Term
| What are the psychological comorbidities of pain? |
|
Definition
| anger, anxiety, loss of self esteem, sleep disturbances, depression |
|
|
Term
| Name some common types of neuropathic pain? |
|
Definition
| trigeminal neuralgia, postherpetic neuralgia, neuropathic low back pain, polyneuropathy (diabetic, HIV) |
|
|
Term
| T/F Diagnosing psychogenic pain is made solely by excluding organic causes of the pain. |
|
Definition
| false, you also need emtional conflict or psychosocial problems |
|
|
Term
| What are the different types of free nerve ending fiber types? |
|
Definition
| A"beta", A"delta", C-fiber |
|
|
Term
| How big are A"beta" fibers? |
|
Definition
|
|
Term
| How big are A"delta" fibers? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Name mediators involved in nociceptive signal initiation? |
|
Definition
| nerve growth factor, interleukins, TNF alpha, protons, PAF, PGE2, substance P, glutamine, bradykinin, histamine, serotonin, adenosine |
|
|
Term
| How many isoforms of the voltage gated sodium channel are there? |
|
Definition
|
|
Term
| The different isoforms of the voltage-gated sodium channels are distinguished by... |
|
Definition
| resistance or sensitivity to tetrodotoxin (TTX), functional characteristics, distribution, when present |
|
|
Term
| What are the characteristics of sodium channel 1.6? |
|
Definition
| predominant isoform in nodes of ranvier; very rapid repriming, produces both persistent, transient and resurgent sodium currents to maintain high frequency firing and rapid conduction of the action potential |
|
|
Term
| What are the characteristics of voltage gated channel 1.7? |
|
Definition
| rapid activation, slow inactivation and repriming; associated with early stages of action potential generation; delayed inactivation allows for summation of depolarization |
|
|
Term
| What are the characteristics of VG sodium channels 1.8? |
|
Definition
| found predominantly in small peripheral neurons; rapidly repriming; associated with initial stages of depolarization in action potential propagation increasing the likelihood of neuronal firing |
|
|
Term
| How fast are impulses transmitted down A-beta system? |
|
Definition
|
|
Term
| How fast are impulses transmitted down A-delta fibers? |
|
Definition
|
|
Term
| How fast do C-fibers transmit impulses? |
|
Definition
|
|
Term
| Describe the neurons of the dorsal root ganglia? |
|
Definition
| pseudounipolar neurons/satellite cells |
|
|
Term
| Are there any synapses in the dorsal root ganglia? |
|
Definition
| no primary afferent synapses but potential from cross-excitation and ectopic firing |
|
|
Term
| Name 2 kinds of glutamate receptors? |
|
Definition
|
|
Term
| Somatic afferent neurons carrying pain sensation decussate at the _____. |
|
Definition
| ventral white commissure of the spinal cord |
|
|
Term
| What are the 2 discrete pathways of the anterolateral funiculus? |
|
Definition
| neospinothalamic tract and the paleospinothalamic tract |
|
|
Term
| Where does the neospinothalamic tract project? |
|
Definition
| direct projection to the VPN, (topography and modality) |
|
|
Term
| Where does the paleospinothalamic tract project to? |
|
Definition
| nucleus raphe magnus, locus ceruleus (spinoreticular tract), periacqueductal grey (spinotectal tract), and posterior and intralaminar thalamic nuclei |
|
|
Term
| At what physical location in the brain does nociceptive stimuli reach consciousness? |
|
Definition
| at the level of the thalamus |
|
|
Term
| After the nociceptive stimuli reaches the thalamus, it is projected to... |
|
Definition
cortical projections= allow for comparison with past experience and current status for interpretation
corticofugal projection=modify perception of pain intensity and determine behavior |
