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Cardio MT2 > MT2_2_Dyslipidemia_Pharmacologic Therapy > Flashcards

MT2_2_Dyslipidemia_Pharmacologic Therapy Flashcards

1
Q

Total Cholesterol Values

A

Normal: less than 200
Borderline: 200-239
High: greater than 240

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2
Q

TG Levels

A

Normal: less than 150
Borderline: 150-199
High: 200-499
Very High: greater than 500

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3
Q

LDL Levels

A 
Optimal: less than 100
Near/Above Optimal: 100-129
Borderline: 130-159
High: 160-189
Very High: greater than 190
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4
Q

HDL Levels

A

Low: less than 40
High: greater than 60

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5
Q

What are the main mechanisms of lipids?

A
  • they stabilize high risk lesions, preserves endothelial function, and controls inflammation
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6
Q

Meds that induce dyslipidemia?

A 
diuretics
cyclosporine
taco
amio
steroids
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7
Q

Meds that induce hypertriglyceridemia?

A 
estrogen
steroids
bile acid resins
protease inhibitors
propofol
sirolimus
BB
atypical antipsychotics
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8
Q

Cholesterol Equation

A

o LDL= TC – (HDL+ TG/5) fyi vldl = tg/5

o Non-HDL = TC – (HDL + TG/5)

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9
Q 
What are fibrates good for?
BARs?
Fish Oil?
PCSK9 Inhibitors
Ezetimibe
A

Fibrates: high TGs
BARs: good for LDL, may increase TGs
Fish Oil may increase LDL,but can greatly lower TG
PSCK9 and Ezetimibe can greatly reduce LDL

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10
Q

High Intensity Statins

A

Lower LDL by 50%
Atorvastatin 40-80mg
Rosuvastatin 20*-40mg

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11
Q

Moderate Intensity Statins

A

Lower LDL by 30-50%

  • Atorvastatin (10*-20)
  • Rosuvastatin (5-10*)
  • Simvastatin (20-40)
  • Pravastatin (40*-80)
  • Lovastatin (40*)
  • Fluvastatin (40*)
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12
Q

How do statins work?

A
  • inhibits HMG-COA reductase
  • up regulates LDL receptors in the liver to take up more
  • decreases secretion of VLDL (to make liver hang on to the cholesterol)
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13
Q

Which statins are metabolized by CYP 3A4? 2C9?

Which statins are lipophilic?

What to give a patient if there is a lot of DDI’s?

A
  • 3A4: Atorvastatin, Lovastatin, Simvastatin
  • 2C9:Fluvastatin, Rosuvastatin
  • ALS, Fluvastatin, Pitavastatin
  • Pravastatin

(CYP3A4 inducers: rifampin, phenytoin, CBZ, SJW)

(CYP3A4 Inhibitors CI: azoles, macrocodes (“cins”), protease inhibitors,cyclo, grapefruit juice) danazol, gemfibrozil, NonDHP CCB, amio

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14
Q

Statins with short half lives?

A
  • Dose at night

- lovastatin, simvastatin, pravastatin, fluvastatin

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15
Q

Statins with longer half lives?

A
  • atorvastain, rosuvastatin, pitavastatin
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16
Q

Common ADRs with statin use?

A

GI, DM, arthalgias, myopathy transaminitis

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17
Q

For myopathies, when do symptoms arise? What do we see? What happens in rhabdomyolysis?

A
  • weeks to months after initiation
  • a rise in creatinine kinase due to the breakdown of muscle
  • rhabdo: MSK with elevation in CK greater than 10% with renal dysfunction
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18
Q

What are the risk factors of myopathies?

A
  • greater than 75
  • female, low body weight
  • hypothyroidism
  • sporadic heavy exercise
  • comorbidities: renal and hepatic dysfunction
  • hx of previous statin intolerance
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19
Q

How to prevent myopathies from occurring? How to deal with myopathies?

A
  • routine CK measurements is not needed
  • educate patients, use lowest dose possible, avoid CYP3A4 inhibitors
  • consider the phillic statins
  • no need to treat unless symptoms appear, even if mild. If pain persists, hold the statin and investigate further (hypothyroidism, renal/hepatic function)
  • reintroduce when symptoms resolve, with a different statin or reduced dose.
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20
Q

When can transaminitis appear? Is routine monitoring needed? Can statins be continued? Is it possible to rechallenge?

A
  • 12 weeks after initiation
  • no
  • yes, but dc if pt develops symptoms
  • can re-challenge
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21
Q

Which anti-hyperlipidemic agents should not be used with statins?

A

niacin, gemfibrozil, fenofibrate…gemfibrozil is completely contraindicated

22
Q

Max dose of amiodarone, verapamil, and dilitazem while on a simvastatin?

A

10mg

23
Q

Max dose of amlodipine and ranolazine on a simvastatin?

A

20mg

24
Q

max dose for danazol, diltiazem, verapamil on lovastatin

A

20mg

25
Q

max dose for amio with lovastatin?

