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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 3: Lipid Lowering Agents > Flashcards

Exam 3: Lipid Lowering Agents Flashcards

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1
Q

Cholesterol is necessary for production of:

A

Cell membranes, bile acids, and steroid hormones

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2
Q

Physical s/s of hyperlipidemia:

A 
Xanthelasma 
Circumferential arcus
PVD
Thickened Achilles
HTN
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3
Q

What is xanthelasma?

A

Nodules in the skin

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4
Q

What is circumferential arcus?

A

Lipid deposits around the iris

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5
Q

Lab tests for cholesterol that are reliable even if non-fasting:

A

Total cholesterol

HDL-cholesterol

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6
Q

Desirable/high total cholesterol levels:

A

Desirable < 200

High > 240

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7
Q

Low/high HDL levels:

A

Low < 40

High > 60

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8
Q

Range of LDL levels:

A

Optimal < 100
Very high > 190

Near optimal, borderline high, high in the middle - 30 pt ranges for each

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9
Q

Describe primary hyperlipidemia:

A

Genetic/inherited and heterozygous

TC > 200, trigs > 500

Aka familial hypercholesteremia

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10
Q

Causes of secondary hyperlipidemia:

A 
Diabetes
Hypothyroid
Obstructive liver disease
Chronic renal failure
Drugs (progestins, steroids)
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11
Q

Effects of ETOH use on lipids:

A

↑ TG, HDL

This is where the “a glass of wine with dinner is good for you” thought comes from!

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12
Q

Effects of HIV/AIDS wasting on lipids:

A

↑ TG

↓ TC, HDL, LDL

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13
Q

Effects of HIV/AIDS on HAART on lipids:

A

↑ TG, LDL, TG

Long-term effects of HAART can be deleterious

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14
Q

Effects of inactivity on lipids:

A

↓ HDL

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15
Q

Effects of obesity on lipids:

A

↑ TG, LDL

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16
Q

Who/when to screen lipids:

A

All adults 20yrs+

4-6 year intervals

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17
Q

What to include in lipid screening:

A 
TC, LDL, HDL, Trigs
ALT
CK
HbA1C
10 year ASCVD risk
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18
Q

Therapeutic lifestyle changes include:

A

↓ saturated fats, cholesterol
↑ physical activity
Weight control

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19
Q

Dietary influences on HDL:

A

HDL ↑ by alcohol, saturated fats, weight loss

HDL ↓ by low fat diets, sugar, excess calories/polyunsaturated fats

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20
Q

Dietary influences on LDL:

A

LDL ↑ by saturated fat, trans fatty acids, dietary cholesterol
LDL ↓ by monounsaturated fats, complex carbs, soy

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21
Q

Dietary influences on total cholesterol:

A

TC ↑ by saturated fats, trans fatty acids

TC ↓ by MUFAs, complex carbs, soy

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22
Q

Dietary influences on triglycerides:

A

TGs ↑ by ETOH, sugar, high carb diet, excess calories

TGs ↓ by weight loss, fish oil

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23
Q

History risk factors for ASCVD:

A 
Hx of coronary heart disease (angina, MI, coronary interventions)
PAD
CAD
AAA
Stroke/TIA
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24
Q

Demographic/comorbidity risk factors for ASCVD:

A

Gender, age, race
Cholesterol
Blood pressure
Diabetes/smoker

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25
Q

Four categories for preventative statin therapy:

A

Clinical ASCVD
LDL > 190
Diabetes
> 7.5% 10yr risk

26
Q

% LDL reduction from moderate intensity statin therapy:

A

30-50%

27
Q

% LDL reduction from high intensity statin therapy:

A

> 50% reduction

28
Q

Two drugs considered high-intensity statin therapy:

A

Atorvastatin 80mg

Rosuvastatin 20mg

29
Q

Statin class of drug:

A

HMG-CoA Reductase Inhibitors

30
Q

Statins MoA:

A

Inhibit the rate-limiting enzyme in formation of cholesterol to ↓ LDL, TGs and ↑ HDLs

31
Q

Statin guidelines for clinical ASCVD:

A

If < 75yo: high intensity statin

If > 75 or contraindications: moderate intensity

32
Q

Statins should be used for primary HLD if LDL ≥:

A

190

33
Q

Reduction of LDL by _____ decreases ASCVD by 20%.

A

39 mg/dl

34
Q

Statin guidelines for DM:

A

Moderate-intensity acceptable

High-intensity if 10yr risk > 7.5%

35
Q

10 year (vs. lifetime) ASCVD risk should be assessed for:

A

Patients without ASCVD/DM and LDL < 190 to determine if preventative statin tx will be useful

36
Q

Additional tx for triglycerides indicated when:

A

TG > 200 and LDL goal achieved

37
Q

Additional tx for HDL indicated when:

A

HDL < 40

38
Q

Bile sequestrant MoA:

A

Binds bile acid in the intestines so liver uses cholesterol to make more; ↓ LDL, ↑ HDL

39
Q

Examples of bile sequestrants:

A

Questran, Colestipol, Colesevelam

40
Q

S/E of bile sequestrants:

A

Oily stools

Low compliance d/t needing to mix powder in drink

41
Q

Nicotinic acid MoA:

A

Reduced production of VLDLs; effect is ↓ LDL, TG and ↑ HDL

42
Q

Examples of nicotinic acid:

A

Niaspan and generics

43
Q

S/E of nicotinic acid:

A

Flushing

44
Q

MoA of fibric acid derivatives:

A

Reduces the synthesis and increases breakdown of VLDLs

45
Q

Examples of fibric acid derivatives:

A

Gemfibrozil (Lopid)
Fenofibrate
Clifibrate

All have -fib-

46
Q

S/E of fibric acid derivatives:

A

Hard on the liver

47
Q

MoA of ezetimibe (Zetia):

A

Inhibits cholesterol/phytosterol aborption from brush border

48
Q

Ezetimibe effect on vitamin absorption and CYP450 enzomes:

A

None!

49
Q

Ezetimibe should be paired with:

A

A statin

50
Q

Statin + ezetimibe = LDL reduction of:

A

25%

51
Q

Statin + bile acid sequestrant = LDL reduction of:

A

8-16%

52
Q

Statin + fibric acid derivative primarily for:

A

Decreasing trigs

53
Q

Statin + fibric acid derivative risks and contraindication:

A

↑ risk of myopathies

C/I in severe hepatic disease

54
Q

Statin + niacin risk:

A

↑ risk of hepatic dysfunction

55
Q

Drug interactions with statins:

A 
Itraconazole/ketoconazole
Erythromycin
Clarithromycin
Gemfibrozil
Grapefruit juice
56
Q

Biggest s/e of statins:

A

Myopathies

57
Q

Relation of statin dose to myopathy incidence:

A

None - any statin, any dose

58
Q

Individuals at risk for statin myopathy:

A

Age > 80
Small body frame/frailty
Impaired renal/hepatic
ETOH abuse

59
Q

Drugs that ↑ risk of statin myopathy:

A 
Niacin
Gemfibrozil
Cyclosporin
HIV protease inhibitors
Verapamil
Amiodarone
60
Q

Lipid-lowering medications safe to use during pregnancy:

A

Only bile acid sequestrants!

61
Q

Four statin tx groups:

A

LDL > 189
Clinical ASCVD
40-75yo with DM, LDL > 70 without ASCVD
40-75yo with DM, LDL > 70, and 10-yr risk 7.5%+

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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