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Endocrinology > Management of Hyperlipidemia > Flashcards

Management of Hyperlipidemia Flashcards

1
Q

Chylomicrons transport fats from where to where?

In the liver, chylomicrons release what? 2
What do they become then?

LDL then carries fat and cholesterol to where?

High-density lipoproteins (HDL) carry fat and cholesterol back where?

When oxidized what increases?
And what forms and what does this cause?

HDL cholesterol is able to go and remove cholesterol from where?

A

the intestinal mucosa to the liver

  1. triglycerides, some
  2. cholesterol and they become low-density liproproteins (LDL)

The body’s cell

back to the liver for excretion

LDL cholesterol increases, and
atheroma formation occurs in the walls of the arteries, which causes atherosclerosis

from the atheroma

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2
Q

Primary (Hereditary)
Causes of Dsylipidemia
3

A
  1. Familial Hypercholesterolemia
  2. Familial Combined Hyperlipidemia
  3. Dysbetalipoproteinemia
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3
Q

What is Familial Hypercholesterolemia?

What are they at high risk for?
4

A

Mutation in LDL receptor, they are absent or defective, resulting in unregulated synthesis of LDL

High risk for

  1. atherosclerosis,
  2. tendon xanthomas (75% of patients),
  3. tuberous xanthomas and
  4. xanthelasmas of eyes.
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4
Q

What is Familial Combined Hyperlipidemia?

A

Autosomal dominant

Increased secretions of VLDLs

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5
Q

What is Dysbetalipoproteinemia?

What does the defective substance usually play a role in?

Increased risk for what?
4

A

Results in apo E2, a binding-defective form of apoE

Usually plays important role in catabolism of chylomicron and VLDL

Increased risk for

  1. atherosclerosis,
  2. peripheral vascular disease
  3. Tuberous xanthomas,
  4. striae palmaris
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6
Q

What are Xanthomas?

Especially likely to be found on skin of patients with what?

A

Soft, yellow skin plaques or nodules that contain deposits of lipoproteins inside histiocytes

Hyperlipidemia

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7
Q

Secondary Causes
of hyperlipidemia?
10

A
  1. Most common cause in developed countries: sedentary lifestyle with excessive dietary intake of saturated fat, cholesterol, and trans fats
  2. Uncontrolled Type 2 DM /
  3. Metabolic Syndrome
  4. Hypothyroidism
  5. Liver Disease
  6. Renal Disease
  7. Corticosteroid Use
  8. Progestin Use
  9. Anabolic Steroid Use
  10. ETOH use / abuse
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8
Q

Metabolic Syndrome
Must meet 3 of the following criteria: 4

Two things that has to be under control to start streating cholesterol?

A
  1. Abdominal obesity (> 40 in men, > 35 in women)
  2. High triglyceride level (> 150)
  3. Low HDL (130/85 mmHg)
  4. Impaired Fasting Glucose level > 100

smoking and diabetes under control

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9
Q

Monounsaturated Effect on Cholesterol levels?

Polyunsaturated Effect on Cholesterol levels?

Saturated effect on cholesterol levels?

Trans fat effect on cholesterol levels?

A

Lowers LDL, Raises HDL

Lowers LDL, Raises HDL

Raises both

Raises LDL

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10
Q

Five major steps which serve as basis for treatment recommendations for hyperlipidemia:

A

1) Obtain fasting lipid profile
2) Identify if there are any CHD risk equivalents
3) Identify if there are major CHD risk factors other than LDL
4) If patient has a CHD risk equivalent, or has 2 or more risk factors (other than LDL), calculate 10 year risk of CHD
5) Determine the risk category, in order to establish the LDL goal, when to initiate therapeutic lifestyle changes, and when to consider drug therapy

  1. fasting lipid profile
  2. CHD risk equivalents
  3. major CHD risk factors other than LDL
  4. Calculate 10 year risk for CHD
  5. risk category
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11
Q

What is the primary and secondary prevention of CVD?

