9 - pain/sensory Flashcards
(121 cards)
1
Q
what is neuropathic pain
A
pain caused by damage to somatosensory nervous system
nerve injury
2
Q
types of neuropathic pain
A
allodynia
dysesthesia
3
Q
dysesthesia
A
abnormal or unpleasant sensation felt when touched, caused by damage to peripheral nerves
4
Q
types of dysesthesia
A
motor
sensory
5
Q
sensory neuropathy
A
tingling numbness shooting pains unable to detect hot or cold pain affect nerves that control feeling
6
Q
motor neuropathy
A
affects motor nerves (nerves that control muscles)
muscle weakness/wasting
muscle twitching/paralysis/cramps
7
Q
how do you treat neuropathic pain
A
antidepressants
anticonvulsants
corticosteroids to relieve pain/pressure
8
Q
spontaneous pain
A
occurs in the absence of a stimulus
9
Q
2 types of spontaneous pain
A
continuous
paroxysmal
10
Q
continuous spontaneous pain
A
steady and on-going (often felt on skin)
ranges from pins and needles sensation to cramping and aching
11
Q
paroxysmal spontaneous pain
A
intermittent pain
no precursor
shooting or stabbing sensation
12
Q
what is phantom pain
A
perception of pain relating to a limb/organ that is not physically part of the body
13
Q
potential mechanisms for phantom pain
A
abnormal growth of injured nerve fibres
neuromas
central sensitisation
14
Q
what are neuromas
A
growth/tumour of nerve tissue
formed from injured nerve endings at stump site and fore abnormal action potentials
15
Q
central sensitisation
A
increased excitability of dorsal horn neurons
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
17
Q
use of antidepressants to treat phantom pain
A
modify neurotransmitters
help you sleep
18
Q
what can anticonvulsants be used to treat
A
epilepsy quiet damaged nerves seizures bipolar disorders neuropathic pain
19
Q
what is a convulsant
A
production of a sudden involuntary muscle contraction
20
Q
how do anticonvulsants work
A
suppress rapid firing of neurons block Na+ channels increase GABA signalling block Glu receptors inhibit Ca2+
21
Q
effect of increase GABAa activity
A
Cl- influx
hyperpolarisation
22
Q
effect of increasing GABAb activity
A
inhibition of VOCCs
opening of GIRK channels
reduce excitability
23
Q
role of sensory neurons
A
afferent neurons that transmit sensory input to CNS
convert external stimuli to electrical impulses
24
Q
what do sensory neurons connect with in the cns
A
interneurons
25
examples of sensory receptors
```
mechanoreceptors
photoreceptors
chemoreceptors
thermoreceptors
nociceptors
```
26
mechanoreceptors
sensory receptor that responds to mechanical pressure
| e.g. touch, auditory vibrations, vestibular
27
photoreceptors
rods and cones in the retina
| sensitive to light
28
chemoreceptors
peripheral chemoreceptors - in blood (aortic and carotid bodies)
central chemoreceptors - detect pH of csf
29
neuromuscular blocks (NMB)
block neuromuscular transmission at the neuromuscular junction
causing paralysis of the affected skeletal muscles
30
when have you achieved a full neuromuscular block
when the muscle is no longer responsive to ACh released by motor neurons
31
depolarising NMB mechanism
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
32
why do depolarising NMBs cause constant depolarisation
NMB is not broken down by AChE
33
non-depolarising NMB mechanism
ACh receptor anatagonist
NMB prevents sufficient binding of ACh to its receptors
prevents normal downstream depolarisation events
34
vision receptos
detect and interpret light stimuli
| wavelenght 400-750nm
35
rods function
for seeing in the dark
function in less intense light
concentrated at outer edges of retina
used for peripheral vision
36
rod structure
long rectangular outer segment made of double membrane discs
| photoreceptive pigment = rhodopsin
37
cone cells
```
interpret colour vision
function best in bright light
```
38
cone structure
shorter triangluar shape outer segment
39
what causes hyperpolarisation of photoreceptor membraen
closure of VOCCs
40
what is released when photoreceptor membrane hyperpolarises
glutamate
41
describe the excitatory response in photoreceptor membrane
Glutamate causes decreased excitatory response at ionotropic receptors
inhibition of horizontal cells and bipolar cells due to hyperpolarisation
42
describe the inhibitory response in photoreceptor membrane
glutamate causes decreased inhibitory response at metabotropic receptors
excitaton of bipolar and horizontal cells due to depolarisation
43
where are hearing receptros found
mechanoreceptors on Organ of corti in cochlea
44
mechanism of hearing
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
45
hair cells
the sensory receptors of the auditory and vestibular systems in the ears
46
where are auditory hair cells found
spiral organ of corti on basilar membrane on cochlea in inner ear
47
role of outer hair cells
mechanically amplify low-level sound that enters the cochlea
48
auditory nerve
relays electrical signals transduced from inner hair cells to auditory brainstem/cortex
49
cochlea
part of inner ear
recieves sound causes stereocilia to move
creates electrochemical potential between sections
important for mechanical sensing an K+ flow
50
organ of corti
made up of hair cells
| lies between tectorial and basilar membranes
51
3 bones of middle ear
malleus
incus
stapes
52
role of bones in middle ear
vibrations introduce pressure waves into the ear
| these waves are amplified by hair cells
53
thermoreceptors
slowly adapting receptors that detect changes in skin temperature
54
transient receptor potential (TRP) channels
when activated, allow depolarisation of the neuron via Ca2+
55
when skin is above 36 degrees
warm receptors activated
| cold receptors quinescient
56
nociceptors
sense noxious and harmful stimuli that require a response
57
types of nociceptors
thermal/mechanical
| polymodal
58
what supplies thermal/mechanical nociceptors
large, fast, myelinated A-delta afferent nerve fibres
