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CPT (My own) > Opioids > Flashcards

Opioids Flashcards

1
Q

How is pain stimulated?

A 
Nociceptors stimulated
Release of substance P and glutamate
Afferent nerve stimulated
Fibres decussate
Action potential ascends
Synapse in thalamus
Project to post central gyrus
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2
Q

Name 2 specific pain afferent nerve fibres

A

A Delta fibre

C fibres

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3
Q

What pain do A delta fibres transmit

A

Sharp pain, myelinated

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4
Q

What pain do C fibres transmit?

A

Dull achey pain

Slower transmission

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5
Q

Which of the 2 types of pain afferent fibres need the higher stimulus

A

c fibres

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6
Q

Which specific parts of the dorsal horn do the 1st order synapse at?

A

Lamina 1 and 5

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7
Q

Which tract do the 2nd order neurones pass through?

A

Ascending lateral spinothalamic tract

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8
Q

Where does the 2nd order neurone synapse?

A

Thalamus

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9
Q

Where do 3rd order neurones synapse?

A

Pre-central gyrus

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10
Q

What is the key pain modulator in the peripheral system?

A

Substantia gelatinosa

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11
Q

What is the key pain modulator in the central system?

A

Peri-aqueductal grey

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12
Q

Describe the stimulatory pathway in peripheral pain?

A

Stimulator alpha and c fibres from damaged tissue to lamina 1 in dorsal horn then to the thalamus

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13
Q

Describe the inhibitory pathway in the peripheral pain

A

Inhibitory afferents towards substantial gelatinosa

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14
Q

How does ‘rub it better’ work?

A

Stimulates substantia gelatinosa, inhibiting lamina 1 and 5

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15
Q

How do we modulate pain centrally?

A

Pain afferents from dorsal horn to the thalamus, then stimulator paths to the cortex from then inhibitory stimulus to periaqueductal grey matter,

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16
Q

Give examples of endogenous opioids

A

Enkpehalins
Gynorphins
Beta-endorphins
Seratonin

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17
Q

What part do the endogenous opioids have on central pain modulation?

A

Inhibition from periaquaductal grey matter to dorsal horn

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18
Q

How are endogenous opioids categorised?

A

According to the class of GPCR receptors

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19
Q

What are the 3 classes of opioid receptors?

A

MOP
DOP
KOP

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20
Q

Where are MOP receptors found?

A

Supraspinal

GI tract

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21
Q

Where are DOP receptors found?

A

Wide distribution

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22
Q

Where are KOP receptors found?

A

Spinal cord
Brain
Periphery

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23
Q

What affect does all the endogenous opioids have on cAMP

A

Decreases it

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24
Q

What effect does MOP receptors have on minerals?

A

Outward flux of potassium

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25
Q

What effect does DOP receptors have on minerals?

A

Influx od calcium

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26
Q

What effect does KOP receptors have on minerals?

A

Efflux od potassium

Influx of calcium

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27
Q

What are the examples of MOP opioids?

A

Enkephalins

Beta endorphins

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28
Q

What are the examples of DOP opioids?

A

Enkephalins

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29
Q

What are the examples of KOP opioids?

A

Dynorphins

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30
Q

What is the order of the WHO analgesic ladder?

A

Simple analgesia- paracetamol NSAIDs

  • -> Weak opioids-codeine
  • -> Strong opioid- morphine, fentanyl
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31
Q

If the pain is neuropathic which analgesics are used preferentially?

A

Anticonvulsants
Tricyclics
Serotonin/NA reuptake inhibitors

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32
Q

What is the main receptor subtype with therapeutic effects?

A

MOP

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33
Q

What are uses od opioids?

A

Mainly to modulate pain
Cough
Diarrhoea
Palliation

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34
Q

Describe the absorption go morphine

A

PO, IV, IM, SC, PR
Gut absorption erratic
Significant first pass effect- 40% oral bioavailability

35
Q

Describe the distribution of morphine?

A

Lipophilic therefore rapidly enters all tissues including foetal
Struggles to cross the blood brain barrier

36
Q

Describe the metabolism of morphine

A

Morphine and glucuronic acid –? M6G and M3G which have neuroexcitatory effects

37
Q

Describe the elimination of morphine

38
Q

Which receptors do morphine have strongest affinity for?

39
Q

What are the actions of Morphine?

A

Analgesia

Euphoria

40
Q

What are the side effects of Morphine?

A

Respiratory depression- medullary res centre less responsive to CO2
Emesis- stimulate chemoreceptor trigger zone
GI tract- decreasing motility, increasing sphincter tone
CVS
Miosis
Histamine release- caution in asthmatics

41
Q

Describe the absorption of Fentanyl

A

IV, epidural, intrathecal, nasal

80-100% bioavailability

42
Q

Describe the distribution of fentanyl

A

Highly lipophilic, highly protein bound
High level of CNS crossing
Has higher distribution than Morphine

43
Q

Describe the metabolism of fentanyl

A

Hepatic via CYP3A4

44
Q

Describe the elimination of fentanyl

A

Half life is 6 mins

Renally excreted

45
Q

What is it compared to mirphine in terms of potency?

