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DDT > 9 - pain/sensory > Flashcards

9 - pain/sensory Flashcards

1
Q

what is neuropathic pain

A

pain caused by damage to somatosensory nervous system

nerve injury

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2
Q

types of neuropathic pain

A

allodynia

dysesthesia

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3
Q

dysesthesia

A

abnormal or unpleasant sensation felt when touched, caused by damage to peripheral nerves

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4
Q

types of dysesthesia

A

motor

sensory

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5
Q

sensory neuropathy

A 
tingling 
numbness
shooting pains 
unable to detect hot or cold pain 
affect nerves that control feeling
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6
Q

motor neuropathy

A

affects motor nerves (nerves that control muscles)
muscle weakness/wasting
muscle twitching/paralysis/cramps

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7
Q

how do you treat neuropathic pain

A

antidepressants
anticonvulsants
corticosteroids to relieve pain/pressure

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8
Q

spontaneous pain

A

occurs in the absence of a stimulus

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9
Q

2 types of spontaneous pain

A

continuous

paroxysmal

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10
Q

continuous spontaneous pain

A

steady and on-going (often felt on skin)

ranges from pins and needles sensation to cramping and aching

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11
Q

paroxysmal spontaneous pain

A

intermittent pain
no precursor
shooting or stabbing sensation

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12
Q

what is phantom pain

A

perception of pain relating to a limb/organ that is not physically part of the body

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13
Q

potential mechanisms for phantom pain

A

abnormal growth of injured nerve fibres
neuromas
central sensitisation

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14
Q

what are neuromas

A

growth/tumour of nerve tissue

formed from injured nerve endings at stump site and fore abnormal action potentials

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15
Q

central sensitisation

A

increased excitability of dorsal horn neurons

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16
Q

treatment of phantom pain

A

antidepressants
anticonvulsants
narcotics - opioid
NMDA R antagonists - block Glu

spinal cord stimulation
hypnosis
acupuncture
mirror box visual feedback

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17
Q

use of antidepressants to treat phantom pain

A

modify neurotransmitters

help you sleep

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18
Q

what can anticonvulsants be used to treat

A 
epilepsy 
quiet damaged nerves
seizures
bipolar disorders
neuropathic pain
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19
Q

what is a convulsant

A

production of a sudden involuntary muscle contraction

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20
Q

how do anticonvulsants work

A 
suppress rapid firing of neurons 
block Na+ channels
increase GABA signalling
block Glu receptors
inhibit Ca2+
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21
Q

effect of increase GABAa activity

A

Cl- influx

hyperpolarisation

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22
Q

effect of increasing GABAb activity

A

inhibition of VOCCs
opening of GIRK channels
reduce excitability

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23
Q

role of sensory neurons

A

afferent neurons that transmit sensory input to CNS

convert external stimuli to electrical impulses

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24
Q

what do sensory neurons connect with in the cns

A

interneurons

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25
Q

examples of sensory receptors

A 
mechanoreceptors
photoreceptors
chemoreceptors
thermoreceptors
nociceptors
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26
Q

mechanoreceptors

A

sensory receptor that responds to mechanical pressure

e.g. touch, auditory vibrations, vestibular

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27
Q

photoreceptors

A

rods and cones in the retina

sensitive to light

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28
Q

chemoreceptors

A

peripheral chemoreceptors - in blood (aortic and carotid bodies)
central chemoreceptors - detect pH of csf

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29
Q

neuromuscular blocks (NMB)

A

block neuromuscular transmission at the neuromuscular junction
causing paralysis of the affected skeletal muscles

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30
Q

when have you achieved a full neuromuscular block

A

when the muscle is no longer responsive to ACh released by motor neurons

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31
Q

depolarising NMB mechanism

A

ACh receptor agonist
NMB binds to ACh receptors, outcompetes ACh
cation influx causes membrane depolarisation
NMB not degraded by AChE
ACh receptor desensitised
prevention of further action potentials

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32
Q

why do depolarising NMBs cause constant depolarisation

A

NMB is not broken down by AChE

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33
Q

non-depolarising NMB mechanism

A

ACh receptor anatagonist
NMB prevents sufficient binding of ACh to its receptors
prevents normal downstream depolarisation events

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34
Q

vision receptos

A

detect and interpret light stimuli

wavelenght 400-750nm

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35
Q

rods function

A

for seeing in the dark
function in less intense light
concentrated at outer edges of retina
used for peripheral vision

