Hyperlipidemia Flashcards
Describe the difference between the secondary and primary prevention of CHD events (Stroke, MI, etc…)
Secondary = patients who have already had one and don’t want another one.
Primary = patients with no history (asymptomatic dyslipidemia)
What is a desirable, high, and very high Total cholesterol, LDL, and Triglyceride?
TC - <200, >240, >280
LDL - <100, >160, >190
Trigs - <150, >200, >500
*all mg/dL
Is routine initiation of statin therapy recommended in patients with class 2-4 heart failure? What about maintenence dialysis?
No, No.
Describe the 4 major statin benefit groups
Secondary prev
- Individuals with ASCVD (stroke, MI hx etc…)
* *High statin if <75, Medium if >75
Primary
- Individuals w/ LDL >190 (or equal)
* *High - 40-75 y/o w/ Diabeetus LDL 70-189
* *Moderate (high risk = high) - No DM or ASCVD hx w/ >7.5% risk LDL 70-189
**Moderate to high
Describe the two high intensity statins including goals for lowering LDL, dose, and possible medium dose.
Atorvastatin 40-80mg
Rosuvastatin 20-40mg
Goal is to lower by 50% or more
Medium dose = high dose divided by 4
Besides Atorvastatin and Rosuvastatin, list the moderate-intensity statins including dose and possible low dose. Also, what is the LDL goal.
LDL goal 30-50% reduction (med)
LDL goal <30% reduc for LOW
Simvastatin 20-40 mg --> 10 Pitavastatin 2-4 --> 1 Pravastatin 40-80 --> 10-20 Lovatatin 40 --> 20 Fluvastatin 40mg BID --> 20-40 Fluvastatin XL 80 --> no low
Describe the role of non statin therapies (with optimized statins) in each of the four catagories.
Use of non statins only if **Less than anticipated response (<50% LDL)
- ASCVD hx patient = Ezetimibe or PCSK9
- > 190 guy = Same as above
- 40-79 DM guy = Ezetimibe
- No ASCVD or DM guy w/ 70-189 = Same as 3
What is the MOA for statins?
Blocks HMG-COA reductase enzyme. A rate limiting step in cholesterol formation.
Causes up regulation in cellular LDL receptors
What time of day are statins given? Which ones are not?
PM dosing due to nightime cholesterol shit
Atorvastatin and rosuvastatin (high/meds) can be any time.
How long do we wait to change doses for statins?
4 weeks.
What are the four cardinal adverse effects for statins?
Myalgia, Myopathy, *Rhabdo, Liver tox
CK >10K or 10 times normal
LFT can raise 1.5 %
What is the schedule for statin monitoring of Fasting lipids, LFT, CK?
Fasting lipids - Base, 4-12 wks, 3-12 months
LFT - Base, 4-12 wks, signs and symptoms
CK - Increased risk person, signs and symptoms
What is the typical patient who is at increased risk of Statin induced myopathy
A *75+ year old *Asian *Woman who has *kidney and *liver dysfunction drinking a *Grapefruit *Cocktail
What two statins do not require dose adjustments for renal function (all others do)
Atorvastatin
Pitavastatin
All statins are highly _______ bound so they may displace ________
Protein
Warfarin (and other protein bound drugs)
You have a patient who is pregnant. She really wants statins. Is that cool? Also, she has acute liver disease… That makes it ok right?
Absolutely not.
No, that is also an absolute contraindication.
Your patient likes grapefruit and red yeast rice, this wont affect a statin right?
It will. It increases risk of myopathy and rhabdo.
Use of Statins with Fibric acid derivatives requires caution. Which one should never be used with statins?
Gemfibrozil
Niacin increases the risk of what with Statin patients?
Muscle shit and liver tox.
How does a Fibrate (Fibric Acid Derivative) work? What is it mainly used for?
Stimulate lipoprotein lipase to remove chylomicrons and VLDL from plasma
PPAR-a Agonist used to lower triglycerides
*can also be used if pt cant handle STATIN or w/ HIV
What are the Fibrates?
Gemfibrozil
FenoFIBRATE (prodrug)
FenoFIBRIC acied
What are the adverse affects of Fibrates? Do we monitor labs with these drugs?
Muscle stuff if Gem + Statin (don’t)
Headache rash
No monitor… Only LFT if combined w/statin
What must be monitored if we take a Fibrate and Warfarin?
INR, fibrates make warfarin efficacy increased.
What patients don’t get Fibrates?
Renal, Hep, Biliary disease patients
Niacin is also called what? What does it do?
Nicotinic acid, Vitamin B3
Inhibit form/secretion of hepatic VLDL = decrease plasma LDL
The main clinical effect of takin Niacin is what?
Increasing HDL…. But* it is comparable to low intensity Statin/Fibrate for LDL and TG
What is the clinical use of Niacin
Pts who cannot take STATIN
Combo drug w/ statin or resin for **Heterozygous familial hypercholesterolemia
What is the most common adverse effect of niacin? What are the other 3?
Most common = Flushing
Liver tox, Hyperglycemia (no uncont DM pts), Hyperuricemia (gout etc…)
What is the LFT monitoring schedule for Niacin?
Baseline, Q6-12 wks, yearly
How does a Bile Acid Sequestrant work?
“Anion exchange resin” binds bile acid and bile salt for excretion. Liver takes cholesterol from bloodstream to make more.
While BAS’s are comparable to low-intensity statin for lowering LDL, what may it increase?
Triglycerides.
What are our Bile Acid Sequestrant agents?
Colistepol - preg B
Colesevelam - preg B
Cholestyramine - preg c
**all sound like chole
What are the BAS adverse effects? Who doesn’t get these drugs?
GI, Decreased absroption of other shit
*Patients with eleveted TG
Ezetimibe is what kind of drug?
Selective cholesterol absorption inhibitor
How does ezetimibe work?
Inhibits absorption of cholesterol and phytosterol at the bush border of intestine..
*Effective even without dietary cholestol (inhibit reabsorption of bile cholesterol)
What is the clinical effect of Ezetimibe? Why would we use it?
Comparable to low intensity statin to LOWER LDL.
Used as adjunctive therapy, causes synergistic decrease of LDL 25% more.
If we take a Bile Acid Sequestrant, how long should we wait to take Ezetimibe?
Take BAS 2 hours befor or 4 hours after.
What is a PCSK9 inhibitor?
Inhibits binding PCSK9 to LDLR –> increased LDLR’s clear more LDL from blood.
PCSK9 inhibitors are highly effective at lowering ________
LDL
PCSK9 drugs include what 2 choices?
Alirocumab (q 2 wks)
Evolocumab (once monthly)
**cumab
PCSK9 inhibitors have a low side effect profile. What effects WILL you see?
Nasopharyngitis
Injection site rxn
Influenza
Omega 3s contain PUFAs… What is their mechanism of action and what do they do?
Unknown MOA, science stuff look it up.
Lowers TG, may raise LDL if TG is high
While Omega 3s are available OTC, what are the two precription options?
Lovaza (preg C and bleeding)
Icosapent ethyl (only EPA)
Think bleeding with all + anticoag/antiplatelet
Psyllium (metamucil) is a ________ that has some ________. What are its adverse affects?
Bulk forming laxative
LDL lowering ability
Flatulance and bloating
