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Pharm > dyslipidemia > Flashcards

dyslipidemia Flashcards

1
Q

5 major lipoproteins

A

VLDL, IDL, LDL, HDL, chylomicrons

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2
Q

HMG CoA reductase inhibitors
patients who benefit

A
  1. Adults with DM
  2. PTs with ASCVD
  3. 10 year risk of ASCVD greater than 7.5%
  4. LDL cholesterol greater than 190 mg/dL
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3
Q

HMG CoA reductase MOA

A

inhibition of HMG-COA reductase decreases cholesterol synthesis,
this results in increased LDL receptors on hepatocytes for increased uptake/degradation

↓ cholesterol → liver ↑ receptors → receptors grab more LDL → cleans the blood → ↓ circulating LDL

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4
Q

When during the day should your patient take the statin? Why?

A

Statins should be taken at night.

Spike of cholesterol is made at night duh

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5
Q

Results of taking a statin

A

Therapeutic Effects
1. ↓ cholesterol synthesis
2. ↑ hepatic LDL receptors
3. ↓ circulating LDL cholesterol level by 50% or more at the HIGHEST doses

also slight ↑ HDL, ↓ triglyceride, ↓ high-sensitivity CRP

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6
Q

What percentage do statins reduce circulating LDL?

A

High-intensity = 50%
(recent cardiac event)
Moderate-intensity = 30-49%
(if they can tolerate low-intensity)

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7
Q

Contraindications of statins

A
  1. PREGNANCY duh
  2. severe hepatic dysfunction
  3. extreme ↑ CPK within a matter of days after starting a statin = severe muscle damage
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8
Q

Which statin intensity is the longest-acting and has the longest half-life?

A

High intensity:
- atorvastatin
- rosuvastatin

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9
Q

Statins with _____ intensity have less side effects and work all day long on the body

A

low-intensity

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10
Q

What is the most common side effect of statins? When would you expect to see the onset?

A

Statin-associated Muscle Symptoms (SAMS)

  • muscle aches with normal serum creatine kinase levels
  • onset = within 4-6 weeks of initiation OR dose increase
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11
Q

In severe cases, starting someone on a statin can lead to the development of ______

A

myositis or rhabdomyolysis

  • CPK >10 times the upper limit

DO NOT use statins moving forward

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12
Q

What Increases the risk of severe adverse effects of taking statins?

A

Co-administration with CYP450 inhibitors (niacin, fibrate, erythromycin, antifungals, nefazodone, cyclosporine)

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13
Q

Your patient started a statin and is experiencing cognitive symptoms including memory loss, forgetfulness, and confusion. What is the next step for this patient?

A

Discontinue statin

Reversible - depending on how long symptoms started

Symptoms typically resolve around 3 wks

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14
Q

With statins, there is a small increased risk of ….

A

DM II

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15
Q

3 statins that inhibit CYP3A4

A

simvastatin, atorvastatin, lovastatin

= higher risk of rhabdo

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16
Q

Adverse effects of statins

A
  1. rhabdo
  2. elevated liver enzymes
  3. cognitive symptoms
  4. DM II
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17
Q

After 4-12 wks of starting a statin, what lab should you run?

A

Fasting lipid panel (FLP)
- check FLP for anticipated clinic response (e.g. high intensity > 50% LDL decrease)
- if LESS than anticipated, verify adherence, lifestyle, secondary causes
- consider lower statin dose if 2 consecutive LDL <40 mg/dL

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18
Q

What class does ezetimibe (Zetia) belong to?

A

absorption inhibitors

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19
Q

MOA of ezetimibe (Zetia)

A

inhibits cholesterol transporters → inhibits intestinal absorption of dietary + biliary cholesterol across intestinal wall → ↓ LDL cholesterol 15-20% when used as monotherapy

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20
Q

When is ezetimibe (Zetia) preferred?

A

best as adjunct with statins IF LDL doesn’t improve by 70 mg/dL

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21
Q

What should you avoid ezetimibe (Zetia) with?

A
  1. moderate-severe liver dysfunction
  2. skeletal muscle effects (when taken with statin)
  3. pregnancy
  4. CHOLELITHIASIS when taken with fibrate
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22
Q

MOA of PCSK9 Inhibitors

A

prevents degradation of LDL receptors so they continue to take up LDL

increase removal of LDL in circulation by liver

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23
Q

PCSK9 lowers cholesterol levels by ______ %. Best for what type of pts?

