Term
| an unpleasent but adaptive experience that signals the body to protect itself from tissue damage |
|
Definition
|
|
Term
| occurs when tissues are being damagedm causes individuals to remove the stimulus or slow down, sleep etc to allow tissues to heal |
|
Definition
|
|
Term
| a protective mechanism of the body |
|
Definition
|
|
Term
| pain is not the same as what? |
|
Definition
|
|
Term
| emotional, affective, and arousal aspects of such stimulation |
|
Definition
|
|
Term
| detection and localization of a stimulated pain receptor |
|
Definition
|
|
Term
| sensory process that provides signals that trigger pain |
|
Definition
|
|
Term
| while nociceptors may fire wildly and continually, what will happen to pain |
|
Definition
|
|
Term
| more than any other system, which qualities of nociception can be controlled from within the brain itself? |
|
Definition
|
|
Term
| what type of pain is generally not felt in the deeper tissues of the body |
|
Definition
|
|
Term
| fast acute pain can be classified as being what (2) |
|
Definition
| nociceptive or neuropathic/neurogenic |
|
|
Term
| nociceptive fast acute pain is due to what |
|
Definition
| activation of peripheral nociceptors in skin/soft tissue in response to tissue injury and inflammation |
|
|
Term
| neuropathic/neurogenic fact acute pain is a result of what more commonly |
|
Definition
| injury/inflammation of peripheral nerves |
|
|
Term
| neuropathic/neurogenic fast acute pain is a result of what less commonly |
|
Definition
| pathological involvement of CNS neurons |
|
|
Term
| what are some PNS disorders that cause neuropathic fast acute pain? (4) |
|
Definition
| herpes zoster, diabetes, trigeminal neuralgia, trauma (CRPS) |
|
|
Term
| what type of fast acute pain is not responsive to Na+ channel blockers? |
|
Definition
|
|
Term
| what type of fast pain is responsive to Na+ channel blockers |
|
Definition
|
|
Term
| Which fast pain is dependent on the presence of Na+ channels and Action potential conduction? |
|
Definition
|
|
Term
| Which fast pain is not dependent on the presence of Na+ channels and Action potential conduction? |
|
Definition
|
|
Term
| What are examples of Sodium channel blockers |
|
Definition
|
|
Term
| slow (chronic) pain examples: (5) |
|
Definition
| burning, itching, throbbing, nauseous, chronic pain |
|
|
Term
| associated with tissue destruction in skin, or deep tissues of the body |
|
Definition
|
|
Term
| pain that is felt or perceived to be in one region of the body but is actually the result of damage to a deeper organ, usually in the same dermatome |
|
Definition
|
|
Term
| when does referred pain occur |
|
Definition
| vague, non-specific information from deeper organs is relayed to spinal cord laminae, as that info ascends the SC the brain interprets it coming from teh more defined limb |
|
|
Term
| pain felt by some individuals with amputations, perception of pain in the amputated limb, related to amount of pain in the limb prior to amputation, and to the number of neuromas in teh stump |
|
Definition
|
|
Term
| what are the 4 types of pain(nociceptors). |
|
Definition
| mechanical, thermal, chemically-sensitive, polymodal |
|
|
Term
| nociceptors that are activated by intense pressure applied to skin |
|
Definition
|
|
Term
| mechanical nociceptor characteristics (4) |
|
Definition
| thinly myelinated, small diamater, A-delta fibers, conduction velocity of 5-30 ms |
|
|
Term
| nocicpetors activated by extreme temperatures |
|
Definition
|
|
Term
| thermal nociceptor characteristics (5) |
|
Definition
| small diamater, thinly myelinated, A-delta fibers, with conduction velocity of 5-30 m/sec |
|
|
Term
| chemically-sensitive nociceptors characteristics (3) |
|
Definition
| unmyelinated C fibers with conduction speeds .5-2m/sec |
|
|
Term
| polymodal nociceptors respond to what |
|
Definition
| intense mechanical, thermal, and chemical stimuli |
|
|
Term
| polymodal nociceptors chracteristics (3) |
|
Definition
| unmyelinated C fibrs with conduction speeds of .5-2m/sec |
|
|
Term
| all nociceptors represent what terminals of fibers? |
|
Definition
|
|
Term
| sharp pain is mediated by what type of fibers? |
|
Definition
|
|
Term
| sharp pain comes form what nociceptors? |
|
Definition
|
|
Term
