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CMT > Lipids > Flashcards

Lipids Flashcards

1
Q

3 types of lipids

A
  1. cholesterol
  2. triglycerides
  3. lipoproteins
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2
Q

what is cholesterol

define/describe

A

essential element of all animal cell membranes and the backbone of steroid hormones and bile acids

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3
Q

what are triglycerides

A

txfr energy from food into cells

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4
Q

what are lipoproteins

A
  • transport lipids
  • classified by density
  • apoprotiein is dense
  • triglyceride is less dense
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5
Q

7 types of lipoproteins

A
  1. chylomicrons
  2. low-density lipoprotein
  3. high-density lipoprotein
  4. very-low-density lipoprotein
  5. Apolipoprotein B (apoB)
  6. Lipoprotein
  7. non-HDL cholesterol
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6
Q

describe chylomicrons

A

least dense
found in blood after fatty meals

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7
Q

describe LDL

A

carry most of our cholesterol

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8
Q

describe VLDL

A

least dense, large
consists mostly of triglycerides that are txfr to cells

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9
Q

describe HDL

A

most dense & smallest
participate in reverse cholesterol transport

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10
Q

describe apoB

A
  • protein that carries LDL and helps it bind to the cell wall
  • contributes to atherogenesis
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11
Q

describe lipoprotein a (lp(a))

A
  • genetically determined subfraction of LDL
  • causal factor in atherosclerosis
  • one-time measurement rec in pts w/ family hx of ASCVD
  • risk enhancing factor favoring early statin tx
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12
Q

describe non-HDL cholesterol

A
  • surrogate marker of apoB
  • measured directly, less sensitive to fasting status
  • better predictor of CV risk than LDL
  • non-HDL Cholesterol = TC - HDL
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13
Q

which lipid value is most sensitive to fasting?

A

triglycerides

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14
Q

which lipoprotein carries the most cholesterol

A

LDL

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15
Q

which lipoprotein is an independent risk for ASCVD

A

Lp(a)

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16
Q

which lipoprotein represents all apoB containing particles?

A

non-HDL calculation

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17
Q

what are the components of a lipid panel?

4

A
  1. total cholesterol
  2. LDL
  3. HDL
  4. triglycerides
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18
Q

which components of a lipid panel are measured directly? which are calculated?

A
  1. direct: TC, HDL, triglycerides
  2. calc: LDL
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19
Q

equation for TC

A

HDL + VLDL + LDL

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20
Q

equation for non-HDL cholesterol

A

TC - HDL

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21
Q

equation for VLDL

& when to use

A

TG / 5

only if TG is < 400

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22
Q

equation for LDL

A

TC - HDL - (TG / 5)

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23
Q

what are benchmarks for LDL levels?

5

A
  • less than 100: optimal
  • 100-129: near optimal/above optimal
  • 130-159: borderline high
  • 160-189: high
  • more than 190: very high
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24
Q

what are benchmarks for TC levels?

3

A
  • less than 200: desirable
  • 200-239: borderline high
  • greater than 240: high
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25
Q

what are benchmarks for HDL cholesterol?

2

A
  • less than 40: low
  • greater than 60: high
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26
Q

benchmarks of triglycerides?

4

A
  • less than 150: normal
  • 150-199: borderline high
  • 200-499: high
  • more than 500: very high
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27
Q

what is the goal of lipid treatment? when does this goal change?

A
  • to reduce LDL
  • when triglycerides are greater than 500
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28
Q

what is the risk of treating when triglycerides are greater than 500?

A

pancreatitis

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29
Q

Atherosclerosis

associated with?

A
  • high LDL
  • low HDL
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30
Q

Atherosclerosis

pathophys

A

plaque w/ large amounts of cholesterol build up in arterial walls

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31
Q

Atherosclerosis

mostly asx until?

A

rupture or vessel occlusion (MI or CVA)

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32
Q

Familial Hypercholesterolemia

associated with which genetic components?

3

A
  1. defective LDL receptors
  2. genetic mutations of apo B
  3. gain of function mutation of PCSK9
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33
Q

Familial Hypercholesterolemia

which lipid is usually elevated?

