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FA17 Cardio 1 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

process of atherogenesis

A

abnormal accumulation of lipids, cells, and extracellular matrix within the arterial wall THESE form plaques

plaques either narrow or rupture causing oxygen deprivation

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2
Q

primary event in atherogenesis

A

vessel injury or endothelial dysfunction (via toxic chemical environments)

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3
Q

endothelial dysfunction causes

A

impairment in permeability, release of cytokines increases desire to clot

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4
Q

atherogenesis is is a chronic ____ condition

A

inflammatory

includes accumulation of lipids in intima, recruitment of leukocytes and smooth muscle cells, deposit in ECM

causing dysfunction

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5
Q

why do we care about hyperlipidemia

A

atherosclerosis can be prevented

primary prevention treatment can get successful results

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6
Q

management strategies provided prior to the onset of CVD related events

A

primary prevention

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7
Q

management plan for those who have already experienced CV event

A

secondary prevention

efforts to prevent progression and/or reoccurrence

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8
Q

modification of identifiable risk factors can…

A

significantly decrease morbidity and mortality

cholesterol reduction leads to consistent reduction in mortality

high cholesterol = atherosclerosis

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9
Q

non modifiable risk factors

A

can’t control or change

family history, male sex,

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10
Q

hereditary and hyperlipidemia

A

runs in family

familial hypercholesterolemia (increased LDL at birth)

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11
Q

age and sex

A

men have higher LDL when younger then when they get older, women have worse

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12
Q

modifiable risk factors

A

blood lipid abnormalities

DM, HTN, sedentary lifestyle. abdominal obesity, cigarette smoking, diet, increased alcohol

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13
Q

lack of physical activity and hyperlipidemia

A

= weight gain, increased LDL, decreased HDL, increased total LDL

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14
Q

hyperlipidemia can result from

A

over production and/or defective clearance of vLDL or increased conversion vLDL to LDL

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15
Q

defective clearance of LDL can be caused by

A

genetically determined structural defects

diminished binding of ApoB to otherwise normal LDL

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16
Q

where do fats typically come from

A

saturated fats, animal products (meat and dairy)

unsaturated fats (seeds, nuts, veggie oils)

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17
Q

sources of cholesterol

A

egg yolks, organ meats and milk

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18
Q

what diet is typically the cause of high cholesterol

A

high in saturated fats and cholesterol

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19
Q

which lipoprotein is exclusively cholesterol

A

LDL

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20
Q

which lipoprotein has more TGs than cholesterol

A

more TG then cholesterol

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21
Q

main source of plasma LDL

A

vLDL

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22
Q

levels of which lipoprotein correlate with atherosclerosis?

A

LDL

high levels in blood cause it to accumulate in the lumen

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23
Q

LDL metabolism

A

liver removes it

hepatocytes that specifically bind to ApoB

ligand associated with LDL that binds with LDL receptors

removes LDL from circulation

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24
Q

LDL and plaque

A

LDL that is not removed from circulation by macrophages

migrate into arterial walls where they become foam cells of atherosclerotic plaques

foam cells harden which causes atherosclerosis

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25
Q

hyperlipidemia and CVD risk

A

increases progressively high levels of LDL cholesterol

this risk declines with high HDL levels

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26
Q

very high LDL levels

A

190 mg/dL and higher

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27
Q

good HDL values

A

40-59 mg/dL

minimum HDL levels for females = 50

28
Q

high TG levels

A

> 500 = risk of pancreatitis

29
Q

declines in serum cholesterol can be skin in ___

A

acute illness

TGs are ELEVATED in presence of pancreatitis

30
Q

CRP

A

Hs-CRP is NOT a screening tool for lipids, it is a produce of hyperlipidemia

high lipids predict CVD

31
Q

Farmingham study

A

predicative score based on age, gender, LDL, HDL. BP, DM, smoking

End points of risk = CHD death, nonfatal MI, unstable angina, stable angina

started with just generational, ID risk factors of everyone

32
Q

smoking cessation

A

programmatic and/or group support with pharmacologic therapy

smoking cessation is most cost effective preventative measures

33
Q

ATPIII

A

elimination of diabetes and addition of wider age range

LDL is still best way to decrease risk

34
Q

predictive variables in ACC?AHA cohort calc

A

age, gender, total cholesterol, HDL, BP, DM, smoking

35
Q

end points of ACC/AHA

A

CHD death
nonfatal MI
fatal stroke
nonfatal stroke

36
Q

treatment decisions based on:

