Pain Flashcards
1
Q
According to WHO, pain is an unpleasant ________ & ________ experience associated with actual or potential ____________
A
sensory
emotional
tissue damage
2
Q
Dysesthesia
A
any abnormal sensation described as unpleasant by patient; may not be pain
3
Q
Hyperalgesia
A
exaggerated pain response from a normally painful stimulus
usually includes aspects of summation w/ repeated stimulus of constant intensity and aftersensation
4
Q
Hyperpathia
A
abnormally painful and exaggerated reaction to a painful stimulus; related to hyperalgesia
5
Q
Hyperesthesia (hypesthesia)
A
exaggerated perception of touch stimulus
6
Q
Allodynia
A
abnormal perception of pain from a normally non-painful mechanical or THERMAL stimulus; usually has elements of delay in perception and of aftersensation
7
Q
Hypoalgesia (hypalgesia)
A
decreased sensitivity and raised threshold to painful stimuli
8
Q
Anesthesia
A
reduced perception of all sensation; mainly touch
9
Q
Pallanesthesia
A
Loss of perception of vibration
10
Q
Analgesia
A
reduced perception of pain stimulus
11
Q
Paresthesia
A
mainly spontaneous abnormal sensation that is not unpleasant; “pins and needles”
12
Q
Causalgia
A
BURNING PAIN in the distribution of one or more peripheral nerves
13
Q
Protopathic sensation
A
noxious
14
Q
Epicritic sensation
A
non noxious; i.e. pressure, light touch; temperature discrimination
15
Q
Fast pain
A
thinly myelinated type AD fibers
- felt ~ 0.1 sec after stimulus
- felt on surface of body: sharp, pricking, electric pain
16
Q
Slow pain
A
unmyelinated type C pain fibers
- felt @ 1 sec after stimulus
- felt in deeper tissue and surface tissue: slow burning, aching, throbbing, chronic
17
Q
What type of painful stimuli goes on both fast and slow pathwathways?
A
mechanical and thermal
18
Q
what kind of painful stimuli goes with slow pain pathways only?
A
chemical
19
Q
What are 5 chemicals that act as painful stimuli?
A
- bradykinin
- ACh
- prostaglandins
- substance P
- proteolytic enzymes ( increase permeability to ions ie K)
20
Q
What are the 4 physiologic processes to nociceptive stimuli?
A
- Transduction
- Transmission
- Modulation
- Perception
21
Q
Transduction
A
Noxious stimuli causes cell damange w/ release of sensitizing chemicals ( ie substance p, bradykinin). These substances activate nociceptors and lead to generation of AP.
noxious stimuli converted to electric activity at the sensory nerve ending
22
Q
Transmission
A
Action potential continues from site of injury to spinal cord; spinal cord; spinal cord to brainstem and thalamus; thalamus to cortex for processing:
propagation of impulses through the sensory nervous system
23
Q
Modulation
A
Neurons originating in the brainstem descend to spinal cord and release substances (endogenous opiods) that inhibit nociceptive impulses:
process of transmission modified by neural influences
24
Q
Perception
A
Conscious experience of pain:
Transduction, transmission, modulation interact w/ the psychology of the patient to create what is perceived as pain
25
primary afferent neurons
first order neurons
send axons into SC via the dorsal (sensory) root
May synapse w/ inter-neurons, sympathetic neurons and ventral horn (motor) neurons
26
Second order neurons
in gray matter of ipsilateral dorsal horn
27
Spinothalamic tract
STT
Spine to thalamus
axons of most 2nd order neurons cross midline and form the spinothalamic tract.
