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Clinical Pharmacology > Opioids > Flashcards

Opioids Flashcards

1
Q

What is nociception?

A

Non concious neural traffic due to trauma or potential trauma to tissue

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2
Q

What is pain?

A

Complex, unpleasant awareness of sensation modified by experience, expectation, immediate context and culture

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3
Q

Explain the seqence that occurs in a painful stimulus

A
  1. Nociceptors are stimulated
  2. Release substance P and Glutamate
  3. Stimulate affernent nerve fibre which synapses in the dorsal horn of the spinal cord
  4. Second order neurone fibres decussate at level of the spinal cord
  5. Synapse in the thalamus onto 3rd order neurone which project to the post central gyrus (sensory area)
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4
Q

Explain how pain is modulated peripherally?

A
  • Tissue damage by alpha delta and C fibres transmits pain to the thalamus
  • Tissue damage inhibits the substantia gelatinosa
  • By rubbing area better, A beta fibres stimulate the subtantia gelatinosa which in turn inhibits laminae 1 + 5 to prevent pain being transmitted to thalamus
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5
Q

How is pain modulated centrally?

A
  • Thalamus recieves input from periphery and activates the cortex and periaqueductal grey matter in the brain
  • Periaqueductal grey sends 5-HT and Enkephalins which are inhibitory signals to the dorsal horn to decrease pain
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6
Q

What are the endogenous opiod receptors in humans?

A
  • mui
  • delta
  • kappa

All GPCR

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7
Q

Where are the different endogenous opiod receptrs distributed throughout the body?

A
  • mui- supraspinal and GI tract
  • delta- wide distribution
  • kappa- spinal cord, brain and periphery
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8
Q

How does stimulation of opiod receptors cause analgesia?

A
  • Hyperpolarisation causes decreased substance P release
  • Increased dopamine release
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9
Q

Which receptors to opiods mainly exert their action by?

A

mui receptors (u)

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10
Q

Give an example of a strong opiod

A

Morphine

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11
Q

How does morphine work?

A
  • Strong affinity to mui receptors (minimal for kappa and delta)
  • Complete activation of mui receptor
  • Causes analgesia and euphoria
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12
Q

Explain the pharmacokinetics of morphine

A

Absorption

  • PO, IV, IM, SC, PR - oral is best for long term, IV for quick effect
  • Gut absorption is erratic
  • Significant first pass effect

Distribution

  • enters all tissues (inc. fetal)
  • struggles to cross blood brain barrier

Elminated

  • Renally
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13
Q

What are the 2 metabolised forms of morphine and the effects of each?

A

Morphine + glucoronic acid → M6G (analgesic) + M3G (euphoric effects)

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14
Q

What are some of the side effects of morphine?

A
  • respiratory depression- medullary resp centre less responsive to CO2
  • emesis - stimulates cehmoreceptor trigger zone
  • GI tract- decreased mobility, increased sphincter tone (constipation)
  • Cardiovascular - decreased BP, syncope
  • Miosis (pupil contriction)
  • Histamine release
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15
Q

Describe the pharmacokinetics of fentanyl (strong agonist)

A

Absorption

  • IV, epidural, intrathecal (CSF), nasal
  • 80-100% bioavailability

Distribution

  • Highly lipophilic, highly protein bound
  • High level of CNS corssing

Metabolised

  • Hepatically by CYP3A4

Elimination

  • short half life (6 hours)
  • renally excreted
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16
Q

What are some of the side effects of fentanyl?

A
  • Respiratory depression
  • Constipation
  • Vomiting
17
Q

How does fentanyl compare to morphine with regards to receptor binding?

A
  • 100x more potent
  • High affinity for mui receptor
  • Will displace morphine if given together
18
Q

Describe the pharmaokinetics of codeine (moderate agonist)?

