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M2 Neuro/Psych > Anxiolytics & Hypnotics - Bloom > Flashcards

Anxiolytics & Hypnotics - Bloom Flashcards

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1
Q

What is the lifetime prevalence of Anxiety disorders?

Of generalized anxiety disorders (GAD)?

A

Very common, 28.8% of people experience it during their lives.

5.7%

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2
Q

What defines generalized anxiety disorder?

What are some symptoms that may be demonstrated?

A

Persistent anxiety for 1+ months, without a diagnosis of a more specific disorder (eg Phobias, OCD).

Apprehension, hyperattentiveness or distractibility, insomnia, impatience. General SNS arousal and muscle tenseness (“Jittery”)

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3
Q

Recall the stages of sleep ranging from Drowsy to REM. Include the EEG wave findings.

A

Drowsy: 8-12Hz Alpha waves
Stage I: 3-7Hz Theta waves
Stage II: 12-14Hz Sleep spindles & K complexes.
Stage III: Like stage II, but deeper.
Stage IV: 0.5-2Hz Delta waves
REM: Low-voltage, fast sawtooth waves (like awake)

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4
Q

Which stage of sleep is most dominant?

What neurotransmitter predominates in deep sleep? REM sleep?

A

Stage 2; about 45% of sleep is in stage 2.

Deep sleep = Serotonin
REM sleep = Norepinephrine

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5
Q

Name 4 classes of medications used presently to treat anxiety and insomnia.

A

Benzodiazepines
SSRIs
Buspirone
Classical Antihistamines (H1 blockers)

Not presently used are barbiturates. “ACO” (alcohol, cannabis, opiates) have also been replaced.

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6
Q

Where is GABA-A found? GABA-B?

From what amino acid precursor is it synthesized?

A

GABA-A is found in the CNS, and is the main target of anxiolytics and hypnotics there.
GABA-B is found in the spinal column, and is targeted for skeletal muscle relaxation (Baclofen).

Glutamate.

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7
Q

Where is GABA localized to in the CNS? Try to name 5-6 structures.

A

Substantia Nigra
Globus Pallidus

Hippocampus
Amygdala

Hypothalamus

Spinal Cord

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8
Q

Describe the structure and function of the post-synaptic GABA receptor.

What results from its activation?

What classes of drugs agonize or antagonize it?

A

It is a pentameric ligand-gated chloride channel.

Influx of chloride, which generates inhibitory post-synaptic potentials (IPSP).

Benzodiazepines and barbiturates, as well as ethanol & inhaled anesethetics agonize it. Flumazenil antagonizes it.

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9
Q

Describe the location, structure, and function of the 5-HT1A receptor.

What relationship does Buspirone have to it? Does it influence any other receptors?

A

Presynaptic; A Gi receptor that also opens a K+ channel.

Buspirone is a partial agonist here, and also binds dopamine receptors.

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10
Q

There are around 7-8 listed benzodiazepines that can treat anxiety.

Compare and contrast Alprazolam and Diazepam.

A

Alprazolam influences the forebrain more, is very short acting, and is appropriate as an antipanic drug.

Diazepam has broader CNS depression, has a long duration, and is also used as a muscle relaxant.

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11
Q

What are the indications for Lorazepam?

What is distinctive about its kinetics? Are there any other benzos that behave this way?

A

For anxiety as well as insomnia (the only mentioned BDZ for both).

It is not a prodrug; only it and Oxazepam are not converted to active metabolites (Note: Oxazepam is an intermediate of many other BDZ including diazepam).

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12
Q

Besides treating anxiety and insomnia, benzodiazepines are indicated to treat many other conditions.

What else is Diazepam indicated for?

Chlordiazepoxide?

Clonazepam?

A

Diazepam is a muscle relaxant.

Chlordiazepoxide is for alcohol withdrawal.

Clonazepam treats acute manic episodes.

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13
Q

Try to name 6 CNS effects of benzodiazepines.

(Hint: A couple make them potentially useful for anesthesia)

A

Anxiolysis
Sedation

Hypnosis
Muscle relaxation
Anterograde amnesia
Anticonvulsant action

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14
Q

What drugs should not be mixed with benzodiazepines?

A

Any other drug that causes CNS depression (ethanol, H1 blockers) due to additive effect.

