Trigger 9 Flashcards
what is the pain pathway
injury - nociceptive, inflammatory mediators
peripheral nerve - afferent neurone, excitatory (glutamate and ATP release)
spinal cord - receptor binding, AMPA (fast), NMPA (slower, release block of prolonged depolarisation)
thalamus
cortex
what are the two types of pain conduction
fast response - A delta fibres
slow response - C fibres
describe the A delta fibres
fast
large myelinated
up to 10m/sec
sharp stabbing pain
describe the C fibres
slow
small unmylinated
1.2m/sec
aching burning pain
How does an agonist of nAChR lead to block?
IV injection of suxamethonium
Depolarisation effect lasts sufficient time to make motor endplate inexcitable
AChE (in situ at motor end plate) does not hydrolyse suxamethonium
Endogenous ACh released in brief spurts & rapidly hydrolysed at the motor endplate by AChE
ACh never causes prolonged depolarisation required for block, unless AChE inhibited
depolarzing muscle relaxant
Structurally two joined ACh
Agonist of nAChR
Metabolised by plasma cholinesterase
- quickly hydrolysed.
Action lasts a few minutes
layers of the eye
Outer fibrous layer (cornea, conjunctiva & sclera)
Middle vascular layer (iris & choroid)
Inner neural layer (retina)
non-depolarzing muscle relaxant
competeive reversible antagonist of nAChR
curare deravitive
prevent Ach binding to receptors
cones
colour vision
high details
activated by
Higher acuity
Higher light threshold
Hundreds off photons
rods
sight in low light
activated by
Low intensity
light (single photon)
steps of photoreception
GPCR and light sensor convalent coupled II cis retinal - light causes it to change to .. all trans retinal metarhodopsin activation of transducin activation of phophodiesterase decreased cyclic GMP closure of Na2+ channels hyperpolarisation of photoreceptor membrane decreased release of glutamate
retina structure
epethilail membrane
photoreceptors
- rods
- cons
what is the effect of decreased release of glutamate
decreased excitatory glutamate response (ionotropoic receptor)
hyperpolarisation of bioplar and horizontal cells
decreased inhibitory glutamate response (metabotrophic receptor)
depolarisation of bioplar and horizontal cells
glutamate iontrophic receptors
NMDA - Ca2+ (blocked by Mg2+)
AMPA - Na
kainate - Na
glutamate metabotrophic receptors
mGlu - Group II/III Presynaptic
Gi/Go
Inhibits VOCCs & opens K+ channels
what is the mian inhibitory neurotransmitter in the brain
glutamate
what are the GABA pathways
both are inhibitory
GABAa - ligand gated chloride channel
hyperpolarisation reduces excitabilty
GABAb - Gi/Go
Inhibits VOCCs & opens K+ channels
= reduces excitability
what is a receptive field
every cell has one
Area of retina that, when stimulated with light, changes cell’s membrane potential
Usually excitatory centre,
inhibitory surround
describe the direct pathway when there is no light
no light photoreceptor depolarised glutamate signals depolarises OFF centre of bipolar cell off centre of ganglion cell more likely to reach threshold action potential more likely
describe the indirect pathway when there is no light
no light
- horizontal cell (from surronding photoreceptors) signal via GABA
hyperpolarises on centre of bipolar cell
- amacrine cell ( from surronding bipolar cell)
on centre ganglion cell less likely to reach threshold
action potentail less likely
describe the direct pathway when there is light
light
photoreceptor hyperpolarised
less glutamate signals hyperpolarises OFF centre of bipolar cell
ON centre ganglion cell less likely to reach threshold
action potentail less likely
describe the indirect pathway when there is light
light
horizontal cells and amacrine cells release less GABA
depolarises ON centre of bipolar cell - release more glutamate
ON centre of ganglion cell more likely to reach threshold
action potential more likely
sound recognition
Vibration of oval window generates fluid wave down scala vestibuli then back through the scala tympani to round window.
Wave conducted to scala media, leading to displacement of basilar membrane.
mechanism of auidtory transduction
sound waves
vibration of organ of corti
bending of cilia on hair cells
change in K+ conductance of hair cell membrane
osciliating receptor potential
intermittent glutamate release
intermittent action potentials in afferent cochlear nerves
how is pitch determined
PITCH is determined by the FREQUENCY of the signal - these are detected at different positions along the cochlea:
higher frequencies closer to the oval window
lower frequencies nearer the helicotrema
how is loudness determined
LOUDNESS is identified by the AMPLITUDE of deflection at a given part of the cochlea
basic response to surgery
peripheral nociceptor stimulation travel vis afferent neurone synapse in dorsal horn +/- modulation lateral STT (contralateral) transmitted to thalamus post-central gyrus
aims of anaesthesia
muscle relaxation immobility hypnosis amnesia analgesia control of stress response
Iv agents benefits
rapid onset and recovery
IV agents disadvanatage
unpredicitable dosing
over dose potential
inhalation agents advantage
reasonably rapid onset and recovery
predicitable dosing
difficult to overdose
factors increasing reticuar activating system
surgery - opiodids, NSAIDs, LAs
stimulatory system - glutamate/NMDA mediated
factors decreasing reticuar activating system
inhibitory system - GABAa/Cl- mediated
opoid receptors
sites - brain, spinal cord, GI tract
G protein linked
- cellular hyper-polarization
- inhibits synaptic transmission of pain
opioid effects
analgesia constipation sadation respiratory depression mood alterations
examples of opioids
morphate
codeine
what are muscle relaxants used for
allow intra-cavity surgery
facilitate intubation/ventilation
paralysis only - no anaesthesia
major compliaction of anaesthesia
failed intubation or ventialtion
pulmonary aspiration of gastric contents
intra-operative awareness
drug error/mishap
what is pain
an unpleasant sensory and emotinal experience assocaited with actual or potentail tissue damage or described in terms of such damage
factors affecting pain
expectation injury infection inflammation stress anxitey gender age culture
positive affect of pain
danger alert - withdrawal protection - rest injury prevention - learning
negative affect of pain
suffering impaired function - motor - respiratory - CVS
nociceptors
bare nerve endings
respond to mechanical, thermal or chemical injury
sensitivity altered by inflammatory mediators - bradykinin, histamin, prostaglandins
visceral pain
iniated by distesion, inflammation and ischaemia
pathways generally via automatic NS
poorly localized
may be perceived in the relevant dermatome - refferred pain
neuroptahic pain
results from nerve damage - trauma - infection often becomes chronic difficult to treat
sites of local anaesthetic
spinal epidural
peripheral nerve
site of injury
how do local anaesthetcis work
administered extracellulary in ionzed form
LA becomes unionized to corss membrane (H+ dissociates)
LA works intracellularly in ionzed form to prevent Na+ channels from opening
what are prostagplandins
part of the eicosaniod system
- local ell signalling
- derivatives of eicosanoic acid
short lived
- systhesized and released almost instantly
involved in peripheral pain sensitization
