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Pharm Test 2 > Analgesia and Pain > Flashcards

Analgesia and Pain Flashcards

1
Q

pain versus nociception

A

pain includes perception, nociception does not

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2
Q

what is neuropathic pain

A

pain caused by a lesion or disease of the somatosensory nervous system.

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3
Q

what is nociplastic pain

A

pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.

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4
Q

types of physiologic pain

A

nociceptive/inflammatory

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5
Q

types of pathophysiologic pain

A

neuropathic and nociplastic

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6
Q

acute pain is carried by:

A

 Carried by large diameter myelinated Aδ fibers

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7
Q

chronic pain is carried by:

A

 Carried by small diameter non-myelinated ‘C’ fibers

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8
Q

somatic pain involves which fibres? which tissues and what characteristics?

A

(fibres A-delta)
* Skin, musculoskeletal
* Superficial or deep

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9
Q

visceral pain involves what fibres?

A

(fibres C)
* Organs

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10
Q

origin of innervcation for visceral vs somatic pain

A

visceral: spinal and vagal
somatic: spinal

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11
Q

noxious stimulus for visceral vs somatic pain:

A

visceral: stretch, inflammation, ischemia
somatic: damage (mechanical)

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12
Q

localization of visceral pain vs somatic pain

A

visceral: poor
somatic: precise

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13
Q

is visceral pain referred? somatic?

A

visceral: yes
somatic: no

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14
Q

1st ORDER NEURONS go from:

A
  • From NOCICEPTORS to the SPINAL CORD
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15
Q

1st ORDER NEURONS go from:

A
  • From NOCICEPTORS to the SPINAL CORD
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16
Q

TYPES OF STIMULI THAT EXCITE NOCICEPTORS

A
  • Thermal
  • Mechanical
  • Chemical
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17
Q

fast pain stimuli? what fibres is it carried on?

A
  • Thermal , Mechanical
  • A-delta Fibers
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18
Q

slow pain stimuli? what fibres is it carried on?

A
  • All three
  • C Fibers
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19
Q

difference in conduction rate between A-delta and C fibres

A

A-delta are fast, C are the slowest (non-myelinated, very thin)

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20
Q
  • A-delta (A-δ) fibers characteristics? what is the neurotransmitter?
A
  • Myelinated
  • Fast
  • 12-30 meters/sec
  • Fast, First pain
  • Neurotransmitter is glutamate
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21
Q

C fibers characteristics? what is the neurotransmitter?

A
  • Unmyelinated
  • Slow
  • 0.5-2 meters/sec
  • Slow, Second pain
  • Neurotransmitter is substance P and glutamate
22
Q

where do pain fibres go in the spinal cord?

A

Dorsal horn:

Aδ fibers
* Laminae I (II is also mentioned)

C fibers
* Laminae I and II

23
Q

what neurotransmitters are used for transmitting pain information? what is the difference between them?

A

Glutamate
* Excitatory
* Lasts only for few milliseconds
* Acts very rapidly

Substance P
* Excitatory
* Released slowly over period of seconds or minutes

24
Q

what is the double pain sensation?

A
  • Glutamate transmitter gives a faster pain
    sensation
  • Substance P transmitter gives more lagging sensation
25
Q

2nd ORDER NEURONS path:

A
  • From DORSAL HORN of spinal cord, THROUGH TRACTS, to THALAMUS
26
Q

3 classes of second order neurons. What are they and which are involved with pain?

A
  1. Low threshold mechanosensitive neuron (LT)
    * Light touch, pressure, proprioception
  2. Nociceptive specific neuron (NS)
    * Noxious stimuli (This are the Aδ and C fibers)
  3. Wide dynamic range neuron (WDRN)
    * Respond to a wide range of stimulus intensities
    from non noxious to noxious
    * They respond like C fibers
27
Q

what is the neospinothalamic tract? what path do the neurons follow? where do they terminate?
What fibres are involved, and what type of pain do they carry?

