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Neurology > Analgesia and Analgesic Drugs > Flashcards

Analgesia and Analgesic Drugs Flashcards

1
Q

Analgesics may reduce nociception by doing what? Give an eg of a drug which acts via each mechanism

A
  • Acting at the site of injury – decrease nociceptor sensitization in inflammation (e.g. NSAIDs)
  • Blocking nerve conduction – (e.g. local anaesthetics) – not considered here
  • Modifying transmission of nociceptive signals in the dorsal horn of the signal cord (e.g. opioids and some anti-depressant drugs)
  • Activating (or potentiating) descending inhibitory controls (e.g. opioids)
  • Targeting ion channels upregulated in nerve damage
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2
Q

Outline the WHO analgesic ladder.

A
  1. NSIAD
  2. Weak opioid
  3. Strong opioid
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3
Q

Give examples of NSAID’s used in step 1 of the WHO analgesic ladder.

A
  • Aspirin
  • Diclofenac
  • Ibuprofen
  • Indometacin
  • Naproxen
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4
Q

Give examples of weak opioids used in step 2 of the WHO analgesic ladder.

A
  • Coedine
  • Tramadol
  • Dextropropoxyphene
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5
Q

Give examples of strong opioids used in step 2 of the WHO analgesic ladder.

A
  • Morphine
  • Oxycodon
  • Heroin
  • Fentanyl
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6
Q

What are opiates?

A

Substances extracted from opium, or of similar structure, to those in opium

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7
Q

What are opioids?

A

ANY agent (including endogenous peptides) that acts upon opioid receptors

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8
Q

What theory is segmental anti-nociception associated with?

A

The gate control theory

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9
Q

What are responsible for Supraspinal Anti-Nociception?

A

Descending pathways from the brainstem

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10
Q

What brain regions are involved in pain perception and emotion? Where do these project back to? To do what?

A

Cortex, amygdala, thalamus, hypothalamus.

Project back to the brainstem and spinal cord to modify afferent input.

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11
Q

Name 3 important brainstem regions in the perception of pain and emotion.

A
  • The Periaqueductal Grey (PAG).
  • Nucleus Raphe Magnus (NRM).
  • Locus Coeruleus (LC).
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12
Q

What cause profound analgesic in PAG?

A

Excitation by electrical stimulation

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13
Q

What drugs can cause such excitation of PAG? How?

A 
Endogenous opioids (enkephalins) or morphine, and related compounds. 
Cause excitation by inhibiting inhibitory GABAergic interneurons ie. disinhibition.
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14
Q

What neurone is NRM made up of?

A

Serotonergic and enkephalinergic neurones

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15
Q

What causes excitation of NRM?

A

Morphine

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16
Q

What type of neurones are found in the LC?

A

Noradrenergic

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17
Q

Segmental anti-nocicpetion….

A

Gate control theory

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18
Q

Supraspinal anti-nociception…

A

Descending pathways from the brainstem

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19
Q

What is opioid action mediated by?

A

G-protein coupled opioid receptors

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20
Q

What do these GPCR’s couple preferentially to?

A

Gi/o

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21
Q

What do G-protein coupled opioid receptors couple preferentially to Gi/o to produce?

A
  • Inhibition of opening of voltage-activated Ca2+ channels.
    (presynaptic effect – suppresses excitatory NT release from nociceptor terminals)
  • Opening of K+ channels.
    (post-synaptic effect – suppresses excitation of projection neurones)
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22
Q

Opioid receptors are widely distributed throughout the __________

A

NERVOUS SYSTEM

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23
Q

What are opioid receptors traditionally classed as? Outline what each of these classes are responsible for.

A
  • μ (mu, aka MOP*) responsible for most of the analgesic action of opioids – but, unfortunately, also some major adverse effects (e.g. respiratory depression, constipation, euphoria, sedation, dependence)
  • δ (delta, aka DOP*) contributes to analgesia but activation can be proconvulsant
  • κ (kappa, aka KOP*) contributes to analgesia at the spinal and peripheral level and activation associated with sedation, dysphoria and hallucinations
  • ORL1 activation produces an anti-opioid effect
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24
Q

As analgesics, how do opioids mainly act?

A

Through prolonged activation of μ-opioid receptors

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25
Q

What kind of pain is morphine used in?

A
  • Acute severe pain

* Chronic pain

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26
Q

How is morphine given in acute pain?

A

IV, IM or SC

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27
Q

In chronic pain, what kind of administration of morphine is most appropriate?