What are our risk equivalent disease? 2

A

Optimum treatment of lipids

Diabetes and any vascular disease

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12
Q

ATP III is based on epidemiologic observations that showed graded relationship between what two things?

A

the total cholesterol concentration and coronary risk

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13
Q

Step 1: Check Lipid Panel
ATP III Guidelines
Healthy adults with no risk factors?

A

Healthy adults, no risk factors – every 5 yrs starting at age 20

Obtain a fasting (9 to 12 hour) serum lipid profile consisting of total cholesterol, LDL, HDL and triglycerides

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14
Q

How do we calculate LDL?

A

LDL = TC – (HDL + TGs / 5)

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15
Q

If on a statin medication, recheck FLP how often and how would we adjust the statin?

A

every 6 wks and uptitrate statin to achieve LDL goal, then q 6 months once at goal

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16
Q 
Lipid Panel Goals
Total Cholesterol?
LDL (low density lipoprotein)?
HDL (high density lipoprotein)?
		in men
		in women
		is considered cardio protective
Triglycerides?
A 
TC- less than 200
LDL- less than 100
HDL
men- less than 40
women- less than 50
cardio protective is less than 60

TG- less than 150 is normal

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17
Q

Identify CHD Risk Equivalents:

5

A 
1. Diabetes
Other forms of clinical atherosclerotic disease
2. Clinical CHD
3. Abdominal Aortic Aneurysm
4. Peripheral arterial disease
5. Symptomatic carotid artery disease
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18
Q

Diabetes is a Risk Equivalent
Men with DM and risk factors?
Without?

Women with DM and risk factors?
Without?

Men or women of any age who have had DM (type I or II) for over how many years with risk factor?
Without?

A

Men over age 40 with type II DM and any other risk factor, or over age 50 with or without other CHD risk factors

Women over age 45 with type II DM and any other CHD risk factor, or over age 55 with or without other CHD risk factors

Men or women of any age who have had DM (type I or II) for over 20 years if they have another risk factor or more than 25 years without another risk factor

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19
Q

Determine Major Risk Factors (other than LDL)?

3

A
  1. Cigarette smoking
  2. HTN (BP > 140/90 mmHg or on antiHTN meds)
  3. Low HDL cholesterol (45 yrs; women >55 yrs)
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20
Q

Assessment of Risk
For persons without known CHD, other forms of atherosclerotic disease, or diabetes:
2

A
  1. Count the number of risk factors.

2. Use Framingham scoring for persons with ≥2 risk factors* to determine the absolute 10-year CHD risk.

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21
Q

Coronary heart disease (CHD) or CHD risk equivalent (10-year risk >20 percent):

LDL goal?

LDL level at which to initiate therapeutic lifestyle changes?

LDL level at which to consider drug therapy

A

LDL- less than100 mg/dL

Initiate therapy- greater than than 100 mg/dL

Drug therapy greater than 130 mg/dL; drug optional at 100 to 129 mg/dL

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22
Q

Determining risk factor:
2 or more risk factors
(10-year risk less than 20%)

LDL goal?

LDL level at which to initiate therapeutic lifestyle changes?

LDL level at which to consider drug therapy

A

LDL- less than130 mg/dL

Initiate therapy- greater than than 130 mg/dL

Drug therapy: 10-year risk 10 to 20 percent: >130 mg/dL 10-year risk less than 10 percent: >160 mg/dL

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23
Q

Determining risk factor:
0 to 1 risk factor
(10 year risk less than 10%)

LDL goal?

LDL level at which to initiate therapeutic lifestyle changes?

