Pain Management Part II

Question 1

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

Answer 1

ion channels or G coupled

Question 2

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

Answer 2

ion channels

Question 3

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

Answer 3

primary afferent sensory neurons

Question 4

what are the 3 primary pain NTs?

Answer 4

substance P, glutamate, and CGRP

Question 5

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

Answer 5

c

Question 6

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

Answer 6

yes
motor and proprioception
low

Question 7

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

Answer 7

yes
touch
moderate

Question 8

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

Answer 8

yes
pain and temperature
high

Question 9

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

Answer 9

no
pain, temp., and touch
very high

Question 10

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

Answer 10

makes it harder for drug to get into neuron

Question 11

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

Answer 11

TRPV1
capsaicin and resiniferatoxin

Question 12

what do capsaicin and resiniferatoxin do?

Answer 12

they deplete substance P to disrupt neuronal function

Question 13

what is strontium used for and how does it work?

Answer 13

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

Question 14

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

Answer 14

bisphosphonates

Question 15

can we use calcitonin for bone pain management?

Answer 15

yes, but it is not efficacious

Question 16

what is the channel target for local anesthetics?

Answer 16

to block voltage-gated sodium channels

Question 17

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

Answer 17

open, active

Question 18

describe the use dependent blockade of local anesthetics (LA)

Answer 18

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

Question 19

which local anesthetics have a short duration of action?

Answer 19

procaine
chloroprocaine
lidocaine
mepivacaine
prilocaine

Question 20

which local anesthetics have a medium duration of action?

Answer 20

benzocaine
cocaine
bupivacaine

Question 21

which local anesthetics have a long duration of action?

Answer 21

etidocaine
ropivacaine

Question 22

which two LAs are the only two without parental use?

Answer 22

benzocaine
cocaine

Question 23

which LAs have topical usage?

Answer 23

benzocaine
cocaine
lidocaine
prilocaine

Question 24

what CNS effects may occur with LA toxicity?

Answer 24

anxiety, nervousness, convulsions, drowsiness, and depressed breathing

Question 25

what cardiovascular effects may occur with LA toxicity?

Answer 25

ventricular arrhythmia and collapse

Question 26

how does increasing sensitization occur? (hyperalgesia)

Answer 26

-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

Question 26

NSAIDs inhibit pain initiation by inhibiting synthesis of sensitizing _______

Answer 26

prostoglandins

Question 27

what are potential neurologic SEs of NSAIDs?

Answer 27

dizziness and tinnitus

Question 28

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

Answer 28

rapid depolarization

Question 29

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

Answer 29

sustained depolarization

Question 30

transmission via primary afferent neurons is ______-dependent

Answer 30

calcium

Question 31

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

Answer 31

3,4,5

Question 32

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

Answer 32

1 and 2

Question 33

C fibers synapse in which layers of the substantia gelatinoasa?

Answer 33

1,2,5

Question 34

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

Answer 34

ascending, interneurons

Question 35

what do NS ascending neurons do?

Answer 35

tell body where pain is located

Question 36

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

Answer 36

wide dynamic range (WDR)

Question 37

what is the function of WDR axons?

Answer 37

transmit an intensity of pain message

Question 38

paleospinothalmic polysynaptic neurons terminate in the _________ others reach the _______

Answer 38

brainstem, thalamus

Question 39

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

Answer 39

thalamus, pain localization

Question 40

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

Answer 40

3-5

Question 41

T/F non-specific neurons only respond to pain

Answer 41

true

Question 42

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

Answer 42

true

Question 43

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

Answer 43

WDRs, enkephalin interneurons

Question 44

GABA/glycine send _______ signals to the WDR neuron

Answer 44

inhibitory

Question 45

cytokines and PGs send ______ signals to the WDR neuron

Answer 45

activating

Question 46

what is the "wind-up" theory causing chronic pain?

Answer 46

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

Question 47

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

Answer 47

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

Question 48

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

Answer 48

immune cells released enhance NT release and lower depolarization threshold

Question 49

what is allodynia?

Answer 49

touch or proprioception turns to pain sensation

Question 50

REVIEW SLIDE 33!!!!

Answer 50

.

Question 51

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

Answer 51

a2 agonists clonidine, dexmedetomidine

Question 52

why can SNRIs/TCAs be useful for pain?

Answer 52

NE activates a2 receptors

Question 53

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

Answer 53

.

Question 54

CGRP receptor antagonists are used to treat?

Answer 54

migraines/headaches

Question 55

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

Answer 55

they also inhibit inhibitory descending pathway

Question 56

what drug is used for trigeminal neuralgia

Answer 56

carbamazepine

Question 57

what drug is used off label for diabetic neuropathy?

Answer 57

Mexiletine

Question 58

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

Answer 58

blocking NMDA receptors will block wind up and treat chronic pain

Question 59

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

Answer 59

thalamus