PHYS: Somatic Sensations (inc. Pain and Temperature) Flashcards

1
Q

exteroception, proprioception, interoception

A
  • exteroception: info abt external world (mechanoreceptors, thermoreceptors, nociceptors) - type of somatic sense
  • proprioception (kinaesthesis): info abt position of body in space (type of somatic sense)
  • interoception: info re: homeostasis e.g. BP, hunger, thirst (type of visceral sense)
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2
Q

3 ways to activate a mechanoreceptor

A
  • stretch
  • tethered: proteins act as elastic strings, press on ion channels and cause them to open
  • indirect gated
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3
Q

how is a mechanoreceptor activated?

A
  • translation: stimulus causes physical change in receptor shape > change in membrane potential
  • transduction: spike region generates AP if stimulus is large enough
  • transmission: conducting region sends message to brain via AB sensory fibres
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4
Q

how does the location of a skin mechanoreceptor determine its function?

A
  • located deeper (pacinian + ruffini) = bigger receptor field size = more crude/delocalised touch and vibration
  • superficial (merkel + meissner’s) = smaller size = finer touch
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5
Q

meissner’s corpuscle:
- structure
- location
- function
- adaptivity

A
  • barrel-shaped, encapsulated, connected to AB sensory fibres
  • dermal papillae (non-hairy/glabarous skin)
  • fine/light touch
  • rapidly adapting (FAI)
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6
Q

pacinian corpuscle:
- structure
- location
- function
- adaptivity

A
  • onion ring, encapsulated, connected to AB sensory fibres, large RF
  • deep dermis (hairy + non-hairy skin)
  • deep pressure + vibration
  • VERY rapidly adapting (FAII)
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7
Q

merkel’s discs:
- structure
- location
- function
- adaptivity

A
  • small receptive field, unencapsulated, connected to AB sensory fibres
  • upper dermis
  • low frequency vibration (Braille), indentation, pressure, texture, VERY FINE DETAIL
  • slow adapting (SAI)
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8
Q

ruffini endings:
- structure
- location
- function
- adaptivity

A
  • large receptive fields, encapsulated, connected to AB sensory fibres
  • dermis
  • detect stretch/tension
  • slow adapting (SAII)
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9
Q

describe fast vs slow adapting receptors, including their alternative names

A
  • fast (phasic): only fire APs @ onset and offset of stimulus - good for detecting changes
  • slow (tonic): fire as long as the stimulus is present - good for sustained stimuli
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10
Q

types of fast/slow adapting receptors

A
  • FA I (meissners - small RF): only respond @ offset and onset
  • FA II (pacinian - large RF): fire during quick changes
  • SA I (merkel’s - small RF): fire APs throughout duration of stimulus
  • SA II (ruffini - large RF): more sparse APs throughout stimulus
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11
Q

3 types of proprioceptors

A
  • cutaneous mechanoreceptors (Ruffini endings)
  • joint receptors (Ruffini endings + pacinian corpuscle)
  • muscle spindles + Golgi tendon organs
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12
Q

muscle spindles
- structure
- afferent fibres
- efferent fibres

A
  • encapsulated proprioceptive structures containing intrafusal muscle fibres, parallel w/ muscle fibres = muscle stretch causes receptor stretch
  • afferent: stretch detected by type 1a (Aa = fast adapting) and type II (AB = slow adapting) sensory fibres
  • efferent: initiate stretch reflex (muscle contraction) to maintain posture and coordination via gamma motor neurons - e.g. patellar jerk
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13
Q

Golgi tendon organs
- location
- afferent fibres
- efferent fibres

A
  • attached to tendons
  • afferent: type 1B sensory fibres detect muscle stretch (type of Aa fibre)
  • efferent: alpha motor neurons initiate INVERSE stretch reflex (muscle relaxation) to prevent injury and overstretching
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14
Q

why does pain exist (short term and long term)?

A
  • short-term pain = withdrawal from source prevents further damage
  • also a social signal to alert others to danger
  • long-term pain = promotes behaviours e.g. sleep and inactivity = recovery
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15
Q

what are nociceptors?
- what do they detect?
- where are they located?

A
  • FREE nerve endings
  • polymodal: can detect thermal, mechanical, chemical stimuli that are painful
  • located everywhere except CNS
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16
Q

4 types of sensory neuron fibres (lvl of myelination + function)

A
  • Aa: heavily myelinated (proprioception + motor)
  • AB: myelinated (touch, pressure, vibration)
  • Adelta: little myelinated (sharp/fast pain, temperature)
  • C: unmyelinated (temperature, slow pain, itch)
17
Q

how is pain felt as ‘ouch’ vs ‘groan’

A
  • Adelta fibres are myelinated so signals are quicker = quick ouch sensation, readily localised b/c all afferent fibres reach the thalamus and somatosensory cortex (NEOSPINOTHALAMIC - SYNAPSE LAMINA I)
  • C fibres are unmyelinated so signals are slower = groan sensation, more poorly localised b/c fibres end in lower brain regions (PALEOSPINOTHALAMIC - SYNAPSE LAMINA II AND III)
18
Q

