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Lab Medicine > Lipid Panel > Flashcards

Lipid Panel Flashcards

1
Q

Three major types of plasma lipids

A
  1. Cholesterol
  2. Triglycerides
  3. Phospholipids
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2
Q

This is the structural component of cell wall membranes. It is the precursor for the synthesis of steroid hormones and bile.

A

Cholesterol

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3
Q

___% of serum cholesterol is synthesized.

A

90%

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4
Q

___% of cholesterol ingested in absorbed.

A

40%

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5
Q

This is the main form of lipid storage in humans.

A

Triglycerides

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6
Q

Where do Triglycerides come from?

A

Calories ingested in a meal and not used immediately by tissues are converted to triglycerides and transported to fat cells to be stored.

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7
Q

Where do endogenous triglycerides come from?

A

Synthesized in the Liver

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8
Q

Where do exogenous triglycerides come from?

A

Dietary fat incorporated into chylomicron in the small intestine.

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9
Q

This is the term for lipid molecules that contain a phosphate group. They are a part of the cell wall membrane and act as donors of phosphate groups for intracellular metabolism and blood coagulation.

A

Phospholipids

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10
Q

Where do phospholipids come from?

A

Originate in the liver and intestinal mucosa

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11
Q

Triglycerides, Cholesterol, and Phospholipids bind with specialized proteins called _____________ to form _____________.

A

Apoproteins; Lipoproteins

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12
Q

Proteins are DENSER than lipids so the greater the composition of lipid within a lipoprotein, the ______ the density of the molecule .

A

Lower

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13
Q

Types of Lipoproteins

Plasma Lipids Bound to Apoproteins

A
  1. Chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
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14
Q

Composition of Chylomicrons

A

Mostly Triglycerides

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15
Q

Composition of VLDL

A

Mostly Triglycerides

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16
Q

Composition of IDL

A

Transitional Form

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17
Q

Composition of LDL

A

Major Carrier of Cholesterol
Makes up 60-70% of Total Cholesterol

Bad Cholesterol

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18
Q

Composition/Function of HDL

A

Makes up 25% of Total Cholesterol

Removes cholesterol from atherosclerotic plaques in arteries.

Good Cholesterol

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19
Q

VLDL and Chylomicrons compose ____% of Total Cholesterol

A

10-15%

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20
Q

People with high total cholesterol have approximately _____ the risk of heart disease as people with optimal levels.

A

Twice

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21
Q

The average total cholesterol level for adult Americans is about ____ mg/dL, which is borderline high risk .

A

200.

The goal is LESS than 200 mg/dL.

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22
Q

There is a ______ relationship between serum cholesterol levels and risk for coronary artery disease .

A

Positive.

Effective tx of Hyperlipidemia has been shown to reduce CV events, Stroke, and Mortality.

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23
Q

This is the term for lipid disorders that are precipitated by other disease states, medications, or lifestyle.

A

Secondary Lipid Disorders

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24
Q

This is the term for genetic defects in the synthesis or metabolism of the lipoproteins. It rarely occurs alone.

A

Primary Lipid Disorders

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25
Q

Diseases that cause Secondary Lipid Disorders

A
  1. Diabetes
  2. Thyroid Disorders
  3. Nephrotic Syndrome
  4. Liver Disease
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26
Q

Lifestyles that cause Secondary Lipid Disorders

A
  1. Obesity
  2. Sedentary
  3. Diet
  4. Smoking
  5. Alcohol
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27
Q

Common Drugs that can Cause Hyperlipidemia

A
  1. Beta Blockers
  2. Thiazide Diuretics
  3. Oral Contraceptives
  4. Steroids

Less Common:

  1. Protease Inhibitors
  2. Immunosuppressive Drugs
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28
Q

Beta Blockers can induce Hyperlipidemia by:

A

May increase TG and reduce HDL

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29
Q

Thiazide Diuretics can induce Hyperlipidemia by:

A

Increase Total Cholesterol, LDL, and TG

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30
Q

Oral Contraceptives can induce Hyperlipidemia by:

A

Increase TG

Effects of HDL and LDL are variable

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31
Q

Steroids can induce Hyperlipidemia by:

A

Increase LDL and TG

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32
Q

Protease Inhibitors can induce Hyperlipidemia by:

A

Increase TG

Decrease HDL

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33
Q

Immunosuppressive Drugs (Cyclosporine, Sirolimus) can induce Hyperlipidemia by:

A

Increase LDL and TG

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34
Q

Physical Exam Findings demonstrating Hyperlipidemia

A
  1. Xanthelasma
  2. Lipemia Retinalis
  3. Achilles Tendon Xanthomas/Thickening of Tendon
  4. Tendon Xanthomas elsewhere
  5. Tuberous Xanthomas
  6. Palmar Xanthomas
  7. Eruptive Xanthomas
35
Q

Total Serum Cholesterol for non-fasting patients 20+ years old:

A
  • Desirable: < 200
  • Borderline: 200-239
  • High: 240+
36
Q

Low Total Serum Cholesterol can be a sign of:

A
  • Hyperthyroidism
  • Malnutrition
  • Chronic Anemia
  • Cancer
  • Severe Liver Disease
37
Q

In all patient populations, lowering serum cholesterol ______ death from CAD and results in _______ of atherosclerotic lesions.

A

Decreases; Regression

38
Q

In young healthy adults, total serum cholesterol is a ______ predictor of clinically relevant CV events occurring 25 or more years later .

A

STRONG

39
Q

Range of HDL

A

40-60

< 40 = Low
> 60 = High

40
Q

For every 1% increase in HDL, what does that cause to CHD in men and women?

A
  • 2% CHD DECREASE in Men

- 3% CHD DECREASE in Women

41
Q

The LDL:HDL Ratio that would be indicative of atherogenic activity would be:

A

4:1 or higher.

Ideally it is less than 3:1, however thi s is NOT a primary target of treatment.

42
Q

T/F: High TG is usually seen with Low HDL

A

True

43
Q

Optimal LDL levels:

A

< 100

44
Q

LDL Levels

A

Near or Above Optimal: 100-129
Borderline High: 130-159
High: 160-189
Very High: 190+

45
Q

T/F: To measure LDL, TG, and HDL effectively, you must have the patient fasting before getting the Lipid Panel.

A

False, Only LDL and TG requires fasting. HDL does not.

However, we normally get the blood at the same time requiring fasting because of LDL and TG.

46
Q

How is LDL measured?

A

Total Serum Cholesterol - HDL - (TG+5)

*If TG is >400, you cannot calculate LDL

47
Q

Causes of Primary Hypertriglyceridemia:

A

Disorders of chylomicrons and VLDL

48
Q

Causes of Secondary Hypertriglyceridemia

A
  • Obesity
  • Uncontrolled DM
  • Liver Dz
  • Alcohol Ingestion
  • Uremia
49
Q

Grading TGs

A

Normal: < 150
Borderline: 150-199
High: 200-499
Very High: 500+

50
Q

What can Very High TG cause?

A
  1. Pancreatitis
  2. Hyperviscosity of the Blood
  3. Thrombus Formation
51
Q

T/F: Hypertriglyceridemia is an INDEPENDENT risk factor for CAD

A

True

Therefore, TG-rich Lipoproteins like Chylomicrons and VLDL are atherogenic.

52
Q

VLDL is estimated to be equal to:

A

TG + 5

53
Q

Non-HDL Goal is:

A

30 mg/dL higher than the LDL goal.

Reminder: LDL goal is < 100 mg/dL

54
Q

_____ cholesterol should be followed as a marker of atherosclerotic risk in all patients with triglycerides greater than 200 .

A

Non-HDL

55
Q

New information about Cholesterol, but no indications to follow these routinely…YET!

A
  • Size of LDL particles
  • Homocysteine Levels
  • Inflammatory Markers (CRP)
  • Thrombogenic Factors
56
Q

A fasting lipoprotein profile is recommended once every ___ years in all adults older than age 20. (Preferably in the absence of acute illness).

A

Five

57
Q

Why does my patient need to fast?

A

Food cause cause:

  1. Increase in TG by 50%
  2. Decrease in LDL of 10-15%
58
Q

What other things can affect lipid profiles/blood work?

A
  • Vigorous Physical Acitivity
  • Pregnancy
  • Recent Weight Loss
  • Acute Coronary Syndrome
59
Q

Guidelines for Screening Men

A
  • 35+

- 20-35 if they have increased risk for CHD

60
Q

Guidelines for Screening Women

A
  • 45+ if they have increased risk for CHD

- 20-45 if they have increased risk for CHD

61
Q

Guidelines for Young Men (<35) or Women WITHOUT Increased Risk of CHD.

A

Neither for or against it.

62
Q

Step-Wise Risk Evaluation:

A
  1. CHD or Equivalent?
  2. How many risk factors?
    - - HDL 60+ negated a positive risk factor
  3. Two or more risk factors? Calculate Framingham Risk Score
    - -> Framingham >20 = CHD Risk Equivalent
  4. Use NCEP Treatment Guidelines based on information gathered.
63
Q

What counts as CHD?

