Pain and analgesics first half of 2 Flashcards

1
Q

Where does peripheral sensitisaiton occur?

A

The primary nociceptive neurons (in the skin etc)

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2
Q

Where in the spinal cord is the first synapse?

A

Most dorsal aspect (lamina 1 or lamina 2)

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3
Q

Which NTs are released from the nociceptive neurons in the spinal cord?

A

Mostly glutamate, also some substance P and a little amount of GCRP

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4
Q

What is CGRP?

A

Calcitonin gene related peptide

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5
Q

Which receptors does glutamate activate?

A

AMPA and NMDA

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6
Q

Which receptor does substance P activate?

A

NK-1 receptor

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7
Q

What type of receptor is NK-1?

A

GPCR

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8
Q

Why is a fast slow time course observed in glutamate transmission?

A

AMPA are fast and NMDA are slow

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9
Q

Which second messenger does NK-1 release?

A

Gq

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10
Q

What does Gq second messenger do regarding PIP2?

A

Breaks down PIP2 into Diacylglycerol (DAG) and inisitol triphosphate (IP3)

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11
Q

What does inositol triphosphate do?

A

Activates calcium stores which leads to an increase in intracellular Ca2+ concentrations

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12
Q

What does DAG do?

A

Activates protein kinase C

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13
Q

What does Gq second messenger do regarding ion channels?

A

Activate Na+, Ca2+ entry ion channels and inhibit K+ exit ion channels–> more depolarisation

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14
Q

What happens if there is a burst of activity from the presynaptic neuron in the spinal synapse part of the pain pathway?

A

The synapse increases in strength over time (i.e. after 11th AP the postsynaptic response is bigger than previous)

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15
Q

What is synaptic plasticity?

A

The strength of a synapse changes over time

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16
Q

Why does the spinal synapse become more sensitive over time?

A

NMDA receptors and NK-1 receptors

17
Q

How is it known that NMDA receptors affect synaptic plasticity?

A

Synaptic plasticity does not occur with AP5 (NMDA agonist) present

18
Q

How is it known that NK-1 receptors affect synaptic plasticity?

A

Synaptic plasticity does not occur with SP antagonist (NK-1 antagonist) present

19
Q

Where in the nociceptive pathway do inhibitory interneurons attach?

A

The dorsal horn projection neuron

20
Q

How are inhibitory interneurons activated in the pain pathway?

A

Offshoots of mechanoreceptors that are in the spinal cord can activate inhibitory interneurons

21
Q

What type of neurons activate inhibitory interneurons in the pain pathway?

A

Glutamatergic

22
Q

What is nursing the injury?

A

Touching an injured part of the body

23
Q

Why do we “nurse an injury”?

A

Touching it activates mechanoreceptors which can cause inhibitory interneurons to be activated, thus inhibiting the pain

24
Q

What is TENS?

A

Transcutaneous electrical nerve stimulation–>An electrical pack that stimulates touch receptors on the skin

25
Why does TENS work?
Activates mechanoreceptors which can cause inhibition of pain
26
Which two types of pathway can inhibit nociception?
Descending inhibitory pathway and ascending inhibitory pathway
27
What is the ascending inhibitory pathway?
Mechanoreceptors causing inhibition
28
What is the descending inhibitory pathway?
Parts of the brainstem, when stimulated, can inhibit pain
29
Which parts of the brain can cause descending inhibitory input?
Periaqueductal grey and raphe nuclei
30
Where does the periaqueductal grey project to in inhibitory input?
The raphe
31
Where does the raphe project to in inhibitory input?
The first synapse in the spinal cord
32
Where in the brain does the periaqueductal grey receive inputs from?
Hypothalamus, amygdala, cortex