A

clinical CV disease or DM
Pt’s age
LDL cholesterol >190
est. 10 yr risk

smoking cessation is most cost effective preventative measures

37
Q

what should an effective diet include

A

giggles, fruits, whole grains

low fat dairy produces, poultry, fish, legumes

healthy oils and nuts

38
Q

pharm management of hyperlipidemia

A

goal is to lower LDL levels (no specific value, just 10%)

should start on ASA

39
Q

HMG-CoA reductase inhibitors

A

aka statins

block rate limiting enzyme in cholesterol synthesis

cholesterol isn’t synthesized in liver so have to increase serum LDL uptake

40
Q

Statin administration and SE

A

take once at night

myalgia, rhabdomyolysis, mysoitis, liver failure

41
Q

high intensity statin therapy

A

Lower LDL by 50%

atorvastatin (Lipitor) 40-80mg
tosuvastatin (Crestor) 20-40,g

42
Q

moderate intensity statins

A

lower LDL by 30-50%

Atorvastatin (Lipitor) 10-20
Rosuvastatin (Crestor) 5-10 
simvastatin (Zocor) 20-40
Pravastatin (pravachol) 40-80
lovastatin (Mevacer) 40
43
Q

low intensity statin therapy

A

lowers LDL by <30%

simvastatin (Zocor)
Pravastatin (Pravachol) 10-20
Lovastatin (Mevacor) 20mg

44
Q

four groups that continually benefit from statins

A
  1. those w/atherosclerotic CV dz
  2. LDL >190
  3. 40-75 DM pos w/ LDL >70
  4. no other dz 40-75, LDL >70-189, 10 yrs factor of 7.5%+
45
Q

ezetemide

A

Zeita

inhibits intestinal absorption of cholesterol, blocks its movement across wall

only med W.O. side effects!!!!

46
Q

bile acid sequestrants

A

Cholestryamine (PRevalite) Colesevelam (Welchol) Colestipol (Colestid)

bile removed, causes liver to use up more LDL to maintain levels

only lipid SAFE in pregos

47
Q

Bile Acid Binding resins SE

A

abdomina discomfort, flats, n/v

INCREASES TG levels and may interfere with fat soluble vitamin absorption

48
Q

Niacin (Nicotinic Acid)

A

known to increase HDL (35-35%)

not used bc increased HDL doesn’t really lower risk, and nasty side effects (FLUSHING< hot flashes and parities)

49
Q

PCSK9 inhibitors

A

ALirocuman (Praluent) Vcolocuman (repatha)

blocks gene that degrades LDL-r on liver, found to lower levels 50-60%

SQ injection, COSTLY but no muscle toxicity

50
Q

Fibric acid derivative

A

Gemfibrozil (lipid)
fenofibrate (Fenoglide, Fibricor, lofibra)

increase vLDL catabolism, fatty acid oxidation and elimination of TG rich particles

increases HDL and reduces TG

51
Q

SE of fibric acid derivatives

A

hepatitis, dyspepsia, n/v, muscle issues (rhabdo, myalgia, myositis)

esp. worse off if you combine with statins

52
Q

Triglyceride specific pharm therapy?

A

Fibric Acid Derivatives if TGs are >500 and pt is at risk of pancreatitis

could add nicotinic acid agent or omega 3

53
Q

if TGs< 499…

A

tx with statin to get to LDL goal

if still high when meet that goal, add nicotinic or intensify statin

54
Q

how to treat elevated TGs

A

primarily diet

avoid alcohol, simple sugar, refined starches, saturated and transfatty acids, monitor calories

55
Q

Tx for pt >21 and LDL >190

A

assess secondary hyperlipidemia cause

initiate statins (highest intensity possible)

56
Q

primary prevention for its w/DM and LDL of 70-189

A

40-75 yr with DM should start or continue statin

if 10 yr risk >7.5% high intensity stain reasonable

57
Q

primary prevention pt w/o diabetes and LDL 70-189

A

moderate intensity statins if reasonable

or could try and work with patient on a treatment plan

58
Q

ASCVD risk

> 7.5%

A

high intensity statin

59
Q

ASCVD risk

5%- 7.5%

A

consider moderate intensity statin

60
Q

what do you asses 4-12 weeks following statin imitation

A

adherence
response to therapy
adverse effects
measure fasting lipid levels

continue w/emphasis on DM management if pt. is DM

61
Q

secondary causes of dyslipidemia

A 
DM
hypothyroidism
excessive alcohol 
liver, renal dz
obesity, smoking, drugs
62
Q

xanthelasma

A

yellowish plaques that occur most commonly near inner cantles of eye and seen more often on upper lid than lower lid

63
Q

eruptive xanthoma

A

skin, red, yellow papular eruptions

firm pea-shaped bumps

found on buttocks, papule may be pyritic

plasma TGs

64
Q

Tendon xanthoma

A

high LDL concentrations found on achilles, patella, back of hand

indicates familial hypercholesterolemia

65
Q

familial hypercholesterolemia

A

increased LDL from birth

causes tendon xanthoma, early onset CVD

impairment in function of these receptors = reduced LDL clearance

increased LDL uptake in marophages = and foam cells

66
Q

homozygous familial hypercholesterolemia

A

VERY rare

high incidence of supra aortic stenosis

67
Q

heterozygous familial hypercholesterolemia

A

high LDL levels form birth, premature CVD, family hx of hypercholesterolemia, tendon xanthomata

FA17 Cardio 1 (6 decks)

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