Dyslipidemia Flashcards

1
Q

Where is cholesterol made? From what?

A

in the liver

made from Acetyl CoA, breakdown product of free fatty acid

rate limiting step: HMG-CoA reductase

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2
Q

Risk factors for dyslipidemia

A

FLASH

  • fam hx
  • low HDL
  • Age (men >45, women >55)
  • smoking
  • HTN, CKD

risk equivalent to CHD= DM, CAD< PAD, AAA

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3
Q

Who benefits from statin therapy?

A

pts with clinical ASCVD

LDL >190

DM age 40-75 with LDL 70-189

LDL 70-189 + 10 yr ASCVD risk >7.5%

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4
Q

TLC to lower LDL and reduce CHD risk

A

reduce intake of saturated fats/cholesterol

increase fiber intake

weight loss

increase physical activity

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5
Q

Fibrates MOA

A

upregulate lipoprotein lipase

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6
Q

Statins MOA

A

interfere with HMG-CoA reductase, the critical enzyme in the biosynthesis of cholesterol

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7
Q

Niacin MOA

A

decrease VLDL and LDL

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8
Q

Bile acid resins MOA

A

bind bile acids, thus increasing the secretion of cholesterol in the stool

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9
Q

Ezetimibe MOA

A

blocks the absorption of cholesterol from the small intestine

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10
Q

Which drugs provide high intensity statin therapy?

A

Atrovastatin 80 mg

Rosuvastatin 40 mg

lower LDL ~50%

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11
Q

Which drugs provide moderate intensity statin therapy?

A

Atrovastin 10 mg

Rousvastatin 20 mg

Simvastatin 20-40mg

Pravastatin 40mg

Fluvastatin 40 mg

Lower LDL ~30-50%

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12
Q

Which drugs provide low intensity statin therapy?

A

Pravastatin 10-20mg

Lovastatin 20mg

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13
Q

Which Statin has the greatest efficacy?

A

Rosuvastatin

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14
Q

Side effects of statin therapy

A

severe: rhabdomyolysis, hepatic failure
mild: arthralgia, myalgia, musculoskeletal pain, increase ALT/AST

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15
Q

Contraindications for statin therapy

A

liver disease, unexplained persistent elevation in ALT/AST, pregnancy, breast feeding

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16
Q

What should you monitor in a pt on a Statin?

A

LFTS, fasting plasma glucose

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17
Q

Atrovastatin drug interactions

A

3A4 inhibitors and inducers

avoid use with: antihepacivirals, Posaconazole, red yeast rice

  • also increases the effects of many drugs, which is why Rosuvastatin is generally the better choice
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18
Q

Rosuvastatin drug interactions

A

2C9 inducers and inhibitors

Avoid use with: Gemfibrozil, Read yeast rice, Ledipasvir or Voxilaprvir (antihepacivirals)

increases effect of Warfarin–> consider Atrovastatin if they need to be on Warfarin

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19
Q

What drug can you add in a pt currently on maximally tolerated statin therapy when additional LDL lowering is desired?

A

Ezetimibe- for <25% additional LDL lowering

PCSK9 inhibitor- >25% lowering ($$$)

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20
Q

Name a cholesterol Absorption Inhibitor (CAI), MOA?

A

Ezetimibe

inhibits cholesterol absorption in the small intestine

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21
Q

Ezetimibe contraindications

A

active hepatic disease, unexplained persistently elevated LFTs

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22
Q

How is Ezetimibe excreted?

A

~ 80% excreted in feces

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23
Q

Side effects of Ezetimibe?

A

severe: cholithiasis
mild: diarrhea, fatigue

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24
Q

What should you monitor in pts on Ezetimibe?

A

LFTs

myositis (rare)

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25
Q

Name 2 PCSK9 inhibitors, MOA?

A

Alirocumab, Evolocumab (Repatha)

abs that inhibits PCSK, reduce LDL in dose dependent manner (can lower up to 70%)

give SQ every 2 weeks

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26
Q

Indications for PCSK9 inhibitors

A

adults with familial hypercholesterolemia

those with ASCVD who need additional LDL lowering

intolerance of statins

27
Q

Side effects of PCSK9 inhibitors

A

hypersensitivity (rare), local rxn, URI sxs

28
Q

Name a Microsomal Triglyceride Transfer Protein (MTP) inhibitor, MOA?

A

Juxtapid (Iomitapide)

binds directly to and inhibits MTP, prevents assembly of apo-B containing-lipoproteins, reduces the production of chylomicrons and VLDL. Reduces LDL concentrations

29
Q

Indication for MTP inhibitor?

A

homozygous familial hypercholesterolemia

30
Q

Juxtapid (Iomitapide) side effects?

A

CP, GI, dyspepsia, V, abd pain, weight loss, constipation/flatulence

31
Q

Contraindications for Juxtapid (Iomitapide)?

