Pain Flashcards
What is pain?
an unpleasant sensory and emotional experience associated with, or resembing that associated with, actual or potential tissue damage
What are the types of pain?
Nociceptive
- pain transmitted by noiceptors
- SOMATIC (soft tissue, bone)
- VISCERAL (less well-localised)
Neuropathic
- pain as a result of damage to the pain system
Noiciplastic
- pain as a result of a modualted pain system eg central sensitisation
What are the 2 types of nociceptors and their differences?
A-delta fibres
ACUTE, SHARP, IMMEDIATE, SHORT LIVED PAIN
- myelianted
- larger iameter
- fast
- sharp/localised
- glutamate is the NT to 2nd order neurone
C-fibres
ACHING/BURNING
- unmyelinated
- smaller diameter
- slow
- dull/diffuse
- substance P is NT to 2nd order neurone
- involved in sensitisation
What triggers nociceptors
chemical:
- prostaglandins
- histamine
- ATP
- Bradykinin
- 5-HT
- H+ ions
specific nociceptors:
- thermal - TRPV1 (heat/capsacin)
- mechanical - crushing, incisions
- chemical - caustic or irritating molecules
THEY MUST REACH A CERTAIN THRESHOLD TO FIRE AN ACTION POTENTIAL
What is sensitisation? When is sensitisation useful? when is it not?
sensitisation = a reduction in the threshold and/or an increase in magnitude of responsiveness
peripheral sensitisation = Long term release of inflammatory mediators –> increased excitability of nociceptors,
Pseudo-unipolar first order neurones produce these inflamamtory mediators suxh as substance P - these are transmitted to either end of neurone
central sensitisation = repetivive inputs into the spinal cord, particualrly c fibres –> subtance P –> “wind up” positive cycle
USEFUL = enables more effective healing and leads to protection of the injury
NOT USEFUL = inappropriate or prolonged sensitistaion = chronic pain, hyperalgesia
pathophysiology of allodynia?
nociceptive A-delta fibres run closely with non-nociceptive A-beta fibres
malformation = pain from mechanical stimuli = allodynia
physiology gate-control theory
a model for ascending pain supression due to mechanical stimulation inhibitinh nociceptive pain
nociceptive A-delta fibres run closely with non-nociceptive A-beta fibres
can interfere with eachother and supress one another
this is the theory behing TENS/rubbing etc.
pathophysiology neuropathic pain
injury to peripheral nerve –> spontaneous signalling in absence of stimulus = stabbing, shock like pain
How does the descending pathway modulate pain?
The periaqueductal gray, or PAG, receives pain information via the spinomescencephalic tract and processes the nociceptive information and relays it to the rostral ventral medulla (RVM). These neurons in the RVM then send a signal down the spinal cord and activate the endogenous opiate system to suppress pain.
main NT= 5-HT, noradrenaline, enkephalins (endogeonous opiods)
what is a pain threshold?
point at which a sensory input is considered “painful”
define chronic pain
> 3 months
