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Clinical Pharmacology > 9.2 opioids > Flashcards

9.2 opioids Flashcards

1
Q

how is pain detected?

A

1) tissue damage = cells release prostaglandins, bradykinin and serotonin into tissue
2) nociceptors stimulated (pain receptors in tissue)
3) Release of substance P (acts locally for inflammation) and glutamate (stimulates afferent nerves for action potential in dorsal horn)

4) afferent nerve stimulated. get
- Sharp pain via A delta fibres = felt quickly as mylinated. will pull hand away from stimulus quickly

  • Dull pain/ throbbing via unmylinated C fibres = have reached AP threshold to stimulate. slower conducting.
    5) first order project onto second order fibres which decussate
    6) action potentials ascends up spinothalamic tract
    7) synapse in thalamus
    8) project to post central gyrus
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2
Q

how can we modulate pain peripherally and how can ‘rubbing it better’ modulate pain?

A

via the substantia gelatinosa in dorsal horn

tissue damage = stimulates afferent fibres of Alpha delta and C fibres. However also has inhibitory fibres that can help modulate pain.

Pain can also be modulated by ‘rubbing it better’ as it stimulates A beta fibres which stimulate the substantia gelatinosa = inhibit lamina = decrease pain signals going up to thalamus

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3
Q

how can we modulate pain centrally?

A

via the periaqueductal grey matter

Tissue damage occours

transmitted up to thalamus via spinothalamic tract

goes to periaqueductal grey matter which is usually inhibited via the cortex, however when we get a pain response the pain detected by cortex and thalamus can stimulate it

Periaqueductal grey matter then sends inhibitory endogenous signals down spinal cord which is mediated by 5HT and endogenous opioids (enkephalins, dynorphins and B endorphins)

this reduces the signal that reaches the thalamus and reduces the pain we are feeling.

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4
Q

where are MOP, DOP AND KOP receptors found and what kind of receptors are they?

A

MOP = suprispinal/GI tract

DOP = wide distribution

KOP = spinal cord/brain/periphery

they are GPCR

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5
Q

what endogenous opioids are released through stimulation of MOP(u) , DOP(a) AND KOP(k)?

A

MOP = enkephalins and B endorphins

DOP = enkephalins

KOPS = dynorphins

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6
Q

what is the mechanism of stimulation of MOP (u) , DOP (a) and KOP (k) receptors?

A

They are GPCRs

so stimulation =

  • reduced cAMP
  • MOP = outflow K
  • DOP = Ca influx
  • KOP = both

Result = hyper polarisation and decreased substance P release

result = analgesia

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7
Q

what effects does MOP(u) stimulation have?

A

MOP = enkephalins and B endorphins

result = analgesia, depression, euphoria, dependence, respiratory sedation

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8
Q

what effect does DOP(a) stimulation have?

A

DOP = enkephalins

result = analgesia, inhibit dopamine

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9
Q

what effect does KOP(k) stimulation?

A

KOP = dynorphins

result = analgesia, diuresis, dysphoria

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10
Q

what are the components of the WHO analgesic ladder?

A

simple analgesic e.g Paracetamol, NSAIDS

weak opioid e.g codine

strong opiid e.g morphine, fentanyl

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11
Q

what type of pain do strong opioids work best with?

A

malignant/ non malignant pain

chronic pain

acute chronic pain

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12
Q

what medication work best of neuropathic pain e.g diabetic feet pain due to damaged nerve?

A
  • anticonvulsants/ anti epileptics
  • tricyclic antidepressants
  • serotonin/ noradrenaline reuptake inhibitors
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13
Q

what are the general principles of opiods?

A

Generally act on MOP(u) (most ADR via stimulation of other receptor)

aim to modulate pain but can also be used in cough and diarrhoea and palliation

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14
Q

how is morphine

  • absorbed
  • distributed
  • eliminated
A

A STRONG OPIOID AGONIST

absorbed

  • PO, IV, IM, SC, PR
  • gut absorption erratic
  • significant first pass effect = 40% oral bioavailability

Distributed

  • rapidly enters all tissue including foetal
  • struggles to cross blood brain barrier

eliminated
- renally

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15
Q

why should you give morphine to pregnant ladies?

A

can get respiratory distress in the new born

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16
Q

what are the actions and side effects of morphine?

A

has strong affinity for MOP (u) receptors

actions

  • analgesia
  • europhia

ADR

  • resp depression as medulla res centre less responsive to CO2 (which drives breathing - won’t be able be to increase breathing rate to compensate)
  • emesis as stimulates chemoreceptor trigger zone
  • Decreased GI motility and increased sphincter tone
  • histamine release via mast cells = caution in asthmatics
17
Q

how is fentanyl

  • absorbed
  • distributed
  • metabolised
  • eliminated
A

A STRONG OPIOID AGONIST

Absorbed

  • IV, epidural, intrathecal, nasal
  • 80-100% bioavailability

Distribution

  • highly lipophilic, highly protein bound
  • high level of CNS crossing

metabolism
- hepatic

Elimination

  • 6 minute half life
  • renally excreted
18
Q

how is fentanyl different to morphine in its action?

A

higher potency
higher affinity for u MOP receptors

less histamine release, sedation and constipation

19
Q

what are the actions and the ADR of fentanyl?

A

action

  • analgesia
  • anaesthetic

side effects

  • respiratory depression
  • constipation
  • vomiting
20
Q

how is codeine

  • absorbed
  • metabolised
  • elimination
A

absorption
- PO, SC administration

metabolism
- codine to morphine via CYP2D6 (if you don’t have much of this enzyme naturally, won’t have any affect as won’t have any circulating morphine)

  • CYP2D6 can be inhibited by fluoxetine

Elimination
- glucoronidation of morphine and renal excretion

21
Q

what is codeines potency compared to morphine?

A

approx 1/10th potency

22
Q

what are the actions and side effects of codeine?

A

actions

  • mild to moderate analgesia
  • cough depressant

side effects

  • constipation
  • respiratory depression (worse in children under 12)
23
Q

how is buprenorphine

  • absorbed
  • distributed
  • metabolised
  • eliminated
A

A MIXED AGONIST ANTAGONIST

Absorbed
- transdermal, buccal, sublingual

distribution
- very lipophilic

metabolism

  • hepatic
  • then glucoronidation before biliary excretion

elimination

  • biliary over renal
  • safe in renal impairment
  • half life 37hrs
24
Q

how does buprenorphine compare to morphine?

A

high affinity for MOP u receptors, low kD

long duration of action

not easily displaced

low Emax as partial agonist = less analgesia but less side effects

lower efficacy

25
Q

what are the actions and side effects of buprenorphine?

A

action

  • moderate to severe pain
  • opioid addiction treatment (titrate down dose slowly)

side effects

  • resp depressio
  • low BP
  • nausea
  • dizziness
26
Q

how is naloxone

  • absorbed
  • distributed
  • metabolised
  • eliminated
A

A MIXED AGONIST ANTAGONIST

Absorbed

  • IV, IM, intranasal, PO
  • very low oral bioavailability as extensive first pass effect
  • rapid onset of action

Distribution
- rapid as very lipophilic

metabolism

  • hepatic
  • renally excreted

elimination
- duration of action 30-60mins

27
Q

what is the action of naloxone compared to morphine?

A
  • affinity for MOP>DOP>KOP

- greater affinity than morphine, less than buprenorphie

28
Q

what are the actions and side effects of naloxone?

A

action
- competitive antagonism of opioid

side effects

  • short half life
  • slow infusion
29
Q

how do synthetic opioids effect the amount of receptors and how can this cause withdrawal symptoms?

A

cells insert more MOP u opioid receptors as a result

more receptors = higher doses needed to fill at least 80% of receptors for a response of analgesia/euphoria.

need to gradually reduce intake and use something like methadone = reduced Emax and side effects e.g resp distress

30
Q

what is the most common cause of death in opioid overdose and how do you treat?

A

resp depression

treat with nalaxone

31
Q

what are the side effects of opioid addiction?

A 
dependence
vomiting
constipation
hypotension and bradycardia
decreased sex drive
resp distress => apnoea 
histamine release
32
Q

who would you avoid giving opioids to?

A 
manual labourers/drivers
elderly
bed bound
asthmatics
resp disease
renal impairment 
pregnant

Ignore in palliative prescribing

33
Q

what dosages can you get cocodamol in?

A

8/500mg = over the counter

30/500mg = prescription only

Clinical Pharmacology (27 decks)

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