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Therapeutics I > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What is dyslipidemia?

A

Presence of one or more of the following:
1. Elevation in total cholesterol
2. Elevation in LDL cholesterol
3. Elevation in triglycerides
4. Low HDL cholesterol

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2
Q

What are the main plasma lipids?

A

Cholesterol, triglycerides, and phospholipids

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3
Q

What is the function of plasma lipids?

A
  1. Essential for cell membrane
  2. Hormone synthesis
  3. Source of free fatty acids
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4
Q

What are the classes of lipoproteins?

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

What is total cholesterol?

A
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6
Q

What is the function of chylomicrons and VLDL?

A

Deliver energy rich triacylglycerol (TAG) to cells in the body -> free fatty acids and monoglycerides

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7
Q

What is the function of just LDL?

A

LDL delivers cholesterol to cells → cholesterol is used in membranes or for the synthe sis of steroid hormones

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8
Q

What is the function of HDL?

A

HDL brings back excess cholesterol to the liver (reverse cholesterol transport)

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9
Q

What are the apolipoprotiens that can be used as lab values?

A

ApoLp(a) and B-100

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10
Q

What are the effects and outcomes of DLD?

A
  1. Excess LDL → atherosclerosis
  2. Excess TG → pancreatitis
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11
Q

What is the function of ApoLp(a)? Where is it located?

A

LDL, HDL

Bound to B100 preventing LDL uptake by B and E receptor

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12
Q

What are the normal functions of vascular endothelium?

A
  1. Control of vascular tone
  2. Maintenance of an antithrombotic surface
  3. Control of inflammatory cell adhesions and diapedesis
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13
Q

What is the function of B100? Where is it located?

A

VDLD, LDL, IDL

Necessary for assembly and secretion of VLVL from the liver

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14
Q

What happens if there is a disruption of vascular endothelium?

A
  1. Inappropriate constriction
  2. Luminal thrombus formation
  3. Abnormal interactions between blood cells (monocytes and platelets)
  4. Activated vascular endothelium
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15
Q

What is an atherosclerotic plaque?

A

Subintimal collections of fat, smooth muscle cells, fibroblasts and intracellular matrix

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16
Q

What is the impact of having atherosclerotic plaques?

A

→ stenosis or rupture → CVD, MI, stroke, PVD, abdominal aortic aneurysm, death

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17
Q

What are the requirements for there to be stenosis?

A
  1. 50% diameter reduction → limitation in ability to meet increased demand
  2. 80% reduction → reduced flow at rest or minimal stress
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18
Q

What is desirable total cholesterol level? High?

A

<200 mg/dL (<5.17 mmol/L)

≥240

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19
Q

What is the optimal LDL level? Very high?

A

<100 mg/dL (<2.59 mmol/L)

≥190

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20
Q

What is considered low HDL? High?

A

<40 mg/dL (<1.03 mmol/L)

≥60

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21
Q

What is considered normal TG levels?

A

<150 mg/dL (<1.70 mmol/L)

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22
Q

What is considered very high TG levels?

A

≥500 mg/dL (≥5.65 mmol/L)

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23
Q

What are clinical signs of heterozygote familial hypercholesterolemia?

A

Development of xanthomas as an adult and vascular disease at 30-50 years

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24
Q

What are clinical signs of homozygote familial hypercholesterolemia?

A

Development of xanthomas as adults and vascular disease in childhood

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25
Q

What are the secondary causes of hypercholesterolemia?

A
  1. Hypothyroidism
  2. Obstructive liver disease
  3. Nephrotic syndrome
  4. Anorexia nervosa
  5. Acute intermittent porphyria
  6. Drugs
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26
Q

What are drugs that can cause secondary hypercholesterolemia?

A
  1. Beta blocker
  2. Immunosuppresants (PI, cyclosporine, mirtazapine, sirolimus)
  3. GC
  4. Progestin
  5. Thiazide
  6. Isotretinoin
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27
Q

What are the clinical signs of familial LPL deficiency?

A

Pancreatisits

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28
Q

What drugs can elevate TG?

A
  1. Alcohol
  2. Estrogens
  3. Isotretinoin
  4. Beta blockers
  5. GC
  6. Bile acid resins
  7. Thiazides
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29
Q

What are the causes of lower HDL? Drugs?