LDL level at which to consider drug therapy

A

LDL- less than 160 mg/dL

Initiate therapy- greater than than 160 mg/dL
Drug therapy: >190 mg/dL;

LDL-lowering drug optional at 160 to 189 mg/dL

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24
Q

Data subsequent to ATP-III
Secondary Prevention Recommendations?
4

A
  1. Intensive statin therapy in patients with acute coronary syndrome recommended as initial therapy
  2. Patients at very high risk (very high risk patients are defined on the next slide) for CHD events should be targeted for LDL below 70 (if unable to achieve with statin alone, second agent should be added)
  3. Usual risk patient with stable CHD unable to achieve LDL goal with statin alone should have second agent added
  4. If they do not tolerate a statin, they should be treated with another lipid-lowering agent
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25
Q

Who is at Very High Risk
for CHD Events?
4

A

Established coronary heart disease
PLUS
Multiple major risk factors (especially diabetes)

OR

Severe and poorly controlled risk factors (continued smoking)

OR

Multiple risk factors of metabolic syndrome (esp TGs> 200 plus non-HDL-C > 130 plus HDL

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26
Q

Remember….very high risk patients!

What should we do?

A

More intensive lipid lowering therapy
LDL below 70 mg/dL
!!!!!!!!!!

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27
Q

After Categorizing Patient
What should we do? 2

What is treating pts with hyerlipidemia based on? 2

A
  1. Initiate Therapeutic Lifestyle Changes (TLC) alone
    OR
  2. TLC and drug therapy
    —The decision to treat hyperlipidemia with drug therapy is based on LDL levels
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28
Q

What are statins?

A

HMG-CoA Reductase Inhibitors

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29
Q

Statins are excellent agents at lowering what?
4

What does it increase?

A

lowering

  1. LDL
  2. cholesterol and decreasing associated
  3. TGs
  4. morbidity and mortality rates for primary and secondary prevention of CAD

HDL

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30
Q

What should our HDL to LDL ratio be?

A

1 to 4

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31
Q

The Statins

7

A
  1. Rosuvastatin (Crestor)
  2. Atorvastatin (Lipitor)
  3. Simvastatin (Zocor)
  4. Lovastatin (Mevacor)
  5. Pravastatin (Pravachol)
  6. Fluvastatin (Lescol)
  7. Simvastatin/Ezetimibe Combo (Vytorin)
32
Q
  1. MOA of Statin Medications
  2. What does it lead to an increase in?
  3. What is more greatly taken up by the liver?
  4. How does this affect LDL in the blood stream?
  5. Is HDL affected?
  6. Low density lipoprotein receptors are also involved with the uptake of what?
    What does this lead to an decrease in?
A
  1. Blocks the conversion of HMG-CoA to mevalonate, which is the rate limiting step in the production of cholesterol in the liver ( the first statin is called Mevacor)
  2. Leads to an increase in the number of LDL receptors in the liver
  3. Larger amounts of LDL cholesterol is taken up by the liver and digested, thereby
  4. decreasing the amount of LDL in the bloodstream
  5. It usually tends to increase
  6. VLDL and IDL
    This leads to a decrease in triglyceride levels
33
Q

What are main
side effects of Statins?
7

A
  1. Hepatotoxicity
  2. Myalgias
  3. Myopathy
  4. Myositis
  5. GI Upset
  6. Headache
  7. Asymptomatic elevation in LFTs
    - They should be checked at baseline, at 6-12 weeks after starting or titrating, and every 6 months after
34
Q

Statin Contraindications?

4

A
  1. Pregnant women
  2. Patient with active / chronic liver disease
  3. Patient with unexplained elevated aminotransferase levels (ALT’s)
  4. CAUTION in patient who consume large amounts of alcohol or a history of liver disease
35
Q

Statins and Myopathy

  1. Check ____ if patient complains of myalgias
  2. Definition of myalgias?
  3. Definition of myopathy?
A

CPK
pain
more breakdown

36
Q

If myopathy occurs with statins what should we do?

A

Change statin and rechallenge

37
Q

When rhabdomyolysis occurs what should we do?

2

A
  1. stop statin use,

2. begin IV fluid hydration to prevent renal failure – usually CKs > 15,000 to cause ARF

38
Q

Meds that increase statin myopathy:

7

A
  • gemfibrozil
  • clarithryomycin
  • verapamil
  • erythromycin
  • amiodarone
  • ketoconazole
  • protease inhibitors
39
Q
  1. Statins and Liver Issues
    Generally well tolerated but some experience elevation in what?
  2. What is it dependant on?
  3. How can it be reversed?
  4. How can we fix this?
  5. When should we stop statin?
A
    • liver transaminases (0.5 – 2.0% of pts)
    • Are dose dependent
    • Usually reversed with lower doses
    • Can change statin and rechallenge
    • Stop statin if LTFs > 3 times baseline
40
Q

Statins and Liver Issues teach pts to report what?
4

When should we monitor LFTs?
4

A
  1. jaundice,
  2. malaise,
  3. fatigue,
  4. lethargy

Monitor LFTs

  1. prior to statin initiation,
  2. at 3 months,
  3. 6 months,
  4. then every year
41
Q

Statins and Renal Issues:

What are they most specific to?

What are we testing? 2

A

Most specific to Rosuvastatin (Crestor)

- Cr at baseline	
- Renal function monitored at dose of 40 mg
42
Q

Take statins in evening or bedtime

- Exception?

A

Atorvastatin

43
Q

What’s the difference in the statins:

  1. All statins have what?
  2. Which are more effective at lowering TG? 2
  3. Which is more effective in raising HDL? 1
A
    • -All statins have an anti-inflammatory effect
    • -All are more potent by 10-15% with evening dosing

Despite same MOA, there are differences between the agents, including their ability to lower cholesterol

  1. Per UpToDate, Atorvastatin and Rosuvastatin have more effective ability to lower TGs
  2. Per UpToDate, Rosuvastatin is more effective in raising HDL-C than atorvastatin, simvastatin, or pravastatin
44
Q

Atorvastatin (Lipitor)

has good effects on what?

A

Lowers LDL 47-65%
Raises HDL 2-9%
Lowers triglycerides 20%

TG

45
Q

Rosuvastatin (Crestor)
has good effects on what?
2

A

Lowers LDL 39-60%
Raises HDL 5-9%
Lowers triglycerides 19-35%

TG
HDL

46
Q

Lovastatin (Mevacor)

compared to the others?

A

Lowers LDL 24-28%
Raises HDL 7%
Lowers triglycerides 10-14%

Not as good

47
Q

Pravastatin (Pravachol)

Compared to other?

A

Lowers LDL 22-34%
Raises HDL 2-12%
Lower triglycerides 11-24%

Not as good

48
Q

Simvastatin (Zocor)

compared to others?

A

Lowers LDL 30-40%
Raises HDL 5-7%
Lowers Triglicerides 10-30%

Still commonly used

49
Q

Elevated transaminases on statins (unless reaching 3x normal) are a reason or not a reason to stop a statin?

Statin side effects are often agent or class specific?

Unexplained myalgias may occur on statins without CK elevation. What should we do?

A

not

Agent

Try a different statin

50
Q

Rhabdomyolysis is uncommon unless what?

A

CK is elevated to 10 x normal. Usually occurs in patients with multiple co-morbidities.

51
Q

Bile Acid Resins MOA?
(what pathway and what do they bind to?)

What does this do to cholesterol return?

Are they absorbed in the Gi tract?

A
  1. Decrease cholesterol absorption through exogenous pathway
  2. These agents bind bile acids in the intestines, forming an insoluble complex that is excreted in the feces

This decreases the return of cholesterol to the liver.

NO

52
Q

How does your body respond to BAR?

What does this process interrupt?
this can cause an increase in what?

