Physiology of Pain Karius Flashcards

(46 cards)

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
How does the insular cortex process of pain in the brain
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
Asymbolia
have physiological signs of pain but can't describe it
27
What happens to pain if there is a lesion in one area that pain is perceived?
does NOT abolish ability to experience pain but the pain experience will change
28
Amygdala impact on pain
receives nociceptive input | important in activating/producing emotional components of pain sensation
29
Clinical significance of synapses in the hypothalamus and medulla for visceral afferents
form basis of physiological changes associated with visceral pain like diaphoresis and altered blood pressure
30
What is the Gate Theory of Pain and how does it work?
Other somatic input can alleviate the pain | Stimulating other senses by changing what info is going to the brain
31
Pathway for gate theory of pain
activate second stimuli (A beta) which will synapse on same interneuron as initial stimuli (A delta or C fiber)
32
What does A beta release to interneuron?
EAA that activates an inhibitory interneuron in the spinal cord
33
What does the inhibitory interneuron release in the gate theory of pain?
glycine to inhibit activity of second order neuron that was initially attached to the interneuron from the A delta/C fiber hyperpolarizes it
34
End result of gate theory of pain?
reduce sensation of pain
35
Descending Mechanism to modify painful inputs
use presynaptic inhibition to reduce activation of second-order nociceptive neuron in spinal cord
36
Step 1 in Pathway for descending influence
Neurons in periaqueductal gray are activated but opiates, EAA, and CB1 cannibinoids
37
Step 2 in Pathway for descending influence
axons from periaqueductal neurons travel to raphe nuclei and release enkephalins and activate raphe neurons
38
Step 3 in Pathway for descending influence
axons from raphe neurons travel to spinal cord and release serotonin which activate inhibitory interneurons causing them to release opiates
39
Step 4 in Pathway for descending influence
Opiates activate receptors on presynaptic terminal of C fiber
40
Step 5 in Pathway for descending influence
*main step* | produces pre-synaptic inhibition that reduces release of substance P from nociceptor and reduce pain transmission
41
Skin pain innervation
both A delta and C fibers
42
Deep pain
periosteum and ligaments dull, achy many C fibers associated with muscle spasm
43
Muscle pain
injury or ischemia during contraction both A and C fibers both fast and slow pain in muscle
44
Visceral pain characteristics
poorly localized C fibers stretch receptors often referred
45
How does visceral pain develop
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
Pneumonia visceral pain
in the lung and the diaphragm so pain is felt in the upper left quadrant