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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
hyperlipidemia and CVD risk
increases progressively high levels of LDL cholesterol this risk declines with high HDL levels
26
very high LDL levels
190 mg/dL and higher
27
good HDL values
40-59 mg/dL minimum HDL levels for females = 50
28
high TG levels
> 500 = risk of pancreatitis
29
declines in serum cholesterol can be skin in ___
acute illness TGs are ELEVATED in presence of pancreatitis
30
CRP
Hs-CRP is NOT a screening tool for lipids, it is a produce of hyperlipidemia high lipids predict CVD
31
Farmingham study
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
smoking cessation
programmatic and/or group support with pharmacologic therapy smoking cessation is most cost effective preventative measures
33
ATPIII
elimination of diabetes and addition of wider age range LDL is still best way to decrease risk
34
predictive variables in ACC?AHA cohort calc
age, gender, total cholesterol, HDL, BP, DM, smoking
35
end points of ACC/AHA
CHD death nonfatal MI fatal stroke nonfatal stroke
36
treatment decisions based on:
clinical CV disease or DM Pt's age LDL cholesterol >190 est. 10 yr risk smoking cessation is most cost effective preventative measures
37
what should an effective diet include
giggles, fruits, whole grains low fat dairy produces, poultry, fish, legumes healthy oils and nuts
38
pharm management of hyperlipidemia
goal is to lower LDL levels (no specific value, just 10%) should start on ASA
39
HMG-CoA reductase inhibitors
aka statins block rate limiting enzyme in cholesterol synthesis cholesterol isn't synthesized in liver so have to increase serum LDL uptake
40
Statin administration and SE
take once at night myalgia, rhabdomyolysis, mysoitis, liver failure
41
high intensity statin therapy
Lower LDL by 50% atorvastatin (Lipitor) 40-80mg tosuvastatin (Crestor) 20-40,g
42
moderate intensity statins
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
low intensity statin therapy
lowers LDL by <30% simvastatin (Zocor) Pravastatin (Pravachol) 10-20 Lovastatin (Mevacor) 20mg
44
four groups that continually benefit from statins
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
ezetemide
Zeita inhibits intestinal absorption of cholesterol, blocks its movement across wall only med W.O. side effects!!!!
46
bile acid sequestrants
Cholestryamine (PRevalite) Colesevelam (Welchol) Colestipol (Colestid) bile removed, causes liver to use up more LDL to maintain levels only lipid SAFE in pregos
47
Bile Acid Binding resins SE
abdomina discomfort, flats, n/v INCREASES TG levels and may interfere with fat soluble vitamin absorption
48
Niacin (Nicotinic Acid)
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
PCSK9 inhibitors
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
Fibric acid derivative
Gemfibrozil (lipid) fenofibrate (Fenoglide, Fibricor, lofibra) increase vLDL catabolism, fatty acid oxidation and elimination of TG rich particles increases HDL and reduces TG
51
SE of fibric acid derivatives
hepatitis, dyspepsia, n/v, muscle issues (rhabdo, myalgia, myositis) esp. worse off if you combine with statins
52
Triglyceride specific pharm therapy?
Fibric Acid Derivatives if TGs are >500 and pt is at risk of pancreatitis could add nicotinic acid agent or omega 3
53
if TGs< 499...
tx with statin to get to LDL goal if still high when meet that goal, add nicotinic or intensify statin
54
how to treat elevated TGs
primarily diet avoid alcohol, simple sugar, refined starches, saturated and transfatty acids, monitor calories
55
Tx for pt >21 and LDL >190
assess secondary hyperlipidemia cause initiate statins (highest intensity possible)
56
primary prevention for its w/DM and LDL of 70-189
40-75 yr with DM should start or continue statin if 10 yr risk >7.5% high intensity stain reasonable
57
primary prevention pt w/o diabetes and LDL 70-189
moderate intensity statins if reasonable or could try and work with patient on a treatment plan
58
ASCVD risk > 7.5%
high intensity statin
59
ASCVD risk 5%- 7.5%
consider moderate intensity statin
60
what do you asses 4-12 weeks following statin imitation
adherence response to therapy adverse effects measure fasting lipid levels continue w/emphasis on DM management if pt. is DM
61
secondary causes of dyslipidemia
``` DM hypothyroidism excessive alcohol liver, renal dz obesity, smoking, drugs ```
62
xanthelasma
yellowish plaques that occur most commonly near inner cantles of eye and seen more often on upper lid than lower lid
63
eruptive xanthoma
skin, red, yellow papular eruptions firm pea-shaped bumps found on buttocks, papule may be pyritic plasma TGs
64
Tendon xanthoma
high LDL concentrations found on achilles, patella, back of hand indicates familial hypercholesterolemia
65
familial hypercholesterolemia
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
homozygous familial hypercholesterolemia
VERY rare high incidence of supra aortic stenosis
67
heterozygous familial hypercholesterolemia
high LDL levels form birth, premature CVD, family hx of hypercholesterolemia, tendon xanthomata

FA17 Cardio 1 (6 decks)

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