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36
Q

rod structure

A

long rectangular outer segment made of double membrane discs

photoreceptive pigment = rhodopsin

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37
Q

cone cells

A 
interpret colour vision
function best in bright light
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38
Q

cone structure

A

shorter triangluar shape outer segment

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39
Q

what causes hyperpolarisation of photoreceptor membraen

A

closure of VOCCs

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40
Q

what is released when photoreceptor membrane hyperpolarises

A

glutamate

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41
Q

describe the excitatory response in photoreceptor membrane

A

Glutamate causes decreased excitatory response at ionotropic receptors
inhibition of horizontal cells and bipolar cells due to hyperpolarisation

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42
Q

describe the inhibitory response in photoreceptor membrane

A

glutamate causes decreased inhibitory response at metabotropic receptors
excitaton of bipolar and horizontal cells due to depolarisation

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43
Q

where are hearing receptros found

A

mechanoreceptors on Organ of corti in cochlea

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44
Q

mechanism of hearing

A

outer hair cells contract in sync with sound and amplify signal
inner hair cells transduce mechanical signal vibration into an electrical signal
open mechanically gated K+ channels

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45
Q

hair cells

A

the sensory receptors of the auditory and vestibular systems in the ears

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46
Q

where are auditory hair cells found

A

spiral organ of corti on basilar membrane on cochlea in inner ear

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47
Q

role of outer hair cells

A

mechanically amplify low-level sound that enters the cochlea

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48
Q

auditory nerve

A

relays electrical signals transduced from inner hair cells to auditory brainstem/cortex

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49
Q

cochlea

A

part of inner ear
recieves sound causes stereocilia to move
creates electrochemical potential between sections
important for mechanical sensing an K+ flow

50
Q

organ of corti

A

made up of hair cells

lies between tectorial and basilar membranes

51
Q

3 bones of middle ear

A

malleus
incus
stapes

52
Q

role of bones in middle ear

A

vibrations introduce pressure waves into the ear

these waves are amplified by hair cells

53
Q

thermoreceptors

A

slowly adapting receptors that detect changes in skin temperature

54
Q

transient receptor potential (TRP) channels

A

when activated, allow depolarisation of the neuron via Ca2+

55
Q

when skin is above 36 degrees

A

warm receptors activated

cold receptors quinescient

56
Q

nociceptors

A

sense noxious and harmful stimuli that require a response

57
Q

types of nociceptors

A

thermal/mechanical

polymodal

58
Q

what supplies thermal/mechanical nociceptors

A

large, fast, myelinated A-delta afferent nerve fibres

59
Q

pain felt by activation of thermal/mechanical nociceptorsq

A

fast response

e.g. stabbing pain

60
Q

what supplies polymodal nociceptors

A

unmyelinated C fibres

61
Q

pain felt by polymodal nociceptos

A

slow response, dull, aching pain

62
Q

polymodal nociceptors

A

perform different functions in combination

63
Q

2 phases of pain

A

phase 1 - medaited by fast, A-delta fibres

phase 2 - polymodal, slow C fibres

64
Q

nociceptors have free nerve endings

A

not connected to specific nerve

connected to area of the body

65
Q

effect of inflammatory mediators on nociceptive signal

A

increase the nociceptive signal
e.g. protons/ATP/histamine
released from tissue damage

66
Q

what is pKa

A

measure of acid strength

the dissociation/ionisation constant

67
Q

when does drug ionisation occur

A

when drugs are dissolved in aqueous solution to weak acidic or basic solutions

68
Q

lower pKa means

A

more acidic

H+ lost more easily

69
Q

lower Ka means

A

less acidic

70
Q

Ka equation

A

[H+][A-] / [HA]

71
Q

can ions pass passivley through membranes

A

no

72
Q

what is peripheral sensitisation

A

increased sensitivity to afferent nerve stimuli
hypersensitivity
can be allodynia or primary hyperalgesia

73
Q

mechanisam of peripheral sensitisation

A

reduction in threshold
increase in responsiveness of peripheral ends of nociceptors
expression on a-adrenoreceptors
inflammatory chemicals released

74
Q

secondary hyperalgesia

A

changes to pain thresholds in the undamaged tissue surrounding the injury, which can become hypersensitive to touch

central sensitisation

75
Q

allodynia

A

peripheral sensitisation
pain threshold decreases
pain from stimulus that normally wouldnt cause pain

76
Q

primary hyperalgesia

A

peripheral sensitisation
changes in the area of injury
responsiveness increases
pain is prolonged and exaggerated

77
Q

central sensitisation

A

increase in excitability of neurons in the cns

can cause secondary hyperalgesia

78
Q

cause of chronic pain

A

central sensitisation

NS in persistent state of high reactivity

79
Q

mechanism of central sensitisation

A

burst of nociceptor activity
strength of synaptic activity changed
different cns neurons activated that would normally only respond to noxious stimuli

