neuro 8.3 pain Flashcards
(109 cards)
1
Q
what are pain receptors called and what do they detect
A
-nocioceptors
-they detect “noxions”
-indicate actual or potential tissue damage
2
Q
what type of nerve endings are nocioceptors
A
-free nerve endings
-A delta or C fibers
3
Q
mechanical nociceptor fibre
A
-A delta fiber
4
Q
thermal nociceptor fibre
A
-A delta fiber
5
Q
what temperatures activate thermal nociceptors
A
-noxious heat: above 45 celcius
-noxious cold: below 5-10 celcius
6
Q
multimodal receptor fibre and what do they respond too
A
- C fiber
- respond to many different stimuli : mechanical, temperature, strong acids
7
Q
what are visceral pain receptors for
A
sensing pain in organs
8
Q
why is pain felt in 2 stages
A
-fast pain: A delta fibers
-slow pain: C fibres
9
Q
first pain characteristics (2)
A
-sharp, well localised
-carried by thin myelinated A delta fibers –> fast
10
Q
second pain characteristics (2)
A
-diffuse , dull, aching/burning
-carried by unmyelinated C fibers –> slow
11
Q
A
12
Q
A
12
Q
A
12
Q
A
13
Q
A
14
Q
A
15
Q
A
16
Q
A
17
Q
A
18
Q
A
19
Q
pain sensation
A
an unpleasant sensory and emotional experience linked to actual or potential tissue damage
20
Q
nociceptive pain
A
pain related to tissue damage caused by noxious stimuli
21
Q
neuropathic pain
A
pain caused by a problem with the free pathway, such as damage to sensory fibers/
22
Q
phantom pain
A
pain felt in a limb that has been amputated - the patient can localize pain in the missing limb
23
deafferentation pain
pain due to degeneration of sensory nerves, leading to abnormal pain signaling
24
central pain
the central pathway of the pain sensory mechanism is affected
25
thalamic pain syndrome
form of central pain caused by damage to the thalamus
26
congenital insensivity to pain
genetic condition where a person cannot feel pain or feels less pain than normal, often linked to shorter life expectancy because pain is a sign of tissue damage
27
acquired pain insensitivity
loss of pain sensation in specific body areas due to damage and disease
28
what is syringomyelia
degeneration of tissue around the central canal of the spinal cord, causing pain insensitivity
29
acute pain
pain caused by noxious stimuli, serving as an alarm for the body
30
chronic or persistent pain
pain that is consistently present over time
31
what are minor analgesics used for and how do they work
used for acute pain, they are inhibitors of prostaglandin synthesis (COX inhibitors)
32
what are major analgesics used for
-chronic pain including morphine and other opioids
33
major system for nociceptive signals
anterolateral system
34
what type of neuron carries pain signals into spinal cord
pseudo unipolar sensory neurons
35
where do central axons of pseudo unipolar neurons enter and what do they synapse with
-dorsal horn of spinal cord
-synapse with 2nd order neurons (projection neurons) and project to thalamus
36
where do A delta fibers synapse
lamina 1,5 of dorsal horn
37
where do C fibers synapse
-with interneurons in lamina 2 called substantial gelatinosa
-signal relayed to lamina 1,5
38
do A beta fibers participate in pain transmission
-no they are mechanoreceptors
-but send collaterals to projection neurons in dorsal horn
39
what are 2 major types of projection neurons in dorsal horn
1-nocicpetive-specific
2-wide-dynamic range (WDR) neurons
40
what do nociceptive-specific neurons respond to
only pain stimuli located in lamina 1
41
what do wide-dynamic range neuron respond too
both pain (A delta) and non-painful (A beta) touch
integrates input from nociceptors and mechanoreceptors
42
where are WDR neurons primarily located
laminate 5 of dorsal horn
43
do A beta fibers ascend only in the dorsal column
they ascend here but also send collaterals to dorsal horn projection neurons
44
what are the 2 divisions of the spinothalamic tract
lateral and ventral (ant) spinothaamic tract
45
what does the lateral spinothalamic tract carry and where does it project
-carries pain sensation
-to the VPL/VPM nuclei of the thalamus
-then to somatosensory cortex
-for sensory experience
46
where does the ventral spinothalamic tract project
-medial (intralaminar) thalamic nuclei
-then somatosensory cortex and association cortices
: cingulate, prefrontal, insula
47
what is the ventral spinothalamic tract responsible for
-emotional component of pain
48
where does the spinoreticular tract project
-reticular formation in medulla and pons
49
what is the function of the spinoreticular tract
-for arousal/alarming reaction caused by pain
50
where does the spinomesencephalic tract project
-to PAG in themesencephalon (midbrain)
51
what does the PAG do
it stimulates descending pathways and regulates pain sensation
52
hyperalgesia
-hieghtened sensitivity to pain
53
primary hyperalgesia and where does it occur
occurs at site of injury and caused by injury itself
54
what do damaged cells release that increases pain sensitivity
-mediators like ions, protons, bradykinin, serotonin, prostaglandins
55
what is the effect of K+ leaking from damaged cells
-causes local hyperkalemia so increase [K+]ec, depolarisation, increased excitability of nociceptors
56
what happens when the area becomes more acidic
-TRP channels on sensory endings become more sensitive leading to increased pain sensitivity
57
what mediators act on GPCRs to increase pain sensitivity
-bradykinin
-serotonin (5-HT)
-prostaglandins (PGs)
58
how do bradykinin, serotonin, and prostaglandins increase excitability
-they activate GPCRs which cause Ca2+ signalling to increase excitability of nociceptors
59
where are prostaglandins derived from
arachidonic acid
60
which enzyme is responsible for prostaglandin synthesis
cyclooxygenase
61
how do drugs e.g aspirin and Tylenol reduce pain
-they inhibit cyclooxygenase, reducing prostaglandin synthesis and lowering pain sensitivity
62
what is secondary hyperalgesia
-heightened sensitivity to pain in areas near the site of injury even without direct damage there
63
what is the axon reflex in secondary hyperalgesia
a mechanism where the stimulus travels backwards along the axon to other terminals, causing mediator release
64
which substances are released during secondary hyperalagesia
-substance p
-CGRP
-bradykinin = vasodilation and capillary permeability increases
-histamine = by mast cells for vasodilation
-serotonin = by platelets
65
what causes central hyperalgesia
-wind up phenomenon, where intense pain stimulation increases neuronal excitability in substantia gelatinosa (dorsal horn)
66
What happens during wind up
-sustained glutamate released= activates NMDA receptors
-leads to long-term potentiation (LTP)
-increases sensitivity of surrounding, non-injured neurons
66
what is allodynia
-when non-noxious stimuli (light pressure) become painful
e.g touch on sunburnt skin
67
what is referred pain
-pain felt in a location different from the actual source
68
why does referred pain happen
-visceral nociceptors send signals to the dorsal horn, which activates projection neurons that normally receive input from body surface, causing diffuse activation
69
gate control theory
a theory that explains how non-nociceptive input can reduce pain transmission by closing the gate in the spinal cord
70
which fibers normally carry nociceptive pain signals
C fibers, synapse on projection neurons in the dorsal horn then go to the spinothalamic tract
71
which fibers are non-nociceptive, and what else do they do
A beta fibers (mechanoreceptors)
-travel in the dorsal column but also give collaterals to the dorsal horn
72
what do A beta fibers activate in the dorsal horn
-they synapse with inhibitory interneurons, which reduce the activity of the projection neurons
73
what is the effect of activating A beta fibers (non-nociceptive pathways)
-
74
what is the practical implication of the gate control theory
-touching or rubbing a painful area can reduce the perception of pain by activating A beta fibers
75
what is DNIC (diffuse noxious inhibitory control)
when noxious stimuli from areas other than the injury site cause analgesia throughout the body
76
what is DNIC mediated by
activation of descending analgesia pathways
77
what activates descending analgesic pathways
stimulation of PAG
78
what neurotransmitters are involved in the descending monoaminergic system
serotonin
norepinephrine
79
where does PAG receive info from
from the cortex and from ascending pain (less effective)
80
where do descending analgesic pathways terminate
in the dorsal horn of the spinal cord - the origin site of pain stimuli
81
what do descending pathways do at the dorsal horn
block the propagation of pain signals toward the cortex
82
what are the key neurons in the endogenous analgesia system
-afferent nociceptive fibers
-projection neurons
83
what neurotransmitters are used between nociceptive fibres and projection neurons
glutamate, with substance P and CGRP as co-transmitters
84
what is the role of inhibitory interneurons in the dorsal horn
-they are the termination site for descending pathways
-they inhibit signal transmission by acting on both pre- and postsynaptic neurons
85
what mediator is released by inhibitory interneurons
enkephalin, an endogenous opiate acting on GCPR opiate receptors
86
what is the primary function of the auditory system
to provide the sense of hearing (conscious experience)
87
what are some uses of hearing in daily life
to identify, localise and communicate
88
what happens if the auditory system is dysfunctional
results in deafness
89
what type of physical stimulus is sensed by the auditory system
rapid vibration, which we perceive as sound
90
what is the audible frequency range in humans
from 20Hz to 20,000Hz
91
how long is the cochlea and how is it shaped
about 35mm long and coiled 2.5 times
92
what is the Scala vestibuli and what does it do
it receives vibrations from the oval window and is separated from the Scala media by reissuers membrane
93
what is the effect of enkephalin at the presynaptic terminal
-activates opioid GPCR (Gi/Go)
-inhibits Ca2+ channels = no Ca2+ influx
result: no neurotransmitter release
94
what is the effect of enkephalin at the postsynaptic terminal
-activates opioid GPCR (Gi/Go)
-opens K+ channels = hyperpolarization
-result = reduced sensitivity of the postsynaptic neuron
95
what are the effects of Gi/Go activation
-decrease cAMP
-increase K+ channels activation
-decrease Ca2+ channel activity
-decrease prostaglandin production
95
what type of GPCRs are opiate receptors
Gi/Go-coupled receptors
96
97
98
99
100
what happens in opioid tolerance
the same dose becomes less effective , requiring a higher dose for the same effect
101
what are the mechanisms of opioid tolerance
-increase metabolism = metabolic tolerance
-receptor desensitisation = phosphorylation & uncoupling
-receptor downregulation = internalisation & degradation
-compensatory mechanisms = counteract morphines effect
102
why do withdrawal symptoms occur after stopping opioids
compensatory mechanisms persist, causing imbalance when morphine is removed
103
what are the types of dependence from opioids
-psychological: cravings
-physiological: BP changes, GI symptoms, etc.
104
what is addiction
-loss of control over intense urges to take the drug despite negative consequences
105
when is addiction diagnosed
when both physical and psychological dependence are present
