Dyslipidemia Flashcards

1
Q

What percentage of death in men >65 y.o is attributed to CHD?

A

50%

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2
Q

What percentage of death in women >65 y.o. is attributed to CHD?

A

56%

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3
Q

Discuss the relationship of serum cholesterol levels to the risk of developing CHD.

A

They are directly proportional; the higher the serum cholesterol levels, the higher the risk of developing CHD.

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4
Q

What can cause your risk for hyperlipidemia to increase?

A
  1. Family history (genetics)
  2. Male >= 45, Female >= 55
  3. Diabetes Mellitus
  4. HTN
  5. diet
  6. exercise level
  7. Smoking
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5
Q

Values of Total Cholesterol

A

< 200 = Desirable

200-239 = Borderline High

> 240 = High

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6
Q

Values of LDL Cholesterol

A

< 100 = optimal

100-129 = near or above optimal

130-159 = borderline high

160-189 = high

> 190 = very high

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7
Q

Values of HDL Cholesterol

A

< 40 = Low

> 60 = High

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8
Q

Values of Triglycerides

A

< 150 = Normal

150-199 = Borderline High

200-499 = High

> 500 = Very High

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9
Q

Primary Prevention of Hyperlipidemia

A

measures targeted to prevent the onset of hyperlipidemia

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10
Q

Secondary Prevention of Hyperlipidemia

A

Identify and treat asymptomatic persons who have hyperlipidemia.

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11
Q

Tertiary Prevention of Hyperlipidemia

A

Minimize the effect of atheroslerosis to prevent disability and prevent complications.

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12
Q

Describe the patient population that has a greater risk for hyperlipidemia?

A

Patients with:

  • clinical ASCVD
  • LDL >= 189 mg/dL
  • diabetes (but without clinical ASCVD) and LDL at 70-189 mg/dL at age 40-75 years
  • LDL at 70-189 mg/dL with an estimated 10-yr risk of ASCVD of 7.5% or higher but without clinical ASCVD or diabetes
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13
Q

What does a calculated risk of 7.5% mean per ACC/AHA guidlines (the ramifications to those at increased risk for hyperlipidemia)?

A

A 10-year risk of 7.5% means that 7.5 out of 100 people with the same predisposing factors will develop atherosclerotic cardiovascular disease.

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14
Q

Atherosclerosis Pathophysiology

A
  • LDL in bloodstream invades blood vessel’s endothelium
  • LDL then accumulates in tunica intima
  • LDL is then oxidized
  • Macrophages phagocytosize oxidized LDL creating foam cells
  • Foam cells form fatty streak
  • collagen migrates over fatty streak, forming a fibrous plaque - rupture- platelet aggregation - thrombin generation-fibrin formation- thrombus and occlusion
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15
Q

According to NCEP, what are the major risk factors for CHD?

A

Current cigarette smoking

Hypertension (BP ≥ 140/90) or on antihypertensive medication

Low HDL (<40mg/dL)

FH of premature CHD (definite MI or sudden death) 1° male relative < 55 y/o, 1° female relative < 65 y/o

Age and Gender (male ≥ 45 y/o and female ≥ 55 y/o)

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16
Q

C-reactive protein (CRP) is a marker for what?

A

inflammation

(the higher the level of CRP, the higher the systemic inflammation and the higher risk for rupture of plaques built up in vessels)

17
Q

What are the serum levels of CRP and related risk for rupture of vascular plaques?

A

serum level risk

 \< 1 mg/l      good

 1-3 mg/l     moderate

 \> 3 mg/l     high risk
18
Q

Reason to initiate a high intensity statin therapy (Atorvastatin 80mg qd)

A

secondary prevention in adults >75

primary prevention in adults with LDLs > 190

primary prevention in adults 40-75 with LDLs 70-189 and estimated 10 yr risk >7.5%

primary prevention in pts with DM age 40-75 with LDLs 70-189 and estimated 10 risk >7.5%

19
Q

Reason to initiate Bile Acid Resin or Nicotinic Acid therapy

A

When LDL needs lowering, can begin with a BAR/Nictotinic Acid and then f/u 6 wks later to determine if tx is working

or

If start with a statin and LDL is not lowered enough at f/u, consider adding a BAR/nicotinic acid

20
Q
A