Pain Flashcards
According to WHO, pain is an unpleasant ________ & ________ experience associated with actual or potential ____________
sensory
emotional
tissue damage
Dysesthesia
any abnormal sensation described as unpleasant by patient; may not be pain
Hyperalgesia
exaggerated pain response from a normally painful stimulus
usually includes aspects of summation w/ repeated stimulus of constant intensity and aftersensation
Hyperpathia
abnormally painful and exaggerated reaction to a painful stimulus; related to hyperalgesia
Hyperesthesia (hypesthesia)
exaggerated perception of touch stimulus
Allodynia
abnormal perception of pain from a normally non-painful mechanical or THERMAL stimulus; usually has elements of delay in perception and of aftersensation
Hypoalgesia (hypalgesia)
decreased sensitivity and raised threshold to painful stimuli
Anesthesia
reduced perception of all sensation; mainly touch
Pallanesthesia
Loss of perception of vibration
Analgesia
reduced perception of pain stimulus
Paresthesia
mainly spontaneous abnormal sensation that is not unpleasant; “pins and needles”
Causalgia
BURNING PAIN in the distribution of one or more peripheral nerves
Protopathic sensation
noxious
Epicritic sensation
non noxious; i.e. pressure, light touch; temperature discrimination
Fast pain
thinly myelinated type AD fibers
- felt ~ 0.1 sec after stimulus
- felt on surface of body: sharp, pricking, electric pain
Slow pain
unmyelinated type C pain fibers
- felt @ 1 sec after stimulus
- felt in deeper tissue and surface tissue: slow burning, aching, throbbing, chronic
What type of painful stimuli goes on both fast and slow pathwathways?
mechanical and thermal
what kind of painful stimuli goes with slow pain pathways only?
chemical
What are 5 chemicals that act as painful stimuli?
- bradykinin
- ACh
- prostaglandins
- substance P
- proteolytic enzymes ( increase permeability to ions ie K)
What are the 4 physiologic processes to nociceptive stimuli?
- Transduction
- Transmission
- Modulation
- Perception
Transduction
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
Transmission
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
Modulation
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
Perception
Conscious experience of pain:
Transduction, transmission, modulation interact w/ the psychology of the patient to create what is perceived as pain
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
Second order neurons
in gray matter of ipsilateral dorsal horn
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
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
alternate pain pathway that causes insomnia due to pain
spinorecticular tract
pathway that activates anti-nociiceptive descending pathways
spinomesencephalic tract
these 2 tracts activate the hypothalamus and evoke emotional behavior
spinohypothalamic and spinotelecephalic tracts
Neospinothalamic tract
fast pain pathway
first order neurons in neospinothalamic tract
travel via AD fibers and terminate on lamina I (lamina marginalis) of dorsal horn of SC
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)
A few of the 2nd order neurons in the fast pain pathway terminate on the ________ causing insomnia
reticular formation
Where do most of the 2nd order neurons from fast pain pathway travel to
ventrobasal complex (VBC) of thalamus
3rd order neurons fast pain pathway
communicate w/ somatosensory cortex
Paleospinothalamic pathway
slow pain pathway
slow pain pathway: 1st order neurons
go via type C to laminae II and III of dorsal horns (together known as substantia gelatinosa)
2nd order neurons: slow pain pathway
take off and terminate in lamina V (also in dorsal horn)
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
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)
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
Fast pain can be localized easily if ____________ are stimulated together with ____________
AD fibers
tactile receptors
Slow pain is poorly _____________
localized
What 3 major components in the brain mediate the analgesia system?
- periaquaductal grey matter (midbrain)
- nucleus raphe magnus (medulla)
- nociception (pain) inhibitory neurons w/in the dorsal horns of SC– act to inhibit pain-transmitting neurons also located in spinal dorsal horn
Epicenter of analgesia in the brain
periaquaductal grey matter
This is afferently stimulated from axons in the SC and cerebellum
nucleus raphe magnus
This area in the brain plays a role in the descending modulation of pain and in defensive behavior
periquaductal grey mater
The main function of the _________ is mostly PAIN MEDIATION; it sends projections directly to the ____________ of the SC
nucleus raphe magnus
dorsal horn
Substance P
released slower; building over a few minutes: slow chronic pain
Glutamate
acts instantly, only lasts a few milliseconds: fast pain
CGRP
calcitonin gene-related peptide
chronic pain: migraines
Where do modulators occur? Do they suppress or aggravate pain?
peripherally at nociceptors
in spinal cord
or supraspinal structures
can suppress or aggravate pain
example of a modulator
NMDA receptor role
Neuroendocrine response
increase secretion of catabolic hormones stress response decrease anabolic metabolism: insulin, testosterone ACTH release hyperglycemia
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
Release of serotonin may induce ______________-
coronary vasospasm
pulmonary responses to pain
increased total body O2 consumption, CO2 production, minute ventilation
What capacities decrease w/ pain?
