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Therapeutics 2 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What are the 4 groups that would benefit from Statin therapy?

A

-secondary prevention for pt with clinical ASCVD
-LDL= 190mg/dL +
-diabetes + age 40-75
-10 year ASCVD risk 7.5% + AND age 40-75

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2
Q

What is the LDL lowering affects of high intensity statin?

A

50%+

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3
Q

What is the LDL lowering affects of moderate intensity statin?

A

30-50%

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4
Q

What is the LDL lowering affects of low intensity statin?

A

<30%

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5
Q

What is a clinical ASCVD?

A

-acute coronary syndrome (MI, stable, and unstable angina)
-coronary or other arterial revascularization
-history of ischemic stroke or transient ischemic attack (TIA)
-peripheral artery disease

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6
Q

What are the high-risk conditions?

A

-age > 65yo
-genetics
-DM
-HTN
-CKD
-smoker
-persistently elevated LDL despite maximally tolerated statin +ezetimibe
-history of congestive heart failure

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7
Q

Which Statin would be best for secondary prevention of ASCVD?

A

high intensity statin, except if pt > 75 yo (possibly use moderate intensity)

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8
Q

When should lipid panel be monitored after Statin initiation or change?

A

4-12 weeks

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9
Q

What is goal LDL of very high risk secondary prevention pt?

A

<55 mg/dL

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10
Q

What is goal LDL of not very high risk secondary prevention pt?

A

< 70mg/dL

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11
Q

What primary prevention groups would benefit from a high intensity Statin?

A

-LDL= 190mg/dL +
-DM AND age 40-75yo
-ASCVD risk 20%+ AND age 40-75yo

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12
Q

What are DM specific risk factor enhancers?

A

-long duration of disease
-albuminuria
-eGFR < 60mL/min
-retinopathy
-neuropathy
-ABI < 0.9

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13
Q

What is the risk of severely elevated triglycerides in pt?

A

pancreatitis

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14
Q

What is the diagnosis criteria for persistent hypertriglyceridemia?

A

fasting TG 150mg/dL+ following 4-12 weeks of lifestyle intervention

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15
Q

What disease may cause hypertriglyceridemia?

A

-poorly controlled DM
-hypothyroidism

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16
Q

What diet/lifestyle choices may cause hypertriglyceridemia?

A

-excess alcohol
-diet high in saturated fat, sugar, high glycemic foods
-sedentary lifestyle

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17
Q

What drugs may cause hypertriglyceridemia ?

A

-propofol
-beta blockers
-glucocorticoids
-oral estrogens
-oncology treatment
-atypical antipsychotics
-immunosuppressants

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18
Q

What lifestyle interventions can be implemented for hypertriglyceridemia?

A

-reduce or eliminate added sugars
-total fat reduction
-weight loss
-decrease alcohol intake
-aerobic activity
-restriction of sugar/refined carbohydrates

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19
Q

What is the MOA of Statins?

A

HMG Co-A Reductase Inhibitor

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20
Q

What is the first-line treatment for LDL lower for ASCVD risk reduction?

A

Statin

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21
Q

What Statins are high intensity?

A

atorvastatin 40-80, rosuvastatin 20-40

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22
Q

What is the major enzyme for Atorvastatin?

A

CYP3A4

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23
Q

What is the major enzyme for Pravastatin?

A

no significant CYP metabolism

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24
Q

What is the major enzyme for Rosuvastatin?

A

CYP2C9

25
Q

What is the major enzyme for Simvastatin?

A

CYP3A4

26
Q

What Statin must be dosed at bedtime?

A

simvastatin

27
Q

Which Statin is the most lipophilic?

A

simvastatin

28
Q

What are the adverse effects of Statins?

A

-statin associated muscle symptoms (SAMS): myalgias, myopathies/rhabdomyolyis MOST COMMON CAUSE OF DISCONTINUATION
-newly diagnosed diabetes (more frequent with diabetes risk factors)
-liver transaminase elevation/hepatic failure
-cognitive impairment

29
Q

What are the drug interactions of Statins?

A

-gemfibrozil
-bile acid sequestrants
-calcium channel blockers
-cyclosporine/tacrolimus
-amiodarone

30
Q

What are the monitoring parameters of Statins?

A

-SAMS, at baseline and then 6-12 week after initiation (each follow-up visit)
-creatinine kinase (CK), possibly at baseline and if muscle symptoms develop
-ALT, AST, if indicated
-TSH, if symptoms develop

31
Q

How can Statin induced myopathies be managed?

A

-decrease statin dose
-switch statin
-nondaily statin dosing
-utilize nonstatins

32
Q

What are modifiable risk factors that increase the risk of statin intolerance?

A

-hypothyroidism
-drug interactions
-alcohol use
-strenuous exercise
-vitamin D deficiency
-obesity
-DM

33
Q

What are the contraindications of Statins use?

A

-active or chronic liver disease
-breastfeeding
-drug interactions
-pregnancy (not complete contraindication, but strongly encouraged to stop statin use)

34
Q

What is the indication for non-statin therapy?

A

-insufficient response to statin therapy
-intolerance to statin therapy
-severe hypertriglyceridemia
-ASCVD risk reduction: icosapent ethyl

35
Q

What is the MOA of Ezetimibe?

A

inhibits NPC1L1 proteins to reduce cholesterol absorption in small intestine

36
Q

What is the indication for Ezetimibe therapy?

A

additive LDL lowering therapy with statin (not to be used alone= no benefit)

37
Q

What are the adverse effects of Ezetimibe?

A

typically well tolerated but may experience, diarrhea, hepatitis, pancreatitis

38
Q

What are the precautions of Ezetimibe?

A

pregnancy/breastfeeding, moderate/severe hepatic disease

39
Q

What is the MOA of PCSK9 inhibitor mAb?

A

binds PCSK9 and increases LDL receptors available to clear circulating LDL

40
Q

What is the indication of PCSK9 inhibitors mAb?

A

combination therapy for high risk patients, statin intolerant patients, genetic dyslipidemia

41
Q

What are the adverse effects of PCSK9 inhibitor mAb?

A

well tolerated but may experience muscle aches, urticaria, injection site reactions

42
Q

What is the MOA of Inclisiran?

A

siRNA that targets PCSK9 messenger RNA to inhibit PCSK9 synthesis (similar to PSCK9 mAb inhibitor)

43
Q

What are the adverse effects of Inclisiran?

A

injection site reaction, arthralgias

44
Q

What is the indication of Bempedoic Acid?

A

adjunct to max tolerated statin for additional LDL lowering therapy

45
Q

What are the adverse effects of Bempedoic Acid?

A

hyperuricemia/gout

46
Q

What are the contraindications of Bempedoic Acid?

A

-pregnancy/breastfeeding
-pediatrics/severe renal impairment/dialysis = not studied

47
Q

What is the MOA of Bile Acid Sequestrants(BAS)?

A

binds bile acid in Gi tract to prevent its reabsorption to encourage cholesterol to be synthesized to bile acid

48
Q

What are the indications of Bile Acid Sequestrants?

A

-add on to statin therapy
-pregnancy

49
Q

What are the adverse effects of Bile Acid Sequestrants?

A

constipation, heartburn, nausea, bloating

50
Q

What are the contraindications of Bile Acid Sequestrants?

A

TG > 300 mg/dL

51
Q

What are the adverse effects of Niacin?

A

-flushing (prostaglandin mediated)
-hyperglycemia
-hyperuricemia/gout
-GI upset

52
Q

What is first line therapy for hypertriglyceridemia?

A

fibric acid derivatives

53
Q

What drugs are fibric acid derivatives?

A

gemfibozil, fenofibrate, fenofibric acid

54
Q

What is the effect of fibric acid derivatives on lipid profile?

A

decrease TG and increase HDL (little impact on LDL)

55
Q

What are the adverse effects of Fibric Acid derivatives?

A

-dyspepsia
-N/V
-skin rash
-gallstones
-myopathy (especially in combo with statins)

56
Q

What are the contraindications of Fibric Acid derivatives?

A

-moderate-severe renal impairment, eGFR <30 (renal adjustment needed if eGFR 30-59)
-hepatic disease

57
Q

What is the indication of Omega-3-fatty acids/Icosapent ethyl?

A

adjunct for TG lowering therapy for pt with very high TG (>500mg/dL)

58
Q

What are the adverse effects of Omega-3-ftty acids?

A

-dyspepsia
-nausea
-prolonged bleeding time (use caution in pt on blood thinners)
-AFib
-DHA can raise LDL, but EPA doesn’t (icosapent ethyl is EPA only)

Therapeutics 2 (13 decks)

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