B7-005 Pain 2 Flashcards

1
Q

acute pain goes through the […] system

A

spinothalamic

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2
Q

carried by unmyelinated C fibers
dull, burning pain-poorly localized

A

slow pain

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3
Q

carried by A-delta thinly myelinated fibers
sharp pricking pain
accurately localized

A

fast pain

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4
Q

slow pain is carried in the […] tract

A

paleothalamic

has several “waypoints” on way to thalamus, envokes “memories” of pain

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5
Q

fast pain is carried in the […] tract

A

neothalamic

goes straight to thalamus

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6
Q

why does slow pain invoke an emotional response?

A

it is diffusely projected throughout the cortex

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7
Q

why does pain persist after the noxious stimuli is removed?

A

peripheral :sensitization by chemical mediators (they depolarize the receptor and make it more sensitive to subsequent stimuli)

central: decreased pain receptor thresholds and changes in synaptic central circuits over time

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8
Q

similar to slow pain, affecting the internal organs

A

visceral pain

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9
Q

why is visceral pain hard to localized?

A

very high percentage of C fibers going through paleothalamic tract which projects diffusely

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10
Q

has characteristics of slow pain
is commonly referred to overlying somatic structures

A

visceral pain

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11
Q

describe the mechanism of referred pain

A

convergence of cutaneous and visceral nociceptors onto same dorsal horn
OR
branching pattern of sensory nerve

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12
Q

secondary to disruption of normal pain physiology caused by abnormal sensitization, conduction, modulation, or perception

A

chronic (abnormal) pain

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13
Q

mildly painful stimuli perceived as more painful that it is

A

hyperalgesia

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14
Q

nonpainful stimuli perceived as pain

A

allodynia

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15
Q

painful tingling (like foot asleep)

A

dysesthesia

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16
Q

persistant hyperpathia associate with vasomotor changes after an injury

usually after a period of immobilization, affected limb may have color changes

A

Complex Regional Pain Disorder

AKA reflex sympathetic dystrophy, causalgia (with nerve injury)

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17
Q

focal area of demyelination with cross talk between bare axons

A

neuralgia

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18
Q

treatment of trigeminal neuralgia

A

carbamezapine
surgery

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19
Q

treatment of Complex Regional Pain Disorder [3]

A

aggressive mobilization
pain control
sympathetic blockade

20
Q

damage to somatosensory systems, associated with numbness

presumed secondary to decreased modulation

A

defferentation pain

21
Q

describe the gate control theory of pain

A

modulation of pain wants the non-painful and painful stimuil to be balanced

a decrease in either one would cause an increase in the other and vice versa

22
Q

loss of non-painful sensory inputs causes a relative pain increase, pain is perceived

A

defferentation pain

23
Q

inhibitory pain pathway
triggered by fight or flight

A

central pain modulation

24
Q

describe the central pain modulation pathway

A

periaqueductral gray –> opiate receptors –> rostroventral medulla –> NE 5HT –> dorsal horn –> enkephalin interneurons

25
Q

treatment used to decrease sensitization [4]

A

early mobility
capsacin
NSAIDs
steroids

26
Q

treatment used to decrease pain conduction [3]

A

nerve block
spinothalamic tractotomy (used for cancer with poor prognosis)
stabilize nerves with anti-epilepsy drugs

27
Q

treatments used to increase pain modulation [2]

A

increase non-painful input: mechanical stimulation, trans-cutaneous stimulator, posterior column stimulator, stimulate periaqueductal gray

medication: antidepressants, opiates

28
Q

treatments used to change pain perception

A

behavior/relaxation therapy
biofeedback
treatment for anxiety/depression

29
Q

recurrent brief episodes of pain in the CN V distribution

A

trigeminal neuralgia

30
Q

most cases of trigeminal neuralgia are caused by

A

vascular compression of the CN V root

31
Q

electric “shock” like pain over the jaw triggered by talking, chewing, or touch

A

trigeminal neuralgia

32
Q

treatment for trigeminal neuralgia

A

carbamazepine (epilepsy drug)

**if no response, they need surgical intervention

33
Q

“burning” pain and allodynia following herpesvirus infection

A

postherpetic neuralgia

34
Q

describe the pathophysiology of postherpetic neuralgia

A

decreased modulation from defferentation

35
Q

used to reduce the risk of postherpetic neuralgia

A

antivirals

**diagnosis must be caught early to have better prognosis

36
Q

damage to descending pain inhibitory pathways can cause

A

decreased modulation

37
Q

treatment of postherpetic neuralgia

A

amitriptyline

38
Q

acute migraine treatment

A

triptans (diptans if risk of stroke)
antiemetics

39
Q

prophylactic migraine treatment

A

beta blocker
amitriptyline
valproate, topiramate (anti-epileptics)
botulinum toxin
anti-CGRP monoclonal antibodies
NSAIDs

40
Q

treatment of deafferentation syndrome

A

tricyclic antidepressant

41
Q

blocks sodium channels in the nerve

A

lidocaine

42
Q

[…] syndrome following a thalamic stroke is common

A

deafferentation pain

43
Q

allodynia with swelling, redness of skin, and skin changes

A

complex regional pain syndrome/reflex sympathetic dystrophy

44
Q

the projection of pain impulses to the cerebral cortex is […]

A

diffuse

extends beyond somatosensory complex

45
Q

physiologic basis of referred pain

A

convergence of primary sensory neurons from the skin and affected organ on the same populations of secondary sensory neurons within the spinal cord