A

Lowers by 50-60%

Best for young pts and extremely high LDL levels

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24
Q

How often do you inject PCSK9?

A

every 2-4 weeks

25
Q

What drug in combo with a statin causes a 15-20% reduction in CV death, MI stroke, hospital admission for unstable angina, or coronary revasc?

A

Evolocumab

26
Q

MOA for bile acid-binding resins

A

bind bile acid in GI → forces body to take up more cholesterol → take cholesterol from the reserves

thank u for ur service

27
Q

Dyslipidemia Rx safe for pregnancy

A

bile-acid binding resins

28
Q

Adverse effects of PCSK9 inhibitors

A
  1. flu-like symptoms
  2. cognitive issues
  3. local injection site rxn
29
Q

Cut off for bile acid-binding resins is a triglyceride level of _____

A

> 500 mg/dL

30
Q

Drug class associated with a lot of GI side effects

A

Bile acid-binding resins

31
Q

Vitamin deficiency may be a consideration with what drug class

A

Bile acid-binding resins

32
Q

Fibric acid derivatives mostly do what

A

lower triglycerides by 40%

33
Q

MOA of fibrates

A

PPAR (peroxisome proliferator-activated receptor-alpha agonists)

genes or whaTeva

34
Q

Gemfibrozil considerations

A

Avoid with any dose of any statin (myopathy)

35
Q

Fenofibrate Considerations

A

avoid with high intensity statin

36
Q

Fibric Acid Adverse effects

A

Dyspepsia, SCr increase, Cholelithiasis, Myopathy, Hepatotoxicity (increase ALT)

37
Q

Fibric acid drug interaction potential

A

Resin: separate dosing
Warfarin: increase INR
Ezetimibe: increase cholelithiasis
Colchicine: increase myopathy

38
Q

Fibrates________ in all statin-treated patients with CVD or diabetes

A

have not been shown to reduce CV events

39
Q

Niacin MOA

A

Reduce production of VLDL particles (LDL precursor), secondary decrease in LDL and increase in HDL cholesterol levels

↓ VLDL, ↓ LDL, ↑ HDL → ↓ cholesterol

40
Q

Niacin adverse effects

A

flushing + skin shiitake
…..
skin flushing
dyspepsia/abdominal pain
nausea, vomiting, diarrhea
pruritus
skin rash/hypersensitivity
hyperglycemia
increased uric acid
dry eyes
myalgia
hepatotoxicity

41
Q

Niacin considerations (how to take/ what to avoid)

A

avoid spicy/hot food
avoid alcohol
take with food
aspirin 30 minutes before dose

42
Q

Omega-3 fatty acid do what

A

lower triglycerides by up to 30%

43
Q

Omega-3 fatty acid preparations

A

Lovaza: DHA and EPA
Vascepa: EPA
Epanova: DHA and EPA

44
Q

Omega-3 fatty acid warnings

A

Hypersensitive to fish or shellfish
Pregnancy/ lactation

45
Q

Omega-3 fatty acid adverse effects

A

GI disturbances: belching, dyspepsia; taste perversion
skin: pruritus, rash
Arthalgia/ joint pain
increased bleeding risk

46
Q

Omega-3 fatty acid monitoring

A

ALT+AST
LDL increase (not with EPA only ie vascepa)
afib/ flutter

47
Q

Vascepa (Icosapent ethyl) is the only preparation shown to

A

reduce CV death, nonfatal MI/ stroke, coronary revascularization, unstable angina 25%

48
Q

Diet therapy goal

A

reduce total fat to 25-30%, saturated fat to <7% of calories, no trans fat

49
Q

LDL-C > 190 mg/dl

A

high intensity statin; no risk assessment

50
Q

DM and age 40-75

A

moderate statin, risk assessment for high intensity

51
Q

age>75

A

clinical assessment

52
Q

0-19y/o

A

lifestyle mod, familial hypercholesterolemia

53
Q

age 20-39

A

lifetime risk assessment/ modification
consider statin with family Hx

54
Q

40-75y/o

A

LDL-C >70 and <190, PT doesn’t have DM
10 year ASCVD assessment

55
Q

low risk

A

<5%

56
Q

borderline risk

A

5-7.5%

57
Q

intermediate risk

A

> 7.5 to <20%, reduce LDL-C by 30-49%

58
Q

high risk

A

> 20%, reduce LDL-C by >50%

Pharm (3 decks)

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