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drugs exam 5 > Sedative Hypnotics and Alcohol > Flashcards

Sedative Hypnotics and Alcohol Flashcards

1
Q

What is a first line agent for treating withdrawal?

A

Benzodiazepines

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2
Q

What is the main pharmacological treatment for sleep disorders?

A

Hypnotics; produces drowsiness, aids sleep onset or maintenance.

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3
Q

At low doses alcohol produces anxiolysis, disinhibition and relaxation through what receptors?

A
  • Agonist activity at GABAa receptors
  • Agonist activity at inhibitory glycol receptors
  • Antagonist at excitatory NMDA (glutamate) receptors
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4
Q

Mesolimbic dopamine pathway

A

Produces euphoria and its rewarding effects through activation

  • alcohol increases firing of dopamine VTA neurons
  • VTA releases dopamine onto NAc, singling reward
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5
Q

Drugs for Management of Alcohol Withdrawal

A

Thiamine

Benzodiazepines

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6
Q

Prevention of alcohol dependence relapse

A
  • naltrexone
  • acamprosate
  • disulfiram
  • topiramate
  • gabapentin
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7
Q

Naltrexone

  • USE?
  • MOA?
A

USE: First line for treating moderate to severe AUD (alcohol use disorder) and preventing relapse

MOA: long- acting mu opioid receptor antagonist, blocks reward signaling on VTA GABA cells

  • Can be used to treat opioid addiction –> screen for concurrent opioid use to avoid triggering opioid withdrawal
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8
Q

Acamprosate

A

Prevents relapse

USE: effective alt. to naltrexone for maintaining alcohol abstinence in those using opioids, or with liver disease- administered 3x daily

MOA: weak NMDA glutamate receptor antagonist; therapeutic effect likely involves slow normalization of compensatory neurochemical changes caused by chronic alcohol use

CONTRAINDICATED in renal dysfunction; renally excreted

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9
Q

Disulfiram

A

Prevents relapse

USE: discourages drinking alcohol; use is limited to certain motivated patients, evidence for efficacy is weaker

MOA: causes unpleasant effects (sweating, HA, N/V) when alcohol is consumed by irreversibly inhibiting ALDH enzyme –> causes aldehyde to accumulate

Required 48 hours of total abstinence before use
Serious side effects are rare but include hepatotoxicity

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10
Q

Topiramate

A

Prevents relapse
- Anticonvulsant drug, also used for migraines

MOA: increases GABAa activity and reduces glutamate signaling

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11
Q

Gabapentin

A

Prevents Relapse
- Anticonvulsant drug, also used for neuropathic pain, interferes with voltage- dependent calcium channel activity in the brain

Good efficacy in patients who failed other options, BUT disadvantage is addictive potential

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12
Q

Sedative Hypnotics

EX?

A

Barbituates
Benzodiazepines
Benzodiazepine antagonist
Other (ethanol)

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13
Q

Barbituates

  • Examples of drugs
  • MOA?
  • USES?
  • Drug interactions?
  • Risks?
A

Thiopental (ultra-short acting)
Secobarbital (short-acting)
Amobarbital (intermediate)
Phenobarbital (long-acting)

MOA:

  • CNS depressants; increase inhibitory neurotransmission
  • Bind GABAa receptor at MULTIPLE sites, distinct from GABA and other drug binding sites; positive allosteric modulates and increase duration of Cl- ion channel opening

USES:

  • seizure disorders: use in partial epilepsy
  • anesthesia induction: thiopental has rapid onset/offset of effect
  • medically- induced coma: pentobarbital or thiopental
  • lethal inj. assisted suicide: secobarbital, pentobarbital

DRUG INTERACTIONS:

  • CNS depression; dose-dependent
  • enzyme induction: chronic barbiturate use markedly increases CYP enzyme levels–> drug interactions
  • can interact with alcohol, certain anticonvulsants, anesthetics, opioids, sedating antidepressants, antipsychotics

RISKS:

  • highest overdose risk; linear dose- response progresses to coma, death
  • dependence risk due to tolerance development
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14
Q 
Benzodiazepines (-pam/-lam)
-Uses?
-Properties?
MOA?
AE/RISK?
A

USES:

  • Status epilepticus: diazepam (IV) or lorazepam are first line
  • pre surgery sedation: midazolam
  • short term treatment of anxiety: alprazolam or beta blockers
  • management of alcohol withdrawal: chlordiazepoxide

PHYSIOCHEMICAL PROPERTIES:

  • time to onset drive by lipophilicity (more lipophilic = more rapid CNS entry)
  • active metabolites extend duration of action

MOA: positive allosteric modulators of GABAa and increase frequency of channel opening (opens at lower GABA conc)
- bind GABAa at a SINGLE SITE

AE/RISK:

  • CNS depression; require caution in elderly
  • risk of abuse: disinhibition, sleep promotion, euphoric effects
  • dependence risk: only recc for short term
  • overdose risk: less dangerous than barbiturates because of 1) shallow dose- response curve 2) availability of an antidote: flumazenil
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15
Q

Flumazenil: benzodiazepine antagonist

A

Only GABAa receptor antagonist; occupies the benzodiazepine binding site without producing any effect

  • reverses CNS depressants effects produced by overdoses of benzodiazepines
  • short acting; additional doses must be administered

Dose NOT reverse barbiturate overdoses because it BINDS at a different site

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16
Q

Hypnotics

A

Treat sleep disorders: conditions that cause persistent interference with sleep amount causing distress and impairment

Choice of drug depends on:

  • type of insomnia (sleep onset vs maintenance)
  • sensitivity to side effects
  • opportunity to co-treat other disorder
17
Q 
Z-Drugs
-EX?
-MOA?
-EFFECTS?
USE?
PK/DOSING?
AE/RISK?
A

“Non-benzodiazepine benzodiazepine receptor agonists”
Eszopiclone
Zaleplon
Zolpidem

MOA:

  • bind to the same site on the GABAa receptor and increase Cl- ion conductance
  • bind selectively between alpha 1 and gamma subunits only

EFFECTS:
shortened time to sleep onset
small increase in sleep time/quality

USE: insomnia

PK+dosing:

  • rapid onset of action
  • effect duration intended to be < 8 hrs

AE/RISKS:

  • dizziness, memory loss, disinhibition, GI upset, hallucinations
  • abuse
  • dependence: after ~2 weeks use, taper down to avoid withdrawal symptoms
  • parasomnias: sleep-related behaviors
18
Q 
Melatonin Receptor Agonists
MOA?
Clinical Use?
Efficacy?
Side effects?
ADV?
A

MOA: RaMELton and tasiMELton

Clinical Use:

  • insomnia with sleep onset difficulty
  • non-24-hour sleep-wake disorder

Efficacy:
- modest improvement in time to sleep onset vs placebo

Side Effects:
Generally mild, headaches and vivid dreams

ADV:
No CNS depressant effects, negligible tolerance/dependence/ abuse risk –> not a scheduled substance

19
Q

Melatonin and Sleep

A

Suprachiasmatic nucleus: found in hypothalamus; major regulator of circadian rhythms

  • activated by light, causing it to suppress melatonin production during the day
  • changes in melatonin levels regulate circadian rhythms
20
Q

Obrexin Receptor Antagonists

A

MOA: SuvOREXant is a dual antagonist at orexin OX1R/OX2R receptors: reduces activity of wake-promoting neurons in hypothalamus

USE: insomnia due to difficulty with sleep onset or sleep maintenance

EFFICACY: reduces sleep latency and increases duration

SIDE EFFECTS: somnolence, HA

WARNINGS: complex sleep behaviors, increased suicide risk

21
Q

Sedatives- Buspirone

A

MOA: serotonin 5HT1A receptor agonist (actual mechanism of anxiolysis unknown)

EFFECTS: anxiolytic effects only

CLINICAL USES:

  • long term treatment of anxiety disorders
  • antidepressants are main drugs for anxiety disorders

DOSING/PK:

  • slow onset of action (3-4 weeks)
  • metabolized by CYP3A4

ADV:

  • No CNS depressant effects
  • negligible tolerance/ dependence abuse risk –> not a scheduled substance
  • safe in pregnancy

SIDE EFFECTS:

  • tachycardia
  • paresthesia
  • nausea

drugs exam 5 (3 decks)

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