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21 Cards in this Set
- Front
- Back
adaptive pain
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nociceptive (protecting org from inj, early warning system for dangerous stimuli), inflammatory (promote healing of injured tissue)
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maladaptive pain
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abnl sensory processing, persistent or current, neuropathic (dmg to pns/cns), fxnal (abnl responsiveness/fxn of ns)
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nsaid effects
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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) |
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nsaid use
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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) |
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aspirin
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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) |
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aspirin poisoning
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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 |
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tx asa poisoning
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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 |
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nsaid ae
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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) |
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ppi
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red h sec, milder ae than misoprostol (diarrhea, constipation, abd pain, ha, long term stomach inf)
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ibuprofen
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equal to aspirin for arthritis (ra, oa), less gi irritation, anti inflamm dose > analgesia
di aspirin (antagonist, x-allergy) |
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indomethacin
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mod-severe arthritis, very potent, very tox (gi), use gouty arthritis, as, oa of hip, close pda
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sulindac
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prodrug related to indomethacin, less ae
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ketorolac
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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) |
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relative analgesia effects
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ketorolac > ibuprofen, naproxen > aspirin
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celecoxib
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cox2 inh, oa/ra, manage acute pain in adults, 1ary dysmenorrhea, fap
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rofecoxib
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cox2 inh, not used due to significant inc risk mi, sudden death, moa inh only pgi2 from endothelium w/o inh platelets
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valdecoxib
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cox2 inh, not used due to significant inc risk mi, sudden death, moa inh only pgi2 from endothelium w/o inh platelets
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best first line nsaid tx
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naproxen + ppi
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acetaminophen
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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) |
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tramadol
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only analgesic, NO anti inflamm or anti pyretic, moa weak opioid agonist, inh ne/5-ht uptake
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overuse ha
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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
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