59
pain felt by activation of thermal/mechanical nociceptorsq
fast response
| e.g. stabbing pain
60
what supplies polymodal nociceptors
unmyelinated C fibres
61
pain felt by polymodal nociceptos
slow response, dull, aching pain
62
polymodal nociceptors
perform different functions in combination
63
2 phases of pain
phase 1 - medaited by fast, A-delta fibres
| phase 2 - polymodal, slow C fibres
64
nociceptors have free nerve endings
not connected to specific nerve
| connected to area of the body
65
effect of inflammatory mediators on nociceptive signal
increase the nociceptive signal
e.g. protons/ATP/histamine
released from tissue damage
66
what is pKa
measure of acid strength
| the dissociation/ionisation constant
67
when does drug ionisation occur
when drugs are dissolved in aqueous solution to weak acidic or basic solutions
68
lower pKa means
more acidic
| H+ lost more easily
69
lower Ka means
less acidic
70
Ka equation
[H+][A-] / [HA]
71
can ions pass passivley through membranes
no
72
what is peripheral sensitisation
increased sensitivity to afferent nerve stimuli
hypersensitivity
can be allodynia or primary hyperalgesia
73
mechanisam of peripheral sensitisation
reduction in threshold
increase in responsiveness of peripheral ends of nociceptors
expression on a-adrenoreceptors
inflammatory chemicals released
74
secondary hyperalgesia
changes to pain thresholds in the undamaged tissue surrounding the injury, which can become hypersensitive to touch
central sensitisation
75
allodynia
peripheral sensitisation
pain threshold decreases
pain from stimulus that normally wouldnt cause pain
76
primary hyperalgesia
peripheral sensitisation
changes in the area of injury
responsiveness increases
pain is prolonged and exaggerated
77
central sensitisation
increase in excitability of neurons in the cns
| can cause secondary hyperalgesia
78
cause of chronic pain
central sensitisation
| NS in persistent state of high reactivity
79
mechanism of central sensitisation
burst of nociceptor activity
strength of synaptic activity changed
different cns neurons activated that would normally only respond to noxious stimuli
80
role of spinal cord areas in withdrawal reflex
sensory neuron sends signal/enters via dorsal-horn of spinal cord
motor neuron leaves cns via ventral horn
81
types of pain conduction
A-delta fibres
| C fibres
82
A-delta fibres
large, fast, myelinated
| sharp, stabbing pain
83
C-fibres
small, slow, unmyelinated
| burning, aching pain
84
interneurons in pain perception
1 type of neuron lets information into brain
1 doesnt
different amounts of the 2 interneurons lead to different perceptions of pain
85
causes of decreased pain threshold
sensitisation
| neuronal plasticity
86
causes of increased pain threshold
habituation
87
where do pain fibres enter spinal cord
dorsal root ganglia
88
what do pain fibres cause release of
glutamate release
89
acute pain
sharp, short-lasting
| directly related to soft tissue damage
90
chronic pain
due to sensitisation of soft tissue damage
91
types of Glu receptor
NMDA
AMPA
Kainate
mGluR
92
excitotoxicity
neuronal damage due to prolonged Glu synaptic transmission
93
synthesis of GABA
from glutamate
| enzyme = glutamate decarboxylase
94
glycine
amino acid neurotransmitter
synthesised from serine
NMDA agonist
95
opioids
drugs involved in analgesia - modulate nociceptic signalling
cause Gi/o signalling
inhibitory effect
96
examples of metabotropic receptors
```
muscarinic cholinergic receptors (M1-M5)
adrenergic receptors (a1, a2, b1, B2)
```
97
ideal pain killers
```
liquid at room temp
high receptor-binding affinity
high bioavailability
ample potency
low solubility in blood tissues
```
98
overall action of botox
prevents ACh release at NMJ to decrease muscle contraction
99
botox heavy chain
allows botox protein to bind and enter pre-synaptic neuron via plasma membrane
100
botox light chain
acts as a protease
| cleaves SNARE proteins required for vesicle docking (SNAP-25)
101
botox mechanism more detail
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
medical uses of botox
treat uncontrolled blinking
treat muscle spasms
treat overactive bladder
reduce wrinkles
103
volume of distribution
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
volume of distribution equation
total amount of drug in the body / drug blood plasma concentration
105
higher Vd
= greater amount of tissue distribution
106
characteristics of drugs with high Vds
low ionisation
high lipid-solubility
low plasma-binding capabilities
107
what may increase Vd
```
liver failure
kidney failure (fluid retention)
```
108
why may decrease Vd
dehydration
109
clinical uses of Vd
determining drug dosages for desired blood concentrations
| estimating blood concentrations when treating overdose
110
total drug clearance is
the volume of plasma which contains the the total amount of drug removed from the body per unit time
111
how do you calculate rate of drug elimination
plasma concentration x total clearance
112
when is clearance at a steady state
when rate of input = rate of elimination
113
what causes drug elimination
liver metabolism
| kidney excretion
114
how do you determine drug clearance
measure teh plasma concentration at intervals during constant rate IV infusion until a steady state is reached
115
how do you calculate drug clearance
rate of elimination of drug / conc. drug left in body
116
drug half life
how long it takes to lose half of a drugs activity
117
low clearance =
less drug in urine
| more drug in body
118
neostigmine
drug that inhibits acetylcholinesterase
119
effect of neostigmine on action potentials
AChE blocked
ACh not broken down
threshold level reached
new AP triggered
120
clincial use of neostigmine
treatment of myasthenia gravis
| treatment of urinary retention
121
myasthenia gravis
not enough ACh receptors
causes weakness in skeletal muscles
autoimmnue disease
