| Term 
 
        | an unpleasant sensory and emotional experience associated with actual or potential tissue damage |  | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 
        | used to be called physiologic and psychologic addiction 
 addiction is a psychologic compusion
 
 dependence is a physiologic, receptor response to an exogenous substance and the result from removing that substance
 |  | 
        |  | 
        
        | Term 
 
        | needing higher doses to elicit the same response |  | Definition 
 
        | tolerance 
 analgesia vs. euphoria:
 tolerance to euphoria develops much quicker than tolerance to analgesia
 
 very difficult to decipher between with short acting analgesics
 
 loss of effect of the medication vs. disease process progressing
 |  | 
        |  | 
        
        | Term 
 
        | exhibition of aberrant or addicted behaviors due to undertreatment of a legitimate pain syndrome |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | another term used for drug seeking |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | central sensitization vs. windup |  | Definition 
 
        | windup is the process which the nervous system acutely prepares nerves for another, similar, noxious stimulus this is physiologically necessary and protective
 
 central sensitization is the process in which the nervous system changes inappropriately due to ongoing, long-term noxious stimulus
 not protective
 
 windup can lead to central sensitization
 |  | 
        |  | 
        
        | Term 
 
        | the physiologic process of nervous system transmission of noxious tissue stimuli |  | Definition 
 
        | nociception 
 pain receptors are called nociceptors
 |  | 
        |  | 
        
        | Term 
 
        | deafferentiation vs. neuropathy |  | Definition 
 
        | neuropathy is generally a result of direct damage or demyelination of a nerve 
 deafferentation refers to afferent nerves being "cut off" from communicating further up the nervous system
 nerve is not intact, but is still firing
 |  | 
        |  | 
        
        | Term 
 
        | a heightened response to a normally painful stimuli |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | perceiving a normally non-noxious stimuli as a noxious stimuli |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | abnormal sensations in the absence of any kind of stimuli |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | classifying pain syndromes |  | Definition 
 
        | pain may be acute or chronic chronic pain is typically defined as pain syndromes lasing > 90 days
 acute pain = postoperative pain, breaking a bone
 
 chronic pain may be malignant or non-malignant pain (cancer or non-cancer pain)
 
 non-malignant chronic pain may be nociceptive or neuropathic
 nociceptive = stomp on toe
 neuropathic = diabetes pain, chemotherapy, shingles, deafferentiation, B12 deficiency, low TSH (hypothyroidism), neurosyphilis
 
 nociceptive pain may be somatic or visceral
 somatic = tissue damage of non-hallow organ
 visceral = pancreatic pain, stomach, intestine, usually deferred pain (liver pain, but right shoulder hurts)
 |  | 
        |  | 
        
        | Term 
 
        | history and physical for pain |  | Definition 
 
        | onset - when did the pain start 
 PQRST
 
 provoking factors:
 chest pain exacerbated by exercise and relieved by rest could be cardiac in origin
 chest pain which is exacerbated by lying down or eating certain foods could be gastrointestinal (GERD)
 
 quality of pain
 may lead to the underlying issues based on the descriptors (i.e. cardiac, musculoskeletal, visceral, psychosomatic, gastrointestinal)
 
 radiation of pain (where does it go)
 
 severity/concurrent symptoms
 intensity
 
 timing/triggers
 
 effect on ADL - a hallmark way to track further therapy and changes
 
 psych - usually limited for chronic pain evaluation
 
 palliation - what has the patient done to treat pain prior
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | diaphoresis tachycardia
 tachypnea
 hypertension
 distraction or silence
 grimacing/groaning
 guarding
 
 chronic pain does not elicit these changes to the degree that acute pain (such as post-op) does
 
 distraction or silence, grimacing and groaning, guarding are all good signs to look for when evaluating the nonverbal or demented/cognitively impaired individual
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | pain is purely subjective 
 difficult to assess multi-dimensional factors
 
 acute pain elicits sympathetic discharge
 
 chronic pain does NOT elicit sympathetic discharge
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | help to guide in the type/etiology of the discomfort: cramping
 dull
 splitting
 sore
 hurting
 crushing
 aching
 stabbing
 tearing
 pressing
 burning (neuropathic pain)
 shooting (neuropathic pain)
 radiating (neuropathic pain)
 sharp(neuropathic pain)
 
