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Pain Flashcards

1
Q

What is pain?

A

An unpleasent sensory and emotional experience associated with real or potential tissue damage, or described in terms of tissue damage.

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2
Q

What are the types of pain?

A
  • Fast, stabbing pain: Result of Aδ fibres due to faster conduction velocities.
  • Slow, burning pain: Result of C fibres with lower conduction velocities.
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3
Q

What are the types of spinal cord neurones that respond to pain?

A
  • Lamina I neurones only receive inputs from nociceptive fibres and only respond to pain so are known as narrow dynamic range (NDR) cells.
  • Lamina V neurones receive inputs from both nociceptive and somoatosensory fibres so respond to touch at low stimuli intensities and pain at high intensities, so are know as wide dynamic range (WDR) cells.
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4
Q

What are the main areas of the cortex that respond to pain?

A
  • Somatosensory cortex: Involved with the sensory component of pain detection.
  • Anterior cingulate cortex (ACC): Part of the limbic system involved with mediating emotional response to pain. Also involved with empathetic pain (pain caused by seeing other people in pain).
  • Insula: Involved in homeostasis and so forms part of the homeostatic response to pain.
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5
Q

Which areas of the brain give descending fibres involved in gate-control of pain?

A
  • Periaqueductal grey (PAG)
  • Raphe nucleus
  • Nuclei of rostral medulla
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6
Q

What is nociception?

A

The neural process of encoding noxious stimuli

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7
Q

What channels are associated with noxious heat?

A
  • TRPV1
  • TRPV3
  • Anoctamin 1 (ANO1)
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8
Q

What channels are associated with noxious cold?

A
  • TRPM8
  • TRPA1
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9
Q

What channels are assciated with protons?

A
  • ASICs (acid-sensing ion channels)
  • TRPV1
  • TASKS
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10
Q

What channels are associated with noxious mechanical stimuli?

A

Peizol 1/2 (possible TRPV4, ASICs)

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11
Q

What channels are associated with noxious ATP?

A

P2X3

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12
Q

What are external noxious stimuli?

A
  • Mechanical
  • Temperature
  • Chemical
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13
Q

What are internal noxious stimuli?

A
  • ATP
  • Bradykinins
  • Acid
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14
Q

What is the pain threshold for heat?

A

~42o

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15
Q

What are the types of pain sensitisations?

A
  • Allodynia: Reduction in pain threshold
  • Hyperalgesia: Same intensity of stimuli causes more pain
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16
Q

What are the important sensitisation factors?

A
  1. NGF
  2. PGE2
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17
Q

What is the general process of pain sensitisation following tissue injury?

A
  1. When stimulated, nociceptor endings themselves release pro-inflammatory substances such as CGRP (calcitonin gene-related product) and SP (substance P).
  2. These chemical mediators cause vasodilation and increased permeability of blood vessels in area of injury.
  3. These chemicals also cause degranulation of mast cells, releasing histamine amongst other pro-inflammatory mediators
  4. Amongst these inflammatory mediators are prostaglandin E2 (PGE2) and nerve growth factor (NGF)
  5. PGE2 and NGF cause sensitisation of local tissues to pain.
18
Q

How does PGE2 cause pain sensitisation?

A
  1. EP4 expression in nociceptive fibres is up-regulated during inflammation.
  2. It is a GPCR that binds to PGE2.
  3. Associated αs subunit activates PKA that phosphorylates ion channels such as Navs, decreasing firing thresholds for nociceptive fibres.
19
Q

What are the main classes of analgesics?

A
  • NSAIDs
  • Opioids
20
Q

What is the mechanism of action of NSAIDs?

A

Inhibits COX enzymes, and thus disrupts production of PGE2 which is one of the main pain sensitisers.

21
Q

What are the functional differences between COX-1 and COX-2?

