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MEDICAL PHYS EXAM FINAL > physiology of pain > Flashcards

physiology of pain Flashcards

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USMLE® Step 1 flashcards
1
Q

define nociception

A
  • sensory response to noxious substance
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2
Q

define pain

A
  • perception of nociceptive sensory info
  • unpleasant sensory and emotional experience associated with actual or potential tissue damage and description in terms of such damage
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3
Q

physical pain (physiological)

A
  • Transient, localized, minimal tissue damage

- warning

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4
Q

inflammatory pain

A
  • acute and chronic that cause tissue damage
  • Inflammatory process mediated
  • HYPERSENSITIVITY is protective and promotes healing
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5
Q

neuropathic pain

A
  • damage/alteration to the nervous system (central/peripheral)
  • generally chronic
  • MALADAPTIVE
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6
Q

somatic pain

A
  • superficial (discrete localization) = skin (pinprick, pinch)
  • -> initial (sharp, A-sigma fibers)
  • -> delay (burning, C fibers)
  • Deep (diffuse localization) = connective tissue, bones, joints, muscles (cramps and headaches)
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7
Q

visceral pain

A
  • conveyed by C-type fibers
  • POORLY LOCALIZED
  • pain is often REFFERED to somatic area following a dermatome pattern
  • often described as ACHING and COLICK
  • EX = angina, colic, ulcer, appendicitis, renal stones
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8
Q

describe characteristics of free nerve endings (nociceptors)

A
  • slowly adapting
  • high threshold
  • SENSITIZATION = alteration of the membrane that brings the resting potential closer to threshold and thus more easily excited
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9
Q

what triggers nociceptors (free nerve endings)

A
  • Activators = K+, H+, substance P, bradykinin
  • Sensitizers = prostaglandins, leukotrienes, ATP, other chemical mediators of inflammation
  • *NSAIDS produce most of thei analgesic effects by REDUCING PROSTAGLANDIN PRODUCTION via inhibition of cyclooxygenase activity**
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10
Q

describe silent nociceptors

A
  • unresponsive to non-noxious and even high intesntiy (noxious) mechanical or temp stimuli unless previously activated or sensitized
  • Responsive to inflammation (chemical) stimuli, which is likely mediating the sensitization of these receptors
  • Once activated by a chemical (inflammatory) stimuli, will then respond to OTHER MODALITIES (temp, pressure)
  • FOUND IN VISCERA
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11
Q

A-alpha/A-beta

A
  • respond to mechanical stimuli
  • LOW THRESHOLD
  • Conduct at 50-120m/s
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12
Q

A-Sigma

A
  • respond to mechanical stimuli
  • HIGH THRESHOLD
  • Conduct at 20 m/s
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13
Q

C fibers

A
  • respond to thermal, chemical, multimodal
  • VERY HIGH THRESHOLD
  • conduct at 1m/s (not myelinated)
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14
Q

role of A-sigma/C fibers in autonomic-induced reflexes

A
  • nociceptors via A-sigma/C fibers activate sympathetic/parasympathetic neruons in the cord and in sympathetic ganglia which innervate the blood vessels and other structures in the region of damage
  • INDUCED ACTIVITY contributes to axon reflex and signs of inflammation
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15
Q

describe primary hyperalgesia (primary/peripheral sensitization)

A
  • Increased sensitivity to noxious and non-noxious stimuli in the area IMMEDIATELY surrounding the primary site of damage due to sensitization of the peripheral nociceptors
  • involves sensitization of peripheral nociceptors by chemical peripheral nociceptors by chemical substances (chemical mediators of inflammation, substance P, glutamate, etc)
  • increased primary nocicpetors sensitivity produced by primary hyperalgesia mechanisms does contribute to allodynia
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16
Q

describe secondary hyperalgesia (secondary/central sensitization)