 help the patient verbalize the quantity or intensity of the discomfort they are experiencing:
 nagging
 agonizing
 annoying
 killing
 tiring
 sickening
 terrifying
 miserable
 torturing
 unbearable
 troublesome
 |  | 
        |  | 
        
        | Term 
 
        | subjective assessment of pain |  | Definition 
 
        | numerous rating and description scales 
 use tool consistently once chosen
 
 clinically reasonable utility
 
 applicable/valid for proposed patient
 
 ordinal information
 
 agreement with clinical outcomes
 
 single vs. multiple dimensional ratings
 
 in assessing the impact of therapy on activities of daily living, both positive and negative effects should be considered
 at low levels of pain, many people can continue to function effectively and few dimensions are affected
 when pain reaches the "worst pain" a number of key functional domains begin to be impaired, including mood and activity levels
 |  | 
        |  | 
        
        | Term 
 
        | the 4 As of pain assessment and documentation |  | Definition 
 
        | analgesia 
 aberrant behavior
 
 adverse effects
 
 activity
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | mediates slow transmission via Ca channels 
 activation dependent
 
 NMDA receptor is associated with opioid tolerance:  most opioids stimulate the NMDA receptor; ideal situation is for opioids to be NMDA receptor antagonists to prevent tolerance
 
 NMDA receptors are involved in central sensitization
 |  | 
        |  | 
        
        | Term 
 
        | NMDA RECEPTOR ANTAGONISTS*** |  | Definition 
 
        | MEMANTINE 
 DEXTROMETHORPHAN
 
 METHADONE
 
 KETAMINE
 
 AMANTADINE
 
 LEVORPHANOL
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | a lesion in a nerve fiber causes axonal "sprouting" 
 channels and receptors are redistributed, upregulated, and there is subtype alteration at the sprout
 
 ectopic discharges result
 
 ectopic discharges can cause impulse propagation on the original neuron
 
 pain laminae = I, II, V
 non-pain laminae = III, IV
 
 light touch fibers may pass through laminae I, II, or V on the way to laminae III, IV; if a sprout causes ectopic discharges in laminae I, II, V then light touch = allodynia
 
 ectopic discharges in the WRONG laminae (terminating in III normally, but the sprout is terminating in laminae II)
 
 also, there can be adjacent membrane remodeling:
 C fiber is injured, and can cause an adjacent A-beta fiber to also start sprouting and causing ectopic discharges
 |  | 
        |  | 
        
        | Term 
 
        | modulation of pain:  excitatory and inhibitory neurotransmitters |  | Definition 
 
        | excitatory: glutamate
 glycine
 
 inhibitory:
 GABA
 5HT
 NE (alpha 2a)
 opioids
 |  | 
        |  | 
        
        | Term 
 
        | opioid receptors and actions |  | Definition 
 
        | MU: analgesia, respiratory, GI, feeding, sedation, prolactin (increased with agonism)
 
 KAPPA:
 analgesia, GI, psychotomimesis, feeding, sedation, diuresis
 
 DELTA:
 analgesia, feeding
 
 drugs that stimulate kappa and antagonize mu = no respiratory depressant effects (only mu control respiration)
 
 kappa doesn't have dopamine activity
 
 never give a kappa agonist to an actively psychotic patient!
 |  | 
        |  | 
        
        | Term 
 
        | opioid receptor signaling |  | Definition 
 
        | decreased adenylyl cyclase 
 increased K current
 
 decreased Na
 
 decreased Ca
 
 increased mapK and PLC
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | codeine naloxone
 heroin
 
 those that lack a 6-OH, possibly decreasing risk of cross tolerance of hypersensitivity:
 hydrocodone
 hydromorphone
 levorphanol
 oxycodone
 oxymorphone
 buprenorphine
 butorphanol
 |  | 
        |  | 
        
        | Term 
 | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 
        | fentanyl sufentanil
 alfentanil
 remifentanil
 |  | 
        |  | 
        
        | Term 
 | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 
        | metabolized by 2D6 to morphine then to morphine-3-glucuronide and morphine-6-glucuronide 
 codeine does not have analgesic activity!  must be metabolized to morphine
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | metabolized by 2D6 and 3A4 to oxymorphone (active) and noroxycodone |  | 
        |  | 
        
        | Term 
 
        | metabolism of hydrocodone |  | Definition 
 
        | metabolized by 2D6 to hydromorphone (active) and then to hydromorphone-3-glucuronide and hydromorphone-6-glucuronide |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | metabolized by 2D6 to M-1 (ACTIVE) 
 tramadol does not have analgesic activity, must be metabolized to active compound!
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | metabolized to normeperidine (may induce seizures) and meperidinic acid |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | gold standard opioid 
 all equianalgesic tables based upon comparison with morphine
 
 undergoes glucuronidation:
 morphine-3-glucuronide (neurotoxicity)
 morphine-6-glucuronide (analgesia)
 
 3:1 oral to parenteral potency ratio
 
 t1/2 of 2-4 hours
 
 onset of action 30 minutes (oral), 5 minutes (IV)
 
 duration of action = 4 hours
 
 NEVER EXCEED 1600 MG DAILY OF AVINZA DUE TO TOXICITIES ASSOCIATED WITH EXCIPIENTS
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | low potency analgesic 
 great for antitussive
 
 must be converted to morphine by 2D6
 
 one of the most constipating opioids
 
 approximate equianalgesic ratio 30:1
 
 no better than IBU
 |  | 
        |  | 
        
        | Term 
 
        | properties of hydrocodone |  | Definition 
 
        | parent and active metabolite are active 
 hydrocodone to hydromorphone by 2D6
 
 little effect of metabolite on analgesia
 
 most highly prescribed med in US
 
 approximately 1/2 as potent as morphine
 
 watch the APAP intake!
 fasting and APAP intake is the most dangerous; body can't make glutethione to take away the bad metabolite of APAP
 |  | 
        |  | 
        
        | Term 
 
        | properties of hydromorphone |  | Definition 
 
        | glucuronidated to similar metabolites as morphine (H-3-G and H-6-G) 
 4:1 oral to parenteral potency ratio
 
 t1/2 of 2-4 hours
 
 onset of action 30 minutes (oral), 5 minutes (IV)
 
 duration of action 4 hours
 
 approximately 4 times a potent as morphine
 |  | 
        |  | 
        
        | Term 
 
        | properties of levorphanol |  | Definition 
 
        | opioid + NMDA activity 
 t1/2 of 2-4 hours
 
 duration of action 4-8 hours
 
 oral morphine equivalent changes with increasing doses of morphine
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | active parent drug 
 metabolized to oxymorphone via 2D6 and 3A4
 
 CYP enzyme inhibition or induction little effect on analgesia
 
 approximately 2x more potent than morphine
 
 t1/2 of 2-3 hours
 
 quick onset and peak, unknown duration
 
 more lipophilic, more abuse potential with this drug
 |  | 
        |  | 
        
        | Term 
 
        | properties of oxymorphone |  | Definition 
 
        | active metabolite of oxycodone 
 undergoes glucuronidation and reduction
 
 little clinical experience to date
 
 onset and duration similar to others
 
 t1/2 of ~7 hours
 
 10:1 oral to parenteral potency ratio
 
 approximately 4x more potent than morphine
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | O-demethylated to active metabolite (M1) 
 weak mu opioid agonist
 
 weak NE/5HT reuptake inhibition
 
 analgesia NOT reversed by naloxone in stuides
 
 caution for seizures and serotonin syndrome
 
 400 mg/day max dose
 300 mg/day mase dose for ER
 |  | 
        |  | 
        
        | Term 
 
        | properties of tapentadol (nucynta) |  | Definition 
 
        | SNRI (mostly norepinephrine) 
 equipotent to oxycodone
 
 mu opioid agonist + NE reuptake inhibitor
 not as much risk for seizure or serotonin syndrome
 will cause BP changes
 |  | 
        |  | 
        
        | Term 
 
        | properties of buprenorphine |  | Definition 
 
        | oral (subutex and suboxone) 
 available as a 7 day patch (Butrans):
 5mcg/hr, 10mcg/hr, 20mcg/hr
 
 do not exceed 20mcg/hr (QTc prolongation)
 
 do not reapply to same site for 21 days
 
 initiation:
 <30 mg oral morphine equivalence start with 5mcg/hr patch (recommended that the patient be weaned to < 30 mg of ORM before starting the patch!!)
 30-80 mg OME start with 10mcg/hr patch
 not recommended for > 80 mg OME
 
 could push morphine off the receptor and cause withdrawal symptoms if the patient isn't tapered down
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | metabolized to inactive metabolites hepatically 
 stimulates kappa, antagonizes mu receptors (use in caution in opioid tolerant)
 
 equianalgesic to morphine, more dysphoria
 
 available only parenterally
 
 use in labor and delivery usually (women have more kappa receptors)
 |  | 
        |  | 
        
