Corticosteroids (Non-DMARD RA Tx) Flashcards

1
Q

What are some advantages of corticosteroids?

A

Inexpensive, can inject into joint spaces

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2
Q

In addition to suppressing signs and sx of RA what else do they do?

A

They appear to have a disease modifying effect, at least in early RA

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3
Q

What happens after discontinuation of treatment with corticosteroids?

A

Disease modifying effects persist, specifically articular erosions

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4
Q

What can be said about the ADE’s of corticosteroids?

A

They are often overestimated

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5
Q

If corticosteroids are give in accordance with physiological circadian rhythms, what happens?

A

It may bring safety and efficacy benefits because it is being administered with normal cortisol which may reduce endocrine suppression that is seen with traditional corticosteroid treatment

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6
Q

What is the MOA of corticosteroids?

A

Binding cytosolic glucocorticoid receptors and translocate to the nucleus where they act to inhibit NF-kB, AP-1, and NFAT which decrease inflammatory cytokines IL-1, IL-6 and TNF-a. This inhibits RANKL, which is responsible for osteoclast activation

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7
Q

What do the majority of anti-inflammatory effects occur via with corticosteroids?

A

cytosolic GC receptors (cGCRs)

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8
Q

Additionally, how may corticosteroids exert effects?

A

Rapid, non-genomic mechanisms (action on Src and intercalation into plasma and mitochondrial membranes)

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9
Q

What are the ADEs of glucocorticoids dependent on and what kind of monitoring must take place?

A

They are dependent on cumulative and daily dose as well as high/low dose; Coadmin of DMARDS can increase ADE’s; Increased monitoring for high doses (monitor everyone for osteoporosis, glaucoma, and ankle edema).

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10
Q

If a corticosteroid is given with an NSAID what can happen?

A

Peptic ulcer dz (give a PPI)

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11
Q

What can the corticosteroids “mess with” in regards to their daily monitoring?

A

It messes with lipid profiles, glucose regulation, and inculin response which increases CV ADE’s (RA pts already at increased risk for CV) and increase risk of infection.

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12
Q

What is the equivalent dose of corticosteroids adjusted on?

A

Potency; only short acting have mineralocorticoid activity (NA/H2O retention)

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13
Q

What is the potency of all corticosteroids based off of?

A

Hydroxycortisone

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14
Q

What is the action duration and activity of Hydroxycortisone?

A

Short acting, Anti-inflamm and salt-rention = 1, oral dose = 20mg (oral/IV)

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15
Q

What is the action duration and activity of Cortisone?

A

Short acting, .8 Anti inflam/salt retention = 25 mg, oral

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16
Q

What is the action duration and activity of Prednisone?

A

Short acting, 4x anti-inflam = 5 mg and .3 salt retention, oral

17
Q

What is the action duration and activity of Triamcinolone?

A

Intermediate acting, 5x anti-inflam = 4mg and 0 salt retention, oral/IV

18
Q

What is the action duration and activity of Betamethasone?

A

Long acting; 25-40x anti-inflam = .6mg and 0 salt retention, oral/IV

19
Q

What is the action duration and activity of Dexamethasone?

A

Long acting; 30x anti-inflam = .75mg and 0 salt retention, Oral/IV