dyslipidemia Flashcards

1
Q

secondary hyperlipidemia

A
Diabetes
Hypothyroidism
Obstructive liver disease
Chronic renal failure
(Live Real Happy Dude)
Drugs that increase LDL and decrease HDL (Progestins, corticosteroids, anabolic steroids)
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2
Q

lipid screening who when

A

Who to Screen?
All adults age 20 years and older
When to Screen/Re-evaluate?
Every 4-6 years

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3
Q

what to screen for lipids

A
Fasting lipoprotein profile
Total cholesterol
LDL cholesterol
HDL cholesterol
Triglycerides
ALT, CK, HbA1c
Estimated 10 year ASCVD Risk
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4
Q

primary prevention

A
**Therapeutic Lifestyle Changes (TLC)
Recommended for all patients regardless of their current state of health
Reduce saturated fats and cholesterol
Increase physical activity
Weight control
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5
Q

influence of diet

A

HDL: want “high” 40-60
Elevated by alcohol, saturated fats, weight loss
Lowered by low fat diet, sugar, excess calories, excess polyunsaturated fats
LDL: >100
Elevated by saturated fat, trans fatty acids, and dietary cholesterol
Lowered by MUFAs, complex carbohydrates, and soy
Total cholesterol: >200
Elevated by saturated fats and transfatty acids
Lowered by substituting MUFAs and complex carbohydrates for saturated fats; lowered by soy
Triglycerides:
Elevated by alcohol, sugar, high carbohydrate diet, and excess calories
Lowered by weight loss and fish oils

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6
Q

Assessing for atherosclerotic cardiovascular disease

A

History of coronary heart disease (CHD): Angina, Myocardial infarction, Coronary interventions (PTCA, Stents, CABG)
Peripheral Arterial Disease: Peripheral (extremity) arterial disease, symptomatic carotid artery disease, abdominal aortic aneurysm
Stroke/TIA

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7
Q

ASCVD risk assessment 11

A
Gender
Age
Race
Total Cholesterol
HDL-Cholesterol
Systolic Blood Pressure
Treatment for High Blood Pressure
Diabetes
Smoker
(Garths STD)
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8
Q

*4 main categories established for statin therapy for 2ndary prevention of ASCVD

A

clinidal ASCVD
LDL>190
DM
>7.5% estimated 10 yrs ASCVD risk

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9
Q

moderate intensity statin therapy

A

approx 30-50% reduction in LDL

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10
Q

high intensity statin therapy

A

approx >50% reduction in LDL

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11
Q

statin therapy in general

A

reduces risk of ASCVD across the spectrum for all those with LDL>70

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12
Q

low intensity statin therapy

A

approx <30% reduction in LDL

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13
Q

Statins MOA

A

Inhibit the rate-limiting enzyme in the formation of cholesterol.
inhibitors of HMG-CoA reductase
(HMG-CoA reductase normally catalyzes the conversion of HMG-CoA to mevalonate- part of the biosynthesis of cholesterol.)
Effect is to decrease LDLs, decrease TGs, and increase HDLs

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14
Q

Statin examples

A
Lovastatin (Mevacor)
Rosuvastatin (Crestor) 
Simvastatin (Zocor) 
Pravastatin (Pravachol)
Atorvastatin (Lipitor)
Fluvastatin (Lescol)
(L FRAPS)
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15
Q

statin therapy for clinical ASCVD age

A

< 75yo receive high-intesnity

> 75 or contraindications to high-intensity therapy should receive moderate

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16
Q

*Statin Therapy for Primary Hyperlipidemia

A

Patients with LDL ≥ 190
Reduction of LDL by 39mg/dl reduces ASCVD by approx 20%
May require additional use of non-statin lipid lowering agents to achieve acceptable lipid reduction
Assess need for addressing hypertriglyceridemia

17
Q

*DM and hyperlipid

A

patients 40-75 with either Type 1 or 2 DM and LDL < 190
Moderate-intensity therapy acceptable unless:
High-intensity therapy if 10yr ASCVD risk > 7.5%

18
Q

*10 year ASCVD risk >7.5%

A

For patients without ASCVD or Diabetes and an LDL < 190, a 10yr ASCVD Risk Assessment should be completed
if high risk Data supports statin therapy for primary prevention and substantial ASCVD risk-reduction

19
Q

*Lipoprotein lowering medications

A

Bile acid sequestrates
Nicotinic acid
Fibric acid derivatives
inhibiting cholesterol and phytosterol absorption

20
Q

*Bile acid sequestrates

A
  • Work by binding to the bile acids in the intestines, resulting in the liver having to use hepatic cholesterol to produce more bile acids. Effect is to decrease LDLs and increase HDLs
    Agents:
    Cholestyramine (Questran), Colestipol, Colesevelam
21
Q

*Nicotinic Acid

A
Works by reducing the production of VLDLs(precursor to LDL) Effect is to reduce LDLs, reduce TGs, and increase HDLs.
Nicotinic acid (Immediate-release, extended-release, and sustained-release or Niaspan)
22
Q

*Fabric acid derivatives

A
Fibrates reduce the synthesis and increase the breakdown of VLDLs. Effect is to reduce LDLs, decrease TGs, and increase HDLs.
Agents:
Gemfibrozil (Lopid)
Fenofibrate
Clofibrate
23
Q

*Ezetimibe (zetia)

A
  • Works by inhibiting cholesterol and phytosterol absorption from the brush border of the intestines.
    No effect on absorption of fat soluble vitamins:
    (A, D, E, K)
    No apparent effect on CYP450 enzymes
    Intended for use in combination with a statin
24
Q

combo therapy

A

statin and exetimibe: approx 25% reduction in LDL

Statin and Bile Acid: approx 8-16% reduction in LDL

25
Statin and Fibric acid derivatives
Primarily assist in decreasing triglycerides * Increased risk of myopathies * Contraindicated with severe hepatic disease
26
Statin and Niacin
increased risk of hepatic dysfunction
27
lovastatin and simvastatin drug interaction
``` Itraconazole (Sporanox) Ketoconazole (Nizoral) Erythromycin Clarithromycin (Biaxin) Gemfibrozil Grapefruit juice Niacin Cyclosporin HIV protease inhibitors Verapamil Amiodarone ```
28
Side effects of statins
``` Myopathies: Can occur with any statin Individuals at risk: Age > 80 Small body frame and frailty Impaired renal or hepatic system Alcohol abuse ```
29
drugs to avoid for pregnancy and nursing women
``` Statins Ezetimibe Niacin Fibric acid derivatives ***Bile acid-binding resins are currently the ONLY lipid-lowering medication safe to use during pregnancy ```
30
Cholesterol necessary for production of
cell membranes bile acids steroid hormones
31
total cholesterol levels
desirable 240
32
HDL level
40-60
33
LDL
<100 borderline high 130-159 high 160--189
34
primary hyperlipidemia
genetic heterozygous condition in elevated TC or TG TC>200 TG>500 familial hypercholesterolemia