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Pharmacology - Exam 2 > Pain (nociception) > Flashcards

Pain (nociception) Flashcards

(52 cards)

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1
Q

what is the somatosensation of pain called

A

nociception

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2
Q

examples of other somatosensations

A

touch

temperature

proprioception

pressure

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3
Q

what does neurophysiology of pain involve?

(3 STEPS)

A

1- initiation 2- propagation 3- perception

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4
Q

what causes initiation of pain sensation

A

activation/depolarization of pain receptors at the site of injury

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5
Q

where does perception of painful stimuli take place

A

somatosensory, emotional, and cognitive regions of the brain

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6
Q

describe propagation of pain sensation

A

depolarization along nerves to spinal cord (switch over in spinal cord:contralateral) and then ascend up spinal cord to thalamus which relays the information to the somatosensory, emotional, and cognitive regions of the brain

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7
Q

how does anesthesia and pain medications work in reference to the ascending pain pathway

A

block the ascending pain pathway at various locations so the pain sensation does not reach the brain

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8
Q

Dorsal column-medial lemniscal pathway (DCML) does what sensations

A

carries the sensory modalities of fine touch (tactile sensation), vibration, and proprioception

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9
Q

The anterior spinothalamic tract of the anterolateral system does what sensations

A

Anterior spinothalamic tract – carries the sensory modalities of crude touch and pressure.

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10
Q

The lateral spinothalamic tract of the anterolateral system does what sensations

A

Lateral spinothalamic tract – carries the sensory modalities of pain and temperature.

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11
Q

why is nociceptive fibers being slow adapting good

A

because it is a protective mechanism you want the pain signal to keep firing so as to learn painful stimuli and not forget the tac in your foot etc

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12
Q

where does the lateral spinothalamic tract cross over

A

spinal cord

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13
Q

what are the two pain fibers of the ascending pain pathway

A

A-delta fibers and C fibers

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14
Q

what chemical stimulates A-delta fibers

A

glutamate

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15
Q

what chemical stimulates C fibers

A

mostly substance P but some glutamate

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16
Q

What binds to receptors of the A-delta and C fibers that leads to sensitization and exacerbation

A

prostaglandins

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17
Q

which fiber A-delta or C fibers has faster conduction and why

A

A-delta fibers be myelinated vs C fibers which are unmyelinated

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18
Q

what “kind” of pain does A-delta fibers elicit

A

sharp, stinging, intense pain (myelinated fast fibers)

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19
Q

what “kind” of pain does C fibers elicit

A

dull, achy, chronic, burning, less intense pain (unmyelinated slow fibers)

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20
Q

what are the three types of pain

A

nociceptive

inflammatory

neuropathic

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21
Q

What is nociceptive pain defined by

Study These Flashcards
A

external irritating or harmful stimulus like heat, cold, acid/chemicals, getting hit with hammer or getting a shot

22
Q

what does the transduction of nociceptive pain rely on

Study These Flashcards
A

activation of distinct TRP channels and other peripheral nocireceptors

23
Q

what is the main TRP channel to know

Study These Flashcards
A

TRPV1 (activated by heat or acid/chemicals like capsaicin)

24
Q

pain treatment options for nociceptive pain

Study These Flashcards
A

local anesthetics

Cox2 inhibitors

opioids/opiates

25
what does TRP stand for
transient receptor potential
26
what activates TRP channels
heat or capsaicin
27
what is capsaicin
compound found in hot peppers that can bind to TRP receptors/channels and elicit sensations of pain
28
how can capsaicin be used for pain management
use capsaicin to target TRP channels for low long activation which then leads to desensitization and management of pain
29
what causes inflammatory pain
tissue or internal organ damage that causes a local or systemic immune response (i.e. release of inflammatory mediators by immune cells)
30
how do inflammatory mediators stimulate pain transduction
they stimulate their respective receptors on nociceptive fibers
31
examples of inflammatory mediators
histamine serotonin bradykinin prostaglandins ATP H+ nerve growth factor TNF alpha endothelins interleukins
32
what do you treat inflammatory pain with
local anesthetics Cox2 inhibitors opioids/opiates
33
locally released inflammatory mediators not only activate pain fibers in inflammatory pain, what else can they do
sensitive pain fibers in both inflammatory and nociceptive pain
34
what are the two forms of sensitization
hyperalgesia allodynia
35
define hyperalgesia
slightly painful stimulus is now perceived as being significantly more painful (this is primarily a peripheral component)
36
define allodynia
enhanced sensitivity and reaction to a stimulus that is normally NOT painful (usually-but not always- at or near the site of primary injury) (this is both due to a peripheral component as well as a central component)
37
how does allodynia work
inflammatory mediators can 'non-specifically' bind to TRP channels and decrease the threshold needed for activation
38
how does hyperalgesia work
inflammatory mediators activate their specific receptors on pain fibers leading to phosphorylation of VGSCs, TRP channels, and other signaling proteins which 'sensitize' these pain fibers thus later phosphorylation events(painful stimulus) are amplified due to increased frequency of firing of APs of these 'sensitized' pain fibers
39
describe neuropathic pain
reflects damage to peripheral or central nervous system which leads to pain perception without persistent external pain stimulus or pain perception in presence of non-painful stimulus (allodynia)
40
what are the treatments for neuropathic pain
atypical analgesics: tricyclic antidepressants, anticonvulsants, calcium channel blockers (drugs that sedate, change mood, or are used for general anesthesia) or opioids/opiates (less effective)
41
can you treat neuropathic pain with opioids/opiates
yes but way less effective
42
what are the two components of pain processing
discriminative (where) and affective (emotional)
43
what does discriminative pain processing determine
magnitude of pain what type of painful stimulus where is the pain coming from
44
what does affective pain processing determine
emotions how unpleasant is the pain how uncomfortable is the pain
45
what is the target of descending pain inhibitory pathways from the brain
dorsal horn in the spinal cord
46
how does the descending pain inhibitory pathways inhibit pain transduction
descending brainstem inputs activate local dorsal horn interneurons that inhibit pain transmission see picture
47
how the descending pain inhibitory pathway works
see picture
48
define referred pain
visceral discomfort/pain interpreted as cutaneous (skin/surface) pain
49
why do we have referred pain
convergence of visceral and cutaneous pain afferents in the spinal cord (onto same spinal thalamic nerves) which then activates central mechanisms that interprets visceral pain as occurring at cutaneous sites
50
describe gate theory
mechanoreceptor activation promotes inhibition of pain relay neurons in the dorsal horn see picture
51
how does phantom limbs/pain work
mis-match between central representation and periphery due to re-wiring of pathways spinothalamic nerves lose innervation from nerves from missing limb then nerves from limb area still there (i.e. lost lower arm so "limb area still there" would be upper arm) rewire and attach to the spinothalamic nerves that once were innervated by the lost limb area now feel pain where no limb is anymore
52

Pharmacology - Exam 2 (14 decks)

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