A
  1. COX-1 is a constitutive enzyme present in most tissues and has basic homeostatic (‘house-keeping’) functions. E.g. producing prostaglandins involved in gastric cytoprotection, platelet aggregation…
  2. COX-2 is mainly activated during inflammation by pro-inflammatory cytokines and produce pro-inflammatory prostaglandins.
22
Q

What are the consequences of inhibition of different types of COX enzymes?

A
  • Inhibition of COX-2 causes main pharmacological effects.
  • Inhibition of COX-1 causes main side-effects.
23
Q

How do NSAIDs inhibit COX?

A

They ener hydrophobic channel in enzyme and form H-bond with Arg120 residue and blocks entry of fatty acid substrate. Prevents catalysis of AA → PGG2 step in PGE production only.

24
Q

What is the mechanism of action of aspirin?

A

Enters active site and acetylates Ser530 and irreversibly inactivates both COX-1 and COX-2.

25
What are examples of NSAIDs?
- Aspirin - Ibuprofen - Paracetamol (no anti-inflammatory effects) - Celecoxib
26
What are the side effects of NSAIDs?
1. GI bleeds: PGs have inhibitory effect on gastric acid secretion and stimulatory effect on secretion of protective mucin. 2. Renal insufficiency: PGE2/PGI2 involved in maintenance of renal blood flow. 3. Stroke/MI (COX-2 selective inhibitors): COX-2 has constitutive role in VSM, producing PGI2, which cause vasodilation, and prevents platelet aggregation. 4. Bronchospasms: Reasons unclear.
27
What are the opioid receptors in the body?
μ, κ, δ, ORL1
28
What types of receptors are opioid receptors?
Gi/o GPCRs
29
Which type of opioid receptor is mainly responsible for mediating analgesic effects of opioids?
μ
30
What are the structural features of opioids that are important to their function?
1. -OH group on 4th benzene ring (clockwise) 2. N- atom linked to 2 carbons on 1st benzene ring
31
What are the effects of opioids on peripheral nociceptive fibres?
1. αi subunit inhibits adenylyl cyclase activity, which counteracts sensitising effects of PGE2. - **Peripheral effect** 2. βγ subunit activates GIRK channels, causing hyperpolarisation of neurones and decreased NT release at from pain fibres in spinal cord. - **Central effect**
32
What are the central analgesic mechanisms of opioids?
1. Inhibits transmission of nociceptive nerve impulses through the dorsal horn of the spinal cord, either pre-synaptically by inhibiting NT release, or post-synaptically by decreasing the excitability of dorsal horn projecting neurones. 2. Stimulates areas of the brain such as the periaqueductal grey, involved in central modulation of pain.
33
What are examples of opioids?
- Morphine - Codeine - Etorphine - Naloxone
34
What are the side effects of opioids and opioid receptors responsible?
- Respiratory depression: Mediated by μ opioid receptors and is a result of suppression of central breathing rhythm. - Nausea/vomiting: Mediated by μ/δ receptors. - Constipation: Mediated by μ, κ and σ receptors.
35
What is placebo analgesia?
Phenomenon whereby a substance which is known not to have any analgesic effects produces analgesic response in subject when given as an analgesic.
36
What is the mechanism behind placebo analgesia?
- Release of endogenous opioids in area where subject believes placebo analgesic is acting causes suppression of pain - There may be a somatotopic representation in the PAG that controls release of endogenous opioids in specific areas of the body.
37
What is the mechanism of analgesic action of gabapentin/pregabalin?
Decreases density of Cav α2δ1 subunit localisation in PM, thus decreasing inward Ca2+ current and spinal cord NT release from nociceptive fibres.
38
What is the mechanism of analgesic action of lidocaine?
Blocks Navs and decreases the spontaneous discharge of nociceptive fibres.
39
What is the mechanism of analgesic action of ziconotide?
Antagonism of N-type Cavs and decreases NT release at spinal cord from nociceptive fibres.
40
What is the mechanism of transcutaneous electrical nerve stimulation (TENS) in pain relief?
Stimulation of Aβ in the area around source of pain causes inhibition of WDR pain response by gate control theory.

Neurophysiology & Human Behaviour (20 decks)

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