A
  • 2nd order neurons
  • Synapses at Lamina I and some in II
  • Long fibres which cross the midline through the anterior commisure and pass upwards in the contralateral anterolateral columns
  • Terminate at the ventral area of the thalamus
  • This is the classic lateral Spinothalamic tract
  • Involves the A-δ fibers
  • Sharp/fast/localized pain
  • “Direct path” from nociceptor to thalamus, without additional synapses besides the 1st to 2nd order neuron
28
Q

what tracts are contained in the paleospinothalamic tract umbrella?

A
  • 1) Spinoreticular tract
  • 2) Spinotectal or spinomedullary tract
  • 3) Spinothalamic tract
29
Q

type of neurons in the paleospinothalamic tract? where do they synapse and where do they go? what kind of fibres?

A
  • 2nd order neurons
  • Synapse in laminae I and then project to IV-VIII (V is most relevant)
  • The innervation of these three tracts is bilateral because some of the ascending fibers do not cross to the opposite side of the cord
  • Ipsi- and contralateral
  • Involves the C fibers
  • Slow/dull/diffuse pain
  • Multiple synapses along the spinal cord
30
Q

where do neurons in the archispinothalamic tract synapse? where do they go? what type of fibres are present?

A

2nd order neurons
* Synapse at laminae II (substantia gelatinosa)
* Then project to laminae IV-VII and ascend to synapse at the mesencephalic reticular formation (MRF) and the periaqueductal gray (PAG)

Involves the C fibers
* Slow/dull/diffuse pain
* Multiple synapses along the spinal cord

31
Q

of the 3 spinal tracts that carry pain: which carry fast pain, and which carry slow pain?

A

Neospinothalamic tract for fast pain Paleospinothalamic tract for slow pain Archispinothalamic tract for slow pain

32
Q

visceral pain is carried in what fibres? in what tracts?

A

VISCERAL PAIN = C FIBERS
* Paleospinothalamic tract
* Archispinothalamic tract
However, note
* C fibers = Somatic and visceral pain

33
Q

somatic pain is carried in what type of fibres? in what tract?

A
  • Pricking or fast pain
  • Neospinothalamic tract
  • Aδ fibers
  • Burning pain
  • Paleospinothalamic tract * C fibers
  • Archispinothalamic tract * C fibers
34
Q

what tract carries pain from the head, face, and intraoral structures? what is the pathway?

A

 Trigeminal tract
 Is also a Neospinothalamic tract

 Noxious stimulus is transmitted to trigeminal ganglion
 Trigeminal fibers enter the pons, descend to the medulla and synapse in the spinal trigeminal nucleus
 Cross midline and ascend as trigeminothalamic tract

35
Q

what type of fibres are present in the trigeminal tract? where do they go?

A

 Aδ fibers go to ventral thalamus and from there to the somatosensory cortex
 Awareness of exact location of pain

 C fibers terminate in the parafasciculus and centromedian thalamus (Intralaminar nuclei)

36
Q

what is the pathway of 3rd order neurons?

A
  • From the THALAMUS to the SOMATOSENSORY CORTEX
37
Q

where do 3rd order neurons of the neospinothalamic tract go? what do they allow us to do?

A
  • From the thalamus, they communicate with the somatic sensory cortex
  • Fast pain can be localized
38
Q

where do 3rd order neurons of the paleospinothalamic tract go? what do they allow us to do?

A
  • From the parafasciculus and centromedian thalamus (Intralaminar thalamic nuclei), these fibers synapse bilaterally in the somatosensory cortex
  • Emotional response to pain
  • Visceral response to pain
  • Also activates brain stem nuclei which are the origin of descending pain suppression pathway regulating noxious input at the spinal cord level
39
Q

where do 3rd order neurons of the archispinothalamic tract go? what do they allow us to do?

A

 Ascend to the PF-CM complex (IL) areas of the thalamus and also send collaterals to the hypothalamus and to the limbic system nuclei
* Mediate visceral, emotional and autonomic reactions to pain

40
Q

what is pain transduction? what affects it?

A
  • Transforms environmental stimuli into an electrical event and generates action potential
  • Chemical, thermal, physical noxious stimuli
  • Characterized by a stimulus threshold
  • Strength and duration of stimulus affects action potential character
41
Q

do nociceptors adapt to continued pain?

