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Neuroendocrine Exam 2 > Sensory Physiology > Flashcards

Sensory Physiology Flashcards

1
Q

Describe type Aå fibers

subtypes

diameter

conduction

supplies

A

afferent

Iå and Ib

large

fast (80-120)

1’ muscle spindles, golgi tendon organs

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2
Q

Describe type Aß fibers

subtypes

diameter

speed

supplies

A

afferent

II

smaller than Aå

less than Aå

2’ muscle spindles, skin mechanoreceptors

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3
Q

Describe type Ad fibers

subtype

diameter

speed

supplies

A

afferent

III

smaller than Aß

slower than Aß

skin mechanoreceptors, thermoreceptors, nociceptors

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4
Q

describe Type C fibers

subtype

diameter

speed

supplies

A

afferent

IV

small

slowest

skin mechanoreceptors, thermoreceptors, nociceptors

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5
Q

Describe type Aä (motor) fibers

supplies

A

efferent

extrafusal skeletal muscle fibers

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6
Q

Describe Ay fibers

supplies

A

efferent

intrafusal muscle fibers

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7
Q

Describe type B fibers

supplies

A

efferent

preganglionic autonomic fibers

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8
Q

Describe type C fibers

supplies

A

efferent

postganglionic autonomic fibers

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9
Q

What do Meissner’s corpuscles sense?

Where are they found?

fast or slow adapting?

A

flutter and tapping

glaborous skin

fast adapting (low threshold)

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10
Q

What do Pacinian corpuscles sense?

Where are they found?

Fast or Slow adapting?

A

high frequency vibration

hairy and glaborous skin

fast adapting (low threshold)

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11
Q

What does a Ruffini Corpuscle sense?

Where is it located?

Fast or slow adapting?

A

Mag/Dir. of stretch, touch, pressure, proprioception

hairy and glaborous skin

slow adapting (low threshold)

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12
Q

What does a Merkel cell sense?

Where is it located?

Fast or slow adapting?

A

Pressure

glaborous skin

Slow adapting (low threshold)

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13
Q

What does a hair-follicle receptor sense?

Where is it found?

Fast or Slow adapting?

A

direction and motion across skin

hair follcles

fast and slow adapting

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14
Q

What do tactile free nerve endings sense?

Fast or Slow adapting?

A

pain and temperature

Slow adapting, high threshold

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15
Q

Describe the significance of receptive fields and compare regions of highest and lowest tactile acuity across the body surface in relation to 2pt discrimination

A
  • allows for spatial resolution of detailed textures
  • acuity is highest in fingertips and lips (smallest receptive field
  • acuity is lowest on the calf, back and thigh (largest receptive field)
  • test is used as a diagnostic of peripheral sensory deficits
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16
Q

Compare and Contrast the functions of SI, SII, and the parieto-temporal-occipital association area in sensory perception

SI

A

somatic sensory area 1

primary sensory cortex in post-central gyrus

first stop for most cutaneous senses

somatotopic preservation

crude identification of sense

17
Q

Compare and contrast the functions of SI, SII, and the parieto-temporal-occiptal association area in sensory perception

SII

A

compares sensations between objects and determines if something becomes a memory

technically, it’s an association area located in teh wall of the sylvian fissure (lateral sulcus)

receives input from SI

somatotopic distribution is less preserved

important for cognitive touch

18
Q

Compare and contrast the functions of SI, SII, and the parieto-temporal-occipital assocation area in sensory perception

Parieto-Temporal-Occipital Association Area

A

high level interpretation of sensory input

input from multiple area

analyses space/coordination of self

ID’s objects

large amount of these assocation areas in humans

19
Q

Describe the Law of Projection as it relates to phantom limb pain

A

“Regardless of the place along an afferent pathway that is stimulated, the sensation is perceived to come from the place that the innervation arises”

essentially, if there is a nerve “highway” from your thumb to your brain, anywhere along that highway that is stimulated is telling your brain that it’s coming from the thumb, even if the thumb has been amputated.

20
Q

Is there a difference between Nociception and Pain?

A

Technically, yes.

Pain is an unpleasent sensory/emotional experience with actual or potential tissue damage

Nociception is the neural process of encoding nocious stimuli (can be related to HTN or withdrawal reflex) and pain is not necessarily implied

21
Q

Define hypersensitivity

Define hyperaesthesia

A

increased responsiveness of nociceptive neurons to their normal input and/or recruitment of a response to normally subthreshold inputs

Increased sensitivity to stimulation, excluding special senses

22
Q

Define hyperalgesia

define allodynia

A

increased pain from a stimulus that normally provokes pain

pain due to a stimulus that does not normally provoke pain (shirt on sunburned back)

23
Q

Compare and contrast Ad fibers and C fibers in regards to pain sensation

A

Ad fibers are fast, myelinated, and have small receptive fields, therefore providing precise, localized pain

C fibers are small, unmyelinated and slow and are activated by chemical/thermal stimuli. They comprise most of the fibers carrying nociception, and have a large receptive field, therefore providing a less precise pain localization

C uses substance P, glutamate/aspartate, CGRP, VIP and NO

24
Q

What is the biphasic response to pain?

