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Medicine Year 2 > Scenario 26 > Flashcards

Scenario 26 Flashcards

1
Q

Where are the cell bodies of nociceptors?

A

Dorsal root ganglia

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2
Q

What are A delta axons responsible for?

A

Fast sharp pain (myelinated)

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3
Q

What are C fibres responsible for?

A

Slow dull pain (unmyelinated)

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4
Q

What type of stimuli do A delta fibres respond to?

A

Tissue damaging- pressure, extreme heat and cold (mechano nociceptors)

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5
Q

What type of stimuli do C fibres respond to?

A

Thermal nociceptors (45 degrees), Chemically sensitive nociceptors (pH irritants), Polymodal nociceptors (thermal, mechanical, chemical)

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6
Q

What is the gate control theory of the pain?

A

Small interneurons in the dorsal horn acts as a gate which controls the amount of excitement in transmission cells
Gate closed- low pain
Gate open- high pain
non-painful input closes the gates to painful input, which results in prevention of the pain sensation from traveling to the CNS

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7
Q

What regulates the gate control theory?

A

Amount of activity in pain fibres, amount of activity in other peripheral fibres (distraction of Abeta fibres), messages descending from the brain (psychological factors influence pain perception)

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8
Q

What is pain hypersensitivity?

A

If pain systems become too sensitive.

Responsivenedd increased so that noxius stimuli produce exaggerated and prolonged pain- hyperalgesia

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9
Q

What is allodynia

A

Thresholds lowered so that stimuli that wouldnt normally cause pain now begin to

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10
Q

What is hyperalgesia?

A

Responsiveness increased so that noxius stimuli produce exaggerated and prolonged pain

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11
Q

What is peripheral sensitisation?

A

Reduction in threshold and increase in responsiveness of peripheral ends of nociceptors
Due to the action of inflammatory cytokines

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12
Q

What is central sensitisation?

A

An increase in the excitability of neurons within the CNS triggered by a burst of nociceptors activity which alters the strength of synaptic connections

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13
Q

What is the function of Abeta fibres?

A

Discriminative touch

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14
Q

What are the functions of nociceptors?

A

Detect stimuli likely to cause tissue damage

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15
Q

What areas of the brain are involved in the pain matrix?

A

Primary and secondary somatosensory, anterior cingulate, insular and prefrontal cortices plus thalamus

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16
Q

What is a nocebo?

A

sensitisation of pain with a false element (think it hurts but it doesn’t)

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17
Q

What percentage of people live with chronic pain and for how long?

A

19% and for 7 years, 36% have inadequate medication

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18
Q

Does everyone feel pain the same?

A

No huge variation in amount of pain felt and the areas that are activated

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19
Q

What is insensitivity?

A

Small number of people (1 in 1million) dont feel pain, sometimes no sweating and fever but normal touch and motor function

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20
Q

What genes are involves in insensitivity?

A

NGF/trkA- lose all small sensory neurons (no nociceptors)
Nav1.7- no inflammatory behaviour in nociceptors
Gainer function in Nav1.9
Transcription factor

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21
Q

How many people are affected by hypersensitivity?

A

1 in 5000-10000 people

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22
Q

What gene is responsible for hypersesitivity

A

Point mutation to cause a gainer function of Nav1.7

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23
Q

What genes alter the normal variation of pain perception?

A

COMT, GCH,MOR,CGRP

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24
Q

How does the mechanical pain threshold change before and after a stimulus?

A

Threshold reduces both in and outside the burn site (hyperalgesia)- CENTRAL mechanism

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25
Q

How does the central mechanism work?

A

Glial cells respond by releasing cytokines which sensitise post-synaptic receptors and increase release of NT from pre-synaptic neuron
Repetitive C fibre activation can result in wind up

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26
Q

How doe the threshold for for thermal hyperalgesia change in and outside the injury?

A

Hyperalgesia at the site but not outside- PERIPHERAL mechanism

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27
Q

How does the peripheral mechanism work?

