Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm SJSM > Block 3 materials (Opioids Drug abuse) > Flashcards

Block 3 materials (Opioids Drug abuse) Flashcards

1
Q

Butorphanol

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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)

A

Butorphanol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pentazocine

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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)

A

Pentazocine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tramadol

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Tramadol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Opioids full agonists

MOA:

Clinical uses:

Adverse effects:

Maintenance vs intoxication

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Full opioid agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Opioid neurons :

Originate:

Project to:

Receptors:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ketamine

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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)

A

Ketamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Intoxication with _________ in High doses causes:

impaired motor function, High BP

A

Ketamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Amantadine

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Amantadine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Barbiturates & Ethanol

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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)

A

Barbiturates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Benzodiazepines

MOA:

Clinical uses:

Adverse effects:

OD:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Buprenorphine

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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)

A

Buprenorphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Opioids mixed agonists-antagonists

MOA:

Clinical uses:

Adverse effects:

A

Nalbuphine & Pentazocine

MOA:
Mostly k agonists & mu antagonists

Clinical uses:
1) Spinal analgesia
2) Dysphoria

Adverse effects:
1) Withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Nalbuphine & Pentazocine

MOA:
Mostly k agonists & mu antagonists

Clinical uses:
1) Spinal analgesia
2) Dysphoria

Adverse effects:
1) Withdrawal

A

Opioids mixed agonists-antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Opioid antagonists

MOA:

Clinical uses:

A

Naloxone, Naltrexone, & Methylnaltrexone

MOA:
Antagonize all opioid receptors

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Naloxone, Naltrexone, & Methylnaltrexone

MOA:
Antagonize all opioid receptors

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

A

Opioid antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MOA:
Anticholinergic activity AVOID IN MI!!!

Clinical uses:
Used to reduce shivering after Halothane anesthesia [by its action on a2 receptor]

Adverse effects:
Tachycardia

A

Pethidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pethidine

MOA:

Clinical use:

Adverse effect:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Nicotine

Intoxication:

Withdrawal:

Treatment options:

A

Intoxication:
Restlessness

Withdrawal:
Irritability
Anxiety
Restlessness
Reduced concentration
Increased appetite

Rx:
Nicotine patch/gun
Bupropion
Varenicline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Intoxication:
Restlessness

Withdrawal:
Irritability
Anxiety
Restlessness
Reduced concentration
Increased appetite

Rx:
Nicotine patch/gun
Bupropion
Varenicline

A

Nicotine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Cocaine

MOA:

Intoxication:

Withdrawal:

Treatment options:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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)

A

Cocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Amphetamine/Methamphetamine

MOA:

Intoxication:

Withdrawal:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

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)

A

Amphetamines/methamphetamiens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

CNS stimulants

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

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

A

CNS Stimulants

35
Q

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

A

Withdrawal:
Benzodiazepines (eg, chlordiazepoxide,
lorazepam, diazepam)

Use disorder:
naltrexone (reduces cravings)

36
Q

THC/cannabis

MOA:

Intoxication:

Withdrawal:

Treatment:

A

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)

37
Q

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

A

THC/cannabis

38
Q

MDMA aka Ecstasy (Phenylethylamines)

Intoxication:

A

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

39
Q

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

A

MDMA aka Ecstasy

40
Q

Phencyclidine (PCP/Angel dust)

MOA:

Intoxication:

Treatment:

A

MOA:
NMDA antagonist

Intoxication:
- Stupor/Violence/Delirium/Psychosis
- Vertical nystagmus/Miosis
- Analgesia
- Coma/Seizures
- Hyperthermia
- Rhabdomyolysis
- HTN/Tachycardia

Treatment:
Diazepam (agitation)
Antipsychotics

41
Q

MOA:
NMDA antagonist

Intoxication:
- Stupor/Violence/Delirium/Psychosis
- Vertical nystagmus/Miosis
- Analgesia
- Coma/Seizures
- Hyperthermia
- Rhabdomyolysis
- HTN/Tachycardia

Treatment:
Diazepam (agitation)
Antipsychotics

A

Phencyclidine (PCP/Angel dust)

42
Q

Lysergic acid diethylamide (Indoleamines)

Intoxication

Treatment:

Dronabinol
Indoleamines (Lysergic acid, LSD, DMT)

A

Intoxication: Most potent
- Bad trips (12+hrs)
- Visual/auditory perception distortion
- Depersonalization
- Anxiety/Paranoia/Psychosis
- Mydriasis

Treat a bad trip with Diazepam

43
Q

Intoxication: Most potent
- Bad trips (12+hrs)
- Visual/auditory perception distortion
- Depersonalization
- Anxiety/Paranoia/Psychosis
- Mydriasis

Treat a bad trip with Diazepam

A

Lysergic acid diethylamide (LSD Hallucinogens)

44
Q

Morphine, Hydromorphone, & Oxymorphone

MOA:

Clinical use:

Adverse effects:

A

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

45
Q

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

A

Morphine, Hydromorphone, & Oxymorphone

46
Q

Codeine

MOA:

Clinical uses:

A

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

47
Q

Drugs that are effective for cough suppressant

A

Codeine, pholcodeine, dextromethorphan

48
Q

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

A

Codeine

49
Q

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

Indicate

A

Acute Opioid intoxication treat it with Naloxone

50
Q

Naloxone

MOA:

Clinical uses:

Adverse effects:

A

MOA:
Short acting competitive opioid antagonist

Clinical uses:
Treat ACUTE opioid or heroin intoxication

Adverse effects:
Withdrawal symptoms at high doses (overshoot)

51
Q

MOA:
Short acting competitive opioid antagonist

Clinical uses:
Treat ACUTE opioid or heroin intoxication

Adverse effects:
Withdrawal symptoms at high doses (overshoot)

A

Naloxone

52
Q

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

A

Withdrawal

53
Q

Buprenorphine
Methadone
Naltrexone (long-term maintenance)
Clonidine

A

Withdrawal treatments

54
Q

Clonidine

MOA:

Clinical use:

A

MOA:
Alpha 2 adrenoceptor agonist

Note Lofexidine has limited side effects

Clinical use:
Withdrawal & addiction

55
Q

MOA:
Alpha 2 adrenoceptor agonist

Note Lofexidine has limited side effects

Clinical use:
Withdrawal & addiction

A

Clonidine

56
Q

Naltrexone

MOA:

Clinical uses:

A

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)

57
Q

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)

A

Naltrexone

58
Q

Methadone (for withdrawal)

MOA:

Clinical uses:

A

MOA:
Long-acting oral opiate

Clinical uses:
1) Reduce cravings
2) Maintenance of opioid addiction

59
Q

Opioids

Full: Morphine, Heroin, Methadone, Fentanyl’s etc

MOA:

Effects:

Toxicity:

Withdrawal:

A

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

60
Q

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

A

Opioids

Full: Morphine, Heroin, Methadone, Fentanyl’s etc

61
Q

Alcohol

Intoxication:

Withdrawal:

Treatment:

A

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

62
Q

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

A

Alcohol (depressant)

63
Q

Barbiturates

Intoxication:

Withdrawal:

Treatments:

A

Intoxication:
Respiratory depression

Withdrawal:
- Delirium
- Cardiovascular collapse

Treatments:
Manage symptoms

64
Q

Intoxication:
Respiratory depression

Withdrawal:
- Delirium
- Cardiovascular collapse

Treatments:
Manage symptoms

A

Barbiturates

65
Q

Benzodiazepines

Intoxication:

Withdrawal:

Treatments:

A

Intoxication:
Ataxia
Minor resp depression

Withdrawal:
Seizures
Sleep disturbances
Depression

Treatment:
Flumazenil

66
Q

Intoxication:
Ataxia
Minor resp depression

Withdrawal:
Seizures
Sleep disturbances
Depression

Treatment:
Flumazenil

A

Benzodiazepines

67
Q

Opioids

Intoxication:

Withdrawal:

Treatment:

A

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

68
Q

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

A

Opioids

69
Q

Varenicline

MOA:

Clinical uses:

Adverse effects:

A

MOA:
Direct acting selective α4β2 Nicotinic Ach Receptor Partial Agonist

Clinical uses:
Nicotine addiction

Adverse effects:
1) Headache
2) Nausea
3) Sleep disturbances

70
Q

MOA:
Direct acting selective α4β2 Nicotinic Ach Receptor Partial Agonist

Clinical uses:
Nicotine addiction

Adverse effects:
1) Headache
2) Nausea
3) Sleep disturbances

A

Varenicline

71
Q

Bupropion

MOA:

Clinical uses:

Adverse effects:

A

MOA:
Inhibits 5-HT, NE, & DA reuptake

Clinical use:
Nicotine addiction

Adverse effects:
Seizures

72
Q

Which Drugs are used to treat ALS?

A

Riluzole & Baclofen

73
Q

Riluzole

MOA:

Clinical uses:

Adverse effects:

A

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

74
Q

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

A

Riluzole

75
Q

Baclofen

MOA:

Clinical uses:

Adverse effects:

A

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

76
Q

Treating Wilson Disease

A

Penicillamine (copper chelator)

77
Q

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

A

Acute Dystonia due to drugs that cause Acute DA antagonism

Treat with centrally acting anticholinergics i.e Benztropine

78
Q

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

A

Akathisia a progression of EPS

Treat by reducing dose of current D2 blocker or changing it
&
giving Clonazepam & Propranolol

79
Q

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

A

Parkinsonism due to dopamine antagonism

Treat by reducing D2 blocker or changing it
&
Giving Anti-parkinson’s drugs

80
Q

Extreme rigidity, fever, unstable BP, myoglobinemia

for weeks-months

A

Neurolept malignant syndrome
(due to Dopamine antagonism)

Treatment:
1) Stop current drug
2) Give Dantrolene & Bromocriptine
3) Supportive care

81
Q

Perioral tremors
Months-years of therapy

A

Perioral tremor aka “Rabbit syndrome”

Treatment:
Antiparkinsonian agents often help. Ex .Amantadine

82
Q

Orofacial dyskinesia, choreoathetosis, dystonia

Months-years of therapy

A

Tardive dyskinesia due to Post- synaptic DA receptor super sensitivity

Treatment:
Give a VMAT 2 Inhibitor like
valbenazine and deutetrabenazine

83
Q

Morphine metabolism

Accumulation of morphine-3-glucuronide causes

A

seizures

84
Q

Morphine metabolism

Accumulation of morphine-6-glucuronide causes

A

somnolence, miosis, decreased respiratory rate

Pharm SJSM (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions