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DDT > Trigger 9 > Flashcards

Trigger 9 Flashcards

1
Q

what is the pain pathway

A

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

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2
Q

what are the two types of pain conduction

A

fast response - A delta fibres

slow response - C fibres

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3
Q

describe the A delta fibres

A

fast
large myelinated
up to 10m/sec
sharp stabbing pain

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4
Q

describe the C fibres

A

slow
small unmylinated
1.2m/sec
aching burning pain

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5
Q

How does an agonist of nAChR lead to block?

A

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

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6
Q

depolarzing muscle relaxant

A

Structurally two joined ACh
Agonist of nAChR

Metabolised by plasma cholinesterase
- quickly hydrolysed.
Action lasts a few minutes

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7
Q

layers of the eye

A

Outer fibrous layer (cornea, conjunctiva & sclera)
Middle vascular layer (iris & choroid)
Inner neural layer (retina)

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8
Q

non-depolarzing muscle relaxant

A

competeive reversible antagonist of nAChR

curare deravitive
prevent Ach binding to receptors

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9
Q

cones

A

colour vision
high details

activated by
Higher acuity
Higher light threshold
Hundreds off photons

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10
Q

rods

A

sight in low light

activated by
Low intensity
light (single photon)

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11
Q

steps of photoreception

A 
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
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12
Q

retina structure

A

epethilail membrane
photoreceptors
- rods
- cons

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13
Q

what is the effect of decreased release of glutamate

A

decreased excitatory glutamate response (ionotropoic receptor)
hyperpolarisation of bioplar and horizontal cells

decreased inhibitory glutamate response (metabotrophic receptor)
depolarisation of bioplar and horizontal cells

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14
Q

glutamate iontrophic receptors

A

NMDA - Ca2+ (blocked by Mg2+)
AMPA - Na
kainate - Na

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15
Q

glutamate metabotrophic receptors

A

mGlu - Group II/III Presynaptic
Gi/Go
Inhibits VOCCs & opens K+ channels

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16
Q

what is the mian inhibitory neurotransmitter in the brain

A

glutamate

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17
Q

what are the GABA pathways

A

both are inhibitory
GABAa - ligand gated chloride channel
hyperpolarisation reduces excitabilty

GABAb - Gi/Go
Inhibits VOCCs & opens K+ channels
= reduces excitability

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18
Q

what is a receptive field

A

every cell has one
Area of retina that, when stimulated with light, changes cell’s membrane potential

Usually excitatory centre,
inhibitory surround

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19
Q

describe the direct pathway when there is no light

A 
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
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20
Q

describe the indirect pathway when there is no light

A

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

21
Q

describe the direct pathway when there is light

A

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

22
Q

describe the indirect pathway when there is light

A

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

23
Q

sound recognition

A

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.

24
Q

mechanism of auidtory transduction

A

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

25
Q

how is pitch determined

A

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

26
Q

how is loudness determined

A

LOUDNESS is identified by the AMPLITUDE of deflection at a given part of the cochlea

27
Q

basic response to surgery

A 
peripheral nociceptor stimulation 
travel vis afferent neurone 
synapse in dorsal horn +/- modulation
lateral STT (contralateral)
transmitted to thalamus 
post-central gyrus
28
Q

aims of anaesthesia

A 
muscle relaxation 
immobility
hypnosis 
amnesia 
analgesia
control of stress response
29
Q

Iv agents benefits

A

rapid onset and recovery

30
Q

IV agents disadvanatage

A

unpredicitable dosing

over dose potential

31
Q

inhalation agents advantage

A

reasonably rapid onset and recovery
predicitable dosing
difficult to overdose

32
Q

factors increasing reticuar activating system

A

surgery - opiodids, NSAIDs, LAs

stimulatory system - glutamate/NMDA mediated

33
Q

factors decreasing reticuar activating system

A

inhibitory system - GABAa/Cl- mediated

34
Q

opoid receptors

A

sites - brain, spinal cord, GI tract
G protein linked
- cellular hyper-polarization
- inhibits synaptic transmission of pain

35
Q

opioid effects

A 
analgesia
constipation 
sadation 
respiratory depression 
mood alterations
36
Q

examples of opioids

A

morphate

codeine

37
Q

what are muscle relaxants used for

A

allow intra-cavity surgery
facilitate intubation/ventilation
paralysis only - no anaesthesia

38
Q

major compliaction of anaesthesia

A

failed intubation or ventialtion
pulmonary aspiration of gastric contents
intra-operative awareness
drug error/mishap

39
Q

what is pain

A

an unpleasant sensory and emotinal experience assocaited with actual or potentail tissue damage or described in terms of such damage

40
Q

factors affecting pain

A 
expectation 
injury 
infection 
inflammation 
stress 
anxitey 
gender 
age 
culture
41
Q

positive affect of pain

A 
danger alert 
- withdrawal 
protection 
- rest injury 
prevention 
- learning
42
Q

negative affect of pain

A 
suffering 
impaired function 
- motor 
- respiratory 
- CVS
43
Q

nociceptors

A

bare nerve endings
respond to mechanical, thermal or chemical injury
sensitivity altered by inflammatory mediators - bradykinin, histamin, prostaglandins

44
Q

visceral pain

A

iniated by distesion, inflammation and ischaemia
pathways generally via automatic NS
poorly localized
may be perceived in the relevant dermatome - refferred pain

45
Q

neuroptahic pain

A 
results from nerve damage 
- trauma
- infection 
often becomes chronic 
difficult to treat
46
Q

sites of local anaesthetic

A

spinal epidural
peripheral nerve
site of injury

47
Q

how do local anaesthetcis work

A

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

48
Q

what are prostagplandins

A

part of the eicosaniod system
- local ell signalling
- derivatives of eicosanoic acid
short lived
- systhesized and released almost instantly
involved in peripheral pain sensitization

DDT (10 decks)

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