NSAIDs II

what are the two propionic acid derivative NSAIDs?
ibuprofen and naproxen
what are the 4 As of ibuprofen? how is it different than asa?
analgesic, antiinflammatory, antipyretic, antiplatelet (reversible – different than ASA, effect is lost within 1-2 days therefore not normally used for this effect)
what are the indications for ibuprofen?
same as asa: pain, inflammation, fever, (pyrogen-induced and CNS response)
what is the M/A of ibuprofen?
competetive inhibition of COX
does it have high blood plasma binding? does it interact with oral hypoglycemics/anticoagulants?
yes, 99%. it does not interact with oral hypoglycemics/anticoagulants <- WITH RESPECT TO BINDING
what are side effects of ibupofen?
GI, nausea/heartburn, some intestinal erosions, not as much occult blood loss, but some ocular disturbances/skin rashes/headache
what are the effects of naproxen? how is it used?
same as ibuprofen: analgesic, antiinflammatory, antipyretic, antiplatelet (reversible – different than ASA, effect is lost within 1-2 days therefore not normally used for this effect). it is indicated for the same symptoms as well: analgesic, antiinflammatory, antipyretic, antiplatelet (reversible – different than ASA, effect is lost within 1-2 days therefore not normally used for this effect)
what is the mechanism of naproxen?
competetive COX inhibitor, inhibits hydrolytic enzymes of lysosomal system, and inhibits migration of PMN leukocytes.
how much does naproxen bind to blood plasma protein? interactions with
high plasma protein binding: 99% it does not interact with oral hypoglycemics/anticoagulants <- WITH RESPECT TO BINDING
what are some side effect with naproxen?
less occult blood loss than asa, drowsiness, vertigo, headache, fatigue, ototoxicity, GI disturbance (emesis, dyspepsia, bleeding), pruritis
what are the heteroaryl acetic acids?
ketorolac (toradol), tolectin (tolectin), diclofenac (voltaren)
what does ketorolac (toradol) do?
it is an analgesic, antiinflammatory, antipyretic, which also prolongs bleeding time (antiplatelet) reversible 24-48 hr)
what is ketorolac used for/how is it adminstered?
short term pain relief via IM injection most commonly
what is the M/A for ketorolac? how well does it bind plasma protein? any interaction with other drugs?
highly potent COX inhibitor. it binds 99% of plasma protein and has little if any interaction with other drugs
what are some side effects of ketorolac?
nausea, dyspepsia, GI pain (can become gastric-erosive w/long term), drowsiness
what are some contraindications for ketorolac?
it has additive side effects with other NSAIDs (synergistic – more GI complaints). ketorolac is contraindicated w/partial or complete syndromw of nasal polyps, angioedema and bronchospasm. also contraindicated with previously hypersensitivity to ketorolac.
what are the effects of tolmetin (tolectin)?
same 4 As: analgesic, antiinflammatory, antipyretic, prolongs bleeding time, and less occult blood than asa (less GI disturbance and less platelet interaction)
what is tolmetin used for?
RA and osteoarthritis ONLY
what is the M/A for tolmetin? what is its plasma protein binding? does it compete with other drugs for binding?
competitive COX inhibitor. 99% plasma protein binding and it does not interact with oral hypoglycemics/anticoagulants <- WITH RESPECT TO BINDING
what are side effects for tolmetin? do many people experience them?
25-40% of people experience epigastric pain, nausea/vomiting, gastric/duodenal ulceration, CNS effects (tinnitus, nervouseness, anxiety, drowsiness). 5-10% discontinue.
what does diclofenac (voltaren) do?
it is an analgesis, antiinflammatory and antipyretic
what is diclofenac prescribed for?
*long term management of RA, osteoarthritis and ankylosing spondylitis. also has been used for post op pain, bursitis, and acute musculoskeletal injury
what is the M/A for diclofenac?
it is a competetive COX inhibitor. it also reduces intracellular concentrations of free arachindonate in leukocytes
what is diclofenac’s protein binding? does it compete with any other drugs? is it subject to first pass effect?
it is 99% plasma protein bound, with minimal competetion with warfarin (if someone is on this and anticoagulant, they need to initially have their levels measured more than once per month). it has a 50% first pass effect
what are side-effects associated with diclofenac?
20% of pts experience epigastric pain/nausea/emesis/gastric ulceration, CNS effects: tinnitus, nervousness, anxiety, drowsiness, and skin rashes/allergies.
what are the 2 enolic acids?
piroxicam (feldene) and phenylbutazone (butazolidin)
what does piroxicam (feldene) do?
