Neuro/Psych-quiz 2-pain

Card Set Information

Author:
Ambestul
ID:
8667
Filename:
Neuro/Psych-quiz 2-pain
Updated:
2010-03-01 17:20:04
Tags:
n p
Folders:

Description:
quiz 2
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user Ambestul on FreezingBlue Flashcards. What would you like to do?


  1. transduction
    cell damage causes release of PG, BK, 5HT, SP(capsaicin, baclofen, opioids, clonidine), and H resulting in formation of action potential
  2. transmission
    action potential travels from the periphery to the spinal cord via afferent nerve fibers, a delta fibers-fast, large, myelinated-sharp well localized pain, c fibers-slow, small, unmyelinated-transmit dull poorly localized pain, local anesthetics
  3. perception
    impulse becomes a conscious experience, pain
  4. modulation
    change or inhibition of pain impulses via descending pathways from teh brainsteam to the spinal cord, endogenous opioids, 5HT, NE, GABA-modify pain experience, tramadol, anticonvulsants, dual-acting ADs
  5. chronic pain
    pain results from damage to the afferent nociceptive nerve fibers, steps 2 3 and 4 in absence of pain(transmission, perception, modulation)
  6. PQRST
    palliative, provocative, quality, radiation/region, severity/intensity, temporal factors
  7. wong-baker faces pain rating scale
    3 and younger or language barrier
  8. APAP
    may inhibit COX-3, centrally located or may inhibit PG via COX-2 and NO in CNS, analgesic and antipyretic, no antiplatelet or antiinflammatory, preferred tx if no inflammation, 325-1000 mg q 4-6 h, max 4000mg, liver toxicity esp with etoh
  9. ASA
    irreversibly inhibits COX-1 and COX-2, decrease PG and thomboxane syn, analg, antipyret, and antiplatelet, no anti-inflamm(only NSAIDs)
  10. NSAIDs
    inhibit COX, decrease PG and thromboxane syn, analg, antipyre, and anti-inflamm, all have ceiling effect, but anti-inflammatory activity may increase as dose is increased
  11. mu
    classical morphine receptor
  12. mu1
    supraspinal analgesia
  13. mu2
    spinal analgesia, resp depression, dependence, tolerance, constipation, euphoria
  14. delta-spinal analgesia
    no cardiovascular effects, almost insens to classical opiates
  15. sigma-no analgesia
    mydriasis, increased HR, halluc, dysphoria
  16. kappa-spinal analgesia, only weakly reversed by naloxone
    no cross-tolerance with morphine, does not precipitate or prevent withdrawal, less euphoria, addiction, resp and CV deprs
  17. morphine
    DOC in severe pain, use IR with SR to control break-thru pain, IM, SQ, PO, phenanthrene
  18. hydromorphone
    use in severe pain, more potent than morphine, IM, SQ, PO, phenanthrene
  19. levorphanol
    use in severe pain, longer half-life useful in cancer tx, IM, SQ, PO, phenanthrene
  20. codeine
    mode pain, weak analgesic, combin with non-opioids, meta to morphine via 2D6, IM and PO, phenanthreene, III
  21. hydrocodone
    mod/sev pain, combine with non-opioids, metab to hydromorphone via 2D6, PO, phenanthrene
  22. oxycodone
    mod/seve pain, combine with non-opioids, PO, phenanthrene
  23. meperidine
    sev pain, poor oral abs, CONTRA renal failure, risk of seizure, myoclonus, not with MAOI(morphine DOC), IM, SQ, PO, phenylpiperadine
  24. fentanyl
    use in sev pain, do not use transdermal patch in acute pain, caution with 3A4 inh, IM, transdermal, lozenge, phenylpiperadine
  25. methadone
    effective in severe chronic pain, sed can be significant, may prolong QT interval, IM and PO, diphenylheptane
  26. propxyphene
    mod pain, weak analg, ?efficacy, combin with non-opioids, increae carbamazepine levels, PO, diphenylheptane
