Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

5BBM0218 Physiology and Pharmacology of CNS > L14: Pain > Flashcards

L14: Pain Flashcards

1
Q

What is pain?

A
  • a unique, unpleasant sensory or emotional experience associated with tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two aspects of pain?

A

Sensory aspect: sensory discriminative, involves threshold intensity and location of pain
Emotional aspect: affective motivational, relates to the emotional experience of pain as unpleasant, threatening, or aversive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the basic pain processing pathway?

A
  • Descending brain pathways from the cortex and limbic brain to the midbrain and spinal cord.
  • NTs released to modify the perception of pain and its intensity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does pain perception occur?

A
  • Pain perception occurs through a dialogue between ascending & descending pathways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is nociception?

A
  • nociception = neural process of encoding noxious stimuli,
  • which includes sensitivity to a noxious tissue-damaging stimulus/stimulus that may become noxious if prolonged.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the four physiological processes involved in pain?

A

Transduction
Transmission
Modulation
Perception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the four physiological processes involved in pain

A
  1. Transduction: Nociceptors respond to tissue-damaging stimuli (mechanical, chemical, and thermal) & transmit the signal to CNS
  2. Transmission: Nociceptive signals are carried from site of tissue injury to brain regions involved in pain perception (involving primary & secondary pain transmission neurons)
  3. Modulation: Descending pain modulatory system alters activity in the spinal cord through monoaminergic NTs, resulting in inhibitory/excitatory effects.
  4. Perception: Pain perception occurs in the brain regions ncl. the cortex, thalamus & limbic brain.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some endogenous inhibitors involved in the modulation of pain?

A
  1. GABA: mediates pain modulation through GABA interneurons & descending inhibitory pathways.
  2. Opioids: Endogenous opioids e.g. enkephalins, beta-endorphins, and dynorphin act as pain modulators.
  3. Noradrenaline (NA): Mediates pain modulation via descending inhibitory pathways originating from the Locus Coeruleus.
  4. Serotonin (5HT): Acts as a pain modulator through descending inhibitory pathways originating from the Raphe Nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the characteristics of acute pain?

A
  • Associated with tissue damage
  • Has an evolutionary advantage
  • Self-limited and doesn’t last more than 12 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the characteristics of chronic pain?

A
  • It is a disease state
  • Outlasts the normal time of healing
  • No evolutionary advantage
  • Includes conditions like neuropathic pain, chronic migraines, and fibromyalgia
  • Results in a negative impact on the quality of life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is peripheral sensitization?

A

an increased sensitivity to afferent nerve stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the effects of peripheral sensitization on pain response?

A
  • increased pain response due to production of neuropeptides like substance P and histamine by nociceptors
  • leads to primary hyperalgesia & allodynia
  • also involves the upregulation of existing and new receptors.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is hyperalgesia and allodynia

A
  • hyperalgesia = heightened pain response to painful stimuli
  • allodynia = pain response to non-painful stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does peripheral sensitization contribute to chronic pain?

A
  • causes a ↓ threshold of firing & ↑ responsiveness of nerve endings, including C-fibers (which respond to heat, pressure, and impact stimuli)
  • activated & sensitized by locally produced inflammatory mediators like bradykinin, histamine, prostaglandins, leukotrienes, Ach, 5HT, and substance P
  • these inflammatory mediators ↓ the threshold for activation of nociceptors, contributing to chronic pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is central sensitization?

A
  • amplification of pain by CNS mechanisms, representing altered function of nociceptors.
    -triggered by peripheral injury or increased nociceptive input
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is central sensitization manifested in the central nervous system?

A

3 ways:
1.↓ in the threshold for activation of neurons, making them more easily excitable.
2. ↑ in receptive field size and recruitment of novel input, making neurons more likely to fire.
3. ↑ in spontaneous background activity of neurons

17
Q

What are the consequences of central sensitization?

