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BB2 > BB2 Revision7 > Flashcards

BB2 Revision7 Flashcards

1
Q

How can neuropathic pain occur due to C-fibre nociceptor pathway malfunctioning? [1]

A

Interneurons (lamina II) can spontaneously become active & fire pain

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2
Q

Specifically, where do axons that transmit pain and form the spinothalamic tract decussate in the spinal cord? [1]

A

Anterior white commissure

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3
Q

Label A

A

White anterior commissure

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4
Q

Which of the folliwng numbers identify where the anterior and lateral spinothalamic tracts run in the spinal cord? [2]

A

5a: lateral spinothalamic tract
5b: anterior spinothalamic tract

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5
Q

Transmission (Anterior Spinothalamic Tract)

Which fibres project within the Anterior STT?

Where does the Anterior STTT project to after travelling up the spinal cord / wheres the third order neurone? [1]

A

Ab, Ad and C fibres

Projects to ventral posterior lateral (VPL) and ventral posterior inferior (VPI) nucleus of the thalamus. (VPL/VPI) on the contralateral anterior STT tract

Third order neurones from VPL/VPI project to the somatosensory cortex (S1 and S2) - Provide exact localisation and physical intensity of noxious stimulus.

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6
Q

Transmission (Lateral Spinothalamic Tract)

Which fibres project within the Lateral STT?

Describe its path

A

Ad and C fibres

Projects contralaterally via LSTT to mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo).

From mediodorsal nucleus of the thalamus (MDvc) innervates anterior cingulate cortex (ACC)

From posterior thalamus (VPI and VMpo) which innervates the rostral insula (unpleasant emotion of pain)

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7
Q

Anterior STT: innervates the [] cortex via []

Lateral STT: innervates the [] & [] via the [] and []

A

Anterior STT
* Innervate the primary and secondary somatosensory cortex via VPL/VPI

Posterior STT:
* Innervates the anterior cingulate cortex and rostral insula via the mediodorsal nucleus of the thalamus (MDvc) and posterior thalamus (VPI and VMpo)

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8
Q

Explain the mechansim of pain modulation at the dorsal horn via the Noradrenaline and serotonin neurons

A

Noradrenaline and serotonin neurons descend from locus coerulus and raphe nucleus respectively & exhibit excitatory repsonse on lamina II neurons

The lamina II neurons present here are inhibitory - so release GABA and ekephalins onto the INCOMING Aδ neurons, which reduces their activity

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9
Q

The unpleasantness (painfull) character of pain is mediated via pain to which are the brain? [1]

A

Limbic systems

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10
Q

Name three types of endogenous opoids and the receptors they can bind to [6]

A

Endogenous opoids:
* endorphins
* enkephalins
* dynorphins

Opoid receptors:
* Mu opioid receptor
* Delta opioid receptor
* Kappa opioid receptor

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11
Q

How does binding of endogenous opiod to opiod receptor inhibit pain? [2]

A

Causes a decrease in Ca2+ release at pre-synaptic terminal

This inhibits release of glutamate and stops pain modulation

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12
Q

How can you modulate pain via Abeta afferents? (e.g. if in pain - rubbing the area might help)

A

Ab afferent from skin also synapse excitably onto lamina II inhibitory cell body, that are used as interneurons from descending pain pathway (from noradrenaline and serotonin)

This causes more inhbitory GABA and enkephalins to be released on INCOMING Aδ neurons, which reduces their activity

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13
Q

Chronic pain

What is allodynia and hyperalgesia?

A

Allodynia: a condition where pain is caused by a non-noxious (non-painful) stimulus (e.g. tickle with a feather).

Hyperalgesia: a condition where an abnormal increased pain sensitivity is caused by a noxious (painful) stimulus (e.g. hot water on sunburn).

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14
Q

Chronic pain

Explain what causes peripheral sensitisation?

A

During injury (esp. inflammation), chemical mediators (i.e. cytokines, H+) can activate nociceptors and activate intracellular signalling mechanism, which can up regulate ion channels, thus increase membrane potential closer to depolarisation threshold.

