Pain Flashcards
What is the IASP definition of pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.
How is pain passed to the brain?
Receptors sense it and generate AP to pass back into the spine and into brain.
Why do we feel pain?
It’s an early warning system, alerts to danger, warning to actual or potential harm.
What are the types of pain?
-Somatic (superficial)
-Somatic (deep)
-Visceral
Cause of superficial somatic pain?
Tissue damage.
Cause of deep somatic pain?
Tissue damage.
Cause of visceral pain?
Distension, lack of O2, inflammation.
Features of superficial somatic pain?
Sharp fast pain, localised and brief, in skin.
Features of deep somatic pain?
Burning, itching slow pain, diffuse and long- lasting, in deep layers of skin and muscles.
Features of visceral pain?
Dull ache, burning slow pain, can cause nausea, in organs.
What is acute pain?
Momentary, lasts for weeks or months (will resolve).
What is chronic pain?
3 months or more. Persistent, remains after healing processes, complex lifestyle implications.
Why is it not good if we can’t feel pain?
Would have to wear protective gear to stop harming ourselves, pain mechanisms disrupted (producing huge amounts of endogenous NTs).
How can some people not feel pain?
Non- functional voltage- gated sodium channels, can’t generate APs as these are dependent on sodium channels.
Therefore, can’t send these back to the brain (no nociception).
What is nociception?
The neural process of encoding noxious stimuli (dangerous stimuli). It is a different phenomenon to pain perception (free nerve endings activated and carried to CNS through spinal tracts).
What is the meaning of polymodal?
The ability to respond to many inflammatory mediators.
What is the process of nociception reaching the CNS?
There are lots of sensory proteins in the free nerve ending (histamine and bradykinin) and if the free nerve ending is activated, it senses damage and depolarise to generate an AP.
Which inflammatory mediators are the activators?
K+, H+, histamine and serotonin (from mast cells).
Which inflammatory mediators are sensitisation?
prostaglandin (vasodilation), bradykinin (coagulation, make nerve endings more sensitive), nerve growth factors.
What is neurogenic inflammation?
Releasing from nerve endings, add to the inflammation response.
What is the purpose of Substance P?
Activates mast cells to release more histamine (very powerful vasodilator)
What is peripheral sensitisation?
Caused by the release of Substance P (if you keep damaging the same area, becomes more and more sensitive)- positive feedback loop.
How does the nociceptive info get into the spine?
Through the spinothalemic pathway (C- fibres and Ad fibres are 1st order and are passed to 2nd order in spine).
What kind of receptor is a C-fibre?
Polymodal, hot and burning sensation (slow pain).
What kind of receptor is A delta fibres?
Mechanical and thermal, mechanothermal. (sharp prickling fast pain).
What is central sensitisation?
Where a 1st order neuron (C fibre) at a pre-synpatic cell releases glutamate which is sensed by the 2nd order neurons.
What are the 2 types of glutamate receptor?
AMPA and NMDA (NMDA if there is lots of glutamate released, otherwise inactive).
What enters the cell if glutamate binds to AMPA receptor?
Na+ enters (allows to generate APs).
What enters the cell if glutamate binds to NMDA receptor (strong stimulation)?
CA2+ (this sensitises the post synaptic cell).
What is the difference between peripheral and central sensitisation?
Peripheral is where the pre synaptic cell is sensitised through the release of Substance P.
Central is where the post synaptic cell is sensitised through Ca2+ entering cell from NMDA.
What type of nerve fibre is used with the indirect spinothalemic pathway?
C- fibre (slower)- limbic system, hypothalamus.
What type of nerve fibres is used with the direct spinothalemic pathway?
Faster A delta fibres- myelinated to carry the AP very fast.
To cortical areas and for better spatial discrimination.
What is referred pain?
This is where you feel pain in other organs (stress and nociceptive signals in places you wouldn’t expect). For example, you can feel an MI in your arm.
What is the reason for referred pain?
When an embryo, the places were originally really close together and as the areas develop, they move further apart but still send sensory info to the same part of the brain.
What is pain modulation?
-Changing the volume of signals coming through
-Changing salience- perception of those signals.
What is the pain gate model?
Both of the 1st order neurons (AB and C) are activated at the same time, AB activates the inhibitory interneuron which reduces the activation and release of GABA.
Therefore, this closes down the 2nd order neuron activity so feel less pain (less nociceptive signals get to the brain).
How can the pain gate model be used for pain modulation?
‘rubbing it better’. Article that shows gentle stroking babies provides pain relief (C fibres are active rated by light stroking).
What are factors that open the pain gate?
-stress, tension, depression, worry, boredom etc.
What are factors that close the pain gate?
relaxation, optimism, happiness, distraction.
What is the difference between nociception and pain perception?
Nociception is the signals coming into the brain and pain perception is interpreting these signals (different depending on the situation).
What are the 2 descending pathways?
serotonergic (release serotonin) and noradrenergic (release adrenaline). These are both inhibitory NTs.
What is the process of these inhibitory NTs for the pain gate?
These inhibitory NTs are released onto the interneurons and they release endorphins onto the chemical synapse between the 1st and 2nd order neurons. This closes the pain gate.
What is the central neuropathic pain (when system goes wrong)?
Things such as stroke, spinal cord injury. Central sensitisation can become pathological as it disrupts the communication between different parts of the brain (inappropriately perceiving pain).
What is the peripheral neuropathic pain?
Physical trauma to the nerve (sends inappropriate signals to the brain to perceive pain).
What happens when a nerve root is crushed?
Stop producing neutrotrophins and start producing nerve growth factors (inflammation response).
What is the impact of a herniated disc?
This is where a nerve root is pressurised and so feel pain.
What is hyperalgesia?
This is increased sensitivity (tissue injury and the area becoming more sensitive).
-Caused by peripheral sensitisation and its an exaggerated response to painful stimuli.
What is allodynia?
This is increased sensitivity to non- noxious (non painful) stimuli.
Central mechanism and switch inhibitory to excitatory (touching with a feather causes pain.
What is the autonomic response to acute pain?
Fight or flight response.
What is the autonomic response to chronic pain?
Often none.
What is psychological component of acute pain?
associated anxiety.
What is psychological component of chronic pain?
Increased irritability, depression, sleep issues, appetite changes.
