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NE Exam 2 > Sensory Physiology Pt 2 > Flashcards

Sensory Physiology Pt 2 Flashcards

1
Q

What are the different locations where pain can occur?

A

Somatic or cutaneous pain, muscle, deep or visceral pain

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2
Q

All pain is signaled through nociceptors which are what?

A

A high threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli

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3
Q

What are mechanical modalities of pain characterization?

A

Response to mechanical forces ranging from moderate pressure with a blunt object to overly tissue damaging stimuli

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4
Q

What are chemical modalities of pain characterization?

A

Response to endogenous or exogenous chemical compounds such as pro-inflammatory mediators, acids or capsaicin (pungent ingredient in chili peppers)

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5
Q

What are the thermal modalities of pain characterization?

A

Response to noxious heat and cold will directly activate thermal receptors expressed by nociceptors

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6
Q

What stimuli can activate nociceptors in skin?

A

Thermal (hot/cold), mechanical (cutting, pinching, crushing) and chemical (inflammatory and other mediators released from or synthesized by damaged skin, and exogenous chemical stimuli such as formalin, carrageenan, bee venom or capsaicin)

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7
Q

Which stimuli/modalities can activate nociceptors in joints?

A

Mechanical (torque/rotation beyond the joints normal ROM) and chemical (inflammatory and other mediators released into or injected into the joint capsule)

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8
Q

What stimuli/modalities can activate nociceptors in muscle?

A

Mechanical (blunt force, stretching, crushing, overuse) and chemical

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9
Q

What stimuli/modalities can activate nociceptors in viscera?

A

Mechanical (dissension, traction on the mesentery) and chemical

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10
Q

What is the characteristic cutaneous pain response?

A

Fast pain (sharp) and slow pain (dull, achy, throbbing)

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11
Q

What kind of pain is characteristic of deep pain?

A

Usually dull and achy

Can be associated with muscle spasm

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12
Q

What type of pain is characteristic in muscle?

A

Both fast and slow pain

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13
Q

What kind of pain is characterized in the viscera?

A

Poor localization, very sensitive to stretch (distends ion)

Associated with referred pain

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14
Q

What are the two reasons why we experience referred pain?

A
  1. Brain requires some experience to localize pain; visceral pain is not experienced often enough in early development to train the brain to localize it
  2. Afferents converge in the dorsal horn
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15
Q

What are TRP receptors?

A

Sense noxious stimuli
Family of receptors including TRPVI, TRPAI and TRPM8
Ligand gated non-selective cation channels permeable to Ca, Na and/or K

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16
Q

Describe TRPV1 receptors

A

Ligand: capsaicin (vanilloid compounds)
Can also be activated by endogenous compound such as bradykinin and by heat greater than 43 degrees C
Activation leads to AP and release of neuropeptides
Sustained activation leads to vasodilation and immune cell recruitment and inflammation

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17
Q

What pain conditions is TRPV1 involved with?

A

Migraines, dental pain, cancer pain, inflammatory pain, neuropathic pain, visceral pain and OA

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18
Q

Describe TRPA1 receptors

A

Ligand: allyl isothiocyanate (in mustard oil, wasabi and horseradish)
Involved in number of inflammatory pain states including allergic contract dermatitis, chronic itch, painful bladder syndrome, migraine, IBS and pancreatitis
Anesthetics often have paradoxical pro-nociceptive effects by acting through TRPA1

19
Q

Describe TRPM8 receptors

A

Can be activated by innocuous cooling (26-15C) and noxious cold (15-8C) as well as by a number of cooling agents (topical and otherwise) such as camphor or menthol which are commonly used for their analgesic properties
Ex. Vicks vapor rub, biofreeze, oral B Orajel

20
Q

What are free nerve endings?

A

Axons of nociceptors have lowly conducting unmyelinated (C fibers) or thinly myelinated (A-delta fibers) axons with peripheral terminals that are not associated with specific structures or cell types
Lack specialized receptor cells or encapsulation structures
Characterization can be broken down by various molecular markers

21
Q

What are the two types of free nerve endings?

A

Peptidergic or non-peptidergic

22
Q

Describe peptidergic nociceptors/free nerve endings

A

Expresses neuropeptides substance P (SP) and CGRP (calcitonin gene related peptide)
Most visceral afferents and half of cutaneous afferents

23
Q

What are non-peptidergic nociceptors/free nerve endings?

