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2nd Year: Drugs and the Mind > Pain > Flashcards

Pain Flashcards

1
Q

List 3 types of pain.

A
  1. Inflammation
  2. Neuropathy
  3. Central pain
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2
Q

What is inflammation?

A

Tissue damage

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3
Q

What is neuropathy?

A

Nerve damage: Na+ channels clustered around areas of damage cause ectopic activity that can spread to the brain and spine.

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4
Q

What is central pain?

A

Pain of the CNS.

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5
Q

What is cancer pain?

A

Pain caused by cancer, a combination of inflammation and neuropathy.

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6
Q

Measuring pain is never accurate. List 4 reasons why.

A
  1. Gender differences
  2. Age increases pain prevalence
  3. Cultural differences in pain expression
  4. Pain can be suppressed under certain condition
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7
Q

Pain is purely a sensation. True or false?

A

False: there is also a psychological component.

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8
Q

The pain scale measures severity. Describe the pain scale.

A

0-3 is mild
3-6 is moderate
6-10 is severe

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9
Q

What is a) acute and b) chronic pain?

A

a) short term

b) long term, +3months

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10
Q

Pain is automatically unpleasant. What kind of afferent fibres are involved in sensing pain?

A

A-delta and C-fibres.

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11
Q

What kind of receptors are these nerve fibres covered in?

A

Nociceptors: these respond to thermal, mechanical and chemical stimuli.

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12
Q

At what kind of pain levels do C-fibres become sensitised?

A

Low pain levels. C-fibres only respond to high levels of excitation.

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13
Q

The actual sensation of pain is often due to the release of chemicals from damaged tissues. Give 3 examples of chemicals released.

A
  1. ATP when cells rupture
  2. Prostaglandins (PGs)
  3. 5HT
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14
Q

How are prostaglandins produced?

A

The activation of cyclooxygenase 1 and 2 (COX 1 and 2)

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15
Q

Pain can also be induced by external chemicals. Give an example of this.

A

Capsaicin from spicy food acts on heat-pain receptors.

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16
Q

How is pain localised i.e. how does the brain realise which part of you is injured?

A

The spinal cord is segmented. Thus the spinal nerves that respond stimulate specific areas of the SS cortex.

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17
Q

What part of the brain produces the emotional response to pain?

A

The limbic brain.

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18
Q

‘Pain is a sensory event that reduces QoL’. Why?

A

Pain impinges upon other physiological processes, thus there is comorbidity of associated disorders with chronic pain.

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19
Q

What disorders are associated with chronic pain?

A

Depression, anxiety, inability to sleep, eat or concentrate etc.

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20
Q

Pain is a hugely important survival signal. You must respond to pain. Failure to respond results in what condition?

A

Central hyper-excitability and hyperalgesia. The senesitivyt increases and the pain gets worse.

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21
Q

What happens if you ignore hyperalgesia?

A

Allodynia arises whereby non-painful stimuli become painful.

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22
Q

What is phantom limb pain?

A

When limbs have been lost nerves are often damaged - these continue to fire and stimulate the SS cortex even when there is no longer a limb there.

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23
Q

What is wind-up?

A

Increased levels of neuronal activity that leads to excitation.

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24
Q

Wind-up leads to central sensitisation. What is central sensitisation?

A

Decreased threshold to stimuli and extension of the receptive field of a neuron.

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25
Q

What does central sensitisation cause?

A

Increased pain perception.

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26
Q

So basically what does wind-up > central sensitisation > increased pain perception mean?

A

Repeated stimulation increases sensitivity so something seems more painful.

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27
Q

a) what are NSAIDS and COXIBS?
b) what kind of pain are they used to treat?
c) how do they work?
d) Give an example of an NSAID.

A

a) Non-steroidal anti-inflammatories and cyclooxygenase inhibitors
b) Inflammation
c) They prevent the activation of COX 1 and 2 to inhibit the production of prostaglandins
d) Ibuprofen

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28
Q

a) what are triptans?
b) what kind of pain are they used to treat?
c) Give an example triptan.

A

a) Drugs that block 5HT receptors
b) Migraine
c) Sumatriptan acts on 5HT1 receptors

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29
Q

Lidocaine is a short-term local anaesthetic. How does it work?

A

In blocks Na+ channels on C-fibres. This prevents the generation of APs. Even though the nociceptors are being stimulated the neuron is unable to communicate this information to the brain.

