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BSO6 Neuro > Workshop 8 > Flashcards

Workshop 8 Flashcards

1
Q

Pain Def

A

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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2
Q

Peripheral Sensation

A

abnormally increased input to the spinal cord

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3
Q

Nociceptors

A

peripheral sensory neurons that detect potenially damaging stimuli

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4
Q

External nociceptors

A

found in tissues, skin, corneas, mucosae

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5
Q

Internal Nocicpetors

A

various organs, mm, joints, viscera

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6
Q

C-Polymodal=C fibres

A

most numerous type
Unmyelinated, slow conducting 2m/second
prolonged burning, aching

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7
Q

Ao Nociceptors

A

thinly myelinated, rapidly conduction 20m/secomd
brief, sharp, stabbing

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8
Q

Somatic Nociceptive Pain characteristics

A

Intermittent
Sharper on Movement, duller at rest
Local to injury
Proportionate to the injury
Proportionate to aggravating and relieving factors

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9
Q

Nociceptors:

A

smallest unmyelinated or lightly myelinated primary afferent nerve fibres

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10
Q

Spatial Summation

A

signals coming from multiple simultaneous input

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11
Q

Temporal Summation

A

summation comes from repeated input

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12
Q

Visceral Nociceptive Pain

A

often diffuse
poorly localised

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13
Q

Visceral Nociceptive Pain- Spatial Summation?

A

large area is stimulated, pain theresold is lowered

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14
Q

Neuropathic Pain def

A

lesion caused by a lesion of the somatosensory Nervous System

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15
Q

Causes of Neuropathic Pain

A

trauma, infection, ischaemia, neoplasia, chemical/drug induced

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16
Q

Central Neuropathic Pain

A

caused lesion or disease of the central somatosensory nervous system

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17
Q

Peripheral Neuropathic Pain

A

caused by a lesion or disease of the peripheral somatosensory nervous system

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18
Q

Neuropathic Pain characteristics

A

constant, intense
Associated positive or negative sensory symptoms
Associated autonomic findings
often aggravated by emotional, stress or sleep related triggers
Very difficult to manage
Responds poorly to typical analgesics
Responds better to neural modulators

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19
Q

Stages in Pain Perception

A

1: Transduction: noxious stimuli are converted into electrophysiological activity
2: Conduction: action potential travels to the dorsal horns of the spinal cord
3: Transmission: info is relayed via spinal cord, to brainstem & thalamus
4: Modulation:
Involves both excitatory and inhibitory mechanisms
5: Perception: Cortex finally registers the modulated sensation of pain
6: Supraspinal Responses: Connections b/w the thalamus and higher cortical centres control perception and integrate the affective responses to pain

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20
Q

Transduction

A

Conversion of Noxious Stimuli into the action potential

Nociceptor Stimulation creates an ion reflux via gated channels

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21
Q

Stages of Transmission

A

Central processes of the nociceptors enter the spinal cord via dorsal roots where they synapse with 2nd oorder neurons in the dorsal horn

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22
Q

Major Pathway involved in the Transmission process

A

Spinothalamic Tract, originated in Rexed laminae 1 and 5-7

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23
Q

Role of Lamina 1 cells

A

Project to the posterior part of the ventromedial nucleus of the thalamus and mediate the autonomic/unpleasant emotional perception of pain

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24
Q

What direction do STT axons cross?

A

Locally and ascend Contra-lateral

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25
Q

Modulation

A

Descending axons from the brainstem synapse in the dorsal horn and modulate nociceptive transmission

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26
Q

Non-Noxious Stimuli?

A

can inhibit ascending pain signals
such as touch/pressure carried by Alphabeta fibres

27
Q

TENS?

A

Transcutaneous Electrical Nerve Stimulation, touch a pressure due to Alphabeta fibres, analgesia achieved by rubbing an affected

28
Q

Perception involves

A

Primary/Secondary Somatosensory Cortices

29
Q

Anterior Cingulate Cortex

A

implicated in several complex cognitive functions, such as empathy, impulse control, emotion, decision-making

30
Q

Insular Cortex

A

responsible for sensory processing, decision-making and motor cortex

31
Q

Modulation of Pain/Perception

A

Nociceptive info is transmitted to brain via spinothalamic

Ascending info can activate info can activate descending pathways from the mid-brain periaqueductal grey area

Exert an inhibitory control over dorsal horn neurons

32
Q

Descending Pain Mechanisms:

A

brainstem plays a crucial role in the modulation of pain processing at the spinal cord levels

Pathway orginaitng in the cortex and thalamus are relayed via the medulla and adjacent areas to the dorsal horn of the spinal cord

33
Q

Brainstem receive afferent input from the

A

superficial dorsal horn
PAG
Nucleus Tractus Solitarius
Parabrachial Nucleus

34
Q

Neurotransmitters Descending Pathways

A

Serotonin, Noradrenaline and endogenous opiods

35
Q

Gate Control Theory

A

Open gate: pain is transmitted
Central Control trigger is inactive allowing the gate remain open
Activity of the A-delta & C fibres produces stimulation that opens the gate in the spinal cord

