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Clinical Medicine II > Cardiology: Hyperlipidemia > Flashcards

Cardiology: Hyperlipidemia Flashcards

1
Q

Is more cholesterol taken in from the diet or produced in the liver?

A

produced in the liver

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2
Q

This lipoprotein carries dietary lipids form the intestine to the liver, skeletal muscle and adipose tissue…

A

Chylomicrons

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3
Q

this lipoprotein carries newly synthesized TAGs from liver to adipose tissue

A

VLDL

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4
Q

This type of lipoprotein is not usually detectable in the blood

A

IDL

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5
Q

This lipoprotein carries cholesterol from the liver to the body’s cells

A

LDL

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6
Q

Why is LDL dangerous?

A

because it delivers cholesterol to the tissues, which can form plaques and lead to atherosclerosis

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7
Q

This lipoprotein collects cholesterol from tissue, including vascular endothelium, and returns it to the liver.

A

HDL

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8
Q

Why is HDL the “good” lipoprotein?

A

its reverse transport from tissues to liver protects against heart disease

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9
Q

Food provides ____ of our cholesterol, while the liver produces the remaining _____.

A

food: 25%

Liver: 75%

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10
Q

Cholesterol from the diet resulting in increased chylomicrons represent the ______ pathway of lipid metabolism

A

exogenous

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11
Q

lipid metabolism in the liver resulting in production of VLDL, LDL, and IDL is the _______ pathway

A

endogenous

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12
Q

HDL pathway of lipid metabolism is also called…

A

reverse cholesterol transport

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13
Q

Familial hypercholesterolemia, polygenic hypercholesterolemia and familial combined hyperlipidemia are examples of what kind of disorder?

A

Inherited increased lipid disorders.

Etiology: genetic

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14
Q

Inherited increased lipid disorders should be suspected in what patient population?

A

1st degree relatives of someone with hx of premature atherosclerotic cardiovascular disease (ASCVD)

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15
Q

Which disorder is the most common autosomal dominant genetic disease?

A

Familial hypercholesterolemia

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16
Q

Familial hypercholesterolemia is ________ meaning it results from a defect in ____ gene(s)

A

monogeneic, 1 gene

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17
Q

What is more common, heterozygous familial hypercholesterolemia or homozygous familial hypercholesterolemia?

A

heterozygous

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18
Q

Heterozygotes can expect a _____x LDL value while homozygotes can exhibit a _____x LDL.

A

Hetero: 2x

Homo: 8x

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19
Q

A patient presents with cardiac sxs and a FH of ASCVD. There father died of an MI at age 45.

What is your suspected dx, how is this confirmed, and how is it treated?

A

Dx: familial hypercholesterolemia

Confirmed by: genetic testing

treat with Statins +/- add-on

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20
Q

These two inherited increased lipid disorders present very similarly, expect this disease is controlled by multiple genes.

A

Polygenic hypercholesterolemia

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21
Q

How do you treat all inherited increased lipid disorders?

A

statin +/- add-on tx

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22
Q

This disease is a polygenic disease that has a wide variety of lipid abnormalities. It is relatively common (1-2% of population) and present in 30-50% of familial CHD

A

familial combined hyperlipidemia

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23
Q

A patient presenting with hx of familial CHD should be screened for _______ because it is most common in the population and is present in 1/3-1/2 of familial CHD.

A

familial combined hyperlipidemia

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24
Q

what is more common, inherited hyperlipidemia or secondary hyperlipidemia?

A

inherited

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25
Q

STEP 1: ATHEROSCLEROSIS

LDL molecules diffuse from blood thru the ________ at a rate that is dependent on _________

A

diffuse thru ENDOTHELIUM

at rate dependent on CONENTRATION

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26
Q

STEP 2: ATHEROSCLEROSIS

________ follows LDL through endothelium, becoming ________cells that contain ________. When they die, they release _________ and form deposits

A

MACROPHAGES follow

become FOAM CELLS

that contain CHOLESTEROL

release CHOLESTEROL when they die

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27
Q

STEP 3: ATHEROSCLEROSIS

what does the body do in reaction to deposit formation from lysed foam cells?

A

increased collagen to form a cap

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28
Q

STEP 4: ATHEROSCLEROSIS

When the ________ ruptures, a ________ can form and lead to _________

A

COLLAGEN CAP ruptures

forming THROMBUS

leading to INFARCT

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29
Q

decision to screen for atherosclerosis should be based on…

A

overall CHD risk, independent of lipid levels

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30
Q 
HTN
DM
TOBB
OBESITY
HDL < 40
HYPERLIPIDEMIA

What type of risk factors are these?

A

Modifiable CHD Risk Factors

31
Q

an HDL of _____ or greater is a negative risk factor for CHD

A

60

32
Q

Why does a fasting lipid panel require a 12 hour fast?

A

TAGs are affected by eating

33
Q

is serum cholesterol affected by eating prior to phlebotomy?

A

no

34
Q

A fasting lipid panel gives you which markers?

A

Total Cholesterol, TAGs, LDL, HDL

35
Q

Acute coronary syndrome and acute MI can do what to a lipid panel?

