Hyperlipidemia Flashcards

1
Q

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

A

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

Primary = patients with no history (asymptomatic dyslipidemia)

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2
Q

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

A

TC - <200, >240, >280

LDL - <100, >160, >190

Trigs - <150, >200, >500

*all mg/dL

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3
Q

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

A

No, No.

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4
Q

Describe the 4 major statin benefit groups

A

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

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5
Q

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

A

Atorvastatin 40-80mg
Rosuvastatin 20-40mg

Goal is to lower by 50% or more

Medium dose = high dose divided by 4

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6
Q

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

A

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
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7
Q

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

A

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
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8
Q

What is the MOA for statins?

A

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

Causes up regulation in cellular LDL receptors

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9
Q

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

A

PM dosing due to nightime cholesterol shit

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

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10
Q

How long do we wait to change doses for statins?

A

4 weeks.

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11
Q

What are the four cardinal adverse effects for statins?

A

Myalgia, Myopathy, *Rhabdo, Liver tox

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

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12
Q

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

A

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

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

CK - Increased risk person, signs and symptoms

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13
Q

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

A

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

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14
Q

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

A

Atorvastatin

Pitavastatin

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15
Q

All statins are highly _______ bound so they may displace ________

A

Protein

Warfarin (and other protein bound drugs)

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16
Q

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?

A

Absolutely not.

No, that is also an absolute contraindication.

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17
Q

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

A

It will. It increases risk of myopathy and rhabdo.

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18
Q

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

A

Gemfibrozil

19
Q

Niacin increases the risk of what with Statin patients?

A

Muscle shit and liver tox.

20
Q

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

A

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

21
Q

What are the Fibrates?

A

Gemfibrozil
FenoFIBRATE (prodrug)
FenoFIBRIC acied

22
Q

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

A

Muscle stuff if Gem + Statin (don’t)

Headache rash

No monitor… Only LFT if combined w/statin

23
Q

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

A

INR, fibrates make warfarin efficacy increased.

24
Q

What patients don’t get Fibrates?

A

Renal, Hep, Biliary disease patients

25
Q

Niacin is also called what? What does it do?

A

Nicotinic acid, Vitamin B3

Inhibit form/secretion of hepatic VLDL = decrease plasma LDL

26
Q

The main clinical effect of takin Niacin is what?

A

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

27
Q

What is the clinical use of Niacin

A

Pts who cannot take STATIN

Combo drug w/ statin or resin for **Heterozygous familial hypercholesterolemia

28
Q

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

A

Most common = Flushing

Liver tox, Hyperglycemia (no uncont DM pts), Hyperuricemia (gout etc…)

29
Q

What is the LFT monitoring schedule for Niacin?

A

Baseline, Q6-12 wks, yearly

30
Q

How does a Bile Acid Sequestrant work?

A

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

31
Q

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

A

Triglycerides.

32
Q

What are our Bile Acid Sequestrant agents?

A

Colistepol - preg B
Colesevelam - preg B
Cholestyramine - preg c

**all sound like chole

33
Q

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

A

GI, Decreased absroption of other shit

*Patients with eleveted TG

34
Q

Ezetimibe is what kind of drug?

A

Selective cholesterol absorption inhibitor

35
Q

How does ezetimibe work?

A

Inhibits absorption of cholesterol and phytosterol at the bush border of intestine..

*Effective even without dietary cholestol (inhibit reabsorption of bile cholesterol)

36
Q

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

A

Comparable to low intensity statin to LOWER LDL.

Used as adjunctive therapy, causes synergistic decrease of LDL 25% more.

37
Q

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

A

Take BAS 2 hours befor or 4 hours after.

38
Q

What is a PCSK9 inhibitor?

A

Inhibits binding PCSK9 to LDLR –> increased LDLR’s clear more LDL from blood.

39
Q

PCSK9 inhibitors are highly effective at lowering ________

A

LDL

40
Q

PCSK9 drugs include what 2 choices?

A

Alirocumab (q 2 wks)
Evolocumab (once monthly)

**cumab

41
Q

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

A

Nasopharyngitis
Injection site rxn
Influenza

42
Q

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

A

Unknown MOA, science stuff look it up.

Lowers TG, may raise LDL if TG is high

43
Q

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

A

Lovaza (preg C and bleeding)

Icosapent ethyl (only EPA)

Think bleeding with all + anticoag/antiplatelet

44
Q

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

A

Bulk forming laxative

LDL lowering ability

Flatulance and bloating