A

Phase 1: Ad fibers are activated with sharp, localized pain

Phase 2: C fibers are activated with dull, throbbing and diffuse pain

25
Q

Where is TRPV1 found?

What is it sensitive to?

Describe its activation

What type of pain is this receptor involved with?

A

C fibers (ligand gated channel)

capsaicin, bradykinin, heat over 43’C

Activation of TRPV1 leads to AP firing, release of CGRP, Substance P, and as it is sustained, releases more, causing vasodilation and migration of proinflammatory cells causing a feed back loop, potentiating TRPV1 and further nociceptive signaling

Pain from migraines, dental, cancer, inflamation, neuropathic, visceral, osteoarthrtis

26
Q

What activates TRPA1?

What pain is it involved in?

How is it involved in anesthetics?

A

many things, notably allyl isothicynate in mustard oil, wasabi and horseradish

inflammatory pain like allergic dermatitis, chronic itch, painful bladder syndrome, IBS, migraine, pancreatitis

many anesthetics have paradoxical pro-nociceptive effects by acting through TRPA1

27
Q

How is TRPM8 activated?

How is it used as an analgesic?

A

activated by innocuous cooling (15-26’C) and noxious cold (8-15’C) as well as “cooling agents” topical or otherwise such as menthol

these “cooling agents” like menthol are commonly used as analgesias

28
Q

What is the gate-control theory of pain modulation

A

“rubbing a spot that hurts makes it feel better”

this is because the inhibitory interneuron is blocking the nociceptive signal from continuing to move forward; aka the gate is closed

the gate opens during strong C fiber activation

29
Q

Describe the physiology of the gate-control theory of pain

A

activte an Aß fiber by normal stimulus and that fiber goes to dorsal horn and synapses on an inhibitory internueron and releases EAA to activate it

activated interneuron releases glycine and inhibits secondary snesory neuron of nociceptive pathway

rubbbing the sore area activates teh Aß fiber to turn on this pathway and reduce pain

30
Q

Describe descending inhibition

A
  • periaquaductal gray is activated by opiates, EAA, and cannabinoids
  • descending projections then travel to locus cerulisu and raphe nucleus
  • serotinin and NE reelased into dorsal horn and acctivate inhibitoru interneurons
  • these local inhibitory interneurons release opiates (enkephalin)
  • these opiates activate Mu receptors on the presynaptic terminals of a C fiber
  • results in reduction of Substance P from C iber and reduces nociception
31
Q

Describe Central Sensitization

What is it?

What does it cause?

A

generates post-injury pain hypersensitivity, usually caused by chronic exposure to peripheral inflammation

type of activity dependent synaptic plasticity of the spinal cord

  • reduced threshold of dorsal horn neurons to nocious stimuli
  • alters receptors/ion channels, cahnges level of synpatic input produced by afferent fiber
  • receptive feild expands
  • persistent stimulation of EAA, ICCa+ nad other signaling cascades
32
Q

Describe peripheral sensitization

A

neuroplastic changes in receptor, ion channel and NTM expression within the PNS

can increase intensity and duration of pain

at site of inflammation, PGE2 sensitizes nociceptors by activating receptors and reducing threshold and increasing responsiveness of the nociceptors

this PGE2 may come from mast cells, neutrophils, macropahges, T cells after Peripheral nerve injury

noninjured afferents can also become sensitized

33
Q

What is expressed by Peptidergic Nociceptors?

What are they responsive to?

What upregulates them?

A

substance P, CGRP

NGF

chornic inflammation

34
Q

Where are peptidergic nociceptors located?

A

visceral afferents (most of them are this type)

cutaneous afferents (about half)

35
Q

What is expressed by non-peptidergic nociceptors?

What do they repsond to?

Where are they found?

involved in what condition?

A

NOT SP or CGRP

GDNF

very few visceral afferents, half of cutaneous afferents

chronic pain, like diabetic neuropathy

36
Q

Describe the cortical processing and wide spread distribution of nociceptive input in the cortex

SI and SII

A

receive input from nocipceptors and play a role in localization of pain

37
Q

Describe the cortical processing and wide-spread distribution of nociceptive input in the cortex

Insular Cortex

A

Particularly important in interpretation of nociception

process info about internal state

contirbutes to autonomic response to pain

integrates all signals related to pain

damage causes asymbolia

lesions in any single area alters experience of pain, but does not abolish it

38
Q

Describe the cortical processing and wide-spread distribution of nociceptive input in the cortex

Amygdala

A

important in emotional component of pain

39
Q

How are the hypothalamnus and medulla involved in processing pain?

A

visceral input travels with autonomic nerves to the hypothalamus and medulla, integrating physiological changes associated with visceral pain

Neuroendocrine Exam 2 (25 decks)

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