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Scientific Basis of Medicine > The Case of the Screaming Agony > Flashcards

The Case of the Screaming Agony Flashcards

1
Q

3 types of pain

A

nociceptive, inflammatory, neuropathic

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2
Q

nociceptive pain

A

normal response to real or threatened non-neuronal tissue damage

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3
Q

is nociceptive pain reversible or irreversible?

A

reversible

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4
Q

how do nociceptors transmit pain to dorsal horn?

A

via ad or c fibres

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5
Q

a-delta fibres

A

fast acting and transmit initial sharp pain, some myelin

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6
Q

c fibres

A

transmit slower, dull pain, no myelin

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7
Q

Where are nociceptors located? (5)

A 
skin
joints
connective tissue
muscle
bone
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8
Q

what does visceral pain feel like?

A

diffuse, aching, cramping, poorly localised

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9
Q

autonomic symptoms associated with visceral pain

A

sweating, nausea, vomiting

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10
Q

which fibres transmit visceral pain?

A

which fibres transmit visceral pain?

autonomic fibres so poorly localised

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11
Q

2 types of nociceptive pain

A

somatic and visceral

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12
Q

inflammatory pain

A

pain that signals some type of tissue damage and inflammation

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13
Q

how does peripheral sensitisation happen?

A

inflammatory mediators e.g. cytokines, substance P sensitive local nociceptors and cause exaggerated responses

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14
Q

what happens at sites of tissue damage?what gets released?

A

cytokines, prostaglandins, ATP, H+, bradykinin, NO released, all directly or indirectly activate or sensitise nociceptors

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15
Q

neuropathic pain

A

pain from damage to neurons of either the peripheral or central nervous system

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16
Q

symptoms of neuropathic pain

A

sharp, stabbing, tingling, burning, electric shock; onset of high intensity (Example: phantom pain)

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17
Q

allodynia

A

Pain due to a stimulus that does not normally provoke pain

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18
Q

Hyperalgesia

A

excessive sensitivity to painful stimuli

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19
Q

hyperpathia

A

pain that continues after stimuli removed

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20
Q

what sensory changes does nerve damage cause?

A

sensory loss

increased responsiveness to noxious and innocuous stimuli

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21
Q

what pain mechanisms involved in vascular pain?

A

all 3: neuropathic, nociceptive and inflammatory mechanisms

22
Q

Define pain

A

unpleasant sensory and emotional experience associated with actual or potential tissue damage

23
Q

factors influencing pain

A

factors influencing pain

physiological, social, psychological, pain tolerance, personality, cultural

24
Q

which inflammatory mediators directly activate nociceptors?

A

ATP and H+

25
Q

what stimuli do a-delta fibres respond to?

A

mechanical or thermal stimuli

26
Q

what stimuli do c fibres respond to?

A

mechanical, thermal or chemical

27
Q

2 spinal pathways which carry pain

A

spinothalamic

spinoreticular

28
Q

path of neurons in spinothalamic pathway

A

1st order neurone enters dorsal horn, ascends 1/2 levels in tract of lissaeur, synapses with 2nd order neurone which crosses over, ascends to thalamus

29
Q

2 spinothalamic tracts

A

lateral neo-spinothalamic tract

medial paleo-spinaothalamic tract

30
Q

what is the dorsal horn divided into?

A

Rexed lamina

31
Q

where do c fibres terminate in dorsal horn?

A

substantia gelatinosa aka lamina 2

32
Q

where do a-delta fibres terminate in dorsal horn?

A

lamina 1 and 5

33
Q

The destination of the neospinothalamic tract is ___________.

A

ventral posterior lateral nucleus of thalamus

34
Q

what does Neo-spinothalamic tract carry?

A

sensory-discriminative aspect of pain

35
Q

destination of paleospinothalamic tract is?

A

medial thalamus, hypothalamus and periaqueductal gray

36
Q

where does spinoreticular tract end?

A

reticular formation in the medulla oblangata, pons, and midbrain

37
Q

Where do 3rd order neurons synapse?

A

primary somatosensory cortex, also may project to insula and anterior cingulate cortex

38
Q

Where is the insula and what does it do?

A

deep within the lateral sulcus, deals with visceral nociceptive input

39
Q

where is anterior cingulate cortex and what does it do?

A

around front of corpus callosum, does attention and memory of pain

40
Q

gate control theory of pain

A

theory that if a-beta fibres are activated by mechanical stimuli they activate inhibitory interneurons which stop c fibres transmitting pain (if you press an injury it may stop hurting)

41
Q

where do descending pain inhibitory pathways originate?

A

periaqueductal gray
reticular formation
nucleus raphe Magnus

42
Q

what receptors are expressed in PAG, reticular formation and nucleus raphe Magnus?

A

endogenous opioid receptors

43
Q

how do descending inhibitory pathways work?

A

serotonin and noradrenaline action inhibit substance P and glutamate release at level of dorsal horn

44
Q

what part of pain pathway do NSAIDs work on?

A

nociceptor terminals

45
Q

what part of pain pathway do antidepressants work on?

A

enhance activity of descending inhibition

46
Q

what parts of pain pathway do opioids work on?

A

brain, nociceptor terminals and dorsal horn

47
Q

what neurotransmitter do alpha delta fibres release?

A

glutamate

48
Q

what neurotransmitter do c fibres release?

A

substance P

49
Q

how does central sensitisation work ?

A

prolonged glutamate release causes more NMDA receptor insertion or hyper responsiveness

50
Q

where is the nucleus raphe Magnus located?

A

in rostroventrolmedial medulla

51
Q

how does endogenous opioid system reduce pain?

A

blocks 1st order neurones from releasing NT
stops release of AP from 2nd order neurones
less pain transmission

Scientific Basis of Medicine (35 decks)

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