2 types of A delta receptors

A
  • mechanical: mediate fast pain response to mechanical stimuli e.g. pin prick
  • thermal: mediate fast pain response to noxious temps, mostly cold
    (both have high threshold b/c only respond to painful stimuli)
19
Q

4 types of C-fibres

A
  • nociceptive (peptidergic and non-peptidergic)
  • silent
  • itch (e.g. histamine)
  • non-nociceptor
20
Q

silent C-fibres

A
  • sensitive to heat but not mechanical stimuli - can be unsilenced by chemical stimuli e.g. capsaicin
21
Q

non-nociceptor C-fibres

A
  • respond to pleasurable touch and cooling stimuli
22
Q

2 divisions of the spinothalamic tract

A
  • anterior: crude touch, pressure, itch
  • lateral: pain, temp, sexual sensations
23
Q

spinothalamic tract pathway

A
  • 1st order sensory neurons synapse w/ 2nd order neurons in the dorsal horn
  • 2nd order neurons decussate contralaterally in spinal cord and synapse w/ 3rd order neurons in thalamus (ventral posterior nucleus) > somatosensory cortex
24
Q

sensory pathway from face and head (trigeminal pain/temp pathway)

A
  • 1st order neurons: three branches (V1, V2 and V3) of trigeminal nerve > synapse w/ 2nd order neurons in spinal trigeminal nucleus
  • 2nd order neurons: decussate in trigeminal lemniscus (brainstem) and synapse in ventral posteromedial nucleus of the thalamus
  • 3rd order neurons: travel via the internal capsule to the primary somatosensory cortex within postcentral gyrus
25
Q

how does sensitisation work during tissue injury?

A
  • nociceptors adapt in response to multiple components of the ‘inflammatory soup’
  • increased chance of activation and electrical activity > hyperalgesia/allodynia
26
Q
  • primary hyperalgesia
  • secondary hyperalgesia
  • allodynia
A
  • primary: pain hypersensitivity in immediate region of injury
  • secondary: pain hypersensitivity in surrounding area of injury
  • allodynia: non-noxious stimuli is perceived as painful e.g. warm water on a sunburn
27
Q

gate control theory

A
  • AB (touch) fibres can inhibit C and A-delta fibres (nociceptive) b/c AB fibres are myelinated = quicker
  • i.e. this is why pain is reduced when you rub the area
28
Q

how do descending pathways inhibit synaptic transmission in the dorsal horn? (pain modulation)

A
  • descending inhibitory neuron releases enkephalin > acts on u-opioid receptors on 1st order neuron coming into dorsal horn
  • reduces release of excitatory neurotransmitters e.g. glutamate to slow pain transmission
  • originates from PAG
29
Q

why does chronic pain (>3 months) occur

A
  • in response to persistent injury, nervous system has increased plasticity > enhanced pain signalling, hypersensitivity and reduction in threshold
  • no physiological purpose unlike acute pain
30
Q

types of pain

A
  • nociceptive: visceral or somatic (deep or superficial)
  • neuropathic: central or peripheral
  • inflammatory: tissue inflammation or hypersensitivity
31
Q

congenital insensitivity vs erythromelalgia

A
  • insensitivity: loss of nav1.7 function
  • erythromelalgia: gain of nav1.7 function (blockage of blood vessels in lower extremities > hyperinflammation)
32
Q

examples of neuropathic pain

A
  • complex regional pain syndrome: develops after injury, surgery, AMI, starts in a limb
  • post-herpetic neuralgia: viral origin e.g. shingles/HIV
  • back/spinal injury
  • diabetic neuropathy
33
Q

which drug blocks NMDA receptor activity?

34
Q

which neurotransmitter is responsible for sensitisation in the dorsal horn?

A
  • glutamate
  • also microglial activation > release BDNF > shift in gradient of pain transmission neurons > more excitability
35
Q

phantom limb pain

A
  • following amputation, nerves that would normally innervate the missing limb can cause pain
  • can arise for peripheral, spinal, central mechanisms
36
Q

referred pain and what might it be caused by?

A
  • when pain in visceral structures radiates to cutaneous areas and sensation arises from body surface
  • may be due to 1st order neurons converging on 2nd order neurons of the same spinal cord region > dorsal horn neurons become hypersensitive > interpreted as coming from the skin
37
Q

thalamic pain

A
  • caused by vascular injury to thalamic neurons (responsible for sensory processing)
  • damaged neurons can initiate excruciating pain signals w/o nociceptive stimulation > referred to contralateral side
  • unresponsive to conventional analgesics so anticonvulsants have to be used
38
Q

DCML pathway

A
  • 1st order – dorsal root ganglion to medulla (decussate here)
  • 2nd order – medulla to thalamus
  • 3rd order – thalamus to primary somatosensory cortex