TV, VC, FRC
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
Pulmonary function __________ w/ abdominal thoracic incision (splinting)
decreases
What happens to the vascular system from stress
platelet adhesion and hyper-coagulability: DVT, pulmonary edema
Where is visceral pain referred to?
somatic sites
What are some other responses to pain your body has?
increased sphincter tone, decreased gastric mobility: ileus; n/v
stress ulcers
urinary retention
Periosteal and somatic irritation initiate reflex motor response leading to ___________
muscle spasm
Chronic pain is pain that persists ______________.
one month longer than expected
T/F: Chronic pain is protective
False
What are the main types of chronic pain?
low back pain, h/a, recurrent facial pain, cancer pain, arthritis
Chronic pain caused by peripheral mechanisms respond to what?
NSAIDs; often from chronic inflammation in periphery
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
Peripheral-Central Mechanism
lesions of peripheral nerves, dorsal roots, or dorsal ganglion cells
Found in: causalgias, other reflex sympathetic dystrophy, phantom pain
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
Chronic nerve compression
i.e. spinal stenosis; these patients often come in for surgery
Central Pain Mechanism
found in lesions to the thalamus and SC injury such as paraplegia
see often in TBIs
Psychophysiologic Mechanism
severe stress: usually seen in chronic tension h/a & chronic pain from muscle spasms in shoulder, back, chest
Learned Mechanisms
secondary gain
These patients frequently develop reactive depression and hypochondriasis
-psychogenic component; difficult to treat
When a person has chronic pain, how do they handle minor injuries? Why?
handle them poorly: serotonin and endorphins are depleted
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
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
What electrolyte would you consider giving a patient w/ chronic pain before surgery? Why?
Magnesium: blocks NMDA receptors so they aren’t active
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
What are 3 common causes of cancer pain?
- tumor invasion of bone: most common
- tumor compression of peripheral nerves: 2nd most common
- treatment: radiaion, chemo
The physical effects are better/worse for cancer pain patients than for other chronic pain patients?
worse
loss of sleep, appetite, n/v
Psychological effects of cancer pain
heightened anxiety, separation and loss, self esteem, life’s goals, effect on family, disfigurement
Cancer patients w/ more emo disturbances & pain ________________ than those whose pain was controlled
died sooner
How does the WHO recommend approaching cancer pain?
- Nonopiod analgesic (mild pain): inhibit prostaglandin syntetase and & antitumor effects in bone mets
- -ASA, tylenol, NSAIDs - “weak” oral opiods (moderate pain)
- -codein, oxycodone - “stronger” opiods (severe pain)
- MSO4; hydromorphone
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
Tolerance of opiods is __________ in cancer patients. THey can require ___________ of morphine IV
normal
200mg/hr
T/F: addiction to pain meds in ca pain patients is rare.
True
What is the goal of chronic pain managment?
sustained pain relief w/ minimal side effects
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
What is a problem w/ using NSAIDS?
celiling effect on analgesia
What parts of the brain are affected in acute stress?
RAS or thalamus
Arcuate nucleus; Locus coeruleus
PVN
Amygdala
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
What happens when the PVN is stimulated in acute stress?
increased CRH–>ACTH (pituitary)–>CORT; NPY/NE (adrenal glands)
What happens at target tissues w/ acute stress?
increased BP/HR
decreased appetite, reproduction; immunity, growth & thyroid function
What is the feedback mechanism w/ acute stress?
CORT inhibits ACTH which inhibits CRH
How are target tissues affected w/ chronic stress?
?? BP/HR
?? appetite
decreased reproduction, immunity & growth/thyroid fx
What is the feedback in chronic stress?
Maladaptive: no negative feedback like in acute
Instead more of the hormones are made