A

Receptor modualation from 2nd messenger, channel modulation, gene expression
NGF antibodies block out pain by expression of trkA channels

Prolonged release of inflamm mediators and neuropeptides that affect ion channels reducing the threshold to painful stimuli

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28
Q

When are stimuli processed spinally?

A

After repeated nociceptor activation

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29
Q

What is neuropathic pain?

A

Pain arising as a direct consequence of a lesion or disease of the somatosensory system

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30
Q

What are some examples of things causing neuropathic pain?

A

Infectious (HIV, post-hepatic neuralgia), metabolic/nutritional (diabetic, alcohol), neurotoxicity, trauma, central lesions (spinal cord injury, stroke)

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31
Q

What are the mechanisms in neuropathic pain?

A

Altered CNS processing (central glial cells contribute), altered gene expression (ectopic), retrograde transport of trophic factors

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32
Q

What is antinociception?

A

Blockade of nociception

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33
Q

What is analgesia?

A

Blockage of pain (nociception and its response)

34
Q

What is the diameter of an A delta fibre

A

2-5 micrometres

35
Q

What is the diameter of a C fibre?

A
36
Q

What is the conduction velocity of an A delta fibre?

A

5-15m/s

37
Q

What is the conduction velocity of a C fibre?

A

0.5-2m/s

38
Q

Where are A delta fibres found?

A

Body surface, muscles and joints

39
Q

Where are C fibres found?

A

Most tissues

40
Q

What type of pain is an A delta fibre?

A

Rapid pricking

41
Q

What type of pain is a C fibreq

A

Slow dull aching diffuse

42
Q

Where is the synapse in the dorsal horn of the spinal cord for A delta?

A

Laminae I and V

43
Q

Where is the synapse in the dorsal horn of the spinal cord for C?

A

Lamina II (substantia gelatinosa)

44
Q

What is chronic pain defined as?

A

Pain for more than 3-6 months?

45
Q

What are the two situations for chronic pain?

A

Due to chronic nociceptive action and respond well to opiods

Neuropathic due to adaptive changes and responds poorly to opiods (new pathways formed)

46
Q

What is the mechanism of action of Local anaesthetics

A

Na channel blockers- no AP generation, fairly lipid soluble so can cross the neuronal membrane where it dissociates and the free bade binds to Na channel.
Have a high affinity for inactive NA channels so slow the rate they revert to resting (remain inactivated for longer)

47
Q

What neurones to local anesthetics have the best effect on?

A

Rapidly firing neurones

48
Q

How are local anaesthetic given?

A

Topically or infused near to the nerve needing to be blocked eg epidurally (injected onto dura of spinal cord) or intrathecally (into thecal space

49
Q

What is the mechanism of NSAIDs

A

Inhibit COX which produced ecosaniods (eg PGE2)
Prostaglandins dont stimulate nociceptors they sensitise them to other mediators so NSAIDs produce analgesia by stopping this

50
Q

What are the effects of NSAIDs?

A

Anti-inflammatory, anti-pyretic, analgesic

51
Q

Are NSAIDs central or peripherally active?

A

Peripherally

52
Q

What are some examples of NSAIDs?

A

Asprin (irreversible), ibuprofen (reversible), paracetamol (indirect inhibitor of COX- no anti-inflamm action)

53
Q

What is the mechanism of action of opiod analgesics?

A

Interaction with the endogenous opiod system. Morphine acts on specific receptors called opiod receptors (blocked by naloxone)

54
Q

What do endogenous ligands for opiod receptors have in common?

A

Tyr-Gly-Gly-Phe-Leu/Met in the first 5 AAs

55
Q

What are the three families of opiods?

A

Endorphins (from POMC with MSH and ACTH), enkephalines (prom proenkephalin) and dynorphins (from prodynorphin)

56
Q

What happens when opiod receptors are activated?

A

Cause neuronal hyperpolarisation inhibiting NT release

57
Q

Which peptides are involved in the pathways that alter NT transmission and what do opiods do to them?

A

PAG (project ro raphe magnus), NRM, NRPG

Opiods increase these causing more interference

58
Q

Which laminae are A beta synapses in?

