Pain Flashcards
(110 cards)
1
Q
Recovering from surgery or with acute medical conditions
A
Acute pain
2
Q
Any abnormal sensation described as unpleasant by the patient
A
Dysesthesia
3
Q
Exaggerated PAIN response from a normally painful stimulus; usually includes aspects of summation with repeated stimulus of constant intensity & aftersensation
A
Hyperalgesia
4
Q
Abnormally painful & exaggerated reaction to a PAINFUL stimulus; related to hyperalgesia
A
Hyperpathia
5
Q
Exaggerated perception of TOUCH stimulus
A
Hyperesthesia (hypesthesia)
6
Q
Abnormal perception of PAIN from a normally NON- PAINFUL mechanical or thermal stimulus; usually has elements of delay in perception
A
Allodynia
7
Q
Decreased sensitivity & raised threshold to painful stimuli Can be Genetic & may require less narcotics
A
Hypoalgesia (hypalgesia)
8
Q
Reduced perception of all sensation, mainly touch
A
Anesthesia
9
Q
Loss of perception of vibration
A
Pallanesthesia
10
Q
Reduced perception of pain stimulus
A
Analgesia
11
Q
Mainly spontaneous abnormal sensation that is not unpleasant/painful; usually described as “pins & needles”
A
Paresthesia
12
Q
Burning pain in the distribution of one or more peripheral nerves I.e. phantom limb pain
A
Causalgia
13
Q
Anesthesia vs. Analgesia
A
Anesthesia is keeping them asleep - patient does not PERCEIVE pain and touch Analgesia is taking way the pain response
14
Q
where does pain start?
A
nociceptors
15
Q
sensation felt as noxious (painful)
A
protopathic
16
Q
sensation felt as non noxious- (high touch, temperature discrimination, light touch)
A
Epicritic
17
Q
Precise location
A
Aδ Fibers
18
Q
fast - 0.1 sec after stimulus
A
Aδ Fibers
19
Q
thinly myelinated
A
Aδ Fibers
20
Q
Felt on surface of body
A
Aδ Fibers
21
Q
Slow- 1 sec after stimulus
A
C fibers
22
Q
felt deeper in tissue and surface tissue
A
C Fibers
23
Q
slow, burning, aching, throbbing
A
C Fibers
24
Q
Chronic pain
A
C fibers
25
sharp, pricking, electric pain
Aδ Fibers
26
Precision in location, know exactly where it is
Aδ Fibers
27
Unmyelinated
C Fibers
28
fast and slow fibers reach threshold to a stimulus
Thermal and mechanical nociceptors
29
Slow pain only
Chemical nociceptors
30
significantly contribute to nociception and neuronal SENSITIZATION durring peripheral inflammation and nerve injury
Chemical nociceptors
31
5 substances Chemical nociceptors release
Acetylcholine, Bradykinin Saubstance P, Prostaglandins and Proteolytic enzymes
32
1. Noxious stimuli causes cell damage and release of sensitizing chemicals (Prostaglandins, Substance P, Bradykinin, Serotonin and histamine) 2. Substances activate nociceptors and lead to the generation of an ACTION POTENTIAL
Transduction
33
Transmission includes the propagation of impulses from the site of injury to the __________ and __________ with projections to the \_\_\_\_\_\_\_\_\_\_\_\_, _____________ and _____________ cortices.
Dorsal horn of the spinal cord Thalamus cingulate, insular and somatosensory
34
Process of altering pain transmission using BOTH inhibitory and excitatory mechanisms
Modulation
35
Three places modulation can take place
Peripherally at the site Dorsal horn of the spinal cord Brain stem
36
when transduction, transmission, and modulation interact with the psychology of the patient
Perception of pain
37
This is thought to be mediated through the thalamus
Perception of pain
38
What is the relay center for nociception
Dorsal horn of spinal cord
39
Name the four types of neurons in the dorsal horn
Primary afferent Intrinsic (Interneuron) Projection Neurons Descending neurons
40
extend caudally from several reions of the brain
terminate in the dorsal horn
have improtant role in modulating nociceptive information
Descending neurons
41
project rostrally into white matter to reach various parts of the brain
Projection neurons- may be synonomous with 2nd order neurons
42
Substania Gelitinosa
Superficial Dorsal Horn
Where C fibers synaps on 2nd order neurons
LOTS of interneurons
Lamina II
43
Two functional groups of interneurons
1. Inhibatory- GABA or Glycine
2. Excitiatory - glutamanergic cells
44
Impotrant in the integration and modulation of incoming nociceptive information
Inerneurons
45
Descending\_\_\_\_\_\_\_\_\_\_ neurons project from the brain througout the dorsal horn.
