Block 3 materials (Opioids Drug abuse) Flashcards
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
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
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)
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
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
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
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
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
Full opioid agonists
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
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)
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
Intoxication with _________ in High doses causes:
impaired motor function, High BP
Ketamine
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
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
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)
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
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
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
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)
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
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
Nalbuphine & Pentazocine
MOA:
Mostly k agonists & mu antagonists
Clinical uses:
1) Spinal analgesia
2) Dysphoria
Adverse effects:
1) Withdrawal
Opioids mixed agonists-antagonists
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
Naloxone, Naltrexone, & Methylnaltrexone
MOA:
Antagonize all opioid receptors
Clinical uses:
IV (reverse respiratory depression)
Oral (reduce alcohol & opiate cravings)
Opioid induced constipation
Opioid antagonists
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
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)
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)
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
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
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
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
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
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
3) Resp depression
4) N/V
5) Constipation & Urine retention
6) Dysphoria
Morphine, Hydromorphone, & Oxymorphone
Codeine
MOA:
Clinical uses:
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.
Clinical uses:
1) Analgesia
2) Cough suppressants
Drugs that are effective for cough suppressant
Codeine, pholcodeine, dextromethorphan
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.
Clinical uses:
1) Analgesia
2) Cough suppressants
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)
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
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)
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
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
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
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
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
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
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
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
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