A
  • Adapt very little OR not at all
  • Excitation of the pain fibers, becomes progressively greater, as the pain stimulus continues
  • Increased sensitivity = hyperalgesia
42
Q

Nociceptors Aδ and C fibers are carried as SNS or PNS components?

A

both SNS and PNS nerves have these fibers

43
Q

what is pain signal modulation? where does this occur?

A

 Peripheral sensory impulses are modified (amplified or suppressed) in the spinal cord by several neurotransmitters

 Peripheral ascending, interneurons, descending pathways
 Excitatory receptors- facilitate excitatory transmission
* ATP, substance P, prostanoids, glutamate (AMPA, KAI, NMDA)
 Inhibitory receptors- inhibit excitatory transmission

44
Q

PROJECTION AND PERCEPTION of pain signals occurs how? what structures are involved?

A
  • Nociceptive information conveyed to the brain by projection nerve tracts (2nd order neurons)
  • RAS (reticular activating system- brainstem) and thalamus are central integrating and transmission points for pain perception and responses
    > Cerebral cortex believed vital in integrating pain perception

PAG (periaqueductal gray is key descending modulatory pathway)
* Opioid activation
* Adrenergic activation
* Gabaergic activation

45
Q

ALLODYNIA

A

 Pain due to a stimulus which does not normally provoke pain

46
Q

HYPERALGESIA

A

 An increased response to a stimulus which is normally painful

47
Q

how does peripheral pain sensitization occur?

A

From tissue damage and inflammation
 Neurochemical alterations

48
Q

how does central pain sensitization arise?

A
  • From frequent (chronic) or severe peripheral nociceptor input
  • Spinal and higher CNS uninhibited neuromodulation
    > Alterations in dorsal horn excitability
    > Long-lasting depolarizations of neurons- “Wind-up”
  • Recruitment of A-beta fibers
    > Normal low-threshold and innocuous stimuli
48
Q

how does central pain sensitization arise?

A
  • From frequent (chronic) or severe peripheral nociceptor input
  • Spinal and higher CNS uninhibited neuromodulation
    > Alterations in dorsal horn excitability
    > Long-lasting depolarizations of neurons- “Wind-up”
  • Recruitment of A-beta fibers
    > Normal low-threshold and innocuous stimuli
49
Q

WIND-UP
-SEQUENCE OF EVENTS

A

Wind-up can happen anywhere in the spinal cord or brain. It means that the pain signal that comes into the central nervous system becomes stronger and longer lasting. This is a physiologic process that involves activation of receptors that are normally dormant on post synaptic nerve endings.

    1. Build-up of Ca2+ in presynaptic terminal
    1. Increases neurotransmitter release of aa and Substance P
    1. Activation of adenosine monophosphate acid (AMPA) postsynaptic receptors and subsequent depolarization releases block of N-methyl-D-aspartate (NMDA) receptors
    1. Activation of NMDA and NK1 receptors induces long-lasting cumulative depolarization
    1. Cytosolic Ca2+ increases due to entry through the NMDA ionophore.
    1. Enhanced performance of NMDA receptors through the increased Ca2+ concentration and the activation of NK1 receptors through second messenger systems
    1. All induced changes result in production of action potentials and wind-up
50
Q

FIBERS AFTER NERVE INJURY

A

 Aβ transmission is coupled with C fibers
> Touch stimulus is interpreted as noxious
* Allodynia

 Due to:
1. sprouting of fibers into laminae II and/or
2. Loss of fiber sheath allows contact with denuded fibers facilitating electrical and chemical cross-excitation, and/or
3. During healing Aβ fibers connect with C fibers

Result at the dorsal root ganglion for Aβ :
 Express substance P in lamina II and activation of NK1 receptor

51
Q

NEUROPATHIC PAIN is what? arises from what?

A
  • Sharp, shooting, devastating, persistent pain
  • Arises from functional changes occurring in the CNS secondary to peripheral nerve injury
  • Once the nerve is damaged, the damaged nerve elicits sustained activation of nociceptors and/or nociceptive afferents
  • The neuropathic pain is due to an abnormal activation of the nociceptive system without specifically stimulating the nociceptors

Pharm Test 2 (16 decks)

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