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Pharmacology Test 1 > Sedative-Hypnotic Agents > Flashcards

Sedative-Hypnotic Agents Flashcards

1
Q

Sedative

A

anxiolytic; anti-anxiety

- indicated for patients experiencing symptoms severe enough to produce functional disability

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2
Q

Hypnotic

A
  • promotes sleep

- requires more pronounced CNS depression (reduce excitability of CNS)

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3
Q

Pharmacologic Therapy of GAD

A
  • Shore Term
  • – reduce severity and duration of anxiety symptoms
  • Long Term
  • – remission with minimal or no anxiety symptoms
  • – no functional impairment
  • – increased quality of life
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4
Q

General Approach to GAD Treatment

  • plan depends on (3 factors)
  • considerations when initiating drug therapy (3 factors)
A
  • develop patient specific treatment plan; psychotherapy and drug therapy

Plan depends on:

  • severity and chronicity of symptoms
  • medication history
  • comorbid medical and psychiatric conditions

Considerations when initiating drug therapy:

  • anticipated adverse effects
  • history of prior response in the patient or a family member
  • patient preference and compliance
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5
Q

Short-Term Pharmacotherapy for Acute Anxiety States

A 
Benzodiazepines (BZ)
- biggest class for ACUTE anxiety treatment
- v. good acute, v. bad long term; v. high risk of dependency
*** act fast, long duration***
(rapid time to peak blood levels; long half-life)
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6
Q

Alprazolam (Xanax)

A

BZs

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7
Q

Max time usage for BZ

A

Max 2-4 weeks (due to risk of physical and mental dependency)

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8
Q

Chlordiazepoxide (Librium)

A

BZs

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9
Q

Clonazepam (Klonopin)

A

BZs

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10
Q

Diazepam (Valium)

A

BZs

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11
Q

Lorazepam (Ativan)

A

BZs

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12
Q

Oxazepam (Serax)

A

BZs

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13
Q

Benzodiazepine Mechanism

A
  • BZs bind to GABA receptor in neuronal membranes
  • – does NOT bind where GABA binds, binds elsewhere and improves GABA function
  • BZs increase the frequency of GABA-gated channel opening events
  • – GABA firing = inhibition of CNS
  • underlies a “GABAergic” mechanism of action, that results in inhibition at all levels of the neuraxis
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14
Q

BZs Clinical Toxicity/Adverse Effects

A
  • can lead to drowsiness, impaired judgement, and diminished motor skills; intensified by alcohol
  • can cause significant dose-related anterograde amnesia, and can impair ability to learn new information
  • at high doses, toxicity can present as lethargy, exhaustion, or as gross symptoms of ethanol intoxication
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15
Q

Prolonged use of BZs

- withdrawal symptoms due to abrupt cessation

A
  • can lead to tolerance, psychologic and physiologic dependence

CLASS IV controlled drugs

Withdrawal symptoms:

  • increased anxiety
  • insomnia
  • CNS excitability that may progress to convulsions
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16
Q

BZ OD

- treatment

A

Flumazenil

  • even at very high doses rarely fatal
  • with severe toxicity, respiratory depression can be complicated by aspiration of gastric contents

Treatment:
- ensure patient airway, maintenance of plasma volume, renal output, and cardiac function

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17
Q

Flumazenil

A
  • competitive antagonist; binds same site as BZ but does nothing
  • approved for use in reversing CNS depressant after BZ overdose
  • requires repeated administration
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18
Q

Advantages of BZ

A
  • rapid onset of action
  • a relatively high therapeutic index and availability of flumazenil for treatment of overdose
  • low risk of drug-drug interactions based on liver enzyme induction
  • minimal effects on cardiovascular and autonomic functions
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19
Q

Disadvantages of BZ

A
  • risk of dependence
  • depression of CNS functions
  • amnesic effects
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20
Q

First-Line Drugs Long-term GAD

A

Newer Antidepressants

  • SSRIs
  • SNRIs
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21
Q

Escitalopram

A

SSRI

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22
Q

Paroxetine (Paxil)

A

SSRI

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23
Q

Sertraline

A

SSRI

24
Q

Duloxetine

A

SNRI

25
Q

Venlafaxine XR (Effexor XR)

A

SNRI

26
Q

SSRI

A

Selective Serotonin Reuptake Inhibitors

27
Q

SNRI

A

Serotonin-Norepinephrine Reuptake Inhibitors

28
Q

Long-Term Treatment GAD Second Line

A
  • TCA
  • Anxiolytic
  • Anticonvulsant
29
Q

TCA

A

Tricyclic Antidepressant

30
Q

Mechanism of Action for Antidepressants for Anxiety

not GABA

A
  • block manifestations of anxiety by increasing amount of serotonin available to interact with postsynaptic 5-HT(1A) receptors Calming-sedative effect
  • downregulates 5-HT(2) receptors which cause anxiety
31
Q