A
  1. Malnutrition
  2. Obesity

Non-ISA beta blockers
Anabolic steroids
Probucol
Isotretinoin
Progestins

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30
Q

What are causes of hypocholesterolemia?

A
  1. Malnutrition
  2. Malabsorption
  3. Myeloproliferative diseases
  4. Chronic infectious diseases (AIDS, TB)
  5. Monoclonal gammopathy
  6. Chronic liver disease
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31
Q

How should we measure LDL-C and Non-HDL-C

A
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32
Q

How do you use the Friedewald equation?

A

LDL-C = (TC) – (triglycerides /5) – (HDL-C)

Not accurate when TG are over 400 or LDL <70

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33
Q

How do you use martin/hopkins equation

A

LDL-C = TC – HDL-C – TG/novel factor

Not accurate when TG are over 400

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34
Q

What are the biomarkers of measuring cholesterol?

A
  1. apoB
  2. Lp(a)
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35
Q

When is apoB used?

A

HyperTG (>200)

> 130 is LDL (≥160)

Expensive and unreliable

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36
Q

When is Lp(a) used?

A

For family and personal hx of premature ASCVD not explained by major risk factors

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37
Q

Why are some cormobidities of lipid abnormality?

A
  1. CVD
  2. Secondary causes
  3. Xanthomas
  4. DM
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38
Q

What are atherosclerosis risk factors?

A
  1. Older age >40
  2. Cigarette smoking
  3. DM
  4. DLD (Increased LDL, low HDL)
  5. HTN
  6. Hyperhomosysteinemia
  7. CKD
  8. CHF
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39
Q

What are ASCVD events?

A
  1. Acute coronary disease (ACS)
  2. MI
  3. Stable/unstable angina
  4. Coronary or revascularization (catheter)
  5. Stroke/transient ischemic attack (TIA)
  6. Peripheral arterial disease (PAD)
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40
Q

The ASCVD risk estimator ____ South Asians while it ____ East Asians

A

underestimate; overestimate

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41
Q

What are ASCVD risk categories?

A

Low: <5%
Borderline: 5-7.4%
Intermediate: 7.5-19.9%
High: ≥20%

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42
Q

What are the clinical presentations of metabolic syndrome?

A
  1. Low HDL
  2. High TG
  3. Visceral obesity
  4. Insulin resistance
  5. HTN
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43
Q

What are the ASCVD prevention groups?

A
  1. Secondary prevention
  2. Severe hypercholesterolemia
  3. DM in adults
  4. Primary prevention
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44
Q

What is secondary ASCVD?

A

Already had a health incident related to atherosclerosis

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45
Q

How falls in secondary prevention?

A

ASCVD risk

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46
Q

What do you always suggest before treating ASCVD?

A

Non-pharm

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47
Q

How do you treat secondary prevention if patients aren’t at high risk?

48
Q

What is the LDL goal for secondary prevention?

49
Q

How do you treat secondary prevention if patients are at high risk?

50
Q

What is considered high risk ASCVD?

A

2 ASCVD events or 1 event and high risk conditions

51
Q

What are the numbers for severe hypercholesterolemia?

52
Q

What the is schedule for treating severe HCA? When is a PCSK9 used?

53
Q

How do we treat secondary prevention in patients with DM?

54
Q

What are DM-specific risk enhancers for ASCVD?

A
  1. ≥10 yr of DMT2 or ≥20 DMT1
  2. Albuminuria (≥30)
  3. GFR <60
  4. Retinopathy
  5. Neuropathy
  6. ABI <0.9
55
Q

What is the LDL goal in DM secondary prevention?

56
Q

What is primary ASCVD?

A

Prevent any occurrence of disease?

57
Q

How do you treat primary prevention based on ASCVD events?

58
Q

How do you treat primary prevention based on age?

59
Q

What are the ASCVD risk enhancers for primary prevention?

A
  1. Family hx of ASCVD
  2. LDL ≥160
  3. CKD
  4. Metabolic syndrome
  5. Women
  6. Inflammatory disease
  7. Ethnicity factors
60
Q

What is coronary artery calcium?

