K3iii: Opioid Syllabus – Opioids

Definitions

  • Alkaloid = nitrogen containing base of a plant origin
  • Opium = dry, powdered mixture of alkaloids obtained from poppy plant
    • The principle alkaloid (50%) is M but there are many alkaloids in the mixture
  • Opiate = a drug derived from opium
  • Opioid = all exogenous substances that bind to opioid receptors to produce some agonist effect
  • Endogenous opioid = family of endogenous opioid peptide ligands which act by binding opioid receptors (endorphins, dynorphins, enkephalins)
  • Narcotic = Gk = stupor, any compound producing ‘numbness’ to external stimuli

Classification

  • ORIGIN
  • CHEMICAL
  • CLINICAL PROFILE

Origin

  • Exogenous/endogenous → endorphins, dynorphins, enkephalins

Chemical

  • Natural alkaloid
    • PHENANTHRENES → morphine, codeine
  • Semi-synthetic
    • Preserved fine ring skeleton (not essential for opioid activity)
    • But alterations to major functional groups → heroin, oxycodone, buprenorphine
  • Synthetic
    • Fine ring structure is altered
    • Do not have structure of Morphine, but contain phenanthrene nucleus of morphine
    • Not a chemically modified version of M, they are manufactured by denovo synthesis

PHENYLPIPERIDINES → PETHIDINE, FENTANYL, REMI, ALFENTANYL

Clinical Profile

  • Latency (time to peak) & duration
    • Ultrashort latency + ultrashort DoA → REMIFENTANYL
    • Ultrashort latency + short DoA → ALFENTANYL
    • Short latency, intermediate DoA → FENTANYL, PETHIDINE
    • Intermediate latency, long DoA → MORPHINE
  • Specificity & efficacy
    • Agonist
    • Partial agonist
    • Antagonist

Properties

  • CEUTIC all opioids are H2O soluble salt preparations

Physical Properties

Drugs

pKa

M

7.9

Pethidine

8.5

F

8.4

Alfentanyl

6.5

REMI

7.1

Methadone

9.3

Drugs

% unionised

M

23%

Pethidine

5%

F

10%

Alfentanyl

90%

REMI

67%

Methadone

1%

Drugs

n-octanol/H2O

M

1.4

Pethidine

39

F

860

Alfentanyl

130

REMI

17.9

Methadone

115

Drugs

VD CC (L/kg)

M

0.2

Pethidine

1.5

F

0.7

Alfentanyl

0.2

REMI

0.07

Methadone

–

Drugs

VD SS (L/kg)

M

3.2

Pethidine

9.4

F

4

Alfentanyl

0.86

REMI

0.4

Methadone

6

Drugs

PPB

M

35%

Pethidine

65%

F

85%

Alfentanyl

90%

REMI

80%

Methadone

85%

Drugs

Clearance

(mL/kg/min)

M

15

Pethidine

10

F

13

Alfentanyl

6.4

REMI

50

Methadone

1.5

Drugs

HER

M

0.7

Pethidine

0.8

F

0.9

Alfentanyl

0.4

REMI

N/A

Methadone

–

Drugs

Dist t ½ (min)

M

15

Pethidine

10

F

13

Alfentanyl

11.6

REMI

1 min

Methadone

0.9

Drugs

Elim t ½ (hrs)

M

3

Pethidine

3 – 5

F

3.6

Alfentanyl

1.6

REMI

5 min

Methadone

35

Drugs

t½ keo (min) 

M

Pethidine

F

4 – 5mins

Alfentanyl

0.6 – 2.3

REMI

1.5 min

Methadone

Drugs

C5HT (after 4hr infusion)

M

Pethidine

F

4hrs

Alfentanyl

60 mins

REMI

4 min

Methadone

  • Ionisation = ↓lipid solubility
  • Low octanol/H2O coefficient = hydrophilic
  • Morphine = poor lipid solubility → because -OH at C3 & C6

Structure

  • Amine group = essential for opioid agonist activity
    • +ve charge necessary to bind strongly to ANIONIC opioid receptor
  • Aromatic ring = phenol group attached to quaternary carbon
  • Quaternary carbon (C13) = carbon atom attached to four others → it is chiral & allows existence of enantiomers → attached to Phenolic Ring & Ethane Chain
  • Ethane chain ( – CH2 – CH2 – ) = separates quaternary carbons from N atom in amine group

Isomerism

  • Dextro & Levo enantiomers possible due to CHIRAL CARBON (C13)
  • Only levoratory exhibits agonist activity

SAR

  • C3 = maximum opioid potency
    • Methylating this group (adding CH3) = makes codeine
    • Codeine x 10 less potent cf. M

But Codeine has reduced Metabolism → ∴ codeine has better OBA cf. M

  • C6 = addition of large side chains to C6 = ↑POTENCY because ↑lipid soluble e. HEROIN has a larger side chain at C6 (but this potency partially offset because also has masked the -OH at C3)
  • N17 = Substitution of phenylethyl group into nitrogen17 ↑agonist activity i.e. FENTANYL, as well as ↑lipid solubility
  • C14 = replacing nitrogen methyl group at N17 is coupled to C14 hydroxylation = formation of PURE ANTAGONIST → Naloxone