Drugs that affect hepatic metabolism (eg Cimetidine inhibits CYPs)

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15
Q

Name 7 symptoms of benzodiazepine withdrawal.

Hint: Two are the conditions they are used to treat.

A

Anxiety
Insomnia

Irritability
Headache
Hyperacusis
Hallucination
Seizures

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16
Q

How should Benzodiazepine abuse be approached?

A

Gradual dose reduction to avoid withdrawal effects. Switch to longer-acting drugs.

If acute toxicity, use flumazenil.

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17
Q

What is the mechanism of action of buspirone?

What is it used to treat?

How long until therapeutic effects occur?

A

5-HT1A receptor agonist

Generalized Anxiety Disorder (GAD)

1-2 weeks

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18
Q

What advantages does busprione have over benzodiazepines?

A
  • Less sedating
  • No cross tolerance
    • i.e., a pt who develops tolerance to a benzo will not have simultanesouly developed tolerance to buspirone
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19
Q

What are some limitations of buspirone regarding its pairing with other drugs?

(Hint: Do not think drug interactions)

A
  • Does not potentiate other sedative-hyponotics
    • I suppose this could also be a benefit given the situation
  • Does not suppress symptoms of withdrawal of other sedative-hypnotics
20
Q

What anxiety disorders can SSRIs and SNRIs be used to treat?

A
  • Panic Attacks
  • Generalized Anxiety Disorder
21
Q

What type of anxiety can beta blockers be used to treat?

A

Performance anxiety

22
Q

What are the daytime sequelae of insomnia?

A

Probably what you’d expect:

  • Tired
  • Fatigued
  • Sleepy
  • Anxious
  • Depressed
23
Q

Compare the pharmacokinetics of Flurazepam with Triazolam.

A
  • Both drugs have **rapid **onset of action
  • Flurazepam has a long duraction of action, while Triazolam’s is ultra short.
24
Q

Benzodiazepines are used to treat insomnia. Describe the specific effects of benzos on sleep and the stages of sleep.

A
  • Cause decreased latency to sleep
  • Increases in Stage 1 and 2 sleep
  • Decreases in Stage 3 and 4, and REM sleep
  • Rebound insomnia upon withdrawal
25
Q

What are the side effects of benzodiazepines?

A
  • Daytime sedation
  • Ataxia
  • Rebound insomnia (after discontinuation)
  • Tolerance & dependence
  • Occasional idiosyncratic excitement & stimulation
  • Increased death rate associated with use???
26
Q

What is the mechanism of action of Zolpidem and Zaleplon?

What are these drugs used to treat?

A

GABA receptor agonist; bind to BDZ receptor but are non-benzos chemically

Insomnia

27
Q

How do the effects on sleep of zolpidem and zaleplon differ from those of benzos?

A
  • Zolpidem and zaleplon preserve stage 3 and 4 sleep and have only minor effects on REM sleep
28
Q

What is the duration of action of zolpidem and zaleplon?

What is the pharmacokinetic difference between zolpidem and zaleplon?

A

5-6 hours, or 7-8 hours with sustained release preparation

Zaleplon has faster onset of action and shorter terminal elimination half-life than zolpidem.

29
Q
  1. What is the mechanism of action of eszopiclone?
  2. What is it used to treat?
A
  1. Similar mech to zolpidem and zaleplon. Non-benzo that binds at or near the BDZ receptor to agonize the GABA receptor complex.
  2. Insomnia
30
Q
  1. How long should a course of eszopiclone last?
  2. How does it compare to similar drugs regarding risk of dependence?
A
  1. Up to 6 months
  2. Lower likelihood of dependence and withdrawal than zolpidem or zaleplon, although still a DEA Schedule IV drug
31
Q

What drug antagonizes zolpidem and zaleplon and can be used to treat overdoses of these drugs?

A

Flumazenil

32
Q

Ramelteon

Mechanism of action?

Use?

A

MT1 & MT2 receptor agonist.

Insomnia characterized specifically by difficulty in falling asleep.

33
Q

Barbiturates

How quickly are they absorbed? Why?

Drug interactions?

Metabolism?

A

Rapidly absorbed & distributed due to high lipophilicity.

Can induce own metabolism and that of other drugs.

Primarily renal excretion.