Major pain pathway to the thalamus, RF, nucleus raphe magnus & periaqueductal gray
LIes anterolaterally in white matter of spinal cord
28
3rd order neurons
located in thalamus and send fibers to somatosensory areas I & II in the parietal cortex, and superior wall of the sylvian fissure
Responsible for perception and localization of pain
29
alternate pain pathway that causes insomnia due to pain
spinorecticular tract
30
pathway that activates anti-nociiceptive descending pathways
spinomesencephalic tract
31
these 2 tracts activate the hypothalamus and evoke emotional behavior
spinohypothalamic and spinotelecephalic tracts
32
Neospinothalamic tract
fast pain pathway
33
first order neurons in neospinothalamic tract
travel via AD fibers and terminate on lamina I (lamina marginalis) of dorsal horn of SC
34
2nd order neurons on fast pain pathway
give rise to long fibers which CROSS midline through anterior white commisure and pass upwards in anterolateral columns (STT)
35
A few of the 2nd order neurons in the fast pain pathway terminate on the ________ causing insomnia
reticular formation
36
Where do most of the 2nd order neurons from fast pain pathway travel to
ventrobasal complex (VBC) of thalamus
37
3rd order neurons fast pain pathway
communicate w/ somatosensory cortex
38
Paleospinothalamic pathway
slow pain pathway
39
slow pain pathway: 1st order neurons
go via type C to laminae II and III of dorsal horns (together known as substantia gelatinosa)
40
2nd order neurons: slow pain pathway
take off and terminate in lamina V (also in dorsal horn)
41
3rd order neurons: slow pain pathway
join fibers from fast pathway and cross opp side via anterior white commissure and travel upwards through the anterolateral pathway
42
2nd order neurons in slow pathway can be _________ or ___________ and can travel up to the brain via __________ or ____________
short or long
| can travel up DC (dorsal column) or STT (mostly uses STT)
43
Where do 3rd order neurons for the slow pathway terminate?
mostly in BRAINSTEM
1/10 in thalamus
rest in medulla, pons, tectum of midbrain mesencephalon periqueductal grey
44
Fast pain can be localized easily if ____________ are stimulated together with ____________
AD fibers
| tactile receptors
45
Slow pain is poorly _____________
localized
46
What 3 major components in the brain mediate the analgesia system?
1. periaquaductal grey matter (midbrain)
2. nucleus raphe magnus (medulla)
3. nociception (pain) inhibitory neurons w/in the dorsal horns of SC-- act to inhibit pain-transmitting neurons also located in spinal dorsal horn
47
Epicenter of analgesia in the brain
periaquaductal grey matter
48
This is afferently stimulated from axons in the SC and cerebellum
nucleus raphe magnus
49
This area in the brain plays a role in the descending modulation of pain and in defensive behavior
periquaductal grey mater
50
The main function of the _________ is mostly PAIN MEDIATION; it sends projections directly to the ____________ of the SC
nucleus raphe magnus
| dorsal horn
51
Substance P
released slower; building over a few minutes: slow chronic pain
52
Glutamate
acts instantly, only lasts a few milliseconds: fast pain
53
CGRP
calcitonin gene-related peptide
| chronic pain: migraines
54
Where do modulators occur? Do they suppress or aggravate pain?
peripherally at nociceptors
in spinal cord
or supraspinal structures
can suppress or aggravate pain
55
example of a modulator
NMDA receptor role
56
Neuroendocrine response
```
increase secretion of catabolic hormones
stress response
decrease anabolic metabolism: insulin, testosterone
ACTH release
hyperglycemia
```
57
Cardiac responses to pain
increased HR, BP, SVR, CO
MI, CHF, dysrrhythmias
decrease myocardial oxygenation secondary pulmonary dysfunction: atelectasis
Coronary artery constriction: high catecholamines
increase plasma viscosity: plt induced occlusion
58
Release of serotonin may induce ______________-
coronary vasospasm
59
pulmonary responses to pain
increased total body O2 consumption, CO2 production, minute ventilation
60
What capacities decrease w/ pain?
TV, VC, FRC
61
what is the most detrimental alteration in post surgical lung volume
FRC: as it decreases, resting lung volume approaches closing volume
as this continues atelectasis results, VQ mismatch and hypoxemia ensue
62
Pulmonary function __________ w/ abdominal thoracic incision (splinting)
decreases
63
What happens to the vascular system from stress
platelet adhesion and hyper-coagulability: DVT, pulmonary edema
64
Where is visceral pain referred to?
somatic sites
65
What are some other responses to pain your body has?
increased sphincter tone, decreased gastric mobility: ileus; n/v
stress ulcers
urinary retention
66
Periosteal and somatic irritation initiate reflex motor response leading to ___________
muscle spasm
67
Chronic pain is pain that persists ______________.
one month longer than expected
68
T/F: Chronic pain is protective
False
69
What are the main types of chronic pain?
low back pain, h/a, recurrent facial pain, cancer pain, arthritis
70
Chronic pain caused by peripheral mechanisms respond to what?
