Corticosteroids (Non-DMARD RA Tx)

Question 1

What are some advantages of corticosteroids?

Answer 1

Inexpensive, can inject into joint spaces

Question 2

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

Answer 2

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

Question 3

What happens after discontinuation of treatment with corticosteroids?

Answer 3

Disease modifying effects persist, specifically articular erosions

Question 4

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

Answer 4

They are often overestimated

Question 5

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

Answer 5

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

Question 6

What is the MOA of corticosteroids?

Answer 6

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

Question 7

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

Answer 7

cytosolic GC receptors (cGCRs)

Question 8

Additionally, how may corticosteroids exert effects?

Answer 8

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

Question 9

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

Answer 9

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).

Question 10

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

Answer 10

Peptic ulcer dz (give a PPI)

Question 11

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

Answer 11

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.

Question 12

What is the equivalent dose of corticosteroids adjusted on?

Answer 12

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

Question 13

What is the potency of all corticosteroids based off of?

Answer 13

Hydroxycortisone

Question 14

What is the action duration and activity of Hydroxycortisone?

Answer 14

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

Question 15

What is the action duration and activity of Cortisone?

Answer 15

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

Question 16

What is the action duration and activity of Prednisone?

Answer 16

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

Question 17

What is the action duration and activity of Triamcinolone?

Answer 17

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

Question 18

What is the action duration and activity of Betamethasone?

Answer 18

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

Question 19

What is the action duration and activity of Dexamethasone?

Answer 19

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