Flashcards in Dyslipidemia Deck (16):
Total Cholesterol Goals
Less than 200mg/dl Optimal
200-240 Borderline High
>240 mg/dl High
*Not a target for therapy
Triglyceride Goals & Lifestyle Modifications
Less than 150mg/dl.
Treatment: Diet, exercise, weight loss of BMI >25, smoking cessation.
60 mg/dl- High
No specific goals for raising HDL-C
LDL Goals & Treatment
Goals: Less than two risk factors 160 mg/dl, 2 or more risk factors (Framingham score 10-20%) goal less than 130mg/dl. Frammingham 20% or CHD risk equivalents 25), Pharmacotherapy (i.e. statins, niacin, ezetimibe, bile acid sequestrants)
Goal is 30 points higher than LDL-C goal.
MOA reduces hepatic cholesterol synthesis and lowers intracellular cholesterol which stimulates the up-regulation of the LDL-C receptor and increases the uptake of non-HDL-C particles from systemic circulation.
Pleiotropic effects: improves endothelial function, inhibit platelet aggreation, decrease LDL oxidation, reduce vascular inflammation, stabilize plaques.
*the most drug interactions.
Monitoring check baseline lipids and again in 608 weeks. Periodically thereafter.
FDA removed LFT monitoring from statin labels in Feb 2012.
MOA: Inhibits the hepatic production of VLDL and consequently it's metabolite LDL-C
Role in therapy: consider adding onto a statin for LDL-C lowering.
Contraindications: 1)Active hepatic dz, 2) Active peptic ulcer dz
1. Flushing, can take ASA 30 min before
2. Elevated LFTs
3. Increased glucose levels
4. Induce hyperuricemia (avoid in gout pts)
MOA: Selective inhibitor of dietary and biliary cholesterol absorption
Only evidence showing outcomes was in a trial of CKD patients 17% reduction in major atherosclerotic events when COMBINED with simvastatin. Never alone has sone any benefit in real outcomes other than LDL lowering!
Use in therapy: third line agent.
Bile Acid Sequestrants
MOA: bind bile acide in intestines, decreasing biliary cholesterol absorption.
Contraindication: Complete biliary obstruction
ADRs, GI constipation, obstruction, etc.
Drug Interactions: can bind many drugs, decreasing absorption.
MOA: PPR-alpha activation, reduced hepatic secretion of VLDL, induction of lipoprotein lipase-mediated lipolysis and clearance of TG.
Clinical use: reserve for patients with high TG >400mg/dl. Clinical evidence for cardiac events seems stronger in Gemfibrozil group.
Sifnificant renal or hepatic dysfunction
In general well tolerated, most common ADR is GI upset.
*Renally CL--> needs dose adjustments!
Omega-3 Fatty acids
DHA and EPA- inhibit hepatic secretion of TG and promote metabolism of TG
Literature supports use of 3-15 g/day. Can initiate DHA and EPA at 1g/day to see TG lowering.
Risk Factors for Calculating LDL-C goal
HTN >140/90 or on therapy
Low HDL-C 60 serves as negative risk
Family Hx of premature CHD, first degree relative, male 45 male, >55 female
CHD Risk Equivalents
DM, PVD, AAA, CAD (TIA Or Stoke), Frammingham >20%
When to initiate drug therapy for dyslipidemia?
High Risk CHD: >100mg/dl
Moderately high risk: 2+ risk factors, frammingham 10-20%, >130mg/dl
Moderate risk, 2+ risk factors, frammingham 190 mg/dl.
Statin Drug Interactions
Cyclosporine: use pravastatin or rosuvastatin (5 mg/dl)
HIV Protease Inhibitors & HCV protease inhibitors- CI with simva or lovastatin
Preferred prava, pitava, or rosuvastatin (10mg/day limit)
Azole antifungals, Clarithromycing, Erythromycin- discontinue statin while on AF therapy or convert to pravastatin or rosuvastatin
Nefazodone: preferred pravastatin or rosuvastatin
Amiodarone: Limit statin doses, Lovastatin 40 mg/day, Simvastatin 20mg/dl or concert o prava or rosuvastatin.
Diltiazem/Verapamil: limite lova to 20mg, simvastatin to 10mg or convert to prava or rosuva
Grapefruit Juice: Limit to less than 1 quart daily. Assess for muscle pain.