        | Term 
 
        | properties of butorphanol |  | Definition 
 
        | metabolized priimarily to hydroxybutorphanol (inactive) hepatically 
 kappa agonist, sigma agonist, mu antagonist
 sigma is a PCP receptor = high abuse potential
 
 available as nasal spray and parenteral
 
 don't convert in opioid tolerant individuals
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | pure opioid antagonist 
 used for opioid overdose reversal
 
 limited data to suggest low doses potentiate analgesia
 
 may be effective orally for opioid bowel syndrome
 |  | 
        |  | 
        
        | Term 
 
        | properties of pentazocine |  | Definition 
 
        | high history of abuse 
 mixed agonist/antagonist:
 agonist at kappa
 antagonist at mu
 
 rarely used in clinical practice today
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | currently being phased out: ceiling dose due to toxic metabolite (normeperidine)
 accumulation in renal insufficiency
 
 caution reversing overdose with naloxone:  seizures may result
 
 still used in acute pancreatitis (no data to support) and post anesthesia rigors
 
 duration of analgesia 2-3 hours
 
 oral meperidine of little analgesic use
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | metabolized via 3A4 to inactive metabolites 
 t1/2 of ~3 hours IV
 t1/2 of ~17 hours transdermal
 t1/2 of ~7 hours transmucosal
 
 onset of analgesia:
 IV is almost instantaneous
 transdermal 12-24 hours
 transmucosal 5-15 minutes
 
 duration of analgesia:
 IV duration ~30-60 minutes
 transdermal not applicable
 transmucosal unknown
 
 fentanyl patches:  matrix vs. reservoir (liquid)
 
 oral transmucosal fentanyl (Actiq) and fentanyl buccal tablet:
 FOR CANCER PATIENTS ONLY THAT ARE OPIOID TOLERANT (buccal tablet)
 titration should always begin at the lowest available dose due to variance in transmucosal absrption
 |  | 
        |  | 
        
        | Term 
 
        | properties of sufentanil, alfentanil, remifentanil |  | Definition 
 
        | rarely used in pain management (anesthesia) 
 sufentanil used in extremely opioid tolerant patients
 
 approximate equianalgesic ratio 0.001:1
 
 parenteral availability only
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | active parent 
 metabolism via N-demethylation:
 3A4, 2C19, 2D6 to inactive metabolites
 
 opioidergic, NMDA antagonism, NE/5HT reuptake inhibition
 
 t1/2 of 7-59 hours
 
 dosing changes dramatically in various clinical situations!!
 
 may cause QTc prolongation and Torsades
 must monitor EKGs!
 
 changes in equianalgesic potency based on previous morphine equivalents
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | CNS: dependence, substance abuse, sedation, psychotomimetic, vertigo, myoclonus, respiratory depression, neurocognitive
 
 GI:
 constipation (need a stool softener and a stimulant laxative), nausea, spinchter of oddi pressure changes, LES/cardiac spinchter changes
 
 GENITO-URINARY:
 urinary retention
 
 INTEGUMENTARY:
 flushing, urticaria, pruritus (opioids cause mast cell lysis -> release of histamine; not an allergic reaction)
 
 METABOLIC:
 stimulate ADH, prolactin, somatotropin, loss of libido
 
 CARDIOVASCULAR:
 hypotension and reflex tachycardia
 
 HEPATIC:
 rare
 
 RENAL:
 rare
 
 OCULAR:
 miosis
 
 IMMUNE:
 decrease in immune function with chronic dosing
 
 OTHER:
 hypogonadism - in men will present with low testosterone levels (depressed, no energy, low libido, elevated pain scores); women will present with ammenorrhea, hair loss, depression, low libido
 |  | 
        |  | 
        
        | Term 
 
        | reasons for using adjuvants |  | Definition 
 
        | analgesia for mild to moderate pain 
 synergy with other adjuvants or opioids
 
 targeted polypharmacy (i.e. neuropathic pain)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | NSAIDs acetaminophen
 antidepressants:  SNRIs, TCAs
 anticonvulsants
 anesthetics
 antipsychotics
 bisphosphonates
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | COX-I is constitutive; blocked by unselective NSAIDs 
 COX-II is inducible/constitutive; blocked by selective NSAIDs
 