A

100 x potency
Higher affinity to mu receptors
Less histamine release, sedation and constipation

46
Q

What implication does the higher potency of fentanyl have on morphine

A

Can shift morphine off, smaller side effects

47
Q

What are the actions of fentanyl?

A

Analgesia

Anaesthetic

48
Q

What are the side effects of fentanyl?

A

Respiratory depression
Constipation
Vomiting

49
Q

What is the absorption of codeine?

A

PO, SC administration sometimes

50
Q

Describe the metabolism of Codeine?

A

Codeine goes to Morphine via CYP2D6 in the liver
CYP2D6 inhibited in Fluoxetine and other SSRI’s
Variable expression throughout the population, so can have no effect or excessive efefcts

51
Q

Describe the elimination of Codeine

A

Glucoronidation of morphine and renal excretion

52
Q

Codeine compared to morphine in terms of potency?

A

1/10th potency

53
Q

What are the actions of Codeine?

A

Mild- moderate analgesia

Cough depressant

54
Q

What are the side effects of Codeine?

A

Constipation

Respiratory depression- worse in children

55
Q

Give an example of a mixed agonist-antagonist

A

Buprenorphine

56
Q

Describe the absorption of Buprenorphine

A

Transdermal, Buccal, Sublingual

57
Q

Describe the distraction of Buprenorphine

A

Very lipophilic therefore distributes everywhere including the brain

58
Q

Describe metabolism of Buprenorphine

A

Hepatic via CYP3A4

Glucoronidation before biliary excretion

59
Q

Describe the elimination of Buprenorphine

A

Biliary > Renal
Safe in renal impairment
Long half life of 37 hrs

60
Q

What is the implications of the long half life?

A

Works as a patch

61
Q

Compare Buprenorphine to Morphine

A

Very high affinity for mu receptor–> low Kd
Long duration of action
Not easily displaced
Lower EMax, as partial agonist–> lower efficacy
Antagonist at K receptors

62
Q

What are the actions of Buprenorphine?

A

Moderate to severe pain
Especially chronic pain
Opioid addiction treatment

63
Q

What are the side effects of Buprenorphine

A

Respiratory depression
Low BP
Nausea
Dizziness

64
Q

Describe absorption of Naloxone

A

IV, IM Intranasal, PO
Very low oral bioavailability as extensive first pass effect
Rapid onset of action
Short onset of action

65
Q

Describe the distribution of naloxone

A

Rapid distribution as very lipophilic

66
Q

Describe the metabolism of Naloxone

A

Hepatic–> Naloxone-3-glucoronide

Renally excreted

67
Q

Describe the elimination of Naloxone

A

Duration of action 30-60 mins

68
Q

Compare Naloxone to Morphine

A

mu>delta>kappa
Greater affinity than morphine
Affinity less than Buprenorphine

69
Q

What are the actions of Naloxone?

A

Competitive antagonism of opioid

70
Q

What are the side effects of Naloxone?

A

Short half life

Slow infusion

71
Q

Why must Naloxone be given in slow infusion?

A

Allowing the stronger drug to be metabolised and excreted to non toxic levels while the competitive inhibitor that Naloxone is able to bind and compete for receptors

72
Q

What are the 2 mechanisms of opioid tolerance?

A

Phosphorylation and uncoupling

cAMP production

73
Q

What is the effect of opioid via phosphorylation and uncoupling?

A

Decreased cAMP which would result to decreased pain via linking with G protein

74
Q

What happens to the phosphorylation and uncoupling process on repeated exposure to opioids?

A

Results in decreased sensisitivty

Arrestin protein binds to the Mu receptors instead and GPCR is displaced so no more downstream cAMP

75
Q

How does repeated exposure to opioids affect cAMP?

A

Rebound effect when opioid removed and instead get flood of cAMP
Decreased neuronal excitability, increased depolarisation
Withdrawal symptoms

76
Q

What can be the effects of opioid overdose?

A

Mu receptor
Variable effects pf doses
Respiratory depression most common cause of death
Can decrease effects- delta agonists and serotonin agonists

77
Q

What is the treatment of opioid overdose?

A

Naloxone infusion

78
Q

Explain the process of respiratory depression in overdose?

A

Drowsyiness decreases breathing–> lowers CO2–> decreased medullary CO2 response–> Decreased respiratory rate –> Increased acidotic state

79
Q

What special considerations are there for opioid prescriptions?

A 
Manual laboureres
Elderly
Asthmatics
Biliary tract obstruction
Resp diseases
Renal impairment
Pregnancy
80
Q

Why do special considerations need to be made with opioids?

A

Make you drowsy

81
Q

What are contraindications of opioids?

A 
Hepatic failure
Acute respiratory distress
Comatose
Head injuries
Raised ICP
82
Q

What indications opioids have on palliative care?

A

Pain

Shortness of breath

83
Q

What side effects are there in opioid usage on palliative care?

A

Nausea

Constipation

CPT (My own) (6 decks)

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