A

Body responds by increasing LDL receptors on the liver, which in turn decreases the amount of LDL cholesterol level in the bloodstream

This process interrupts enterohepatic recirculation of bile acids and affects enzyme systems – which can cause an increase in TGs

53
Q

Bile Acid Resins:

What kind of therapy is it commonly used for?
Pregnancy cat?

Max effects seen when?

Effects are related to what?

Taken with or without food?

A

Adjunct therapy

Safe in pregnancy and pediatrics

Maximum effects are seen in approx 3 weeks

Effects are dose related

Should be taken with meals
Meds should be taken at least 1 hr before or 4 hours after the bile acid resin

54
Q

Bile Acid Resin – Side Effects 4

Which one is less likely to cause GI effects?

A 
Use is often limited by side effects
1. Nausea, 
2. bloating, 
3. cramping
4. Increase in liver enzymes
Colesevalam is better – less likely to cause GI effects
55
Q

Bile Acid Resins
2

Which one has better numbers?

A
  1. Cholestyramine (Questran)
    Lowers LDL 15-30%
    Raises HDL 3-5%
    Lowers triglycerides 0-15%
  2. Colestipol (Colstid)
    Lowers LDL 12-25%
    Raises HDL 0-1%
    Triglycerides 0-24%
56
Q

What is Niacin?

Can improve cholesterol levels when used at doses how many times the recommended daily dose?

What kind of effects on LDL?
HDL?
TG?

A

Naturally occurring B vitamin (B3)
(BEST DRUG TO INCREASE HDL)

100-300 times

Lowers LDL 15-25%
Raises HDL 35%
Lowers triglycerides 50%

57
Q

MOA for Niacin?

A

Uncertain

Appears to decrease VLDL synthesis in liver and increase lipoprotein lipase activity

58
Q

Absolute Contraindications for Niacin?

2

A
  • Hepatic dysfunction

- Severe gout

59
Q

Relative Contraindications for niacin?

3

A
  • Peptic ulcer disease
  • Gout - can elevate uric acid levels
  • Diabetes - can worsen glucose control
60
Q

Niacin side effects? 7

What might help certain side effects? 2

A
  1. Increased prostaglandin activity leading to pruritis and flushing to the face and neck
    A dose of ASA taken 30 - 60 minutes before the Niacin may help
    Niaspan, an extended release, may help
  2. Hepatotoxicity – monitor LFTs
  3. Uric acid and
  4. glucose increases – get baseline labs
  5. Orthostatic hypotension
  6. Dyspepsia,
  7. GI side effects
61
Q

Cholesterol Absorption Inhibitors
1

MOA:

  1. Where does it act?
  2. What does it inhibit and what does this lead to?
  3. What does it cause a reduction of and an increase of?
  4. This mechanism is complementary to that of the what?
A

Ezetimibe (Zetia)

  1. Appears to act at the brush border of the small intestine
  2. Inhibits the absorption of cholesterol leading to a decrease in the delivery of intestinal cholesterol to the liver
  3. Causes a reduction of hepatic cholesterol store and an increase in clearance of cholesterol from the blood
  4. This mechanism is complementary to that of the STATINS
62
Q

Cholesterol Absorption Inhibitors
affects on LDL used on mono therapy?
In combination with statin?

Contraindications?2

Side effects? 3

A

Lowers LDL up to 18% (monotherapy)
Lowers LDL up to 35% with a statin

Contraindications
If used with a statin
1. Active hepatic disease
2. Elevated ALT’s

Side effects
Headache
Diarrhea
Abdominal pain

63
Q

Fibric Acid Derivatives
2 drugs?

Not considered a major class of lipid-lowering drugs because of what?

What is it good for?

What should be monitored?

A

Gemfibrozil (Lopid)- can cause rhabo!- dont use it
Fenofibrate (Tricor, Trilipix)

they have minimal effect on LDL.

Good for lowering triglycerides

LFT’s need to be monitored

64
Q

Fibric Acids / Fibrates MOA?