  27. mixed opioid agonist/antag drugs
    may precipitate withdrawal in opiate-dep pts, generally 2nd line for mod to sev pain, ceiling effect for analgesia, lower resp dep, sed, and abuse potential
  28. pentazocine
    talwin, weak mu antag, k & s agonist, 3rd line for mod/sev pain, IM SQ PO, IV
  29. butorphanol
    stadol, k & s agonist,? partial mu agonist, 2nd line for mod/sev pain, IM IN, schedule IV
  30. nalbuphine
    nubain, mu antag, k partial agon, s agon, 2nd line mod/sev pain, IM, RX
  31. buprenorphine
    buprenex, suboxone, mu parti ag, 2nd line mod/sev pain, IM, SL, III
  32. tramadol
    central analg, mild opiate agonist, inhibitor of NE and/or 5-HT uptake, mu ago, blocks 5-HT reup, blocks NE reupta, PO, RX, mod/sev pain, less resp depre, lower abuse?, can lower seizure threshold, use in caution in combo with serotonin enhancing drugs (SSRIs, TCAs, MAOIs)
  33. tapentadol
    nucynta, mu ag, also inhibits NE reupta(no 5-HT) PO, II, mod/sev, fewer GI SEs vs. oxycodon
  34. sedation
    reduce dose in half, give less often, d/c other sedating meds, add stimulant, tolerance within 4-5 days of steady dose
  35. respiratory depression
    more common in opioid-naiive, throught to be antagonized by pain, can occur with inititiation and inceaswe of dose, toler can develop with chronic dosing, reversible with naloxone but last 30-60 min
  36. N/V
    stimulation of CTZ, tolerance within sev days, add anti-emetic (prochloroperazine, meto, hydroxyzine-also can enhance analgesia), switch
  37. constipation
    tolerance NOT the norm, bowel regimen, stimulant lax (senna, bisacodyl) w/w out stool softener, bulk forming lax CONTRA, bupre and transdermal fentanyl may have lower risk
  38. itching/rash
    hist release and mast cell degran, morphine associated with most hist release, oxy and fentanyl least, use differnt class if true or possible allergy
  39. tolerance
    decrease of drug effect over time, doses typically stabilize unless condition worsens
  40. dependence
    withdrawal sx occurs w/out adequate level of the drug
  41. addiction
    impaired control over drug use, continued use despite harm, craving, compulsive use
  42. ADs with less sedation and antichol for neuropathic pain
    desipramine and nortrityline, others to use are amit, dulox first then venla, SSRIs disappointing results, gabapentin(need high doses), structurally related to GABA, dizz, somn, wt gain, edema, nausea(similar eff to ami)pregabilin, similar to gaba in mech and SE, MORE evidence in chronic pain, some studies show fast onset and greater effic compared to gaba, others: carb, oxcarb, dival, and lamotr, milnasipran(Savella) same efficacy as previous
  43. meta analysis
    preg statistically sig adv vs. duloxetine, dulox adv in causing less dizziness vs. preg, no sign differences btwn dul and gaba
  44. methadone for chronic pain
    long half-life, NMDA antag in addition to opioid rec action, may attenuate neuropathic pain signal transmission and wind-up phenomenon(pain amplification due to CNS sensitization to pain signals)
  45. lidocaine SE
    dizz, drows, disorient, muscle twitching, seizures, resp arrest, HOTN, brady, heart block, ventricular arr, cardiac arrest
  46. acute severe pain tx:
    morphine/other opioid
  47. mild (1-3) to mod (4-6) pain tx
    ASA, NSAIDs, codeine
  48. bone pain tx
    NSAIDs
  49. neuropathic pain tx
    gaba, preg, dulo, other anticonvulsants or ADs
  50. pain due to muscle strain tx
    NSAIDs, muscle relaxants

What would you like to do?

Home > Flashcards > Print Preview