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Neuro Review by Minnie > Pain (78b, 81b, 82b) > Flashcards

Pain (78b, 81b, 82b) Flashcards

Actually all of this module could be called this

1
Q

Which anesthetic does not interact with the GABA receptor?

A

Ketamine

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2
Q

What is the role of antidepressants in pain?

A

Treat neuorpathic pain by enhancing the descending inhibitory pathway

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3
Q

Which IV anesthetic is anti-emetic?

A

Propofol

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4
Q

Which pain medication is an NMDA antagonist?

A

Ketamine

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5
Q

During an operation, the patient’s aneurysm bursts

What should the anesthesiologist do?

A

Give a bolus of IV anesthetic to decrease cerebral blood flow so the bleed can be managed

Do not give inhaled bolus - these increase cerebral blood flow!

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6
Q

What is the role of nerve blocks in treating chronic pain?

A
  • Diagnostic
    • Figure out which nerve is the problem
  • Prognostic
    • Figure out if surgery will work
  • Treatment
  • Adjunctive
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7
Q

Which receptor is involved in “wind up”?

A

NMDA receptor (on the 2nd order neuron)

Results in a burst of nociceptive signals with C-fiber stimulation (even if many of the C-fiber signals are blocked by opioids)

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8
Q

What are the indications for ketamine during anesthesia?

A

High risk patinets with hemodynamic instability

Increases cerebral blood flow - do NOT use in patients with intracranial hypertension

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9
Q

Do NSAIDs or opioids have a role in neuropathic pain?

A

No

  • Use antidepressants, anticonvulsants, or muscle relaxants instead
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10
Q

What is the MOA of barbituates for anesthesia?

What are they used for?

A
  • Activates GABA-A receptor AND facilitates the binding of endogenous GABA to the GABA-A receptor
    • Cl- conductance increases
    • Hyperpolarization
  • Used for induction of anesthesia
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11
Q

Normally, C-fibers go to lamina ___ of the dorsal horn, while A-beta fibers go to lamina ___

A

Normally, C-fibers go to lamina 2 of the dorsal horn, while A-beta fibers go to lamina 3

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12
Q

Effect on cerebral blood flow of…

  • Most IV anesthetics:
  • Volatile anesthetics:
A
  • Most IV anesthetics: Decrease cerebral blood flow
    • ​Except ketamine - increases flow and O2 demand
  • Volatile anesthetics: Increase cerebral blood flow
    • Due to vasodilation

Both decrease cerebral O2 demand (except ketamine)

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13
Q

The anterolateral tract transmits pain up the spinal cord, and then splits into 3 different pathways

  • The _______ tract is for processing pain
  • The _______ tract activated our emotional response to pain (fear)
  • The _______ tract increases our awareness
A
  • The neospinothalamic tract is for processing pain
  • The paleospinothalamic tract activated our emotional response to pain (fear)
  • The spinoreticular tract increases our awareness
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14
Q

What is the MOA of propofol for anesthesia?

A
  • Activates the GABA-A receptor
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15
Q

Which method of central sensitization results in allodyina?

A

Neural sprouting

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16
Q

Which antiepileptic is most commonly used for neuropathic pain?

A

Gabapentin

17
Q

Is the placebo effect a psychological phenomenon, or can it be explained by physiological changes in the body?

A

The placebo effect is NOT purely a psychological phenomenon

  • There are endorhin-mediated phsyiologic changes that occur as a result of a placebo
  • However, the placebo itself is not responsible for these changes
    • Likely due to the brain’s reward system/what we expect from taking a medication??
18
Q

What is the mechanism of action of ketamine?

A

NMDA receptor antagonist

  • Works to treat pain even if wind up (central sensitization) has occurred
19
Q

What is the mechanism of oral skeletal muscle relaxants?

A

Nonspecific supression of CNS polysynaptic pathways

20
Q

Which drug would you give to counteract the hypotension (and reflex tachycardia) associated with propofol?

A

An alpha-1 agonist (ex: phenylephrine)

  • Propopfol vasodilates
  • Alpha-1 agnoists counteract by vasoconstricting
21
Q

How do antiepileptic drugs work to treat chronic pain?

A

Block voltage-sensitive Na+ channels

  • Decreases excitation and increases inhibition
    • Fewer action potentials
    • Increased threshold for repetitive action potential generation
    • Prevents firing of burst neurons (wind up)
  • Use for neuropathic pain!
22
Q

What is the MOA of TCAs and SNRIs in treating pain?

A
  • Block reuptake of 5HT and NE to enhance the descending inhibitory pathway
  • Works to treat neuropathic pain
23
Q

What is the MOA of etomidate?

In which patients would we use etomidate rather than propofol?

A
  • Activates GABA-A receptors
    • -> Increased Cl- conductance
    • -> hyperpolarization
  • More CV stability with etomidate than propofol, but causes nausea, vomiting, and adrenal cortical suppression
    • Use in patients with ischemic heart disease who probably can’t tolerate propofol
24
Q

How do opioids decrease pain?

A
  • Decrease C-riber transmission
  • Increase the activity of the descending inhibitory system
25
Q

When is ketamine indicated for pain management?

A
  • When opioids and NSAIDs are failing
  • Other adjuncts have been tried
  • Regional anesthesia (epidural, wound infiltration) is contraindicated
  • The patient is in the hospital
    • Given IV
26
Q

What are the 3 major neurotransmitters of pain?

A

Glutamate

Substance P

CGRP

27
Q

Which class of drugs promotes sedation, hypnosis, amnesia, and anxiolysis?

What is it used for?

A

Benzodiazapines

Used pre-op to reduce anxiety and promote amnesia

Note - NOT an analgesic; cannot activate the GABA receptor without endogenous GABA

28
Q

What is the MOA of muscle relaxant drugs to treat chronic pain?

A
  • GABA agonists potentiate the descending inhibitory system
    • Cause sedation, centrally acting
    • Tolerance in 2 weeks :(
  • Alpha-2 agonists
    • Tizanidine
    • No tolerance :)

Don’t use soma!! (addictive tranquilizer)

Neuro Review by Minnie (8 decks)

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