antiinflammatory drugs Flashcards
H1 antagonists
competitive inhibitors (ineffective at high histamine levels), require hepatic activation. most cross the BBB and placenta.
use of H1 antagonist
type I HSR. motion sickness, vertigo. nausea, vomiting, preop sedation. OTC sleep aids, and cold remedy
SE of the H1 antagonisrts
M block and sedation.
diphenhydramine
strong M block. antimotion sickness. widely used OTC.
SE of diphenhydramine
SEDATION
promethazine
antihistamine. strong M block. some antimotion. does cause sedation. anesthetic.
chlorpheniramine
some M block, some sedation, some antimotion, CNS stimulation.
meclizine
some M block, some sedation, HUGE antimotion sickness. highly effective for antimotion sickness
cetirizine/loratadine/fexofenadine
no CNS entry, no M block, no sedation. ONLY FOR USE ON ALLERGIES
what inhibits phospholipase A2 and thus decreases all inflammatory mediators?
glucocorticoids
what do NSAIDs do
nonselective inhibitors of COX1/2 decrease prostaglandins and thromboxanes. all have analgesic, antipyretic, and antiinflammatory as well as antiplatelet function by definition.
what is the mechanism for NSAID
irreversible inhibition by binding covalently to serine hydroxyl
functions of the low dose NSAID
antiplatelet. also decrease tubular secretion of uric acid and thus cause hyperuricemia.
functions of moderate dose NSAID
analgesics and antipyresis.
functions of high dose NSAID
antiinflammation. this also decreases the reabsorption of uric acid and causes uricosuria.
what is the hallmark of reaching the antiinflammatory range of NSAID treatment
tinnitus.
what is REYE syndrome
high dose ASA toxicity of children with viral illness. this is caused by ETC uncoupling.
SEof ASA
acute gastritis, ulcers, bleeding. salicylism (tinnitus, vertigo, decrease hearing). bronchoconstriction (never use in asthmatics), HSR. increases bleeding time.
what can we use to combat ASA gastritis
misoprostal.
what is chronic ASA use associated with
papillary necrosis of renal tubules. this causes renal dysfunction.
which is the worst NSAID to use for analgesia? what is the best
Aspirin. ketorolac
what is the NSAID with NO renal dysfunction
sulindac
what are the other SE of sulindac
SJS, hematoxic
what is indomethicin
strong NSAID.
what are the SE of indomethicin
hematoxicity thrombocytopenia, agranulocytosis.
what is celecoxib
COX2 selective. there is no more efficacy than the others. but there is less GI irritation, less antiplatelet activity.
what is the huge negative about celecoxib
it is associated with endothelial cell dysfunction MI and stroke.
acetominophen
there is no inhibition of COX. it is completely devoid of antiinflammatory affects. it is equivalent in analgesic and antipyretic effects.
what does acetominophen have NO functions at doing
no antiplatelet activity, not implicated in reye syndrome, no effects on uric acid, not bronchospasmatic, GI is low.
what is the major SE of acetominophen
hepatotoxicity through depletion of glutathione
what is the antidote to acetominophen toxicity
N-acetylcysteine within the first 12 hours.
