NR 546 Week 6 Assignment Addiction Medication Table

Drug Name

Indication

Neurotransmitter(s) Affected

Target Symptoms

Half-life (T1/2), Metabolism (CYP 450 enzyme)

Considerable Side Effects (connection to NT or to circuit in affected brain)

Initial Dosing Reflection

Special lifespan considerations (age, pregnancy, breastfeeding)

Buprenorphine (Subutex)

Induction and maintenance of opioid use disorder; other formulations used to treat pain.

Half-life: ~24–60 hours (sublingual, variable). Metabolism: primarily CYP3A4 (N-dealkylation) and UGT glucuronidation

Sedation, respiratory depression (m-agonism at brainstem respiratory centres). Constipation (m receptors in GI). Sweating (autonomic/monoaminergic effects), headache. Hepatic enzyme increase (metabolism). Precipitated withdrawal when administered to an individual using full agonists (competitive partial agonism).

Induction when in moderate withdrawal (COWS ≥8–12). Typical initial 2–4 mg SL, reassess in 1–2 hr and titrate. Common maintenance 8–16 mg/day (up to 24–32 mg/day in some cases). Caution in severe hepatic impairment; preferred monoform in pregnancy when indicated; coordinate OB care.

Buprenorphine/Naloxone (Suboxone, Zubsolv, Bunavail)

Opioid use disorder (maintenance and outpatient). Combination reduces misuse/IV use.

Neurotransmitters/Target symptoms:
Buprenorphine: partial μ‑agonist. Naloxone: opioid antagonist (μ). Modulates dopaminergic reward pathways.

Buprenorphine half-life ~24–60 hrs (sublingual). Naloxone has low sublingual bioavailability; IV half-life 30–80 min. Buprenorphine is metabolised by CYP3A4; naloxone is primarily metabolised via hepatic glucuronidation.

As with buprenorphine: constipation, sedation, and nausea. In sublingual administration, Naloxone is insignificant systemically but may cause withdrawal when intravenously administered (antagonism at m receptors).

Begin at withdrawal: dosage 2-4mg SL, increase to effect; usual maintenance dosage 8-16mg buprenorphine component/day. Not a preferred drug to become pregnant with (monoform buprenorphine is commonly used).

Methadone (Dolophine, Methadose)

The use of opioids (maintenance through licensed clinics) and acute severe pain (specialty).

Neurotransmitters/Target symptoms:
Full μ‑opioid receptor agonist; NMDA antagonist at higher doses. Affects dopaminergic reward circuits.

Highly variable half-life: ~8–59 hours (commonly 24–36+ hrs). Metabolism: CYP3A4, CYP2B6, CYP2D6 (interactions common).

Respiratory depression (μ‑agonism). QT prolongation/torsades (cardiac ion channel effects). Sedation, constipation (μ receptors). Hypogonadism with chronic use (endocrine suppression).

Treatment for OUD should be initiated in clinics; most often, the starting dose is 20-30mg, followed by strict monitoring and gradual increase of the dose. Maintenance individualised( usually 60-120 mg/day). Watch interactions and QT protraction; take precautions with the geriatric and during pregnancy, and seek specialist attention.

Naltrexone (Revia, Vivitrol) 

Neurotransmitters/Target symptoms:
Full μ‑opioid receptor agonist; NMDA antagonist at higher doses. Affects dopaminergic reward circuits.

Highly variable half-life: ~8–59 hours (commonly 24–36+ hrs). Metabolism: CYP3A4, CYP2B6, CYP2D6 (interactions common).

Respiratory depression (μ‑agonism). QT prolongation/torsades (cardiac ion channel effects). Sedation, constipation (μ receptors). Hypogonadism with chronic use (endocrine suppression).

Starting in OUD at the clinic, the starting dose is usually 20-30 mg, and close monitoring and gradual increase are done. Maintenance individualised (usually 60-120mg/kg/day). Keep an eye on the interactions and QT prolongation; be careful with the elderly and pregnancy under the supervision of a specialist.

Acamprosate (Campral)

Alcohol use disorder – justifies abstinence following detoxification.

Neurotransmitters/Target symptoms:

Adjusts glutamatergic (NMDA) and GABAergic transmission – assists in restoring balance in excitatory/inhibitory interfaces due to chronic alcoholism.

Half-life ~20–33 hours. Not metabolised by CYP450; eliminated primarily unchanged by the kidneys (renal excretion).

Diarrhoea, GI upset. Anxiety, insomnia (CNS glutamate/GABA modulation). Rare reports of suicidal ideation (monitor mood).

Normal adult dose 666 mg as three doses per day ( 333 mg tablet TID). Correct renal impairment; should not be used in severe renal inadequacy. Begin during the abstinence of a patient.

Disulfiram (Antabuse)

Alcohol use disorder — aversion therapy to deter drinking by causing an unpleasant reaction with alcohol.

Neurotransmitters/Target symptoms:
Inhibits aldehyde dehydrogenase (ALDH) → acetaldehyde accumulation; produces peripheral and central aversive/autonomic effects.

The long-term effects are caused by the irreversible inhibition of ALDH; it may take days to weeks to wear off. Liver metabolism (metabolised through many pathways, not determined by a single CYP enzyme).

Facial flushing, tachycardia, nausea, vomiting (acetaldehyde accumulation). Hepatotoxicity (rare but serious) — monitor LFTs. Neuropathy, psychosis (rare). Drowsiness, metallic/garlic taste.

Normal: 500 mg single daily 1-2 weeks loading, 250mg/kg maintenance (125-500 mg/day). Make patient abstinent (12-48 hrs) prior to beginning. Should not be used during pregnancy and should be used with hepatic disease.