A

40mg

26
Q

Meds CI with lovastatin?

A

similar to simvastatin, including boceprevir, telaprevir, nefazodone

  • avoid cyclosporine and gemfibrozil and a lot of grapefruit juice
27
Q

When are stains CI?

A
  • acute liver disease
  • pregnant (category X)
  • breastfeeding
  • concurrent use of CYP3A4 inhibitor
28
Q

What to monitor for when a patient is on a statin?

A

FLP at baseline, 4-12 weeks after initiation or adjustment, q3-12 months

Baseline transaminases and CK..only get repeat levels if there is a concern for stain toxicity

Check 3 months if pt is taking niacin or vibrate

routeine DM screening

29
Q

For fibrates, what do we have to monitor for?

A
  • might have to renally adjust due to excretion through urine
30
Q

What is the general MAO of fibrates?

A

activates PPARalpha, increases synthesis of apoCIII, increases synthesis of LDL receptors

31
Q

ADRs of fibrates?

A

GI, Rash, Cholelithiasis, Cr increase w/o renal dysfunction, myopathy

32
Q

What are the main CI of fibrates?

A
  • severe hepatic or renal dysfunction
  • biliary cirrhosis or preexisting gallbladder disease

may enhance anticoag effect of warfarin, hypoglycemic effect on sylfonylureas

33
Q

What to monitor for fibrates?

A
  • renal function at baseline, q3 months, q6months therefore after
  • transaminases at baseline and 3 months after initiation
34
Q

for fenofibrate, what is the monitoring parameter?

A

CrCl less than 30, DC

greater than 30-80, limit dose to max 54mg/day

35
Q

For gemfibrozil what are the parameters?

A

less than 10, avoid or admin 50% of the dose

10-60, admin 75% of the dose

36
Q

What are the MOAs of bile acid resins?

A
  • bile acids facilitate digestion and absorption of lipids from the GI tract, synthesized in the liver
  • BARs sequester bile acids in the GI tract, increasing elimination, so the liver is then stimulated to produce more bile acids, and the reduced cholesterol concentrations upregulate LDL receptors.
37
Q

Major ADR with bile acid resins?

A

GI, improve adherence by taking apple or orange juice

38
Q

What are the complete CI for BAR?

A
  • hypertriglyceridemia
  • biliary or bowel obstruction
  • reduces the absorption of warfarin, levothyroxine, thiazide, BBs, therefore give drugs time apart
  • can decrease absorption of fat-soluble vitamins
39
Q

What is the main monitoring parameter for BARs?

A
  • TGs, repeat q4-8 weeks
  • use w caution if TG is over 250, do not initiate if over 300
  • dc if TG is over 400
40
Q

What is the MOA of niacin?

A
  • inhibits the mobilization of FFA from peripheral adipose to liver
  • reduces synthesis and secretion of VLDLC, and LDLC
  • promotes HDL retention of apolipoprotein AI
41
Q

What are the ADRs of Niacin?

A
  • Based on the metabolic pathway. Amidation follows hepatotoxicity, and conjugation causes vasodilatory effects.
42
Q

How to deal with flushing with Niacin?

A
  • start at a low dose w food
  • premedicate with aspirin 325mg 30 min prior
  • avoid hot things
43
Q

CI for Niacin

A
  • active hepatic disease, transaminitis
  • active peptic ulcer disease
  • severe gout
  • consider: BARs can decrease [niacin], niacin may enhance myopathic effects of statins, may interact w anticoags and antiplatetlets
44
Q

Monitoring parameters for niacin?

A
  • hepatic trans aminases
  • uric acid
  • diabetes
    at baseline and repeat when dose is changed or every 6 months
45
Q

ADRs of Omega 3 fatty acids?

A
  • GI, fishy burps

- increase in bleeding time, abnormal plate function (therefore watch out for DDIs with anti-platelets and warfarin)

46
Q

How do PCSK9 inhibitors work? (alirocumab, evolocumab)

A

inhibiting PCSK9 will allow more LDL receptors to remain in the membrane to uptake more lipids

47
Q

Main ADRs associated with PCSK9 inhibitors?

A
  • respiratory, injection site reaction, myalgia, increased transaminases w alirocumab
48
Q

How does ezetimibe work?

A

blocks NPC1L1 (a cholesterol absorption blocker) stimulating hepatic cholesterol and bile acid synthesis, and up regulates LDL receptor expression

49
Q

What are ADRs with exetimibe?

A
  • GI, arthalgias, cough, fatigue

- transaminases greater than 3x

50
Q

CI to ezetimibe?

A
  • hypersensitivity
  • concomitant use with a statin in patients with hepatic disease or transaminits
  • severe hepatic disease (class C)
51
Q

What to monitor for ezetimibe?

A
  • hepatic transaminases baseline, routine if on use with statin or fenofibrate
  • DC if transaminits is greater than 3x
52
Q

for diet, what should be avoided to improve LDL levels?

A

reduce both saturated and trans fats

Cardio MT2 (12 decks)

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