A

3-6

59
Q

What is the ascending pain pathway?

A

activation of the nociceptive primary afferents which enter dorsal horn and synapse onto interneurons and projection neurons. Projection neurons travel to the brain in the spinothalamic tract

60
Q

What affect do opiods have on the asc pain pathway?

A

Opiods inhibit firing and stop the transduction of the signal to the brain and inhibit the release of glutamate and substance P from primary afferents

61
Q

What is the descending inhibitory pathway and what is the effect of opiods?

A

Axons frmo PAG synapse in nucleus raphe magnus and cause descending inhibition the dorsal horn
Activation of PAG and NRM by morphine causes increased desc pathway firing but involves many serotenergic neurons so depeletion of 5HT decreases anti-nociceptive effect of morphine.

62
Q

What are the side effects of morphine?

A

Emesis, constipation, resp depression, cough suppresion, pin point pupils, euphoria, itching (histamine release), hypotension/ hypothermia, gall bladder contraction, tolerance

63
Q

Which substrate is for the mu receptor?

A

Morphine (beta endorphins)

64
Q

Which substrate is for the delta receptor?

A

Enkephalins

65
Q

Which substrate is for the kappa channels

A

Dynorphin

66
Q

What do the activation of all these channels lead to?

A

Increased K conductance, inhibit adenylate cyclase and voltage gated Ca channels

67
Q

What are some examples of mu-agonists (strong opiods)

A

Buprenorphine (partial agonist- less resp depression), diamorphine (more potent), fetanyl (very short acting), methadone (long acting(, oxycodone, pethidine (metabolised quickly- labour and minor surgery, no pin point pupils)

68
Q

What are some examples of weak opiods?

A

Codeine, dihyfrocodeine (nurofen and solpadeine are this and an NSAID), tramadol and tampentadol (less resp depression)

69
Q

What antagonists are used to treat overdose?

A

Naloxone, naltrexone, alvimopam (in gut not brain- opiod induced constipation)

70
Q

How do we treat opiod addicts?

A

Replacement therapy- methadone to prevent relapse and lofexidine to decrease withdrawal signs

71
Q

What are some other miscellaneous drugs?

A

Nitrites for angina (glycerol trinitrite)- veno dilation
Triptans (sumatriptan) for migraine
Na channel blocker for epilepsy for trigeminal neuralgia (cambamazepine)
Tricyclic antidepressants to treat neuropathic pain
Anticonvulsants (pregabalin) for neuropathic pain

72
Q

Why can the placebo effect not be measured correctly in clinical trials?

A

Need to tell them 50% chance of placebo for ethical reasons

73
Q

What is the conscious mechanism for placebo?

A

Expectation of less pain causes dopamine release in nucleus acumbens, increased mu opiod activity and descending pain inhibition (PAG) also anxiety modulation in orbitofrontal region

74
Q

What is the unconscious mechanism for placebo?

A

Classical conditioning- repeated association with the pill and environment etc and the active drug the stimulus alone is able to cause the response without the active drug- dorsolateral prefrontal cortex

75
Q

What is the evidence for classical conditioning in the placebo effect?

A

If conditioning performed by opiods then placebo analgesia by opiod if by non-opiod then analgesia by cannabinoid

76
Q

Other possibilites of placebo response?

A

Spontanous remission, false positive errors, see dr at worst point anyway

77
Q

What is the effect of injecting saline and saying it is a painkiller

A

Same as 6-8mg of morphine

78
Q

If you are told something is a placebo but its active what is the effect?

A

Treatment effect only, more effect when told it is active (+placebo)

79
Q

The larger the difference between the open and hidden administration

A

The larger the placebo component

80
Q

The smaller the difference between open and hidden administration

A

the larger the specific effects of the treatment

81
Q

Do areas with higher cognition have higher placebo effect?

A

Yes

82
Q

Do Alzheimers patients experience the placebo effect?

A

No- need larger doses

Medicine Year 2 (19 decks)

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