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CNS CLERKSHIP > Analgesic Drugs > Flashcards

Analgesic Drugs Flashcards

1
Q

How may the analgesics NSAIDs reduce nociception and pain?

A
  • Act at site of injury to decrease nociceptor sensitisation in inflammation.
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2
Q

How may the analgesics - local anaesthetics, reduce nociception and pain?

A
  • Block nerve conduction.
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3
Q

How may the analgesics - opioids and some anti-depressants, reduce nociception and pain?

A

Suppress transmission of nociceptive signals in dorsal horn of spinal cord.

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4
Q

How may the analgesics - opioids reduce nociception and pain?

A

Activate/potentiate descending inhibitory controls.

  • Suppress transmission of nociceptive signals in dorsal horn of spinal cord.
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5
Q

How may the analgesics - anti-epileptics, reduce nociception and pain?

A
  • Target ion channels that are upregulated in nerve damage.
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6
Q

Give examples of strong opioids.

A
  • Morphine, oxycodone, hydromorphone, heroin, fentanyl.
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7
Q

Give examples of weak opioids.

A
  • Codeine, tramadol, dextropropoxyphene.
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8
Q

Give examples of NSAIDs.

A
  • Aspirin, diclofenac, ibuprofen, indometacin, naproxen.
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9
Q

What is an opiate?

A

Substance extracted from opium OR of similar structure to substances in opium.

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10
Q

What is an opioid?

A

ANY agent (including endogenous peptides) that act upon opioid receptors.

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11
Q

How do nociception and pain differ?

A
  • Pain is the awareness of suffering.

- Nociception may occur in absence of pain and vice versa.

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12
Q

Why is pain perception highly variable?

A

For same degree of nociceptor activity, more or less pain may be perceived depending on level of concurrent innocuous sensory input and behavioural context.

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13
Q

Pain is triggered by what?

A
  • Nociceptor stimulation (C- and Aδ- fibres).
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14
Q

How may nociceptor stimulation (C- and Aδ-) be reduced?

A

Simultaneous excitation of low threshold mechanoreceptors (LTMs: Aβ-fibres).

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15
Q

Describe the Gate Control Theory of Melzack and Wall.

A

Nerve impulses stimulated by injury are influenced in the spinal cord by other nerve cells which act as gates to either prevent or facilitate the passage of these impulses.

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16
Q

Certain neurones within the Substantial Gelatinosa are thought to be excited by both large diameter (Aβ) sensory axons and unmyelinated (C/Aδ-) nociceptive axons.

To where do these project?

A

The spinothalamic tract.

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17
Q

Inputs to projection neurones within the Substantial Gelatinosa are inhibited by?

A

An interneurone.

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18
Q

What excites the interneurone that inhibits input to projection neurones within the Substantial Gelatinosa?

A

Aβ axon.

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19
Q

What inhibits the Aβ axon that excites the interneurone responsible for inhibiting input to projection neurones within the Substantial Gelatinosa.

A

C/Aδ-.

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20
Q

What is the overall outcome of the gate control theory?

A

Activity in nociceptive axon maximally excites the projection neurone, allowing nociceptive signals to rise to the brain.

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21
Q

Supraspinal anti-nociception is relayed via which pathways and from where?

A

Descending pathways from the brainstem.

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22
Q

What brain regions are involved in pain perception and emotion?

A
  • Cortex.
  • Amygdala.
  • Thalamus.
  • Hypothalamus.
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23
Q

The brain regions involved in pain perception and emotion project back to the brainstem and spinal cord to modify?

A

Afferent input.

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24
Q

Excitation by electrical stimulation of the Periaqueductal grey (PAG) region produces what?

A

Profound analgesia.

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25
Q

The periaqueductal grey (PAG) area may be excited by what - other than electrical stimulation?

A
  • Endogenous opioids (enkephalins).

- Morphine and related compounds.

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26
Q

How do endogenous opioids, morphine and related compounds cause excitation of the periaqueductal grey area?

A

By inhibiting inhibitory GABAergic interneurones i.e. disinhibition.

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27
Q

What causes excitation of Nucleus raphe magnus?

A

Morphine.

