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21 Cards in this Set

  • Front
  • Back
adaptive pain
nociceptive (protecting org from inj, early warning system for dangerous stimuli), inflammatory (promote healing of injured tissue)
maladaptive pain
abnl sensory processing, persistent or current, neuropathic (dmg to pns/cns), fxnal (abnl responsiveness/fxn of ns)
nsaid effects
analgesic: mostly periph (also central), use mild-med dull pain, can use w/ opioid, moa block pge2 synth (sensitize nn to chemical mediators at inflamm site)

anti-inflamm: red vasodilation/erythema (not acetaminophin), use ra (higher conc), moa inh pg from wbc (vasodilate, inc permeability)

antipyretic: red fever due to inc pge2 in hypothalamic thermoreg area (doesn't dec nl temp or non-pg e.g., exercise, heat stroke)
nsaid use
acute: pain relief, red inflamm, red fever, use ha, minor inj, dysmenorrhea, sxs/fever of cold/flu, acute bursitis

chronic: oa, ra, as (relieve sxs, do not modify dz prog)
aspirin
irreversible cox inh (via acetylation, can reverse w/ esterase but platelets can't synth pro), from willow bark, dec risk mi/cva (80 mg, inh txa), tx low intensity pain, red fever, anti-inflamm (325-650 mg), ra (1-4 g), long term use at low dose inh colon/other cancer

readily abs stomach (weak acid), small intestine (more sa, sol), wide dist (csf, peritoneal, synovial), acetylates albumin, deacetylated in liver/plasma to salicylic acid (also nsaid), nl dose 3 hr hl, high dose 15 hr (0-order kinetics), ph dep renal excrete (bicarb inc)

ae gi upset (bleed, ulcer, perf), 15% hs-like rxn, airway hyperreactivity, nasal polypse, reye's syndr (w/ virus), salicylism (tinnitus, sweating, vomit, epigastric pain, vision blur), acid/base imbalance, anticoag, renal fail (w/ ckd, chf, diuretics), gout (dec ua elim, inc elim at toxic levels)
aspirin poisoning
high tx dose: uncouple oxphos in skeletal --> dec o2, inc co2 --> resp stim co2 and direct effect on resp center --> hyperventilation --> resp alkalosis --> metab compensation excrete bicarb

toxic dose: depress resp center --> retain co2 --> bicarb already low w/ metab comp --> uncompensated resp acidosis superimposed on metab acidosis (inc pyruvic/lactic/acetoacetic acids), uncharged (enter cns faster), sxs fever/dehydration, hypokalemia
tx asa poisoning
mild salicylism (500-750 ug/ml) only needs po/iv rehydration, k supp

marked salicylism (750+) need elim tx: po activated charcoal (may choke), simple alkalinization (1L 26% na bicarb over 2 hr, keep urine ph 7.5+), hd if 1000+, persistant acidosis, or loss of consciousness
nsaid ae
renal effects: in a state of dec bv (cirhosis, nephrosis, hf, diuretics) or dec renal blood flow --> inc vasoconstrictor (angii, catecholamines, vasopressin) --> comepnsation by pg dilator inh by nsaid --> acute renal failure

gi: topical effect (minor, trap h in mucous) and systemic (inh pg synth --> dec mucous sec, inc h sec, antiplatelet)
ppi
red h sec, milder ae than misoprostol (diarrhea, constipation, abd pain, ha, long term stomach inf)
ibuprofen
equal to aspirin for arthritis (ra, oa), less gi irritation, anti inflamm dose > analgesia

di aspirin (antagonist, x-allergy)
indomethacin
mod-severe arthritis, very potent, very tox (gi), use gouty arthritis, as, oa of hip, close pda
sulindac
prodrug related to indomethacin, less ae
ketorolac
only nsaid im, mod-severe pain (post op), analgesia eq to morphine, not for anti-inflamm

ae gi upset, renal, bleeding (don't use pre op)
relative analgesia effects
ketorolac > ibuprofen, naproxen > aspirin
celecoxib
cox2 inh, oa/ra, manage acute pain in adults, 1ary dysmenorrhea, fap
rofecoxib
cox2 inh, not used due to significant inc risk mi, sudden death, moa inh only pgi2 from endothelium w/o inh platelets
valdecoxib
cox2 inh, not used due to significant inc risk mi, sudden death, moa inh only pgi2 from endothelium w/o inh platelets
best first line nsaid tx
naproxen + ppi
acetaminophen
antipyretic, analgesic, NOT anti inflamm, moa unknown (cox 3?)

ae due to p450 metab --> benzoquinone imine --> elim w/ glutathione sh group, a large dose depletes glutathione --> metabolites react w/ sulfhydryl groups in hepatic pro --> necrosis

tx tox w/ free sh groups (n-acetyl cysteine)
tramadol
only analgesic, NO anti inflamm or anti pyretic, moa weak opioid agonist, inh ne/5-ht uptake
overuse ha
if use nsaid 15+ days/mo get daily ha that varies in severity/type/location, predictable early morning (2-5am) ha, low pain threshold on phys/cog exertion