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Cardiology Exam > Lipid Lowering Meds > Flashcards

Lipid Lowering Meds Flashcards

1
Q

dyslipidemic drug classes

A
  1. HMG CoA reductase inhibitors (“statins” & bempedoic acid
  2. cholesterol absorption inhibitor (ezetimibe)
  3. PCSK9 inhibitors (monoclonal anibodies & siRNA)
  4. niacin
  5. fibrates/fibric acid derivatives
  6. omega 3 fatty acid derivatives
  7. bile acid binding resins (BABR)
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2
Q

citrate pathway to cholesterol synthesis within hepatocyte (important steps)

A
  1. ATP citrate lyase catalyzes conversion of citrate → acetyl-CoA
  2. acetyl-CoA → HMG Co-A
  3. HMG CoA REDUCTASE catalyzes conversion of HMG Co-A → mevalonic acid
  4. mevalonic acid → cholesterol
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3
Q

HMG CoA reductase inhibitors (statins) - MOA

A

*block HMG CoA reductase (one of the rate-limiting enzymes in the cholesterol synthesis pathway; normally converts HMG CoA to mevalonic acid)
*reversible inhibition

*results in decreased total cholesterol levels & increased LDL receptor expression

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4
Q

bempedoic acid - MOA

A

*blocks ATP citrate lyase (enzyme in the cholesterol synthesis pathway; normally converts citrate to acetyl-CoA)
*reversible inhibition

*results in decreased total cholesterol levels & increased LDL receptor expression (dose-dependent fashion)

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5
Q

HMG CoA reductase inhibitors - examples

A

*simvastatin
*ATORVASTATIN
*pravastatin
*ROSUVASTATIN

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6
Q

HMG CoA reductase inhibitors - ADEs

A

*headache
*fatigue
*N/V/D
*MUSCLE ACHES & PAINS (myopathies, myalgias, myositis)
*increased LFTs
*rhabdomyolysis

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7
Q

atorvastatin - MOA & metabolism

A

*HMG CoA reductase inhibitor → decreased total cholesterol & increased LDL receptor expression
*hepatic metabolism (CYP3A4 minor)

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8
Q

rosuvastatin - MOA & metabolism

A

*HMG CoA reductase inhibitor → decreased total cholesterol & increased LDL receptor expression
*hepatic metabolism (mixed enzymes [2C9]) & some renal

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9
Q

pravastatin - MOA & metabolism

A

*HMG CoA reductase inhibitor → decreased total cholesterol & increased LDL receptor expression
*hepatic GLUCURONIDATION (& some renal) metabolism

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10
Q

statin metabolism

A

*CYP3A = lovastatin, simvastatin, ATORVASTATIN (highest risk of drug interactions)
*CYP2C9 = fluvastatin, pitavastatin
*other enzymes/renal = pravastatin
*ROSUVASTATIN = CYP2C9/other enzymes/renal

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11
Q

dose-dependent effects of statins on LDL levels

A

*lower doses of statins result in a baseline reduction of LDL; increasing doses of statins results in a dose-dependent reduction of LDL
*2 high-intensity statins (cause the most marked reduction of LDL) = atorvastatin & rosuvastatin
*high doses of high intensity statins result in decreased triglycerides
*rule of 7: if you double the dose of the statin, you do NOT double the reduction of LDL levels (decrease it by about 7-8 mg/dL)

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12
Q

unintended benefits/consequences of statins

A

*mild increases in HDL
*decreased triglycerides if using high doses of high-intensity statins (atorvastatin, rosuvastatin)
*anti-inflammatory
*plaque stabilization or regression
*increased blood sugar
*dementia risk?

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13
Q

bempedoic acid - metabolism

A

*hepatic glucuronidation (lower risk of drug interactions)

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14
Q

bempedoic acid - ADEs

A

*tendon rupture
*hyperuricemia/gout
*increased serum creatinine/BUN
*anemia (decreased Hb)
*increased LFTs

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15
Q

ezetimibe - drug class & MOA

A

*cholesterol absorption inhibitor
*MOA: inhibits cholesterol absorption at the brush border of the small intestine
*mildly lowers LDL

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16
Q

ezetimibe - metabolism, ADEs, uses

A

*hepatic metabolism
*ADEs: N/V/D
*mainly used as an add-on therapy to a statin to achieve additional LDL reduction or in statin intolerance

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17
Q

PCSK9 inhibitors - examples

A
  1. monoclonal antibodies = alirocumab, evolocumab
  2. small interfering RNA (siRNA) = inclisiran
18
Q

PCSK9 inhibitors (monoclonal antibodies) - MOA

A

*normally, PCSK9 binds to LDL receptors to prevent them from being recycled to the cell surface (resulting in decreased LDL receptors)
*monoclonal antibodies against PCSK9 allows for an INCREASE IN LDL RECEPTOR RECYCLING TO THE CELL SURFACE, so there are more receptors available to bind LDL (causing DRAMATIC LDL REDUCTION)