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28
Q

Opioid action is mediated by?

A

G-protein-coupled opioid receptors.

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29
Q

G-protein-coupled opioid receptors preferentially signal to?

A

Gi/o.

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30
Q

G-protein-coupled opioid receptors preferentially signal to Gi/o to produce?

A
  • Inhibition of opening of voltage-activated Ca2+ channels.
  • Opening of K+ channels.
  • Inhibition of adenylate cyclase.
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31
Q

How does opioid action inhibit opening of voltage-activated Ca2+ channels?

A
  • By suppressing excitatory neurotransmitter release from nociceptor terminals.
  • Mediated by Gi/oβγ subunit.
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32
Q

How does opioid action openq K+ channels?

A
  • Suppresses excitation of projection neurones.

- Mediated by Gi/oβγ subunit.

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33
Q

What mediates opioid action in the inhibition of adenylate cyclase?

A
  • Mediated by Gi/oα subunit.
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34
Q

Opioid receptors are distributed throughout the nervous system. Name the three traditional classes.

A
  • μ (mu/ mop).
  • δ (delta/ dop).
  • κ (kappa/ kop).
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35
Q

Decribe the following opioid receptor.

- μ (mu/ mop).

A
  • Responsible for most analgesic action of opioids.

- Also responsible for some major adverse s/e.

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36
Q

Decribe the following opioid receptor.

- δ (delta/ dop).

A
  • Contributes to analgesia but activation can be pro-convulsant.
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37
Q

Decribe the following opioid receptor.

- κ (kappa/ kop).

A
  • Contributes to analgesia at spinal and peripheral level.

- Activation associated with sedation, dysphoria and hallucinations.

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38
Q

What effect do opioids have on the following system:

- Respiratory?

A
  • Apnoea.
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39
Q

What effect do opioids have on the following system:

- Cardiovascular.

A
  • Orthostatic hypotension.
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40
Q

What effect do opioids have on the following system:

- Gastrointestinal.

A
  • Nausea, vomiting, constipation, increased intrabiliary pressure.
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41
Q

What effect do opioids have on the following system:

- Central nervous system.

A
  • Confusion, euphoria, dysphoria, hallucinations, dizziness, myoclonus, hyperalgesia (with excessive use).
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42
Q

Describe the mechanism that results in the following effect of opioids:
- Apnoea.

A
  • Blunting of medullary respiratory centre to CO2 (hypercapnic response).
  • Involves μ (mu/ mop) and δ (delta/ dop) receptors.
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43
Q

Describe the mechanism that results in the following effect of opioids:
- Orthostatic hypotension.

A
  • Reduced sympathetic tone and bradycardia (via actions on medulla).
  • Histamine-evoked vasodilation.
  • Morphine, but NOT all opioids cause mast cell degranulation which can trigger bronchospasm in asthmatics.
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44
Q

Which opioids cause mast cell degranulation that can trigger bronchospasm in asthmatics?

A

Morphine.

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45
Q

Describe the mechanism that results in the following effect of opioids:
- GI s/e: nausea, vomiting, constipation, increased intrabiliary pressure.

A
  • Act on chemoreceptor trigger zone (CTZ - outside the BBB).
  • -> Increased smooth muscle tone and decreased motility via enteric neurones.
  • Involves μ (mu/ mop) and δ (delta/ dop) receptors.
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46
Q

Describe the mechanism that results in the following effect of opioids:
- CNS s/e: confusion, euphoria, dysphoria, hallucinations, dizziness, myoclonus, hyperalgesia.

A
  • Varying degrees dependent upon specific opioid drug and the receptor subtypes activated.
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47
Q

How does analgesia provided by opioid agonists mainly occur?

A

Through prolonged activation of μ-opioid receptors.

48
Q

Where is morphine metabolised?

A

In the liver.

49
Q

How is morphine metabolised?

A

In the liver by Glucuronidation at 3 and 6 positions.

50
Q

Morphine is metabolised into what?

A

Inactive M3G and analgesic active M6G.

51
Q

Morphine is excreted by what?

A

The kidneys.

52
Q

When may morphine be given IV?