A
  • total cholesterol
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34
Q

Familial Hypercholesterolemia

describe clinical manifestation of heterozygous pts

A
  • up to 3x normal levels of LDL
  • LV disease begins in 30s or 40s
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35
Q

Familial Hypercholesterolemia

describe clinical manifestation of homozygous pts

A
  • extremely high LDL (up to 8x normal)
  • atherosclerosis in childhood
  • may require plasmapheresis to remove cholesterol
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36
Q

Familial Chylomicronemia

AKA

3 things

A
  1. Lipoprotein Lipase Deficiency (LPLD)
  2. Fredrickson Type 1 Hyperlipoproteinemia
  3. Familial Hypertriglyceridemia
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37
Q

Familial Chylomicronemia

caused by?

A

abnormality of LPL that is responsible for ability of itssues to take up triglycerides (TG) from chylomicrons

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38
Q

Familial Chylomicronemia

characterized by?

A

hypertriglyceridemia

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39
Q

Familial Chylomicronemia

complications

2

A
  • recurrent pancreatitis
  • hepatosplenomegaly
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40
Q

Familial Chylomicronemia

important to abstain from?

A

EtOH

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41
Q

Dysbetalipoproteinemia

elevated levels of?

A

reminant lipoproteins

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42
Q

Dysbetalipoproteinemia

associated with?

A

premature ASCVD

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43
Q

Familial Combined Hyperlipidemia

most commonly affected genes?

3

A
  • LDLR
  • APOB
  • PCSK9
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44
Q

Conditions that affect lipids

AKA- secondary causes of dyslipidemia- 11

A
  1. metabolic syndrome
  2. type 2 diabetes
  3. uncontrolled hyperglycemia
  4. obesity
  5. hypothyroidism
  6. liver disease
  7. renal disease
  8. corticosteroid use
  9. progestin use
  10. anabolic steroid use
  11. alcohol use/abuse
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45
Q

conditions that increase TC

10

A
  1. obesity
  2. uncontrolled DM
  3. hypothyroidism/Cushing
  4. nephrotic syndrome
  5. CKD
  6. obstructive liver disease
  7. corticosteroid use
  8. OCPs
  9. Diuretics
  10. Beta Blockers
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46
Q

conditions that decrease TC

3

A
  1. hyperthyroidism
  2. cirrhosis
  3. malignancy
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47
Q

factor that increases LDL

1

A
  1. alcohol use
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48
Q

conditions that decrease HDL

4

A
  1. obesity
  2. sedentary lifestyle
  3. metabolic syndromes
  4. beta blockers
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49
Q

conditions that increase triglycerides

6

A
  1. DM
  2. alcohol use
  3. nephrotic syndrome
  4. CKD
  5. OCP
  6. diuretics
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50
Q

you are treating a pt for high cholesterol. Current LDL is non-calculable, other values are:
* TG > 450
* HDL: 40
* TSH: 10 (normal < 4)
* HgA1C: 9.8

why is her cholesterol not at goal in spite of compliance with cholesterol medications?

A

must correct DM and TSH

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51
Q

Clinical Presentation

4- but really labs are best dx tool

A
  1. eruptive xanthomas/xanthelasma
  2. tendinous xanthomas
  3. lipemia retinalis
  4. corneal arcus
52
Q

Screening Guidelines Children

A
  • selective screening for children age > 2 y/o with family hx, lipid disorder, or premature ASCVD
  • first screen between ages 9-11 and again between 17-21
53
Q

Screening Guidelines Adults

A
  • first at age 20 if not done as a child
  • every 5 years for those at low risk after age 35 (men) or 45 (women)
  • more often screenings based on relative risk
54
Q

Screening Guidelines for Older Adults

A
  • screening not recommended for those over age 75
55
Q

Describe Pooled Cohort Equations

A
  • estimates 10 year risk of MI, CVA, CV death
  • does over-estimate risk of middle/higher SES pts
  • separate calculator for white/black pts
56
Q

Pooled Cohort Equation risk levels defined

A

10 year risk is….
* less than 5%: low
* 5-7.5%: borderline
* 7.5-20%: intermediate
* more than 20%: high

57
Q

Risk enhancing factors- basically who will benefit the most from therapy?