Response time for antidepressants

A

2-4 weeks+

32
Q

Buspirone

A
  • Anxiolytic (anxiety only; doesn’t help with depression)
  • second-line treatment GAD
  • does NOT interact with GABAergic systems
  • takes 2+ weeks to take effect * NOT good for acute anxiety treatment*
33
Q

Pregabalin

A
  • Anticonvulsant
  • second-line treatment GAD
  • increases GABA synthesis and release
  • DOES NOT BIND TO GABA RECEPTORS
  • produces effects similar to BZs and anti-depressants
  • controlled substance; dependence risk (V) (less than BZs)
  • is GABAergic
34
Q

Imipramine

A
  • TCA
  • second line treatment GAD
  • acts like SNRI
  • higher toxicity and adverse effect rates than newer antidepressants
35
Q

Imipramine Side-effects

A
  • antihistamine (sedation/somnolence)
  • anticholinergic (dry mouth; constipation; burred/double vision/ tachycardia)
  • antiadrenergic (orthostatic hypotension/BP dips)
  • risk of serious toxicity (including seizures, rapid heart rate, and cardiac arrest) with high doses
36
Q

Hypnotics

A
  • drugs used for treatment of insomnia

- SHORT t1/2: want to be able to get up in the morning

37
Q

GABAergic Hypnotics

A
  • Benzodiazepines (higher doses than used for anxiety)

- Non-Benzodiazepines hypnotics (also bind to GABA receptors)

38
Q

Triazolam (Halcion)

A

BZ Hypnotic

39
Q

Temazepam (Restoril)

A

BZ Hypnotic

40
Q

Estazolam (ProSom)

A

BZ Hypnotic

41
Q

Flurazepam (Dalmane)

A

BZ Hypnotic

42
Q

Quazepam (Doral)

A

BZ Hypnotic

43
Q

Zaleplon

A

Non-BZ Hypnotic

- help fall asleep DOESNT help KEEP asleep

44
Q

Zolpidem (Ambion)

A

Non-BZ Hypnotic

- helps fall asleep & stay asleep

45
Q

Eszopiclone

A

Non-BZ Hypnotic

- helps fall asleep & stay asleep

46
Q

Newer Non-GABAergic Hypnotics

A
  • Melatonin (MT) Receptor Agonists

- Orexin (OX) Receptor Antagonist

47
Q

Ramelteon

A

Melatonin (MT) Receptor Antagonist

48
Q

Tasimelteon

A

Melatonin (MT) Receptor Antagonist

49
Q

Suvorexant (Belsomra)

A

Orexin (OX) Receptor Antagonist

50
Q

Goals of Treatment for Hypnotics

A
  • correct underlying sleep complaint
  • consolidate sleep (fall asleep and stay asleep)
  • improve daytime functioning (can wake up and function)
  • avoid adverse effects from drug therapies

** Drug therapy should be used in the LOWEST possible dose for the SHORTEST possible period of time **

51
Q

BZ as Hypnotic Agents

A
  • decreases number of awakenings
  • higher dose than used for GAD
  • after prolonged use, can result in withdrawal and increased insomnia
52
Q

Non-BZ Hypnotics

A
  • bind to same site on GAGA receptor as BZs; exhibit similar effects
  • all decrease time to persistent sleep
  • rapid onset of activity, short half lives, few amnesic effects
  • schedule IV controlled substance: SHORT TERM USE ONLY
53
Q

All Non-BZ Hypnotics Increase Total Sleep Time EXCEPT

A

Zaleplon

- helps fall asleep, does not help stay asleep

54
Q

MT Receptor Agonists

A
  • Ramelteon & Tasimelteon
  • act as agonists at MT1 and MT2 receptors
  • NO GABAergic effects in the CNS
  • no risk of dependency
  • promote sleep
55
Q

Tasimelteon is uniquely approved for:

A

non-24 hour sleep-wake disorder

56
Q

Orein (OX) Receptor Antagonist

A
  • BLOCKER of WAKE receptor
  • acts as antagonist at OX1 and OX2 receptors in the brain, with non GABAergic CNS effects
  • BLOCKS WAKEFULNESS
  • schedule IV controlled substance
  • “sleep-driving” behavior and amnesic effects

Pharmacology Test 1 (8 decks)

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