| chronic pain is carried by what fibers? |
|
Definition
| unmyelinated slower conducting C fibers |
|
|
Term
| chronic pain is activated by what nociceptors? |
|
Definition
|
|
Term
| refers to an innocuous stimulus mediated by A-beta fibers evokes the perception of pain |
|
Definition
|
|
Term
| responsiviness of nocicpetors to painful stimuli such that the response is lessened or heightened |
|
Definition
|
|
Term
| sensitization can occur where |
|
Definition
| in the CNS (drosal horn neurons) and PNS |
|
|
Term
| increased/exaggerated sensitivity (lower threshold) of pain receptors to noxious stimuli, reectpors fire more easily |
|
Definition
|
|
Term
| occurs within the area of damaged tissue, caused by peripheral sensitization |
|
Definition
|
|
Term
| occurs when the tissues surrounding the damaged tissue become supersenstive, caused by central sensitization |
|
Definition
|
|
Term
| primary hyperalgesia is caused by what |
|
Definition
|
|
Term
| primary hyperalgesia is caused by what |
|
Definition
|
|
Term
| secondary hyperalgesia is caused by what |
|
Definition
|
|
Term
| periphereal sensitization is a result of direct release of chemical mediators into the inflamed area such as what |
|
Definition
| mast cells (histamine and serotonin) and prostaglandins (fibroblasts) |
|
|
Term
| peripheral sensitization: mast cells and prostanglandins released into the inflamed area act directly on what? |
|
Definition
| receptive membrane of nociceptores |
|
|
Term
| peripheral sensitization: what are other mediators that are released indirectly? |
|
Definition
|
|
Term
| peripheral sensitization: what do the macrophages release |
|
Definition
| leukotrienes (interleukin-1) |
|
|
Term
| peripheral sensitization: macrophages release leukotrienes which signal what |
|
Definition
| fibroblasts to relase prostaglandins |
|
|
Term
| peripheral sensitization: where is substance P released from? |
|
Definition
| nociceptor terminals themselves |
|
|
Term
| peripheral sensitization: where is substance P synthesized? |
|
Definition
| cell bodies (Dorsal root ganglion, trigeminal ganglia) of primary C-fiber afferents |
|
|
Term
| peripheral sensitization: after synthesis of substance p in cell bodies of primary c-fiber afferents where is it transported? |
|
Definition
| centrally onto 2nd order dorsal horn neurons and peripherally onto the nociceptor |
|
|
Term
| peripheral sensitization: release of substance P contributes to primary hyperalgesia by causng what? |
|
Definition
| mast cells to degranulate and release histamine |
|
|
Term
| peripheral sensitization: how does the release of histamine from mast cells contribute to primary hyperalgesia? |
|
Definition
| decreases teh threshold for activation of nociceptors |
|
|
Term
| peripheral nerve damage results in what? |
|
Definition
| afferent pathway conducting pain to the CNS is compromised |
|
|
Term
| if the afferent pathway conducting pain to the CNS is compromised what would one expect? |
|
Definition
| pain to be depressed not augmented |
|
|
Term
| Peripheral nerve damage often results in many intractable pain states such as what (5) |
|
Definition
| diabetic neuropathy, causalgia, phantom limb pain, trigeminal neuralgia, CRPS |
|
|
Term
| after axotomy, or segmental demyelination, may afferent axons become what? |
|
Definition
|
|
Term
| after axotomy, or segmental demyelination, many afferent axons become hyper excitable and do what? |
|
Definition
| generate an ongoing spontaneous discharge that originates from the site of injury |
|
|
Term
| after axotomy, or segmental demyelination, many afferent axons become hyper excitable and generate an ongoing spontaneous discharge that originates from the site of injury. What is this discharge called? |
|
Definition
|
|
Term
| discharge which originates from the site of injury not from the initial segment of the axon |
|
Definition
|
|
Term
| in those with peripheral neuropathies, there is a directly correlation between complaints of pain and paresthesia and what |
|
Definition
|
|
Term
| an accumulation of voltage-regulated/gated Na+ channels in the injured region due to a remodeling of the neuronal membrane results in what |
|
Definition
|
|
Term
| the amount of stimulus necessary for one to experience pain |
|
Definition
|
|
Term
