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Pharm 225A > Hyperlipidemia/Hypertriglyceridemia > Flashcards

Hyperlipidemia/Hypertriglyceridemia Flashcards

1
Q

“-Statin” drug route/MoA

A
  • PO
  • MoA: inhibits HMG CoA reductase –> less cholesterol in liver –> increased removal of LDL from blood into liver
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2
Q

“-Statin” drug indications

A
  • homo/heterozygous high cholesterol
  • PRIMARY prevention of cardiovascular events
  • ex. atorvaSTATIN, simvaSTATIN, rosuvaSTATIN
    1ST LINE
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3
Q

“-Statin” AEs

A
  • Common: arthralgia/myopathy/myositis
  • Less: hepatitis/jaundice
  • Significant: rhabdomyolysis, hepatic failure (rare)
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4
Q

Ezetimibe route/MoA

A
  • PO
  • MOA: blocks transport of cholesterol from intestine to liver –> increase of LDL receptors on liver –>more LDL removed from circulation
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5
Q

Ezetimibe indications

A
  • homozygous high chol.
  • PRIMARY high cholesterol
  • off label: secondary prevention of cardiovascular events
    ADJUNCTIVE to -statins or can also be used alone
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6
Q

Ezetimibe D-D interactions

A
  • Fibrates –> avoid combination
  • Bile acid sequestrants –> impaired absorption
  • cyclosporine
  • Warfarin –> possible increase of INR
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7
Q

Ezetimibe AEs

A
  • Common: Diarrhea, Myalgia, resp infection
  • Less: elevated AST/ALT
  • Sig: rhabdomyolysis, pancreatitis, cholecystitis, anaphylaxis
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8
Q

PCSK9 Inhibitor drug types (2)

A
  • monoclonal antibodies: AlirocuMAB
    EvolocuMAB
    &
  • RNA type
    Inclisiran
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9
Q

PCSK9 Inhibitors route/MoA (-MABs)

A
  • SubQ
  • blocks PCSK9 from degrading LDL receptors –> more LDL receptors to clear LDL from bloodstream
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10
Q

PCSK9 Inhibitors route/MoA (inclisiran)

A

-SQ
- blocks mRNA that encodes for PCSK9 production –> less PCSK9 = more LDL receptors –> more LDL removed from circulation

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11
Q

PCSK9 Inhibitors Indications

A
  • Homozygous familial high chol.(-MABs)
  • heterzygous (RNA)
  • primary hyperchol. (-MABs)
  • secondary prevention of cardiovascular events
  • ADJUNCTIVE after statins/ezetimibe stop working
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12
Q

PCSK9 Inhibitor AEs

A
  • common: injection site reaction
  • Less: liver disorder
  • Sig: hypersensitivity, angioedema
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13
Q

ATP Citrate Lyase (ACL) inhibitor drug/route/MoA

A
  • Drug: Bempedoic Acid
  • route: PO
  • MoA: activated in liver; inhibits cholesterol synthesis in liver –> increase in LDL receptor –> increase clearance of LDL from circulation
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14
Q

ACL inhibitor indication

A
  • heterozygous familial chol
  • atherosclerotic CVD
    -ADJUNCTIVE when -statins/ezetimibe stops working
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15
Q

ACL inhibitor AEs

A

do not use if pregnant
- Common: gout, hyperuricemia
- Less: liver disorder, BPH in men
- Sig: tendon rupture, A-fib, anemia/thrombocytopenia

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16
Q

Bile Acid Sequestrants route/MoA

A
  • PO
  • MoA: promotes bile excretion in feces–> decreased bile acid availability–> increased uptake of LDL to liver, less in circulation
17
Q

Bile Acid Sequestrants Drug & indication

A
  • Colesevelam
  • Heterozygous familial high chol.
  • atherosclerotic CVD
  • ADJUNCTIVE when -statins and ezetimibe stop working
18
Q

Bile Acid Sequestrants AEs

A
  • Common: “belly effects” abd pain; constipation, N/V
  • Less: vitamin A, D, E, K deficiency
  • Sig: hyper-triglyceridemia, pancreatitis, gallbladder calculi
19
Q

Contraindications of Bile Acid Sequestrants (colesevelam)

A
  • when TG > 500
  • if hx of pancreatitis caused by high TG
  • bowel obstruction
20
Q

Fibric Acid derivatives Inidications

A
  • hypertriglyceridemia
  • prevention of CVD
  • ADJUNCTIVE/alternate to omega 3; also if TGs>500
21
Q

Fibric Acid derivatives (drugs/route/MoA)

A
  • Gemfibrozil/fenofibrate
  • PO
  • MoA: activates PPAR-alpha –> more LPL (lipoprotein lipase) –> less fatty acids available in liver to release triglycerides
22
Q

Contraindications of Fibric acid derivative

A
  • severe renal impairment
  • active liver dx
  • gallstones
  • breast feeding
23
Q

Fibric Acid derivative SEs

A
  • Common: abdominal pain; N/V/D; dyspepsia; rash/itching; mylagia; increased liver enzymes
  • Less: photosensitivity
  • Sig: rhabdomyolysis; delayed hypersensitivity
24
Q

VLDL Synthesis Inhibitors indications

A
  • CV risk reduction with hypertriglyceridemia
  • ADJUNCTIVE if statins stop working; also for CVD/DM
25
Q

VLDL synthesis inhibitors (drugs/route/MoA)

A
  • omega 3/fish oil & icosapent ethyl
  • PO
  • MoA: inhibition of acyl-CoA –> decreased triglyceride synthesis –> decreased VLDL –> decreased LDL mediated plaque formation
26
Q

Omega 3 AEs

A
  • common: eructation/dypepsia
  • Less: skin rash, increase liver enzymes
  • Sig: bleeding tendency disorder; A-fib/A-flutter
27
Q

Microsomal TG transfer protein (MTP) inhibitor indication

A
  • homozygous familial high chol.
  • ADJUNCTIVE to other cholesterol lowering meds, when statins stop working
  • only if high chol. is their only condition
28
Q

MTP inhibitor drug/route/MoA

A
  • Lomitapide
  • PO
  • MoA: binds MTP in liver & intestine –> blocks transport/formation of VLDL/chylomicron particles –> decrease level of both in blood stream –> decreased LDL formation
29
Q

MTP inhibitor (lopitamide) AEs

A
  • major GI issues (abd distension, constipation, D/N/V)
  • Increased liver enzymes –> additional hepatic lab monitoring required
30
Q

Angiopoietin-Like Protein 3 (ANGPTL3) inhibitor indication

A
  • Homozygous familial high cholesterol
  • ADJUNCTIVE to other LDL lowering meds
31
Q

(ANGPTL3) inhibitor drug/route/MoA

A
  • Evinacumab
  • route: IV
  • MoA: inhibits ANGPTL3 –> promotes clearance of VLDL remnants before they are metabolized to LDL
32
Q

(ANGPTL3) inhibitor AEs

A
  • infusion related rxns
  • hypersensitivity/anaphylaxis
  • also respiratory infections, GI issues, dizziness, limb pain
  • avoid pregnancy during use and for 5 months after last admin

Pharm 225A (7 decks)

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