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Internal Medicine > JH IM Board Review - Lipid Disorders I > Flashcards

JH IM Board Review - Lipid Disorders I Flashcards

1
Q

Lipoproteins are:

A

Spherical complexes consisting of a lipid core and an outer protein monolayer.

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2
Q

The role of lipoproteins is to …

A

Transport lipids, such as cholesterol and TGs, in the circulation.

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3
Q

Lipoprotein particles are classified according to increasing density;

A patient’s cholesterol levels are most commonly expressed as the concentration of cholesterol in each of the listed individual lipoprotein particle groups:

A
  1. Chylomicrons.
  2. VLDL.
  3. IDL.
  4. LDL.
  5. HDL.
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4
Q

Chylomicrons are:

A

TG-rich lipoproteins responsible for transporting dietary fat and CH into the body.

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5
Q

Chylomicrons are synthesized by … cells from dietary FAs absorbed via the … transporter.

A

INTESTINAL EPITHELIAL CELLS.

NPC1L1.

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6
Q

… releases FFAs from chylomicrons, leaving chylomicron remnants.

A

Lipoprotein lipase.

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7
Q

VLDL is synthesized where?

A

In the liver.

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8
Q

VLDL is synthesized from … (2)

A
  1. FFAs — obtained from chylomicrons [DIETARY FAT].

2. Endogenously produced TGs (generated from excess dietary protein and carbs).

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9
Q

VLDL is hydrolyzed by …

A

Lipoprotein lipase and converted to smaller particles (IDL).

Then to LDL.

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10
Q

The peripheral tissue clears …%, and the liver takes up …% of serum LDL, primarily via LDL transporters.

==> LDL transports cholesterol to peripheral tissues.

A

25%

75%

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11
Q

Cholesterol homeostasis is regulated by hepatic LDL receptor expression:

A
  1. Decreased hepatocyte CH levels leads to an increase in LDL receptor expression ==> greater clearance of serum LDL.
  2. Increased dietary saturated FFAs decreases hepatic LDL receptors and leads to increased serum LDL levels.
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12
Q

Dietary CH inhibits the production of endogenous CH, but once endogenous CH production is fully suppressed, additional dietary CH …

A

May also result in increased serum CH.

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13
Q

HDL is …

A

Small lipoprotein that transports CH from the arteries back to the liver (reverse CH transport).

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14
Q

HDL is POTENTIALLY atheroprotective because …

A

It is instrumental in REVERSE CH TRANSPORT and has intrinsic anti-inflammatory, anti-thrombotic, anti-apoptotic, anti-oxidative, and endothelial function-enhancing properties.

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15
Q

Apolipoproteins are a …

A

Major component embedded in the lipoprotein surface monolayer.

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16
Q

Apolipoproteins affect lipoprotein metabolism by …

A

Activating different enzymes and mediating cellular uptake through interactions with cell-surface receptors.

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17
Q

Apolipoproteins are divided into … classes:

A

5

Apo-A — Apo-E

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18
Q

Apo A-containing lipoproteins are a/w …

A

Reduced atherosclerosis.

major protein component of mature HDL

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19
Q

Apo B-containing lipoproteins are a/w:

A

Increased atherosclerosis.

Major protein component of LDL

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20
Q

Apo CII-containing lipoproteins are on the …

A

Surface of VLDL and

==> activate lipoprotein lipase to promote TG hydrolysis.

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21
Q

**Apo CIII inhibits …

A

Lipoprotein lipase.

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22
Q

Lipoprotein(a) [Lp(a)] is …

A

An LDL-like particle with Apo B covalently linked to apo A.

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23
Q

Elevated Lp(a) levels are a/w an …

A

Increased risk of atherosclerotic events.

==> Especially in those with a personal FHx of premature ASCVD.

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24
Q

In a large prospective study of women >45y, increased Lp(a) levels correlated with …

A

Higher coronary events when LDL-cholesterol (C) levels were above average levels.

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25
Q

Familial lipoprotein lipase deficiency (I) - Defect?

A

Lipoprotein lipase deficiency

==> Incr. Chylomicrons.