A

Scan measuring the amount of calcium in the wall of the coronary arteries using a specialized x-ray machine

Deposits with plaque buildup

61
Q

What is the scoring for CAC?

A

CAC score of 0 = low ASCVD 10-year risk (w/o cancelling high risk comorbidities)

CAC score of ≥ 100 = 10-year risk of ASCVD ≥ 7.5%

62
Q

What is primary prevention in older adults

A
  1. 75+ with LDL of 70-189 → moderate intensity statin
  2. 75+ reasonable to stop stain if risk outweighs benefits
  3. 76-80 with LDL of 70-189 → measure CAC (avoid statin if score is 0)
63
Q

What is primary prevention for young adults?

A

Teach them how to eat healthy

Eliminate risk factors

Be aware of elevations

64
Q

When should you screen for primary prevention?

A
  1. familial hx of genetic dyslipidemia or early CVD
  2. Obesity or metabolic risk
  3. screened once between ages 9-11 and then again between 17-21 years
65
Q

What do you do when abnormalities are contributed to obesity? Genetics?

A

Intense lifestyle therapy

Statin initiation

66
Q

What should ASCVD diets consist of? Exclusions?

A

Veggies, fruit, whole grains, fiber, low fat dairy, protein, veggie oils

Sweets, sugary beverages, red meats, saturated fats and cholesterol

67
Q

What type of diet is associated with HLD?

68
Q

Exercise rec?

A

150 min/week

69
Q

Statin contraindications?

A

Pregnancy and nursing

70
Q

High intensity statins? Dosing?

A

Atorvastatin (Lipitor): 40, 80 mg
Rosuvastatin (Crestor): 20, 40 mg

71
Q

Moderate intensity statins? Dosing?

A

Atorvastatin (Lipitor): 10, 20
Rosuvastatin (Crestor): 5, 10
Simvastatin (Zocor): 20-40
Pravastatin (Pravachol): 40, 80
Lovastatin (Mevachor): 40, 80
Fluvastatin (Lescol): 40 BID

72
Q

Low intensity statin? Dosing?

A

Pravastatin (Pravachol): 10-20
Lovastatin (Mevachor): 20

73
Q

What are the t1/2 of high intensity statins?

A

Crestor: 19hr
Lipitor: 14hr

74
Q

What statins are metabolized by CYP3A4?

A
  1. Atorvastatin
  2. Fluvastatin (minor)
  3. Lovastatin
  4. Simvastatin
75
Q

What statins are metabolized by CYP2C9?

A
  1. Fluvastatin
  2. Pitavastatin
  3. Rosuvastatin
76
Q

What are DDIs of statins?

A

Fenofibrate (less ADR) < Gemfibrozil (rhabdomyolysis)

77
Q

Equivalence of Atovstatin:Rosuvastatin

78
Q

What is 1st line for all patients with DLD?

79
Q

What statins can be doses at anytime?

A
  1. Atorvastatin
  2. Fluvastatin XL
  3. Pitavastatin
  4. Rosuvastatin
80
Q

Why are most statins given at night?

A

Maximum LDL-C reduction

81
Q

Short t1/2 statins?

A

Fluvastatin, Lovastatin, Pravastatin, Simvastatin

82
Q

What are the major enzymes that metabolize statins?

A

CYP3A4, 2C9

83
Q

What populations have no sensitivity to statins?

A

Hispanic, AA

84
Q

How do Asians respond to statins?

A
  1. Higher rosuvastatin plasma levels are seen in Japanese, Chinese, Malay, and Asian Indians as compared with whites → lowering of dose
  2. Japanese may be sensitive to statins
  3. Caution with titrating up
85
Q

What are the non stain classes?

A
  1. Zetia
  2. BAS
  3. PCSK9 Inhibitors and Inclisiran
  4. Bempedoic Acid
86
Q

What is the second line agent of DLD?

A

Ezetimibe (Zetia)

87
Q

Effect and ADRs of Zetia?

A
  1. LDL and TG reduction
  2. HDL raise

Mild GI complaints like diarrhea

88
Q

BAS effect? ADRs? CI?

A
  1. LDL reduction
  2. HDL and TG raise
  3. Colesevelam is for DMT2 to reduce AIC

Constipation and nausea

TG>300

89
Q

What is the first line agent for pregnancy?

90
Q

Counseling point of BAS?

A
  1. binding of other medications → separate administration
    1 hr before or 4 hrs after
  2. Take w/ food
91
Q

PCSK9? Effects? ADRs? Dosing?

A

Alirocumab (Praluent), Evolocumab (Repatha)

LDL reduction

Flu-like symptoms (decrease by room temp before use)

Expensive (Not first line for insurance); Bi-weekly or once a month

92
Q

What is Inclisiran?

A

Leqvio is a siRNA that reduces the production of PCSK9 by inhibiting mRNA

LDL reduction

Add on to statin, SQ injection

93
Q

What are effects and ADRs of bempendoic acid?

A

Modest LDL reduction

Hyperuricemia and tendon rupture

94
Q

What are the populations at risk for DLD?

A
  1. Ethnicity
  2. HyperTG
  3. Women
  4. CKD
  5. Chronic inflammatory disorders and HIV
95
Q

Asian with ASCVD, Lipid, Metabolic Issues?

A

South asia have increased risk

Lower levels of HDL, and higher LDL and TG prevalence

Increased MetA with lower waist circumference

96
Q

Hispanic with ASCVD, Lipid, Metabolic Issues?

A

Women have low HDL
DM is disproportionally present

97
Q

AA with ASCVD, Lipid, Metabolic Issues?

A

Women increases ASCVD risk

High levels of HDL and low TG

Increased DM and HTN

98
Q

What is the difference between moderate and severe hyperTG?

A

Moderate: Excess TG are carried in VLDL
Severe: Elevated VLDL plus chylomicrons

99
Q

How do you treat hyperTG?

A
  1. 20 or older with hyperTG → lifestyle factors, secondary factors, medications
  2. 4-75 moderate and ASCVD 7.5% or higher → favoring initiation or intensification of statin therapy
  3. 40-75 sev
  4. severe and ASCVD 7.5% or higher → statin therapy
  5. Fasting TG ≥1000 → non pharm and vibrate therapy
100
Q

How should women be treated with DKD?

A
  1. No statins for pregnancy
  2. Stop statins 1-2 months before pregnancy is attempted
101
Q

CKD recommendations of DLD?

102
Q

CKD that is considered elevated risk of ASCVD?

A

Reduced eGFR (<60)
Presence of albuminuria ≥30

103
Q

What is the treatment for chronic inflammatory disorders and HIV?

A

Lifestyle improvements should be tried for 3-6 months after diagnosis

104
Q

What are statin alternatives?

A
  1. Niacin
  2. Fibrates
  3. Omega 3
  4. Lomitapide
  5. Mipomersen
105
Q

Niacin effects? ADRs? Counseling points?

A

LDL and TG decrease, HDL increase

GI intolerance, flushing/itching, lab abnormalities

Use of aspirin, taking with meals, and slowly titrating the dose upward may minimize flushing/itching

106
Q

Fibrate effects? ADRs?

A

Decrease TG and LDL, Raises HDL

Dose adjustment for renal dysfunction

Gallstones, bleeding risk

107
Q

Omega 3 effects?

A

Lower TG, raise LDL and HDL

108
Q

Vascepa vs Lovaza?

A

Viscera supports CV risk reduction

109
Q

ADR of Omega 3?

A

Fishy burps, Increased bleeding with anti-platelets and coags

110
Q

Lomitapidide?

A

Only for HoFH → REMS due to hepatotoxicity

111
Q

Mipomersen?

A

Only for HoFH → REMS due to hepatotoxicity

112
Q

When to monitor efficacy?

A
  1. Follow up about 3-6 months after lifestyle therapy modifications
  2. Follow up about 4-12 weeks after pharmacologic therapy initiation or titration
  3. Once stable, monitoring is done every 6 months to a year
113
Q

Lab monitoring of DLD toxicity?

A
  1. LFTs
  2. Glucose
  3. CBC/BMP
  4. CK
114
Q

Last line for Primary DLD?

A
  1. Partial ileal bypass
  2. Portocaval shunts
  3. Plasma exchange
  4. LDL-apheresis
  5. Liver transplantation

Therapeutics I (32 decks)

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