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Neuroscience and Rehabilitation 5MPT2015 (Y2) > Pain e.g. Analgesic and anti inflammatory drugs > Flashcards

Pain e.g. Analgesic and anti inflammatory drugs Flashcards

1
Q

Define nociception.

A

Process by which nociceptive information is detected by the brain.

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2
Q

Define Antinociception.

A

Blockade of nociception.

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3
Q

Define Analgesia

A

Blockade of pain

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4
Q

What are 4 types of Analgesic drugs?

A
  • Local anaesthetics e.g. Lidocaine
  • Non-steroidal anti-inflammatory drugs (NSAIDs) e.g. Aspirin, ibuprofen, paracetamol.
  • Opioids e.g. Morphine, codeine
  • Miscellaneous drugs (These relieve the pain by relieving the cause of the pain) e.g. Nitrates, triptans, angina etc.
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5
Q

How does acute pain respond to the 3 types of analgesic drugs?

A

Responds well to all 3 types of drugs.

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6
Q

Define chronic pain?

A

Pain for more than 3-6months duration.

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7
Q

How does chronic pain respond to different analgesic drugs?
For:
- Neuropathic pain
- Nociceptive pain.

A
  • Due to chronic nociceptive activation, responds well to opioids.
  • neuropathic pain due to adaptive changes responds poorly to opioids.
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8
Q

What are the 4 different types of chronic pain?

A
  • Nociceptive
  • Neuropathic
  • Visceral
  • Mixed
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9
Q

Give examples of chronic Nociceptive pain.

A
  • OA

- RA

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10
Q

What are the two types of Neuropathic pain, and give examples of each.

A

Central;

  • Post-stroke
  • Multiple sclerosis
  • Spinal cord injury
  • Migraine
  • HIV related neuropathic pain.

Peripheral;

  • Post-herpetic neuralgia
  • Diabetic neuropathy
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11
Q

Give examples of chronic Visceral pain.

A
  • Internal organ
  • Pancreatitis
  • Inflammatory bowel syndrome
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12
Q

Give examples of chronic Mixed pain.

A
  • Lower back
  • Cancer
  • Fibromyalgia
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13
Q

How do local anaesthetics work?

A
  • Local anaesthetics are Na+ channel blockers
  • They slow the rate at which channels revert to resting state.
  • Local anaesthetics block action potential generation by decreasing the number of Na + channels available to open
  • They have greatest effect in rapidly firing neurons
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14
Q

How can local anaesthetics be administered?

A
  • They’re given topically or infused near to the nerve to be blocked.
  • Can be administered locally to spinal cord to produce regional block, either; Epidurally or intrathecally i.e. during child birth.
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15
Q

What is the mechanism of action of NSAIDs?

A
  • Activation of the prostaglandins (messengers)
  • In the membrane there are phospholipids, which are acted upon by PLA₂, which splits Arachidonic acid from the membrane.
  • Arachidonic acid is the substrate for cyclooxygenase, which causes the production of the proteinoid’s (might be wrong term but idk) the three main ones are:
  • Tx (Thromboxane)
  • PG (Prostaglandin)
  • PGI₂ (Prostacyclin)
  • These are involved in mediating various phases of the inflammatory response.
  • As for the nociceptive effect, PGE₂ that is responsible for nociceptive responses.
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16
Q

How do NSAIDs work?

A
  • They inhibit cyclo-oxygenase (COX)

- COX produces eicosanoids e.g. PGE₂ from arachidonic acid.

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17
Q

What are the 3 main effects of NSAIDs?

A
  • Anti-inflammatory
  • Anti-pyretic i.e. anti-fever
  • analgesia
18
Q

What do prostaglandins do?

A
  • They do not stimulate nociceptors, they sensitise them to other mediators.
  • NSAIDs produce analgesia by preventing this sensitization.
19
Q

Which are the main NSAIDs that are used as analgesics?

A
  • Aspirin
  • Ibuprofen
  • Paracetamol
20
Q

What type of inhibitor to COX is aspirin?

And what is its duration?

A

A irreversible inhibitor, this is because it binds to COX and blocks its active site.

  • 4 hours
21
Q

What type of inhibitor to COX is ibuprofen?

And what is its duration?

A

A reversible inhibitor as it binds to the active site of COX, and is an alternative substrate and is eventually broken down by COX.

  • 4 hours
22
Q

What type of inhibitor to COX is paracetamol?

And what is its duration?

A

A indirect inhibitor of COX, don’t need to know why, seems like they’re not too certain either.

23
Q

What is one way to increase the effectiveness of NSAIDs?

A

Combine them with a weak opioid such as; Codeine in OTC medicines.

24
Q

How do Opioid analgesics work?

A

They produce analgesia by interaction with the endogenous opioid system.

  • Morphine acts on specific opioid receptors.
25
Q

what is the endogenous opioid system?

A
  • Innate pain-relieving system. It controls pain sensitivity under various conditions.
26
Q

What are the mediators used for the endogenous opioid system?

What are the main/ the first 2 to be isolated?

A
  • Peptides which activate the opioid receptors.

- The main 2 are Leu⁵ & met⁵- enkephalin.

27
Q

What are the 3 families of opioid peptides

A
  • endorphins e.g. b-endorphin
  • enkephalins e.g. [Met5]enkephalin, [Leu5]enkephalin.
  • dynorphins e.g. dynorphin A, dynorphin B
28
Q

What are the 3 types of opioid receptor?

A
  • (Mu the symbol of a U but with a tail going down on the right)
  • δ = delta
  • κ = Kappa
29
Q

What do opiates do?

A

They act with receptors to activate inhibitory pathways and inhibits nociceptive transmission.

30
Q

Describe in a flowchart like way the Ascending pathway of pain.

A

Afferent neurons –> DRG –> Spinal cord dorsal horn –> Thalamus –> Prefrontal cortex/ somatosensory cortex/ cingulate cortex.

31
Q

Describe in a flowchart like way the Descending pathway of pain.

A

From midbrain= Periaqueductal gray/ Raphe nuclei –> Dorsolateral funiculus (Opioids take effect on the neurons from PAG/RN —> DF).

DF—> spinal cord dorsal horn–> Thalamus—> Prefrontal cortex/ somatosensory cortex/ cingulate cortex.

32
Q

Where are opioid receptors found?

A
  • Periaqueductal gray (PAG)
  • Nucleus raphe magnus (NRM)
  • NRPG
  • dorsal horn of the spinal cord, especially lamina ll
33
Q

Describe in full the ascending pain pathway.,

A
  • Activation of nociceptive primary afferents (Ad or C fibres) which enter dorsal horn and synapse onto interneurons or projection neurons
  • Activation of projection neurones in the dorsal horn which travel to the brain in the spinothalamic tract
  • If one records firing of dorsal horn neurones, opioids inhibit firing and stop transduction of the signal to the brain. Inhibit release of glutamate and substance P from primary afferents
34
Q

Describe in full the descending pain pathway.,

A
  • Activation of PAG and NRM by morphine causes increase firing of descending pathway to dorsal horn.
  • This involves mainly serotonergic neurons and depletion of 5HT or 5HT antagonists decrease anti-nociceptive effect of morphine.
  • Effect in PAG and NRM is due to inhibition of release of GABA from local interneurons. This leads to dis-inhibition of the descending serotonergic pathway which decreases transmission of nociceptive information through the dorsal horn.
35
Q

At which receptor is Morphine a selective agonist for?

A

Mu.

36
Q

What are the effects of Morphine? pt.1

There’s 5

A

ANALGESIA

  • All kinds of acute & severe pain
  • Reduces sensation of pain (nociception) and the emotional response

EUPHORIA
- Depends on circumstances, varies with different opioids

RESPIRATORY DEPRESSION
- Selective depression of sensitivity to PCO2

MIOSIS

  • Pin-point pupils, diagnostic for opioid overdose
  • Parasympathetic stimulation via the Edinger Westphal nucleus

EMESIS
- Due to stimulation of chemical trigger zone in area postrema

37
Q

What are the effects of Morphine? pt.2
(There’s 7)
(Includes psychological effects)

A

CONSTIPATION

  • Increase in gut tone, decreased gut transit, due to high level of receptors on enteric neurons
  • Kaolin and morphine used to treat diarrhoea, loperamide (Imodium)

OPIOID-INDUCED HYPERALGESIA
- Roeckel et al. (2016). Neurosci. 338, 160-182.

COUGH SUPPRESSION
- All opioids suppress cough reflex, not an opioid effect, possibly due to stimulation of dextromethorphan receptor

HISTAMINE RELEASE

HYPOTENSION

TOLERANCE

  • Decrease response with repeated administration
  • High emesis > analgesia Low miosis, constipation

DEPENDENCE

  • Physical dependence
  • Withdrawal syndrome
  • Psychological dependence
38
Q

What are some Mu agonists

A

DIAMORPHINE (diacetylmorphine) – more lipophilic and more potent than morphine

BUPRENORPHINE – very lipophilic, given sublingually, partial agonist

OXYCODONE – cancer pain

FENTANYL - very lipophilic, very short acting, used as part of pre-medication for surgery. Fentanyl patches used for long term relief in cancer patients.

PETHIDINE – labour, minor surgery. No pin-point pupils

METHADONE – long acting, once daily dosing, used for maintenance of addicts

39
Q

What are 2 opioid drugs that are mixed opioid agonists/ uptake inhibitors?

A

mu -receptor agonist and noradrenaline and 5HT uptake inhibitor:

  • TRAMADOL
  • TAPENTADOL

(cause less respiratory depression?)

40
Q

What are 2 weak opioids used for mild pain.

A
  • CODEINE
  • DIHYDROCODEINE

(combined with NSAID in OTC preparations)

41
Q

What 2 drugs are used to treat opioid overdose as they are antagonists?

A
  • Naloxone

- Naltrexone (Longer duration of action)

42
Q

What drugs are used to treat opioid induced constipation?

A

Peripherally active antagonist

ALVIMOPAM
also paralytic ileus

QUATERNARY NALOXONE

Neuroscience and Rehabilitation 5MPT2015 (Y2) (20 decks)

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