Sensory Physiology Flashcards

1
Q

How are peripheral nerves classified?

A

Contribution to compound AP

Fiber diameter, myelin thickness, and conduction velocity

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2
Q

What does conduction velocity determine?

A

Fiber’s contribution to the ocmound AP

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3
Q

How can you you test for peripheral nerve disease ?

A

Conduction velocity and compound AP

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4
Q

What is the correlation of fiber diameter and conduction velocity?

A

Large diameter correlates to faster conduction velocity

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5
Q
What kind of receptor is 
             Meissner Corpuscle? 
RA or SA? 
In what kind of skin?
Sensation type?
A

RA in glabrous skin

Touch and vibration. Flutter and tapping

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6
Q
What kind of receptor is 
             Pacinian Corpuscle? 
RA or SA? 
In what kind of skin?
Sensation type?
A

RA

Both hairy and glabrous

Rapid indentation of skin - vibration

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7
Q
What kind of receptor is 
             RUffini Corpuscle? 
RA or SA? 
In what kind of skin?
Sensation type?
A

SA

Both hairy and glabrous

Stretch, touch, pressure and proprioception

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8
Q
What kind of receptor is 
             Merkel Corpuscle? 
RA or SA? 
In what kind of skin?
Sensation type?
A

SA

Glabrous skin

Pressure sensation

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9
Q
What kind of receptor is 
             Hair follicle receptor? 
RA or SA? 
In what kind of skin?
Sensation type?
A

RA and SA

Motion across skin and directionality of motion

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10
Q
What kind of receptor is 
             Tactile free nerve endings? 
RA or SA? 
In what kind of skin?
Sensation type?
A

(High threshold)

SA

Pain and temperature

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11
Q

What are receptive fields?

A

Areas of innervation where individual mechanoreceptors fibers convey info from a limited area of skin

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12
Q

What part of the body have a high density of small receptive fields?

What does this allow for?

A

High density of small receptive field

Allows for fine discrimination of sensory inputs

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13
Q

Where is tactile acuity lowest?

A

Calf, back and thigh

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14
Q

What is S1 involved in?

A

Integration of info for position sense, size and shape discrimination

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15
Q

What is S2 responsible for?

A

Comparison b/w objects, different tactile sensations, determining whether not something becomes a memory

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16
Q

What is the parietal temporal occipital association area responsible for?

A

High level interpretation of sensory inputs

Analysis rs sptial coordinates of self in environments

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17
Q

What is phantom limb pain?

A

Describes pain in a body part that is no longer present

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18
Q

What is the Law of Projection?

A

Sensation along an afferent pathway (no matter where it is stimulated) will always go back to the origin

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19
Q

What is nociceptin?

A

Neural process of encoding noxious stimuli

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20
Q

What is hypersensitivity caused by?

A

Increased RESPONSIVENESS of nociceptive neurons to NORMAL INPUT

21
Q

What is hyperaesthesia?

A

Increased sensitivity to stimulation

22
Q

What is hyperalgeisa?

A

Increased pain from a painful stimulus

23
Q

What is allodynia?

A

Pain due to stimulus that does NOT normally provoke pain

24
Q

What are the characterizations of A-delta fibers?

What info does it carry?

A

Myelinated
Faster conduction velocity than C fibers

Carries pain info from MECHANICAL Rs.

Small receptive fields

25
What are the characterizations of the C fibers?
Unmyelinated Slow conduction velocity Activated by CHEMICAL and thermal stimulation Larger receptive field
26
What do C fibers release upon receiving chemical or thermal stimuli?
``` Release: Substanc P Glutamate Aspartate CGRP VIP NO ```
27
What kind of pain is elicited by A fibers? C Fibers? What do these two responses comprise?
A fibers: Sharp and localized C fibers: dull, throbbing, and less localized Bi-phasic response to pain
28
What can nociceptors be activated by?
Mechanical (pressure) Thermal (noxious heat and cold) Chemical (endogenous or exogenous compounds)
29
What is TRPV1? What expresses it? What is it sensitive to? What can it be activated by?
Ligand gated non-selective cation channel C fibers Vallinoid compounds Activated by inflammatory mediators, bradykinin and heat
30
What does activating TRPV1 do? Leading to what?
AP firing Release of Neuropeptide like CGRP, Neurokinins, Substance Leads to vasodilation and activation of immune and other cell types
31
What does the release of pro-inflammatory mediator release by TRPV1 cause?
Potentiation of TRPV1 channel (a positive feedback loop)
32
What kind of pain is TRPV1 involved w/?
``` Migraine Dental pain Cancer pain Inflammatory pain Neuropathic pain Visceral pain OA ```
33
How is TRPA1 activated? What can act thru TRPA1?
Alkyl isothicyanate in mustard oil, wasabi, and horseradish Anesthetics act thru TRPA (A1 sauce - has wasabi in it)
34
What is TRPM8 activated by?
Innocuous cooling Noxious cold Cooling agents (TRMP8 = Temper8)
35
What happens when the Gate is closed in the Theory of Pain?
Inhibitory interneuron is blocking nociceptive pathway Not allowing nociceptive signal to move forward
36
According to the gate control theory of pain, what happens if Pain is sensed?
Gate opens during strong c-fiber activation Allows strong signal to be sent to the brain
37
According to the Gate control theory of pain, How is pain modulated?
Rubbing that spot, activates an A beta fiber To dorsal horn and synapses on an inhibitory interneuron, releases EAA Inhibitory interneuron activated and releases glycine INHIBITS secondary sensory neuron of pain path NO MORE PAIN
38
How do opiates, EAA and cannibinoid work?
``` Opiates, EAA, canniboid —> PAG —> Locus Ceruleus RAphe NUclei —> NE and 5HT to dorsal horn —> Activated inhibitory interneurons —> Local inhibitory interneurons release opiates —> Mu receptors of C Fibers —> Reduction of AP from C fibers —> Reduction of nociception ```
39
What is central sensitization?
Generates post injury pain hypersensitivity via cellular and molecular mechanisms By reducing threshold of dorsal horn neurons to noxious stimulation
40
What is peripheral sensitization?
Neuroplastic changes of PNS
41
What is a key phenomenon of peripheral sensitization?
PGE2 sensitizes peripheral nociceptors, reduces firing threshold, and increases responsiveness
42
What are peptidergic nociceptors? What are they responsive to? What are peptidergic afferents?
Express Neuropeptides like Substance P and CGRP Responsive to nerve growth factors Most are visceral 1/2 of cutaneous are peptidergic
43
What upregulates the neuropeptides released by peptidergic nociceptors?
Chronic inflammation
44
What are non-peptidergic nociceptors? What are its associated afferents?
Do not express neuropeptides Responds to GDNF 1/2 of cutaneous afferents Very few are visceral afferents
45
Where are non-peptidergic nociceptors seen?
Diabetic neuropathy
46
What is S1 and S2 role in pain?
Receive input from nociceptors Play role in localization of pain
47
What is the insular cortex in regards to pain? What does damage to this cortex cause?
Important for interpretation of nociception And processes info about internal state of body Damage = asymbolia
48
What is the amygdala in the pain pathway?
Emotional component to pain
49
What is the hypothalamus and medulla’s role in the pain pathway?
Visceral input travels w/ autonomic nerves to here Integrates physiological changes associated w/ visceral pain