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Clinical Pharmacology > Lipid Therapeutics > Flashcards

Lipid Therapeutics Flashcards

1
Q

Newer statins

A

-Rosuvastatin* -Atorvastatin* -Simvastatin* -Pitavastatin -Pravastatin

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2
Q

Statins MOA

A

-Inhibition of HMG CoA reductase leads to the prevention of mevalonate being converted into cholesterol -Expression of the LDL receptor gene is upregulated and this leads to increased endocytosis of LDL -End result is lower serum LDL

Know the word mevalonate and HMG-CoA reductase*

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3
Q

What percent do statins lower LDL and TGs?

A
  • Decrease LDL by 30-60%
  • Decrease TGs 20-40%
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4
Q

Other beneficial effects of statins

A
  • Improve endothelial function
  • Reduce plasma viscosity
  • Plaque stabilization
  • Reduce inflammation
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5
Q

Statin indications

A
  • Primary prevention & secondary prevention
  • Start statins in DM patients at diagnosis (secondary)
  • Post AMI (secondary)
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6
Q

When should statins be taken?

A
  • Lovastatin, fluvastatin, and simvastatin* should be taken qhs when most cholesterol synthesis occurs due to shorter half life
  • the rest can be taken any time (atorvastatin)
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7
Q

Drug monitoring - statins

A
  • LFTs: At baseline and if there is evidence of liver dysfunction
  • Fasting BS/HgBA1c
  • CPK
  • FLP: 1-3 months after initiation and then every 3-12 months after that
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8
Q

Drug interactions - statins

A
  • Simvastatin and atorvastatin are major CYP3A4 substrates
  • Simvastatin most affected, especially with strong CYP3A4 inhibitors
  • Increases myopathy risk 5x -Simvastatin also a Pgp substrate –> Pgp inhibitors may increase myopathy risk as well
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9
Q

what drugs when mixed with a statin can cause additive interactions?

A

-Niacin + statin = additive myopathy -Fibrates + statin = additivt Hepatotoxicity/myopathy ***Specifically gemfibrozil (blocks hepatic clearance)

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10
Q

What antibiotic should you not mix with a statin?

A

-Daptomycin!!!!! Increased myopathy risk

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11
Q

What is the most common ADR from statins?

A
  • Myopathy (up to 30%)
  • Risk and severity often secondary to drug interactions or higher doses
  • Stop drug if CK >10x ULN (rhabdo)
  • Eval for Vit D deficiency, thyroid disorder, or PMR
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12
Q

Where do myalgias most commonly occur?

A

-Big muscles (thighs)

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13
Q

What gene (SNP) puts the patient at high risk for myopathy

A

SCL01B1

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14
Q

Strategies to work through myalgia/myopathy symptoms

A
  1. Eval RF 2. Eval med list for interacting drugs 3. Try CoQ10 4. Lowering dose may help 5. Change statin to low dose rosuvastatin 6. Try alternate day dosing*** 7. Add non-stain drug (Ezetimibe)
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15
Q

Myalgia and exercise

A

-Go slow and work up to 30 min of exercise/day -Increase duration of activity before intensity

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16
Q

Other HMG-CoA reductase inhibitor ADRs

A
  • Increased conc. of aminotransferase
  • DM (usually seen in pts with traditional RF*, don’t stop giving a statin when DM is dx)
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17
Q

What statin is a great option for someone with renal impairment?

A

Atorvastatin

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18
Q

Cholesterol absorption inhibitor, drug and MOA

A

-Ezetimibe -Blocks absorption in the small bowel, without affecting triglyceride or fat soluble vitamin absorption

19
Q

Clinical indications of cholesterol absorption inhibitor

A

Decrease LDL 20-25%

20
Q

Cholesterol absorption inhibitor drug interactions

A

-May increase warfarin effect -Do not mix with fibrates*

21
Q

Bile acid sequestrants, drug and MOA

A

-Colesevelam* -MOA: binds bile acids in intestines, grabs cholesterol and drags it through the intestines, get a reflexive TG bump

22
Q

Clinical use of bile acid sequestrants, when is it contraindicated?