36
Q

Proximally Mediated Gate Closure

A

Central control trigger is active, sending messages from the brain to close the gate in the spinal cord

eg. Distraction, relaxation causes the gate to close, decreasing the perception

37
Q

Peripherally mediated gate closure

A

Activity in the Alpha Beta Fibres produces inhibition closing the gate in the spinal cord
eg. Stimulation of touch sensors (alpha-beta fibres) in the skin by rubbbing

38
Q

Peripheral Sensitisation defin

A

increased responsivenss and reduced thresold of PNS nocicpetive neurons to the stimulation of their receptvie fields

39
Q

Due to the Peripheral Senstation

A

injury of the mast cell,s macrophages, neutrophils release a mixture of pro-inflammatory substances

40
Q

injury of the mast cells macrophages, neutrophils release a mixture of pro-inflammatory substances results in

A

increased efficacy of tranducting ion channels
reduced firing th of voltage-gated channels
an exaggereted responses following activation of these channels

Exaggerated responses following activation of these channels

activation and sensation of peripheral nociceptors occurs

41
Q

Brain Plasticity/ Central Sensitiation def

A

Central sensitation decrisbes the changes that occur in the brain in response repeatednerve stimulation

42
Q

Repeated Nerve Stimulation causes

A

neurotransmitter levels and the brain electrical signals change as neurons develop a memory

43
Q

increased responsiveness of nocicpetors in the CNS to either normal or sub-threshold afferent input resuts in

A

Hypersensitivity to stimuli (HYPERALGESIA)
Responsiveness to non-noxious stimuli (ALLODYNIA)
Increased output to nociception
Expanded receptive field: ie increased pain respone evoke by stimuli outside the area (2nd Hyperalgesia)

44
Q

Allodynia

A

Pain due to stimulus that doesn’t normally provoke pain

45
Q

Hyperalgsia

A

Perception of a painful stimulus as more painful than normal
caused by peripheral/central senstiation

46
Q

Hyperalgsia

A

Perception of a painful stimulus as more painful than normal
caused by peripheral/central senstiation

47
Q

Hyperparthia

A

painful syndrome characteries by an abnormal painful reaction to a stimulus espically a repetitive stimulus as well as reduced thershold

48
Q

Dysasesthia::

A

Unpleasant abnormlal sensations

49
Q

Central Sensitiaton

A

increases responsivenss to nociceptive neurons in theCNS to their normal or sub-thershold afferent input

50
Q

Peripheral Sensitisation

A

Increased responsivenss and reduced threshold of nociceptive PNS neurons to the stimulation of their receptive field

51
Q

Analgesic Strategies that target following aspects of pain include

A

Transduction-inhibtion of nocicpetor activation

Conduction/Transmission- inhibition of nocicpetor activation

Modulation-inhibition of CNS neurons

Perception: inhbitons of CNS neurons

52
Q

Analgesic Drugs

A

Anti-Inflam(Non-Sterodial anti-inflammaotry drugs, Corticosteroids)
Opioids
Paracetamol
Antiepileptics
Antidepressants

53
Q

NSAIDS what are they

A

inhbiit prostaglandin synthesis by inhibiiting cycclooxygenase(COX) key enzyme in inflammatory cascade

54
Q

NSAID Actions

A

anti-inflammatory
analgesic (treatment of mild-moderate)
anti-pyretic
anti-platelet aggregation
duration of action 6-8hr

55
Q

Opioids definitions

A

agonists of central and peripheral receptors which are located on the cell membranes of neurons

56
Q

where opioid receptor cell membrane located in the Cns and PNS

A

CNS: Brain and Spinal Cord
PNS: mytenteric plexus and submucos plexus in the wall of the gut
Peripheral Sensory and Autnomic nevers

57
Q

Glucocorticoids def

A

synthesised in the adrenal cortex manufactured as a pharmaceutical.

58
Q

Glucocorticoids effects

A

immediate vasodilation

59
Q

Glucocorticoids function

A

reduce pain by inhibiting prostaglandin synthesis which turn in reduces inflammation
useful in arthritis

Reduce spontaneous discharge in injured nerves hence thier use in the treatment of neuropathic pain

60
Q

Where are Glucocorticoids receptors

A

neuron membranes on the CNS/PNS

61
Q

Most Commonly prescribed corticosteroid for pain

A

Dexaemthasone

62
Q

Gluocorticoid reduced pain by

A

down-regulation the expression of pro-inflammatory proteins, prostaglandins

Up-regulating the expression of anti0inflmmatory proteins

63
Q

Paracetamol works on mainly?

A

CNS

64
Q

Mainly on the CNS it induces?

A

COX inhibition which reduces prostaglandin synthesis
Activation of descending sertonergic, opioid, nitric oxide and cannabinoid pathways

BSO6 Neuro (9 decks)

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