A
  • involves WIDER somatic area of HYPERSENSITIVITY than observed with Primary hyperalgesia and is SLOWER in developing
  • thought to be central phenomena involving a change in the responsiveness of the spinothalamic neurons (mediated by Substance P, glutamate, etc)
  • promoted by sustained high intensity input from A-sigma and C fibers
17
Q

describe allodynia

A
  • Pain resulting from non-noxious stimulus
  • Predominately produced by facilitation of second-order spinal neuron responsiveness to non-noxious stimuli through a WIND UP or similar phenomenon elicited from intense noxious input
  • Increased primary nociceptor sensitivity produced by primary hyperalgesia mechanisms does contribute to this phenomenon as well
18
Q

Paleospinothalamic tract

A
  • located more medially in spinothalamic tract
  • projects primarily to central lateral nucleus of the thalamus and from there into the cerebral cortex and medullary regions
  • associated with LARGER RECEPTIVE FIELDS
  • associated with INCREASED AROUSAL, AFFECTIVE and AUTONOMIC Responses
  • -> sharp, severe pain results in sympathetic excitation type of response (increased HR, sweating etc)
  • -> severe, dull crushing pain results in sympathetic depression type response (bradycardia, vasodialtion)
19
Q

Neospinothalamic tract

A
  • more laterally in spinothalamic tract
  • projects predominately to the VPL (trunks/limbs) and VPM (trigeminal head) nuclei of the thalamus and from there somatotopically to the somatosensory cortex
  • associated with SMALLER peripheral receptors
  • Assocaited with LOCALIZATION, QUALITY and TYPE of “PAIN”
  • Colaterals from the thalamus also project to other cortical areas invovled in appreciation of “pain perception”
  • Consistent with sensory-discrimination of pain
20
Q

Dorsal column

A
  • in additon to proprioceptive info, provides an IPSILATERAL ASCENDING PATHWAY for VISCERAL PAIN
21
Q

Descending columns

A
  • endogenous control of pain
  • evidence for spinal and supraspinal influence on pain and nociception
  • -> conscious control
  • -> stress induced analgesia
  • -> stimulation-produced analgesia (SPA) = electrical stimulation of selected foci will produce profound analgesia
  • -> Periaqueductal gray (PAG) = involved in ALL CIRCUITS OF PAIN CONTROL and MODULATION
22
Q

what are analgesic meds and how do they work

A
  • Non-opioids/NSAIDS = inhibit prostglandin production/peripheral chemical mediation of nociception (also in spinal cord
  • Opioids/morphines = activate opioid receptors which enhance the action of met-enkephalin through the opioid receptors in the dorsal horn as well as higher centers in Brainstem, thalamus and other areas
23
Q

PAG

A
  • can activate the raphe and locus ceruleus descending systems
  • can modulate the ascending pathways and through indirect ascending projections, attenuate the response to the noxious information
24
Q

Raphe

A
  • serotonin (5-HT)
25
Q

Locus ceruleus

A
  • Norepinephrine (NE)
26
Q
  • nucleus reticularis paragigantocellularis (NRPG)
A
  • Norepinephrine (NE)
  • activation of descending 5-HT and NE projections from raphe and LC results in activation of INHIBITORY INTERNEURONS at the dorsal horn as well as direct modulation of incoming nociceptive info
  • provides the basis for EFFICACY of ANTIDEPRESSANTS AS ADJUCTS in the management of chronic and neuropathic pain syndromes (tricyclic antidepressants act to reduce the uptake of NE and 5-HT)
27
Q

describe the pain enhancing projections

A
  • rostral medullary raphe –> 5-HT projection to dorsal horn of spinal cord provides sensitization of neruons to noxious and non-noxious sensory input
  • -> system is active for transient period when strong noxious stimuli is first presented but after a period of time becomes quiescent (WARNING ALARM to INCREASE SIGNAL INTENSITY relative to background noise)
  • continued activation contributes to secondary or CENTRAL HYPERALGESIA/ALLODYNIA and even neuropathic pain syndromes
28
Q

