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COM Neuro 3 > Physiology of Pain Karius > Flashcards

Physiology of Pain Karius Flashcards

1
Q

What is fast pain associated with?

A

immediate injury

sharp pain

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2
Q

What is slow pain associated with?

A

dull or achy pain

occurs after the injury

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3
Q

Pain characterized by location

A

deep, muscle, visceral, somatic/cutaneous

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4
Q

Sensory Receptor characteristics

A

base nerve endings with ion channels that open in response to stimuli

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5
Q

Two types of nociceptor fibers

A

Adelta and C fibers

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6
Q

A delta fiber characteristics

A

small, sparsely myelinated

fast, sharp pain

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7
Q

C fiber characteristics

A

unmyelinated

slow, dull pain

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8
Q

Types of Nociceptors

A

sensitive to thermal and mechanical
sensitive to only thermal
sensitive to only mechanical
silent/sleeping

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9
Q

Silent/sleeping nociceptors

A

detect pain to same spot
ex. if I hit my hip against table and then a day later I hit it again
not active under most conidions

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10
Q

Mutations in mechanosensitive Na+ channel

A

lead to absence of pain sensation or paroxysmal pain syndrome

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11
Q

Paroxysmal pain syndrome

A

experience overwhelming pain but nothing happened to cause it

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12
Q

Function of ligand gated channels on nociceptors

A

alter sensitivity of the nociceptors to input

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13
Q

What receptors are associated with ligand gated channels?

A

Substance P, kinins (bradykinin), ATP, H+

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14
Q

What happens when substance P, bradykinin, ATP, and H+ receptors are bound to?

A

activate silent nociceptors

change the sensitivity of nociceptors

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15
Q

Spinothalamic tract to the brain

A

fast pain

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16
Q

Spinoreticulothalamic system to brain

A

slow pain

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17
Q

How does the spinal cord sense noxious stimuli from A delta fibers?

A

release EAA (NT) from A delta fibers which act on non-NMDA receptors

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18
Q

How does the spinal cord sense noxious stimuli from C fibers?

A

substance P and EAA

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19
Q

Pathway of spinoreticulothalamic pathway

A

slow pain

nociceptors synapse on interneuron in spinal cord before crossing and ascending to the reticular formation

20
Q

What can modify the spinoreticulothalamic pathway?

A

opiods and sensory information

21
Q

How can modulations of spinoreticulothalamic be made?

A

local (gate theory)

descending (opiod pathway)

22
Q

How is visceral pain sensed?

A

visceral afferents travel with autonomic nerves

has some synapses in the hypothalamus and medulla

23
Q

Where is nociceptive input distributed in the brain’s cortex?

A

thalamus, mediofrontal cortex, post-central gyrus, insular cortex
this makes pain impossible to ignore

24
Q

S1 and S2 input on processing of pain in the brain

A

receive input from nociceptors and play a role in localizing pain

25
Q

How does the insular cortex process of pain in the brain

A

Interpretation of nociceptive inputs
Process internal state of body “yes everything is okay or no everything is not okay”
Autonomic response to pain “sympathetic reaction”
Integrates all signals related to pain (asymbolia)

26
Q

Asymbolia

A

have physiological signs of pain but can’t describe it

27
Q

What happens to pain if there is a lesion in one area that pain is perceived?

A

does NOT abolish ability to experience pain but the pain experience will change

28
Q

Amygdala impact on pain

A

receives nociceptive input

important in activating/producing emotional components of pain sensation

29
Q

Clinical significance of synapses in the hypothalamus and medulla for visceral afferents

A

form basis of physiological changes associated with visceral pain like diaphoresis and altered blood pressure

30
Q

What is the Gate Theory of Pain and how does it work?

A

Other somatic input can alleviate the pain

Stimulating other senses by changing what info is going to the brain

31
Q

Pathway for gate theory of pain

A

activate second stimuli (A beta) which will synapse on same interneuron as initial stimuli (A delta or C fiber)

32
Q

What does A beta release to interneuron?

A

EAA that activates an inhibitory interneuron in the spinal cord

33
Q

What does the inhibitory interneuron release in the gate theory of pain?

A

glycine to inhibit activity of second order neuron that was initially attached to the interneuron from the A delta/C fiber
hyperpolarizes it

34
Q

End result of gate theory of pain?

A

reduce sensation of pain

35
Q

Descending Mechanism to modify painful inputs

A

use presynaptic inhibition to reduce activation of second-order nociceptive neuron in spinal cord

36
Q

Step 1 in Pathway for descending influence

A

Neurons in periaqueductal gray are activated but opiates, EAA, and CB1 cannibinoids

37
Q

Step 2 in Pathway for descending influence

A

axons from periaqueductal neurons travel to raphe nuclei and release enkephalins and activate raphe neurons

38
Q

Step 3 in Pathway for descending influence

A

axons from raphe neurons travel to spinal cord and release serotonin which activate inhibitory interneurons causing them to release opiates

39
Q

Step 4 in Pathway for descending influence

A

Opiates activate receptors on presynaptic terminal of C fiber

40
Q

Step 5 in Pathway for descending influence

A

main step

produces pre-synaptic inhibition that reduces release of substance P from nociceptor and reduce pain transmission

41
Q

Skin pain innervation

A

both A delta and C fibers

42
Q

Deep pain

A

periosteum and ligaments
dull, achy
many C fibers
associated with muscle spasm

43
Q

Muscle pain

A

injury or ischemia during contraction
both A and C fibers
both fast and slow pain in muscle

44
Q

Visceral pain characteristics

A

poorly localized
C fibers
stretch receptors
often referred

45
Q

How does visceral pain develop

A

Brian is taught that the shoulder is more likely to experience pain than the heart, the nociceptors may converge on the same interneuron of the spinal cord

46
Q

Pneumonia visceral pain

A

in the lung and the diaphragm so pain is felt in the upper left quadrant

COM Neuro 3 (3 decks)

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