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Pharmacology and Therapeutics 2 Y2 > Opioids > Flashcards

Opioids Flashcards

1
Q

What is an opiate

A

An alkaloid derived from the poppy, Papaver somniferum

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2
Q

What is an opioid

A

Opioids are anything that behaves like an opiate (natural or synthetic)

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3
Q

Re opiate structure, what is important for the analgesic effect?

A

Tertiary nitrogen

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4
Q

What part of an opioid binds to receptor

A

Tertiary nitrogen

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5
Q

How to turn an opioid into an antagonist?

A

Extend tertiary nitrogen side chain by 3 carbons

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6
Q

What is the second most important part of an opioid for it to bind to a receptor

A

Hydroxyl group at position 3

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7
Q

Intravenous bioavailability of opioids?

A

100%

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8
Q

Opioids pKa? Implication for GI absorption?

A

More than 8, weak bases. So, poorly absorbed in stomach

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9
Q

Ionised or unionised in blood? Implication for tissue absorption? Opioids

A

Ionised, so not readily absorbed

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10
Q

How does lipid solubility effect potency, generally?

A

More lipid soluble, faster into brain, more powerful effect

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11
Q

What makes morphine the least lipid soluble?

A

The OH groups

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12
Q

how active are metabolites of morphine?

A

Active

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13
Q

Why are people who metabolize morphine poorly more likely to see negative side-effects

A

Because Morphine seems more likely to cause negative side-effects than the active metabolites

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14
Q

Which opioids are basically prodrugs? What are they metabolised into?

A

Heroine and codeine. Metabolised into morphine

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15
Q

Where is heroine metabolised into morphine?

A

In the brain

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16
Q

Active metabolite of morphine?

A

Morphine 6 glucoronide

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17
Q

Speed of metabolism and clearance of fentanyl? Impact on its effect

A

metabolized quickly and cleared, so it has a fast but short-lasting effect

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18
Q

Speed of metabolism and clearance of methadone? Impact on its effect

A

is metabolized slowly, so it accumulates in blood and fat, so it has a long-lasting effect (one of the reasons it’s used to ween people off of heroin)

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19
Q

Where is codeine metabolised into morphine?

A

liver

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20
Q

What metabolises codeine

A

2 cytochrome p450s

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21
Q

What is codeine metabolised into, %’s of each metabolite?

A

Norcodeine (90-95%, inactive) and morphine (active, 5-10%)

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22
Q

Why are some people good/some people bad metabolisers of codeine

A

common polymorphisms in the 2DY enzyme - People can be good or bad metabolizers of codeine

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23
Q

What receptors do opioids target

A

Opioid receptors

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24
Q

Endogenous opioids? (3/4)

A
  • Endorphins
  • Enkephalins
  • Dynorphins/neoendorphins
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25
Q

What function do endorphins regulate?

A

Pain/sensorimotor

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26
Q

What function do Enkephalins regulate?

A

Motor/cognitive function

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27
Q

What function do dynorphins regulate?

A

Neuroendocrin

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28
Q

What receptors do dynorphins activate?

A

Kappa

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29
Q

What receptors do Enkephalins activate?

A

Delta

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30
Q

What receptors do endorphins activate?

A

Mu or Delta and Mu again

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31
Q

How do opioids slow cellular activity? (3)

A
  1. Hyperpolarizing cells (increasing K+ efflux) – so nerves affected can’t fire again till the effect wears off
  2. Reducing the inward calcium current (impacts exocytosis and release of neurotransmitters
  3. Decreasing adenylate cyclase activity
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32
Q

Positive effects of opioids? (3)

A
  • Analgesia
  • Euphoria
  • Depression of cough centre (anti-tussive)
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33
Q

Negative effects of opioids?

