Pain physio / assessment Flashcards
What are the definitions of pain / nociception
Pain = Unpleasant sensory and emotional experience, associated with actual or potential tissue damage
(associated with sensory and affective components)
Nociception = neural process of encoding noxious stimuli (unconscious)
What are the 2 types of fibers responsible for nociception
- A-delta fibers (“fast pain”)
- C-fibers (“slow pain, unmyelinated)
+/- A-beta fibers but mostly sensory not pain
What are the 2 types of C-fibers
- Peptidergic (releasing substance P and CGRP = calcitonin gene related peptide)
- Non-peptidergic (expressing c-Ret neurotrophin receptor targeted by glial-derived neurotrophic factors)
Describe the pathway of nociception
- Primary afferent nerve fibers = A-delta and C-fibers, their free nerve endings are the nociceptor
(= “primary afferent neuron”) - Synapse in dorsal horn of spinal cord (neurotransmitters = substance P, glutamate):
- A-delta fibers synapse in lamina I and V
- C-fibers synapse in lamina I and II - Ascending pathways in the spinal cord:
- spinothalamic tract (from laminae I & V)
- spinoreticular tract (from laminae II, IV, V)
- spinomesencephalic tract (from laminae I & V)
(= “projection neuron”) - Synapse in thalamus / reticular activating system / midbrain (periaqueductal gray)
(= “supraspinal neurons”) - Integration:
- Thalamus ->relay to somatosensory cortex
- Reticular activating system -> projection to thalamus and limbic system + autonomous and endocrine responses
- Periaqueductal gray -> descending inhibitory function, modulation of nociception
What is the definition of hyperalgesia / allodynia
- Hyperalgesia = exaggerated and prolonged response to a noxious stimulus
- Allodynia = pain response to a low‐intensity, normally innocuous stimulus
Hyperalgesia and allodynia are a conse quence of peripheral and central sensitization.
What are mechanisms of peripheral sensitization and central sensitization
- Peripheral sensitization:
- Tissue damage / inflammation changing the micro-environment of nociceptor (release of neurotransmitters and mediators sensitizing nerve terminals)
- Changes in ion channels expression on nerve endings of primary afferent neurons -> hyperexcitability - Central sensitization:
- Activation of NMDA receptors
- Transcriptional changes in dorsal horn of spinal cord (expression of COX-2)
- Activation of microglial cells upregulating COX-2
What are the 5 steps leading to pain
- Transduction (conversion of nociceptive signal into action potential)
- Transmission (through A-delta and C-fibers to spinal cord)
- Modulation (involving interneurons in dorsal horn of spinal cord)
- Projection (spinothalamic, spinoreticular and spinomesencephalic tracts)
- Perception (cortex, hypothalamus, limbic system, PAG)
What are the 2 major excitatory neurotransmitters involved in the pathway of pain
- Glutamate
- Substance P
Name 3 composite pain scales for assessment of acute pain and the categories they assess
- Glasgow Composite Measure Pain Scale (GCMPS): posture, activity, vocalization, attention to wound / painful area, demeanor, mobility, response to touch
- Validated in dogs
- Colorado State University Veterinary Teaching Hospital Pain Score for Cats and Dogs: comfort, movement, appearance, unprovoked behavior, interactive behavior, vocalization, HR and RR
- Not really validated
- UNESP-Botucatu Multidimensional Composite Pain Scale (UNESP-Botucatu MCPS): 10 variables assessed over pain expression, psychomotor change and physiological variables
(also exists as a short form) - Validated in cats
Name 3 pain scales validated in cats for assessment of acute pain
- UNESP-Botucatu Multidimensional Composite Pain Scale (UNESP-Botucatu MCPS)
- Grimace Scale: ear position, orbital tightening, muzzle tension, whiskers position, head position
- Glasgow Composite Measure Pain Score Feline (GCMPS-F)
What are 4 big types of pain
- Visceral pain (from visceral nociceptors)
- Somatic pain (from skin, blood vessels, muscles, connective tissues nociceptors)
- Neuropathic pain (from nerve fibers, spinal cord, CNS themselves)
- Psychogenic pain (emotional, anticipatory)
What substances released in tissues contribute to transduction of a painful stimulus
- Substance P
- Prostaglandins
- Serotonin
- Bradykinin
- Histamine
- Leukotrienes
- Potassium
What are the main endogenous mechanisms of modulation of pain
- Descending inhibitor nervous system ->acts in spinal cord
- Endogenous opioid system
- Segmental inhibition / gate control theory (stimulation of sensory pathway to “overwhelm” the nerves and decrease the transmission of pain) -> acts on primary afferent nerves
- Peripheral modulation of nociceptors -> acts on nociceptors (decreased iCa entry)
Where is the origin of the Descending inhibitory nervous system? What are the neurotransmitters?
Periaqueductal gray (PAG) in the midbrain with relay in the Rostral ventral medulla (RVM)
Transmitters = serotonin and norepinephrine
What are the 3 groups of endogenous cannabinoids? What receptors to they bind?
- Enkephalins (leucine-enkephalin, methionine-enkephalin) -> kappa receptors
- Endorphins (beta-endorphin) -> mu receptors
- Dynorphins (dynorphin-A) -> delta receptors
What categories of analgesics act on transduction / transmission / modulation / perception
- Transduction: local anesthetics, NSAIDs
- Transmission: local anesthetics
- Modulation: local anesthetics, ketamine, opioids, alpha2-agonists
- Perception: opioids, alpha2-agonists, general anesthetics
Name 3 unidimensional pain scoring systems
- Simple descriptive scale
- Numeric rating scale
- Visual analog scale
Which sensory fibers are myelinated and which aren’t?
A- beta & A-delta are myelinated
C nociceptors are not myelinated
What is decussation?
During transmission, after 1st order neuron goes to dorsal horn, information travels to the contralateral ventral horn and then up the spinothalamic tract
Associate the opioid receptor to the endogenous ligand:
Opioid receptor:
1. Mu
2. Kappa
3. Delta
Endogenous ligand:
A. Dynorphine A
B. B-Endorphine
C. Leucine and methionine-enkephalin
1 - B
2 - C
3 - A