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26
Q

Familial lipoprotein lipase deficiency - Clinical findings:

A
  1. Eruptive xanthomas.
  2. Lipemia retinalis.
  3. Abdo pain.
  4. HSM.
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27
Q

Familial lipoprotein lipase deficiency - Risk of CHD:

A

0

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28
Q

Familial hyperCH (IIa) - Defect:

A

Defective LDL receptor or apo B-100.

==> Incr. LDL.

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29
Q

Familial hyperCH - Clinical findings:

A
  1. Tendinous xanthomas.
  2. Xanthelasma planar.
  3. Xanthomas.
  4. Corneal arcus.
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30
Q

Combined hyperlipidemia (IIb) - Defect?

A

Incr. Secretion of apo-B-containing particles.

==> Incr. VLDL, LDL.

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31
Q

Combined hyperlipidemia - Clinical findings:

A

Often asymptomatic except for CHD.

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32
Q

Familial dysbetalipoproteinemia (III) - Defect?

A

Apo-E polymorphism.

==> Incr. VLDL, IDL.

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33
Q

Familial dysbetalipoproteinemia (III) - Clinical findings:

5

A
  1. Tuberoeruptive xanthomas.
  2. Hyperuricemia.
  3. Glucose intolerance.
  4. Corneal opacities.
  5. Yellow-orange discoloration of palmar creases.
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34
Q

Familial hypertriglyceridemia (IV, V) - Defect?

A

IV ==> Decr. Activity of lipoprotein lipase.

==> Incr. VLDL. Often asx.

V ==> Acquired lipoprotein lipase dysfunction, and chylomicronemia.

==> Incr. VLDL, chylomicrons. Often asx.

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35
Q

Tangier disease - Defect?

A

Decr. Ability to esterify CH.

==> Decreased HDL.

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36
Q

Tangier disease - Clinical findings:

A
  1. Corneal opacities.
  2. Polyneuropathy.
  3. Orange tonsils (!).
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37
Q

Gain of function of proprotein convertase subtilisin-like kexin type 9 (PSCK9) - Defect?

A

Increased LDL receptor degradation.

==> Incr. LDL.

Asx. No CAD risk.

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38
Q

A tendinous xanthoma is highly suggestive of …

A

Familial hyperCH (if LDL-C >190mg/dL).

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39
Q

Lipemia retinalis is a …

A

Creamy and/or pink discoloration of both arterioles + venules in the retina.

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40
Q

Lipemia retinalis is seen on fundoscopic exam in pts w/

A

Severe hypertriglyceridemia.

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41
Q

Primary dyslipidemias can be classified into …

A

Fredrickson types I through V

==> based on levels of LDL, normal and abnormal VLDL, and fasting chylomicrons.

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42
Q

Secondary dyslipidemias are caused by a concomitant disorder.

For example:

A

Severe TGemia is a/w an underlying genetic lipid disorder exacerbated by excessive alcohol consumption, diabetes, or pregnancy.

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43
Q

Elevated LDL-C ddx:

5

A
  1. Hypothyroidism.
  2. Chronic liver disease.
  3. Cholestasis.
  4. Nephrotic syndrome.
  5. Pregnancy.
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44
Q

Hypertriglyceridemia ddx:

7

A
  1. Alcohol.
  2. Obesity.
  3. Pregnancy.
  4. DM.
  5. Hypothyroidism.
  6. Chronic renal failure.
  7. Medications.
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45
Q

Drugs that may cause hyperTG:

4

A
  1. Nonselective beta-blockers.
  2. High-dose diuretics.
  3. Oral estrogen replacement therapy.
  4. Oral contraceptives.
46
Q

Low HDL-C ddx:

6

A
  1. Tobacco use.
  2. DM.
  3. Obesity.
  4. Sedentary lifestyle.
  5. HyperTG.
  6. Drugs.
47
Q

Drugs that lower HDL:

A
  1. Progestins.
  2. Anabolic steroids.
  3. CS.
48
Q

Type B pattern means …

A

Apo B numerically nearly equal to or greater than LDL-C.

==> Indicating the presence of small, dense, atherogenic particles.