|
|
Term
| What happens when nociceptive signals reach the periacqueductal grey? |
|
Definition
| site of endorphin/enkephalin peptide and high opioid receptor density, projections inhibit inhibition that suppress descending projections |
|
|
Term
| Which endocannabanoids are most studied? |
|
Definition
|
|
Term
| What is the MOA of endocannabanoids such as anandamide and 2-AG? |
|
Definition
| agonists at CB1/CB2 receptors as well as TRPV1 to produce inhibition of descending control; metabolize FAAH and MGL (monoacylglycerol lipase) |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Describe the descending pathway of the nucleus raphe magnus? |
|
Definition
| site of 5-HT production: reticulospinal projections to dorsal root entry zone |
|
|
Term
| Describe the descending pathway of the locus ceruleus? |
|
Definition
| site of NE production: reticulospinal projections to dorsal root entry zone |
|
|
Term
| What are the descending pathways amonth primary and secondary afferents and interneurons? |
|
Definition
| inhibit transmitter release from primary afferent directly and via release of dynorphin, enkephalin, glycine or GABA |
|
|
Term
| How does the sympathetic nervous system respond to nocious stimulation? |
|
Definition
| norepinephrine release from post-ganglionic sympathetic neurons produce vasoconstriction, decreased gastrointestinal motility and reduced firing threshold of primary afferents. Increases number, frequency and duration of discharge volleys and sensitizes second order second order afferents |
|
|
Term
| What happens do voltage gated sodium channels of somatic afferent neurons after axotomy? |
|
Definition
| 1.8, 1.9 and delayed rectifier K+ conductance are down-regulated in DRG following axotomy, but increase distally in CCI proximal to ligation. Nav 1.3 is expressed |
|
|
Term
| Describe the MOA of allodynia? |
|
Definition
| loss of C-fiber input to lamina I and IIo. A"beta" afferents in lamina IIi sprout new terminals that extend into the vacated synpases in IIo and allow low threshold afferent stimulation direct access to nociceptive pathways |
|
|
Term
| HOw can allodynia be prevented? |
|
Definition
| addition of NGF preserves C-fiber afferents which prevents the sprouting of a"beta" fibers |
|
|
Term
| What mutation is responsible for a congenital insensitivity to pain? |
|
Definition
| nonsense mutations in the SCN9A gene (chromosome 2q), cause loss of function of the Nav 1.7 resulting in a congenital insensitivity to pain. |
|
|
Term
| What happens when there is a single mutation in the Nav 1.7 gene? |
|
Definition
| can produce hyperexcitability or hypoexcitability depending upon the cell type in which teh mutation occurs; hyper- sensotry neurons, hypo-sympathetic neurons |
|
|
Term
| What is the mutation that causes inherited primary familial erythromelalgia? |
|
Definition
| autosomal dominant condition caused by a mutation in teh SCN9A gene resulting in a gain of function |
|
|
Term
| What are the symptoms of inherited primary familial erythromelalgia? |
|
Definition
| burning dysesthesia of hands, feet, and ears is debilitating, significantly impairing quality of life |
|
|
Term
| How do you treat inherited primary familial erythromelalgia? |
|
Definition
| tends to be refractory to treatment although sodium channel blocking agents and prostagladin analogs have shown promise |
|
|
Term
| What is the mutation that causes paroxysmal extreme pain disorder? |
|
Definition
| autosomal dominant condition caused by a mutation in the SCN9A gene encoding Nav 1.7 resulting in a gain of function |
|
|
Term
| What are the symptoms of paroxysmal extreme pain disorder at birth? |
|
Definition
| flushing of the skin of the buttocks, posterior thigh, and feet |
|
|
Term
