Week 9 - Sensory Processing P2 Flashcards
(19 cards)
What is pain
an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
What is the difference between acute and chronic pain
acute pain is normally more short term (less than 3-6 months) due to a clear, identifiable injury or illness.
Chronic pain is long term (beyond normal healing time > 3-6 months) and may persist after an injury has healed or without clear cause
Information regarding pain is transmitted through what 2 types of nociceptive nerve fibers
- C fibres
- Aδ (A-delta) fibers
What are the properties of C fibres
- unmyelinated
- conduction speed is slow
- pain type: dull, burning, aching pain
- stimuli: mechanical, thermal and chemical
Function: delivers ongoing, longer lasting pain often associated with tissue injury or inflammation - causes nauseous, chronic pain usually associated with tissue damage and destruction
What are A-delta fibers
- thin myelinated
- small diameter
- conduction speed is fast
- pain type: sharp, localized, immediate pain
Stimuli: mechanical and thermal (e.g. pinprick, burn)
Function: Alerts you quickly to harmful stimuli so you can react (e.g. pulling hand away from hot surface)
What neurotransmitters do nociceptive nerves use
Peptide neurotransmitters (substance P, neurokinin A, CGRP)
- peptides synthesized in ganglia and transported both centrally and peripherally
central release - nociceptive transmission
Peripheral release - neurogenic component of inflammation
What do A-delta fibres mainly innervate
- mainly innervates the skin
- not normally associated with deeper structures
Where do C-fibres innervate
- associated with skin but also innervate deep tissue and organ systems
What is the conduction velocity for A-delta fibres
20m/sec
takes 0.1 sec to send a signal
What is the conduction velocity for C fibres
0.5m/sec
3-4 sec to send a signal
are A-delta fibres sensitive to pressure and low dose local anesthetics
relatively sensitive to pressure
relatively insensitive to low dose of local anesthetics
are C fibres sensitive to inhibition by pressure and low dose local anesthetics
relatively insensitive to inhibition by pressure
sensitive to low does of local anesthetics
what happens if you block the activity of A delta fibres in response to a noxious stimulus
you may block the sharp pain but the pain associated with C fibres activation becomes much stronger and more aversive
- Conversely it appears that is AO fibres are active, they may reduce the nociceptive sensations associated with the stimulation of C fibres
What is a nociceptive signal
signal sent in the nociceptive nerves
what is TRPV1
A receptor protein that is only located on pain sensing neurons in the periphery
It is polymodal and responds to:
- Capsaicin
- Temperature
- H+
- Lipids
- Mechanical stimuli
How are nociceptive nerves activated
- Capsaicin stimulates nociceptive C-fibres by acting on a specific receptor/ion channel – TRP vanilloid receptor subtype 1-TRPV1R
- 6-transmembrane cation channel – opening allowing influx of mostly Ca2+ and Na+
- causes membrane depolarisation - if depolarisation reaches certain threshold then it generates an action potential in the nociceptive neuron
- This receptor is responsible for much of the “polymodal” natural of these nerves
- Nociceptive nerve terminals also express receptors for a wide range of mediators including glutamate, GABA, Ach, Serotonin, ATP, bradykinin, noradrenaline, histamine, somatostatin, opioids ect
blocking TRPV1 will cause what
specifically block pain but not motor or autonomic acitivty
why does pain persist longer after the initial event e.g. injury or infection
because nociceptive nerves are subject to ongoing chemical stimulation
what factors ma be responsible for the ongoing chemical stimulation of nociceptive nerves
- various neurotransmitters -serotonin, histamine and acetylcholine
- kinins - 2 peptides, bradykinin and kallidin, are released under conditions of tissue injury -potent pain producing substances
- Metabolic -= lactic acid, K+ ion, H+ ions, ATP and ADP – released by damaged cells and hypoxic tissues