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Neuroendocrine Test Two > Sensory Physiology Pierce T#2 > Flashcards

Sensory Physiology Pierce T#2 Flashcards

1
Q

Describe Aalpha sensory fiber type.

A

Ia and Ib, they have a large diameter and fast conduction velocity 80-120

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2
Q

Describe Abeta sensory fiber.

A

Fiber type II

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3
Q

Describe Adelta sensory fiber type

A

Fiber type III

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4
Q

Describe C sensory fibers.

A

Fiber type IV small diameter and slow conduction velocity 0.5-2

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5
Q

What are the 4 motor fiber types?

A

Aalpha Agamma B C

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6
Q

What are the two types of skin?

A

Hairy skin or non hairy aka Glabrous

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7
Q

What is receptor adaptation?

A

When stimulus is constant over time the neural response diminishes and sensation is lost over time. It can be rapid adapting or slowly adapting.

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8
Q

What is the difference between slowly adapting and rapidly adapting receptors?

A

Receptors that respond to prolonged and constant stimulation are slowly adapting while receptors that respond only at the beginning or end of the stimulus are rapid and only active when stimulus intensity increases or decreases.

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9
Q

What happens to free nerve endings with diabetic neuropathy?

A

They begin to die off and retract into the dermis so they are no longer innervating the epidermal layers. You can easily damage the epidermis and not feel pain as a consequence.

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10
Q

What are the slowly adapting mechanoreceptors?

A

Ruffini corpusscle Merkel cell Tactile Hair follicle receptor

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11
Q

Rapidly adapting mechanoreceptors?

A

Meissners corpuscle or hair follicle receptor

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12
Q

Very rapidly adapting mechanoreceptors?

A

Pacininan corpuscle

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13
Q

What sensation is associated with a meissner corpuscle, where is it located and what type of receptor?

A

Touch and vibration flutter and tapping. It is a rapid adapting receptor located in glaborous skin.

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14
Q

Sensation, location and receptor type for pacinian corpuscle?

A
  • Rapid indentation of skin with high frequency vibrations
  • Located in hairy and glaborous skin
  • rapid adapting receptor
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15
Q

Sensation location receptor type for ruffini corpuscle?

A
  • Touch and pressure proprioception
  • Found in glaborous skin
  • slow adapting receptor
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16
Q

Merkel cell sensation, location, receptor?

A
  • Pressure
  • found in glaborous skin
  • slow adapting
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17
Q

Hair follicle receptor sensation and receptor?

A
  • Rapid and slow adapting
  • detects motion across skin and directionality of it
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18
Q

Tactile free nerve ending sensation and receptor?

A

slow adapting and detects pain and temperature

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19
Q

What is a receptive field?

A

Areas of innervation where a mechanoreceptor fiber conveys information. Can be large or small.

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20
Q

How do you test the function of the receptive fields? Where is tactile acuity highest and lowest?

A

Through the 2 point discrimination test. There are prongs spaced specific amount of mm apart and you place it on patients skin and ask if they feel one or two prongs touching their skin. If you touch a single receptive field the person will only feel one prong. If you are touching two receptive fields the patient will feel two prongs. The finger tips and lips have the highest acuity as they have the smallest receptive fields. The calf back and thigh have the lowest tactile acuity as they have the largest receptive fields.

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21
Q

Where is the primary somatosensory cortex (S1), what does it do, what info does it receive?

A

Located in post central gyrus. It is the first stop for most cutaneous sensations. involved in integration of proprioception and size shape discrimination

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22
Q

Where is the secondary somatosensory cortex (S2), what does it do, what info does it recieve?

A

Located in wall of sylvian fissure receives input from S1 and has less detailed somatotopic representation than S1. It is involved in cognitive touch, compares btw objects, differnet tactile sensations and determs whether it becomes a memory.

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23
Q

What does the parieto-temporal-occipital association cortex do?

A
  • High level of interpretation for sensory inputs
  • Receives inpupt from multiple sensory areas
  • Analyze spatial coordinates of self
  • Names objects
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24
Q

What is phantom limb pain?

A
  • Pain in a body part that is not actually there
  • Law of projection is most basic principle to this
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25
Q

What is the law of projections?

A

No matter where along the afferent pathway a stimulation is applied the perceived sensation arises from the origin of sensation. Even if there is no longer X body part the pathway the sensation once took is still present and can be stimulated making the brain think there is pain in a limb that doesn’t exist.

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26
Q

What is pain?

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

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27
Q

What is nociception?

A

Neural process of encoding noxious stimuli. Consequences of encoding can be autonomic such as elevated BP or bahavioural suc has motor withdrawl reflex. Pain sensation is not implied.

28
Q

What is hypersensitivity?

A

Increased responsiveness of nociceptive neuron responses &/or recruitment of a response to what would normally be below threshold

29
Q

What is Hyperaesthesia?

A

Increased sensitivity to stimulation, doesnt include special sensess

30
Q

What is hyperalgesia?

A

increased pain from a stimulus that normally induces pain

31
Q

What is Allodynia?

A

Pain due to stimulus that shouldn’t normally provoke pain. For example when you are sunburnt and put clothes on it hurts, but normally getting dressed would not be painful.

32
Q

Which fiber C or Adelta transmit pain faster and why

A

Adelta transmits sharp pain quickly as it is a larger fiber and it is myelinated. C fiber has a small diameter and not myelinated.

33
Q

What is biphasic response to pain?

A

Combination of Adelta and C fibers. The inital response to pain will be Adelta as they are quick to respond as they are myelinated, it will be a sharp quick pain. There will be a second response a few seconds later and this is the C fiber response, they are slower and this pain will be a long throbbing pain

34
Q

What are the four types of pain

A
  • somatic or cutaneous
  • muscle
  • deep
  • visceral

All signaled through nociceptors

35
Q

What are the three stimuli nociceptors respond to?

A
  • Mechanical: response to mechanical forces
  • Chemical: respond to endogenous or exogenous chemicals
  • Thermal: response to noxious heat and cold
36
Q

What pain are joints receptive to?

A
  • Mechanical and chemical pain
37
Q

What kind of pain is muscle pain

A
  • Mechanical pain such as overuse blunt trauma stretching….
  • Chemical such as infflammatory mediators
38
Q

What kind of pain is visceral pain?

A
  • Mechanical something like distension of organs
  • Chemical such as inflammatory mediators or acids
39
Q

What kind of pain is felt with cutaneous pain?

A
  • Biphasic pain
  • fast sharp pain first followed by dull achy throbbing pain
40
Q

Deep pain is described as __.

A
  • Usually dull and achy
41
Q

What kind of pain is felt with muscle pain?

A
  • Both fast and slow pain
42
Q

With visceral pain what kind of pain is felt?

A
  • Poor localization
  • very sensitive to distension
  • associated with referred pain
43
Q

why do we have referred pain?

A
  • The brain needs experience to localize pain, the visceral pain is not experienced enough in early development to train the brain to precisely localize the pain.
  • Afferents converge in the dorsal horn
44
Q

What is TRPV1?

A
  • Activated by Capsaicin, found in chili peppers
  • Also activated by endogenous substances such as bradykinin and heat greater than 43 degrees Celcius
  • Leads to AP and releaase of neuropeptides
  • Sustained activation leads to vasodilation and immune cell recruitment and inflammataion
  • involved in migraine dental pain cancer pain inflammatory, neuropathic, visceral and osteoarthritis
45
Q

What are the TRP receptors?

A

They sense noxious stimuli

  • Ligand gated non selective cation channel permeable to Ca, Na, and K
  • TRPV1
  • TRPA1
  • TRPM8
46
Q

What is TRPA1?

A
  • allyl isothiocyanate found in mustard oil, wasabi, and horseradish, garlic, cinnnamon
  • Involved in inflammatory pain states such as allergic contact dermatitis, chronic itch, painful bladder system, IBS and pancreatitis, migraines
  • Anesthetics have paradoxial pro-nociceptive effects by acting through TRPA1
47
Q

TRPM8

A
  • Activated by innocuous cooling and noxious clod tems and cooling agens such as vics, biofreeze, orajel
  • Mint and Methanol or camphor
48
Q

Free nerve ending s lack specialized receptor cells and encapsulations. They are split into two categories by molecular markers, what are they?

A
  • Peptidergic
  • Non Peptidergic
49
Q

What are peptidergic free nerve endings?

A
  • Express neuropeptides such as substance P or CGRP
  • Most visceral afferents and half of cutaneous afferents are peptidergic
    • Chronic inflammation
    • Visceral pain
    • Chronic inflammation upregulates neuropeptides!
  • Neuropeptides can communicate with other cells and go out into the system
50
Q

What are non peptidergic free nerve endings?