80
Q

role of spinal cord areas in withdrawal reflex

A

sensory neuron sends signal/enters via dorsal-horn of spinal cord

motor neuron leaves cns via ventral horn

81
Q

types of pain conduction

A

A-delta fibres

C fibres

82
Q

A-delta fibres

A

large, fast, myelinated

sharp, stabbing pain

83
Q

C-fibres

A

small, slow, unmyelinated

burning, aching pain

84
Q

interneurons in pain perception

A

1 type of neuron lets information into brain
1 doesnt

different amounts of the 2 interneurons lead to different perceptions of pain

85
Q

causes of decreased pain threshold

A

sensitisation

neuronal plasticity

86
Q

causes of increased pain threshold

A

habituation

87
Q

where do pain fibres enter spinal cord

A

dorsal root ganglia

88
Q

what do pain fibres cause release of

A

glutamate release

89
Q

acute pain

A

sharp, short-lasting

directly related to soft tissue damage

90
Q

chronic pain

A

due to sensitisation of soft tissue damage

91
Q

types of Glu receptor

A

NMDA
AMPA
Kainate
mGluR

92
Q

excitotoxicity

A

neuronal damage due to prolonged Glu synaptic transmission

93
Q

synthesis of GABA

A

from glutamate

enzyme = glutamate decarboxylase

94
Q

glycine

A

amino acid neurotransmitter
synthesised from serine
NMDA agonist

95
Q

opioids

A

drugs involved in analgesia - modulate nociceptic signalling
cause Gi/o signalling
inhibitory effect

96
Q

examples of metabotropic receptors

A 
muscarinic cholinergic receptors (M1-M5)
adrenergic receptors (a1, a2, b1, B2)
97
Q

ideal pain killers

A 
liquid at room temp
high receptor-binding affinity 
high bioavailability
ample potency
low solubility in blood tissues
98
Q

overall action of botox

A

prevents ACh release at NMJ to decrease muscle contraction

99
Q

botox heavy chain

A

allows botox protein to bind and enter pre-synaptic neuron via plasma membrane

100
Q

botox light chain

A

acts as a protease

cleaves SNARE proteins required for vesicle docking (SNAP-25)

101
Q

botox mechanism more detail

A

heavy chain allows botox to enter pre-synaptic
light chain cleaves SNAP-25
NT-filled vesicle cannot dock to membrane
no ACh released
no muscle contraction

102
Q

medical uses of botox

A

treat uncontrolled blinking
treat muscle spasms
treat overactive bladder
reduce wrinkles

103
Q

volume of distribution

A

volume of liquid required (containing total drug) to match concentration of drug in blood plasma

the degree to which a drug is distributed in body tissue rather than the plasma

104
Q

volume of distribution equation

A

total amount of drug in the body / drug blood plasma concentration

105
Q

higher Vd

A

= greater amount of tissue distribution

106
Q

characteristics of drugs with high Vds

A

low ionisation
high lipid-solubility
low plasma-binding capabilities

107
Q

what may increase Vd

A 
liver failure
kidney failure (fluid retention)
108
Q

why may decrease Vd

A

dehydration

109
Q

clinical uses of Vd

A

determining drug dosages for desired blood concentrations

estimating blood concentrations when treating overdose

110
Q

total drug clearance is

A

the volume of plasma which contains the the total amount of drug removed from the body per unit time

111
Q

how do you calculate rate of drug elimination

A

plasma concentration x total clearance

112
Q

when is clearance at a steady state

A

when rate of input = rate of elimination

113
Q

what causes drug elimination

A

liver metabolism

kidney excretion

114
Q

how do you determine drug clearance

A

measure teh plasma concentration at intervals during constant rate IV infusion until a steady state is reached

115
Q

how do you calculate drug clearance

A

rate of elimination of drug / conc. drug left in body

116
Q

drug half life

A

how long it takes to lose half of a drugs activity

117
Q

low clearance =

A

less drug in urine

more drug in body

118
Q

neostigmine

A

drug that inhibits acetylcholinesterase

119
Q

effect of neostigmine on action potentials

A

AChE blocked
ACh not broken down
threshold level reached
new AP triggered

120
Q

clincial use of neostigmine

A

treatment of myasthenia gravis

treatment of urinary retention

121
Q

myasthenia gravis

A

not enough ACh receptors
causes weakness in skeletal muscles
autoimmnue disease

DDT (12 decks)

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