12

A
  1. family hx of premature disease
  2. metabolic syndrome
  3. chronic inflammatory conditions
  4. high risk race/ethnicity
  5. elevated hsCRP
  6. elevated apo B
  7. primary hypercholesterolemia
  8. CKD
  9. hx of pre-eclampsia or premature menopause
  10. presistently high TG
  11. elevated apo(a)
  12. low ankle brachial index
58
Q

Cardiac Calcium Score

is the……

best….

A

single best test for additional risk stratification

59
Q

Cardiac Calcium Score

what type of imaging?

A

noncontrast cardiac gated CT

60
Q

Cardiac Calcium Score

repeat how often?

A

every 3 to 7 yrs based on risk

61
Q

Cardiac Calcium Score

how to interpret a cardiac calcium score

5 categories

A
  • 0: no evidence of CAD
  • 1-10: minimal evidence of CAD
  • 11-100: mild evidence of CAD
  • 101-400: moderate evidence of CAD
  • 400 + : severe evidence of CAD
62
Q

A pt with which of the following characteristics will a cardiac calcium score be most useful in a shared decision-making model?
* aged 75
* intermediate 10-year risk of heart disease
* LDL of 194
* type 2 DM
* smoker

A

intermediate 10 year risk of heart disease

63
Q

The Pooled Cohort Equation is used to estimated the 10-year risk of heart disease or stroke for an individual. The risk is reported to be 10%. What risk category is the result?
* borderline
* high
* intermediate
* low

A

intermediate

64
Q

CV Disease Prevention

what is primary prevention

A
  • refers to therapy in persons with no known cardiovascular disease
65
Q

CV Disease Prevention

what is secondary prevention

A
  • therapy in persons with known CV disease
66
Q

CV Disease Prevention

At what age do you stop primary prevention?

A

75

67
Q

CV Disease Prevention

What shouldn’t you use as primary prevention in pregnant women?

A

statins

68
Q

CV Disease Prevention

When do you consider lifestyle factors and drug therapies in someone with 0-1 risk factors?

A
  • Lifestyle changes: LDL > 160
  • Drug therapies: LDL > 190
69
Q

CV Disease Prevention

When do you consider lifestyle factors and drug therapies in someone with 2+ risk factors?

A
  • Lifestyle: LDL > 130
    Drug therapies
  • 10-year risk 10-20%: LDL > 130
  • 10-year-risk < 10%: LDL > 160
70
Q

CV Disease Prevention

When do you consider lifestyle factors and drug therapies in someone with CHD?

A
  • Lifestyle: LDL > 100
  • Drug Therapies: LDL > 130
71
Q

CV Disease Prevention

Who gets high intensity statins for primary prevention?

A
  • LDL > 190
  • Age 40-75 with diabetes AND risk enhancing factors or 10-year risk >20%
  • Age 40-75 without diabetes with LDL 70-189 and intermediate or high risk with additional risk factors
72
Q

CV Disease Prevention

Who gets moderate intensity statins for primary prevention?

A
  • Age 40-75 with diabetes
  • Age 40-75 without diabetes with LDL 70-189 and intermediate or high risk
73
Q

CV Disease Prevention

Descisions to continue statin therapies in pts older than 75 y/o should be based on:

4 things

A
  1. functional status
  2. life expectancy
  3. comorbidities
  4. pt preference
74
Q

CV Disease Prevention

who is very high risk?

4 things

A
  1. ACS within past 12 mo
  2. MI other than event listed above
  3. hx of ischemic stroke
  4. symptomatic PAD
75
Q

CV Disease Prevention

what is considered high risk>

8 things

A
  1. > 65 y/o
  2. heterozygous familial hypocholesterolemia
  3. DM
  4. hypertension
  5. CKD
  6. current smoker
  7. CHF
  8. LDL >100 with statin and ezetimibe
76
Q

CV Disease Prevention

who gets a statin in secondary prevention?

A

EVERYONE

77
Q

Lipid Treatment

What lifestyle changes should be made? what lipid does component act on?

5 general measures

A
  1. exercise (increases HDL)
  2. wt loss (decreases LDL, increases HDL)
  3. tobacco cessation (increases HDL)
  4. modest alcohol use (increases HDL)
  5. Aspirin (not rec for all)
78
Q

Lipid Treatment

after how long should you recheck lipids after lifestyle changes?

A

4-6 wks

79
Q

Lipid Treatment

Desired dietary intake for lifestyle changes?