| the amount of pain one can withstand |
|
Definition
|
|
Term
|
Definition
| rubbing arm after getting it pinched |
|
|
Term
| A-fiber input reaches SC first and turns on inhibitory interneurons. This inhibition then turns off/decreaces teh ascending pain input |
|
Definition
|
|
Term
| what is required for the gate theory to continue working? |
|
Definition
| continued activation of the A-beta fibers, once the activation stops, pain returns |
|
|
Term
| the gate theory can have a short duration, what mechanism has longer-acting gating? |
|
Definition
|
|
Term
| pain modulation occurs via a system in which direction? |
|
Definition
|
|
Term
| pain modulation descending system: Origin |
|
Definition
| cerebral cortex and hypothalamus |
|
|
Term
| pain modulation descending system terminates where |
|
Definition
| neurons in the periaqueductal gray |
|
|
Term
| pain modulation: cortical input originates from what lobes? |
|
Definition
|
|
Term
| pain modulation: frontal lobe is responsible for what |
|
Definition
| cognitive activation of the pain modulating system |
|
|
Term
| pain modulation: insular lobe is responsible for what |
|
Definition
| modulates the autonomic response to pain that reciprocally influences the emotional response |
|
|
Term
| pain modulation: projections from the periaqueductal gray descend to what |
|
Definition
|
|
Term
| pain modulation: projections from the periaqueductal gray descend to raphe nuclei where? |
|
Definition
| in the medullary reticular formation |
|
|
Term
| pain modulation: from raphe nuclei, axons descend to synapse where |
|
Definition
| dorsal horn spinal cord neurons |
|
|
Term
| pain modulation: other brainstem centers project to spinal cord levels and inhibit nociceptive projections neurons in the dorsal horn both directly and indirectly. Where are these brainstem centers lcoated? |
|
Definition
| pons and medulla (eg locus coeruleus) |
|
|
Term
| pain modulation: other brain stem centers on the pons and medulla project into the SC level and inhbit nociceptive projection neurons in the dorsal horn directly and indirectly through interneurons in what |
|
Definition
|
|
Term
| pain modulation: which tract contains receptors for endogeneous opiate neurotransmitters ie endorphis |
|
Definition
| paleo-spinothalamic tract |
|
|
Term
| what is the role of endogenous opiods? |
|
Definition
| modulate our response to pain |
|
|
Term
| how do endogenous opioids modulate our response to pain? |
|
Definition
| extent to which pain is percieved, one's emotinal response including affecting and motivational components |
|
|
Term
| how is the pain-modulating system activated? |
|
Definition
| noxious stimulation can activate the system |
|
|
Term
| noxious stimulation can activate the pain modulation system via what tracts? |
|
Definition
|
|
Term
| noxious stimulation can activate the pain modulation system via tracts of the Paleospinaothalamic tract to what structure? |
|
Definition
|
|
Term
| what is the importance of the brainstem structures which the tracts of the paleo spinothalamic tract connect to? |
|
Definition
| whose neurons represent the source of the descending modulating network |
|
|
Term
| what can depress the modulating system? |
|
Definition
|
|
Term
| what happens when the modulating system is depressed? |
|
Definition
|
|
Term
| what is a conditioned reaction to pain modulation? |
|
Definition
| an expectation of relief as in the placebo effect from a prior experience |
|
|
Term
| opiods reduce pain and produce what |
|
Definition
|
|
Term
| opiods as exeogenous drugs bind with opium receptors where |
|
Definition
| in teh periaqueductal gray and other areas |
|
|
Term
| oral administration of exogenous opiods effects the entire body and can have negative side effects, so where would these drugs be administered to reduce these side effects |
|
Definition
|
|
Term
| spinal blocks admininstered to the spinal cord are place where? |
|
Definition
| subdural space (intrathecally) or superficial to the dura mater (epidurally) |
|
|
Term
| which is the least successful pain modulation technique |
|
Definition
|
|
Term
| example of a peripheral surgical attempt to control pain |
|
Definition
|
|
Term
| example of a central surgical procedure to control oaun |
|
Definition
|
|