4 As (equivalent to asa, indomethacin or naproxen, but much better tolerated)
what is piroxicam used for?
osteoarthritis, RA, acute gout
what is the M/A of piroxicam?
it is a potent COX inhibitor that also inhibits activation of neutrophils and hemostasis
how does piroxicam bind to plasma protein? does it compete with other drugs?
piroxicam binds 99 to plasma protein that may compete with warfarin and has enterohepatic recycling
do pts on piroxicam experience side effects?
11-46% experience GI symptoms, along with a 1% incidence of peptide ulcers. 4-12% discontinue
what does phenylbutazone do?
analgesic (though inferior to asa for non-rheumatic pain), antiinflammatory (most prominent) antipyretic, very toxic and uricosuric similar to asa (helps with excretion of uric acid)
what is phenylbutazone used for?
acute gout and RA (infrequently these days due to toxicities)
what is the mechanism of phenylbutazone? how well does it bind plasma protein? does it compete with other drugs for plasma protein binding?
it is a COX inhibitor. it binds plasma protein 98% and competes with other NSAIDs, warfarin, oral hypoglycemic, and sulfonamides
what are the side effects of phenylbutazone?
10-45% of pts commonly experience epigastric pain, nausea, emesis and skin rashes. gastric ulceration, CNS effects (vertigo, insomnia, euphoria, nervousness), nephritis, hepatitis, aplastic anemia, agranulocytosis can also occur. 10-15% discontinue
what are contraindications for phenylbutazone?
phenylbutazone is contraindicated for pts w/ cardiac, hepatic or renal dysfunction, blood dyscrasias. it can promote retention of Na+ and Cl- w/water leading to cardiac decompensation and pulmonary edema in some pts
what are the indole and indene acetic acids? what do they do?
the indole and indene acetic acids are indomethacin (INDOCIN) and sulindac (CLINORIL). they are analgesic, antiinflammatory, antipyretic and antiplatelet (leading to significant occult blood loss)
what are indomethacin or sulindac used for?
RA, ankylosing spondylitis, acute gout. it can be used to close patent ductus arteriosus (all NSAIDs can do this, which is why they are used with caution in pregnancy)
what is the M/A of indomethacin? how is it administered?
MOST potent inhibitor of COX, also inhibits mobility of PMN lymphocytes. it can be taken PO or IV. it is used only in short term (8 days), or low doses for gout
well does indomethacin bind plasma protein?
indomethacin/sulindac bind 90% plasma protein (can also bind extensively to tissues).
what are the side effects of indomethacin?
35-50% experience abdominal pain, nausea, anorexia, gastric ulceration, significant occult blood loss, CNS effects: severe frontal headache, vertigo, mental clouding, depression, psychosis, skin rashes, allergic rxns, nephritis, aplastic anemia, thrombocytopenia. 20% discontinue.
what is indomethacin contraindicated for?
concurrent administration with warfarin/asa b/c of increased risk of GI bleeding
does indomethacin interact with any drugs?
antihypertensives of thiazide diuretic class, beta-blockers and ACE inhibitors
what is sulindac? how does it compare to indomethacin?
a congener of indomethacin, a prodrug where a sulfide metabolite is the active agent. it is less irritating to the gastric mucosa than indomethacin, (but still more irritating to the gastric mucosa than other NSAIDs). its toxic effect is also similar to indomethacin
what are the selective COX2 inhibitors? what do they inhibit?
celecoxib (celebrex) and rofecoxib (vioox, pulled off market) are both selective inhibitors of COX2 (inflammatory tissue) and do not inhibit COX1 (stomach), at therapeutic conditions
what does celecoxib do?
anti-inflammatory, analgesic, analgesic, (not antiplatelet b/c platelets do not get inflamed)
how is celecoxib administered? when does it reach peak plasma levels, steady state? how much plasma protein does it bind? what is it metabolized by? how is it excreted?
celecoxib is absorbed following PO. it reaches peak plasma levels at 3 hours and steady state at day 5. it binds plasma protein 97% and is metabolized by P450 (unlike any other NSAID but acetaminophen). celecoxib is excreted in feces and urine
what are side effects of celecoxib?
can cause GI ulceration, bleeding, and perforation (but with a lower incidence than other NSAIDs). may cause a premature closure of the ductus arteriosus
what generically available NSAID was close to celecoxib in terms of low GI ulcer incidence?
diclofenac
what is a contraindication for celebrex?
sulfa allergies
what is misoprostol (cytotec)? what is a major contraindication for it?
PGE1 analog, used to suppress gastric ulceration for pts with chronic NSAID treatment. it has a abortifacient property and therefore should not be used in pregnancy.
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