Physiology - Fractures and Dislocation Flashcards
Nociceptors
Peripheral receptors of pain (noxious stimuli)
Types of nociceptors
Mechanical nociceptors
Polymodal nociceptors
Thermal nociceptors
Mechanical nociceptors
Stimulated by intense pressure
Have fast conducting myelination - give rise to sharp fast (1st) pain (localised)
Polymodal nociceptors
Respond to multiple stimuli
Afferents are C fibres
C fibres
Slower than A delta fibres - unmyelinated
Result in slow (2nd) pain - aching or burning natures
High threshold thermo, mechano and chemical receptors
Thermal nociceptors
C fibre afferents
Respond to extremes of hot and cold
Primary hyperalgesia
Occurs within areas of damaged tissue
Secondary hyperalgesia
Occurs ~ 20mins after an injury, tissues surrounding a damaged area may become supersensitive
What is pain proportionate to
Nociceptive input
Pain pathways
A delta and C fibres enter dorsal horn and interact w/ projection neurons
Ascension via spinothalamic tract to thalamus
3rd order neurons project and terminate in the 1’ somatosensory centre - determine which region of body is experiencing pain
Limbic cortex
Emotional centre
Tells us pain is unpleasant and concerning
Molecular sensor for noxious heat stimuli
TRPV1 (capsaicin - chilli)
Molecular sensor for noxious mechanical stimuli
TRPA1
TRPV4
Piezo
Molecular sensor for noxious chemical stimuli
ASIC
TRPA1
TRPV1
Molecular sensors for noxious cold stimuli
TRPM8 (menthol)
TRPA1
Molecular sensor for ATP
ATP comes from damaged tissue
P2X3
What happens when molecular sensor channels have been opened
Triggers an influx of Na+ —-> causing an action potential
Mediated by Na channels (1.8 and 1.9)
Where do projection neurons cross to
Cross to diagonal side of dorsal horn (ventral aspect)
Anatomy of pain pathways
Transduction
Transmission
Modulation
Perception
Transduction
Conversion of noxious stimuli into electrical energy
Transmission
Electrical stimulus is sent to the dorsal horn of the spinal cord and synapse at the 2nd order neuron
Modulation
Inhibition vs amplification of signal (facilitated by EAA)
Inflammatory soup
ATP Bradykinin PGE2 Serotonin Histamines COX-2 activation Substance P
PGE2
Prostaglandins
NGF
Nerve growth factor
What happens during transduction
Afferent fibres enter into dorsal horn and transmit signal to WDR neurons at diff laminae
WDR neurons
Wide Dynamic Range neurones
Receive stimulation from both small diameter and big diameter fibres
Found in lamina V
EAA
Excitatory Amino Acids
Endogenous relievers of pain
Opioids
Gate theory (TENS)
NSAIDs
Local anaesthetic
How do opioids work as an endogenous relievers of pain
Produce analgesia via binding and acting on opioid receptors causing body to produce endorphins - inhibit ascending pathway
Types of pain
Physiological (nociceptive) pain
Pathological (neuropathic) pain
Psychogenic pain
Pathological pain
Caused by damage of nerve pathway
Psychogenic pathway
In depression and anxiety
Main pain gates
Spinal gate
Brain stem gate
Thalamic gate
Gate control theory
Concurrent activity in large-diameter (Aβ) primary afferents reduces the transmission of pain signals in small-diameter (Aδ and C) afferents due to inhibitory neuron at lamina II
Explains why rubbing skin (exciting tactile and pressure receptors) relieves pain
Spinoreticular pathway
Ascension tract for pain detected by C fibres
Where do pain pathways pass before reaching thalamus
Medulla, pons and midbrain
Spinothalamic and spinoreticular pathways cross at diff levels
A- alpha fibres
Motor neurones
A-beta fibres
Large diameter fibres
Transmit info about touch and pressure - mechanoceptor
When is infl soup released
In response to injury form leaky blood vessels and damaged tissues
Directly excites nociceptors or makes them more sensitive to other agents
NSAIDs pain relieving mechanisms
Inhibit COX enzymes - no PGE2 or leukotrienes produced
Local anaesthetic pain relieving mechanism
Reversibly blocks the conduction of action potentials by blocking Na+ channels on axon
Stimulation of inhibitory interneuron at lamina II
Stimulated by A-beta fibres