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Pharm Management of Dyslipidemia
Terms in this set (22)
Old ATP III guidelines targeted ___ to categorize patients according to risk.
LDL. This is no longer used due to lack of evidence. The benefit of statins was from appropriate INTENSITY, not from certain LDL levels.
How are ACC/AHA guidelines different from ATP III guidelines?
1. No more LDL goals.
2. New Pooled Cohort equation to replace Framingham risk score.
3. Four statin benefit groups (specific patient populations--determines intensity of statin needed)
4. Safety and monitoring
5. Non-statin therapies lack outcomes data--only used in specific cases
What are the 4 statin benefit groups?
1. Clinical ASCVD (coronary HD--ACS, MI, angina, coronary vascularization; Cerebral vascular disease--stroke or TIA that are ischemic; Peripheral vascular disease--PAD due to atherosclerosis)
2. LDL> or = 190 mg/dL
3. Age 40-75 with diabetes and LDL 70-189 mg/dL
4. Age 40-75 with LDL 70-189 mg/dL and 10-year ASCVD risk> or = 7.5%
I have diabetes and am 60 yo. What intensity statin should I be on?
MODERATE-intensity statin unless estimated 10 y ASCVD risk >7.5%--high-intensity statin.
What is the optima intensity of statin therapy for a 64 yo man with STEMI?
ASCVD and <75 yo
HIGH INTENSITY statin therapy for optimal risk reduction in those who tolerate it.
Moderate-intensity if >75 yo (OR if high-intensity statin isn't safe or tolerated)
What is the optimal intensity of statin therapy for a 36 yo woman with elevated LDL-C of 260 mg/dL, noted in teens and family history CHD?
LDL>190 mg/dL with secondary causes ruled out.
statin therapy for optimal risk reduction in those who can tolerate it.
(If LDL-C levels remain very high after intensity of statin therapy has been achieved, addition of a non-statin drug may be considered to lower LDL-C further (evidence is weak).)
What is the optimal intensity of statin therapy for a 52 yo woman with diabetes, well-controlled HTN and albuminuria with a 10 year ASCVD risk of <7.5%?
Diabetes, 40-75 yo, LDL-C 70-189 mg/dL.
High intensity if estimated 10-year ASCVD risk calculated >7.5%
I inhibit HMG-CoA reductase. What am I? What are the results?
Statin--prevents conversion of mevalonate preventing cholesterol synthesis. Primarily lowers LDL (lowers TGs and raises HDL)
Why are each of the statins different? How do you know which one to use?
Differ in POTENCY.
Differ in METABOLISM (drug-drug interaction)
Which 3 statins are responsible for drug-drug-interaction? Why?
Simvastatin, Atorvastatin, Lovastatin.
All use CYP450 3A4 as a metabolic pathway (majority of metabolism).
Risk of myopathy increases when coadministered with meds that inhibit their metabolism
Why do you take statins in the evening?
Cholesterol synthesis is HIGHEST in the evening
T/F: Statins have been linked to a moderate risk of developing diabetes.
NOT moderate--VERY SMALL RISK compared to benefits of the meds.
When should you consider decreasing a statin dose?
When 2 consecutive values of LDL-C are <40 mg/dL.
What are some basic risks of statins?
COntraindications: pregnancy and lactation; active/chronic liver disease
Gemfibrozil. What type of drug am I? How often should I be taken?
Fibrate. Decreases TGs by up-regulating liprotein lipase. Primarily reduces TGs. Reserved for patients with HIGH TGs despite lifestyle modifications. Unlike other fibrates, must dose TWICE daily and 30 min before food.
What is the mechanism of action of niacin?
Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation. Primarily increases HDL. LIMITED USE (risks>benefits)
I am on a non-statin drug that resulted in flushing.
What is the drug? How do you minimize the flushing?
Reduce flushing: Take food or aspirin 30 mins before administration; Nighttime administration; Slow-dose titration.
What is the only non-statin drug that affects exogenous production of cholesterol?
Ezetimibe (Zetia). INhibits intestinal absorption of exogenous cholesterol. Lowers LDL. Well tolerated. Contraindicated with active hepatic disease.
Does NOT affect cholesterol made by the liver.
What are some adverse side effects of Bile Acid sequestrates?
GI side effects
; Adverse drug reactions
What is the mechanism of action of fish oil?
Diminish synthesis of TGs in the liver and promote metabolism of TGs! Lowers TGs.
How do PCSK-9 inhibitors work? (may not need to know)
Monoclonal antibody that binds PCSK9. Decreases LDLR degradation, improves LDL-C clearance and lowers plasma LDL-C. Administered subq.
Recent cardiac events can falsely (lower/raise) lipids for up to 12 weeks after the event.
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