A

falsely low levels 24-48 hrs after MI, persisting for 60 days

36
Q

Cholesterol Values-

Desirable:

High Risk:

A

Desirable: < 200

High Risk: > 240

37
Q

Triglyceride Values-

Desirable:

High Risk:

A

Desirable: < 150

High Risk: 200-499

38
Q

HDL Values-

Desirable:

High Risk:

A

Desirable: 60

High Risk: < 35

39
Q

LDL Values-

Desirable:

High Risk:

A

Desirable: 60-130

High Risk: 160-189

40
Q

soft, yellow plaques in various places like eyelids, palms, axilla and chin.

A

Plane Xanthoma

41
Q

Plane xanthomas are associated with…

A

familial or secondary hypercholesterolemia

42
Q

yellow-orange nodules commonly located over knees and elbows

A

tuberous xanthoma

43
Q

a tuberous xanthoma found on tendons is called….

A

tendinous xanthoma

44
Q

tuberous xanthoma is associated with…

A

familial hypercholesterolemia

45
Q
  • small red-yellow papules
  • abrupt onset
  • located on extensor surfaces and buttocks
A

Eruptive xanthomas

46
Q

what causes eruptive xanthomas?

A

elevated TAGs, > 1500

47
Q

eruptive xanthomas are associated with…

A

familial hyperlipidemia

48
Q

a white or grey ring around the cornea

A

cornal arcus

49
Q

a patient exhibits corneal arcus without elevated lipids. Age is >40. Is this concerning?

A

no, common finding in pts over 40

50
Q

The DASH diet has demonstrable effects on what markers?

A

BP, LDL, and risk of CHD/Stroke

51
Q

An exercise program to address CHD should include…

A

3-4 40 minutes sessions/week of moderate to vigorous exercise

52
Q

The only class of drugs to demonstrate clear improvements in overall mortality in primary and secondary prevention of CHD.

A

statins (HMG CoA reductase inhibitors)

53
Q

What tests should be obtained to measure a baseline prior to initiating statin therapy?

A

lipid panel

LFTs

CK

54
Q

To assess adherence and percent response to statins and lifestyle changes, a repeat lipid panel should be done every_______

A

4-12 weeks after starting or does adjustment

55
Q

when a statin does has been titrated to the preferred therapeutic response, how often should monitoring via lipid panel, LFTs and CK take place?

A

every 3-12 months

56
Q

What are three appropriate responses to an intolerance or poor response to statin therapy?

A
  1. reinforce importance of adherence to meds and lifestyle changes
  2. exclude secondary hyperlipidemia
  3. investigate tolerance
57
Q

are bile acid sequestrants safe during pregnancy?

A

yes

58
Q

The four statin benefit groups are:

A
  1. clinical ASCVD Dx
  2. LDL 190 or higher
  3. DM 40-75 yo with LDL 70 or higher
  4. LDL 70-189 and 10 yrASCVD risk 7.5% or greater
59
Q

LDL 190 or higher is treated with…

A

high intensity statin, no risk assessment needed to start tx

60
Q

DM aged 40-75 pt. is treated with…

A

risk assessment to determine moderate or high intensity statin

61
Q

If a patient is 40-75 with LDL 70-190 and no DM… treat with…

A

calculate 10 year ASCVD risk

62
Q

uncomplicated 40-75 yo pt. with LDL 70-190. ASCVD risk “low” (< 5%)… tx?

A

lifestyle factors only

63
Q

uncomplicated 40-75 yo pt. with LDL 70-190. ASCVD risk “borderline” (5-7.4%)… tx?

A

moderate intensity statin

64
Q

uncomplicated 40-75 yo pt. with LDL 70-190. ASCVD risk “intermediate” (7.5-20%)… tx?

A

moderate intensity statin to reduce LDL 30-49%

65
Q

uncomplicated 40-75 yo pt. with LDL 70-190. ASCVD risk “High” (< 50%)… tx?

A

initiate statin to reduce LDL 50%

66
Q

This drug:

lowers LDL

SE: liver toxicity, myopathy, drug interactions

A

Statins

67
Q

This drug:

decreases TGs

Toxicity when used with statin

most useful with hyperTGemia

A

Fibrates

68
Q

If myositis is suspected during statin therapy, what should be done?

A

stop therapy, check CK and LFTs

69
Q

This drug:

Raises HDL, Lowers LDL

don’t use w/ statin, must monitor LFTs

must be titrated slowly to moderate side effects

SE: flushing

A

niacin

70
Q

This drug:

lowers LDL

safe in pregnancy

Can increase TGs

SE: diarrhea and other GI issues

A

bile acid sequestrants

71
Q

This drug:

statin add-on

decreases LDL

A

Ezetamibe

72
Q

when shouldn’t you combine ezetamibe and statins?

A

pts with liver disease

73
Q

This drug:

profoundly decreases LDL

used as statin adjunct or in statin intolerance

Expensive, injection

A

PCSK9 inhibitors

Clinical Medicine II (31 decks)

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