49
Q

Type B pattern is a/w …

A

Impaired fibrinolysis, endothelial dysfunction, and accelerated ASCVD.

50
Q

Type B pattern is a/w … syndrome.

A

Metabolic.

51
Q

Clinical ASCVD is dx when pts have …

7

A
  1. ACS.
  2. MI.
  3. STABLE OR UNSTABLE ANGINA.
  4. Coronary or other arterial revascularizations.
  5. Stroke.
  6. TIA.
  7. Peripheral arterial disease.
52
Q

In pts >20y and w/o clinical ASCVD, what should be checked at least once every 5y?

A

Fasting lipoprotein levels.

==> Total CH, LDL-C, HDL-C, and TGs.

53
Q

In NON fasting samples, which lipoproteins are accurate?

A

TC

HDL-C.

NON-HDL-C (TC/HDL-C).

54
Q

Both TC and HDL-C (NOT LDL-C) are used in the 2013 ACC/AHA risk estimator.

Hence, nonfasting lipid levels are …

A

Acceptable in determining 10y (ages 40-79y) + Lifetime (20-59y) global ASCVD.

55
Q

2013 ACC/AHA guidelines identify 4 major groups who have favorable risk/benefit ratios when treated w/ statins in preventing ASCVD:

A
  1. Clinical ASCVD.
  2. Primary elevation of LDL 190mg/dL or higher.
  3. Diabetics aged 40-75y w/ an LDL of 70-189mg/dL.
  4. LDL of 70-189mg/dL + estimated 10y ASCVD risk greater than 7.5%.
56
Q

Group 4 pts at lower risk should …

A

NOT be treated w/ a statin w/o a clinician-patient risk discussion, addressing other risk factors ==>

Smoking, HTN, lifestyle etc.

57
Q

Of note, previous guidelines (Adult Treatment Panel III) used the …

A

Modified Framingham risk score (FRS) to set thresholds for lipid management.

==> The new guideline uses a different global risk equation derived from pooled NHLBI cohorts.

58
Q

NHLBI Pooled Cohort Equations (PCEs) - PCEs do what?

A

Identify the RISK of fatal and nonfatal coronary heart disease (CHD) and strokes.

59
Q

PCE risk factors include:

7

A
  1. Age.
  2. Sex.
  3. Race (AA vs Non AA).
  4. TC, HDL-C.
  5. SBP.
  6. Tx for HTN.
  7. Smoking.
60
Q

PCE lipid risk factors include specifically which markers?

A

Untreated CH and HDL-C and are used for both short-term (10y) and long-term (30y or lifetime) risk estimations.

==> Emphasis on NON-HDL-C (TC minus HDL-C).

==> Do NOT use LDL-C in risk estimation.

61
Q

Non-HDL-C correlates …

A

MUCH MORE STRONGLY than LDL-C w/ atherogenic apo B and other LDL particles.

62
Q

The PCE 10y risk calculation should be performed every …-… in individuals aged …-… w/o DM or ASCVD w/ LDL-C 70-189mg/dL.

A

4-6y.

40-75y.

63
Q

5 other factors that should be considered in evaluating the need for drug tx:

A
  1. FHx of premature ASCVD ==> <55y in male 1o relative/ <65y in female 1o relative.
  2. LDL-C 160mg/dL or higher.
  3. High-sensitivity CRP (hsCRP) 2mg/dL or higher.
  4. Coronary artery calcium (CAC) score greater than 300 Agatston units or greater than the 74th percentile for age, sex, and ethnicity.
  5. Ankle to brachial index greater than 0.9.
64
Q

hsCRP 2mg/dL or higher is a/w with a …-…% increase in predicted risk (JUPITER trial).

A

30-40%.

65
Q

If hsCRP is elevated, statin therapy can be considered in men >50y of age or women >60y with a LDL-C >130mg/dL who are …

A
  1. Not on lipid-lowering, hormone replacement, or immunosuppressant therapy.
  2. Who do not have clinical CHD, DM, CKD, severe inflammatory conditions, or contraindications to statins.
66
Q

Coronary artery calcium is highly specific for …

A

Atherosclerosis.

