4. Pain Flashcards
Pain definition?
Pain is an unpleasant sensory and emotional experience associated with either actual or potential tissue damage.
It is actually subjective and not a substantive construct of the real World
Functions to protect the _____
The sense of Pain only occurs in your _____, prior to that its just a code
Pain is therefore highly ______ and contextual
Functions to protect the body
The sense of Pain only occurs in your brain, prior to that its just a code
Pain is therefore highly subjective and contextual
Signal perception is modulated by…
Situation, Emotion, Genetic susceptibility, previous experience
Peripheral aspect on pain detection al nocireceptors?
1.Nociceptive receptors 2.Nociceptive activation 3.Sensitization of receptors 4.Nociceptive fibres
Nociceptive nerves have free ……….. with……….
Nociceptive nerves have free unspecialised nerve endings with ‘pain’ channels inserted in the membrane
Most common nocireceptor?
The most common is the Transient Receptor Potential family of channels (TRP)
Sensitivity of the TRP channels
Sensitive to (amongst others) O2, pH osmolarity and valinoids (capsicum) and heat (NB potentially involved in infra red vision in reptiles) Can be sensitised by substance P, bradykinins, serotonin, pH, ATP, NO etc
Structure of TRP channel?
Composed of a 6 unit trans-membrane portion and a ‘basket’ of regulatory complex in the cytoplasm.
Allows Ca2+ into the cell
Temperature, mechanical and chemical activation of nociceptors?
Temperature:
Extreme heat and extreme cold open ‘Transient receptor potential vanilloid’ (TRPV) channels inserted in the membrane.
Allows Na2+ and Ca2+entry and so depolarises the cell to give an action potential
Mechanical :
Actual mechanism still unknown. Presumed to be a form of insensitive mechanoreceptor which allows Na entry when activated.
Chemical:
Apart from TRPV receptors, it’s largely unknown but chemical transmission can cause sensitisation of pain receptors
Describe the sensitisation process of pain receptors?
All these processes increase the sensitivity to pain and non pain stimuli.
- Bradykinin activates pain fibres directly and causes increase in prostaglandins
- Tissue damage produces H ions which give muscle ache (e.g. weight lifting)
- Prostaglandin E2 is made by cyclooxygenase. Aspirin and other NSAIDs act to inhibit this enzyme
- Calcitonin gene related peptide (CGRP )and SP both recruit silent receptors which increase summation in the dorsal horn.
- Histamine causes hyperalgesia through its effects on blood vessels.
Purpose of pain sensitisation
To prevent future damage to area via memory
features of a-delta fibres?
Myelinated
Sharp 1st pain
Mechanical pinching
Extreme hot or cold
Features of c fibres?
Unmyelinated
Secondary slow pain (diffuse)
Mechanical pinching, Thermal and Chemical stimuli (polymodal)
Mode of nocirecptive singal transmission?
Via a-delta and c fibres
USE neurotransmitters:
On stimulation they release…
1. Glutamate
2. Substance P
3. Calcitonin gene-related peptide (CGRP)
@ both central synapses and peripheral synapses.
Peripheral release (recall histamine practical) give the red flare and tenderness associated with pain.
Substance P & CGRP release is responsible for the 3 local physiological signs of pain
- Calor (heat)
- Rubor (redness)
- Tumor (swelling)
1 & 2 caused by local hyperaemia and the third by plasma extravasation
What are the anteolateral tracts for ascending pain?
Spinothalamic tracts:
- Paleo (dull, old pain via the DM intralaminar of Thalamus to the limbic system association cortices)
- The neo (fast, sharp via VPL of thalamus to the primary somatosensory cortex)
Nociceptive fibres synapse in the dorsal horn (quick to cross) with 2 types of ascending axons. Name the axons?
- Nociceptive specific (NS) – C and Aδ only and
- Wide dynamic range neurons (WDR)- any sensory input including pain, can fire in a graded fashion based on C fibre frequency of input (higher the pain higher the input)
The NS and WDR neurons are points of descending pain modulation from PAG in the brainstem