This makes the sensory primary afferent fibres more sensitive to activation.

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15
Q

Explain what causes central sensitisation

A

Continuous activation of the projection neurones can activate intracellular signalling mechanism, which can up regulate ion channels, thus increase membrane potential closer to depolarisation threshold.

This makes the projection neurones more sensitive to activation.

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16
Q

Peripheral sensitisation

Explain what ectopic and ephatic activation of nocifibres are

A

In peripheral sensitisation:

Ectopic activation: spontaneous activation of fibres causing pain

Ephatic: lateral contact causes generation of AP on neighbouring fibre and cause pain

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17
Q

Central sensitsation of pain

Explain what Abeta fibres collateral sprouting-induced pain is [1]

A

Abeta fibres (which dont normall cause paincan sprout in dorsal horn - which directly activates projection neurons which causes chronic pain

18
Q

What is functional pain? [2]

A

no underlying lesion found despite investigation

pain is disproportionate to the degree of any clinically discernable tissue injury

19
Q

Referred pain

Severe pain down a leg (sciatica) may be caused by a []

Hip problem may give rise to []

Gall bladder pain may be felt in the []

A

severe pain down a leg (sciatica) may be caused by a slipped disk in the back

a hip problem may give rise to knee pain

gall bladder pain may be felt in the right shoulder

20
Q

[] & [] are the most common mental disorders associated with chronic pain.

What are the NTs that are involved in these mental disorders and how do the influence pain? [3]

A

Depression & anxiety are the most common mental disorders associated with chronic pain

Serotonin (5HT) & Norepinephrine (NE); generally suppress sensations of normal bodily functions

Dopamine (DA); modulates pain perception & dampens pain

21
Q

Peripheral sensitization

How does Capsaicin reduce pain?

A

The relief of pain that may follow this topical treatment is thought to be related to the temporary deactivation of heat-sensitive epidermal nociceptors expressing the Transient Receptor Potential Vanilloid 1 (TRPV1)

Capsaicin excites pain and heat rececptors; but then desensitization the receptors and reduces pain

22
Q

Explain the mechanism that causes peripheral sensitisation to pain

A

Primary afferent attracts substance P

Substance P attracts mast cells or neutrophils & releases histamines

Histamines, alongside other chemicals like prostaglandins, ATP, 5-HT, bradykinin

Substance P also dilates the blood vessels

This will excite the pain terminals

The nociceptor terminals become more sensitive to the same quantity of the chemical mediators.

23
Q

What is the physiological effect of the molecule CGRP? [1]

A

CGRP is a highly potent vasodilator

24
Q

Explain how Nav 1.7 sodium channel influences pain

A

When there is an injury, there is receptor potential in the primary afferent and if the potential is big enough it will create an action potential and pain (via Na & Ca2+ channels)

Nav 1.7 sodium channel is a threshold channel because it amplifies the receptor potential of DRG ganglions to reach the threshold for the Nav 1.8 channel found in DRG (which causes AP)

25
Q

Describe the characteristics of primary erythromelalgia [2]

What is the pathophysiology of behind primary erythromelalgia? [2]

A

Primary erythromelalgia is a rare autosomal dominant neuropathy characterized by the combination of recurrent burning pain, warmth and redness of the extremities.

It is a channelopathy (genetic etiology) caused by mutations ofSCN9A, the encoding gene of the voltage-gated sodium channel subtype Nav1.7 - causes the channel to open with less depolarisation
.

