PH3113 - Pain and Analgesia 3 Flashcards
What is the treatment for IBS in the UK?
Anti-spasmodics
Anti-motility drugs
Osmotic laxatives
Drugs for constipation
Anti-depressants
What is pain?
Nociception
- sensitivity to and awareness of noxious/harmful stimuli
Suffering
- cerebral awareness, interpretation and anxiety of pain
What is the emotional component of pain?
Suffering
What are the components of pain?
Sensory
- perception of pain characteristics
- intensity
- quality
- location
Affective
- negative emotion
- anxiety
- fear
- unpleasant sensation
Congnitive
- interpretation of pain
Behavioural
- coping strategies used to express, void or control pain
Physiological
- nociceptive and stress response
How is pain intensity characterised?
Pain intensity is subjective
- can be measured in a variety of ways
How is pain duration characterised?
Acute
- less than 3 - 6 months
- short
- normally non-traumatic
Sub-acute/inflammatory
- local inflammatory changes
- intensity affected by inflammatory mediator
Chronic malignant
- more than 3 - 6 months
- caused by cancer
- progressive and substantial
- peripheral and central sensitisations
Chronic non-malignant
- often neuropathic
- long-term
- unrelated to peripheral injury
- tissue
- pathology in pathways
Give examples of different types of pain
Nociceptive
- visceral
- somatic
- deep
- superficial
Neuropathic
- peripheral
- central
Inflammatory
- tissue inflammation
- hypersensitivity
What are the different types of neuropathic pain?
Hyperalgesia
- increased pain to a mildly noxious stimulus
- central facilitation
- peripheral sensitisation
Allodynia
- pain to a non-noxious stimulus
- should not be painful
(not usually perceived as painful but is)
Spontaneous pain
- pain without stimulus
What is referred pain?
Reflective pain
What are some examples of referred pain?
Upper chest/left limb
- myocardial infarction
Head ‘ice cream’ headache
- vagus nerve
General
- phantom limb pain
Right shoulder
- liver
- gall bladder
Left
- thoracic
- diaphragm/lung
What is phantom pain?
Pain felt by a majority of amputees
- 50 - 80%
Sensations often map to other areas of the body
- related to proximity in cortex
- trigeminal nerve severed
- map of face on hand
- same effect can be seen with other senses
- some are helped by mirror therapy
How do we feel pain?
3 levels of pain information
Nociception
- where it is
- peripheral activation and release of pain mediators
- primary nociceptors
- C and A-delta fibres
- A-delta fibres myelinated
- C fibres unmyelinated
Pain gating
- neurones influence how pain signal is transmitted to ascending and descending secondary fibres
- dorsal horn of spinal cord
Pain perception
- brain
- thalamus
- limbic
- cortical systems
How is pain detected in the periphery?
Stimulants
- noxious factors
- bradykinins
- prostaglandins
- nerve growth factors
- serotonin
- ATP
- H+
Give examples of pain receptor stimulants
Bradykinin
Histamine
5-HT
What effect do pain receptor stimulants have on the sensitivity of sensory neurones to other transmitters? (prostaglandins and opioids)
Prostaglandins
- increase the sensitivity of sensory neurones
Opioids
- decrease the sensitivity of sensory neurones
- TRPV 1 channel
How is pain transmitted from the nociceptor to the spinal cord?
A delta fibres release
- glutamate
C fibres release
- substance P
- neurokinin A
- calcitonin gene-related peptide
- CGRP
What is the gate control theory of pain?
States that the sensation of pain is transmitted from periphery of the body along ascending nerve paths to the brain
- an alternate activity can replace the travel of pain sensation closing the gate control at the spinal cord and reduce pain impulses
• Incoming C fibre= secondary afferent neurone sending info up ascending pain fibre into the brain
• Here the nociceptor released glutamate or other neurotransmitter like substances to activate/stimulate neurone
• But also a collection of inhibitory interneurons which would normally prevent these secondary afferents from firing.
• Don’t want pain signals firing from spinal cord if there is no pain stimulus.
• They will release GABA and prevent fibres from being activated when no pain stimulus
• When we have a pain sensation- same time as stimulating secondary afferent there is an off shoot of the primary afferent fibre which inhibits the inhibitory interneuron (releasing inhibitory neurotransmitters)
• prevent firing of inhibitory neurones allowing the stimulatory sensation to be transmitted up secondary neurone
• AB fibres (mechanoskin receptor fibres) – respond to touch
• Stimulation of these AB fibres= you can counteract activity at the inhibitory interneurons – turn on inhibitory neurone.
• Stimulate inhibitory neurones (fire more) to counteract the positive stimulus coming from the sensory neurone
• Eg. Mild pain= turn on inhibitory neurones (release Glutamate) and dampen down the pain signal going up to the secondary afferent neurone.
• Gated theory of pain, gated mechanism, gated by inhibitory neurone.
• Severe pain: Can overwhelm the system and then the pain stimulus will be transmitted up to the brain.
How does the descending pathway control pain mechanisms?
Periaqueductal grey receives input from different brain areas
- hypothalamus
- somatosensory cortex
- amygdala
Gate keeper!
Locus coeruleus
- noradrenaline
Raphe nuclei
- serotonin
