BMS11004 WEEK 11 - TUESDAY Flashcards

pain, nociceptors, afferent fibres, tracts

1
Q

define specificity theory

A

pain is a distinct sensation, detected/transmitted by specific receptors to distinct brain area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define convergence theory

A

pain is integrated, plastic state represented by pattern of convergent somatosensory activity within distributed network (neuromatrix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what type of fibre (a, b, y) are lightly myelinated nociceptors, what modality are they, how fast

A

Aδ (alpha delta)
fast (20m/s)
mechanosensitive, mechanothermal-sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what type of fibre (a, b, y) are unmyelinated nociceptors, what modality are they, how fast

A

C fibre
slow (2m/s)
polymodal= mechanical, thermal, chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

when are nociceptors most easily demonstrated

A

in heat response- find afferent whose activity correlate with pain perception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what fibre types mediates fast pain

A

sharp, immediate
mimicked by direct stimulation of Aδ (delta) fibre nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what fibre types mediates slow pain

A

diffuse, delayed, long-lasting
mimicked by stimulating C fibre nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when you cut yourself, what nociceptors activate

A

first sharp pain = Aδ
replaced by long dull pain = C fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are molecular pain receptors

A

specific molecular receptors associated with nociceptive nerve endings and activated by heat, hot chillis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

capsaicin receptor (TRPV1) is a specific molecular receptor. describe what fibres it is activated in, how

A

activated in nociceptive Aδ and C fibres at 45c by capsaicin (vanilloid, active component in chilli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

name the 2 ways that molecular receptors can respond in pain

A

responds to heat directly and fire
capaicin can bind and cause it to fibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

name the 2 components of central pain pathways

A

sensory discriminative - signals location, intensity, stimulus type (involve spinothalamic tract)
affective motivational- signal unpleasant, enables fight/flight autonomic response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is spinothalamic tract also known as

A

anterolateral system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

explain topological maps of pain

A

topologically represented in cortex, region responding to painful stimulus and response correlates to pain intensities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

explain what brain areas are linked to affective-motivational response to pain

A

insula, cingulate cortex (limbic system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

explain topographical maps of affective-motivational pathway, and locations

A

little mapping
share pathways with anterolateral system
neurons in paracrachial nucleus respond from any body surfaces

17
Q

what is hyperalgesia

A

increased response to painful stimuli (hypersensitivity of damaged skin to normally tolerable pain stimulus eg: pin prick)

18
Q

what is allodynia

A

painful response to normally innocuous stimulus (painful sensitivty of subburnt skin to brush)

19
Q

what is hyperalgesia due to, and peripheral effects

A

lowered nociceptor threshold
damaged tissue releases inflammatory substances, affecting nerve function, attract mast cell, neutrophils, increase blood flow

20
Q

what are prostaglandins (inflammatory response in hyperalgesia)

A

lower threshold for AP generation
in analgesic painkillers

21
Q

what is hyperpathia

A

variant of hyperalgesia/allodynia
due to fibre/axonal loss/damage
cause raised detection threshold, when exceeded causes explosive pain
can occur when central pathway damaged- shingles, diabeters, MS, stroke

22
Q

when is neuropathic pain experienced

A

post amptutation

23
Q

what can phantom limb pain suggest regarding central representations

A

illusion of limb being present
suggest central representation of body isnt passive, and occur when born without limb suggesting central map pre-formed

24
Q

what is referred pain

A

due to damage in viscera, perceived as coming from specific location according to location of organ eg: heart attack in shoulder
reflect convergence of visceral afferent onto pathway as cutaneous afferent in CNS
useful in clinical diagnosis

25
Q

what does stimulation of PAG do

A

activates brainstem nuclei modulating activity in dorsal horn neurons
activating enkephalin releasing interneurons, presynaptically inhibiting nociceptive fibres

26
Q

why does rubbing injury (modulation) work

A

locally inhibit mechanoreceptive (A-beta fibres) of nociceptive (C fibres) in spinal cord
suggests pain perception due to integration of convergent sensory info