A
  • Depression of respiration (medulla)
  • Stimulation of chemoreceptor trigger zone (nausea/vomiting)
  • Pupillary Constriction
  • G.I. Effects
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34
Q

How does pain reach the thalamus (start from pain reception)

A
  • Pain is usually sensed peripherally by sensory neurons
  • These relay information to the spinal cord (dorsal horn)
  • This information is then relayed along spino-thalamic neurons to the brain
  • The first place it reaches is the thalamus, which decides where to direct the information
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35
Q

What is the role of the PAG - PERIAQUEDUCTAL GRAY in the pain tolerance pathway

A

PAG region is the integrating centre for the PTP – it receives all the information and determines output

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36
Q

What does PAG stand for

A

PERIAQUEDUCTAL GRAY

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37
Q

Where does the thalamus send its pain sensory information

A

cortex and PAG

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38
Q

What does NRPG stand for

A

NUCLEUS RETICULARIS PARAGIGANTOCELLULARIS

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39
Q

Where does the dorsal horn send its pain information, and along what

A

along the spinothalamic tract to the NRPG (NUCLEUS RETICULARIS PARAGIGANTOCELLULARIS ) and thalamus

40
Q

Where does the cortex send its pain sensory information

41
Q

Where does the PAG send its information

A

TO the NRM

42
Q

What does NRM stand for

A

Nucleus raphe magnus

43
Q

What is the role of the NRM - nucleus raphe Magnus - in the pain tolerance pathway

A

which is the effector arm of the PTP. From there, the descending neurons try to depress the feelings of pain in the spinal cord

44
Q

What is the role of the hypothalamus in the pain tolerance pathway

A

constantly relaying information on your general state of health and can also activate the PAG The hypothalamus reduces pain tolerance if someone is in a lot of pain (so they still feel a lot of pain) in order to stop the body from wasting resources on doing anything other than healing i.e. moving around or being active

45
Q

What is the role of the locus conealeus in the pain tolerance pathway

A

the SNS effector, which is largely independent of the PTP It signals to the dorsal horn of the spinal cord to dampen the pain (think about when you’re playing sport – the LC is active and you feel little pain until after you finish when the SNS switches off releasing its inhibition on the spinothalamic nuclei),

46
Q

What is the role of the substantia gelatinosa in the pain tolerance pathway

A

which can process the information from the LC and modify the signal, to determine how much inhibition of the pain you actually get

47
Q

Where is the substantial gelatinosa found

A

in the dorsal horn

48
Q

Where does the thalamus put it signals out to in the PTP?

A

Cortex and PAG

49
Q

Where does the cortex put it signals out to?

50
Q

Where does the hypothalamus put it signals out to?

51
Q

Where does the PAG put it signals out to?

52
Q

Where does the NRM put it signals out to?

A

dorsal horn

53
Q

Where does the NRPG put it signals out to?

54
Q

Where does the LC put it signals out to?

A

Dorsal horn

55
Q

Are signals from the NRPG excitatory/inhibitory/both?

A

excitatory

56
Q

Are signals from the thalamus excitatory/inhibitory/both?

A

excitatory

57
Q

Are signals from the cortex excitatory/inhibitory/both?

58
Q

Are signals from the PAG excitatory/inhibitory/both?

A

excitatory

59
Q

Are signals from the NRM excitatory/inhibitory/both?

A

inhibitory

60
Q

Are signals from the hypothalamus excitatory/inhibitory/both?

61
Q

Are signals from the LC excitatory/inhibitory/both?

A

inhibitory

62
Q

Are signals from the dorsal horn excitatory/inhibitory/both?

A

excitatory

63
Q

Are signals from the substantia gelatinosa excitatory/inhibitory/both?

A

inhibitory

64
Q

What does LC stand for

A

locus coeruleus

65
Q

Where does the PAG receive signals from

A

Thalamus, cortex and hypothalamus

66
Q

Where does the dorsal horn receive signals from

A

LC, NRM and substantia gelatinosa

67
Q

Where do opioids act in the PTP

A

PAG, NRPG, Dorsal horn and periphery

68
Q

What receptors do opioids act on

A

Mew and opioid receptors

69
Q

How do opioids cause analgesia

A

Disinhibition - it switches off GABA in the PAG and NRPG which fires on NRM which suppresses pain

70
Q

How do opioids cause euphoria

A
  • Opiates enter the brain and bind to opioid receptors
  • They depress the firing rate of GABA neurons - DISINHIBITION
  • Remember GABA suppresses reward neurons
  • This means that the dopaminergic neurons increase their firing rate and euphoria is experienced
71
Q

Neurologically why do we cough? (what fibres, NT and nerve)

A
  • Ach/neurokinin (NK) C-fibres relay cough information via the vagus nerve to the cough centre
72
Q

Anti-cough NT?