| What are the symptoms of paroxysmal extreme pain disorder in childhood? |
|
Definition
| paroxysmal burning dysesthesia of rectum with erythema of pubic region, scrotum, perineum, buttocks, posterior thigh and feet |
|
|
Term
| Besides the perineum, posterior thigh, rectum and feet, where else do patients with paroxysmal extreme pain disorder experience burning dysesthesia and erythema? |
|
Definition
| sclera, temporal, ocular, mandibular + rhinorrhea, salivation and lacrimation |
|
|
Term
| What drug has shown some benefit in treating paroxysmal extreme pain disorder? |
|
Definition
|
|
Term
| T/F Patients with congenital insensitivity to pain have a normal response to non-noxious sensory stimulation with intact proprioception, vibratory sense, and tactile discrimination between sharp and dull. |
|
Definition
|
|
Term
| Which numbers on the pain scale are considered mild vs. moderate vs. severe? |
|
Definition
| 1-3=mild; 4-6=moderate; 7-10=severe |
|
|
Term
| The WHO states that mild pain should be treated with... |
|
Definition
| nonopiods (NSAIDS, salicylates, acetaminophen) |
|
|
Term
| The WHO states that you should treat moderate pain with... |
|
Definition
| weak opiods (codeine and hydrocodone) and adjuvants |
|
|
Term
| How does the WHO state you should treat severe pain? |
|
Definition
| strong opiods +/- adjuvants (strong opioids= morphine, oxycodone, hydromorphone, fentanyl transdermal) |
|
|
Term
| What is physical dependence? |
|
Definition
| withdrawal syndrome arises if drug discontinued, dose substantially reduced or antagonist administered |
|
|
Term
|
Definition
| greater amount of drug needed to maintain therapeutic effect, or loss of effect over time |
|
|
Term
|
Definition
| behavior suggestive of addiction; caused by undertreatment of pain |
|
|
Term
|
Definition
| (psychological dependence):psychiatric disorder characterized by continued compulsive use of substance despite harm |
|
|
Term
| What is the maximum time frame you can treat pain with ketorolac? |
|
Definition
|
|
Term
| What is the prodrug to valdecoxib? |
|
Definition
|
|
Term
| What is tramidol used for? |
|
Definition
|
|
Term
| What is the MOA of tramadol? |
|
Definition
| acts at opiate receptor and blocks reuptake of NE and serotonin |
|
|
Term
| What are the adverse effects of tramadol? |
|
Definition
| similar to opiates, usually milder |
|
|
Term
| What is tapentadol used for? |
|
Definition
| unique analgesic for moderate to severe pain |
|
|
Term
| What is the MOA of tapentadol? |
|
Definition
| acts at opiate receptors and blocks reuptake of norepinephrine |
|
|
Term
| What are the adverse effects of tapentadol? |
|
Definition
| similar to opiates, usually milder |
|
|
Term
|
Definition
| weak opiate preparation with poor efficacy and opiate adverse effects |
|
|
Term
| Which weak opiates are often used in combo with acetaminophen for synergistic effect? |
|
Definition
| codeine, hydrocodone, oxycodone |
|
|
Term
| What are the different preparations of morphine sulfate? |
|
Definition
| immediate release for breakthrough pain, sustained release=12 hour preparation, sustained release 24 hour preparation |
|
|
Term
|
Definition
| a sustained release morphine preparation that, when crushed/chewed/dissolved releases the mu-antagonist naltrexone, thereby blocking morphine's effect |
|
|
Term
|
Definition
| methadone (delayed toxicity), hydromorphone (parenteral formulation), meperidine (not preferred for chronic pain), oxymorphone (oral, rectal, and injectable forms available), levorphanol (long half-life), buprenorphine (combination with naloxone) |
|
|
Term
|
Definition
| immediate and extended release oxymorphone that is 5-10x more potent that morphine |
|
|
Term
| What are the indications for "Opana"? |
|
Definition
| persistent moderate to severe pain |
