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Pharm '14 test 2 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

Triglycerides serve what function in the body?

A

Essential energy source

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2
Q

Cholesterol is needed for what in the body?

A

Cell membrane structure, bile acid formation, steroid hormone synthesis

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3
Q

Hyperlipidemia can be..

A

Hypercholesterolemia

Hypertriglyceridemia

Elevated LDL

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4
Q

Physical exam findings in hyperlipidemia

A

Xanthelasma

Circumferential arcus

PVD

Thickened achilles

HTN

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5
Q

If not fasting for lab testing, which values should you pay attention to?

A

Only Total and HDL. If TC are over 200mg/dl or HDL<40, retest

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6
Q

Total cholesterol numbers

A

Good- 240 mg/dl

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7
Q

HDL numbers

A

Low- 60 (very good)

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8
Q

LDL numbers

A

Optimal- 190

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9
Q

Are numbers supposed to be important anymore?

A

No, should be focusing on RISK

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10
Q

What are the typical total cholesterol and TC in someone with primary hyperlipidemia?

A

Total >200, TC often >500

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11
Q

Causes of secondary hyperlipidemia

A 
DM
Hypothyroid
Obstructive liver disease
Chronic renal failure
Drugs such as progestins, corticosteroids, anabolic steroids
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12
Q

When should lipid screening start? When to re-screen?

A

All adults 20 and older. Every 4-6 years if numbers/risk normal.

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13
Q

A lipid screen should include which tests?

A

Total, LDL, HDL, TC, ALT, CK, HbA1c. Complete 10 year estimated ASCVD risk assessment.

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14
Q

What intervention should everyone receive, regardless of risk or numbers?

A

Therapeutic lifestyle changes. Reduce saturated fats/cholesterol, increase activity, control weight.

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15
Q

Diet effects on HDL

A

ETOH, saturated fats, and weight loss RAISE HDL

Low fat diet, sugar intake, excess calories, and excess polyunsaturated fats LOWER HDL

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16
Q

Diet effects on LDL

A

Saturated fat, trans fatty acids, and cholesterol RAISE LDL

MUFAs, complex carbs, and soy LOWER LDL

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17
Q

Diet effects on total cholesterol

A

Saturated fats and trans fatty acids RAISE total cholesterol

Substituting MUFAs and complex carbs for saturated fats, soy LOWER total cholesterol

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18
Q

Diet effects on TC

A

ETOH, sugar, high carb diet, excess calories RAISE TC

Weight loss, omega 3 fatty acids LOWER TC

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19
Q

Total fat recs

A

25-35%

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20
Q

Total carb recs

A

50-60%

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21
Q

Daily fiber recs

A

20-30 grams

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22
Q

Total protein recs

A

15%

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23
Q

Total daily cholesterol intake should be

A

less then 200mg

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24
Q

ASCVD risk factors

A

Gender, age, race, total cholesterol, HDL, systolic BP, treatment for BP, diabetes, smoker

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25
Q

What drug class is the focus of ASCVD prevention?

A

Statins

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26
Q

Name the four main categories established for statin therapy for secondary prevention of ASCVD

A

Clinical ASCVD

LDL >/= 190

Diabetes

> /= 7.5% estimated 10-yr ASCVD risk

27
Q

You would expect to see an LDL reduction of _____ in moderate intensity statin therapy

A

30-50%

28
Q

You would expect to see an LDL reduction of _____ in high intensity statin therapy

A

50% or greater

29
Q

What is the LDL level at which there is generally a reduction in ASCVD risk with statin therapy

A

LDL >70

30
Q

Primary agents and doses for low intensity statin therapy

A

Pravastatin 10-20mg

Lovastatin 20mg

31
Q

What reduction in LDL can be expected with low intensity statin therapy?

A

<30%

32
Q

What are the primary agents and doses for moderate intensity statin therapy?

A

Atorvastatin 40mg

Rosuvastatin 10mg

SImvastatin 20-40mg

Pravastatin 40mg

Lovastatin 40mg

Fluvastatin 40mg BID

33
Q

Which agents and doses are used in high intensity statin therapy?

A

Atorvastatin 80mg

Rosuvastatin 20mg

34
Q

How do statins work?

A

Inhibition of HMG-CoA reductase, which is the rate limiting enzyme is the formation of cholesterol

35
Q

What effect do statins have in general on lipid profile

A

Decrease LDL
Decrease TG
Increase HDL

36
Q

Statin therapy recs for clinical ASCVD

A

75 and under- high intensity statin therapy

Over 75 or unable to tolerate high intensity therapy- moderate intensity therapy

37
Q

In primary hyperlipidemia, a reduction in LDL of 39mg/dl results in ASCVD risk reduction by

A

~20%

38
Q

Statin therapy for primary hyperlipidemia is for patients with an LDL of

A

190 or more

39
Q

What is a secondary concern for patients with primary hyperlipidemia?

A

High TG level, which may require therapy in addition to statins

40
Q

When considering statin therapy for ASCVD risk reduction in diabetes, does the type (I or II) matter?