A

pregnancy, hepatic impairment

32
Q

Juxtapid (Iomitapide) PK?

A

99.8% protein bound

hepatic metabolism CYP3A4

renal elimination

33
Q

Boxed warning for Juxatapid (Iomitapide)?

A

hepatotoxity

only prescribed through restricted program called the Juxtapid Rems Program

34
Q

What should you monitor in pts on Juxtapid?

A

transaminases (liver enzymes)

baseline preg test

35
Q

Why should someone on Juxtapid maintain a low fat diet?

A

to avoid GI effects

36
Q

Mipomersen sodium (Kynamro) MOA?

A

inhibits apolipoprotein B-100 synthesis, used with other lipid lowering meds

37
Q

Indication for Mipomersen sodium?

A

pts with homozygous familial hypercholesterolemia

38
Q

Adverse rxns of Mipomersen sodium?

A

injection site rxn (Admin 200mg SQ/wk)

flu like sxs

39
Q

Mipomersen sodium contraindications?

A

hepatic impairment, unexplained persistent elevated LFTS, sensitivity to produce components

40
Q

Boxed warning for Mipomersen sodium?

A

hepatotoxicity

prescribed only through restricted program called Kynamro rems

41
Q

What should you monitor in a pt taking Mipomersen sodium (Kynamro)?

A

ALT, AST, alkaline phosphatase, total bilirubin

42
Q

fibrates MOA?

A

Upregulates lipoprotein lipase-> increases catabolism of VLDL, eliminates TG rich particles, fatty acid oxidation

Modulation of apolipoproteins - increases catabolism/clearance of TG rich particles

43
Q

Effects of fibrates?

A

35-50% lowering of TG

5-20% decrease in LDL (may increase in pts with elevated TG)

5-20% increase in HDL

44
Q

Name 2 fibrates

A

Fenofibrate, Gemfibrozil

45
Q

Side effects of Fenofibrate

A

Severe: acute renal failure, cholelithiasis

mild: increase LFTs, abd pain, dyspepsia, HA< drowsiness

46
Q

Fenofibrate contraindications

A

hepatic dysfunction, severe renal impairment, existing gallbladder disease, pregnancy, breast feeding

47
Q

What should you monitor in pts taking Fenofibrate?

A

LFTs, renal function, Lipid panel

48
Q

Fibrates drug interactions?

A

Statins- avoid combo (increases risk of myopathies)

Sulfonylureas

Warfarin

49
Q

Nicotinic Acid MOA?

A

Inhibits synthesis & secretion of VLDL and LDL

useful in most dyslipidemias

50
Q

Effects of Nicotinic Acid?

A

LDL lowering 10-15%

Increases HDL 15-35%

TG lowering 25-30%

51
Q

Niacin formulations?

A

OTC: Niacin (immediate and slow release)

Rx: Niaspan (extended release)

52
Q

Side effects of Nicotinic Acid?

A

severe: hepatotoxicity

Mild: flushing/warmth/tingling (can take with NSAID), hyperglycemia, hyperurecemia

53
Q

Contraindications of Nicotinic Acid

A

active hepatic disease, unexplained persistent elevated LFTs, active peptic ulcers, arterial hemorrhage

54
Q

What should you monitor in a pt on a Nicotinic Acid?

A

LFTs, Lipid panel

55
Q

Nicotinic Acid drug interactions?

A

anticoagulants (may increase bleeding time)

Statins

56
Q

Bile Acid Substrates (BASs) MOA?

A

cholesterol is a precursor to bile acids, BASs bind with bile acids in the intestine –> eliminates via feces

57
Q

Effect of BASs?

A

decreases LDL 15-30%

minimally increases TG and HDL

58
Q

Name 2 BASs, when should they be taken?

A

Cholestyramine (Questran, Prevalite), Colestipol

with meals

59
Q

BASs contraindications? Side effects?

A

hypersensitivity

Severe: bleeding with chronic use

mild: abd pain, bloating, constipation, flatulence, nausea

60
Q

What should you monitor in a pt taking BAS? Drug interactions

A

lipid panel

will bing with other meds, decreasing their absorption administer meds 1 hr before or 4 hrs after BASs

61
Q

Omega 3 Fatty Acids MOA? Name one.

A

uncertain, thought to inhibit VLDL and triglyceride synthesis in the liver

Omega 3 Acid Ethyl Esters (Lovaza)

62
Q

O3FA side effects? Contraindications?

A

Eructation “fish burp”, dypepsia, increase in LFTs

fish hypersensitivity

63
Q

O3FA drug interactions?

A

anticoagulants and antiplatelets (may enhance bleeding time)

64
Q

What should you monitor in a pt taking O3FA?

A

LFTs, lipid panel