A
  • Doesn’t express CGRP or SP
  • very few visceral afferents
  • Half of cutaneous are non peptidergic
  • Involved in somatic chronic pain states such as diabetic neuropathy
51
Q

If a fiber is releasing Substance P or CGRP what kidn of fiber could it be?

A

C fiber

52
Q

Adelta fibers only release ___,

A

EAA (so glutamate)

53
Q

How are nociceptors modulated?

A
  • Local systems-Gate control theory of pain (when you rub a sore spot to alleviate pain)
  • Descending inhibition- dampening input on way to cortex
    • Pre synatptic inhibitbion is ex.
54
Q

What is the Gate control theory of pain laymens terms?

A

Rubbing spot where it hurts to relieve pain.

It is a signal theory from Melzack and Wall, they believed there was a transmission station in the dorsal horn of sc that influencces transmission to cortex. It acts as a gate and can be open and closed.

  • Phantom limb pain
  • Acupuncture
  • TENS unit
55
Q

Describe the Gate control theory in the absence of pain

A
  • In the absence of C fiber activation (pain), the inhibitory interneuron is tonically active and supresses the pain pathway, it releases glycine which is inhibitory.
  • This results in NO pain being sent to the brain
56
Q

Describe the Gate control theory with pain and how it decreases it.

A
  • With a painful stimuli C fibers inhibit the inhbitory interneurons by releasing Gly onto the interneuron. So the signal is then able to be sent to the brain via EAA being released to the second neuron!
  • In regards to the gate theory when you begin to touch the painful area with NON PAINFUL stimuli the ABeta fiber sends activating activity to the inhibitory interneuron that the C fiber is currently inhibiting. The inhibitory interneuron is partially active and can release a little bit of glycine.
  • This slightly decreases the pain!
57
Q

What is Pre-Synaptic inhibition?

A
  • Most powerful form of inhibitory control in all primary afferent fibers
  • The inhibition is a diminished excitatory signal coming in
    • for ex there are 100 signals entering and you can decrase it by 25, so now there are 75 signals. So the signal only reaches 75 neurons.
  • GABAergic associated influx of Cl- into axon results in hyperpolarization and less Ca+ enters the cytosol. This leads to a decrease in NT release.
58
Q

What is descending inhibition?

A
  • Peri aquaeductal Grey mater is activated by opiates EAA and cannabinoids
  • PAG sends a branch down the spinal cord to LC or raphe nucleus
    • If goes to locus cerulieus it activates a neuron the LC sends neuron to the dorsal horn and releases NE. (Noreadrenergic path)
    • If goes to RN it releases EAA and activates cell body which projects to the dorsal horn and releases serotonin. (Serotonergic path)
  • Both activate inhibitory interneurons to release opoids such as enkephalin
  • opiates activate mu receptors on the pre synaptic side (or post) at the level where C fibers will synapse with secondary neuron
  • Results in reduction of NT reducing nociception
59
Q

What is released from the locus cerileus ?

A

NE

60
Q

What ways do the descending serotonergic and noradrenergic neurons work?

A
  1. Activates local interneurons
  2. Suppresses spinothalamic projection neurons therefore reducing pain intensity
61
Q

Central sensitization?

A

Affects activity at synapse level in CNS along nerve pathways that transmit the nociceptive signals. Can be in SC or higher up in the brain.

  • Impacts synaptic plasticity
  • Reduces threshold of neurons to noxious stimuli, meaning that it takes less signals to induce pain response
  • Proinflammatoru singals from glial cells contribute to neuroimmune activation that senstiizes neurons
62
Q

What is peripheral senzitization?

A
  • Neuroplastic changes related to function chemical profile or structure of the peripheral ns that encompasses changes in receptor ion channel and NT expression levels.
  • The inflammatory mediators can sensitize nociceptor specifically prostaglandin E2 and bradykinin. They will decrease firing threshold and increase responsiveness
  • Thermal sensitivity can be increased that normal body temps induce pain via TRPV1
63
Q

What is the insular cortex imporatant for regarding pain?

A
  • Interpretation of nociception
  • integrates all signals related to pain
  • damage causess asymbolia
64
Q

What is the amygdala imporant for with pain?

A

It is the emotional response to pain

65
Q

Where does pain with a visceral input travel and do?

A

Travels to hypothalamus and medulla with the autonomic nerves integrating physiological changes seen with visceral pain

Neuroendocrine Test Two (15 decks)

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