A

In acute severe pain as incremental doses in high dependency areas.

53
Q

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

A

Oral.

  • Immediate: Oramorph.
  • Sustained release: MST Continus.
54
Q

Specialist administration of morphine by epidural and intrathecal routes provides what?

A

Profound analgesia.

55
Q

What is Diamorphine?

A
  • 3,6-diacetylmorphine.

- Heroin.

56
Q

How does diamorphine differ from morphine?

A

More lipophilic than morphine.

57
Q

What is the benefit of administering Diamorphine via IV?

A
  • Rapid onset of action as it enters CNS rapidly.
58
Q

What is codeine?

A

A naturally occurring weak opioid for mild/moderate pain.

59
Q

How is codeine metabolised?

A

In the liver by demethylation (in small amounts).

60
Q

Codeine undergoes hepatic metabolisation into?

A

Morphine by CYP2D6 and CYP3A4.

61
Q

What useful properties in addition to analgesia does codeine possess?

A
  • Anti-diarrhoeal (but may cause constipation).

- Anti-tussive.

62
Q

What semi-synthetic derivatives of codeine have higher potency?

A
  • Oxycodone.

- Hydrocodone.

63
Q

Which drug is 75-100x more potent than morphine?

A

Fentanyl.

64
Q

When is Fentanyl given and how?

A

IV to provide analgesia in maintenance anaesthesia.

65
Q

Fentanyl is suitable for which forms of administration in chronic pain states, but not in acute pain?

A
  • Transdermal.

- Buccal.

66
Q

When is pethidine used?

A

Acute pain esp. labour.

67
Q

Pethidine has rapid onset of action when given in which form?

A

IV, IM or SC.

68
Q

Why is pethidine not suitable for controlling chronic pain?

A

Rapid onset, but short duration of action.

69
Q

Pethidine should not be used in conjunction with what?

A

MAO inhibitors.

70
Q

Pethidine used in conjuntion with MAO inhibitors will cause what?

A
  • Excitement, convulsions and hyperthermia.
71
Q

What is a neurotoxic metabolite of pethidine?

A

Norpethidine.

72
Q

Norpethidine, the neurotoxic metabolite of Pethidine, maycause what?

A

Seizures.

73
Q

Buprenorphine is a partial agonist, useful in what types of pain?

A

Chronic pain.

74
Q

How is buprenorphine administered to those with chronic pain?

A

Patient controlled injection systems.

- Injection or sublingually.

75
Q

Describe the onset and duration of action of Buprenorphine.

A

Slow onset but long duration of action.

76
Q

Describe tramadol.

A
  • Weak μ-receptor agonist.

- Opioid.

77
Q

How is Tramadol thought to exert significant analgesic action?

A

By potentiation of descending serotonergic and adrenergic systems.

78
Q

How is tramdol administered?

A

Orally.

79
Q

Tramadol use should be avoided in patients with which condition?

A

Those with epilepsy.

80
Q

Describe methadone.

A

Opioid.

  • Weak μ-agonist of phenylheptylamine class.
  • Action at K+ channels, NMDA glutamate receptors and some 5-HT receptors.
81
Q

How is methadone adminstered?

A

orally.

82
Q

Describe the duration of action and half-life of methadone.

A
  • Long duration of action.

- Plasma half-life >24hours.

83
Q

Methadone can be useful in treating patients with which conditions?

A
  • Chronic pain in terminal cancer.

- Withdrawal from strong opioids e.g. heroin.

84
Q

Etorphine is used in who?

A

Large animals - elephants, rhinos.

Reversed by diprenorphine.

85
Q

Generally, the more addictive opioids with abuse potential have which kind of half-life?

A

Shorter half-life opioids tend to be more addictive than those with long half-lives.

86
Q

Name an antagonist of opioids.

A
  • Naloxone.
  • Naltrexone.
  • Alvimopan.
  • Methylnaltrexone.
87
Q

How does naloxone work?

A

As a competitive antagonist at μ-receptors.

88
Q

What is naloxone used for?

A

To reverse opioid toxicity.

- i.e. respiratory +/or neurological depression.

89
Q

How is naloxone administered?

A

Incrementally IV.

