Flashcards
Week 3
Cards in this deck (29)
- 1What is pain?-An unpleasant sensory and emotional experience associated with actual/potential tissue damage
-Combination of sensory and emotional components
-Subjective - 2What is nociception?Sensory component of pain alone (no emotional component)
- 3How is pain perceived peripherally?-Free nerve endings in skin, muscle and viscera
-Activated by noxious (intense) stimuli
-Stimulus intensity is shown via the firing rate - 4Describe mechanical nociceptors-Activated by a strong shearing force in the skin
-eg. cut, strong blow
-Sharp pain
-A delta fibres (excitatory) - 5Describe polymodal nociceptors-Respond to many stimuli eg. sharp blow, damaging heat >46 degrees
-Activated by chemicals released by damaged tissue eg. k+, H+, histamine, prostaglandins, bradykinin
-Dull burning pain
-C fibres (excitatory) - 6How does sharp pain occur?-Fast transmission by myelinated A delta fibres
-Well localised pain
-Faster propagation of AP - 7How does dull, burning pain occur?-Exists as a 'second pain'
-Slower transmission
-Goes along unmyelinated C fibres - 8Describe the substantia gelatinosa/lamina II-Laminar organisation
-Somatotopic organisation (localisation in somatosensory cortex)
-Synapsing with second order neurones occurs here
-Directly/indirectly (via interneuron) passes signal to projection neurones - 9What is the gate theory of pain?-Local interneurones modulate activity of projection neurones
-Majority of these are inhibitory
-Pain signal must therefore overcome inhibition to be sent to the brain - 10Describe the signals present in the Gate Theory of Pain (resting state)Gatekeeper neurone in the substantia gelatinosa has an inhibitory effect on the projection neurone which ascends to the brain
- 11Describe the signals present in the Gate Theory of Pain (non-noxious input)-Signal arrives along the AB mechanoreceptor fibres
-Fibre excites both the gatekeeper and projection neurone
-Since the gatekeeper neurone is stimulated, the inhibitory effect is still present
-No signal is propagated to the projection neurone - 12Describe the signals present in the Gate Theory of Pain (noxious stimulus)-Signal arrives along the AB mechanoreceptor fibres and excites both the gatekeeper and projection neurone
-A delta/C fibres also excite the projection neurone
-An inhibitory interneurone is present between the A delta/C fibres and the gatekeeper interneurone. This is stimulated, removing the inhibitory effect of the gatekeeper neurone
-Signal is propagated to the projection neurone and into the brain - 13Where is pain perceived/localised in the ascending spinothalamic pathway?Perceived: subcortical level
Localised: cortical level - 14What is the intrinsic analgesic system?-Descending pathways release 5-HT, noradrenaline and enkephalin (endogenous opioid)
-These close the spinal gate, allowing initial pain relief - 15What is facilitated pain?-Normal physiological pain ie. acute, phasic
-Duration and intensity depends on the number of AP fired
-Chronic pain can increase pain sensitivity, resulting in facilitated pain - 16How does peripheral and central sensitisation occur?Modification of neurotransmission plasticity
- 17What is the difference between an innocuous and noxious stimulus?Innocuous: no pain sensation
Noxious: pain sensation - 18What is hyperalgesia?Enhanced painful response to a normally painful stimulus
- 19What is allodynia?Painful response to a normally non-painful stimulus
- 20How does sensitisation of peripheral nociceptors occur?-Substance P and CGRP is released from nerve endings
-This results in plasma extravasation (results in redness and swelling)
-Immune cells migrate and activate
-Inflammatory soup is released eg. prostaglandins, H+ etc
-Polymodal nociceptor is sensitised so it has a lower threshold - 21What is the point of polymodal nociceptors?-Promotes protective behaviours
-Promotes healing - 22Difference between primary and secondary hyperalgesia?Primary: increased pain sensitivity that occurs directly in the damaged tissue
Secondary: increased pain sensitivity distant from the site of injury - 23How is acute pain signalled?-Only needs glutamate neurotransmitter and AMPA receptors
-Duration and intensity is matched in the ascending signalling - 24How does secondary hyperalgesia signalled?-High frequency input stimulates Substance P and glutamate release
-Combined effect of substance P/NK-1 receptor and glutamate/AMPA receptor produces sufficient depolarisation
-Mg2+ is released, removing the voltage-dependent block
-Glutamate is also able to bind to NMDA receptor resulting in Ca2+ entry and intracellular signalling - 25Why is paracetamol not classified as an NSAID?-Not a good anti-inflammatory
-Does not share platelet or gastric side effects that other NSAIDs have - 26What are the 3 main therapeutic effects of NSAIDs?-Analgesic
-Antipyretic (reduces/prevents fever)
-Anti-inflammatory - 27Why do these effects occur?Decreases prostaglandin levels so:
-less vasodilation and oedema
-less sensitivity of nociceptor nerve endings to inflammatory mediators
-decreased hypothalamic set point for temperature control - 28What are the side effects associated with NSAIDs?GI mucosa: peptic ulcers, GI bleeding, lost mucosal protection
Kidney: Na/water retention, hypertension, vasodilation (collapse of glomeruli)
CVD: stroke, MI - 29Side effects associated with morphine use?-Nausea
-Respiratory depression
-Constipation
-Bronchoconstriction
-Sedative