A

inhibit cholesterol absorption from small intestine by inhibiting Niemann-Pick C1-like 1 on intestinal epithelial cells.

47
Q

What are AE of ezetimibe?

A

GI upset, slight increase risk of hepatic enzyme elevation with statin

48
Q

What are drug drug interactions with ezetimibe?

A

cyclosporine, decrease effect with cholestyramine

49
Q

What is the MOA of PCSK9 (alirocumab, evolulcumab) inhibitors?

A

inhibit PSCK9- facilitations degradation of LDL receptors in the liver-> LDL receptor recycling-> increase number of available receptors to remove LDL from blood

50
Q

How much is esetimibe expected to lower cholesterol

A

LDL 18-20%, TG 5-10%, raise HDL 1-5%

51
Q

How much does PCSK9 inhibitors lower cholesterol

A

LDL 60% down

52
Q

What are adverse effects of PCSK9 inhibitors

A

injection site reactions

53
Q

In primary hypercholesterolemia (LDL>190), what is the indicated therapy

A

maximally tolerated statin (look to add ezetimibe (>20yo) / bile acid sequestrate (>20yo)/ PCSK9 inhibitor (>30yo) with <50% reduction)

54
Q

What are the 3 bile acid sequestrants

A

cholestyramine, colestipol, colesevelam

55
Q

What is the MOA of bile acid sequestrants

A

bind to bile acids to disrupt enterohepatic recirculation. this binds to other drugs

56
Q

What is the effect of cholesterol on bile acid sequestrant

A

LDL down 15-26%
TG up to 10%
HDL up 3-6%

57
Q

What is the indicated therapy for patients with diabetes with regard to ASCVD

A

20-39y.o- consider moderate statin
40-75yo- calculate PCE- (if indicated) either high intensity or high intensity with ezetimibe
>70yo- should probably just take statin

58
Q

What should be done for primary prevention for statin therapy

A

low risk- life style
borderline risk- moderate intensity stain
intermediate risk- moderate intensity. want 30-49% LDL, can add ezetimibe or BA sequestrate to achieve goal
high risk- start statin

59
Q

What is moderate hypertriglyceridemia and what is the treatment indication

A

177-499mg/dL

ASCVD, age >40 with DM-> maximize statin therapy and add icosapent ethyl

60
Q

What is severe hypertriglyceridemia and what is the treatment indication

A

> 500 mg/dL
40-75y.o and ASCVD risk >5%-> up statin therapy, push low fat diet, fibrate, or icosapent ethyl to reduce risk of pancreatitis
20-39 y.o or 40-75yo with ASCVD risk <5% + no DM-> low rate diet, fibrate, icosapent ethyl to reduce risk of pancreatitis

61
Q

What is icosapent ethyl and how does it work

A

An omega 3 fatty acid. decrease VLDL-TG synthesis in liver and up TG clearance by circulating VLDL particles
EPA, lowers TG by 33%

61
Q

What is icosapent ethyl and how does it work

A

An omega 3 fatty acid. decrease VLDL-TG synthesis in liver and up TG clearance by circulating VLDL particles
EPA, lowers TG by 33%

62
Q

Fibrate MOA (fenofibrate, gemfibrozil)

A

activates lipoprotein lipase and reduces apoprotein C-III-> increased lipolysis.
decrease LDL, TG, and raise HDL

63
Q

AEs in fibrates

A

interact with statins (more myalgias)

64
Q

When do you use fibrates really only

A

reducing TG

65
Q

Niacin is ______ for LDLC lowering or increasing HDL due to _____

A

not recommended
lack of clinical benefit
(also has no benefit for TG)

66
Q

Niacin MOA

A

inhibit mobilization of free FA from peripheral adipose tissue-> reduce VLDL synthesis

67
Q

Bempedoic acid MOA

A

inhibit ATP citrate lyase (upstream from HMG-CoA)

68
Q

How much does bempedoic acid decrease LDL when added onto statin

A

15-25% reduction

69
Q

Is there a definitive effect of bempedoic acid on ASCVD

A

no

70
Q

Inclisiran MOA

A

siRNA-> prevents formation of PCSK9 proteins-> promote degradation of LDL

71
Q

What is the effect of Inclisiran on LDL when added to again therapy

A

50%

72
Q

What is inclisiran approved for

A

adults with established ASCVD and HeFH

73
Q

Can a women who is trying to become pregnant be on a statin

A

no, they are contraindicated

74
Q

What is the dyslipidemia drug of choice for someone who is pregnant

A

bile acid sequestrants

FPC2 Exam 8 (5 decks)

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