 various COX-II/COX-I selectivities
 |  | 
        |  | 
        
        | Term 
 
        | order of COX-II to COX-I selective |  | Definition 
 
        | most COX-II selective to most COX-I selective 
 more COX-II selective:
 lumiracoxib, etoricoxib, rofecoxib, valdecoxib, etodolac, nimesulide, diclofenac, celecoxib, meloxicam
 
 more COX-I selective:
 fenoprofen, ibuprofen, tolmentin, naproxen, aspirin, indomethacin, ketoprofen, flurbiprofen, ketorolac
 |  | 
        |  | 
        
        | Term 
 
        | NSAID ADRs and monitoring parameters |  | Definition 
 
        | gastric/duodenal ulceration and bleed 
 hypertension
 
 acute renal failure/insufficiency
 
 bleeding diathesis/increased INR
 
 cardiovascular
 NSAID associated CV risks appear to be COX selective associated (more COX-II selective = increased CV risks)
 cardiac collateralization
 stress priming
 
 monitoring parameters:
 
 creatinine at baseline and 1-2 weeks post initiation
 
 annual Hbg/Hct or if symptomatic (to tell if the patient is bleeding
 
 BP
 |  | 
        |  | 
        
        | Term 
 
        | NSAID induced GI bleed:  risk factors and prevention |  | Definition 
 
        | risk factors: prior peptic ulcer disease
 prior NSAID GI complication
 advanced age
 concurrent corticosteroid or anticoagulant use
 high doses of NSAIDs
 combination of NSAIDs
 
 prevention:
 eradication of H. pylori
 PROTON PUMP INHIBITORS OR MISOPROSTOL
 |  | 
        |  | 
        
        | Term 
 
        | what pain drugs should be used for patients with CV risk factors? |  | Definition 
 
        | 1st line:  opioids, tramadol, acetaminophen 
 2nd line:  non-acetylated salicylate
 
 3rd line:  non-selective NSAID (safest is naproxen)
 |  | 
        |  | 
        
        | Term 
 
        | propertiesw of acetaminophen |  | Definition 
 
        | dosing of 4gm/24 hours (3gm/24 hours OTC) 
 dosing of 2400mg/24 hours in elderly and alcohol abuse
 
 evidence to suggest LFT spikes at 4gms or less in healthy adults
 |  | 
        |  | 
        
        | Term 
 
        | antidepressants: SNRIs vs. SSRIs
 secondary vs. tertiary amine TCAs
 |  | Definition 
 
        | SNRIs vs. SSRIs need the NE more than the 5HT (NE is always inhibitory for pain, 5HT may or may not be inhibitory for pain)
 
 secondary amine TCAs are just as effective as tertiary amines with less ADRs
 |  | 
        |  | 
        
        | Term 
 
        | antidpressants used for pain |  | Definition 
 
        | TCAs (NE>5HT): amitriptyline
 nortriptyline
 imipramine
 desipramine
 
 SSRIs (5HT > NE):
 generally ineffective
 
 SNRIs (NE = 5HT)
 venlafaxine (dapaminergic)
 desvenlafaxine
 duloxetine
 milnacipran (savella) - for fibromyalgia
 
 atypicals (NE>5HT)
 mirtazapine (alpha adrenergic) - makes you hungry, sleepy
 bupropion (dopaminergic) - avoid in seizure disorder, eating disorder, anxiety disorder
 |  | 
        |  | 
        
        | Term 
 
        | chochrane review of anticonvulsants in DPN |  | Definition 
 
        | CBZ appears more efficacious than GBP 
 GBP better tolerated than CBZ
 
 no clear advantage of GBP over CBZ
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | saturable gut and CNS kinetics 
 somnolence
 
 renally eliminated unchanged
 
 minimum effective dose for neuropathy:  900 mg/day (initial target)
 1800 mg (600 mg TID) is the max dose (not much response above this
 
 of the anticonvulsants, gabapentin has become the generally accepted first line agent for PDN
 
 in clinical studies, response to therapy evidenced by statistically significant reductions in pain scores within as short as several weeks
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | correlation between pain and serum concentrations is unknown 
 hepatic enzyme elevation
 
 weight gain
 
 causes teratogenicity
 
 may be used in patients with comorbid seizure disorder
 |  | 
        |  | 
        
        | Term 
 
        | properties of carbamazepine |  | Definition 
 
        | unequivocal efficacy in studies for almmost every subtype of neuropathic pain 
 difficult to interpret target dose
 
