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PHYSL 372 > Pain System 2 > Flashcards

Pain System 2 Flashcards

1
Q

What does damaged tissue or inflammation release?

A

NGF, bradykinin, serotonin, ATP, histamine, prostaglandins, H+, K+, cytokines (IL6 and IL1beta, TNFalpha)

(inflammatory soup)

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2
Q

Describe how the chemical sensitization of nociceptors occurs.

A
  • damaged tissue or inflammation releases inflammatory soup
  • inflammatory soup sensitizes the nociceptor
  • nociceptor releases CGRP and Substance P
  • vasodilation occurs

“backwards release” (ask someone to explain)

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3
Q

What are TRP channels?

A

variety of ligand gated ion channels activated at different temperatures

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4
Q

What kind of neurons can TRPV1 be found on? What are they activated by? At what temperature are they activated?

A
  • on small nociceptive neurons
  • activated by: capsaicin, moderate thermal stimuli, H+ ions
  • temperature: 43 degrees celcius
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5
Q

Which channels do chili peppers activate?

A

TRPV1

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6
Q

What kind of neurons can TRPV2 be found on? What are they activated by (temperature) ?

A
  • on A-delta cells (to lamina I)
  • activated by intense noxious heat >52 degree celcius
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7
Q

At what temperature are TRPM8 receptors activated? What are they activated by?

A
  • cold/cool temperatures –> 8-22 degree celcius
  • activated by menthol and icilin
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8
Q

Which substance increases sensitivity of all TRP channels?

A

bradykinin

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9
Q

label the diagram on slide 7.

A

flare, mechanical hyperalgesia

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10
Q

When inflammatory factors are release at an injury, an area of ____________________ develops around the original injury.

A

hyperalgesia

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11
Q

excitation of which type of pain fiber causes release of substance P and CGRP? Where are they released from?

A
  • C-fiber
  • released from sensory nerve endings
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12
Q

What are the effects of the release of substance P and CGRP?

A
  • excite other C-fibers
  • axon reflex
  • vasodilation (redness)
  • extravasation of plasma proteins (add to inflammatory soup)
  • oedema (swelling)
  • migraine pain
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13
Q

Provide an overview on how neurogenic inflammation can cause sensitization of sensory nerve fibers.

A

DETAILS:
- prostaglandin sensitizes TRP channels via PKA –> phosphorylate Na+ channel –> TRP channel open at lower temperature threshold –> generate more APs
- bradykinin sensitizes TRP channels –> reduce threshold for activation –> increased output to a given stimulus

OVERVIEW:
1. CGRP and substance P stimulate mast cell
2. mast cell release histamine
3. bradykinin and prostaglandin sensitize the axon
4. axon further releases CGRP and substance P to stimulate blood vessel

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14
Q

If pain signals tissue damage, why do we have endogenous analgesic mechanisms? What substance play a role in the analgesia?

A
  • central mechanisms that suppress pain have a significant survival value
  • endogenous opioids (enkephalin, dynorphin, endorphin, endomorphin) dampen pain signals
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15
Q

Where are pain signals modified in the descending top down inhibitory pain path?

A
  • PAG
  • RVM
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16
Q

What mechanism hold the descending analgesic pathways in check so that we can feel pain?

A

tonic GABAergic inhibition in RVM and PAG

17
Q

draw the descending analgesic pathway from amygdala to spinal opioid INs.

A

slide 12

18
Q

What is the prototypical substance for analgesia

A

opioids

19
Q

What are the 3 endogenous opioids? What are the 3 pro-hormones?

A
  • endogenous opioids: endorphin, dynorphin, enkephalin
  • pro-hormones: POMC, prodynorphin, proenkephalin
20
Q

What are the 3 MAIN endogenous opioid receptor types?

A

mu, kappa, delta

21
Q

What were the initial opioid receptor types identified?

A

mu, kappa, sigma

22
Q

Which opioid receptor type is bound by enkephalins? endorphins?

A
  • delta bound by enkephalins
  • epsilon bound by endorphins
23
Q

What is the mechanism of action of opioid receptors?

A
  • GPCR
  • inhibit adenylyl cyclase
  • open K+ channels
  • hyperpolarization
24
Q

Which opioid receptor is most widely expressed?

A

mu opioid receptors

25
Q

What is the main action of mu1 vs mu2 receptors? peripheral or spinal/supraspinal?

A
  • mu1: analgesia (peripheral and spinal/supraspinal)
  • mu2: respiratory depression, bradycardia, euphoria, ileus (spinal/supraspinal)
26
Q

What does binding of the kappa opioid receptor produce? peripheral or spinal/supraspinal? Which effects are negative?

A
  • analgesia
  • sedation
  • dysphoria (negative)
  • psychomimetic effects (negative)
  • inhibit ADH release (promote diuresis) (negative)
  • peripheral and spinal/supraspinal
27
Q

What is the function of delta opioid receptors?

A
  • potentiate effects of both mu1 and mu2
  • analgesia and undesirable effects
28
Q

TRUE or FALSE: it is thought that mu and kappa receptors exist together as a complex

A

FALSE: mu and delta

29
Q

TRUE or FALSE: ketamine is an opioid

A

FALSE: anesthetic induction agent that possesses analgesic properties

30
Q

How does ketamine affect the sympathetic nervous system?

A
  • activate sympathetic nervous system
  • maintain blood pressure and heart rate; bronchodilation
31
Q

What is ketamine a derivative of?

A

phencyclidine derivative (PCP, angel dust)

32
Q

What kind of anesthesia does ketamine produce?

A

dissociative anesthesia

33
Q

what kind of state does ketamine resemble?

A

cataleptic state

34
Q

What are the mechanisms of action of ketamine? Where does it bind?

A
  • binds non-competitively to PCP recognition site on NMDARs –> blocks NMDARs (KEY)
  • effects on opioid receptors
  • monoaminergic receptors –> voltage-gated Na+ channels
35
Q

How does ketamine affect NMDARs

A

ketamine binds a site in the channel pore (acts similar to Mg2+ ion) to block conductance through channel (Ca2+)

note: even if Mg2+ block removed from NMDAR, if ketamine still present, ions still cannot flow through

36
Q

What is the action of NSAIDs in analgesia? does it act centrally or peripherally? When is the best time to use it in terms of surgery?

A
  • block prostaglandin synthesis –> take away sensitization (decrease hyperactivity)
  • central and peripheral
  • best if used pre- or perioperatively
37
Q

What is the pro and con of NSAIDs in comparison to opioids?

A
  • pro: not as dangerous as opioids bc no respiratory depression
  • con: inhibition is not as direct
38
Q

classify the following as acting centrally or peripherally:
- NSAIDs
- mu1
- mu2
- kappa

A
  • NSAIDs = central and peripheral
  • mu1 = central and peripheral
  • mu2 = central
  • kappa = central and peripheral

(check notes again)

PHYSL 372 (21 decks)

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