Block 3 materials (Opioids Drug abuse) Flashcards by isabelle courtney

Butorphanol

MOA:

Clinical uses:

Adverse effects:

Mixed opioid agonist-antagonist

MOA:
κ-opioid receptor agonist & μ-opioid receptor partial agonist.

Nasal formula

Clinical uses:
Severe pain (i.e migraines & labor)

Adverse effects:
1) Respiratory depression (less than full opioid agonists)
2) Withdrawal symptoms if used with a full agonist (not easily reversed with naloxone

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Mixed opioid agonist-antagonist

MOA:
κ-opioid receptor agonist & μ-opioid receptor partial agonist.

Clinical uses:
Severe pain (i.e migraines & labor)

Adverse effects:
1) Respiratory depression (less than full opioid agonists)

Butorphanol

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Pentazocine

MOA:

Clinical uses:

Adverse effects:

Mixed opioid agonist-antagonist

MOA:
κ-opioid receptor agonist & weak μ-opioid receptor antagonist/partial agonist.

Clinical uses:
1) Analgesia for moderate-severe pain

Adverse effects:
1) Opioid withdrawal symptoms if taking a full opioid agonist (due to competition for opioid receptors)

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Mixed opioid agonist-antagonist

MOA:
κ-opioid receptor agonist & weak μ-opioid receptor antagonist/partial agonist.

Clinical uses:
1) Analgesia for moderate-severe pain

Adverse effects:
1) Opioid withdrawal symptoms if taking a full opioid agonist (due to competition for opioid receptors)

Pentazocine

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Tramadol

MOA:

Clinical uses:

Adverse effects:

MOA:
A very weak opioid agonist that inhibits the reuptake of norepinephrine & serotonin

Clinical use:
Chronic pain

Adverse effects:
1) Seizures (reduced threshold)
2) Serotonin syndrome

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MOA:
A very weak opioid agonist that inhibits the reuptake of norepinephrine & serotonin

Clinical use:
Chronic pain

Adverse effects:
1) Seizures (reduced threshold)
2) Serotonin syndrome

Tramadol

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Opioids full agonists

MOA:

Clinical uses:

Adverse effects:

Maintenance vs intoxication

Morphine (oxymorphone & hydromorphone), Heroin (diacetylmorphine), & Meperidine
(all long acting)

Fentanyl, Codeine (oxycodone & hydrocodone), & Methadone

MOA:
Full agonists at opioid receptors
μ (β-endorphin),
δ (enkephalin), & κ (dynorphin)

They close presynaptic Ca2+ channels & open postsynaptic K+ channels to reduce synaptic transmission & inhibit the release of ACh, Norepi, 5-HT, Glutamate, & Substance P.

Clinical uses:
1) Analgesia
2) Euphoria
3) Sedation
4) Cough suppressants (Codeine)

Adverse effects:
1) Constipation (all)
2) Bacteremia, HEP B & C, HIV (Heroin)
3) Miosis (all except Meperidine = mydriasis)
4) Resp & CNS depression
5) Dependence
6) Biliary colic (sphincter of Oddi spasms)

Maintenance:
Methadone, Buprenorphine, Clonidine, Naltrexone

Intoxication : Naloxone

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Morphine (oxymorphone & hydromorphone), Heroin (diacetylmorphine), & Meperidine
(all long acting)

Fentanyl, Codeine (oxycodone & hydrocodone), & Methadone

MOA:
Full agonists at opioid receptors
μ (β-endorphin),
δ (enkephalin), & κ (dynorphin)

They close presynaptic Ca2+ channels & open postsynaptic K+ channels to reduce synaptic transmission & inhibit the release of ACh, Norepi, 5-HT, Glutamate, & Substance P.

