Corticosteroids Flashcards

1
Q

In addition to suppressing signs/symptoms of RA, corticosteroids also appear to have?

A

Disease modifying effects

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2
Q

Do the dz modifying effects of CS stop once you stop the therapy?

A

No, they persist after therapy is stopped!

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3
Q

CS get a bad rap for having severe systemic adverse effects. But come on, are low dose CS really that bad?

A

No, docs and pts probably overestimate the risk of AE’s in LOW DOSE corticosteroids.. Due to the serious AE’s of HIGH potency CS. So go ahead, give a low dose CS, it aint that big a deal

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4
Q

So you’re gonna give a low dose CS, what should you consider about WHEN the drug is absorbed and distributed in the body?

A

Consider circadian rhythms. Endogenous cortisol peaks when we sleep. It makes sense, then, that tx with CS should aim to make the drug distribute at night (slow release tablets before bed, perhaps)

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5
Q

Overall big picture MOA of CS?

A

Regulate transcription activity of inflammatory and anti-inflammatory cytokines

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6
Q

In which cellular compartment do CS work? How do they get there?

A

CS work in the nucleus (duh, they regulate transcription). They get there by binding to cytosolic glucocorticoid receptors which translocate the CS to the nucleus

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7
Q

Which transcription factors do CS inhibit? And therefore which inflammatory cytokines are down-regulated?

A

CS inhibit NF-kB, AP-1, and NFAT. This causes down-regulation of the inflammatory cytokines: TNF-alpha, IL-1, & IL-6

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8
Q

The reductions of those specific cytokines in CS tx leads to reduction of what?

A

Decreases RANKL –> decreased osteoclast –> decreased breakdown of bone (Good for RA!)

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9
Q

CS have adverse effects on pretty much everything. What can they do to bone?

A

Osteoperosis

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10
Q

What does DMARD co-administration with CS do?

A

Increases CS adverse effects

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11
Q

What does NSAID co-administration with CS do?

A

Increase risk for Peptic ulcer disease (GI bleeds)

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12
Q

What can you give to prevent osteoporosis in patients taking CS?

A

Bisphosphonate

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13
Q

What can you give to prevent PUD in patients taking CS?

A

Proton pump inhibitor

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14
Q

What other ADEs do corticosteroids have?

A
  1. Messes with lipid profiles
  2. Messes with sugars (glucose regulation and insulin response)
  3. CV adverse effects
  4. Increased risk of infection
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15
Q

What are the short acting CS and what is unique about them?

A

Hydrocortisone, Cortisone, Prednisone/Prednisolone, & Methylprednisone. Have mineralocorticoid activity –> salt & water retention

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16
Q

What is the intermediate acting CS? What is it’s anti-inflammatory potency relative to Hydrocortisone?

A

Triamcinolone. 5x as potent as Hydrocortisone

17
Q

What are the long acting CS? What is their potency relative to Hydrocortisone?

A

Betamethasone: 25-40x
Dexamethasone: 30x

18
Q

Which CS are available in injectable form?

A

Hydrocortisone, Triamcinolone, Betamethasone, DExamethasone

19
Q

Which CS are available in oral form only?

A

Cortisone, Prednisone

**Sweatman actually never talks about Prednisolone or Methyprednisone in his document