67
Q

2013 ACC/AHA guidelines specifically favor CAC greater than or equal to … as the cutoff for high-risk status.

A

300.

==> Strong observational data that supports a cutoff of CAC greater than or equal to 100.

68
Q

In contrast, a CAC score of … is a/w low short-term event rates and reclassifies risk downwards.

A

0.

69
Q

The 3 following risk factors are of uncertain benefit in assessing the risk for future ASCVD:

A
  1. Carotid artery intimal-medial thickness w/o assessment of the presence of carotid plaque ==> No longer considered reasonable.
  2. Lipoproteins, apolipoproteins, and particle size and density measurements ==> Not recommended in asx patients.
  3. GFR, albuminuria, or cardiorespiratory fitness measurements ==> No data show improvement in net ASCVD risk reclassification.
70
Q

Metabolic syndrome criteria:

A
  1. Abdo obesity = waist circumference (in men >40inches, in women >35inches).
  2. TGs >150.
  3. HDL <40 in men, <50 in women.
  4. BP >130/85mmHg.
  5. Fasting glucose >100.
71
Q

Metabolic syndrome is not as good as a global risk score for predicting ASCVD risk, but …

A

It does indicate a group who are prone to develop diabetes as well as cardiovascular disease.

==> All these factors improve with adherence to a healthy lifestyle that leads to modest weight loss.

72
Q

Dyslipidemia tx (to decrease ASCVD) - Statins - All are generic except?

A

Rosuvastatin and pitavastatin.

73
Q

Statins lower LDL-C by …-…%, raise HDL-C by …-…%, and lower TGs by …-…%.

A

20-60%.

3-12%.

10-35%.

74
Q

2013 ACC/AHA guidelines emphasize the use of statin tx for ASCVD prevention.

Compared with previous guidelines, non-statin therapies for the initial management of hyperCH are …

A

No longer recommended.

75
Q

The 2013 guidelines classify statins into 3 groups:

A
  1. High-intensity statin tx ==> Lowers LDL by >50%.
  2. Moderate-intensity ==> Lowers LDL by 30-50%.
  3. Lower-intensity ==> Lowers LDL by <30%.
76
Q

High-intensity statin therapy involves:

A

Daily dose lowers LDL cholesterol by approx. >50%.

==> Recommended: ATORVASTATIN 40-80mg/ ROSUVASTATIN 20-40mg.

77
Q

Moderate-intensity statin therapy involves:

A

Daily dose lowers LDL by approx. 30-50%.

Recommended: atorvastatin 10-20mg, rosuvastatin 5-10mg, simvastatin 20-40mg, …, pitavastatin 2-4mg.

78
Q

2013 cholesterol tx guidelines no longer recommend treating to …

A

DEFINED LDL targets.

==> Rather, they recommend globally lowering LDL and non-HDL w/ proven therapy to reduce ASCVD.

**Controversial = Some experts recommend aiming therapy to an LDL goal.

79
Q

Statins SE - Increased in pts with:

6

A
  1. Multiple or serious comorbidities, including impaired renal or hepatic function.
  2. History of statin intolerance or muscle disorders.
  3. Genetic polymorphisms (eg SLCO1B1) or concomitant use of drugs affecting statin metabolism.
  4. Age older than 75y.
  5. Asian ancestry.
  6. Hx of hemorrhagic stroke.
80
Q

Monitoring of statin tx - Initial fasting lipid panel, followed by …

A

A repeat lipid panel 4-12wks after statin initiation to determine pt’s response and adherence.

==> Repeat testing should be considered every 3-12months.

==> Beneficial changes in values could be b/o statins and lifestyle modifications.

***A 10% LDL increase may be caused by statin nonadherence or weight gain.

81
Q

Baseline hepatic function panel during statin tx?

A

No need to monitor after initiating tx.

Check if sx suggesting hepatotoxicity develop.

82
Q

Bile acid sequestrants (BAS —cholestyramine, colestipol, colesevelam) - Lower LDL by …-…%

A

10-25%.

83
Q

BAS can decrease the …

A

Absorption of other drugs.

==> Should be taken at least 90min before or 4h after BAS administration.

84
Q

BAS can raise …

A

TGs!

