Cardiovascular Risk Reduction: Lipids Flashcards

1
Q

True or false: there is no evidence to support treating to a specific LDL or HDL target.

A

true

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2
Q

What are the four statin benefit groups? (people who benefit from statins)

A
  1. people with clinical CV disease
  2. People with LDL over 190
  3. People 40-75 yo with diabetes (even with normal LDL and no CV disease)
  4. People who have an estimated 10 yr CV disease risk over 7.5% (even without clinical CV disease or diabetes)
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3
Q

High intensity statin therapy will reduce LDL on average by what percent?

A

greater or equal to 50%

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4
Q

Moderate intensity statin therapy will reduce LDL by what?

A

30-50%

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5
Q

Low intensity statin therapy will reduce LDL by what?

A

less than 30%

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6
Q

What are the two high-intensity statin regimens?

A

Atorvastatin 40-80 mg

Rosuvastatin 20-40mg

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7
Q

What are some secondary causes of hyperipidemia?

A

diet (and alcohol)

drugs: diuretics, cyclosporine, steroids, amiodarone, estrogens, beta blockers, thiazides

biliary obstruction, nephrotic syndrome, chronic renal failure

hypothyroidism, pregnancy

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8
Q

What are the factors that go into calculating the CV risk status?

A

age, gender, blood pressure, diabetes, hypertension (treated or not) and smoking

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9
Q

In patients with diabetes, what intensity of statin therapy should you use?

A

moderate is recommended, but you should consider high-intensity if their CV disease risk is over 7.5%

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10
Q

In benefit group 4 (CV risk over 7.5% but no diabetes and normal ldl), what intensity of statin therapy should you use?

A

moderate or high

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11
Q

How often should you estimate someone’s CV risk if they’re not on a statin?

A

every 4-6 years

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12
Q

What are some patient characteristics that would make you think a patient may not be able to tolerate a high-intensity statin?

A
  1. medical comorbidities like liver and renal disease
  2. baseline ALT > 3x normal
  3. Age over 75
  4. on interacting drugs
  5. hx hemorrhagic stroke (IDK why)
  6. Asian ancestry (I assume it’s a metabolism thing)
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13
Q

What is the most complicated problem of statin safety?

A

myopathy (ranges from myalgia to rhabdomyolysis and renal failure)

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14
Q

Because of the risk of myopathy, should you routinely check a baseline CK?

A

no, but consider if they’re at risk for muscle disease (family hx of statin intolerance or muscle disease)

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15
Q

So when should you measure a CK then?

A

if they have symptoms develop (pain, stiffness, cramping, fatigue)

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16
Q

If the symptoms are mild to moderate, what other causes should you consider?

A
hypothyroid
PMR
steroid myopathy
Vit D deficiency
primary muscle disease
17
Q

True or false: if someone has a statin intolerance, you should never use the same statin again.

A

false - after symptoms resolve, you should rechallenge with the original or lower dose of the same statin to establish causality

then is symptoms recur, you should change to a different statin at a low dose

18
Q

You should get a baseline ALT before starting a statin, but do you need to routinely check it?

A

nope - not recommended unless the patient has symptoms suggesting hepatotoxicity (fatigue, loss of appetite, abdominal pain, dark urine, jaundice)

19
Q

True or false: statin use has been associated with a modest excess risk of new-onset diabetes in RCTs and meta-analyses.

A

true

but it’s confined to those with other risk factors

ultimately the small risk of DM outweight the potential ASCVD risk reduction

20
Q

True or false: there is evidence for memory impairment/confusion with statin use.

A

false - no proven link

21
Q

What are the three pharmacologic categories you can use in patients who can’t take a statin or didn’t respond adequately to a statin?

A

ezetimibe
bile acid sequestrants
PCSK-9 inhibitors

22
Q

How does ezetimibe work?

A

it modifies cholesterol absorption in small intestine

23
Q

Bile acid sequestrants can have an added benefit in what patient population?

A

diabetics

coleselavan has been shown to lower A1c by 0.5%

24
Q

What are the limiting factors for bile acid sequestrants

A

GI side effects and pill burden

25
Q

How do the PCSK-9 inhibitors work?

A

they’re monoclonal antibodies against PCSK-9, which increases LDL receptors/clearance

26
Q

What is the main drawback for the PCSK-9 inhibitors?

A

cost (13K/yr)