|
|
Term
| How is Opana administered? |
|
Definition
| 1 hr prior to or 2 hours after eating; can give immediate release every 6 hours or extended release twice daily |
|
|
Term
| What are the various ways in which fentanyl can be administered? |
|
Definition
| transdermal patches, oral "lollipop", buccal disc, buccal film |
|
|
Term
| Name the anticonvulsants that can be used to treat neuropathic pain? |
|
Definition
| gabapentin, oxcarbazine, topiramate, levetiracetam, zonisamide, lamotrigine, carbamazepine, phenytoin, clonazepam |
|
|
Term
| What is the MOA of pregabalin? |
|
Definition
| blocks alpha-2-delta voltage-gated calcium channels thereby reducing release of excitatory neurotransmitters |
|
|
Term
| What are the pharmocokinetics of pregabalin? |
|
Definition
| like gabapentin is not protein bound, is not subject to hepatic metabolism, is cleared unchanged by the kidney |
|
|
Term
| What is the t1/2 of pregabalin? |
|
Definition
|
|
Term
| What are the adverse effects of pregabalin? |
|
Definition
|
|
Term
| What is the t1/2 of lacosamide? |
|
Definition
|
|
Term
| What is the MOA of lacosamide? |
|
Definition
| enhances Nav slow inactivation, lower repetitive firing. May offer disease modifying benefit by binding to collapsin-response mediator protein 2 (CRMP-2) that is involved in neuronal differentiation and axonal outgrowth |
|
|
Term
| What are the adverse effects of lacosamide? |
|
Definition
| dizziness, diplopia, headache, and somnolence |
|
|
Term
| Name some tricyclic antidepressants that can be used for neuropathic pain? |
|
Definition
| amitriptyline, nortriptyline, doxepine, imipramine, desipramine |
|
|
Term
| Name some antidepressants that are potentially beneficial in treating neuropathic pain although there has been limited testing. |
|
Definition
| venlafaxine, trazadone, bupropion, mirtazapine |
|
|
Term
| Which is more effective in the management of pain, TCAs or SSRIs? |
|
Definition
|
|
Term
| What is the MOA of duloxetine? |
|
Definition
| blocks serotonin and NE reuptake |
|
|
Term
| How is duloxetine metabolized? |
|
Definition
| metabolized in the liver by CYP2D6 and CYP1A2 |
|
|
Term
| What is the half life of duloxetine? |
|
Definition
|
|
Term
| What are the adverse effects of duloxetine? |
|
Definition
| insomnia, somnolence, fatigue, dizziness, nausea, dry mouth, constipation |
|
|
Term
| What is the MOA of milnacipran? |
|
Definition
| selectively block 5-HT and NE reuptake |
|
|
Term
| What are the adverse effects of milnacipran? |
|
Definition
| insomnia, somnolence, fatigue, dry mouth, headache, nausea, dizziness |
|
|
Term
| What antispasmodic agents can be used for neuropathic pain? |
|
Definition
|
|
Term
| What is the MOA of baclofen? |
|
Definition
|
|
Term
| What are the side effects of baclofen? |
|
Definition
| drowsiness, lightheadedness, dizziness |
|
|
Term
| What are the MOA of tizanidine? |
|
Definition
|
|
Term
| What are the adverse effects of tizanidine? |
|
Definition
| drowsiness, orthostatic hypotension |
|
|
Term
| How does mexiletine treat neuropathic pain? |
|
Definition
|
|
Term
| How does clonidine treat neuropathic pain? |
|
Definition
| by being an alpha-2 agonist |
|
|
Term
| T/F Lidocaine can be used to treat neuropathic pain. |
|
Definition
|
|
Term
| What is the MOA of capsaicin for treating neuropathic pain? |
|
Definition
|
|
Term
| What is the MOA of delta-9-tetrahydrocannabinol/cannabidiol? |
|
Definition
|
|
Term
| How is delta-9-tetrahydrocannabinol/cannabidiol administered? |
|
Definition
| sublingual/oral mucosal spray |
|
|
Term
| T/F Most patients become tolerant to delta-9-tetrahydrocannabinol/cannabidiol. |
|
Definition
| false; not shown to produce tolerance |
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