A
  1. total fat 25-30% of cals
  2. saturated fats < 7% of cals
  3. dietary cholesterol < 200 mg/d
  4. 20-30g of soluble fiber daily
  5. 2g of plant stanols and sterols daily
  6. antioxidants
80
Q

Lipid Treatment

which diet is most moften recommended for cholesterol reduction?

A

mediterranean

81
Q

A 45 y/o woman with no risk factors for CHD is found to have cholesterol levels of 165 mg/dL. What nutrition advice should you give?
1. abstain from all alcohol
2. begin a fish oil supplement
3. cut carbohydrate intake to < 30% of cals
4. decrease saturated fat to < 15% of cals
5. increase fiber to 20g daily

A

increase fiber to 20g daily

82
Q

Which of the following “natural” interventions has not been proven to reduce cholesterol?
1. almonds
2. walnuts
3. increased fiber
4. Co-Q 10
5. Plant stanols
6. Red-yeast rice extract

A

Plant stanols

83
Q

Lipid Treatment

first, second, third line for hyperlipidemia?

A
  1. statins
  2. ezetimibe
  3. PCSK9 inhibitors
84
Q

Lipid Treatment

first, second, third line for hypertriglyceridemia?

A
  1. fibrates
  2. niacin
  3. fish oil
85
Q

Lipid Treatment

names for fish oil tx

A
  1. icosapent ethyl (vascepa)
  2. omega-3-acid ethyl esters (lovaza)
86
Q

Lipid Treatment

Benefits of fish oil tx

A
  • reduce TG up to 30%
87
Q

Lipid Treatment

dosage for fish oils

CAD tx vs TG

A
  1. 1g/d for CAD
  2. 2-4g/d for TG reduction
88
Q

Lipid Treatment

Contraindications of fish oils

A
  1. fish/shellfish allergy
  2. increased bleeding risk
  3. discontinue for surgery
89
Q

Lipid Treatment

benefit of niacin (niaspan)?

A
  • reduces LDL 15-25%
  • increases HDL 25-35%
90
Q

Lipid Treatment

what to take 1 hr before Niacin?

A

Aspirin or NSAID

91
Q

Lipid Treatment

Contraindications of Niacin?

A
  • caution with cyclosporine, macrolides, anti-fungals, and other CYP metabolites
92
Q

Lipid Treatment

names for fibrates that might be prescribed?

A
  1. gemifibrozil (Lopid)
  2. fenofibrate (Tricor, Triglide, Lipofen)
93
Q

Lipid Treatment

benefits of fibrates

A
  • reduce TG 40%
  • reduce LDL 10-15%
  • Increase HDL 15-20%
94
Q

Lipid Treatment

contraindications of fibrates?

A
  1. impaired renal function
  2. caution w/ cyclosporine, macrolides, anti-fungals, and CYP450 metabolites
95
Q

Lipid Treatment

MOA of statins

A
  • inhibit the rate-limiting enzyme in the formation of cholesterol in the liver and increases hepatic LDL receptors
96
Q

Lipid Treatment

risks of statins

6

A
  1. myalgias
  2. CK elevations
  3. myositis
  4. rhabdomyolysis
  5. elevated transaminases
  6. DM development
97
Q

Lipid Treatment

contraindications of statins?

A
  • Liver function
  • niacin, fibrates, EES, anti-fungals, nefazodone, cyclosporin
98
Q

Lipid Treatment

by how much do low intensity statins reduce LDLs? which meds/doses are low intensity?

A
  1. < 30%
  2. Pravastatin, 10-20mg
  3. Lovastatin, 20mg
99
Q

Lipid Treatment

by how much do moderate intensity statins reduce LDLs? which meds/doses are moderate intensity?

A
  1. 30-50%
  2. Pitavastatin, 2-4mg
  3. Simvastatin, 20-40mg
  4. Pravastatin, 40-80mg
  5. Atovastatin, 10-20mg
  6. Rosuvastatin, 5-10mg
100
Q

Lipid Treatment

by how much do high intensity statins reduce LDLs? which meds/doses are high intensity?

