Quiz 1 Flashcards

1
Q

AB fibres

A

found in muscle spindle, 100m/s.

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2
Q

A-delta fibres

A

well localised, first pain, 40m/sec, Sharp, pricking pain

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3
Q

Type 1 pain

A

Pain from chemical or mechanical stimuli

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4
Q

Type 2 pain

A

Pain to thermal stimuli

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5
Q

C fibres

A

Slow second pain, 1-2m/s, dull burning quality

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6
Q

TRPV1 channels

A

Heat and chemical (approx 43 deg), capascin an acid sensiing (H+) V1 cars= hot

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7
Q

TRPM8

A

cold (+0), both noxious and innocuous, menthol M8 its cold

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8
Q

TRPA1

A

cold (-0deg)ad GI tract smooth muscle A for anus

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9
Q

ASIC 1

A

Git smooth muscle, cmustard, garlic, smoke

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10
Q

ASIC 2/3

A

cardiac and skeletal muscle, can be activated by anaerobic metabolism ASCIS is a sport shoe

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11
Q

naV channels

A

influence flow of sodium and therefore influence resting membrane potentials and thresholds.
NaV 1.7- in sympatetic and C fibres, upregulated in inflammatory conditions

Nav 1.8- c fibres, action potential in cold conditions

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12
Q

Nerve growth factor

A

released by macrohages and t lymphocytes
Tyrosine kinase is reeptor
1. binds directly to nociceptors
2. activates mast cells- degranulate- release histamie
3. increase sympathetic sprouting of nerves- increased receptive field

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13
Q

Interneurons

A

Excitatory glutamergic or inhibitory GABA/ glycine

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14
Q

Effects of intracellular Ca2+ on CS

A
  1. Increased Ca2+- activation of kinases- phosphorylate NMDA and AMPA- increased channel open times, quikcer Mg2+ remova, inreaed sensitivity
  2. Ca2+ activates Calmodulin (CaMK)- phosphorylates AMPA and makes modified AMPA receptors that are more efficient and open at loer activation levels
  3. PKC activation reduces effects of GABA and glycine and descending inhibition from PAG
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15
Q

Astrocytes

A

homestasis, neurotransmitter release and uptake, release NO, PGE2 and glutamate in inflammatory conditions

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16
Q

Microglia

A

like macrophages, accumulate in dorsal horn at injured nerve, neurotransmitter/cytokine release, activate in nerve injury, release SP, ATP, glutamate

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17
Q

Spinomesencephallic tract

A

travels to PAG, parabrachial, amydala. Involve in emotional response to pain

18
Q

Spinoreticular tract

A

travels to hypothalmus, ANS, involved in stress and motivaional affective and autonomic centres of pain

19
Q

Thalamus

A

involved in the sensory discriminative and motivational affective part of pain

20
Q

Lateral nociceptive thalamus

A
contains 2 nucle
VPL: nociception from body
VPM: nociception from face
sends info to s1 and S2
Nuclei have lower thresholds during inflammation
21
Q

Medial nociceptive thalamus

A

Recieve input frm SMT and SRT, responds to nociception from all parts of body, wide receptive field, play a role in intensity
Project to limbic system, motivational affective part of the thalamus

22
Q

Lateral pain system

A

refers to the sensory discrimintaroy aspet of pain from s1 and s: localisation, intensity and quality

23
Q

S1 vs S2

A

S1: localisation and intensity of pain
s2: bilateral receptive fields, vague localisation, projections to limbic system therfore emotional

24
Q

Medial pain system

A

refers to everything other than S1 and S2
PAG, amygdala, cingulate cortices, insular cortices
affective and emotional aspects of pain

25
Q

ACC

A

connected to thalamus, involved in attention and escape from pain and emotion

26
Q

Insula cortex

A

awarenss and withdrawal from pain

27
Q

Amydala

A

puts emotions and meaning onto everythig, behavioural adaptations, also has inputs from SMT

28
Q

Lateral nucleus

A

(In amygdala) recieves affective, cognitive and sensory informatoion from thalamus, somatosensory and limbic reas.`

29
Q

Central nucelus

A

recieves processed info from lateral nucleus.
recives info about anixiety and fear
recieves raw information from spinal cord via parabrachial nucleus (pons)
also connectedto PAG, dorsal reticular nucleus, substantia nigra, locus coeruleus and raphe nucleus

30
Q

Rostro-ventral medulla

A

includes nucleus raphe magnus and reticular formation. inhibitory and excitatory function. Shifts ON cells ON.

31
Q

ON cells

A

produce facilitatory impulse that increases glutamate and substance P

32
Q

PAG-RVm axis

A

PAG releases opiods– RVM releases serotonin– serotonin stops transmission of nociceptor signal at dorsal horn, namely c fibre

33
Q

PAG RVM axis influenes

A

influenced by cognition (ACC), emotion (M/ACC), stress (hypothalamus) and fear (amygdala)

34
Q

Diffuse noxious inhibitory control

A

phenomenon whereby pain in one body region can inhibit pain in another body region

35
Q

COnditioned pain modulation

A

tests for diffuse noxious inhibitory control as there is said to be a loss of this in chronic pain. Conditioned stimulus of cold water and test stimulus of thermal/ mechanical pressure. in chronic pain there will be absent or increased sensitity to test stimulus

36
Q

Stress and pain ST

A

ST: Adrenal glands release cortisol- macrophage and SNS activity increased and decreased threshold for inflammatory response-_ macrophages active microglia

37
Q

stress and pain LT

A

chronic release of cortisol= chronic inflammatory response= cytokines producing systemic response = affecting serotonin, adrenaline, opiods

38
Q

Development of widespread pain

A

due to increase in receptive fields and referred pain. and opening of inactive/ adjacent synapses in DH.

39
Q

features of CS pain

A

pain is widespread, allodynia, spontaneous, hyperalgesia, chnages in mood, unrefreshed sleep, poor concentration, fatigue

40
Q

Spinomesencephalic tract and supraspinal descending modulation

A

SMT arises as 2nd order neuron > decussate to anterolateral system > ascend up spinal cord in white matter > terminate at PAG > synapse with descending neuron > descend down MB, decussate at pons > continue down spinal cord in lissaurs tract > terminate at lamina 2 > release Ca > inhibit SP and G from 1 order neuron > decrease pain transmission.