Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Stack #4564884
nuero 3
| Term | Definition |
|---|---|
| what is pain? | “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.” |
| Nociception” involves the transmission of | information about potential tissue damage through neurons of the ALS |
| When nociception is originated from free nerve endings that information is transferred into the CNS through Aδ afferents associated with the | spinothalamic tract or through C fibers |
| what is fast pain? | AS fibers |
| what is slow pain? | C fibers |
| In addition to speed, the spinothalamic projections to the | to the primary somatosensory cortex allow for precise localization of the site where potential tissue damage is occurring. |
| pain perception exist for nociceptive information initiated on the surface of the body, termed | superficial pain |
| nociceptive information arising from internal structures, including muscles, tendons, joint capsules, and internal organs, referred to as | deep pain |
| When a noxious stimulus is applied to the surface of the body... | free nerve endings in the skin are activated and transmit the nociceptive information into the spinal cord through Aδ and C afferents. |
| Aδ afferent nociceptors respond to | noxious thermal (heating) and mechanical stimuli, |
| C afferent nociceptors respond to a wide range of | thermal, chemical and mechanical stimuli, leading to them being called C polymodal nociceptors |
| where are AS receptors mainly located | the skin |
| Activation of Aδ nociceptors also activates the | withdraw reflex |
| the withdraw reflex results in | in activation of lower motor neurons that innervate flexors |
| Noxious stimuli that impact muscles, bones, or internal organs often results from | injury,overuse, or strain |
| The free nerve endings in internal locations are mainly the | C polymodal type of nociceptor |
| “slow pain” pathways | spinolimbic, spinoreticular, spinomesencephalic |
| central sensitization | increased signaling of nociceptive information at synapses in the CNS |
| this pain feels as if it originates in the tissues overlying the affected organ, rather than being interpreted as coming from the organ itself, a process called | reffered pain |
| Pain perception is considered to be acute if it lasts for | 2 weeks or less |
| acute pain is associated with | short-term damage to a body structure that often subsequently heals |
| acute pain mechanisms involve activation of | Aδ afferent nociceptors. |
| Because of the direct involvement of nociceptors in mediating the sensation, acute pain perception is usually in | proportion to the amount of damage |
| chronic pain is | over 2 weeks |
| Chronic pain can be either | nociceptive or neuropathic |
| When you break a bone, C polymodal nociceptors are activated at the site of the break and | include mechanonociceptors thermonociceptors, and chemonociceptors |
| The nociceptive information is passed through the CNS pathways to the brain for | the interpretation of pain proportional to the damage sustained in the broken bone |
| As mentioned, neuropathic chronic pain can develop from | normal, nociceptive pain, most commonly existing as persistent pain after an injury has healed. |
| Mechanisms leading to neuropathic chronic pain include those associated with damage to primary nociceptive neurons, most often seen with peripheral nerve injury | ectopic foci, ephaptic transmission) |
| Ectopic foci is... | When there is damage to a peripheral nerve, which would damage primary nociceptors, |
| Ephaptic transmission is... | One way to get ephaptic transmission is through demyelination. This allows action potentials in Aβ touch afferents to generate action potentials in the neighboring nociceptive afferents |
| Central sensitization is... | This mechanism for neuropathic pain involve plastic increases in the amount of neurotransmitter released from primary nociceptors, or in the number of neurotransmitter receptors on the secondary nociceptive projection neurons in the dorsal horn. |
| Structural rearrangements is... | These structural changes increase synaptic efficiency by creating more synaptic sites, perhaps through unmasking of silent synapses. |
| Pain matrix dysregulation. | Increases in pro-nociceptive or decreases in antinociceptive signaling in the pain matrix can maintain neuropathic pain |
| When the sympathetic, flight or fight, system is activated, a person’s perception of pain is | damaged |
| the intensity theory is | In this theory, pain is defined as an emotion brought on by stimulation of sensory systems (e.g., tactile sensation) by stronger than normal stimuli that are summed in the CNS, specifically the spinal cord dorsal horns |
| the specificity, or labeled line, theory of pain is | This theory states that pain is a unique sensation with specific receptors (nociceptors) that transmit pain information to a center in the brain. |
| The pattern theory of pain | there are no specialized receptors for pain and that pain is mediated through specific patterns of firing of the neurons associated with other sensations. |
| gate-control theory of pain is | In gate-control theory, painful stimuli activate small fibers that reach a “gate” in the dorsal horn of the spinal cord. The gate consists of larger fibers that either allow or prohibit further transmission of the pain information |
| The nociceptive pathways involve secondary projection neurons that have axons that ascend in the spinal cord... | contralateral to the side where the noxious stimulus is applied. |
| the pain matrix controls how | noxis stimuli are perceived |
| ALS nociceptive pathways that carry nociceptive information to the brain | descending pro- and anti-nociceptive pathways that can alter transmission of nociceptive information at synapse |
| The activation of nociceptive pathways can | be altered at the site of the painful stimulus |
| lammation-mediated activation of the cyclooxygenase enzymes causes local release of | prostaglandins, which activate C polymodal chemonociceptor |
| All of the ALS pathways have synapses in the spinal cord dorsal horn ipsilateral to where | where the nociceptors are activated, making the dorsal horn an important site for controlling nociception. |
| Neurons in the limbic cortex, including those in the amygdala, and those in the ventral medial hypothalamus project to the | periaqueductal gray (PAG) matter. |
| Norepinephrine released in the dorsal horn inhibits nociceptive transmission, | , while serotonin can either facilitate or inhibit nociceptive transmission |
| treatment with anti-depressants, like serotonin and norepinephrine reuptake inhibitors (SNRIs), can | mimic the effects of releasing serotonin and norepinephrine in the dorsal horn. |
| . Enkephalins are substances that act on | opioid receptors. |
| Since hormones released from glands travel throughout the body using the vascular system, they can access | important sites of nociceptive transmission, like the dorsal horn. |
| Nociception is the transmission of information about... | potential tissue damage through neurons of the ALS. |
| Spinothalamic tract | fast pain |
| Spinomesencephalic, Spinoreticular, and Spinolimbic tracts | slow pain |
| Damaged neurons form | dystrophic endings or painful neuromas |
| Central sensitization occurs when | increase of NT or post synaptic receptors are available |
Created by:
ecoesfeldd