A

Does not express CGRP or SP neuropeptides
Very few visceral afferents are of this type
Half of cutaneous afferents are non-peptidergic
Involved in somatic chronic pain states such as that of diabetic neuropathy

24
Q

What substances can C fibers release at a synapse as signaling transmitter?

A

EAA (bound to non-NMDA receptors) and SP/CGRP

25
Q

What signaling transmitters do A-delta fibers release?

A

EAA only (bound to non-NMDA receptors)

26
Q

What are nociceptors modulated by?

A

Descending systems (local system or descending inhibition) and interneurons in the dorsal horn

27
Q

What is the local system?

A

Gate control theory of pain (rubbing the spot that hurts to ease the pain) published by Malzack and Wall
TENS unit, phantom limb pain, apuncture

28
Q

What is descending inhibition

A

Dampens input on its way up to the cortex

Ex. Pre-synaptic inhibition

29
Q

In the gate control theory, what happens when the gate is closed?

A

No pain is sensed because the inhibitory interneuron is blocking the nociceptive signal from continuing to move forward
No pain = no signal from C fibers

30
Q

In the gate control theory, what happens when the gate opens (during pain)?

A
  1. Activate an A-beta fiber by normal stimuli. The central process of this fiber branches in the dorsal horn and synapses on an inhibitory interneurons upon which it releases EAA.
  2. The activated interneuron releases glycine and inhibits the secondary sensory neuron of the nociceptive pathway
  3. Rubbing an area of affected skin activates the A-beta fiber and reduces the sensation of pain
31
Q

What is pre-synaptic inhibition?

A

Primary afferent neurotransmission is controlled by pre and postsynaptic inhibitory mechanisms
Probably the more powerful form of inhibitory control in all primary afferent fibers

32
Q

What are the steps of pre-synaptic inhibition?

A
  1. GABAergic associated influx of Cl- into the axon
  2. Results in hyperpolarization
  3. Less Ca enters cytosol
  4. Leads to less NT release
    A diminished excitatory signal
33
Q

What is descending inhibition?

A
  1. PAG are activated by opiates, EAA and cannabinoids
  2. Descending projections travel to locus coeruleus (NE) and raphe nucleus (serotonin)
  3. Serotonin and Ne released into dorsal horn and activate inhibitory interneurons
  4. Local inhibitory interneurons release opiates (like enkephalin)
  5. Opiates activate mu receptors on pre-synaptic (and post-synaptic) terminals of a C fiber
  6. Results in reduction of SP from the C-fiber and reduces nociception
34
Q

What do descending serotonergic and nor-adrenergic neurons lead to?

A

Activate local interneurons

Suppress spinothalamic projection neurons

35
Q

Describe central sensitization

A

Activity dependent synaptic plasticity in the SC that generates post injury pain hypersensitivity together with the cellular and molecular mechanisms responsible for this form of neuronal plasticity
Can be at the level of the SC, higher brain regions or both

36
Q

What are the characteristics of central sensitization?

A 
Reduces threshold of involved neurons to noxious stimuli 
Involves synaptic plasticity (persistent stimulation of EAA receptors like NMDA and intracellular signaling cascades) 
Central inflammation (pro-inflammatory signals from glial cells contribute to neuroimmune activation that can sensitize neurons)
37
Q

What is peripheral sensitization?

A

Neuroplastic changes relating to the function, chemical profile or structure of the PNS that encompasses changes in receptor, ion channel and NT expression levels

38
Q

Describe peripheral sensitization

A

Results in inflammation that develops in injured tissues which sensitize the nociceptor and can increase intensity and duration of pain
Prostaglandins and bradykinin eventually reduce firing threshold and increase nociceptor responsiveness
Thermal sensitivity can increased so that normal body temps activate nociceptors like TRPVI

39
Q

Which two things can cause chronic pain?

A

Central and/or peripheral signals/sensitization

40
Q

Describe the insular cortex

A

Important in interpretation of nociception
Processes information about internal state of the body
Contributes to autonomic response to pain
Integrates all signals related to pain
Damage causes asymbolia

41
Q

The amygdala is important to what?

A

The emotional response to pain

42
Q

A lesion in any single area alters the experience of pain but does not what?

A

Abolish it completely

43
Q

Visceral input travels with autonomic nerves and goes to what?

A

Hypothalamus and medulla, integrating physiological changes associated with visceral pain

NE Exam 2 (19 decks)

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