IM or SC if IV not practical.

90
Q

Naloxone has a short half-life. Why is this important?

A
  • Opioid toxicity can recur due to strong opioid agonsts with a longer duration of action.
  • Titrate individual dose and frequency to that required to reverse opioid toxicity. MUST monitor effect closely and do NOT leave patient unattended.
91
Q

In opioid addicts, Naloxone may trigger what?

A

Acute withdrawal response.

92
Q

In patients requiring high dose opioid analgesia regularly, Naloxone may trigger what?

A

Acute withdrawal response.

93
Q

If pethidine is given to a mother during labour, and the newborn has opioid toxicity, what may be administered?

A

Naloxone.

94
Q

What advantage does Naltrexone have over Naloxone?

A
  • Oral availability.

- Much longer half-life.

95
Q

Describe the action of the opioid antagonists: Alvimopan and Methylnaltrexone.

A
  • Do not enter CNS.

- Reduce GI effects of surgical and chronic opioid agonist use.

96
Q

Non-selective NSAIDs have which actions?

A
  • Analgesic.
  • Antipyretic.
  • Anti-inflammatory.
97
Q

Non-selective NSAIDs actions are largely due to what?

A

Inhibition of synthesis and accumulation of prostaglandins by cyclo-oxygenase (COX) enzymes COX-1 and COX-2.

98
Q

Prostaglandins cause what symptoms?

A
  • Hyperalgesia.
  • Allodynia.
  • Pain.
99
Q

COX-2 is induced where and by what?

A

Locally at sites of inflammation by various cytokines.

100
Q

Therapeutic benefit of NSAIDs mainly derives from?

A

Inhibition of COX-2.

101
Q

Why do NSAIDs decrese recruitent of leukocytes?

A

These produce inflammatory mediators.

102
Q

Why do NSAIDs suppress prostaglandin activity on nociceptors?

A

Prostaglandins act on peripheral terminals of nociceptors to decrease activation threshold.

103
Q

If NSAIDs cross the BBB, what are they able to do?

A

Suppress production of pain-producing prostaglandins in the dorsal horn of the spinal cord.

104
Q

Why is paracetamol not an NSAID?

A

Lacks anti-inflammatory activity and only acts centrally.

105
Q

Why do NSAIDs have limited analgesic efficacy?

A

Multiple signalling pathways cause nociceptor sensitisation.

106
Q

Why can nephrotoxicity arise as a result of long-term NSAID administration?

A

COX-2 is inhibited, but constitutively expressed by the kidney.

107
Q

Inhibition of COX-2 by NSAIDs can have what effect in renal disease?

A

Compromise renal haemodynamics.

108
Q

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

A

They are prothrombotic.

109
Q

Treatment of neuropathic pain?

A
  • Gabapentin and Pregabalin (anti-epileptics).
  • Amitryptyline, Nortryptiline and Desipramine (TCAs).
  • Carbamazepine.
110
Q

Neuropathic pain does not respond to?

A
  • NSAIDs.

- Opioids unless in high doses.

111
Q

How do Gabapentin and Pregabalin help in neuropathic pain?

A

Reduce cell surface expression of subunit α2δ of some voltage-gated Ca2+ channels that are upregulated in damaged sensory neurones.

112
Q

Reduction of cell surface expression of α2δ by gabapentin and pregabalin presumably has what effect on neurotransmitters?

A

Decreases neurotransmitters e.g. Glutamate and substance P from central terminals of nociceptive neurones.

113
Q

Gabapentin is often used in which condition?

A

Migraine prophylaxis.

114
Q

Pregabalin is often useful in which condition?

A

Painful diabetic neuropathy.

115
Q

Action of Amitriptyline, Nortryptiline and Desipramine in neuropathic pain?

A

Act centrally by decreasing reuptake of noradrenaline.

116
Q

Action of Carbamazepine in neuropathic pain?

A

Blocks subtypes of voltage-activated Na+ channels upregulated in damaged neve cel.

117
Q

First line treatment to control pain intensity and frequency of attacks in trigeminal neuralgia?

A

Carbamazepine.

CNS CLERKSHIP (43 decks)

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