NSAIDs; often from chronic inflammation in periphery
71
What is the reflex role in chronic pain?
excessive muscle tension and tendon stretch
| SNS hyperactivity can create local ischemia and persistent disruption of the microcirculation
72
Peripheral-Central Mechanism
lesions of peripheral nerves, dorsal roots, or dorsal ganglion cells
Found in: causalgias, other reflex sympathetic dystrophy, phantom pain
73
Circle Mechanism
intense stimulation of nerve fibers in spinal cord activated internuncial neurons creating an abnormal reverberatory activity in a closed loop
Difficult to treat: don't know what is stimulating the nerve
74
Chronic nerve compression
i.e. spinal stenosis; these patients often come in for surgery
75
Central Pain Mechanism
found in lesions to the thalamus and SC injury such as paraplegia
see often in TBIs
76
Psychophysiologic Mechanism
severe stress: usually seen in chronic tension h/a & chronic pain from muscle spasms in shoulder, back, chest
77
Learned Mechanisms
secondary gain
These patients frequently develop reactive depression and hypochondriasis
-psychogenic component; difficult to treat
78
When a person has chronic pain, how do they handle minor injuries? Why?
handle them poorly: serotonin and endorphins are depleted
79
How does chronic pain affect a person's personality?
show signs of neuroticism (from loss of control over pain)
However, these s/s often go away if pain is relieved
Longer duration of pain= greater psychological changes
80
What happens to pain fibers in chronic pain? What does this lead to?
tonic activity of C fibers: leads to enhanced postsynaptic effects by NMDA-receptor sensitization
81
What electrolyte would you consider giving a patient w/ chronic pain before surgery? Why?
Magnesium: blocks NMDA receptors so they aren't active
82
Treatment of chronic pain
steroid epidural injections with or without trigger point injections, peripheral nerve blocks w/ neurolytics, acupunture
high levels of analgesics
rehabilitation: physically, psychosocially, psychologically
83
What are 3 common causes of cancer pain?
1. tumor invasion of bone: most common
2. tumor compression of peripheral nerves: 2nd most common
3. treatment: radiaion, chemo
84
The physical effects are better/worse for cancer pain patients than for other chronic pain patients?
worse
| loss of sleep, appetite, n/v
85
Psychological effects of cancer pain
heightened anxiety, separation and loss, self esteem, life's goals, effect on family, disfigurement
86
Cancer patients w/ more emo disturbances & pain ________________ than those whose pain was controlled
died sooner
87
How does the WHO recommend approaching cancer pain?
1. Nonopiod analgesic (mild pain): inhibit prostaglandin syntetase and & antitumor effects in bone mets
- -ASA, tylenol, NSAIDs
2. "weak" oral opiods (moderate pain)
- -codein, oxycodone
3. "stronger" opiods (severe pain)
- MSO4; hydromorphone
88
What are some adjuncts to treating chronic/cancer pain?
corticosteroids: prevents release of steroids; stimulates appetite
antidepressants: elevate mood; help w/ sleep; block reuptake of serontonin, potentiate narcotic analgesics
89
Tolerance of opiods is __________ in cancer patients. THey can require ___________ of morphine IV
normal
| 200mg/hr
90
T/F: addiction to pain meds in ca pain patients is rare.
True
91
What is the goal of chronic pain managment?
sustained pain relief w/ minimal side effects
92
What are other treatment modalities of chronic pain?
regional: but short term relief only
Neurolytics: permanent destruction of nerve; often get some motor loss too but pts often willing to handle this
93
What is a problem w/ using NSAIDS?
celiling effect on analgesia
94
What parts of the brain are affected in acute stress?
RAS or thalamus
Arcuate nucleus; Locus coeruleus
PVN
Amygdala
95
What happens when the amygdala, arcuate nucleus, and locus coerculeus are activated in acute stress?
Amygdala: behavioral changes
| Arucate nucleus & Locus coeruleus: NPY, NE excretion
96
What happens when the PVN is stimulated in acute stress?
increased CRH-->ACTH (pituitary)-->CORT; NPY/NE (adrenal glands)
97
What happens at target tissues w/ acute stress?
increased BP/HR
| decreased appetite, reproduction; immunity, growth & thyroid function
98
What is the feedback mechanism w/ acute stress?
CORT inhibits ACTH which inhibits CRH
99
How are target tissues affected w/ chronic stress?
?? BP/HR
?? appetite
decreased reproduction, immunity & growth/thyroid fx
100
What is the feedback in chronic stress?
Maladaptive: no negative feedback like in acute
| Instead more of the hormones are made