From the pontene neuron(locus Cerueus) __________ is released onto interneuorns
From the Raphe Nuclei ___________ is released onto interneurons.
The interneurons then release _____________ on the opiate receptors which increase ___________ conductance. They are our bodies natural \_\_\_\_\_\_\_\_.
Monoaminiergic
Norepinepherine
Serotonin
Enkephalins
Potassium
Opioids
46
1st order neurons enter the spinal cord via the dorsal root ganglion and can synapse in three places
1. Interneuons
2. Sympathetic neurons
3. ventral horn (motor) neurons
47
**Modulate** the pain at the level of the dorsal horn by releaseing NE which is an antialgesic/algesic
Cause a **response** to the pain by integration of incoming nociceptive stuimuli
1st order neurons synapsing on **Sympathetic** neurons in the dorsal horn of the spinal cord
48
Where information is coming in and has the ability to transtfer it to SNS neurons to get a response
Can modulate pain from th acsending and descending tracts
in the spinal column in the **gray matter** between 1st and 2nd order neurons
**Interneurons** in the dorsal horn of the Spinal Cord
49
Interneurons synapsing on motor neurons in the **ventral horn** of the spinal cord
Causes muscle spasms
50
2nd order neurons start in the gray matter of the ___________ dorsal horn
ipsilateral
51
Pain will usually synapse in the __________ dorsal horn then cross over to the _________ and travel to the thalamus via the __________ tract.
gray matter of the ipsilateral
WHITE MATTER
Spinothalamic tract
52
Another name for spinothalamic tract
Anterolateral tract
53
what percentage of 2nd order neurons cross the midline and form the spinothalamic tract?
90%
54
Spinal thalamic tract is the major pain pathway to the thalamus, \_\_\_\_\_\_\_\_\_\_\_, \_\_\_\_\_\_\_\_\_\_\_\_\_\_, and \_\_\_\_\_\_\_\_\_\_\_.
It lies _____________ in the white matter of the spinal cord
reticular formation
nucleus raphe magnus
periaquaductal gray
anterolaterally
55
Feels the sensation
1st order neuron
56
responsible for the perception and localization of pain
3rd order neuron
57
located in the thalamus and send fibers to somatosensory areas I and II
Third order neurons
58
location of somatosensory areas one and two
parietal cortex
superior wall of the sylvan fissure
59
there is no perception of pain until...
it arrives at the somatosensory cortex via the third order neurons
60
Pathway that couses insomnia r/t pain infomation being sent to the reticular activating system (RAS)
Spinoreticular tract
61
Responsible for chronic pain patients needing sleep aids
Spinoreticular tract
62
Activates anti-nociceptive decending pathway to the spinal cord that calms the pain at the level of the spinal cord
Spinomesencephalic tract
63
The same as activating our intrinsic opoid system
Spinomesencephalic tract
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65
Evoke emotional behavior by activating the hypothalamus where the stress reponse is located
Causes chronic pain patients to have physiologic psychological changes
Spino**hypo**thalamic Tract
Spino**telen**cephalic Tract
66
Chronic pain causes personality changes, communicates with the amygdala, when chronic pain goes away, personality back to normal
Spino**telen**cephalic Tract
67
What fibers are inhibatory on the STT nuron in the dorsal horn of the spinal cord?
A- Beta
68
What fibers are excitatory on the STT nuron in the dorsal horn of the spinal cord?