A
  • input from low-threshold, non-nociceptive fibers activates nociceptive-specific neurons
  • Activates nociceptive pathways
  • can lead to clinical pain characterized by allodynia & hyperalgesia & spontaneous pain
18
Q

What are the types of pain?

A
  1. Nociceptive Pain - Arises from tissue damage and inflammation
  2. Neuropathic Pain - Arises from damage to nerve fibers
  3. Other Pain - Arises from neurological dysfunction in the CNS
19
Q

What are the mechanisms in inflammation related to pain?

A
  • PGE2 (Prostaglandin E2) and PGI2 (Prostacyclin) are important pain-producing or enhancing mediators.
  • Considered enhancers of pain perception.
20
Q

How does nerve laceration contribute to pain?

A
  • Surgical trauma can cause nerve laceration, leading to neuropathic pain.
  • Neuropathic pain is difficult to treat with analgesics
21
Q

How are inflammatory pain and neuropathic pain treated differently?

A
  • Inflammatory Pain: Preferably treated at the source, where inflammatory mediators are being released.
  • Neuropathic Pain: Usually arises due to changes in the spinal cord and CNS. Treating at the source may not be effective
22
Q

What makes neuropathic pain challenging to treat?

A
  • Nerves take longer to recover from damage
  • making neuropathic pain often chronic & difficult to treat with analgesic medications
23
Q

What are the coreleased neurotransmitters in certain pain pathways?

A
  • Substance P and glutamate are coreleased.
  • Substance P activates NK1 receptors, which prolongs the activity of glutamate in pain transmission
24
Q

How do NSAIDs work as pain relievers?

A
  • NSAIDs inhibit COX enzymes, preventing the production of prostaglandins
  • COX-2 is expressed in inflammation, and by blocking it, NSAIDs reduce pain and inflammation
25
Q

What is the mechanism of action of paracetamol as a pain reliever?

A
  • mild analgesic that lacks anti-inflammatory effects.
  • exact mechanism of action unclear
  • it weakly inhibits the synthesis of prostaglandins
26
Q

What happens to ion channels in neuropathy, and how does it contribute to pain?

A
  • ion channels behave abnormally, leading to the unnecessary transmission of electrical impulses
  • Na+ channels can accumulate at the site of injury and seem to be found only in the CNS
  • contributes to the development of neuropathic pain
27
Q

What are the different types of nerve fibers?

A

Aδ fibers
C fibers
Aß fibers

28
Q

describe Aδ fibers

A
  • thinly myelinated
  • transmit info rapidly at around 15m/s, and are responsible for sharp and intense pain perception
  • cell bodies located in the dorsal root ganglion.
29
Q

describe C fibers

A
  • non-myelinated
  • transmit info at slower rate of around 1m/s, & responsible for dull and throbbing pain perception
  • cell bodies located in the dorsal root ganglion.
30
Q

describe Aß fibers?

A
  • heavily myelinated
  • small diameter
  • fast-conducting fibers that are activated by non-noxious stimuli e.g. pressure & touch
31
Q

Why are secondary messengers necessary for the response to extracellular chemical signals?

A
  • because they amplify cellular responses
  • act as intermediaries between cell surface receptors & intracellular processes - allowing a single extracellular signal to trigger multiple intracellular responses
32
Q

How do secondary messengers amplify cellular responses to extracellular signals? Provide examples.

A
  • amplify cellular responses by propagating and amplifying the initial signal
  • can activate multiple intracellular pathways and regulate various cellular processes
  • EXAMPLES: cAMP, IP3/DAG, and Ca2+ ( which activate various kinases, enzymes & TFs to mediate cellular responses to single extracellular signal)
33
Q

What is the normal role of glutamate at synapses, and how does it contribute to neurodegeneration in disease?

A
  • major excitatory neurotransmitter in the brain
  • important in synaptic transmission & plasticity (learning & memory)
  • excessive glutamate release and receptor activation can lead to excitotoxicity (contributing to neurodegeneration in diseases e.g. PD & AD)

5BBM0218 Physiology and Pharmacology of CNS (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions