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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
Q

What are the characterizations of the C fibers?

A

Unmyelinated
Slow conduction velocity
Activated by CHEMICAL and thermal stimulation

Larger receptive field

26
Q

What do C fibers release upon receiving chemical or thermal stimuli?

A 
Release: 
Substanc P 
Glutamate
Aspartate
CGRP
VIP
NO
27
Q

What kind of pain is elicited by A fibers?
C Fibers?

What do these two responses comprise?

A

A fibers: Sharp and localized

C fibers: dull, throbbing, and less localized

Bi-phasic response to pain

28
Q

What can nociceptors be activated by?

A

Mechanical (pressure)

Thermal (noxious heat and cold)

Chemical (endogenous or exogenous compounds)

29
Q

What is TRPV1?

What expresses it?

What is it sensitive to?

What can it be activated by?

A

Ligand gated non-selective cation channel

C fibers

Vallinoid compounds

Activated by inflammatory mediators, bradykinin and heat

30
Q

What does activating TRPV1 do?

Leading to what?

A

AP firing

Release of Neuropeptide like CGRP, Neurokinins, Substance

Leads to vasodilation and activation of immune and other cell types

31
Q

What does the release of pro-inflammatory mediator release by TRPV1 cause?

A

Potentiation of TRPV1 channel (a positive feedback loop)

32
Q

What kind of pain is TRPV1 involved w/?

A 
Migraine
Dental pain
Cancer pain
Inflammatory pain
Neuropathic pain
Visceral pain
OA
33
Q

How is TRPA1 activated?

What can act thru TRPA1?

A

Alkyl isothicyanate in mustard oil, wasabi, and horseradish

Anesthetics act thru TRPA

(A1 sauce - has wasabi in it)

34
Q

What is TRPM8 activated by?

A

Innocuous cooling
Noxious cold
Cooling agents

(TRMP8 = Temper8)

35
Q

What happens when the Gate is closed in the Theory of Pain?

A

Inhibitory interneuron is blocking nociceptive pathway

Not allowing nociceptive signal to move forward

36
Q

According to the gate control theory of pain, what happens if

Pain is sensed?

A

Gate opens during strong c-fiber activation

Allows strong signal to be sent to the brain

37
Q

According to the Gate control theory of pain, How is pain modulated?

A

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
Q

How do opiates, EAA and cannibinoid work?

A 
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
Q

What is central sensitization?

A

Generates post injury pain hypersensitivity via cellular and molecular mechanisms

By reducing threshold of dorsal horn neurons to noxious stimulation

40
Q

What is peripheral sensitization?

A

Neuroplastic changes of PNS

41
Q

What is a key phenomenon of peripheral sensitization?

A

PGE2 sensitizes peripheral nociceptors, reduces firing threshold, and increases responsiveness

42
Q

What are peptidergic nociceptors?

What are they responsive to?

What are peptidergic afferents?

A

Express Neuropeptides like Substance P and CGRP

Responsive to nerve growth factors

Most are visceral
1/2 of cutaneous are peptidergic

43
Q

What upregulates the neuropeptides released by peptidergic nociceptors?

A

Chronic inflammation

44
Q

What are non-peptidergic nociceptors?

What are its associated afferents?

A

Do not express neuropeptides

Responds to GDNF

1/2 of cutaneous afferents
Very few are visceral afferents

45
Q

Where are non-peptidergic nociceptors seen?

A

Diabetic neuropathy

46
Q

What is S1 and S2 role in pain?

A

Receive input from nociceptors

Play role in localization of pain

47
Q

What is the insular cortex in regards to pain?

What does damage to this cortex cause?

A

Important for interpretation of nociception

And processes info about internal state of body

Damage = asymbolia

48
Q

What is the amygdala in the pain pathway?

A

Emotional component to pain

49
Q

What is the hypothalamus and medulla’s role in the pain pathway?

A

Visceral input travels w/ autonomic nerves to here

Integrates physiological changes associated w/ visceral pain

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