230 - Pain Flashcards
What defines chronic pain?
> 6 months pain - as this is longer than natural healing processes
What is chronic pain syndrome?
Chronic pain + additional issues: depression, sleep issues, anxiety
What occurs in the chronic pain cycle?
Pain - fear of movement - avoidance - rest - distress + frustration - physically deconditioned - pain
How can you asses pain?
Use IMPACT guidelines
- Pain intensity
- Physical function
- Emotional function
- Rating of improvement
What is the difference between acute and chronic pain?
Acute - always a cause - aim to find cause and cure damage using a medical model
Chronic - no longer a clear cause - the pain has no function
What are the 2 types of pain?
Nociceptive - stimulus - pain pathway
Neuropathic - doesn’t need nociceptive stimulus, generalised within nervous system.
What is a nocicepter?
A receptor in a reflex arc + pathway
- the free nerve endings of a sensory nerve, can be speciallised to feel particular stimuli
- Thermal (TRPV1 receptor)
- Chemical (Histamines + bradykinin mediated)
- Mechanical (stretch receptors)
What are the 2 types of sensory nerve fibres involved in pain?
A-delta: myelinated, fast pain sensation, unimodal
C fibres: Unmyelinated, slow lingering pain, polymodal
(A-beta fibres inhibit nociceptive transmission)
How does inflammation affect pain?
Contributes to nociceptive pain - as inflammatory mediators sensitise nociceptive pathways - makes 1st order neurones more likely to fire.
- so use anti-inflams in pain drug therapy (eg. aspirin inhibits prostaglandins)
Describe the path that pain takes up the pain pathway
Pain sensed by a 1st order nocicepter, travels into the spinal cord. It synapses there with 2nd order neurone, ascends the spinothalamic tract to the thalamus. In the thalamus it synapses with a 3rd order neurone which forms the thalamocortical projection
- ends in:
- insula + cingulate cortex (makes pain unpleasant)
- Primary somatosensory cortex at post-central gyrus (localises pain - homunculus)
What is the role of the descending pathway in nociception?
Where does it project from?
It modulates the ascending pathway
Mediates endogenous analgesia - by giving microinjections of opioids.
Projects from 3 places:
- PAG (in midbrain) - opiodergic
- Nucleus of Raphe magnus - serapheneric and opiodergic
- Locus Coernelus - noradrenergic
Describe the endogenous opioid system
Gives endogenous pain relief
Has 3 receptors - Mu (addictive), Delta and Kappa
They are all metabotropic and G-protein coupled.
The endogenous opioids are all peptides:
- endorphins
- Enkephalins
- Dynorphins
As well as pain relief you get euphoria, sedation, cough suppression, respiratory depression. You can become tolerant.
How does the opioid system modulate pain?
Spinal interneurones release enkephalins into the synapse of 1st or 2nd order nociceptor neurones, which shuts down their activity.
The interneurones are activated by the descending pathway
What is neuropathic pain?
Pain caused by neuronal damage, eg. inflammation.
It sensitises nociceptive pathways - pain more readily transmitted.
What is hyperalgesia?
Pain hurts more than it should
What is allodynia?
Stimulus hurts when it shouldn’t
What is parasthesia
pain in absence to stimulus
What is stress induced analgesia?
Stress -> amygdala -> projections into the PAG which stimulates opioid modulation of pain.
? evolutionary advantage?
What is phantom limb pain?
Perfection of pain on a missing limb.
Often limbs that have been amputates, paralysed or in a fixed position.
Caused by sensory confusion - there is a massive sensory loss including 1st order neurone loss, so the remaining 2nd order neurones reorganise in the dorsal horn.
A Beta fibres (touch) may synapse with the 2nd order neurones, so touch sensation viewed as pain.
The sensory homunculus in the somatosensory cortex also may be reorganised, with adjacent areas merging.
What is one way of trying to treat phantom limb pain?
Mirror visual feedback - try to correct the sensory perception in the somatosensory cortex.
What are 4 main theories behind pain?
Intensive: pain is an emotional state cuased by intense stimuli.
Single-wire theory: Disterbance passed along one nerve fibre to brain
Specificity: pain has its own independant system
Bio-psycho-social: no simple relationship between damage and pain
Gate-theory: Opioids are involved in gating pain
Describe the theory of delay discounting
The subjective value of reward is reduced when there is an increased delay, uncertainty or duration of task.
What is dolorimetry?
Measurement of pain
What is the peak-end rule of pain?
Different parts of the painful experience carry different weights - we remember the peak and end pain levels.
- Kahnman - cold water experiements
- Redelmeier + Kahnman - colonoscopy experiments
What are the 3 steps in the WHO pain ladder?
1: non-opioid +/- adjuvants
2: Weak opiod +/- non-opioid +/- adjuvant
3: Strong opioid +/- non-opioid +/- adjuvant
What are 2 classes of non-opioid analgesia used?
Paracetamol (reduces central prostaglandin synthesis ?COX3 action)
NSAIDS - ibuprofen, naproxen (Competitive COX inhibitors - reduces prostaglandins but also affects other COX actions - side effects: GI damage, kidney damage, NA+ Water retention, worsening of asthma)
If the COX1 action in NSAIDS is what causes the side effects, why don’t we use selective COX2 inhibitors instead of NSAIDS?
They were developed (Celecoxib, etoricoxib, Vioxx-withdrawn) but withdrawn/not used so much due to cardiovascular complications.
Weigh up risks.
What are examples of weak opioids?
Codeine
Dihydrocodein
Tramadol (only 20% opioid, also non-opioid by increasing serotonin)
If you are using what class of drug must you be careful with tramadol?
SSRIs
What are examples of strong opioids?
Morphine - gold standard Fentanyl - lipophilic Diamorphine - heroin, quick, euphoria Methadone - long acting Remifentanl - short half life, sedative in ITU
What side effects do you get with opioids?
N+v
Drowsiness
Unsteadiness
Consipation
occasionally sweating, dry mouth
Name 4 classes of aduvant drugs used in analgesia
Anti-epileptics (gabapentin, carbamizapine)
Anti-depressants (amitriptyline)
NMDA-R antagnoists (Ketamine)
Anaesthetics (lidocaine, entonox)