A

No, Type I or II treated the same for ASCVD risk

41
Q

Which level of therapy is acceptable for diabetics with an LDL greater than 190?

A

Moderate intensity therapy

42
Q

When is high intensity therapy needed in diabetes?

A

LDL greater than 190 and 10yr ASCVD risk > 7.5%

43
Q

When should a 10yr ASCVD risk assessment be completed?

A

In patients without ASCVD or DM with an LDL<190

44
Q

Why are statins so great?

A

They demonstrate substantial ASCVD risk reduction across all LDL levels, especially for those with high ASCVD risk

45
Q

What are some areas that need additional investigation in the new ASCVD risk reduction guidelines?

A
  • Other biomarkers to guide treatment
  • Best non-invasive imaging for risk assessment
  • Lifetime vs 10yr risk and optimal age to begin statins
  • Other subgroups such as HF, ESRD on HD, HIV, solid organ transplant, etc.
46
Q

What are the secondary treatment goals of the guidelines?

A

Treat TG >200 if LDL goal has been achieved

Treat low HDL (<40)

47
Q

Cholestyramin (Questran), Colestipol, and Colesevelam are all _____ and work by

A

Bile acid sequestrants

Bind bile acids in the intestines –> liver uses more hepatic cholesterol to produce bile –> decreased LDL and increase in HDL

48
Q

What effect does nicotinic acid have on blood lipoproteins?

A

Causes a reduction in the synthesis of VLDLs which results in decreased LDLs and TGs and an increase in HDLs

49
Q

Gemfibrozil (Lopid), Fenofibrate, and Clofibrate are all ________. How do these agents work?

A

Fibric acid derivatives

They reduce synthesis and increase the breakdown of VLDLs which results in decreased LDLs and TGs and an increase in HDLs

50
Q

How does Ezetimibe (Zetia) work?

A

Inhibits absorption of cholesterol and phytosterol at the brush border.

Has little effect on vitamin A,D,E, and K (fat soluble vitamins) or the CYP450 system.

Used in conjunction with a statin

51
Q

Statin plus Ezetimibe results in an LDL reduction of ______

Statin plus bile acid sequestrant results in an LDL reduction of ______

A

~25%

~8-16%

52
Q

Nasty risk associated with statin use

A

Myopathies

53
Q

Statin plus fibric acid derivative is used for _______, increases the risk of ________ and is contraindicated in _________.

A

decreasing TGs

myopathies

severe hepatic disease

54
Q

Statin+Niacin=

A

:-(

Also, increased risk of hepatic dysfunction

55
Q

Significant drug interactions with Lovastatin and Simvastatin

A 
Itraconazole (Sporanox)
Ketoconazole (Nizoral)
Erythromycin
Clarithromycin (Biaxin)
Gemfibrozil
Grapefruit juice
56
Q

Individuals at increased risk for statin induced myopathies

A 
>80
Small body frame
Frailty
Impaired renal/hepatic function
ETOH
57
Q

Drug combos with statins that increase myopathy risk

A 
Niacin
Gemfibrozil
Cyclosporin
HIV protease inhibitors
Verapamil
Amiodarone
58
Q

Currently the only lipoprotein lowering agent safe for use during pregnancy

A

Bile acid sequestrants

59
Q

In the future we’ll be using

A

Cholesteryl ester transfer protein inhibitors (CETP)

Exchanges lipoprotein particles in a reverse cholesterol transport process (Sounds pretty serious…)

Significant DROP in LDL along with a bump in HDL

Anacetrapib and Dalcetrapib are possible candidates

(Fun fact- Anacetrapib can stick around in the body for 4 years after cessation of therapy, kind of freaks some researchers out, but YOLO, right?)

60
Q

Another potential future therapy for altering lipoprotein profile is Eprotirome. Whats it do?

A

Thyroid hormone acts to mediate lipid lowering activity. Eprotirome is an analog of thyroid hormone.

Up to an additional 30% reduction in lipoproteins when added to statin therapy

(Apparently the company developing this drug pulled the plug a year ago due to really bad “unwanted effects after long term exposure”…why are we learning this crap?)

61
Q

Microsomal triglyceride transfer protein inhibitors, another possible future treatment, does what

A

Reduces the secretion of VLDL in the liver

Provides up to 50% reduction in plasma LDL levels

62
Q

Mipomersen, future therapy candidate, does what

A

May reduce plasma levels of lipoprotein A

Being tested in severe hypercholesterolemia and statin intolerant pts

63
Q

Take home message-
The focus should be on assessing a patient’s risk for Atherosclerotic Cardiovascular Disease and whether they fall into one of the four statin therapy groups, which are…..

A

Clinical ASCVD

LDL > 189

Individuals 40-75 with Diabetes and LDL 70-189 without ASCVD

Individuals 40-75 with Diabetes and LDL 70-189 and a 10-year ASCVD risk of 7.5% or higher

64
Q

What determines the intensity of statin therapy?

A

Presence of Clinical ASCVD

Risk of Developing ASCVD

Presence of Diabetes with/without hyperlipidemia

Presence of isolated hyperlipidemia (genetic component)

Pharm '14 test 2 (5 decks)

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