Hyperlipidemia

Question 1

Describe the difference between the secondary and primary prevention of CHD events (Stroke, MI, etc…)

Answer 1

Secondary = patients who have already had one and don’t want another one.

Primary = patients with no history (asymptomatic dyslipidemia)

Question 2

What is a desirable, high, and very high Total cholesterol, LDL, and Triglyceride?

Answer 2

TC - <200, >240, >280

LDL - <100, >160, >190

Trigs - <150, >200, >500

*all mg/dL

Question 3

Is routine initiation of statin therapy recommended in patients with class 2-4 heart failure? What about maintenence dialysis?

Answer 3

No, No.

Question 4

Describe the 4 major statin benefit groups

Answer 4

Secondary prev

1. Individuals with ASCVD (stroke, MI hx etc…)
   * *High statin if <75, Medium if >75

Primary

1. Individuals w/ LDL >190 (or equal)
   * *High
2. 40-75 y/o w/ Diabeetus LDL 70-189
   * *Moderate (high risk = high)
3. No DM or ASCVD hx w/ >7.5% risk LDL 70-189

**Moderate to high

Question 5

Describe the two high intensity statins including goals for lowering LDL, dose, and possible medium dose.

Answer 5

Atorvastatin 40-80mg
Rosuvastatin 20-40mg

Goal is to lower by 50% or more

Medium dose = high dose divided by 4

Question 6

Besides Atorvastatin and Rosuvastatin, list the moderate-intensity statins including dose and possible low dose. Also, what is the LDL goal.

Answer 6

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

Question 7

Describe the role of non statin therapies (with optimized statins) in each of the four catagories.

Answer 7

Use of non statins only if **Less than anticipated response (<50% LDL)

1. ASCVD hx patient = Ezetimibe or PCSK9
2. > 190 guy = Same as above
3. 40-79 DM guy = Ezetimibe
4. No ASCVD or DM guy w/ 70-189 = Same as 3

Question 8

What is the MOA for statins?

Answer 8

Blocks HMG-COA reductase enzyme. A rate limiting step in cholesterol formation.

Causes up regulation in cellular LDL receptors

Question 9

What time of day are statins given? Which ones are not?

Answer 9

PM dosing due to nightime cholesterol shit

Atorvastatin and rosuvastatin (high/meds) can be any time.

Question 10

How long do we wait to change doses for statins?

Answer 10

4 weeks.

Question 11

What are the four cardinal adverse effects for statins?

Answer 11

Myalgia, Myopathy, *Rhabdo, Liver tox

CK >10K or 10 times normal
LFT can raise 1.5 %

Question 12

What is the schedule for statin monitoring of Fasting lipids, LFT, CK?

Answer 12

Fasting lipids - Base, 4-12 wks, 3-12 months

LFT - Base, 4-12 wks, signs and symptoms

CK - Increased risk person, signs and symptoms

Question 13

What is the typical patient who is at increased risk of Statin induced myopathy

Answer 13

A *75+ year old *Asian *Woman who has *kidney and *liver dysfunction drinking a *Grapefruit *Cocktail

Question 14

What two statins do not require dose adjustments for renal function (all others do)

Answer 14

Atorvastatin

Pitavastatin

Question 15

All statins are highly _______ bound so they may displace ________

Answer 15

Protein

Warfarin (and other protein bound drugs)

Question 16

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?

Answer 16

Absolutely not.

No, that is also an absolute contraindication.

Question 17

Your patient likes grapefruit and red yeast rice, this wont affect a statin right?

Answer 17

It will. It increases risk of myopathy and rhabdo.

Question 18

Use of Statins with Fibric acid derivatives requires caution. Which one should never be used with statins?

Answer 18

Gemfibrozil

Question 19

Niacin increases the risk of what with Statin patients?

Answer 19

Muscle shit and liver tox.

Question 20

How does a Fibrate (Fibric Acid Derivative) work? What is it mainly used for?

Answer 20

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

Question 21

What are the Fibrates?