Indications, Administration, Dosing

Indications

  1. Analgesia
  2. Premed
  3. Attenuate CV response to laryngoscopy
  4. As a primary anaesthetic agent
  5. Tx heroin withdrawal

Route

  1. Enteral
    • Oral → M, Codeine, Endone, Tramadol, Methadone
    • PR → Oxycodone
  2. Parenteral
    • SC, IM, IV → M, F, Pethidine
    • Neuraxial → M, F, Pethidine
      • Epidural = 10% IV dose
      • Intrathecal = 10% epidural dose
  1. Topical
  • F, Buprenorphine

Dose → google ANZCA opioid dose equivalent for their PDF statement

Opioid

Morphine

Oral

30mg

Parenteral

10mg

Codeine

200mg

120mg

Endone

15mg

15mg

Pethidine

240mg

100mg

Fentanyl

–

100mcg

Alfentanil

–

1mg

Remifentanil

–

100mcg

Mechanism of Action

  • Opioids produce effect by binding µ opioid receptor
  • µ opioid receptor located throughout CNS, but concentrated in periaqueductal grey matter near 4th ventricle & substantia gelatinosa of dorsal horns of SC
  • Gi GPCR
    • Closure of voltage sensitive Ca2+ channels on presynaptic membrane → ↓intrac Ca2+
    • Post-synaptic stimulation of K-efflux → hyperpolarisation
    • Inhibition of AC → ↓cAMP
  • OVERALL → ↓cell membrane excitability, ↓transmission of nociceptive signals

Opioid Receptors

M receptor

2 subtypes

  1. µ1 = supraspinal analgesia
  • Analgesia
  • Miosis
  • Euphoria
  1. µ2 = spinal analgesia
  • Resp D
  • Inhibits GI motility
  • Euphoria
  • Dependence
  • Urinary retention
  • Pruritus

Prototype agonist = MORPHINE

δ-receptor

2 subtypes

  • Activation results in analgesia & resp depression
  • Spinal analgesia

Prototype agonist = ENKEPHALINS

k-receptor

3 subtypes

  • Activation results in:
  • Miosis
  • Dysphoria
  • Inhibition ADH release (diuresis)
  • Less analgesia
  • Dependence

Prototype against = DYNORPHINS

Opioid Receptor Activation

  • Endogenous peptide opioids (Endorphins, dynorphins, enkephalins) activate their specific opioid receptor
  • Overall ↓ neurotransmission
    • PRESYNAPTIC INHIBITION of NT release (Ach, DA, NA, sub P)
    • POST-SYNAPTIC INHIBITION of NT release
  • Opioid drugs mimic the actions of endogenous ligands
  • The effect the drug produces depends on:
    1. Affinity for opioid receptor
      • +ve charged amine essential to bind anionic opioid R
      • ↑opioid receptor occupancy = ↑opioid effects
    2. Specificity of binding: µ, k, δ receptor
    3. Efficacy of opioid
  • Full agonist = maximal biological response
  • Partial agonist = submaximal response
  • Antagonist = no biological effect
  • Mixed agonist-antagonist = simultaneously an agonist one receptor & an antagonist at another

Affinity & Efficacy of Opioids at Different Receptors

Full Agonist

Morphine

µ

+++

k

+

σ

Pethidine

+++

+

Fentanyl

+++

+

Alfentanil

+++

+

Remifentanil

+++

+

Partial Agonist

Buprenorphine

Partial Agonist

Nil

Tramadol

Partial Agonist

Nil

Antagonist

Naloxone

−−−

−

Pharmacodynamic Effects

CNS

  • Analgesia
    • Mainly due to peripheral opioid rec activation
    • ↑pain threshold (↑ stimulus required to activate nociception)
    • ∆ pain perception/response → Europhia
    • Sedation
    • Dull C fibres > Sharp Aδ fibres
  • Sedation
  • Miosis
    • ↑parasymp outflow of CNS

Resp

  • Ventilatory depression
    • ↓CO2 responsiveness
      • Dose dependent respiratory depression
      • µ receptor of ventrally medulla agonism
      • ↓brainstem response to CO2
  • Airway effects
    • Antitussive → by central opioid α agonism
    • Bronchospasm → histamine release provoked by opioids
    • ↓ciliary activity
  • CVS
    • – VE INOTROPY
        • Pethidine causes marked myocardial depression
    • – VE CHRONOTROPY
        • Central vagal (X) excitation
        • Depression of AV Nodal Conduction (exception pethidine → tachycardia)
    • ↓SVR
        • Histamine release → VD
  • GU
    • Urinary retention
    • Ureteric colic
    • Uterine contraction

∴ opioids cause SMOOTH MUSCLE CONTRACTION

NB: Opioids can worsen pain of ureteric colic ∴ pethidine is preferred 

  • GI
    • N&V → stimulation of µ receptors on CTZ floor 4th ventricle
    • ↑smooth m. tone → delayed gastric emptying, reflux, constipation, biliary colic
  • Immunological
    • Histamine release (M > Pethidine > F)

NB: histamine release is not opioid R mediated & true allergy to opioids is uncommon

 

  • MSK
    • Pruritus → due to central effects & some histamine release
      • Usually post neuraxial administration
      • Intrathecal opioids cause pruritus by segmental excitation within SC
    • Muscle rigidity → esp thorax/abdomen
      • Due to excitation
      • Especially with high dose opioid