2013 guidelines discourage BAS tx in pts with TG 300mg/dL or higher, and caution if TG 250mg/dL.

85
Q

BAS - Absolute contra if … (3):

A

TG >500mg/dL.

Hx of TG-induced pancreatitis.

Hx of bowel obstruction.

86
Q

Colesevelam is especially useful in those w/

A

DM ==> Helps function of beta-cells.

87
Q

Ezetimibe - MoA:

A

Inhibition of CH absorption in the small intestine through inhibition of the NPC1L1 transporter.

88
Q

Ezetimibe lowers LDL by …-…%.

A

15-25%.

89
Q

Ezetimibe SE (uncommon):

A
  1. Transaminitis.
  2. Abdo and back pain.
  3. Diarrhea.
  4. Fatigue.
90
Q

A recent study showed a modest decrease in CVD events in pts with ACS when ezetimibe was added to …

A

SIMVASTATIN.

91
Q

Fibrates (gemfibrozil, fenofibrate) - Lower TG by …-…%.

Raise HDL-C by …-…%.

Lower LDL-C by …-…%.

A

25-50%.

10-20%.

5-20%.

92
Q

Fibrates - Reduce CHD events but do not reduce …

A

CHD mortality rates.

93
Q

Fibrates are especially useful in pts with …

A

DM.

94
Q

Gemfibrozil should NOT be given with …

A
  1. Atorvastatin.
  2. Simvastatin.
  3. Lovastatin.

***They all compete for the glucuronidation pathway.

95
Q

Of note, … can be used with statins.

A

Fenofibrate.

96
Q

What is the role of fibrates in the management of hyperlipidemia and ASCVD risk management?

A

Unclear.

97
Q

Role of fibrates - The 2013 guidelines recommend use in …

A

High-risk patients who are either intolerant or have a suboptimal response to statins.

***Some experts favor fibrate tx in addition to statins in DM pts with low HDL and high TGs.

98
Q

Niacin lowers LDL by …-…% and raises HDL by …-…%.

Lowers TGs by …-…%

A

5-25%.

15-35%.

20-40%.

99
Q

Niacin caused … decrease in mortality rates in post-MI pts in the prestatin era:

A

Modest.

100
Q

Niacin showed … when used with statins.

A

No benefit.

101
Q

Flushing of niacin is ameliorated with …

A

Aspirin pretx.

102
Q

Role of niacin in the management of hyperlipidemia and ASCVD risk management?

A

Uncertain.

103
Q

Pts treated with statins should not also be given niacin because …

A

2 large scale clinical trials have documented NO INCREMENTAL benefits in pts with low levels of LDL.

104
Q

Summary - Approach to the patient - Measurement of lipids:

A
  1. Fasting lipid profile beginning at age 21y.
  2. If nonfasting, TC and HDL values remain accurate and are adequate for ASCVD risk estimation with the ACC/AHA PCE risk estimator.
  3. If normal, repeat measurement at approx. every 5y.
  4. If abnormal, pursue intensive lifestyle modification therapy first.
105
Q

All pts hospitalized for an ASCVD event should have a lipid profile checked within …

A

24h.

106
Q

Do not routinely measure emerging risk factors (5):

A
  1. Lp(a).
  2. HsCRP.
  3. Apo B.
  4. LDL particle number.
  5. Other prothrombotic and proinflammatory factors.
107
Q

Management of TG disorders - Classification (4):

A

Normal <150.

Borderline high 150-199.

High 200-499.

Very high >500.

108
Q

TG disorders - Tx:

A
  1. Lifestyle = weight reduction, exercise, decr alcohol intake.
  2. Omega-3 + fibrates (= initial tx if TG >500).
109
Q

Low HDL is defined as …

A

<40.

110
Q

Most effective drug to increase HDL is …

A

Niacin.

BUT 2013 guidelines do NOT recommend niacin therapy.

==> Instead, statin tx should be used in pts with low HDL and an ASCVD risk >7.5%.

111
Q

The pharmacologic raising of HDL has …

A

NOT BEEN SHOWN TO REDUCE ASCVD EVENTS TO DATE.

Internal Medicine (107 decks)

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