Term
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Definition
inhibits COX1 and 2. inhibits granulocyte adherence and chemotaxis. Used for prophylaxis of CAD, DVT, unstable angina, MI, and Stroke.
At low doses uric acid secretion is decreased -> gout.
Reyes syndrome (liver dysfunction and encephalopathy)
GI bleeds, hypersensitivity, salycylism, bronchoconstriction, renal dysfunction |
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Term
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Definition
Used for mild to moderate pain relief
No antiinflammatory, platelet, or GI effects
Used when aspirin can't be used and for antipyresis in children |
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Term
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Definition
Highly anti-inflammatory and analgesic
symptomatic treatment of gout, RA, OA |
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Term
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Definition
Effective for OA and musculoskeletal sprains analgesia.
Irreversibly inhibits thromboxane production in platelets. Long half life and more potent than aspirin |
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Term
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Definition
potent NSAID rapidly and completely absorbed from the GI. highly plasma bound. Anti-inflammatory, anti-pyretic, and analgesic
Used for all arthritis's and closing of PDA |
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Term
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Definition
prodrug 90% absorbed.
Highly potent COX inhibitor
Used for acute and long term treatment of OA, RA, bursitis, and acute gouty arthritis. |
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Term
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Definition
Long term treatment for RA, OA, and gout.
Long half life allows once daily dosing
High COX-2 affinity |
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Term
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Definition
potent analgesic (non-opiod option)
Do not use for more than 5 days for risk of GI bleeding. Contraindicated in GI bleeding pts. |
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Term
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Definition
highly selective for COX-2.
accumulates in synovial fluid and used for OA and ankylosing spondylitis. |
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Term
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Definition
only drug selective for COX-2.
Low GI side effects. No effect on platelets are bleeding. Long half life allows once daily dosing
Used for dysmenorrhea, OA, RA, and post-op.
Contraindicated in HTN or any cardiovascular condition. |
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Term
list in order of strength of analgesia.
ibuprofen, naproxen aspirin, and ketorlac |
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Definition
| ketorlac, naproxen, ibuprofen and aspirin is the weakest |
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Term
| Shared toxic effects of NSAIDs? |
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Definition
GI: dyspepsia, abd pain, diarrhea, ulcers
Cardiovascular: COX-2 inhibitors increase risk of thrombosis, stroke, and MI.
Acute renal failure in pts w/ decreased renal function
Hypersensitivity: rhinitis, angioedema, urticaria, bronchoconstriction, flushing, hypotension
Pregnancy: contraindicated in 3rd trimester from hemorrhage and delayed labor |
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Term
| How do you prevent GI effects of NSAIDs? |
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Definition
| Use a COX-2 inhibitor, prescribe low as possible dose, administer cotherapy such as misoprostol, H2 receptor antagonist or PPI. |
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Term
| What drugs will precipitate a gouty attack? |
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Definition
diuretics because you're removing water and concentrating the uric acid.
Aspirin because at low doses, secretion is decreased. |
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Term
What enzyme does allopurinol block?
Why used in chemo pts? |
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Definition
xanthine oxidase
in chemo pts it blocks tumor lysis syndrome which precipitates gout attacks. |
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Term
| what are some consequences of hyperuricemia? |
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Definition
| gout, tophi, renal lithiasis, acute tubular blockade |
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Term
| What are the initial NSAIDs of choice for the treatment of gout? |
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Definition
| indomethacin and ibuprofen. |
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Term
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Definition
microtubular blocker. Stops mitotic spindles, arrests cell division, mobility, and release of chemotactic factors. .Inhibits migration of leukocytes, and decreases mast cell degranulation
Dramtic relief for acute gout attacks but must be given w/in first few hours of attack.
SEs - N/V/D and bone marrow suppression limit dose and duration of therapy |
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Term
Corticosteroids given in gouty attack?
When? |
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Definition
intra-articular triamcinolone and oral prednisone
Given if pt unresponsive to NSAIDs, or colchicine and polyarticular involvment. |
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Term
| Metabolism of allopurinol? |
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Definition
metabolized in liver to active drug called oxypurinol and excreted via the kidney.
dosage adjustment needed in pts w/ hepatic and renal impairment. |
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Term
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Definition
blocks tubular reabsorption of uric acid. lowers blood levels of uric acid.
indicated for underexcretors |
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