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brain and behaviour > Pain > Flashcards

Pain Flashcards

-learn anatomy and physiology of pain - learn treatment options for pain

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The Brain flashcards
1
Q

how does acute pain occur?

A

activity of nociceptor in response to potentially harmful stimuli

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2
Q

what informations do A-delta and C fibres respectively carry?

A

A-delta fibres: myelinated; first pain, fast, sharp, prickling and well-localised pain
C-fibres: unmyelinated; slow,, dull and diffuse pain

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3
Q

what does mutation in Nav1.7 or TrkA cause?

A

congenital indifference to pain

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4
Q

what information does the anterior spinothalamic tract carry?

A

2nd order neurons carrying input from A-delta fibres (lamina V)

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5
Q

which thalamic nuclei does the anterior spinothalamic tract innervate?

A

VPL and VPM –> somatosensory localisation and intensity of pain
VPI–> secondary somatosensory cortex - cognition and planning

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6
Q

what information does the paleospinothalamic tract carry?

A

2nd order neurons from lamina I with input from C fibres mostly

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7
Q

which thalamic nuclei does the paleospinothalamic tract innervate?

A

mediodorsal nucleus (ventral caudal part) –> anterior cingulate cortex - affective and motivational aspects
medial subnucleus of the posterior group (POm) –> anterior/rostral insular – quality/emotion
these projection bring about the punishing aspects of pain

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8
Q

what is peripheral sensitisation?

A

inflammatory mediators released by damaged tissue make the nociceptors more sensitive to pain and decrease threshold depolarisation - primary hyperalgesia - pain is felt more intensely

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9
Q

what is central sensitisation?

A

prolonged activity of nociceptive afferents increase the excitability of dorsal horn neurons - hyperalgesia
low threshold mechanoreceptors input to second order neurons lead to pain in response to innocuous stimuli - allodynia

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10
Q

what neurotransmitters and receptors are involved in central sensitisation

A
  • activation of Ca2+ channels
  • removal of Mg2+ from NMDA receptor increases its sensitivity to glutamate
  • nociceptors release glutamate substance P, CGRP and BDNF to dorsal form neurons
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11
Q

wha tis chronic pain?

A

pain lasts for more than 12 weeks

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12
Q

how does TENS work?

A

stimulation of non-noxious large afferents (A-beta fibres) activate lamina II inhibitory interneurons which suppresses transmission of neurotransmitters from C fibres to 2nd order neurons and blocks the pain (that’s why rubbing area of injury provides relief)

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13
Q

describe the descending inhibitory control of pain.

A

PAG receive input from nociceptor afferents and act on raphe nuclei and locus coruleus which release 5-HT and noradrenaline. these act on lamina II interneuron which releases enkephalins and GABA to inhibit A-delta and C fibres and dorsal horn neurons.

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14
Q

why does acupuncture work?

A

pain in one area inhibits pain in other areas. painful stimulus activates descending inhibtiory control pathways

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15
Q

which brain structures are involved in the perception of intensity of pain?

A

superior parietal lobe –> insula–> amygdala

  • control cognition and attention
  • amygdala is involved in the labelling of pain as aversive*
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16
Q

which brain structures are involved in the perception of unpleasantness of pain?

A

ACC–> PFC–> PAG

control of emotion

17
Q

what are the three types of pain?

A

nociceptive
inflammatory
neuropathic

18
Q

what is the mechanism of action of morphine (opioids)?

A

acts on mu-opioid receptors to produce analgesia
increase K+ conductance - decreased excitability and decreases Ca2+ influx - decreased neurotransmitter release
-activates descending inhibitory pathways

19
Q

what are the side effects of opioids?

A

respiratory depression, nausea and vomiting, mitosis, euphoria/dysphoria, drowsiness/lethargy
reduced GI motility, constipation, reduced biliary/pancreatic excretions
urinary urgency, itching

20
Q

name other opioids besides morphine.

A

fentanyl sufentanil, methadone, heroin, pentazocine, pethidine, dextromoramide, meptazinol

21
Q

what is the mechanism of action of paracetamol?

A

reduces active oxidised form of COX-2

  • decreases PGE2 induced reduction of glycine inhibition of spinal cord cells
  • may also inhibit endocannabinoids reuptake
22
Q

why is diclofenac contraindicated in individuals in cardiovascular complication?

A

significant COX-2 selectivity - inhibits Prostacyclin formation without inhibiting TXA2 production, risk of clotting (stroke MI)

23
Q

what is the mechanism of action of tramadol?

A

mu-opioid receptor agonist

serotonin and noradrenaline reuptake inhibition

24
Q

what are the side effects of tramadol?

A

itching, nausea and vomiting, sweating, constipation

25
Q

what drugs are used to treat neuropathic pain?

A

anticonvulsants and antidepressants

26
Q

what is the mechanism of action of pregabalin?

A

binds to alpha-2-delta subunit of n-type ca2+ channels and inhibits calcium influx and therefore reduces neurotransmitter (glutamate, substance P, noradrenaline) release

27
Q

what the side effects of pregabalin?

A

drowsiness, headache, dizziness,

confusion, dry mouth, constipation, tremor, peripheral oedema ,

28
Q

how do carbamazepine and phenytoin reduced neuropathic pain?

A

decrease activity of sodium channels - less neuronal excitation

29
Q

what is the mechanism of action of amitriptyline (TCA) in treating pain?

A
  • SNRI –> serotonin and noradrenaline involved in descending inhibitory control
  • acts on NMDA receptor and blocks Na+ and Ca2+ channels
  • also acts against depression and insomnia associated with chronic pain
30
Q

name some local anaesthetics?

how do they work?

A

prilocain, bupivacaine, lignocaine

- block Na+ channels

31
Q

what are the side effects of local anaesthetics?

A

hypotension, respiratory depression, bradycardia

32
Q

name some inhaled and IV general anaesthetics.

how do they act?

A

inhaled: enflurane, isoflurane, sevoflurane, desflurane, halothane, NO and xenon
IV: propofol, etomidate, ketamine

33
Q

what is a side effect of general anaethetics?

A

CV depression

34
Q

what is trigeminal neuralgia?

how does it occur?

A

sudden, paroxysmal attacks pop pain, electric shock like, sharp, stabbing pain in the face
compression, distortion or stretching of Trigeminal nerve fibres by PICA or AICA

35
Q

how is trigeminal neuralgia treated?

A

carbamazepine, phenytoin, sodium valproate –> decrease sodium conductance
baclofen, clonazepam –> positive allosteric modulator of GABAa receptor

36
Q

which opioid drug is active sublingually?

A

dextromoramide

37
Q

which opioid has less risk of respiratory depression?

A

meptazinol

38
Q

which opioid has increasing half life after every administration?

A

methadone

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