Clinical uses:
1) Analgesia
2) Euphoria
3) Sedation
4) Cough suppressants (Codeine)

Maintenance:
Methadone, Buprenorphine, Clonidine, Naltrexone

Intoxication : Naloxone

Full opioid agonists

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Opioid neurons :

Originate:

Project to:

Receptors:

Origin:
Arcuate nucleus

Projection:
Ventral Tegmental Area & Nucleus accumbens

Receptors:
μ (β-endorphin): “SACRUM”
- Sedation
- Analgesia
- Constipation
- Resp depression
- truncal Rigidity
- eUphoria
- Miosis

δ (enkephalin):
- Spinal analgesia
- Modulation of hormone & neurotransmitter release

κ (dynorphin): “DCA”
- Dysphoria
- Constipation
- Analgesia

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Ketamine

MOA:

Clinical uses:

Adverse effects:

NMDA antagonist (PCP analog)

MOA:
Inhibits excitation by glutamate at NMDA receptors to decrease neural conduction

AVOID in HTN & Ischemic heart disease

Clinical uses:
1) Analgesia
2) Amnesia & Catatonia in conscious patients
3) Cardiovascular stimulation (bronchodilation, elevated BP & HR)

Adverse effects:
1) Dissociative anesthesia
2) Increased intracranial pressure
3) Emergence reactions (reduced with Midazolam)

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NMDA antagonist (PCP analog)

MOA:
Inhibits excitation by glutamate at NMDA receptors to decrease neural conduction

AVOID in HTN & Ischemic heart disease

Clinical uses:
1) Dissociative Analgesia
2) Amnesia & Catatonia in conscious patients
3) Cardiovascular stimulation (bronchodilation, elevated BP & HR)

Adverse effects:
1) Dissociative anesthesia
2) Increased intracranial pressure
3) Emergence reactions (reduced with Midazolam)

Ketamine

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Intoxication with _________ in High doses causes:

impaired motor function, High BP

Ketamine

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Amantadine

MOA:

Clinical uses:

Adverse effects:

NMDA receptor antagonists (antiviral)

MOA:
Blocks muscarinic receptor to increase dopamine release & reduce its uptake

Clinical uses:
1) Parkinson disease
2) Influenza virus A
3) Reduce levodopa induced dyskinesias toxicity
(peripheral edema, livedo reticularis, & ataxia)

Adverse effects:
1) Insomnia
2) Dizziness/Confusion
3) Ankle edema
4) Atropine-like symptoms
5) Livedo reticularis

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NMDA receptor antagonists (antiviral)

MOA:
Blocks muscarinic receptor to increase dopamine release & reduce its uptake

Clinical uses:
1) Parkinson disease
2) Influenza virus A
3) Reduce levodopa induced dyskinesias toxicity
(peripheral edema, livedo reticularis, & ataxia)

Adverse effects:
1) Insomnia
2) Dizziness/Confusion
3) Ankle edema
4) Atropine-like symptoms
5) Livedo reticularis

Amantadine

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Barbiturates & Ethanol

MOA:

Clinical uses:

Adverse effects:

Phenobarbital & Pentobarbital

MOA:
Facilitates GABA(A) action by increasing the duration of Cl- channel opening to reduce neuron firing

AVOID in patients with porphyria

Clinicals:
Sedative (anxiety, seizures, & insomnia)

Adverse effects:
1) Respiratory & Cardiovascular depression
2) Severe CNS depression (worse with alcohol)
3) Dependence
4) Drug interactions (induces CYOP450)

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Phenobarbital & Pentobarbital

MOA:
Facilitates GABA(A) action by increasing the duration of Cl- channel opening to reduce neuron firing

AVOID in patients with porphyria

Clinicals:
Sedative (anxiety, seizures, & insomnia)

Adverse effects:
1) Respiratory & Cardiovascular depression
2) CNS depression (worse with alcohol)
3) Dependence
4) Drug interactions (induces CYOP450)

Barbiturates

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Benzodiazepines

MOA:

Clinical uses:

Adverse effects:

OD:

Alprazolam, Chlordiazepoxide, Diazepam, Lorazepam, Midazolam, Oxazepam & Triazolam

MOA:
Facilitates GABA(A) action by increasing the frequency of Cl- channel opening & reducing REM sleep

Give LOT for patients with liver disease

Clinicals:
1) Anxiety, Panic disorders, Spasticity, & Status epilepticus (Diazepam, Lorazepam, Midazolam)

2) Eclampsia & supervised withdrawal (Chlordiazepoxide, Diazepam)

3) Night terrors
4) Sleep walking
5) General anesthetic

Adverse effects:
1) Dependence
2) CNS depression with alcohol or Barbs
3) Respiratory depression (less than Barbs)
4) Anterograde amnesia

OD:
treat with Flumazenil

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Alprazolam, Chlordiazepoxide, Diazepam, Lorazepam, Midazolam, Oxazepam & Triazolam

MOA:
Facilitates GABA(A) action by increasing the frequency of Cl- channel opening & reducing REM sleep

Give LOT for patients with liver disease

Clinicals:
1) Anxiety, Panic disorders, Spasticity, & Status epilepticus (Diazepam, Lorazepam, Midazolam)

2) Eclampsia & supervised withdrawal (Chlordiazepoxide, Diazepam)

3) Night terrors
4) Sleep walking
5) General anesthetic

Adverse effects:
1) Dependence
2) CNS depression with alcohol or Barbs
3) Respiratory depression (less than Barbs)
4) Anterograde amnesia

OD:
treat with Flumazenil

Benzodiazepines

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Buprenorphine

MOA:

Clinical uses:

Adverse effects:

MOA: Opioids partial agonists
Partial μ opioid receptor agonist &
κ / δ receptor antagonists
Buprenorphine binds with high affinity but low activity at the receptor

Combined with Naloxone

Clinical uses:
1) Analgesia (combined with naloxone to prevent abuse)
2) Wean patients off full opioid agonists
(while avoiding withdrawal from sudden termination of opioids)

Adverse effects:
1) Opioid withdrawal
2) Resp & CNS depression (not as severe)

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MOA: Opioids partial agonists
Partial μ opioid receptor agonist &
κ / δ receptor antagonists
Buprenorphine binds with high affinity but low activity at the receptor

Combined with Naloxone

Clinical uses:
1) Analgesia (combined with naloxone to prevent abuse)
2) Wean patients off full opioid agonists
(while avoiding withdrawal from sudden termination of opioids)

Adverse effects:
1) Opioid withdrawal
2) Resp & CNS depression (not as severe)

Buprenorphine

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Opioids mixed agonists-antagonists

MOA:

Clinical uses:

Adverse effects:

Nalbuphine & Pentazocine

MOA:
Mostly k agonists & mu antagonists

Clinical uses:
1) Spinal analgesia
2) Dysphoria

Adverse effects:
1) Withdrawal

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Nalbuphine & Pentazocine

MOA:
Mostly k agonists & mu antagonists

Clinical uses:
1) Spinal analgesia
2) Dysphoria

Adverse effects:
1) Withdrawal

Opioids mixed agonists-antagonists

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Opioid antagonists

MOA:

Clinical uses:

Naloxone, Naltrexone, & Methylnaltrexone

MOA:
Antagonize all opioid receptors

Clinical uses:
IV (reverse respiratory depression)
Oral (reduce alcohol & opiate cravings)
Opioid induced constipation

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Naloxone, Naltrexone, & Methylnaltrexone

MOA:
Antagonize all opioid receptors

Clinical uses:
IV (reverse respiratory depression)
Oral (reduce alcohol & opiate cravings)
Opioid induced constipation

Opioid antagonists

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MOA: Anticholinergic activity AVOID IN MI!!! Clinical uses: Used to reduce shivering after Halothane anesthesia [by its action on a2 receptor] Adverse effects: Tachycardia

