Summary Table of Drugs Used in Dyslipidemia Flashcards

1
Q

Which drug: MOA

Inhibit HMG-CoA reductase

A

Statins

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2
Q

Which drug: MOA

Peroxisome proliferator- activated receptor-alpha (PPAR-α) agonists

A

Fibrates

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3
Q

Which drug: MOA

  • Binds bile acids in gut
  • prevents reabsorption
  • increases cholesterol catabolism
  • upregulates LDL receptors
A

Bile acid sequestrants

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4
Q

Which drug: MOA

Blocks sterol transporter NPC1L1 in intestine brush border

A

Cholesterol absorption inhibitor

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5
Q

Which drug: MOA

  • Decreases catabolism of apo AI
  • reduces VLDL secretion from liver
A

Niacin

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6
Q

Which drug: MOA

Complexes PCSK9

A

PCSK9 humanized monoclonal antibodies

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7
Q

Which drug: Effects

  • Reduce cholesterol synthesis and upregulate low-density lipoprotein (LDL) receptors on hepatocytes
  • modest reduction in triglycerides
A

Statins

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8
Q

Which drug: Effects

  • Decrease secretion of very- low-density lipoproteins (VLDL)
  • increase lipoprotein lipase activity
  • increase high- density lipoproteins (HDL)
A

Fibrates

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9
Q

Which drug: Effects

Decreases LDL

A

Bile acid sequestrants

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10
Q

Which drug: Effects

  • Inhibits reabsorption of cholesterol excreted in bile
  • decreases LDL and phytosterols
A

Cholesterol absorption inhibitor

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11
Q

Which drug: Effects

  • Increases HDL
  • decreases lipoprotein(a) [Lp(a)], LDL
A

Niacin

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12
Q

Which drug: Effects

Inhibits catabolism of LDL receptor

A

PCSK9 humanized monoclonal antibodies

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13
Q

Which Drug: Clinical Applications

  • Atherosclerotic vascular disease (primary and secondary prevention)
  • acute coronary syndromes
A

Statins

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14
Q

Which Drug: Clinical Applications

Hypertriglyceridemia, low HDL

A

Fibrates

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15
Q

Which Drug: Clinical Applications

Elevated LDL, digitalis toxicity, pruritus

A

Bile acid sequestrants

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16
Q

Which Drug: Clinical Applications

Elevated LDL, phytosterolemia

A

Cholesterol absorption inhibitor

17
Q

Which Drug: Clinical Applications

  • Low HDL
  • elevated VLDL, Lp(a); elevated LDL in statin- unresponsive or intolerant patients
A

Niacin

18
Q

Which Drug: Clinical Applications

Familial hypercholesterolemia not responsive to oral therapy

A

PCSK9 humanized monoclonal antibodies

19
Q

Which Drug: PK, Toxicities, Interactions

  • Oral
  • Duration 12-24 h
  • Toxicity: Myopathy, hepatic dysfunction
  • Interactions: CYP-dependent metabolism (3A4, 2C9) interacts with CYP inhibitors/competitors
A

Statins

20
Q

Which Drug: PK, Toxicities, Interactions

  • Oral
  • duration 3–24 h
  • Toxicity: Myopathy, hepatic dysfunction
A

Fibrates

21
Q

Which Drug: PK, Toxicities, Interactions

  • Oral
  • taken with meals
  • not absorbed
  • Toxicity: Constipation, bloating
  • interferes with absorption of some drugs and vitamins
A

Bile acid sequestrants

22
Q

Which Drug: PK, Toxicities, Interactions

  • Oral
  • duration 24 h

• Toxicity: Low
incidence of hepatic dysfunction, myositis

A

Cholesterol absorption inhibitor

23
Q

Which Drug: PK, Toxicities, Interactions

  • Oral
  • large doses
  • Toxicity: Gastric irritation, flushing, low incidence of hepatic toxicity
  • may reduce glucose tolerance
A

Niacin

24
Q

Which Drug: PK, Toxicities, Interactions

  • Parenteral
  • Cost ~ $14,000/year
  • Toxicity: injection site reactions, nasopharyngitis, flu-like symptoms, rarely myalgia, neurocognitive and ophthalmologic events
A

PCSK9 humanized monoclonal antibodies