Answer 21

Gemfibrozil
FenoFIBRATE (prodrug)
FenoFIBRIC acied

Question 22

What are the adverse affects of Fibrates? Do we monitor labs with these drugs?

Answer 22

Muscle stuff if Gem + Statin (don’t)

Headache rash

No monitor… Only LFT if combined w/statin

Question 23

What must be monitored if we take a Fibrate and Warfarin?

Answer 23

INR, fibrates make warfarin efficacy increased.

Question 24

What patients don’t get Fibrates?

Answer 24

Renal, Hep, Biliary disease patients

Question 25

Niacin is also called what? What does it do?

Answer 25

Nicotinic acid, Vitamin B3 Inhibit form/secretion of hepatic VLDL = decrease plasma LDL

Question 26

The main clinical effect of takin Niacin is what?

Answer 26

Increasing HDL.... But* it is comparable to low intensity Statin/Fibrate for LDL and TG

Question 27

What is the clinical use of Niacin

Answer 27

Pts who cannot take STATIN Combo drug w/ statin or resin for **Heterozygous familial hypercholesterolemia

Question 28

What is the most common adverse effect of niacin? What are the other 3?

Answer 28

Most common = Flushing Liver tox, Hyperglycemia (no uncont DM pts), Hyperuricemia (gout etc...)

Question 29

What is the LFT monitoring schedule for Niacin?

Answer 29

Baseline, Q6-12 wks, yearly

Question 30

How does a Bile Acid Sequestrant work?

Answer 30

"Anion exchange resin" binds bile acid and bile salt for excretion. Liver takes cholesterol from bloodstream to make more.

Question 31

While BAS's are comparable to low-intensity statin for lowering LDL, what may it increase?

Answer 31

Triglycerides.

Question 32

What are our Bile Acid Sequestrant agents?

Answer 32

Colistepol - preg B Colesevelam - preg B Cholestyramine - preg c **all sound like chole

Question 33

What are the BAS adverse effects? Who doesn't get these drugs?

Answer 33

GI, Decreased absroption of other shit *Patients with eleveted TG

Question 34

Ezetimibe is what kind of drug?

Answer 34

Selective cholesterol absorption inhibitor

Question 35

How does ezetimibe work?

Answer 35

Inhibits absorption of cholesterol and phytosterol at the bush border of intestine.. *Effective even without dietary cholestol (inhibit reabsorption of bile cholesterol)

Question 36

What is the clinical effect of Ezetimibe? Why would we use it?

Answer 36

Comparable to low intensity statin to LOWER LDL. Used as adjunctive therapy, causes synergistic decrease of LDL 25% more.

Question 37

If we take a Bile Acid Sequestrant, how long should we wait to take Ezetimibe?

Answer 37

Take BAS 2 hours befor or 4 hours after.

Question 38

What is a PCSK9 inhibitor?

Answer 38

Inhibits binding PCSK9 to LDLR --> increased LDLR's clear more LDL from blood.

Question 39

PCSK9 inhibitors are highly effective at lowering ________

Answer 39

LDL

Question 40

PCSK9 drugs include what 2 choices?

Answer 40

Alirocumab (q 2 wks) Evolocumab (once monthly) **cumab

Question 41

PCSK9 inhibitors have a low side effect profile. What effects WILL you see?

Answer 41

Nasopharyngitis Injection site rxn Influenza

Question 42

Omega 3s contain PUFAs... What is their mechanism of action and what do they do?

Answer 42

Unknown MOA, science stuff look it up. Lowers TG, may raise LDL if TG is high

Question 43

While Omega 3s are available OTC, what are the two precription options?

Answer 43

Lovaza (preg C and bleeding) Icosapent ethyl (only EPA) Think bleeding with all + anticoag/antiplatelet

Question 44

Psyllium (metamucil) is a ________ that has some ________. What are its adverse affects?

Answer 44

Bulk forming laxative LDL lowering ability Flatulance and bloating