Neuro/Psych-quiz 2-pain

cell damage causes release of PG, BK, 5HT, SP(capsaicin, baclofen, opioids, clonidine), and H resulting in formation of action potential

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

impulse becomes a conscious experience, pain

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

pain results from damage to the afferent nociceptive nerve fibers, steps 2 3 and 4 in absence of pain(transmission, perception, modulation)

palliative, provocative, quality, radiation/region, severity/intensity, temporal factors

3 and younger or language barrier

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

irreversibly inhibits COX-1 and COX-2, decrease PG and thomboxane syn, analg, antipyret, and antiplatelet, no anti-inflamm(only 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

classical morphine receptor

supraspinal analgesia

spinal analgesia, resp depression, dependence, tolerance, constipation, euphoria

no cardiovascular effects, almost insens to classical opiates

mydriasis, increased HR, halluc, dysphoria

no cross-tolerance with morphine, does not precipitate or prevent withdrawal, less euphoria, addiction, resp and CV deprs

DOC in severe pain, use IR with SR to control break-thru pain, IM, SQ, PO, phenanthrene

use in severe pain, more potent than morphine, IM, SQ, PO, phenanthrene

use in severe pain, longer half-life useful in cancer tx, IM, SQ, PO, phenanthrene

mode pain, weak analgesic, combin with non-opioids, meta to morphine via 2D6, IM and PO, phenanthreene, III

mod/sev pain, combine with non-opioids, metab to hydromorphone via 2D6, PO, phenanthrene

mod/seve pain, combine with non-opioids, PO, phenanthrene

sev pain, poor oral abs, CONTRA renal failure, risk of seizure, myoclonus, not with MAOI(morphine DOC), IM, SQ, PO, phenylpiperadine

use in sev pain, do not use transdermal patch in acute pain, caution with 3A4 inh, IM, transdermal, lozenge, phenylpiperadine

effective in severe chronic pain, sed can be significant, may prolong QT interval, IM and PO, diphenylheptane

mod pain, weak analg, ?efficacy, combin with non-opioids, increae carbamazepine levels, PO, diphenylheptane

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

talwin, weak mu antag, k & s agonist, 3rd line for mod/sev pain, IM SQ PO, IV

stadol, k & s agonist,? partial mu agonist, 2nd line for mod/sev pain, IM IN, schedule IV

nubain, mu antag, k partial agon, s agon, 2nd line mod/sev pain, IM, RX

buprenex, suboxone, mu parti ag, 2nd line mod/sev pain, IM, SL, III

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)

nucynta, mu ag, also inhibits NE reupta(no 5-HT) PO, II, mod/sev, fewer GI SEs vs. oxycodon

reduce dose in half, give less often, d/c other sedating meds, add stimulant, tolerance within 4-5 days of steady dose

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

stimulation of CTZ, tolerance within sev days, add anti-emetic (prochloroperazine, meto, hydroxyzine-also can enhance analgesia), switch

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

hist release and mast cell degran, morphine associated with most hist release, oxy and fentanyl least, use differnt class if true or possible allergy

decrease of drug effect over time, doses typically stabilize unless condition worsens

withdrawal sx occurs w/out adequate level of the drug

impaired control over drug use, continued use despite harm, craving, compulsive use

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

preg statistically sig adv vs. duloxetine, dulox adv in causing less dizziness vs. preg, no sign differences btwn dul and gaba

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)

dizz, drows, disorient, muscle twitching, seizures, resp arrest, HOTN, brady, heart block, ventricular arr, cardiac arrest

morphine/other opioid

ASA, NSAIDs, codeine

NSAIDs

gaba, preg, dulo, other anticonvulsants or ADs

NSAIDs, muscle relaxants