Pethidine

Pethidine MOA: Clinical use: Adverse effect:

MOA: Anticholinergic activity AVOID IN MI!!! Clinical uses: Pethidine is used to reduce shivering after Halothane anesthesia [by its action on a2 receptor] Adverse effects: Tachycardia

Nicotine Intoxication: Withdrawal: Treatment options:

Intoxication: Restlessness Withdrawal: Irritability Anxiety Restlessness Reduced concentration Increased appetite Rx: Nicotine patch/gun Bupropion Varenicline

Nicotine

Cocaine MOA: Intoxication: Withdrawal: Treatment options:

MOA: Long-acting Monoamine transporter inhibitor that blocks Dopamine, Norepi, & 5HT reuptake Intoxication: Acute - Impaired judgment - Mydriasis - Diaphoresis - Hallucinations - Paranoia - Angina/sudden cardiac death Chronic - Perforated nasal septum Withdrawal: 1) Restlessness 2) Hunger 3) Severe depression 4) Sleep disturbance Treatments: 1) Benzodiazepines 2) Beta or mixed alpha beta blockers (HTN & heart)

Cocaine

Amphetamine/Methamphetamine MOA: Intoxication: Withdrawal:

MOA: Indirectly inhibits reuptake of NE & DA from a mobile pool (considered weak MAO inhibitors) Intoxication: - Euphoria/Grandiosity/Paranoia - Mydriasis - Hyper-alertness/Insomnia - HTN/Cardiac arrest - Fever/Seizures - Fractured teeth Withdrawal: Nonspecific CRASH - Depression - Increased appetite - Vivid nightmares/disturbances Treatments: 1) Benzodiazepines (agitations & seizures)

Amphetamines/methamphetamiens

CNS stimulants MOA: Clinical uses: Adverse effects:

Methamphetamines/amphetamines, & Methylphenidate MOA: Increase catecholamines in the synaptic cleft (esp norepi & dopamine) Clinical use: ADHD Narcolepsy Binge-eating disorder Adverse effects: 1) Nervousness/Agitation/Anxiety 2) Tachycardia/HTN 3) Insomnina 4) Anorexia 5) Tics 6) Bruxism

CNS Stimulants

Drugs of choice for alcohol withdrawal? vs Alcohol use disorder?

Withdrawal: Benzodiazepines (eg, chlordiazepoxide, lorazepam, diazepam) Use disorder: naltrexone (reduces cravings)

THC/cannabis MOA: Intoxication: Withdrawal: Treatment:

MOA: Acts on CB1 (brain) & CB2 (immune) receptors to trigger more dopamine release in nucleus accumbens Intoxication: - Euphoria/Hallucinations - Anxiety/Paranoid delusions - Impaired judgement/Slowed time - Social withdrawal - Increased appetite - Dry mouth - Red eyes Withdrawal: - Irritability - Anxiety - Depression - Insomnia/Restlessness - Reduced appetite Treatment: Dronabinol (maintenance) Rimonabant (inverse CB1 agonsit)

Intoxication: - Euphoria/Hallucinations - Anxiety/Paranoid delusions - Impaired judgement/Slowed time - Social withdrawal - Increased appetite - Dry mouth - Red eyes Withdrawal: - Irritability - Anxiety - Depression - Insomnia/Restlessness - Reduced appetite

THC/cannabis

MDMA aka Ecstasy (Phenylethylamines) Intoxication:

Intoxication: - Euphoria/Disinhibition - Hallucinations/Distorted sensory/time - Hyperactivity - Thirst - Bruxism - HTN/Tachycardia - Hyperthermia - Hyponatremia - Serotonin syndrome Withdrawal: - Depression - Fatigue - Change in appetite - Concentration issues - Anxiety

MDMA aka Ecstasy

Phencyclidine (PCP/Angel dust) MOA: Intoxication: Treatment:

MOA: NMDA antagonist Intoxication: - Stupor/Violence/Delirium/Psychosis - Vertical nystagmus/Miosis - Analgesia - Coma/Seizures - Hyperthermia - Rhabdomyolysis - HTN/Tachycardia Treatment: Diazepam (agitation) Antipsychotics

Phencyclidine (PCP/Angel dust)

Lysergic acid diethylamide (Indoleamines) Intoxication Treatment: Dronabinol Indoleamines (Lysergic acid, LSD, DMT)

Intoxication: Most potent - Bad trips (12+hrs) - Visual/auditory perception distortion - Depersonalization - Anxiety/Paranoia/Psychosis - Mydriasis Treat a bad trip with Diazepam

Lysergic acid diethylamide (LSD Hallucinogens)

Morphine, Hydromorphone, & Oxymorphone MOA: Clinical use: Adverse effects:

MOA: Full opioid agonists They close presynaptic Ca2+ channels & open postsynaptic K+ channels to reduce synaptic transmission & inhibit the release of ACh, Norepi, 5-HT, Glutamate, & Substance P. AVOID in head injury, hepatic/renal dysfunction Clinical uses: 1) Visceral, dull & constant pain (best) 2) MI & acute pulmonary edema (IV) Adverse effects: 1) Miosis 2) Infant dependency

Morphine, Hydromorphone, & Oxymorphone

Codeine MOA: Clinical uses:

Drugs that are effective for cough suppressant

Codeine, pholcodeine, dextromethorphan

Codeine

Euphoria to depression Depressed respirations & Bowel sounds Miosis Seizures (tramadol or meperidine) Indicate

Acute Opioid intoxication treat it with Naloxone

Naloxone MOA: Clinical uses: Adverse effects:

MOA: Short acting competitive opioid antagonist Clinical uses: Treat ACUTE opioid or heroin intoxication Adverse effects: Withdrawal symptoms at high doses (overshoot)

Naloxone

Occurs in opioid dependent people (6-12hrs post high) Reversal of CNS, eye, skin, & Gi effects Restlessness/Yawning Rhinorrhea & Lacrimation Piloerection N/V/abdominal cramps/Diarrhea Pupil dilation Indicate

Withdrawal

Buprenorphine Methadone Naltrexone (long-term maintenance) Clonidine

Withdrawal treatments

Clonidine MOA: Clinical use:

MOA: Alpha 2 adrenoceptor agonist Note Lofexidine has limited side effects Clinical use: Withdrawal & addiction

Clonidine

Naltrexone MOA: Clinical uses:

MOA: Long-acting opioid antagonist that blocks the effects of opioids if taken Clinical uses: 1) Prevent opioid relapse 2) Treating alcohol withdrawal (long term)

Naltrexone

Methadone (for withdrawal) MOA: Clinical uses:

MOA: Long-acting oral opiate Clinical uses: 1) Reduce cravings 2) Maintenance of opioid addiction

Opioids Full: Morphine, Heroin, Methadone, Fentanyl's etc MOA: Effects: Toxicity: Withdrawal:

MOA: Full opioid agonists They close presynaptic Ca2+ channels & open postsynaptic K+ channels to reduce synaptic transmission & inhibit the release of ACh, Norepi, 5-HT, Glutamate, & Substance P. Effects: 1) Euphoria 2) Analgesia 3) Sedation 4) Cough suppression (codeine) 5) Constipation 6) Miosis (except meperidine) Toxicity: 1) Severe respiratory depression (reverse with NALOXONE) 2) N/V Withdrawal: Lacrimation, yawning, sweating, restlessness, diarrhea, depressionetc

Opioids Full: Morphine, Heroin, Methadone, Fentanyl's etc

Alcohol Intoxication: Withdrawal: Treatment:

Intoxication: Emotional lability Slurred speech Ataxia Coma/Blackouts Elevated AST Withdrawal: - Tremors, Insomnia, Gi upset, Agitation, Diaphoresis (within 36 hrs) - Seizures (within 48 hrs) - Halucinations (within 48hrs) - Delirium tremens (within 96hrs) Treatment: Long acting benzodiazepines

Alcohol (depressant)

Barbiturates Intoxication: Withdrawal: Treatments:

Intoxication: Respiratory depression Withdrawal: - Delirium - Cardiovascular collapse Treatments: Manage symptoms

Barbiturates

Benzodiazepines Intoxication: Withdrawal: Treatments:

Intoxication: Ataxia Minor resp depression Withdrawal: Seizures Sleep disturbances Depression Treatment: Flumazenil

Benzodiazepines

Opioids Intoxication: Withdrawal: Treatment:

Intoxication: - Euphoria - Resp/CNS depression (impaired gag & pupil reflex) - Seizures - Reduced Gi motility Withdrawal: - Sweating - Mydriasis - Piloerection - Rhinorrhea/Lacrimation - Yawning - Flu-like signs Treatment: Intoxication: Naloxone Withdrawal: Methadone & Buprenorphine Maintenance: Naltrexone

Opioids

Varenicline MOA: Clinical uses: Adverse effects:

MOA: Direct acting selective α4β2 Nicotinic Ach Receptor Partial Agonist Clinical uses: Nicotine addiction Adverse effects: 1) Headache 2) Nausea 3) Sleep disturbances

Varenicline

Bupropion MOA: Clinical uses: Adverse effects:

MOA: Inhibits 5-HT, NE, & DA reuptake Clinical use: Nicotine addiction Adverse effects: Seizures

Which Drugs are used to treat ALS?

Riluzole & Baclofen

Riluzole MOA: Clinical uses: Adverse effects:

MOA: NMDA antagonist MOA: Reduces the release of glutamate by blocking voltage-gated Na+ channels & reducing neuronal cell death by decreasing glutamine excitotoxicity. Clinical uses: Slows the progression of ALS Adverse effects: 1) Dizziness 2) Nausea 3) HTN

Riluzole

Baclofen MOA: Clinical uses: Adverse effects:

GABA(B) receptor agonist MOA: It facilitates the spinal inhibition of motor neurons in by activating pre & postsynaptic GABA(B) receptors Clinical uses: 1) muscle spasticity 2) dystonia 3) MS

Treating Wilson Disease

Penicillamine (copper chelator)

Spasm of muscles of face, tongue, neck, back within 1-5 days

Acute Dystonia due to drugs that cause Acute DA antagonism Treat with centrally acting anticholinergics i.e Benztropine

Restlessness and intense urge to move, onset between 5-60 days

Akathisia a progression of EPS Treat by reducing dose of current D2 blocker or changing it & giving Clonazepam & Propranolol

Bradykinesia, rigidity, tremor, mask facies, shuffling gait Onset between 5-30 days

Parkinsonism due to dopamine antagonism Treat by reducing D2 blocker or changing it & Giving Anti-parkinson's drugs

Extreme rigidity, fever, unstable BP, myoglobinemia for weeks-months

Neurolept malignant syndrome (due to Dopamine antagonism) Treatment: 1) Stop current drug 2) Give Dantrolene & Bromocriptine 3) Supportive care

Perioral tremors Months-years of therapy

Perioral tremor aka “Rabbit syndrome" Treatment: Antiparkinsonian agents often help. Ex .Amantadine

Orofacial dyskinesia, choreoathetosis, dystonia Months-years of therapy

Tardive dyskinesia due to Post- synaptic DA receptor super sensitivity Treatment: Give a VMAT 2 Inhibitor like valbenazine and deutetrabenazine

Morphine metabolism Accumulation of morphine-3-glucuronide causes

seizures

Morphine metabolism Accumulation of morphine-6-glucuronide causes

somnolence, miosis, decreased respiratory rate