Pain and analgesia Flashcards
what is the World Health Organisations definition of pain?
1) an unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage
how are patients asked to indicate the degree of pain they are experiencing?
1) Pain scales where patient is asked to indicate degree of pain in relation to extremes
- can be a numerical scale 0 (no pain) to 10 (worse pain)
- Visual Analogue Scale ( mark along the scale)
2) Rating scales: patient asked to indicate degree of pain:
- word descriptor scales ( e.g. 0= no pain, 2 = distressing pain, 5 = excruciating pain…)
- verbal scale (On a scale of 0 to 10…)
other scales used to indicate pain are functional and categorical scales. describe these scales
1) functional scales:e.g. 0= no pain, 1 = tolerable and pain does not prevent any activities, 5 = intolerable and pain prevents verbal communication
2) Categorical scale: Mild (1-3) , Moderate (4-6), Severe (7-10)
Graphic scales can also be used to rate pain. what are graphic scales and when would they be used?
1) uses smiley faces: 0 = Very happy, no hurt :), 10= Hurts as much as you can imagine :(.
2) used for young/disabled patient
list five scales used to indicate pain
1) word descriptor scale
2) verbal scale
3) functional scale
4) Categorical scale
5) graphic scale
Pain is multifactorial, but can be divided into 2 broad sub-classes. name the two sub-classes
1) Nociceptive pain
2) Neuropathic pain
1) what is Nociceptive pain ?
2) give examples of Nociceptive pain
1) Peripheral visceral or somatic pain due to direct activation of pain-sensing receptors (nociceptors) in response to a noxious stimulus that alerts the organism of impending tissue damage
2) Examples: inflammation, fractures, burns, bumps & bruises
what are the two types of Nociceptive pain?
1) acute : lasting < 3-6 months, desirable defence mechanism
2) chronic : lasting >6 months, undesirable
1) what is Neuropathic pain ?
2) give examples of Neuropathic pain
1) Pain produced by damage to, or dysfunction of, nerves in the peripheral or central nervous system
2) Examples: trigeminal neuralgia, nerve trauma, peripheral neuropathy, phantom limb pain
Is Neuropathic pain chronic or acute?
1) Neuropathic pain tends to be chronic, but can also be acute
(e. g. following surgery)
Nociceptive pain perception may be viewed as a three-stage process. outline these 3 stages
1) Detection of pain in the periphery. Noxious stimuli (to skin or subcutaneous tissue) activates sensory nociceptors
2) Transmission of pain signals from the periphery to spinal cord, predominantly by C-fibres and Aδ -fibres. Signals are amplified or inhibited by local neuronal circuits and descending inhibitory pathways from higher brain centers
3) Reception of signal by higher central brain centers, afferent activity generates a pain sensation and initiates an appropriate response
Name the three mine types of fibres involved in sensory transduction and state their function.
1) Aβ: touch/pressure (mechanoreception). Likely target of TENS and acupuncture
2) Aδ: signal sharp pain (nociceptors)
3) C: Dull, burning pain (nociceptors)
- Temperature (thermoceptors)
state the diameter, conduction velocity and myelination for the following fibres.
1) Aβ
2) Aδ
3) C
1) Aβ: diameter= 5-10ɥm
- conduction velocity (m/s)= 30-70
- myelination: thick
2) Aδ: diameter= 2-5ɥm
- conduction velocity (m/s)= 5-30
- myelination: thin
3) C: diameter= ~1ɥm
- conduction velocity (m/s)= < 1
- myelination: none
outline the gate control theory proposed by Melzack and Wall
1) perception of pain may be controlled by a ‘gate
2) The gate is formed by transmission neurones which supply the thalamus and are affected by small inhibitory neurones (substantia gelatinosa SG interneurones) and by nociceptive (C and Aδ fibres) and mechanoreceptor (Aβ) fibre input.
( The smaller, unmyelenated A (delta) and C nerve fibers sense pain such as sharp burning and aching feelings. Larger, myelenated A (beta) skin nerves which carry senses of touch, heat, cold and pressure. the A (beta) nerves are faster, and also have priority which effectively blocks out the pain messages to the brain and closes the gate.) -> google
summarise the role of the following in the gate control theory:
1) SG (substantia gelatinosa)
2) C/Aδ fibres
3) Aβ
4) Descending inhibitory pathways from the CNS
1) SG interneurones inhibit (close) the gate: reduce pain
2) Activation of C/Aδ fibres open the gate (increase pain) by: direct excitation of the gate, inhibition of SG interneurones
3) Activation of Aβ fibres close the gate by: excitation of SG interneurones
4) Descending inhibitory pathways from the CNS close the gate by: inhibition of the gate, direct activation of SG interneurones
targeting inflationary mediators is the basis for designing analgesic drugs. list the Inflammatory mediators of peripheral pain and state their function.
1) Bradykinin activates :
- B₂ receptors in nociceptive neurones
- B₁ receptors: via the metabolite des-Arg⁹BK; ‘upregulated’ by inflammation
2) Substance P: activate NKA (neurokinin) receptors in nociceptive neurones
3) Adenosine triphosphate (ATP): activate P₂X₃ receptors
4) Protons (H+): activate Acid-Sensing Ion Channels (ASICs)
5) Endogenous activators of TRPV1 vanilloid receptors also heat, target of capsaicin . TRPV1 upregulated by BK and Nerve Growth Factor (NGF)
6) Prostanoids
1) what are Prostanoids and when are they released?
2) what do Prostanoids cause?
3) how can the release of these mediators be blocked?
1) Prostanoids are released in inflammation (prostaglandins and thromboxane) produced from precursors in cell membrane
2) cause release of two mediators, PGE2 and PGF2 released in inflammation, greatly increase responses to bradykinin and 5-HT = sensitization (more painful)
3) Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) such as aspirin block the cyclooxygenase enzyme which breaks down arachidonic acid into all of the above mediators.