Affect on TGs?
Affect on HDL?
Affect on LDL?

A

Unclear
Principal effect of triglyceride lowering appears to result from the stimulation of lipoprotein lipase, which enhances the breakdown of VLDL to LDL
May inhibit hepatic VLDL production and triglyceride synthesis

Lower triglycerides up to 60%
Raise HDL up to 30%
Lowers LDL up to 20% (Tricor most effective at LDL reduction)

65
Q

Fibric Acid Derivatives
Contraindications?3
Adverse affects?6

A

Contraindications

  1. History of gallstones
  2. Severe hepatic or
  3. renal dysfunction
Adverse effects
1. GI related
2. Myopathy chance increased if taken with statins
3. Jaundice
4. Increases the effects of 
Warfarin
5. Gallstones
6. Hepatotoxicity
66
Q

Hypertriglyceridemia
Borderline levels and treatment?
HIgh levels and treatment?

A

Borderline (150-199 mg/dL): calorie restriction and exercise

High (>200 mg/dL): diet and medications

67
Q 
Hypertriglyceridema Therapy
Diet? 4
Limit what? 4
Supplement? 1
Pharm? 4
A
  1. Low fat diet /
  2. calorie restriction /
  3. increase fiber
  4. Exercise

Limit

  1. alcohol,
  2. simple sugars,
  3. refined starches,
  4. saturated and trans fatty acids

Omega 3 fatty acid (Lovaza) – fish oil:
2 – 4g/day recommended; higher dose can increase LDL

Pharm therapy with

  1. niacin,
  2. fibric acid derivative,
  3. lovaza, or
  4. statins
68
Q

Fish Oil Supplementation (Omega-3):

Limited by what?

FDA approval is limited to what?
why?

A

Use is often limited by metabolic and gastrointestinal side effects

The commercial preparation Lovaza, which has been available for many years in Europe and is now also available in the United States, is 90 percent omega-3 fatty acids.

US FDA limited approval for Lovaza to the treatment of severe hypertriglyceridemia (>500) because of concerns that it appears to increase LDL levels

69
Q

a

A

a

70
Q

Possible Benefits From Other Therapies. What are they?

4

A
  1. Soluble fiber in diet (2–8 g/d) (oat bran, fruit, and vegetables)
  2. Soy protein (20–30 g/d)
  3. Stanol esters (1.5–4 g/d) (inhibit cholesterol absorption)
  4. Fish oils (3–9 g/d)
    (n-3 fatty acids)
71
Q

Diabetes:
Remember, DM is considered what?

CARE trial and Heart Protection Study found significant improvement in outcomes with what?

A

Remember, DM is considered a CHD equivalent

CARE trial and Heart Protection Study found significant improvement in outcomes with statin therapy even at LDL-cholesterol values below 116 (Goal for LDL is less than 70)

72
Q

ACC/AHA: 4 Statin Benefit Groups Identified

A
  1. Patients with clinical atherosclerotic disease
  2. Patients with LDL > 190 (typically pt with FH)
  3. Patients with diabetes 40-75 yo with LDL levels of 70 – 189 and without evidence of ASCVD
  4. Patients without evidence of ASCVD or DM but who have LDL levels of 70 – 189 and a 10-year risk of ASCVD > 7.5%
73
Q

Statins reduce risk of what by 20%? 2

HOw should we think of statins as providers?
2

A

CV disease and stroke by about 20%, regardles of baseline lipid profile

  1. Think of statins as risk-reduction meds the same way we consider aspirin
  2. No longer treating to a target LDL level; we are treating to lower risk
74
Q

Why should we choose the lowest dosage that will get you the biggest LDL reduction?

A

Since statin harm is dose related

75
Q

In hyperlipidemia what should be the order of importance in treatment? 3

A

get LDLs down
Get HDLs up
Get TGs down

Endocrinology (23 decks)

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