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Year 3 Exam 2 > Pain > Flashcards

Pain Flashcards

1
Q

What chemical activates B2 receptors on nociceptors?

A

Bradykinin

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2
Q

What chemical activates prostanoid receptors on nociceptors?

A

Prostaglandin

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3
Q

What chemical activates P2X receptors on nociceptors?

A

ATP

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4
Q

What activates TRPV1? [4]

A

pH<5.5
Heat>43 degrees C
Capsaicin (chilli)
Allyl isothiocyanite (wasabi, mustard)

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5
Q

How is an action potential generated in nociceptors?

A
  1. Trauma causes the release of chemical mediators e.g. bradykinin, prostaglandin, ATP, protons etc…
    2a. ATP activates the P2X receptor leading to depolarisation
    2b. Protons activate ASIC also leading to depolarisation.
    2c. TRYPV1 becomes activated and also contributes to depolarisation
    2d. Bradykinin activates B2 receptors causing PKC activation which then causes phosphorylation of TRPV1 …
    2e. Prostaglandins activate prostanoid receptors which stimulate PKA activity, PKA contributes to phosphorylation of ion channels and further contributes ot depolarisation
  2. Once enough depolarisation has occurred, this triggers the opening of voltage gated sodium channels, resulting in action potential generation
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6
Q

Is nociceptor A myelinated?

A

Yes

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7
Q

Is nociceptor C myelinated?

A

No

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8
Q

Which nociceptor is responsible for first pain?

A

A gama

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9
Q

Which nociceptor is responsibe for second pain?

A

C

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10
Q

What is first pain?

A

Intense, quick pain that occurs soon after the painful event.

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11
Q

What is second pain?

A

Duller, longer lasting pain that occurs some time after the painful event has occurred.

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12
Q

Where do ascending pathways originate?

A

Nociceptor fibres where trauma occurs.

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13
Q

Where do descending pathways originate?

A

The brain

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14
Q

What NT is present in ascending pathways?

A

Glutamate

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15
Q

What NTs are present in descending pathways?

A

5-HT and NA

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16
Q

Are the ascending pathways excitatory or inhibitory?

A

Excitatory

17
Q

Are the descending pathways excitatory or inhibitory?

A

Inhibitory

18
Q

Loss of activity in which sodium channel results in no feeling of pain?

A

NAv 1.7

19
Q

Where on the spinal cord do pain fibres from nociceptors enter? [generally=

A

Dorsal horn

20
Q

Which laminae do pain fibres A delta enter the dorsal horn at?

A

1 and 5

21
Q

Which laminae do pain fibres A beta enter the dorsal horn at?

A

3, 4 and 5

22
Q

Which laminae do pain fibres C enter the dorsal horn at?

A

1 and 2

23
Q

What are the 4 processes of nociception?

A

Detection
Transmission
Perception
Modulation

24
Q

What areas of the brain are activated during the perception stage of nociception?

A

Reticular system, somatosensory cortex, limbic system

25
Q

What information is processed by the somatosensory cortex in the perception stage of nociception?

A

Location and intensity

26
Q

What is the gate control theory of nociception?

A

The theory that there are ‘gates’ in the spinal cord that can either increase or decrease the pain signal before it reaches the brain.

27
Q

What are the four opioid receptors?

A

DOR
MOR
KOR
ORL1

28
Q

What kind of receptors are opioid receptors?

A

GPCRs

29
Q

What can cause neuropathic pain? [5]

A
  • Stroke
  • Multiple sclerosis
  • Diabetic neuropathy
  • Shingles
  • Traumatic/surgical amputation
30
Q

Why are gabapentin and pregabalin effective at treating neuropathic pain?

A

They are thought to bind to voltage gated calcium channel α2δ subunit and reduce neurotransmitter release

31
Q

Why are amitriptyline and desipramine thought to be effective at treating neuropathic pain?

A

They potentiate descending inhibition by modulating 5-HT and NA levels.

32
Q

Why is ketamine thought to be effective at treating neuropathic pain?

A

It is an NMDA receptor blocker (glutamate sensitive receptor, inhibits ascending pathways)

Year 3 Exam 2 (19 decks)

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