Pain Management and OUD Flashcards
What area of the brain do opioids effect?
They produce feelings of pleasure by activating the ventral tegmental area and releasing dopamine from the nucleus accumbens
What is a PDMP?
Prescription Drug Monitoring Program is an electronic database that relays information on filled prescriptions for controlled substances and can assist in identifying opioid misuse in an individual patient.
Buprenorphine MOA
Partial agonist of the mu receptor.
Weak kappa receptor antagonist.
Delta receptor agonist.
Potent analgesic acting on the CNS producing a ceiling effect on respiratory depression.
Buprenorphine Pharmacokinetics
Bioavailability: PO = high first-pass effect, SL bypasses the first-pass effect.
Absorption: Peak effect 3-4 hours
Distribution: highly lipophilic, crosses blood-brain barrier
Metabolism: metabolism by cytochrome CYP3A4 enzymes after it enters the body and forms an active metabolite, norbuprenorphine, with weak intrinsic activity.
Half-Life: 38 hours
Excretion: fecal excretion
Urine: high levels of norbuprenorphine metabolite.
Buprenorphine Dosing
SL: 2-4mg and titrate up to 8mg-24mg
IM: 300mg extended release monthly
Induction: when patients experience mild to moderate withdrawal symptoms
Buprenorphine Special Considerations
Renal: no contraindication
Liver: reduced dose to prevent toxicity
Buprenorphine Adverse Effects
Anticholinergic: CNS depression, QT prolongation, HypoTN, lowered Sz threshold.
N/V, Drowsy, Dizzy, HA, memory loss, diaphoresis, dry mouth, myosis, sexual adverse effects, urinary retention.
CYP3A4 Agonists = metabolize Buprenorphine Faster
Carbamazapine
Phenytoin
Rifampin
CYP3A4 Antagonists = metabolize Buprenorphine Slowly
fluvoxamine
ketoconazole
indinavir
erythromycin
saquinavir
Buprenorphine vs Methadone
The drug is safer even at high doses.
Optional therapeutic doses can be achieved relatively quickly.
There is a lower risk of substance misuse and diversion.
The drug is associated with less stigma than methadone.
Patients can obtain the medication from any healthcare provider, eliminating the need for specialized methadone clinics.
Due to its partial opioid receptor agonist activity, buprenorphine is less likely to cause euphoria compared to full agonists such as methadone or morphine, reducing the likelihood of misuse or diversion.
Buprenorphine treatment typically lasts 3 to 6 months or even 1 to 2 years, whereas methadone treatment is often lifelong.
Buprenorphine/Naloxone MOA
Buprenorphine is a long-acting opioid that binds with high affinity at the mu receptor.
Naloxone is a pure opioid receptor antagonist combined with buprenorphine to reduce abuse potential.[3] Naloxone competes and displaces other opioids from the mu, kappa, and delta receptors, diminishing their effects.
Buprenorphine/Naloxone Pharmacokinetics
Absorption: Bioavailability is higher for SL for buprenorphine and lower for Naloxone.
Distribution: Buprenorphine high plasma binding, Naloxone weak plasma binding
Metabolism: metabolism by cytochrome CYP3A4 enzymes after it enters the body and forms an active metabolite, norbuprenorphine, with weak intrinsic activity.
Half-Life: 38 hours
Excretion: fecal excretion
Urine: high levels of norbuprenorphine metabolite.
Anticholinergics to avoid while on Buprenorphine/Naloxone
Benztropine, oxybutynin, diphenhydramine, scopolamine, antipsychotics, and tricyclic antidepressants as they can increase the risk of urinary retention and constipation
MOA’s to avoid while on buprenorphine/naloxone
Phenelzine, tranylcypromine, and linezolid with opioids, including buprenorphine, may result in serotonin syndrome.
Methadone MOA
Binds to opiate receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression. Methadone has also been shown to have N-methyl-D-aspartate (NMDA) receptor antagonism.
Methadone Pharmacokinetics
Onset of action: Oral: Analgesic: 0.5 to 1 hour; Parenteral: 10 to 20 minutes.
Peak effect: Parenteral: 1 to 2 hours; Oral: Continuous dosing: 3 to 5 days.
Distribution: Lipophilic, highly protein bound.
Metabolism: Hepatic; N-demethylation primarily via CYP3A4, CYP2B6, CYP2C19, CYP2C9, and CYP2D6 to inactive metabolites.
Excretion: Urine
Methadone Adverse Effects
Anticholinergic: CNS depression, QT prolongation, HypoTN, lowered Sz threshold.
N/V, Drowsy, Dizzy, HA, memory loss, diaphoresis, dry mouth, myosis, sexual adverse effects, urinary retention.
Methadone Dosing Precautions
Dose cautiously if renal or liver impairment is present
Why is Methadone effective in treating OUD?
It reduces cravings. Methadone is effective in treating OUD due to its very long half-life, which reduces cravings and dulls the euphoric effects of other opioid agonists. Because of its full mu opioid agonist properties, methadone is also efficacious in pain control and is thought to be less likely to produce tolerance due to its antagonistic effects at the N-methyl-d-aspartate (NMDA) receptor.
Which medication is not routinely used in the management of chronic pain?
Naltrexone: Medications used in OUD include buprenorphine, methadone, and naltrexone. Naltrexone, an opioid antagonist, is not routinely used in the management of chronic pain.
Patient Education on OUD treatment
Proper administration.
Discuss common side effects.
Drug take-back programs
Pain Definition
“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”
Nociceptive Pain
Occurs as a result of nerve receptor stimulation following a mechanical, thermal, or chemical insult.
Includes: Somatic, visceral, and central pain.
Somatic Pain
Nociceptive pain associated with muscle, skin, or bone injury.
Visceral Pain
Nociceptive pain associated with the visceral organs.
Central Pain
Nociceptive pain that is from MS, SCI’s, Migraine, and Post-stroke syndrome
Neuropathic Pain
Caused by abnormal signal processes in the CNS.
Peripheral Pain
Neuropathic pain that is from DM and postherpetic neuralgia.
Inflammatory Pain
A subtype of nociceptive pain that results from the release of proinflammatory cytokines at the site of tissue injury.
Present in acute pain and chronic pain.
A patient complains of pain from a migraine. How would the practitioner classify this type of pain?
Central Neuropathic Pain: Examples of central neuropathic pain syndromes include pain from multiple sclerosis, spinal cord injuries, migraine, and poststroke syndrome. Peripheral neuropathies include pain from diabetes and postherpetic neuralgia. Inflammatory pain may be present in acute pain from bruises or infection and chronically in pain from rheumatoid arthritis or osteoarthritis. Somatic pain is associated with muscle, skin, or bone injury and is often well localized.