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Flashcards in Pain and Thermosensation Deck (35)
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1
Q

what is pain?

A

unpleasant sensory and emotional experience associated with actual tissue damage or described in terms of such damage

2
Q

3 forms of pain?

A

nociceptive (adaptive - immediate protective response, short lived) inflammatory pain (adaptive - assists in healing, lasts days-weeks) pathological (maladaptive - no physiological purpose, lasts months-years-lifetime)

3
Q

pathological pain is defined as what?

A

pain lasting over 3 months with no physiological cause

4
Q

alternative drug classes used as analgesics (often in neuropathic pain)?

A

antidepressants (e.g amitriptyline ) anticonvulsants (e.g gabapentin) local anaesthetics

5
Q

what are nociceptive neurones?

A

primary sensory afferent nerves which can only be activated by intense noxious stimuli (mechanical, chemical or thermal) can also be activated by lesser stimuli in inflammation

6
Q

primary neurotransmitter of nociceptive neurones?

A

glutamate

7
Q

where are terminals of nociceptive neurones found?

A

central terminal in CNS

peripheral terminal in peripheral location

8
Q

subtypes of nociceptive neurones?

A

A delta fibres C fibres

9
Q

describe A delts fibres

A

mechanical/thermal noceiceptors thinly myelinated respond to noxious thermal and mechanical stimuli mediate first or fast pain - lancinating, stabbing, pricking sensations

10
Q

describe C fibres

A

unmyelinated collectively respond to all noxious stimuli (polymodal) mediate second or slow pain - burning, throbbing, cramping, aching sensations

11
Q

why is 2nd pain slower to arise?

A

results from developing inflammatory response so takes time for inflammatory mediators to arise

12
Q

what 3 types of receptor are present at polymodal receptors?

A

mechanoreceptors (mechanical stimuli) heat/cold sensitive receptors (temperature) ASIC, P2X, P2Y, B2 receptors (chemical stimuli)

13
Q

many types of thermal receptors, what are the main family of thermal receptors?

A

transient receptor potential (TRP) family

14
Q

nociceptive pathway?

A

free nerve ending> depolarization > axon > dorsal horn of spinal cord > glutamate released > 2nd order neuron excited > axon crosses over immediately at spinal cord level and ascends spinal cord in spinothalamic and spinoreticulothalamic tracts

15
Q

where is soma of nociceptor neurone found?

A

dorsal root ganglion

16
Q

peptidergic polymodal nociceptors (subtype of C fibres) hhave afferent and efferent functions, describe the afferent function

A

Transmit nociceptive information to the CNS via release of glutamate and peptides (substance P, neurokinin A) within the dorsal horn

17
Q

repeated stimulation of the efferent branch of peptidogergic polymodal nociceptors can result in what?

A

AP is conducted around the terminal branches of the peripheral terminal causing release of peptides - substance P, CGRP

these peptides act as proinflammatory mediators causing inflammation and pain but can also stiulate further APs in the peripheral terminal which travel back to the spinal cord causing perception of pain

= hyperalgesia (slight pain becomes intense pain) and allodynia (pain from non-noxious stimuli)

18
Q

///

A

///

19
Q

course of neurogenic inflammation?

A

peptides released from free nerve ending of peptidergic nociceptor due to tissue damage or inflammatory mediators > SP (peptide) causes - vasodilation and extravasation of plasma proteins promoting formation of bradykinis and prostaglandins - release of histamine from mast cells - sensitises surrounding nociceptors > CGRP induces vasodilation > primary and secondary hyperalgesia and allodynia ensue

20
Q

describe the path of neurotransmission between the primary sensory afferent and 2nd order neurone in the dorsal horn of the spinal cord?

A

AP > opening go voltage gated calcium channels > calcium influx > glutamate release > activation of glutamate receptors > membrane depolarization > ng of voltage gated sodium channels > AP

21
Q

what are the 2 types of glutamate receptor?

A

AMPA

NMDA

22
Q

Action of glutamate on each type of glutamate receptor?

A

AMPA = fast graded e.p.s.p large enough to trigger an AP in the post synaptic cell

NMDA usually blocked by magnesium, when cell is depolarized by AMPA, magneisum moves and opens up NMDA to contribute to synaptic transmission when afferent input is intense (peptides can also remove Mg and cause slight depolarization)

NMDA can allow calcium influx which alters gene transcription in cell causing increased sensitivity to glutamate

23
Q

C fibres path to spinal cord?

A

synapse on most superior part of dorsal horn (lamina 1) on NS cells and interneurone which has cell body in lamina 2, this interneurone synpases on WDR neurone

24
Q

path of A delta fibres?

A

synapse on lamina 1, 2 and directly on WDR neurones

25
Q

path of A beta fibres?

A

loop round and synapse on medial side of laminas 3, 4, and 5

26
Q

paradox of A beta fibres synapse?

A

A beta fibres are non noxious but synapse on same cells (WDR) as fibres carryinf noxious stimuli (A delta and C) brain could get confused

27
Q

what are WDR neurones?

what are A beta fibres?

A

wide dynamic range neurones

recieve input from all 3 types of fibre so respond to wide range of stimuli

A beta fibres carry information about touch

28
Q

visceral pain comes from what actions of the viscera?

A

stretching, twisting, inflammation and ischaemia (not cutting or burning) originates from nociceptors covering tissues (peritoneum, pleura etc)

29
Q

path of visceral pain?

A

visceral afferents follow sympathetic pathways before entering the dorsal horn

30
Q

how can visceral pain be felt as cutaneous?

A

some visceral and cutaneous affernts converge upon the sam spinothalamic neurones in the spinal cord (all cells with a visceral RF also have a separate cutaneous RF)

31
Q

visceral vs viscerosomatic pain?

A

visceral = poorly localised, often associated autonomic features, often referred, consistent viscerosomatic = sharp and well localised, occurs when inflammatory exudate from diseased organ contacts somatic (body wall) structures, pathology may be present with diffuse visceral pain that progresses to sharp viscerosomatic pain

32
Q

pain vs nociception?

A

pain = awareness of suffering, can occur in the absence of nociception or can have nociception with no pain nociception = may occur in the absence of pain, just the conduction of a noxious (or even non-noxious) stimulus

33
Q

describe the gate control theory?

A

physiological gate in spinal cord when open, nociceptive signals can enter dorsal horn and ascend spinal cord if closed, even the most intense stimuli cant enter (no pain felt) whether open/closed depends on the activity of A beta fibres compared to A delta and c fibres - high A beta activity by comparison = closed (explains phenomenon why pain isn’t felt if heavily distracted)

34
Q

where is the “gate” located?

A

substantia gelatinosa

35
Q

how does the gate work?

A

AB synapse on projection neurone which could cause pain, however an earlier branch of AB excites inhibitory interneurone which inhibits action of projection neurone

AD and C fibres also synapse on projection neurone and can cause pain. The earlier branch of these fibres however is inhibitory in nature so inhibits the inhibitory interneurone, so the projection neurone is not inhibited so is therefore excited and pain can be percieved