Anti-Inflammatories Flashcards
Cardinal signs of inflammation
- redness
- swelling
- heat
- pain
- loss of function/ROM
Prostaglandins
- chemical mediators
- vasodilation, relaxation of smooth muscle, increased capillary permeability, sensitization of nerve cells to pain
- synthesis causes inflammation and pain at site
Cyclooxygenase (COX) enzyme
- converts arachidonic acid into prostaglandins
- COX1 - protects stomach lining and regulates platelets; decreases fever
- COX2 - triggers inflammation and pain
Salicylates
- inhibits biosynthesis of prostaglandins
- inhibits COX1 –> decreases protection of stomach lining
- inhibits COX2 –> decreases inflammation and pain
- increased risk of ulceration, bleeding
- therapeutic serum level –> 15 - 30 mg/dL
- do not give to children w/ flu or virus symptoms –> Reye’s syndrome
- S/E: tinnitis/hearing loss, blood dyscrasias, hepatotoxicity, GI distress
- interacts w/ anticoags, oral antidiabetics, glucocorticoids, ACE inhibitors, loop diuretics, corticosteroids
Aspirin (acetylsalicylic acid, ASA)
severe toxicity over 50 mg/dL
Para-chlorobenzoic Acid
- inhibits prostaglandin synthesis
- 99% protein bound
- used for RA, OA, gouty arthritis, trauma pain
- Causes Na and H2O retention –> not for unmanaged/unstable HTN
indomethacin
be careful w/ warfarin, gemfibrazil, diphenhydramine
Phenylacetic acid derivatives
- inhibit prostaglandin synthesis
- used for RA, OA, ankylosing spondylitis, pain
- no antipyretic effect
- S/E: GI issues, hard on kidneys if PO
diclofenace sodium, ketorolac (toradol)
black box warning for ketorolac, recommended for short-term pain management, not for kids
Proprionic acid derivatives
- most widely used NSAID, OTC
- inhibits prostaglandin synthesis, COX1&2 inhibitor
- used for pain, RA, OA
- S/E: GI issues (not as severe as other NSAIDs), tinnitus, dysrhythmias, nephrotoxicity
- interacts w/ warfarin, phenytoin, sulfonamides, cephalosporins, aspirin, oral antidiabetics/insulin, calcium channel blockers
- may take 1-3 weeks for therapeutic effects (depending on reason for taking)
ibuprofen, aleve, motrin, naproxen, ketoprophen
Fenamates
- inhibits prostaglandin synthesis
- for OA, RA, pain, dysmenorrhea (may make bleeding worse initially)
- S/E: tinnitus, edema, renal dysfunction, elevated hepatic enzymes, stroke, GI distress
- avoid w/ Hx of peptic ulcer
meclofenamate
Oxicams
- inhibits prostaglandin synthesis
- some COX2 selectivity
- for OA, RA
- S/E: GI distress, renal dysfunction, angioedema, elevated hepatic enzymes, stoke
meloxicam
Selective COX2 inhibitors
- selectively inhibits COX2 w/o inhibition of COX1
- for OA, RA, ankylosing spondylitis, pain, dysmenorrhea
- S/E: Gi distress, peripheral edema, renal dysfunction
celecoxib, nabumetone similar
Corticosteroids
- control inflammation by supressing many components of inflammatory process at injured site
- used for arthritic flare-ups, not drug of choice d/t SE
- must taper off over 5-10 days, otherwise fatal
prednisone, prednisolone, dexamethasone
Disease-modifying antirheumatic drugs
- -mab
- immunosuppressive, immunomodulators
- alleviate symptoms of RA, OA when other treatments fail
- S/E: infection, elevated hepatic enzymes, blood dyscrasias
infliximab
Gout
- defect in purine metabolism leads to uric acid crystal accumulation (calculi)
- can be affected by diet
Colchicine
- inhibits migration of leukocytes to inflammed site (part of inflammation process)
- alleviates gout symptoms
- contra w/ severe renal, cardiac, or GI problems
Uric Acid inhibitors
- decreases uric acid synthesis, prevents gout attacks
- not anti-inflammatory
- S/E: arthralgia, ED, blood dyscrasias, SJS, GI issues, renal/hepatic impairment
allopurinol, febuxostat
advise yearly eye exam, vision can change on allopurinol