describe GATE CONTROL THEORY OF PAIN

A
  • Low threshold, faster conducting MECHANORECEPTOR activation enchances the activity of an INHIBITORY INTERNEURON which reduces excitability of the pain conveying spinothalamic and spinoreticulothalamic projection neurons
  • Higher threshold and slower conduction A-sigma and C fibers reduce the inhibitory interneuron activty and excite the pain conveying spinothalamic and spinoreticulothalamic neurons
  • However since mechanoreceptors input arrives faster, the excitability of spinothalamic neurons is reduced
  • Rubbing your arm makes pain go away
29
Q

OPIOIDS

A
  • met-enkephalin
  • found at many site throughout CNS and periphery
  • Analgesia-mediating sites appear to involve opioid receptors and interneurons in the dorsal horn of spinal cord, LC, raphe, and PAG
  • activate opioid receptors, enhancing the action of met-enkephalin trhoguh the opioid receptors in the dorsal horn as well as higher centers in the brainstem, thalamus etc
30
Q

Reffered pain

A
  • localization of the pain to a site unrelated and often distant to its actual origin
  • -> CONVERGENCE of afferent signals from viscera to spinothalamic neruons receiving other somatic info
  • -> follows a dermatomal arrangement
31
Q

projected pain

A
  • pain produced by irritation of an axon (nerve) at an ectopic site and localized to the site of the nociceptors of the axon (nerve) and along the tract of the peripheral nerve
  • -> project pain provides evidence in support of labeled line theory of sensory processing
  • -> example would be hitting your crazy bone at the elbow and perceiving the pins and needles sensation localized to the hand and fingers
32
Q

define central pain

A
  • pain originating from a central process
  • form of neuropathic pain
  • includes thalamic pain, phantom limb pain
33
Q

define thalamic pain

A
  • lesion involving the VPL/VPM nucleus of the thalamus

- manifestation of severe pain to the CONTRALATERAL SIDE OF BODY, typically involving the entire side of body

34
Q

define phantom limb pain (sensations)

A
  • pain and other sensations localized to missing areas of an amputated or deafferented limb or somatic area
  • projected pain plays some role as neuroma may form in the peripheral nerve remnants which may serve as an ectopic source of activity
  • reorganization of the somatosensory cortex and probably other subortical areas including the spinal cord is also thought to contribute greatly to the formation of phantom pain and other types of phantom sensations
35
Q

neuropathic pain

A
  • does NOT require any apparent peripheral or central pathology
  • associated with damage or alteration of nervous system, central and or peripheral
  • may be spontaneous or induced by an otherwise mild stimulus (allodynia) resulting in intense pain
  • hyperalgesia, an exaggerated PAIN perception relative to the intensity of the noxious stimulus is a common feature
  • *EX = diabetic neuropathy**
36
Q

Sympathetic mediated pain (SMP)

A
  • continuous BURNING pain that may develop following a traumatic peripheral injury
  • -> pain is greatly exacerbated by innocuous stimuli (allodynia) and sympathetic activation (intact sympathetic system is required to maintain this disorder)
37
Q

describe the mechanisms of sympathetic mediated pain

A
  • actiavtion of nociceptors can enhance sympathetic activity
  • -> nociceptors contribute to segmental axon reflex
  • -> nocicpetive information in the spinal cord influences reflex sympathetic pathways
  • following DAMAGE and REPAIR of afferent fibers in damaged peripheral nerve the nociceptors may elaborate alpha adrenergic receptors
  • tonic release of NE by the sympathetic fibers can then activate/sensitize the nocepeptors eliciting pain
38
Q

Complex regional pain syndrome (reflex sympathetic dystrophy RSD)

A
  • Hyperpathia
  • dystrophic changes in skin, nails, hair, muscles and or bone
  • sympathetic hyperactivity (variable), including temp. changes and hyperhidrosis

MEDICAL PHYS EXAM FINAL (14 decks)

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