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Pharmacology - Exam 2 > Pain (nociception) > Flashcards

Pain (nociception) Flashcards

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

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

A

activation of distinct TRP channels and other peripheral nocireceptors

23
Q

what is the main TRP channel to know

A

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

24
Q

pain treatment options for nociceptive pain

A

local anesthetics

Cox2 inhibitors

opioids/opiates

25
Q

what does TRP stand for

A

transient receptor potential

26
Q

what activates TRP channels

A

heat or capsaicin

27
Q

what is capsaicin

A

compound found in hot peppers that can bind to TRP receptors/channels and elicit sensations of pain

28
Q

how can capsaicin be used for pain management

A

use capsaicin to target TRP channels for low long activation which then leads to desensitization and management of pain

29
Q

what causes inflammatory pain

A

tissue or internal organ damage that causes a local or systemic immune response (i.e. release of inflammatory mediators by immune cells)

30
Q

how do inflammatory mediators stimulate pain transduction

A

they stimulate their respective receptors on nociceptive fibers

31
Q

examples of inflammatory mediators

A

histamine

serotonin

bradykinin

prostaglandins

ATP

H+

nerve growth factor

TNF alpha

endothelins

interleukins

32
Q

what do you treat inflammatory pain with

A

local anesthetics

Cox2 inhibitors

opioids/opiates

33
Q

locally released inflammatory mediators not only activate pain fibers in inflammatory pain, what else can they do

A

sensitive pain fibers in both inflammatory and nociceptive pain

34
Q

what are the two forms of sensitization

A

hyperalgesia

allodynia

35
Q

define hyperalgesia

A

slightly painful stimulus is now perceived as being significantly more painful (this is primarily a peripheral component)

36
Q

define allodynia

A

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
Q

how does allodynia work

A

inflammatory mediators can ‘non-specifically’ bind to TRP channels and decrease the threshold needed for activation

38
Q

how does hyperalgesia work

A

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
Q

describe neuropathic pain

A

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
Q

what are the treatments for neuropathic pain

A

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
Q

can you treat neuropathic pain with opioids/opiates

A

yes but way less effective

42
Q

what are the two components of pain processing

A

discriminative (where) and affective (emotional)

43
Q

what does discriminative pain processing determine

A

magnitude of pain

what type of painful stimulus

where is the pain coming from

44
Q

what does affective pain processing determine

A

emotions

how unpleasant is the pain

how uncomfortable is the pain

45
Q

what is the target of descending pain inhibitory pathways from the brain

A

dorsal horn in the spinal cord

46
Q

how does the descending pain inhibitory pathways inhibit pain transduction

A

descending brainstem inputs activate local dorsal horn interneurons that inhibit pain transmission

see picture

47
Q

how the descending pain inhibitory pathway works

A

see picture

48
Q

define referred pain

A

visceral discomfort/pain interpreted as cutaneous (skin/surface) pain

49
Q

why do we have referred pain

A

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
Q

describe gate theory

A

mechanoreceptor activation promotes inhibition of pain relay neurons in the dorsal horn

see picture

51
Q

how does phantom limbs/pain work

A

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
Q
A

Pharmacology - Exam 2 (14 decks)

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