A- Delta
69
How are the laminal divided in the dorsal horn of the spinal cord
they are from lamina I- VIII
they start with 1 on the outside and progressively go to 8 on the inside
70
The neospinothalamic tract is most clely associated with
the location and perception of pain
71
the paleospinothalamic tract is most closely associated with
the initiation of unplesant aspects of pain as well as the autonomic response
72
Pathway of fast pain\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
## Footnote
1. **\_\_\_** fibers pass through the DRG to lamina\_\_\_and __________ in the dorsal horn
2. synapse with **\_\_\_\_\_\_\_\_\_\_** or **\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_.**
3. 2nd order neurons **\_\_\_\_\_** to white matter and **\_\_\_\_\_\_\_\_\_\_**
4. some of the 2nd order neurons will terminate on **\_\_\_\_\_\_\_\_\_\_\_\_\_\_**, **MOST** travel to **\_\_\_\_\_\_\_\_\_\_\_\_** of thalamus and synapse with 3rd order neurons
5. 3rd order neurons go to the **\_\_\_\_\_\_\_\_\_\_\_** where pain can be
**\_\_\_\_\_\_\_\_\_\_** and **\_\_\_\_\_\_\_\_\_\_.**
**Neospinothalamic** Tract
## Footnote
1. **Aδ** fibers pass through the DRG to lamina **I and V (lamina marginalis)** in the dorsal horn
2. synapse with **interneurons** or **2nd** order neurons
3. 2nd order neurons **cross** to white matter and **join the STT**
4. some of the 2nd order neurons will terminate on **reticular fomation (sleep centers)**, MOST travel to **ventobasal Complex (VBC)** of thalamus and synapse with 3rd order neurons
5. 3rd order neurons go to the **somatosensory cortex** where pain can be **perceived** and **located**
73
Pathway of slow pain\_\_\_\_\_\_\_\_\_\_\_\_\_
## Footnote
1. **\_\_** fibers pass through the DRG to lamina **\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_** in the dorsal horn
2. **\_\_\_\_\_\_\_\_** has lots of internurons that connect with\_\_\_\_\_\_\_\_\_. most of the 2nd order neurons go up **\_\_\_\_\_\_\_\_** crossing. Very few **\_\_\_\_\_\_\_** and join the STT
3. 2nd order neurons terminate widely in the **\_\_\_\_\_\_\_\_**, 1/10th of their fibers stop in the **\_\_\_\_\_\_\_\_** the rest stop in the **\_\_\_\_\_\_\_\_, \_\_\_\_\_\_\_\_** and tectum of the midbrain **\_\_\_\_\_\_\_\_\_\_\_\_\_\_**.
4. There are **\_\_\_\_\_\_\_\_\_\_\_\_\_\_** but the 2nd can communicate with other parts of the brain,
5. This system is responsible for the unpleasant aspects of pain, the **\_\_\_\_\_, \_\_\_\_\_** pain and the **\_\_\_\_\_\_\_\_\_\_** response to pain.
**Paleospinothalamic tract**
## Footnote
1. **C** fibers pass through the DRG to lamina **II and III (II = substantia gelatinosa)** in the dorsal horn
2. **Lamina II** has lots of internurons that connect with **lamina IV-VII**. most of the 2nd order neurons go up **without** crossing. Very few **cross** and join the STT
3. 2nd order neurons terminate widely in the **brainstem**, 1/10th of their fibers stop in the **thalamus**, the rest stop in the **medulla, pons** and tectum of the midbrain **periaquaductal grey**.
4. There are **NO 3rd order neurons** but the 2nd can communicate with other parts of the brain,
5. This system is responsible for the unpleasant aspects of pain, the **slow, dull** pain and the **autonomic** response to pain
74
lamina V
lamina marginalis
75
lamina II
substantia geitinosa
76
Fibers from the **\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_** tract teminate alot lower, in the reticular area of the **\_\_\_\_\_\_\_\_\_** this is the reason for their autonomic response and processing of **\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_** pain
Fibers from the **\_\_\_\_\_\_\_\_\_\_\_\_\_** tract terminate in the **\_\_\_\_\_\_\_** and thus they are able to **\_\_\_\_\_\_\_\_\_** and **\_\_\_\_\_\_\_\_\_\_** pain.
Fibers from the **Paleospinothalamic** tract teminate alot lower, in the reticular area of the **brainstem** this is the reason for their autonomic response and processing of **slow, dull (chemical and heat)** pain
Fibers from the **Neospinothalamic** tract terminate in the **cortex** and thus they are able to **perceive** and **locate** pain.
77
Fast pain can be localized easily if A-delta fibers are stimulated together with \_\_\_\_\_\_\_\_\_\_\_\_
tactile receptors
78
Slow pain of C-fibers is __________ visceral and slow pain
Poorly localized
79
What are the three areas that mediate the brain analgesia system
1. Periaquaductal grey matter in the midbrain
2. nucleaus raphae magnus in the medulla
3. nocioception inhibitory interneurons within the dorsal horn of the spinal cord
80
Epicenter of analgeisa
prominent role in descending pain modulation
plays a role in defensive behavior-such as protecting an injury
sends fibers from brain to spinal cord
to the sides of the cerebral aquaduct in th midbrain
Periaquaductal Grey
81
pain modulator in the midbrain
periaquaductal gray
82
pain modulator in the medulla
nucleus raphe magnus
83
pain modulator using serotonin
Nucleus Raphe Magnus
84
Afferently stimulated from axons in the spinal cord and cerebellum
It gets the signals crossing the cerebellum and the spinal cord
Sends projections to the dorsal horn of the spinal cord to directly inhibit pain using serotonin
Nucleus Raphe Magnus
85
neurotransmitters directly involved in endogenous pain supression system
enkephalins and seorotonin
86
releases serotonin to stimulate interneuron to release enkephalin tonto theopiate receptors
Nucleus Raphe Magnus
87
releases NE onto interneuron that releases enkephalins onto opiate receptor - these then send messages to the periphery to modulate pain locally
Pontene neuron (locus ceruleus)
88
what is the role of the descending pathway?