A
  • Angina
  • MI
  • Coronary Angioplasty
64
Q

What counts as CHD Risk Equivalents?

A
  • DM
  • PAD
  • TIA
  • Stroke
  • 10 year risk greater than 20%
65
Q

What counts as Risk Factors?

A
  • 45+ Male
  • 55+ Female
  • Family Hx of Premature CHD in first degree relatives. (< 40
66
Q

Non-Pharmacologic Treatment of Hyperlipidemia

A
  • Lifestyle Modifications are appropriate for ALL patients
  • Reducing Saturated Fat in Diet to < 7% of calories gives a LDL reduction of 8-10%
  • Reduction of dietary cholesterol to <200 mg/day provides an additional 3-5% reduction.
67
Q

T/F: For patients with zero or one major risk factor and serum LDL cholesterol concentrations between 160 and 189 mg/dL, six weeks of diet and exercise is recommended before lipid levels are reevaluated .

A

TRUE!

68
Q

This drug class:

  • Lowers total cholesterol and LDL.
  • It may increase HDL.
  • It may decrease TG
  • Maximum Effect seen after 4-6 weeks.
A

Statins

69
Q

How do statins work?

A

Inhibits the enzyme that catalyzes the rate-limiting step in cholesterol synthesis.

70
Q

When starting statins what do you NEED to do with LFTs? And what are you looking for?

A

LFTs before starting Statins
LFTs at 6 weeks post
LFTs at 12 weeks post
LFTs twice years after that.

Searching for AST or ALT rise 3x greater than baseline. If that happens STOP meds.

71
Q

When starting statins what do you NEED to do with CPK? And what are you looking for?

A

CPK before starting Statins
Routine Monitoring isn’t Indicated

If patient complains of myalgia or weakness, check CPK.

If 10x high, d/c drug.

72
Q

Facts about Statins:

A
  • Myalgia and Weakness = 2-7% of patients on statins
  • Myopathy occurs in 0.1-0.2% of patients on statins
  • Statins can lead to Rhabdo
73
Q

Benefits of Statins

A

Reduction in:

  • Major Coronary Events
  • CHD Deaths
  • Need for Coronary Procedures
  • Stroke
  • Total Mortality
74
Q

These statins are the most potent and affect LDL.

A

Rosuvastatin and Atorvastatin

75
Q

These statins are the second most potent and affect LDL.

A

Simvastatin and Pravastatin

76
Q

In a subtherapeutic response to a statin, what should you do?

A

Move to a more potent statin.

Doubling the statin will only produce about a 5% decrease in Total Cholesterol and a 7% decrease in LDL.

77
Q

This drug selectively inhibits the intestinal absorption of cholesterol. It is often used in combination with statins to further decrease LDL.

Sadly, it has higher incidences of elevated LFTs and GI Side Effects.

A

Ezetimibe

78
Q

These drugs bind with cholesterol-containing bile acids in the intestines and are then eliminated in the stool. They lower LDL by 15-30% buy can raise TG.

A

Bile Acid Sequestrants

  • Cholestyramine
  • Colesevalam
  • Colestipol
79
Q

When are Bile Acid Sequestrants not recommended? Contraindicated?

A

Not Recommended: >200

CI: > 400

80
Q

Bile Acid Sequestrants can interfere with absorption of fat soluble vitamins and some drugs, such as:

A
  • Digoxin
  • Thyroid Supplements
  • Coumadin
81
Q

This drug:

  • Decreases the Total Serum Cholesterol, LDL and TG.
  • Increases HDL
  • Increases Serum Glucose
  • Increases Serum Uric Acid
  • Increases LFTs
  • Can Decrease Serum T4

Has been shown to decrease mortality and incidence of coronary events.

A

Niacin

82
Q

Side Effects of Niacin:

A
  • Flushing
  • Itching
  • GI Distress
83
Q

These drugs:

  • Lower elevated TG (~20-50%) by increasing lipoprotein lipase activity
  • Increases HDL levels (10-20%) through peroxisome proliferator-activated receptor binding.
  • LDL changes are unpredictable
  • Can cause transaminase and CPK elevations
  • Will affect PT/INR
A

Fibric Acid Derivatives

  • Gemfibrozil
  • Fenofibrate
84
Q

These drugs:

  • Target TG
  • Increase HDL
  • Increase LDL
  • Antithrombic Potential, but studies have not shown significant changes in PT INR
A

Omega 3 Fatty Acids

Lab Medicine (7 decks)

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