34
Q

Give an example of a barbiturate that is:

  1. Ultrashort-acting?
  2. Short- to intermediate-acting?
  3. Long-acting?
  • What is each category used for?
  • What determines these differences in onset of action?
A
  1. Thiopental: Induction of anesthesia; seizures
  2. Secobarbital: Insomnia
  3. Phenobarbital: Seizures; insomnia

Differences in onset and length of action are explained by degree of lipophilicity (longer acting drugs have a longer onset; they are less lipophilic than the rapid-/shorter-acting drugs)

35
Q

Barbiturates

Adverse Effects

A
  • CNS depression
    • Sedation
    • Hypnotic (well, it had better be!)
    • Anesthesia
  • Respiratory depression
  • Higher-than-hypnotic doses can produce CV effects
    • Decreased MAP and pulse pressure
  • Induction of hepatic drug metabolism
  • Tolerance, dependence & withdrawal
36
Q

Barbiturates

What are the side effects of barbiturate withdrawal?

How should withdrawal in chronic users be handled?

A
  • Anxiety
  • Agitation
  • Insomnia
  • Tremor
  • Potentially life-threatening seizures

Abrupt withdrawl is contraindicated for chronic (ab)users - wean them off gradually.

37
Q

What are the symptoms of barbiturate toxicity / overdose?

How should such an overdose be treated?

A
  • Sxs: About what you’d expect.
    • Stupor
    • Coma
    • Respiratory depression
  • Treatment:
    • Remove any unabsorbed drug
    • Support respiration
    • Prevent complications
38
Q

Barbiturates: Drug Interactions?

A
  • Additive with other CNS depressants such as:
    • Alcohol
    • other Sedative hypnotics
    • Antihistamines
  • Drugs that affect microsomal drug metabolism
39
Q

Chloral Hydrate

What is the active metabolite of this drug?

What other class of sedatives is its pharmacology most similar to?

Sleep side effects?

A

Trichloroethanol is the active form

Similar to barbiturates

Less effects on stages of sleep than BDZs and barbiturates

40
Q

Nonprescription/OTC sleep medications tend to belong to what drug class?

Name a common drug in this class.

A

Antihistamines

Diphenhydramime

41
Q

Suvorexant

Mechanism of action?

Use?

Adverse effects?

A
  • Orexin receptor (OX1 & OX2) antagonist.
    • Orexins are neuropeptide central promotors of wakefulness.
    • Suv-orex-ant(agonist)
  • Used for insomnia
  • Adverse effects similar to other hypnotics
42
Q
  1. What is spasticity?
  2. What components of the nervous system are involed in spasticity?
  3. What class of drugs are used to treat spasticity?
A
  1. An increase in tonic stretch reflexes and flexor muslce spasms, often together with overall muscle weakness
  2. Involves both the stretch reflex arc and higher centers in the brain
  3. Skeletal muscle relaxants
43
Q

Compare the skeletal muscle relaxants Diazepam and Baclofen in terms of their mechanisms of action. Be specific.

Bonus: Which drug is more sedating?

A
  • Diazepam - more sedating
    • ​Binds GABAA receptor
      • ligand-gated ion channel
      • Facilitates GABA-mediated presynaptic inhibition
  • Baclofen - less sedating
    • Binds GABAB receptor
      • G protein-coupled receptors
      • Interferes with release of excitatory transmitters (e.g. glutamate)
44
Q

Tizanidine

  1. Mechanism of action?
  2. Use?
  3. Adverse effects?
  4. Drug interactions?
A
  1. Alpha2-adrenergic agonist (related to clonidine)
    • Enhances both pre- and postsynaptic inhibition
  2. Muscle spasm
  3. S/Es:
    • Hypotension
    • Dry mouth
    • Asthenia
  4. Interacts with ciprofloxacin and fluvoxamine (CYP1A2 inhibitors)
45
Q

Other than GABAergic and adrenergic agents, what are some other drugs used to treat skeletal muscle spasticity?

[Likely somewhat low-yield]

A
  • Botulinum toxin - long acting local effect
  • Carisoprodol
  • Cyclobenzaprine
  • Metaxalone
  • Orphenadrine
  • Dantrolene
    • Decouples excitation and contraction in muscle fibers; also used for malignant hyperthermia!

M2 Neuro/Psych (45 decks)

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