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30
Q

Give 2 drugs used for neuropathy. How do they work?

A
  1. Carbemazepine: Na+ blocker so APs cannot be generated.

2. Gabapentin: Ca2+ blocker that prevents the release of NTs so APs cannot be communicated between neurons.

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31
Q

a) how does ketamine affect pain?
b) What are the side effects of ketamine usage?
c) When is ketamine used and why?

A

a) Ketamine blocks NMDA glutamate receptors. These are involved in wind-up, thus ketamine decreases the perception of pain.
b) NMDA receptors are also involved in memory and cognition so it can cause unpleasant side effects.
c) It is used intra-operatively: the dissociative side effects are not a problem if the patient is unconscious.

32
Q

Endogenous opioids modulate the pain response. Give examples of opiate drugs, what is the difference between them?

A

Morphine, heroin, codeine, pethidine etc.

All opiate drugs are pharmacologically identical in the sense that they are all metabolised into morphine in the body. Thus opiates (that are not morphine) are often called pro-drugs.

33
Q

Some people do not gain pain relief from drugs like codeine. Why?

A

They are lacking in enzymes from the cytochrome P450 mono-oxygenase family and cannot effectively metabolise it into morphine.

34
Q

What is the chemical name for heroin?

A

Diacetylmorphine: it has 2 acetyl groups that render it inactive until they are lost, at which point heroin rapidly penetrates the CNS.

35
Q

Heroin is a weak pro-drug and codeine is strong. True or false?

A

False: heroin is v. strong and codeine is weak.

36
Q

When is pethidine used?

A

In childbirth.

37
Q

There are 4 receptors for endogenous opioids. What are they?

A

Mu, delta, kappa and ORL-1

38
Q

a) What are the endogenous opioids of the Mu receptor? What effects do these produce?
b) What are its synthetic agonists?
c) What kind of receptor is it?

A

a) Endomorphins, these act to reduce pain
b) Morphine, codeine etc. (most opiate drugs target Mu)
c) a GPCR that opens K+ channels. This is hyperpolarising.

39
Q

a) What are the endogenous opioids of the delta receptor? What effects do these produce?
b) What are its synthetic agonists?
c) What kind of receptor is it?

A

a) Enkephalins, these act to reduce pain
b) Same as the Mu receptor, morphine/codeine etc.
c) a GPCR that opens K+ channels. This is hyperpolarising.

40
Q

If mu and delta receptors are hyperpolarising, how does this act to reduce pain?

A

They reduce the amount of APs generated. Opening K+ channels causes K+ to leave the cell and the inner axon to become more negative. It is thus harder to generate an AP so pain stimulation is lessened.

41
Q

a) What are the endogenous opioids of the kappa receptor? What effects does this produce?
b) What kind of receptor is it?

A

a) Dynorphins, these have been found to both reduce and stimulate pain
b) a GPCR that closes Ca2+ channels. This inhibits NT release.

42
Q

a) What are the endogenous opioids of the ORL-1 receptor? What effects does this produce?
b) What kind of receptor is it?

A

a) nociceptin, this has been found to increase pain sensation in hyperalgesia
b) a GPCR that opens K+ channels. This is repolarising.

43
Q

Why is it that ORL-1 receptors are repolarising and increase pain sensation?

A

They open K+ channels to allow K+ into the cell. This increases the speed of repolarisation of the neuron, shortening the refractory period and allowing APs to be generated more quickly. As AP frequency denotes stimulus size, then more frequent APs indicate more severe pain.

44
Q

What is naxolone?

A

An antagonist to the mu, delta and kappa receptors that can be used to reverse OD on opiate drugs.

45
Q

Does naxolone work on ORL-1 receptors?

A

No.

46
Q

How must naxolone be administered if it is to reduce opiate OD?

A

Repeatedly, as it has a very short half-life, and immediately.

47
Q

Are the majority of opioid receptors in the CNS pre or post-synaptic?

A

Pre-synaptic, approx. 75%.

48
Q

Opiate drugs are useful in treating which kinds of pain?

A

Inflammation and central pain.

49
Q

Why are opiates not useful for neuropathy?

A

The excessive activity of NMDA glutamate receptors and cholecystokinin associated with neuropathy interfere with opioid action in the spine.

50
Q

Does naxolone only block synthetic opioids?

A

No, it can also block endogenous opioids.

51
Q

What kind of NTs are endogenous opioids?