A
  • reduce LDLs by ~50%
    1. Atovastatin, 40-80mg
    2. Rosuvastatin, 20-40mg
101
Q

which of the following statin medications and doses is high intensity intervention?
1. Atorvastatin, 40mg
2. Lovastatin, 20mg
3. Pravastatin, 40mg
4. Simvastatin, 40mg
5. Rosuvastatin, 10mg

A

Atorvastatin, 40mg

102
Q

Select all statins that could be used to reduce LDL by 35-50%
1. atorvastatin, 40mg
2. atorvastatin, 80mg
3. rosuvastatin, 10mg
4. rosuvastatin, 20mg
5. simvastatin, 10mg

A

rosuvastatin 10 mg

103
Q

Lipid Treatments

what meds are bile acid sequestrants?

A
  • cholestryamine (Questran)
  • colesevelam (Welchol)
  • colestipol (Colestid)
104
Q

Lipid Treatments

moa of bile acid sequestrants

A

binds bile acids in the intestine which increases bile acid synthesis and LDL receptor activity

105
Q

Lipid Treatments

benefits of bile acid sequestrants?

A
  1. reduces LDL by 15-25%
  2. safe in pregnancy
  3. can use with liver disease
106
Q

Lipid Treatments

risks of bile acid sequestrants?

A

TG may increase

107
Q

Lipid Treatments

contraindications of bile acid sequestrants?

NOT A MED

A

TG >500 mg/dL

108
Q

Lipid Treatments

what med is a cholesterol absorption inhibitor?

A

ezetimibe (zetia) 10 mg daily

109
Q

Lipid Treatments

MOA of ezetimibe

A

inhibits intestinal absorption of dietary and biliary cholesterol by inhibiting cholesterol transport.

can use as monotherapy or add to statin

110
Q

Lipid Treatments

benefits of ezetimibe

A
  • reduced LDL 15-20%
  • reduces hsCRP
  • well tolerated, QD
111
Q

Lipid Treatments

contraindications of ezetimibe

A

liver failure

112
Q

Lipid Treatments

which meds are PCSK9 inhibitors

A
  • alirocumab (Praluent)
  • evolocumab (Repatha)
113
Q

Lipid Treatments

moa of PCSK9 inhibitors

A

human monoclonal antibodies that inhibit LDL receptor degradation

use as a monotherapy or with statins

114
Q

Lipid Treatments

benefits of PCSK9 inhibitors

A
  • decrease LDL 50-60%
  • decrease Lp(a) 20-30%
115
Q

Lipid Treatments

which meds are adenosine triphosphate-citrate lyase inhibitors? (ACL)

A

Bempedoic Acid (nexletol)
Bempedoic Acid + ezetimibide (Nexlizet)

116
Q

Lipid Treatments

moa of ACL inhibitors

A
  • targets cholesterol synthesis in the liver (two steps upstream of statins)
  • up regulation of LDL receptors in the liver
117
Q

Lipid Treatments

benefits of ACL inhibitors

A
  • lowers LDL by 17-20%
  • combo w/ ezetimibe: 38%
118
Q

Lipid Treatments

contraindications of ACL inhibitors

A
  • not to be used with simvastatin 20mg or pravastatin 40mg
119
Q

Lipid Treatments

which med is angiopoietin-like 3 (ANGPTL3) inhibitor?

A

evinacumab

120
Q

Lipid Treatments

moa of ANGPTL3 Inhibitors

A
  • monoclonal antibody
  • activates lipoprotein lipase and endothelial lipase to increase lipid metabolism
121
Q

Lipid Treatments

benefits of ANGPTL3 inhibitors

A
  1. reduces TG
  2. reduces non-HDL cholesterol
  3. LDL redution by 49%
122
Q

Lipid Treatments

which med is small interfering RNA?

A

inclisiran (leqvio)

123
Q

Lipid Treatments

moa of small interfering rna

A

silences RNA involved in the synthesis of PCSK9 that controls synthesis of LDL cell surface receptors

124
Q

Lipid Treatments

indications of inclisiran

A
  1. maximally tolerated statin dose
  2. clinical CV disease
  3. pts with heterozygous familal hypercholesterolemia
125
Q

Lipid Treatments

use small interfering RNA meds in combo with? to do what?

A
  • adjunct to statins
  • to address LDL
126
Q

Lipid Treatments

how often to check lipids? how often after desired levels achieved?

A
  • check 12 wks after therapy initiation
  • after at goal: check anually

CMT (72 decks)

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