 need to monitor:
 serum concentrations (autoinduction), CBC, lytes
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | dizziness and somnolence 
 works exactly the same as gabapentin
 
 can titrate this quicker than gabapentin and tends to have less edema
 
 if a patient fails gabapentin, they can still respond to pregabalin
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | paresthesias, renal stones, cognitive slowing 
 improvement in Hgb A1c
 
 causes weight loss
 
 drink copious amounts of water with this drug!  risk of kidney stones
 |  | 
        |  | 
        
        | Term 
 
        | anesthetics used for pain |  | Definition 
 
        | lidocaine transdermal patch: lidoderm
 available as 4%
 may cut
 do not exceed 3 patches at once (for risk of cardiac arrhythmias)
 patches cannot be on longer than 12 hours!!!
 
 continuous intraincisional anesthetic:
 OnQ pain pump and others
 lidocaine, bupivacaine, mepivacaine
 
 capsaicin:
 zostrix
 Qutenza - every 3 month patch; have to apply a topical anesthetic before applying Qutenza; leave on for 1 hour and it's good for 3 months
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | acute (<30 days) chronic (3-6 months)
 nociceptive (tissue injury)
 neuropathic (nerve injury)
 bone (prostaglandin mediated metastasis)
 sympathetic pain - COMPLEX REGIONAL PAIN SYNDROME = SYMPATHETICALLY MAINTAINED PAIN; drugs that will work = adrenergic blockers (clonidine)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | second leading cause of surgical avoidance 
 most common reason for readmission
 
 new data on empiric analgesia:  peri operative pregabaline or gabapentin
 
 control pain with IV push opioids
 
 maintain with IV patient controlled analgesia (PCA)
 IV PCA is the mainstay of postop pain management
 
 basal rate infusions should be reserved only for opioid tolerant patients (those that came into the hospital on opioids)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | chronic low back pain failed back surgery syndrome
 neuropathic pain syndromes
 sympathetically maintained pain syndromes
 central pain syndromes (pain arises from the CNS; result of damage to the CNS i.e. stroke)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | incidence of 10-15% 
 herniation or degeneration of lumbar disk
 
 risk factors include:  depression, disputed compensation issues, other chronic pain, and job dissatisfaction
 
 controversy over need for imaging and what type (MRI vs. radiography)
 
 pharmacologic therapy:
 NSAIDs - no good data
 muscle realxants - no data to support use for greater than 6-8 weeks for pain management
 TCAs - have been shown to be effective
 opioids/tramadol - have been shown to be effective; tramadol is probably the best
 
 non-pharm therapy:
 surgery
 physical therapy +/- cognitive behavioral treatment
 |  | 
        |  | 
        
        | Term 
 
        | failed back surgery syndrome |  | Definition 
 
        | unrelieved pain following lumbar spine surgery 
 epidural corticosteroid gold standard despite equivocal data
 
 opioids outperform NSAIDs
 
 spinal cord stimulation:
 new "hot" therapy
 based on gate control theory
 
 evidence to support surgery is poor
 |  | 
        |  | 
        
        | Term 
 
        | neuropathic pain syndromes |  | Definition 
 
        | peripheral: painful diabetic neuropathy
 post-herpetic neuralgia
 trigeminal neuralgia
 complex regional pain syndrome
 sciatica/radiculopathy
 phantom limb pain
 HIV
 
 central:
 central poststroke pain
 multiple sclerosis
 spinal cord injury pain
 |  | 
        |  | 
        
        | Term 
 
        | painful diabetic neuropathy |  | Definition 
 
        | prevention with strict glycemic control (A1c < 7) 
 treatment:
 duloxetine - only FDA approved therapy
 TCAs (class A)
 anticonvulsants (class A)
 opioids (class A)
 tramadol (class A)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | prevention: antiviral within 72 hours
 oral corticosteroids ineffective
 epidural bupivacaine blockade
 
 treatment:
 TCAs (class A) - amitriptyline, nortriptyline, desipramine, maprotiline
 gabapenting and pregabalin (class A)
 opioids (class A) - tramadol, oxycodone, morphine
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | therapies with class A evidence: carbamazepine
 baclofen
 
 therapies with uncontrolled or anecdotal evidence:
 phenytoin
 clonazepam
 valproate
 oxcarbazepine
 gabapentin
 IV lidocaine
 tizanidine
 microvascular decompression surgery
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | experienced by 8% of stroke patients 
 characterized by abnormal temperature and pain in area affected by stroke
 
