Acute and Chronic Pain Flashcards

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1
Q

analgesia

A

absence of spontaneous report of pain or pain behaviors in response to stimulus normally expected to be painful

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2
Q

dysesthesia

A

and unpleasant abnormal sensation, whether spontaneous or evoked

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3
Q

hyperesthesia

A

increased sensitivity to stimulation, excluding special senses

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4
Q

hypoalgesia

A

diminished pain in response to a normally painful stimulus

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5
Q

neuropathic pain

A

pain arising as a direct consequence of a lesion or disease affecting the somatosensory system

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6
Q

nociceptor

A

a receptor preferentially sensitive to tissue or trauma or to a stimulus that would damage tissue if prolonged

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7
Q

nocioception

A

activation of sensory transduction in nerves by thermal, mechanical, or chemical energy impinging on specialized nerve endings

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8
Q

plasticity

A

nociceptive input leading to structural and functional changes that may cause altered perceptual processing and contribute to pain chronicity

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9
Q

What is the gate control theory?

A

an modulate pain at the spinal chord

Rubbing of large fibers will gate pain fibers at the spinal cord

highlights the importance of the spinal cord dorsal horn in modulating increasing pain signals, can be gated to eliminate pain signal from C-fibers

Descending pathways are also involved

three components: sensory, affective, evaluative

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10
Q

What is the neuromatrix theory?

A

individuals develop their own “neurosignature” as part of a neural netowrk which is influenced by a number of inputs (previous physical or psychological trauma), genetic susceptibility, cognitive and evaluative, that feed into a network of brain structures in creatin g”outputs” over time in one’s life manifesting as pain, one’s action program, and long term effects on the stress regulation or endocrine system

updated Gate Control Theory

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11
Q

transduction

A

detection of noxious or damaging stimuli

this signal is transduced into electrical activity by various types of nociceptors

thermal nociceptors detect extreme temperatures, chemical nociceptors detect noxious substances, and mechanical nociceptors detect high-intensity pressure

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12
Q

conduction

A

detection of noxious or damaging stimuli

resulting electrical signals are conducted via primary afferent nociceptive neurons to the dorsal horn of the spinal cord

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13
Q

transmission

A

synaptic transfer of input to neurons with specific laminae of DH

two ascending pathways - spinothalamic and spinoparabrachial tracts

spinothalamic tract relays through the thalamus to the somatosensory cortex and related areas

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14
Q

modulation

A

the sensation of pain and the response to pain are affected not only by pain transmission from affected neurons (via ascending pathways) but also by the brain’s response to that transmission (via the descending pathways)

inhibitory spinal interneurons and projections from the brainstem to the dorsal horn of the spinal cord modulate pain signaling by limiting the transfer of incoming snesory input to the brain

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15
Q

perception

A

the spinothalamic tract relays pain information through the thalamus to th esomatosensory cortex and associated areas, allowing for localization of pain, avoidance behavior, and cognitive processing of pain

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16
Q

affective response

A

the spinoparabrachial tract relays the pain stimulus to the parabrachial nucleus of the brainstem, continuing on to the ventral medial nucleus of the hippocampus and the central nucleus of the amyglada, brain regions involved in the affective response to pain

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17
Q

allodynia

A

a pain due to astimulus which does not normally provoke pain.

Temperature or physical stimuli can provoke allodynia, (which may feel like a burning sensation), and it often occurs after injury to a site.

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18
Q

hyperalgesia

A

an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves

what is normally painful becomes much more painful

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19
Q

What are the outcomes of healing to injury with plasticity?

A

hyperalgesia and allodynia

will lead to chronic pain

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20
Q

What are Abeta fibers?

A

large, thickly myelinated fibers that are non-nocioceptive

  • normally responds to non-painful (mechanical) stimuli
  • can be recruited into pain processing over time
21
Q

What are Adelta fibers?

A

small, thinly myelinated nociceptive fibers

  • respond to heat, cold, and high-intensity mechanical stimuli
22
Q

What are C fibers?

A

unmyelinated, nociceptive fibers

responds to head, mechanical, and chemical stimuli

23
Q

What is the response for non-painful stimuli?

A

specificity for a particular stimulus

high degree of gain to amplify weak signals

rapid adaptation to increasing intensities

24
Q

What is the response for painful stimuli?

A

specificity is less important

high threshold receptors - thermal, chemical, and mechanical stimuli (polymodal)

threshold for firing may decrease

25
Q

What is the framework for acute/subacute injuries?

A

clinical alterations - symptoms

anatomical alterations - tissue injuries and overload

functional alterations - biomechanical deficits and subclinical adaptations

26
Q

What are the clinical symptoms of musculotendinous overload?

A

pain

instability

dysfunction

27
Q

What are functional biomechanical deficits of musculotendinous overload?

A

muscular weakness

inflexibility

scar tissue

muscle strength imbalance

28
Q

What is the signaling cascade in peripheral nerve terminals?