A

Oral - as immediate release Oramorph or as modified release MST continue

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28
Q

What other name does diamorphine go by?

A

3,6-diacetylmorphine.
or
Heroin

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29
Q

What is more lipophilic, morphine or diamorphine?

A

DIAMORPHINE

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30
Q

When given IV, what is the onset of action of diamorphine like?

A

RAPID - enters CNS rapidly

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31
Q

How is fentanyl given? Why?

A

Given IV to provide analgesia in maintenance anaesthesia

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32
Q

In what way is fentanyl suitable for in chronic pain states but not in acute pain?

A

Transdermal delivery

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33
Q

What is buprenophine useful in?

A

Chronic pain, with patient-controlled injection systems

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34
Q

What type of drug is buprenophine?

A

A partial agonist

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35
Q

What is the onset and duration of buprophine like?

A

Slow onset and long duration of action

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36
Q

Via what 2 routes can bupropion be given?

A

By injection, or sublingually

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37
Q

What is pethidine used in?

A

Acute pain, especially labour

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38
Q

What is pethidine NOT suitable for when given IV, IM or SC? Why?

A

Not suitable for control of chronic pain – due to short duration of action

39
Q

What should pethidine not be used in conjunction with? Why?

A

MAO inhibitors – may cause excitement, convulsions, hyperthermia.

40
Q

What is norpethidine?

A

A neurotoxic metabolite of pethidine

41
Q

What are Codeine (3-methoxymorphine) + Dihydrocodeine?

A

Weaker opioids used in mild/moderate pain

42
Q

HEPATIC METABOLISM occurs in relatively small amounts. What does this convert codeine/dihydrocodeine into?

A

Morphine and Dihydromorphine

43
Q

How is codeine given?

A

ORALLY - not IV

44
Q

Describe how tramadol (possibly) works.

A
  • A weak μ-receptor agonist
  • Probably exerts significant analgesic action by potentiation of the descending serotonergic (from NRM) and adrenergic (from LC) systems
45
Q

How is tramadol given?

A

ORALLY

46
Q

Who should never be given tramadol?

A

Patients with epilepsy

47
Q

What type of drug is methadone?

A

A weak μ-agonist with additional actions at other sites in the CNS, including potassium channels, NMDA receptors and some 5-HT receptors

48
Q

How is methadone given?

A

ORALLY

49
Q

In terms of drugs with an abuse potential, which ones are generally more addictive?

A

Those with a short half life

50
Q

What is the duration of action of methadone?

A

Long duration of action – plasma half-life of > 24h

51
Q

What is the main use of methadone?

A

To assist in withdrawal from ‘strong opioids,’ such as heroin

52
Q

What is the mechanism of action of naloxone?

A

A competitive antagonist at μ-receptors (to a lesser extent κ- and δ-receptors)

53
Q

What is naloxone used for?

A

To REVERSE OPIOID TOXICITY (ie respiratory +/- neurological depression) associated with ‘strong opioid’ overdose

54
Q

How is naloxone given?

A

Incrementally IV

  • IM and S/C routes may be employed if the route isn’t practical
55
Q

What is the half life of naloxone like?

A

SHORT

56
Q

Why is it clinically important that Naloxone has a short half-life?

A

Since opioid toxicity can recur to ‘strong opioid’ agonists with a longer duration of action (clinically, you must monitor the effect of naloxone very carefully, titrating the individual dose, and frequency, to that required to reverse opioid toxicity)

57
Q

In opioid addicts or those pts requiring high dose opioid analgesia regularly, what may the administration of naloxone do?

A

Trigger an acute withdrawal response

58
Q

When else may naloxone be given?

A

May be given to a newborn displaying opioid toxicity (e.g. respiratory depression) as a result of administration of pethidine to mother during labour

59
Q

What drug is similar to naloxone, but has a much longer half life?

A

Naltrexone

60
Q

What do NSAID’s diminish?

A

Nociceptive sensitisation

61
Q

What are NSAID’s, especially ibuprofen and naproxen used for?

A

To reduce mild/moderate inflammatory pain

62
Q

What action do non-selective NSAID’s have? How do they achieve this?

A

Analgesic, antipyretic and anti-inflammatory actions

  • achieved largely by inhibiting the synthesis and accumulation of prostaglandins by cyclo-oxygenase (COX) enzymes – COX-1 and COX-2
63
Q

Give 5 examples of non-selective NSAID’s.