19
Q

alirocumab - drug class, MOA

A

*PCSK9 inhibitor (monoclonal antibody)
*inhibition of PCSK9 → increased LDL receptors on the cell surface → marked LDL reduction

20
Q

evolocumab - drug class, MOA

A

*PCSK9 inhibitor (monoclonal antibody)
*inhibition of PCSK9 → increased LDL receptors on the cell surface → marked LDL reduction

21
Q

PCSK9 inhibitors (monoclonal antibodies) - metabolism, ADEs

A

*reticulo-endothelial system metabolism
*ADEs: injection site reactions, flu-like symptoms, myalgias, increased LFTs

22
Q

inclisiran - drug class, MOA

A

*indirect PCSK9 inhibitor (siRNA)
*MOA: binds to ASPGR receptor & endocytosed → endosome is degraded, releasing siRNA → siRNA loaded into RISC complex → complex binds to PCSK9 mRNA and destroys it

*result: increased LDL receptors at the cell surface → marked LDL reduction

23
Q

inclirisan - metabolism, ADEs

A

*metabolism: catalytic breakdown of mRNA for PCSK9 production
*ADEs: injection site reactions, flu-like symptoms, arthralgias, anti-drug antibodies

24
Q

niacin - MOA & uses

A

*unclear; decreases synthesis and secretion of VLDL by the liver
*RAISES HDL (best drug to raise HDL), lowers LDL, lowers TG
*place in therapy:
-mixed hyperlipidemia
-combination therapy
-hypertriglyceridemia

25
Q

niacin - ADEs

A

*dyspepsia
*FLUSHING
*itching
*urticaria
*increased LFTs
*use with caution in PUD and diabetes

26
Q

niacin - metabolism

A

*hepatic conjugation (drug interactions: simvastatin, gemfibrozil)

27
Q

fibrates (fibric acid derivatives) - examples

A

*gemfibrozil
*fenofibrate

28
Q

fibrates (fibric acid derivatives) - MOA

A

*increase lipoprotein lipase activity (LPL)
*increase catabolism of VLDL
*variable effects on LDL, moderate rise in HDL, significant reduction of triglycerides
*BEST DRUG TO LOWER TRIGLYCERIDES

29
Q

fibrates (fibric acid derivatives) - ADEs

A

*myalgias
*increased LFTs
*N/V/D

30
Q

fibrates (fibric acid derivatives) - metabolism

A

*gemfibrozil: hepatic (drug interactions with lovastatin, simvastatin, and niacin)
*fenofibrate: hepatic (lower risk of drug interactions)

31
Q

gemfibrozil - drug class, MOA

A

*class: fibrates (fibric acid derivatives)
*MOA: increase LPL activity & VLDL catabolism → REDUCTION OF TRIGLYCERIDES primarily

32
Q

fenofibrate - drug class, MOA

A

*class: fibrates (fibric acid derivatives)
*MOA: increase LPL activity & VLDL catabolism → REDUCTION OF TRIGLYCERIDES primarily

33
Q

omega 3 fatty acid derivatives - MOA

A

*decrease VLDL-TG synthesis and increase TG clearance (decrease lipogenesis, increase LPL)
*DECREASE TRIGLYCERIDES; increase HDL

34
Q

omega 3 fatty acid derivatives - examples

A

*icosapentaenoic/docosahexenoic acids
*icosapent ethyl

35
Q

omega 3 fatty acid derivatives - ADEs

A

*icosapentaenoic/docosahexenoic acids: taste disturbances, dyspepsia, increased risk of developing atrial fibrillation, increased risk of bleeding

*icosapent ethyl: peripheral edema, gout, increased risk of developing atrial fibrillation, increased risk of edema

36
Q

bile acid binding resins (BABR) - examples

A

*cholestyramine
*colestipol
*colesevalm

37
Q

bile acid binding resins (BABR) - MOA

A

*binds bile acids in the GI tract
*upregulation of LDL receptors
*lowers LDL, +/- HDL, raises triglycerides

38
Q

bile acid binding resins (BABR) - uses

A

*mild to moderate LDL elevation
*combination therapy

39
Q

bile acid binding resins (BABR) - ADEs

A

*N/V/D
*dyspepsia
*increased triglycerides

40
Q

drugs to use to significantly reduce total cholesterol & LDL

A
  1. statins (high intensity - atorvastatin, rosuvastatin)
  2. PCSK9 inhibitors (alirocumab, evolocumab)

*second line: bempedoic acid, ezetimibe, BABRs, niacin

41
Q

drugs used to significantly reduce triglycerides

A
  1. statins (high intensity - atorvastatin, rosuvastatin)
    2nd line: fibrates, omega 3’s, niacin
42
Q

drugs used to raise HDL levels

A
  1. NIACIN
    2nd line: statins, omega 3’s

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