Exam 3: Lipid Lowering Agents Flashcards Preview

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Flashcards in Exam 3: Lipid Lowering Agents Deck (61):
1

Cholesterol is necessary for production of:

Cell membranes, bile acids, and steroid hormones

2

Physical s/s of hyperlipidemia:

Xanthelasma
Circumferential arcus
PVD
Thickened Achilles
HTN

3

What is xanthelasma?

Nodules in the skin

4

What is circumferential arcus?

Lipid deposits around the iris

5

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

Total cholesterol
HDL-cholesterol

6

Desirable/high total cholesterol levels:

Desirable < 200
High > 240

7

Low/high HDL levels:

Low < 40
High > 60

8

Range of LDL levels:

Optimal < 100
Very high > 190

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

9

Describe primary hyperlipidemia:

Genetic/inherited and heterozygous

TC > 200, trigs > 500

Aka familial hypercholesteremia

10

Causes of secondary hyperlipidemia:

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

11

Effects of ETOH use on lipids:

↑ TG, HDL

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

12

Effects of HIV/AIDS wasting on lipids:

↑ TG
↓ TC, HDL, LDL

13

Effects of HIV/AIDS on HAART on lipids:

↑ TG, LDL, TG

Long-term effects of HAART can be deleterious

14

Effects of inactivity on lipids:

↓ HDL

15

Effects of obesity on lipids:

↑ TG, LDL

16

Who/when to screen lipids:

All adults 20yrs+
4-6 year intervals

17

What to include in lipid screening:

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

18

Therapeutic lifestyle changes include:

↓ saturated fats, cholesterol
↑ physical activity
Weight control

19

Dietary influences on HDL:

HDL ↑ by alcohol, saturated fats, weight loss
HDL ↓ by low fat diets, sugar, excess calories/polyunsaturated fats

20

Dietary influences on LDL:

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

21

Dietary influences on total cholesterol:

TC ↑ by saturated fats, trans fatty acids
TC ↓ by MUFAs, complex carbs, soy

22

Dietary influences on triglycerides:

TGs ↑ by ETOH, sugar, high carb diet, excess calories
TGs ↓ by weight loss, fish oil

23

History risk factors for ASCVD:

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

24

Demographic/comorbidity risk factors for ASCVD:

Gender, age, race
Cholesterol
Blood pressure
Diabetes/smoker

25

Four categories for preventative statin therapy:

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

26

% LDL reduction from moderate intensity statin therapy:

30-50%

27

% LDL reduction from high intensity statin therapy:

> 50% reduction

28

Two drugs considered high-intensity statin therapy:

Atorvastatin 80mg
Rosuvastatin 20mg

29

Statin class of drug:

HMG-CoA Reductase Inhibitors

30

Statins MoA:

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

31

Statin guidelines for clinical ASCVD:

If < 75yo: high intensity statin
If > 75 or contraindications: moderate intensity

32

Statins should be used for primary HLD if LDL ≥:

190

33

Reduction of LDL by _____ decreases ASCVD by 20%.

39 mg/dl

34

Statin guidelines for DM:

Moderate-intensity acceptable
High-intensity if 10yr risk > 7.5%

35

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

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

36

Additional tx for triglycerides indicated when:

TG > 200 and LDL goal achieved

37

Additional tx for HDL indicated when:

HDL < 40

38

Bile sequestrant MoA:

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

39

Examples of bile sequestrants:

Questran, Colestipol, Colesevelam

40

S/E of bile sequestrants:

Oily stools
Low compliance d/t needing to mix powder in drink

41

Nicotinic acid MoA:

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

42

Examples of nicotinic acid:

Niaspan and generics

43

S/E of nicotinic acid:

Flushing

44

MoA of fibric acid derivatives:

Reduces the synthesis and increases breakdown of VLDLs

45

Examples of fibric acid derivatives:

Gemfibrozil (Lopid)
Fenofibrate
Clifibrate

All have -fib-

46

S/E of fibric acid derivatives:

Hard on the liver

47

MoA of ezetimibe (Zetia):

Inhibits cholesterol/phytosterol aborption from brush border

48

Ezetimibe effect on vitamin absorption and CYP450 enzomes:

None!

49

Ezetimibe should be paired with:

A statin

50

Statin + ezetimibe = LDL reduction of:

25%

51

Statin + bile acid sequestrant = LDL reduction of:

8-16%

52

Statin + fibric acid derivative primarily for:

Decreasing trigs

53

Statin + fibric acid derivative risks and contraindication:

↑ risk of myopathies
C/I in severe hepatic disease

54

Statin + niacin risk:

↑ risk of hepatic dysfunction

55

Drug interactions with statins:

Itraconazole/ketoconazole
Erythromycin
Clarithromycin
Gemfibrozil
Grapefruit juice

56

Biggest s/e of statins:

Myopathies

57

Relation of statin dose to myopathy incidence:

None - any statin, any dose

58

Individuals at risk for statin myopathy:

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

59

Drugs that ↑ risk of statin myopathy:

Niacin
Gemfibrozil
Cyclosporin
HIV protease inhibitors
Verapamil
Amiodarone

60

Lipid-lowering medications safe to use during pregnancy:

Only bile acid sequestrants!

61

Four statin tx groups:

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