A
  • Aspirin
  • Ibuprofen
  • Naproxen
  • Diclofenac
  • Indomethacin
64
Q

Give 3 examples of COX-2 selective inhibitors?

A
  • Etoricoxib
  • Celecoxib
  • Lumiracoxib
65
Q

What do prostaglandins mediate?

A

Hyperalgesia

66
Q

What is thromboxane-A2 responsible for?

A
  • Platelet aggregation

* Vasoconstriction

67
Q

What is prostacyclin (PGI2) responsible for?

A
  • Platelet disaggregation

* Vasodilation

68
Q

COX-1 is __________ active

A

CONSTITUTIVELY (always)

69
Q

When is COX-2 induced?

A

During inflammation

70
Q

What derives from inhibition of COX-2?

A

Therapeutic benefit

71
Q

What problems occur through inhibition of COX-1?

A

GI toxicity

72
Q

What do most cells generate PGE2 in response to?

A

Mechanical, thermal or chemical injury

73
Q

What is the effect of PGE2?

A

It sensitizes nociceptive neurones, and causes hyperalgesia

74
Q

What is paracetamol also known as?

A

Acetoaminophen

75
Q

Why is paracetamol not classed as an NSAID?

A

Because it lacks anti-inflammatory activity, and only weakly inhibits COX isoenzymes

76
Q

What is the analgesic effect of paracetamol due to?

A

Its metabolites (e.g. N-acetyl-p-benzoquinoneimine, which is also responsible for hepatotoxicity in overdosage). (TRPA1 has emerged as a recent, novel, target that is activated by such metabolites)

77
Q

Why do NSAID’s have limited analgesic efficacy?

A

Because multiple signalling pathways, several of which don’t involve arachidonic acid metabolism, cause nociceptor sensitization

78
Q

What are the main 2 side effects to be aware of with long-term administration of non-selective NSAIDs?

A
  • GI damage

* Nephrotoxicity

79
Q

Why can GI damage result from long term use of non-selective NSAID’s?

A

Because PGE2 produced by COX-1 protects against the acid/pepsin environment.
(and NSAIDs inhibit COX-1.)

80
Q

Why can nephrotoxicity result from long term use on non-selective NSAID’s?

A

Because of inhibition of COX-2 constitutively expressed by the kidney

81
Q

What kind of nephrotoxicity results from NSAID use?

A

Compromise renal haemodynamics in renal disease

82
Q

Why is the use of selective COX-2 inhibitors limited?

A

They are pro-thrombotic

83
Q

In what conditions does severe and debilitating neuropathic pain occur in?

A
  • Trigeminal neuralgia.
  • Diabetic neuropathy.
  • Post-herpetic neuralgia.
  • Phantom limb pain.
84
Q

Is neuropathic pain easy to treat?

A

NO – it doesn’t respond to NSAIDs, and appears to be relatively insensitive to opioids (unless given at high doses)

85
Q

What are the 3 groups of treatment options for neuropathic pain?

A
  1. Gabapentin + Pregabalin (anti-epileptics).
  2. Amitriptyline, Nortryptiline + Desipramine (tricyclic anti-depressants).
  3. Carbamazepine
86
Q

What do gabapentin and pregabalin not act via?

A

The GABAergic system

87
Q

What is the mechanism of action of gabapentin and pregabalin?

A

Reduce the cell surface expression of a subunit (α2δ) of some voltage-gated Ca2+ channels (high-voltage-activated subgroup) which are upregulated in damaged sensory neurones

88
Q

What is gabapentin used in?

A

Migraine prophylaxis

89
Q

What is pregabalin used in?

A

Painful diabetic neuropathy

90
Q

What does the action of gabapentin and pregabalin ultimately cause?

A

A decrease of neurotransmitters, such as glutamate and substance P, from the central terminals of nociceptive neurones.

91
Q

How do Amitriptyline, Nortryptiline + Desipramine act?

A

Act centrally by decreasing the reuptake of noradrenaline

92
Q

Additionally, what do duloxetine and venlafaxine do?

A

Decrease the reuptake of 5-HT (but selective serotonin reuptake inhibitors (SSRIs) do not provide analgesia).

93
Q

How does Carbamazepin work?

A

Blocks subtypes of voltage-activated Na+ channel that are upregulated in damaged nerve cells.

94
Q

What is Carbamazepin the first line treatment for?

A

Control of pain intensity and frequency of attacks in trigeminal neuralgia

Neurology (42 decks)

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