A

Absorption: PO and Subcut

Metabolism

  • Pro drug metabolised to morphine via CYP2D6
  • CYP2D6 inhibited by Fluoxetine (+ other SSRIs)

Elimination

  • glucoronidation of morphine and renally excreted
19
Q

How does codeine compare to morphine with regards to potency?

A

1/10 th potency of morphine

20
Q

What are some of the side effects of codeine?

A
  • Constipation
  • Respiratory depression - worse in children
    • contra indicated in under 12s
21
Q

What is buprenorphine?

A

A mixed agonist-antagonist opiod

Has very high affinity for mui recepor (mui), has long duration of action but only a partial agonist

Acts as an antagonist at kappa receptors

22
Q

When is buprenorphine used?

A
  • Moderate to severe pain
  • Opiod addiction treatment
23
Q

What are some of the side effects of buprenorphine?

A
  • Respiratory depression
  • Low BP
  • Nausea
  • Dizziness
24
Q

Describe the pharmacokinetics of buprenorphine?

A

Absorption: transdermal (most common), buccal, sublingual

Distribution: very lipophilic

Metabolism: hepatic (CYP3A4) then glucoronidated

Elimination: mainly biliary, safe in renal impairment, t1/2 37 hours

25
Q

What kind of opiod is Naloxone?

A

Antagonist

26
Q

Describe the pharmacokinetics of Naloxone

A

Absorption

  • IV, IM, Intranasal, PO
  • Very low bioavailability (extensive 1st pass)
  • Rapid onset of action

Distribution: very lipophilic

Metabolism: hepatic → naloxone-3-glucuronide

Elimination: duration of action 30-60 mins, renally excreted

27
Q

How does Naloxone compare the morphine and buprenorphine with regards to affinity for the mui receptor?

A
  • Affinity mui > delta > kappa
  • Greater affinity than morphine
  • Affinity less than buprenorphine
28
Q

What are some of the side effects of naloxone?

A
  • Short half life → patients can go back into overdose as effects reverse
  • Give by slow infusion → allows morphine/ heroin to be excreted whilst nalazone is bound
29
Q

Explain how phosphorylation and uncoupling causes opiod tolerance?

A
  1. Opiods bind to mui receptor causes decrease cAMP → decreases pain
  2. Repeat exposure causes intracellular phosphorylation
  3. Arrestin binds which uncouples the G protein so there is no downstream signalling
  4. No decrease in cAMP → no decrease in pain
30
Q

How does opiod removal cause withdrawl symptoms?

A
  • Binding of opiod causes decrease in cAMP
  • When opiod is removed, get a rebound effect where cell floods with cAMP
  • Neurone excitability- excessively fire causing withdrawl symptoms
31
Q

What are some of the symptoms of opiod withdrawl?

A
  • Agitated
  • Anxious
  • Sweating
  • Vomiting
  • Diorrhoea
32
Q

What are some of the effects of overdose with opiods?

A
  • Dependence
  • Vomiting
  • Constipation
  • Hypotension/ bradycardia
  • Decreased sex drive
  • Histamine release
  • Miosis
  • Drowsiness
  • Respiratory depression → apnoea
33
Q

What is the major cause of death of opiod overdose?

A

Respiratory depression

Depressed respiratory centre can’t recognise increased CO2 , patient becomes more acidodic and apnoeic

34
Q

In which patients should opiods be used with caution?

A
  • Manual labourers/ Drivers
  • Elderly (less fat so tissue distribution different)
  • Bedbound
  • Asthmatics
  • Biliary tract obstruction
  • Respiratory Diseases
  • Renal Impairment
  • Pregnancy
35
Q

In which patients are contraindicated?

A
  • Hepatic failure
  • Acute respiratory distress
  • Comatose
  • Head injuries
  • Raised ICP
36
Q

When are opiods indicated in palliative care?

A
  • Pain
  • Shortness of breath
  • Manage side effects; nausea, constipation

Clinical Pharmacology (25 decks)

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