dyslipidemia Flashcards
secondary hyperlipidemia
Diabetes Hypothyroidism Obstructive liver disease Chronic renal failure (Live Real Happy Dude) Drugs that increase LDL and decrease HDL (Progestins, corticosteroids, anabolic steroids)
lipid screening who when
Who to Screen?
All adults age 20 years and older
When to Screen/Re-evaluate?
Every 4-6 years
what to screen for lipids
Fasting lipoprotein profile Total cholesterol LDL cholesterol HDL cholesterol Triglycerides ALT, CK, HbA1c Estimated 10 year ASCVD Risk
primary prevention
**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
influence of diet
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
Assessing for atherosclerotic cardiovascular disease
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
ASCVD risk assessment 11
Gender Age Race Total Cholesterol HDL-Cholesterol Systolic Blood Pressure Treatment for High Blood Pressure Diabetes Smoker (Garths STD)
*4 main categories established for statin therapy for 2ndary prevention of ASCVD
clinidal ASCVD
LDL>190
DM
>7.5% estimated 10 yrs ASCVD risk
moderate intensity statin therapy
approx 30-50% reduction in LDL
high intensity statin therapy
approx >50% reduction in LDL
statin therapy in general
reduces risk of ASCVD across the spectrum for all those with LDL>70
low intensity statin therapy
approx <30% reduction in LDL
Statins MOA
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
Statin examples
Lovastatin (Mevacor) Rosuvastatin (Crestor) Simvastatin (Zocor) Pravastatin (Pravachol) Atorvastatin (Lipitor) Fluvastatin (Lescol) (L FRAPS)
statin therapy for clinical ASCVD age
< 75yo receive high-intesnity
> 75 or contraindications to high-intensity therapy should receive moderate
*Statin Therapy for Primary Hyperlipidemia
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
*DM and hyperlipid
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%
*10 year ASCVD risk >7.5%
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
*Lipoprotein lowering medications
Bile acid sequestrates
Nicotinic acid
Fibric acid derivatives
inhibiting cholesterol and phytosterol absorption
*Bile acid sequestrates
- 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
*Nicotinic Acid
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)
*Fabric acid derivatives
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
*Ezetimibe (zetia)
- 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
combo therapy
statin and exetimibe: approx 25% reduction in LDL
Statin and Bile Acid: approx 8-16% reduction in LDL
Statin and Fibric acid derivatives
Primarily assist in decreasing triglycerides
- Increased risk of myopathies
- Contraindicated with severe hepatic disease
Statin and Niacin
increased risk of hepatic dysfunction
lovastatin and simvastatin drug interaction
Itraconazole (Sporanox) Ketoconazole (Nizoral) Erythromycin Clarithromycin (Biaxin) Gemfibrozil Grapefruit juice Niacin Cyclosporin HIV protease inhibitors Verapamil Amiodarone
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
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
Cholesterol necessary for production of
cell membranes
bile acids
steroid hormones
total cholesterol levels
desirable 240
HDL level
40-60
LDL
<100
borderline high 130-159
high 160–189
primary hyperlipidemia
genetic heterozygous condition in elevated TC or TG
TC>200
TG>500
familial hypercholesterolemia