 burning, scalding, freezing
 
 may manifest up to 6 months following stroke
 
 treatment:
 carbamazepine (class A)
 gabapentin (anecdotal)
 amitriptyline (class A)
 levorphanol (class A)
 |  | 
        |  | 
        
        | Term 
 
        | complex regional pain syndrome |  | Definition 
 
        | SYMPATHETICALLY MAINTAINED!!! 
 treatment:
 gabapentin (class A)
 IV lidocaine (class A)
 phentolamine (class A) - alpha blocker
 spinal cord stimulation (class A)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | presence of 11 or more of the 18 tender points identified 
 nociceptive flexion reflex
 
 central sensitization vs. inflammatory mediators
 disinhibition syndrome - body does not have enough descending pathway activity
 no inflammatory process
 
 ALL FIBROMYALGIA PATIENTS have insomnia!
 first thing to treat is sleep
 then cardiovascular exercise
 then drugs
 
 treatment:
 pregabalin (strong, FDA approved)
 amitriptyline (strong)
 cyclobenazaprine (strong)
 tramadol (modest)
 fluoxetine (modest)
 venlafaxine (modest)
 duloxetine (modest)
 |  | 
        |  | 
        
        | Term 
 
        | epidemiology of cancer pain |  | Definition 
 
        | up to 70% of patients with cancer will present with pain 
 over 50% report moderate to severe pain in the last months of life
 
 43% of patients with cancer reported being unsatisfied with their pain treatment
 |  | 
        |  | 
        
        | Term 
 
        | etiology of malignant pain |  | Definition 
 
        | acute: occuring at the time of diagnosis
 
 chronic:
 associated with tumor progression or treatment
 
 co-morbid chronic pain syndromes
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | by the mouth 
 by the clock
 
 by the ladder:  for severe pain, give a potent opioid
 
 for the individual
 
 with attention to detail
 |  | 
        |  | 
        
        | Term 
 
        | 3 step analgesic ladder for cancer |  | Definition 
 
        | STEP 1: non opioid:  aspirin or APAP
 
 STEP 2:
 opioid for mild to moderate pain - codeine
 PLUS
 non opioid - aspirin or APAP
 
 STEP 3:
 opioid for moderate to severe pain - morphine
 PLUS
 non opioid - aspirin or APAP
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | direct nociceptive pain neuropathic pain
 bone pain - hardest type of cancer pain to treat; opioids will work, but anti-inflammatory drugs are the mainstay of treatment (high dose IBU, indomethacin, corticosteroids); it is a prostaglandin mediated pain
 visceral pain - designed to sence expansion, stretch, contortion; gabapentin, TCAs, pregabalin
 breakthrough pain
 spiritual pain (anxiety driven)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | caused by: tumor invasion of the nervous system
 chemotherapy
 
 managed same as non-cancer patients
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | may be due to direct prostaglandin involvement or tumor infiltration 
 most common primary malignancies:
 breast, prostate, lung
 
 most common sites of metastasis:
 thoracolumbar spine, pelvis, lower limbs
 
 treatment options:
 NSAIDs
 bisphosphonates - stablize bone metastases; pamidronate first line, zolendrenic acid
 corticosteroids (especially if spinal cord stenosis)
 opioids
 radiation - fights the cancer directly, not immediately effective for pain
 radiopharmaceuticals (strontium or samarium = "radioactive bisphosphonates")
 
 NSAIDs logically make sense but...we get nervous about using NSAIDs in patiens on cancer chemotherapy due to potentially low platelet counts
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | continued escalation of opioids w/o relief 
 pain and opioid utilization decreased with counseling, especially clergy
 
 address anxiety and depression specifically as contributors to spiritual pain
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | 3 types recognized: idiopathic
 incident
 end of dose
 
 pain diary will assist classification
 
 breakthrough doses should be 10-20% of total 24 hour opioid intake
 
 remember pure mu opioids preferred
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | rapid titration of IV opioids 
 1st dose should be 10-20% of previous 24 hour use of opioids
 
 reassess patient after 15 minutes (morphine starts working in 5 minutes, peaks in 15 minutes); if the pain hasn't changed at all, you double the dose of the bolus
 
 if the pain decreases but less than 50% repeat the dose
 
 if the pain decreases by > 50% is considered a success
 
 amount of opioids it takes to control pain is 4 hour equivalent
 
 patients pain must be stable prior to conversion to home pain regimen
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