A

Peptide NTs.

52
Q

Describe the synthesis of peptide NTs.

A

They are synthesised in the cell body as large, inactive precursors. They are then transported to the nerve terminals, with processing en route so that they are fully active when they arrive and are released into the synapse.

53
Q

Mu and delta receptors are hyperpolarising and thus reduce the amount of APs generated. If these receptors are pre-synaptic, how does this reduce pain sensation?

A

Neurotransmitter release is controlled by APs: APs cause Ca2+ channels to open, causing the vesicles to fuse with the membrane and release NTs into the synapse. If there are no APs there is no Ca2+ influx, thus no NTs are released.

54
Q

Epidurals are the delivery of anaesthetics to the dura mater of the spinal cord. Why do epidurals have few side effects?

A

The effects are localised to that region of the spine, no drugs enter the PNS.

55
Q

How do opioids impact on the psychological experience of pain?

A

There are opioid receptors in the 5HT and noradrenaline regions of the brain, e.g. the raphe nuclei (serotonin). When opioid receptors are triggered by pain it modulates the release of these NTs. 5HT is largely associated with mood and sleep and noradrenaline with arousal.

56
Q

Define a) ascending and b) descending control pathways.

A

a) (PNS to) spinal cord to brain = sensation

b) brain to spinal cord = response

57
Q

Opioids affect descending control pathways. List 5 side effects of therapeutic doses.

A
  1. Anxiety relief
  2. Respiratory depression
  3. Anti-tussive effects
  4. Constipation
  5. Nausea and vomiting
58
Q

Why is anxiety relief useful for therapeutic opioid usage?

A

It is used pre-surgery to relax patients.

59
Q

Why are the anti-tussive effects useful for therapeutic opioid usage?

A

Used post chest surgery to prevent aggravation.

60
Q

Why is constipation useful for therapeutic opioid usage?

A

Used post bowel surgery. Opioids cause a maintained contraction of the smooth muscle in the gut, causing a reduction in peristalsis. They also reduce gut secretion.

61
Q

How do opioids cause respiratory depression?

A

They reduce the sensitivity of receptors in the brainstem to pCO2.

62
Q

How do opioids cause nausea and vomiting?

A

They activate receptors in the chemoreceptor trigger zone.

63
Q

Why can street useage of opioids create dependence?

A

They increase noradrenaline levels in the locus coeruleus and dopamine in the nucleus accumbens. Both these monoamine nuclei are involved in reward systems.
Therapeutic useage of opioids does not create dependence as pain switches off the reward pathway.

64
Q

All clinical opioids target which receptor?

A

The mu receptor.

65
Q

Pentazocine, a therapeutic opioid, does not target mu. Instead it targets…?

A

Kappa

66
Q

Mu opioids are all pharmacologically identical but differ in potency and pharmacokinetics. True or false?

A

True: they are all metabolised to morphine but vary in receptor affinity and speed of absorption/action.

67
Q

Why does heroin penetrate the CNS more rapidly than other opioids?

A

It is highly lipophilic.

68
Q

Why is tramadol (opioid) a good analgesic?

A

It is a weak opioid that blocks noradrenaline and 5HT reuptake. It appears to produce less side effects than other opioids.

69
Q

What happens in opioid OD?

A

The subject falls asleep, often vomits and chokes on it. Also respiratory depression is severe and can cause breathing to stop completely.

70
Q

Anti-depressant drugs are actually very effective in pain relief. How?

A

They block the reuptake of noradrenaline and 5HT. This causes synaptic levels of NT to increase.

71
Q

What kind of pain are ADs most effective in treating?

A

Neuropathy.

72
Q

Which areas of the brain do afferent C-fibres innervate?

A

The thalamus and cortex for perception. The limbic system is also involved for the emotional response to pain.

73
Q

What kind of NTs do C-fibres produce?

A

Peptide (opioid) and amino acid (glutamate) NTs.

74
Q

What kind of stimulation does the release of peptide NTs from C-fibres produce?

A

Slow depolarisation via GPCRs (opioid receptors).

75
Q

What kind of stimulation does the release of glutamate from C-fibres produce?

A

Fast depolarisation via AMPA receptors and slow via NMDA receptors (wind-up).

76
Q

How is swelling produced in inflammatory pain?

A

Plasma leaks out blood vessels and causes swelling.

2nd Year: Drugs and the Mind (12 decks)

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