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IDT Fall > Pain Management Part II > Flashcards

Pain Management Part II Flashcards

1
Q

chemical senses on neurons are sent via which type of receptors? (ion? G-coupled?)

A

ion channels or G coupled

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2
Q

mechanical and thermal senses on neurons are sent via which type of receptors? (ion? G-coupled?)

A

ion channels

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3
Q

initiation of a pain signal is conducted by what type of neurons?

A

primary afferent sensory neurons

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4
Q

what are the 3 primary pain NTs?

A

substance P, glutamate, and CGRP

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5
Q

primary afferent sensory neurons are:
a. Unipolar
b. Multipolar
c. Pseudo-unipolar
d. Bipolar

A

c

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6
Q

A alpha fibers:
Myelinated?
function?
sensitivity to block?

A

yes
motor and proprioception
low

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7
Q

A beta fibers:
Myelinated?
function?
sensitivity to block?

A

yes
touch
moderate

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8
Q

A delta fibers:
Myelinated?
function?
sensitivity to block?

A

yes
pain and temperature
high

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9
Q

C dorsal root fibers:
Myelinated?
function?
sensitivity to block?

A

no
pain, temp., and touch
very high

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10
Q

how does myelin affect a drug’s ability to block the sensory neuron?

A

makes it harder for drug to get into neuron

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11
Q

the activation of what receptor can block nociceptive receptors?
which 2 chemicals are agonists at this receptor?

A

TRPV1
capsaicin and resiniferatoxin

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12
Q

what do capsaicin and resiniferatoxin do?

A

they deplete substance P to disrupt neuronal function

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13
Q

what is strontium used for and how does it work?

A

it treats bone pain by entering in place of calcium to potentially reduce pain and inflammation

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14
Q

what class of drugs can we use for bone pain that are also primarily used for osteoporosis?

A

bisphosphonates

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15
Q

can we use calcitonin for bone pain management?

A

yes, but it is not efficacious

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16
Q

what is the channel target for local anesthetics?

A

to block voltage-gated sodium channels

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17
Q

local anesthetics have a high affinity for _____ channels, and thus ____ nerves are more affected by blockade

A

open, active

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18
Q

describe the use dependent blockade of local anesthetics (LA)

A

-LAs increase the refractory period of sodium channel
-they incr. threshold for depolarization
-each depolarization leads to more channel blockade
-eventual loss of excitability

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19
Q

which local anesthetics have a short duration of action?

A

procaine
chloroprocaine
lidocaine
mepivacaine
prilocaine

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20
Q

which local anesthetics have a medium duration of action?

A

benzocaine
cocaine
bupivacaine

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21
Q

which local anesthetics have a long duration of action?

A

etidocaine
ropivacaine

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22
Q

which two LAs are the only two without parental use?

A

benzocaine
cocaine

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23
Q

which LAs have topical usage?

A

benzocaine
cocaine
lidocaine
prilocaine

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24
Q

what CNS effects may occur with LA toxicity?

A

anxiety, nervousness, convulsions, drowsiness, and depressed breathing

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25
Q

what cardiovascular effects may occur with LA toxicity?

A

ventricular arrhythmia and collapse

26
Q

how does increasing sensitization occur? (hyperalgesia)

A

-sensitizing chemicals are released from surrounding cells which lower the threshold for depolarization
- pain NTs are released with lower stimuli
-substance P activates the immune cells to release sensitizers creating a feedback loop

26
Q

NSAIDs inhibit pain initiation by inhibiting synthesis of sensitizing _______

A

prostoglandins

27
Q

what are potential neurologic SEs of NSAIDs?

A

dizziness and tinnitus

28
Q

what effect does glutamate have when released by primary sensory afferents?

A

rapid depolarization

29
Q

what effect does substance P/ CGRP have when released by primary sensory afferents?

A

sustained depolarization

30
Q

transmission via primary afferent neurons is ______-dependent

A

calcium

31
Q

A beta fibers synapse in which layers of the substantia gelatinoasa?

A

3,4,5

32
Q

A delta fibers synapse in which layers of the substantia gelatinoasa?

A

1 and 2

33
Q

C fibers synapse in which layers of the substantia gelatinoasa?

A

1,2,5

34
Q

C fibers and A delta fibers in substantia gelatinoasa activate non-specific (NS) _______ neurons and ________

A

ascending, interneurons

35
Q

what do NS ascending neurons do?

A

tell body where pain is located

36
Q

C and A delta fibers also influence the activity of _____ secondary neurons

A

wide dynamic range (WDR)

37
Q

what is the function of WDR axons?

A

transmit an intensity of pain message

38
Q

paleospinothalmic polysynaptic neurons terminate in the _________ others reach the _______

A

brainstem, thalamus

39
Q

neospinothalamic pathways mostly ascend directly to the ______ with a focused message of _____ _____________

A

thalamus, pain localization

40
Q

A beta and A alpha fibers synapse in which layers of the substantia gelatinoasa?

A

3-5

41
Q

T/F non-specific neurons only respond to pain

A

true

42
Q

T/F wide dynamic range neurons respond to all sensations including pain

A

true

43
Q

NE and 5-HT from descending reaction paths inhibit _____ or activate inhibitory __________ __________ to inhibit pain transmitter release and 2nd order pain transmission

A

WDRs, enkephalin interneurons

44
Q

GABA/glycine send _______ signals to the WDR neuron

A

inhibitory

45
Q

cytokines and PGs send ______ signals to the WDR neuron

A

activating

46
Q

what is the “wind-up” theory causing chronic pain?

A

overtime there is increased glutamate release which leads to repeated depolarization leading to activation of NMDA Receptors
NMDA receptor activation makes the post-synaptic neurons more easy to depolarize

47
Q

what is the theory of loss of inhibitory neurons causing chronic pain?

A

overstimulation of too much calcium activation can kill inhibitory neurons which will increase excitability/sensitization of relay neurons

48
Q

what is the theory of spinal/central sensitization causing chronic pain?

A

immune cells released enhance NT release and lower depolarization threshold

49
Q

what is allodynia?

A

touch or proprioception turns to pain sensation

50
Q

REVIEW SLIDE 33!!!!

A

.

51
Q

what drug class has synergistic effects with opioids which mediate spinal analgesic actions?
name the 2 we use

A

a2 agonists
clonidine, dexmedetomidine

52
Q

why can SNRIs/TCAs be useful for pain?

A

NE activates a2 receptors

53
Q

note: tramadol and tapentadol are reuptake inhibitors with some opioid agonism

A

.

54
Q

CGRP receptor antagonists are used to treat?

A

migraines/headaches

55
Q

GABA agents inhibit pain NT release and should inhibit pain transmission. What is the issue that makes them not effective at inhibiting pain?

A

they also inhibit inhibitory descending pathway

56
Q

what drug is used for trigeminal neuralgia

A

carbamazepine

57
Q

what drug is used off label for diabetic neuropathy?

A

Mexiletine

58
Q

what is the mechanism of action of ketamine which is an NMDA receptor blocker?

A

blocking NMDA receptors will block wind up and treat chronic pain

59
Q

what portion of the brain is the primary distributor of pain signals?

A

thalamus

IDT Fall (29 decks)

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