antiarthritics Flashcards
(34 cards)
Hydroxychloroquine Sulfate (Plaquenil)
Nonbiologic Disease Modifying Antirheumatic Drugs (DMARDs)
half-life: 6-7 days! long!
deposits in tissues (eyes)–>irreversible ocular toxicity
retinopathy
fetal uveal tissue (CI in preg.)
may use in combo with corticosteroids and salicylates
Methotrexate (Trexall, Rheumatrex)
non-bio DMARD
- see immune lecture
v. common, cheap
Sulfasalazine (Azulfidine)
non-bio DMARD
split in intestine–>5-ASA*(active) and SP (danger)
SP–>acetyl-SP: slow or fast metabolizers–>slow metabs @ risk for adverse events
affin. for CT, immunosuppr.
* reversible* neutropenia (vs. hydroxchloraquine)
Leflunomide (Arava®)
non-bio DMARD
inhibits dihydroorotate dehydrogenase (pyrimidine biosyn.)
antiproliferative,
anti-inflamm, tx for RA
6-12 hr onset, 2wk half life!!!
hepatotoxicity- black box (FDA warning)
not used in pregnancy
Etanercept
bio DMARD
TNF inhibitor
dimeric fusion protein: human rec. P75 attached to Fc of IgG–>attaches TNF-a or B and inhibits their binding to TNF receptors
risks: infections, sepsis and malignancies
tx: RA, JRA
can use in combo with methotrexate
Infliximab (Remicade)
bio DMARD
TNF inhibitor
chimera: human Fc IgG, murine variable region-binds TNF-a (NOT TNF-B)
half life about 9.5 days
tox: hypersn to murine portion
immunosuppr: TB, fungal infections, OIs
infusion-rel. reactions: dev. human anti-chimeric Abs (HACAs)
tx: RA, Crohn’s
used in combo with methotrexate
Anakinra
bio DMARD
non-TNF inhibitor
IL-1 receptor antagonist
non-bio DMARDs already know
Azathioprine (Imuran®)
Cyclosporine (Sandimmune, Neoral)
arthritis
assoc. with spondylitis
degen. joint disease
assoc. with infection
initial tx??
then move on to ??
aspirin, salicylates, NSAIDs (if do not tolerate/respond to salicylates)
disease‐modifying antirheumatic drugs (DMARDs)
use ?? for flares
glucocorticoids, don’t want to use chronically
prednisone, prednisolone
ASA dosage
3 gs/day
3-6 for significant anti-inflam.
GI intolerance
NSAIDs
same affects as ASA
*indomethacin: less GI complaints
combo therapy of DMARDs
synergistic
reduce resistance and toxicity
*agent of choice det. by pt and physician
70-80% of individuals w. RA show…
RF
B‐cells that secrete immunoglobulins, including the autoantibody rheumatoid factor, which can be identified in 80% of affected individuals.
inflammatory mediators present in RA
complement cleavage products, leukotrienes, prostaglandins, histamine, serotonin, proteases, platelet‐activating factor and cytokines (TNF‐), IL‐1, IL‐6, etc)
neutrophils–>lysosomal enz. TOI, AA cascade products
progressive RA therapy
a. Reduce pain, swelling and inflammation
b. Maintain joint mobility and range of motion
c. Prevent deformity
d. Retard disease progression
start pt w. education, PT, OT…then
salicylates (ASA) and NSAIDS
use ??? btw 1st and 2nd line agents
low-dose corticosteroids
“bridge”
DMARDs
2nd line
slow onset, more toxic
agent det. by Dr., pt
consider: convenience, monitoring, costs, time of onset, adverse effects
early RA (
mild:
DMARD monotherapy: methotrexate/Cl on its own
mod or high:
DMARD combo
+/- TNF inhibitor
established RA (>6 mos)
mild:
DMARD combo
mod or high:
DMARD combo
+ TNF inhibitor OR
+ non-TNF inhibitor
JRA tx: ASA ?
concern for Reyes w. ASA
JRA tx: NSAIDs?
use Tolmetin and Naproxen