Pain modulation - they will let us know if we need to fo to the emergency room if they cannot moculate pain enough via the opoid receptors.
89
three naturally occuring opioids
endorphins
enkephalins
dinorphins
90
Excitatory neurotransmitter released by the pain fiber isn the substantia gelatinosa of the spinal cord
Cause neurogenic inflammation
Released slower- over a few minutes
Involved in slow chornic pain
Substance P
91
acts on mast cells releasing histmaine- produce smooth muscle contraction and mucous secretion
Substance P
92
Excitatory Neurotransmitter that acts instantly
lasts only a few milliseconsds
associated with fast pain
immediate release when hammer hits hand
gutamate
93
Neuropeptide released by sensory neurons that causes neurogenic inflammation
releases slowly
It is a protien involved in pain modulation
Potent Vasodialator
CGRP
94
where does pain modulation occur
peripherally at nociceptors
in the spinal cord
supraspinal
95
pre synaptic receptor on a 2nd order neuron blocekd by a magnesium ion
NMDA receptor
96
Under normal conditions neuron isnt depolarized long enough to allow this receptor to pass Ca++ ions
NMDA receptor
97
persistant pain causes glutamate to build up in the synaptic cleft and the 2nd order neuron is depolarized long enough for this receptor to open
NMDA receptor opens because the magnesium pore blocker is knocked off
98
in acute pain, this is cleared fast enough from the synaptic cleft and 2nd order neuron is not depolarized long enough to knock magnesium from the NMDA receptor
Gultamate
99
this receptor being activated is associated with chronic pain
NMDA receptor
100
substance p activates
NK1 n (neurokinin-1)
101
EAA (excitatory amino acids) like glutamate immediatly activate ____________ receptors causing a transient depolarization of the \_\_\_\_\_\_\_\_\_\_\_\_\_. The \_\_\_\_\_\_\_\_\_\_\_receptor is never activated in ____________ pain becuse the neuron is not depolarized long enough to dislodge the \_\_\_\_\_\_\_\_\_.
AMPA
2nd order neuron
NMDA
Acute pain
Mg++
102
1. In response to intense or prolonged barrages of incoming nocioceptive infomation neurons become **\_\_\_\_\_\_\_\_** and over respond to incoming pain signals.
2. This barrage from **\_\_\_\_\_\_\_\_** depolarizes the 2nd order neuron long enough to allow **\_\_\_\_\_\_** ions to exit the **\_\_\_\_\_\_\_** receptors.
3. This resuts in an i**\_\_\_\_\_\_\_\_** which in turn activates **\_\_\_\_\_\_\_\_\_\_\_\_** which converts **\_\_\_\_\_\_\_\_** to **\_\_\_\_\_\_\_**.
4. Because NO is a gas it rapidly difuses out of the neurons
and acts **\_\_\_\_\_\_\_\_\_\_\_\_\_\_.**
1. **sensitized**
2. **gluamante**, **Mg++,** **NMDA**
3. i**nflux of Ca++ ions,** **nitric oxide synthase eNOS,** **L-Argenine,** **NO**.
4. **pre and postsynaptically.**
103
When AMPA receptor are anctivated and Nitric oxide acts presynaptically what does it do?
Causes an exagerated release of substance P and Excitory Amino Acids (ie Glutamate)
104
When AMPA receptor are anctivated and Nitric oxide acts postsynaptically what does it do?
Causes neurons to become hyperexcitable
Ask
105
increased NO levels also cause _________ to be released intracellularly leading to increased \_\_\_\_\_\_\_\_\_\_\_.
cGMP
excitation/ sensitization
106
How does morphine work
stops excitation by binding to the mu receptors and increasing potassium conductace which will hyperpolarize the cell
107
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Response to Pain
increased **\_\_\_\_\_\_\_\_** hormones
Decreased **\_\_\_\_\_\_\_\_\_** metabolism, insulin, testosterone
hyperglycemia then leads to increased **\_\_\_\_\_\_\_\_** which leads to an increase in **\_\_\_\_\_\_\_\_\_\_**
Neuroendocrine
catobolic
anabolic
ACTH
108
Coronary artery constrictionion is caused at
high catchecholamine levels
109
release of this may incduce coronary vasospasm
serotonin
110
