PH3113 - Pain and Analgesia 3 Flashcards

1
Q

What is the treatment for IBS in the UK?

A

Anti-spasmodics
Anti-motility drugs
Osmotic laxatives
Drugs for constipation
Anti-depressants

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2
Q

What is pain?

A

Nociception
- sensitivity to and awareness of noxious/harmful stimuli
Suffering
- cerebral awareness, interpretation and anxiety of pain

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3
Q

What is the emotional component of pain?

A

Suffering

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4
Q

What are the components of pain?

A

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

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5
Q

How is pain intensity characterised?

A

Pain intensity is subjective
- can be measured in a variety of ways

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6
Q

How is pain duration characterised?

A

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

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7
Q

Give examples of different types of pain

A

Nociceptive
- visceral
- somatic
- deep
- superficial
Neuropathic
- peripheral
- central
Inflammatory
- tissue inflammation
- hypersensitivity

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8
Q

What are the different types of neuropathic pain?

A

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

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9
Q

What is referred pain?

A

Reflective pain

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10
Q

What are some examples of referred pain?

A

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

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11
Q

What is phantom pain?

A

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

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12
Q

How do we feel pain?

A

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

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13
Q

How is pain detected in the periphery?

A

Stimulants
- noxious factors
- bradykinins
- prostaglandins
- nerve growth factors
- serotonin
- ATP
- H+

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14
Q

Give examples of pain receptor stimulants

A

Bradykinin
Histamine
5-HT

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15
Q

What effect do pain receptor stimulants have on the sensitivity of sensory neurones to other transmitters? (prostaglandins and opioids)

A

Prostaglandins
- increase the sensitivity of sensory neurones
Opioids
- decrease the sensitivity of sensory neurones
- TRPV 1 channel

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16
Q

How is pain transmitted from the nociceptor to the spinal cord?

A

A delta fibres release
- glutamate
C fibres release
- substance P
- neurokinin A
- calcitonin gene-related peptide
- CGRP

17
Q

What is the gate control theory of pain?

A

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.

18
Q

How does the descending pathway control pain mechanisms?

A

Periaqueductal grey receives input from different brain areas
- hypothalamus
- somatosensory cortex
- amygdala
Gate keeper!

Locus coeruleus
- noradrenaline
Raphe nuclei
- serotonin