73
Q

What receptors are found on the vomiting centre

74
Q

How are opioids anti-tussive? (3)

A
  • Opioids decrease the firing rate of C-fibres - Decreased sensory relay
  • They also have a direct depressant effect on the cough centre itself
  • They also inhibit the 5HT1A receptors, so you have more serotonin in the cough centre, which is anti-cough
75
Q

What senses blood CO2

A

Chemoreceptors

76
Q

Where is the resp control centre

77
Q

what coordinates respiratory rhythm generation (determines respiratory rate)

A

PRE-BOTZINGER COMPLEX

78
Q

How do opioids REDUCE RESPIRATORY RATE significantly (2)

A
  • Opioids inhibit the central chemoreceptors (reduce information relay to the medulla)
  • They also reduce rhythm generation in the pre-Botzinger complex
79
Q

how do opioids stimulate nausea/vomiting

A
  • Opiates cause disinhibition (of GABA) of the chemoreceptor trigger zone
  • The chemoreceptor trigger zone sends a signal of nausea to the medullary vomiting centre which leads to nausea and vomiting
  • There are also signals from the higher centres and the gut to the chemoreceptor trigger zone
80
Q

Where do opioids act to stimulate nausea/vomiting

A

chemoreceptor trigger zone

81
Q

How do opioids stimulate miosis

A
  • Opioids switch on the parasympathetic nerve which starts in the Edinger-Westphal nucleus
  • The parasympathetic nerve causes constriction of the pupils
  • The effect is disinhibition again by switching off GABA
82
Q

What is a good sign of heroine OD

A

Pinpoint pupils

83
Q

What effect do opioids have on the GI system

A
  • They inhibit secretions and gut contraction by effecting motor actions
  • Cause heavy constipation
84
Q

What is urticaria

A
  • Histamine release in a non-allergic response to opioids
  • Some kind of direct interaction of opioids with mast cells which causes histamine release
  • Seems to involve PKA
  • Doesn’t seem to need opioid receptors
  • Opioids needs to have an OH group on C6
85
Q

What does an opioid need to stimulate urticaria

A

Opioids needs to have an OH group on C6

86
Q

Key mechanism for opioid tolerance?

A

receptor internalization

87
Q

What proteins drive receptor internalisation

88
Q

High opioid exposure leads to … (arrestin conc.)

A

If opioids are constantly suppressing cells, the cell tries to desensitise itself to opioids
- Arrestin concentration increases and more receptors are internalized

89
Q

Explain the physical withdrawal effects of opioids

A

rebound effect of cells - They respond to opioids decreasing cellular activity by increasing adenylate cyclase – if you remove the opioid you then have cells with overactive adenylate cyclase – this causes a lot of the side-effects seen with withdrawal

90
Q

How do you combat the physical withdrawal effects of opioids

A

You need cellular adenylate cyclase to return to normal before withdrawal symptoms disappear and use methadone to ween people off it

91
Q

Why is opioid OD common

A

users who try to come off of the drugs, and then go back to them and have the same dose as before (even though their tolerance has decreased)

92
Q

Signs of opioid OD? (4)

A
  • Coma
  • Respiratory depression The major problem – difficult to reverse
  • Pin-point pupils
  • Hypotension Excessive histamine release
93
Q

Main problem of opioid OD

A

Respiratory depression The major problem – difficult to reverse

94
Q

treatment of opioid OD?

A

NALOXONE (opioid antagonist)

95
Q

What about naloxone makes it an opioid antagonist

A

3 carbon++ side chain on the tertiary nitrogen

96
Q

What is naloxone

A

NALOXONE (opioid antagonist)

Pharmacology and Therapeutics 2 Y2 (24 decks)

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