A

chemical, mechanical, or thermal activation of peripheral nociceptors via nonselective cation or Na+ channels

influx of calcium and sodium ions depolarizes the membrane

voltage-gated sodium channels open and further depolarize the membrane

burst of action potentials

29
Q

What are the key neurotransmitters and modulators involved in pain processing?

A

increased processing: glutamate and substance P

decreased processing: norepinephrine, serotonin, GABA, glycine, endocannabinoids, endorphins, monoamines

30
Q

What are the features of central sensitization?

A

development of or increases in spontaneous neural activity

reduced threshold for activation by peripheral stimuli or for dorsal horn neural activation

increased receptive field of nociceptive afferents or dorsal horn neurons

increased response of dorsal horn neurons to painful stimuli

31
Q

What are the potential mechanisms for central sensitization?

A

cellular processes such as decreased inhibition, increased membrane excitability, and synaptic facilitation

microglial activation

32
Q

What are some of the effectors altered in central sensitization?

A

changes in threshold and activation kinetics of NMDA and AMPA receptors

changes in AMPA receptor membrane trafficking

alterations in ion channels to increase inward currents and reduce outward currents

reductions in the release or activity of GABA and glycine

altered gene expression in dorsal horn neurons

33
Q

What is the function of calcium channels in the nervous system? What are drugs that modify its function?

A

inward channel, primary driver for most intracellular responses to stimulation

drugs: pregabalin, gabapentin, ziconotide

34
Q

What is the function of potassium channels in the nervous system? What are drugs that modify its function?

A

outward channels - efflux of potassium makes the membrane potential more negative (hyperpolarized)

drugs: baclofen, clonidine, opioids

35
Q

What is the function of sodium channels in the nervous system? What are drugs that modify its function?

A

inward channel - influx of sodium through open channels makes membrane potential less negative, bringing it closer to the threshold potential necessary to initiate an action potential

drugs: local anesthetics, carbamazepine, phenytoin

36
Q

What is the function of chloride channels in the nervous system? What are drugs that modify its function?

A

inward channel: influx of chloride makes the membrane potential more negative (hyperpolarized)

drugs: benzodiazepines (amplify GABA, induced opening of channel)

37
Q

What are the key steps in pain mechanisms?

A

sensitization and abnormal peripheral input

leads to…

sensitization and amplification of peripheral input in the dorsal horn

leads to…

sensitization of neuron in the brain

38
Q

What are the mechanisms of nocioceptive central pain?

A

autosensitization of receptors

ectopic firing of dorsal root ganglion cell

calcium-induced molecular cascades from excess glutamate

phenotypic change of A-ß cells and DRG

changes in gene expression of sodium channels and neuropeptides

anatomic changse at dorsal horn

39
Q

Where is pain processed?

A

center just for pain: thalamus

center for pain and emotion: somatosensory cortex, insular cortex, hippocampus, amyglada, anterior cingulate cortex

40
Q

What is catastrophizing?

A

definition: exaggerated negative orientation toward a noxious stimulus

rumination - “I can’t seem to get it out of my mind”

magnification - “I become afraid that the pain will get worse”

helplessness - “I feel I can’t stand it anymore”

41
Q

What is Gatchel’s 3-stage model for acute to chronic pain?

A

state I - normal emotional reaction during acute phase

stage II - behavioral and psychological reactions and problems

stage III - acceptance or habituation to “sick role”

42
Q

What are the symptoms of central sensitization?

A

hyperalgesia

spontaneous pain

allodynia

decreased threshold to peripheral stimuli

expansion of receptive field

increased spontaneous activity

43
Q

What are the features of muscle pain?

A

aching and cramping

difficult to localize and refers to other deep somatice tissues (fascia, muscles, joints)

muscle nocioceptive activity is processed differently in the CNS

inhibited more strongly by descending pain-modulating pathways than cutaneous pain

44
Q

What is myofascial pain?

A

characterized by regional areas of muscle weakness or dysfunction many times associated with an area of acute or chronic injury that has characteristic referral patterns of pain, many times mimicking a “pinched nerve” or radicular spine syndrome

45
Q

symptoms of myofascial pain

A

local and referred pain

pain with iso contraction

stiffness, limited ROM

muscle weakness

paresthesia and numbness

propioceptive disturbance

autonomic dysfunction

46
Q

What are the physical findings of myofascial pain?

A

local tenderness

single or multiple muscles

palpable nodules

firm or taut bands

“twitch response” (LTR)

jump sign

muscle shortening

limited joint motion

muscle weakness

47
Q

What are some causes of chronic pain?

A

trauma

congenital or familial abnormalities

nerve or nervous system injury

osteoarthritis

muscle or visceral injury

other systemic disorders where pain continues to persist for at least 3 to 6 months with characteristic central or peripheral nervous system changes

48
Q

What is the treatment for chronic pain?

A

relies on pharmacologic therapies to help reduce pain, improve mood, improve sleep quality, and return patients to previous lesure activities and work

49
Q

What are teh characteristics of organ pain?

A

the viscera have lower densities of sensory nerve innervation and share sympathetic and parasympathetic convergence in the central nervous system

visceral or organ pain is usually more poorly localized