A

-Decrease LDL up to 20%, can raise TG -DON’T USE if TG’s > 300 mg/dL

23
Q

Bile acid sequestrant ADRs

A

GI intolerance

24
Q

PCSK9 inhibitors, drugs and MOA

A

-Alirocumab -Evolocumab -MOA: modulates receptor degradation, prevents the LDL-C clearance from blood, and increased serum LDL

25
Q

Clinical indication and pearls of PCSK9 inhibitors

A

-Adjunct to diet/max tolerated statin for pts with familial hypercholesterolemia -Decrease LDL by 60% (very potent) -$$$

26
Q

ATP-Citrate Lyase inhibitors, drug and MOA

A

-Bempedoic acid (can add ezetimibe) -Activated by ACSVL1, this is basically like an upstream version of a statin that blocks at its precursor

27
Q

ACL inhibitors clinical indiciations

A

Same as PCSK9, adjunct to diet and max tolerated statin therapy in pts with hetero familial hypercholesterolemia or ASCVD who need extra LDL lowering

28
Q

If you combine Bempedoic acid with a statin, you are at in increased risk of..?

A

Myopathy

29
Q

Common ADRs of ACL inhibitors

A
  • Muscle spasms and back/extremity/abd pain
  • Anemia/leukopenia
  • Elevated LFTs
  • Increases urate*
  • Tendon rupture******** (also FQ)
30
Q

Targeting HDL and TG, drug and MOA

A
  • Niacin (extended-release -> least flushing and HTX)
  • Inhibits the mobilization of free fatty acids from peripheral adipose tissue to the liver, hence VLDL decreased
31
Q

What drug favorably modifies all plasma lipoproteins and lipids?

A

Niacin (increase HDL 15-35%, decrease TG 10-50%, decrease LDL 5-25%)

32
Q

How should you dose niacin?

A

Very slowly

33
Q

What is the one thing Robert Downey junior said to know regarding monitoring with niacin?

A

Glucose (baseline, 3 months, then annually)

34
Q

ADRs of niacin

A
  • FLUSHING (induced by local production of prostaglandins)
  • HTX
  • Aggravate glucose and gout
35
Q

Targeting TG, drug and MOA

A
  • Fibric acid derivatives (fenofibrate*, gemfibrozil)
  • MOA: Agonizes PPAR-alpha (the glitazones also do this)
36
Q

Clinical use of the fibric acid derivatives

A
  • Persistent hyperTG, severe, at risk of pancreatitis (>800)*
  • Uricosuric activity, gout prevention
37
Q

CYP interactions with gemfibrozil

A

2C9 and 2C19 inhibitors

38
Q

ADRs of fibric acid derivatives

A

N/V, dyspepsia MC

39
Q

Clinical use of fish oils

A

-Decrease TG 20-50% -Long term may increase HDL

40
Q

Drug interactions to be aware of with fish oils

A

High doses have antiplatelet effects

41
Q

Lipid Management

A
  1. Decide if therapy is indicated 2. Start moderate to high risk statin therapy
42
Q

Steps in statin intolerant patients

A
  1. CVD pt who cannot tolerate a high-intensity (ezetimibe, only non-statin that improves CV outcomes) 2. Monotherapy, high CV risk who CAN’T take a statin (PCSK9 inhibitors for very high-risk pts)
43
Q

What is the overall approach to metabolic syndrome?

A

-A: assessment of CV risk and ASA therapy -B: BP control -C: cholesterol mgmt -D: DM prevention and diet therapy -E: exercise therapy

44
Q

Pregnancy and Statins

A
  • Category X -D/c statin 2/3 months before planning on becoming pregnant
  • Just don’t treat lipids in pregnant pts

Clinical Pharmacology (54 decks)

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