Exam 3: Lipid Lowering Agents Flashcards

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
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%+