26
Q

The difference between central and peripheral sensitization can be identified quite easily. How? [2]

A

The difference between central and peripheral sensitization can be identified quite easily, as peripheral sensitization becomes heat-sensitive whereas central sensitization does not

27
Q

Explain the mechanism of how sensing pain in the face occurs

A

spinal trigeminal nucleus in the lateral medulla of the brainstem

Incorporates sensory information principally from the three extracranial divisions of the trigeminal nerve (V1, ophthalmic; V2, maxillary; V3, mandibular)

The SN projects both contralaterally and ipsilaterally to the ventral posteromedial nucleus of the thalamus (via the ventral and dorsal trigeminothalamic tracts)

This sensory information will be relayed from the thalamus to the primary motor cortex via the primary sensory cortex, allowing response to stimuli of the face

(instead of the DRG, face uses trigeminal nucleus to conduct pain)

28
Q

Which type of receptors is the midbrain periaqueductal gray full of? [1]

Which nuclei does this receptor type influence? [4]

A

Opoid receptors - influences the:

  • parabrachial nucleus
  • medullary reticular formation
  • locus coerruleus
  • raphe nuceli
29
Q

Describe the distribution of endocannabinoid receptors [3]

A

in the pain pathway at the peripheral and central (spinal and supraspinal) levels

in areas of the brain and brainstem nuclei involved in nociceptive perception as thalamus, amygdala, and periaqueductal grey matter.

Both CB1and CB2receptors have been detected in non-neuronal cells participating in immune and inflammatory processes in the proximity of the primary afferent neurons nerve terminals.

30
Q

Explain the main function of the endocannabinoid receptors

A

Activate Via retrograde transmission:

  • Post synaptic neuron sends a message to pre-synaptic neuron to stop release of GABA and glutamate (e..g if GABA activated - will stop release of glutamate)

E.g. Activation of GABA receptor causes release of endocannabinoid, which goes retrogradly (to the pre-synaptic terminal) and decrease release GABA)

31
Q

What is important to consider about the symptoms of depression? [1]

A

symptoms may present differently in people with different ethnic backgrounds raising the issue of how best to assess depression cross-culturally for research purposes

32
Q

Name a scale used to rate depression [1]

A

Hamilton Rating Scale for Depression

33
Q

Which are the brain regions associated with depression? [6]

A

Amygdala
Ventrolateral prefrontal cortex
Dorsolateral prefrontal cortex
Medial prefrontal cortex
Striatal regions (ventral striatum)
Hippocampus

34
Q

Where is the subgenual anterior cingulate cortex ? [1]

How is the subgenual anterior cingulate cortex effected during depression? [1]

What structural implications does this have? [1]

A

Decreased metabolism: significant reduction in glucose consumption

The mean gray matter volume of the subgenual anterior cingulate cortex is reduced

35
Q

Describe a relationship between genetics and environments that causes depression:
What occurs at a higher risk of major depression after significant life events? [1]

A

5-HT transporter polymorphism (impact on 5-HT signalling) is associated with a higher risk of major depression after significant life events

The different alleles may lead to different levels of transcription of the transporter
Therefore, the genetic variation modulates the response to stressful events

36
Q

What is the DMD like in patients with depression? [2]

In which particular areas? [2]

A

Major depression have an increased functional connectivity within DMN

increased connectivity between DMN and fronto-parietal networks: especially left subgenual cingulate area

involved in self-reference thoughts and negative recurrent thoughts = worse :(

37
Q

Neurotransmitter systems associated with mood disorders

Which NT systems are implicated with depression? [2]

A

monoaminergic pathways: noradrenergic and serotonergic

(but not the only players)

38
Q

What happens to the hippocampus during stress in depression? [1]

A

Shrinks

39
Q

Overview of changes to brain during depression [3]

A
  • Decreased cortical thickness
  • Decreased mean grey matter in ACC due to decreased glucose metabolism
  • Volumes of hippocampal white matter decrease in patients with a first episode of depression
40
Q

Between which two areas of the brain have a reduced connectivity in patients of depression who also carry higher active MAO risk alleles? [2]

A

Amygdala–prefrontal connectivity reduced

may affect the course of major depression by disrupting cortico-limbic connectivity.

41
Q

Describe interactions between key structures that involved in depression that cause an increase in depressive ruminations:

Which areas of the brain become hyperactive? [4]

Which areas of the brain become hypoactive

A

Hyperactive:
* amygdala
* hippocampus
* subgenual cingulate cortex
* medial prefrontal cortex

Hypoactive:
* Dorsolateral prefrontal cortex
* ventrolateral prefrontal cortex

BB2 (65 decks)

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