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Pharmacology II Exam 1 > Hypnotic Agents > Flashcards

Hypnotic Agents Flashcards

1
Q

Benzodiazepines (2nd generation GABA hypnotics) to know (3)

A

Flurazepam, temazepam, triazolam

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2
Q

Non-benzodiazepine BZD agonists (3rd generation GABA hypnotics) to know (3)

A

Eszopiclone, zolpidem, zaleplon

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3
Q

Melatonin receptor agonists

A

Ramelteon

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4
Q

Orexin receptor antagonists (newest class)

A

Suvorexant

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5
Q

Ultra-short hypnotics: half-life

A

2-3 H

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6
Q

Ultra-short hypnotics use

A

Patients having trouble falling asleep

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7
Q

Advantage of ultra-short hypnotics (half-life 2-3 H)

A

Little daytime drowsiness

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8
Q

Disadvantages of ultra-short hypnotics (half-life 2-3 H)

A

Rebound insomnia and REM rebound in early morning, tendency to use higher doses to achieve longer DOA

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9
Q

Short hypnotics half-life

A

5+ H

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10
Q

Short hypnotics use

A

Patients wake up in the middle of the night

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11
Q

4 advantages of short hypnotics

A
  • Does not accumulate in the body
  • low incidence of residual effects
  • not metabolized by CYPs
  • tolerance to hypnotic effect is slow
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12
Q

Disadvantage of short hypnotics

A

Rebound insomnia and REM rebound in early morning

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13
Q

Long hypnotics half-life

A

24-120 H

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14
Q

Long hypnotics use

A

Patients wake up early in the morning

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15
Q

3 advantages to long hypnotics

A
  • Maybe more effective on the 2nd night
  • rebound insomnia and REM are less intense after DC
  • residual daytime anti-anxiety effects may be helpful
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16
Q

2 disadvantages of long hypnotics

A
  • Residual daytime drowsiness (may be severe)

- potential for drug accumulation

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17
Q

Ultra-short acting BZ to know

A

Triazolam (half-life 1.5-5 H, eliminated in 12-15 H)

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18
Q

1 good and 1 bad about triazolam

A
  • Low incidence of daytime drowsiness;

- rebound insomnia and REM rebound can occur in a single night

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19
Q

**Incidence of anterograde amnesia is higher than with other hypnotics

A

Triazolam (ultra-short acting BZ)

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20
Q

Short acting BZ to know

A

Temazepam (half-life 3-18 H)

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21
Q

Why would temazepam be presented for use especially in elderly patients?

A

Eliminated by conjugation (Phase II processes fairly unaffected by age)

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22
Q

2 good and 1 bad about temazepam

A
  • Little or no tolerance over 2 weeks
  • low incidence of daytime drowsiness
  • insomnia and REM rebound are possible (short acting BZ)
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23
Q

Long acting BZ to know

A

Flurazepam (half-life 2.3 H, but active metabolites have 74-90 H half lives)

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24
Q

Residual anti-anxiety effect, maybe more effective on second night

A

Flurazepam (long acting BZ)

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25
Q

At what rate does tolerance develop to flurazepam?

A

Slowly (long acting BZ)

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26
Q

Describe the daytime drowsiness AND rebound insomnia/REM likeliness with flurazepam.

A

Causes daytime drowsiness, but rebound insomnia/REM is unlikely (long-acting BZ)

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27
Q

T/F: Non-benzodiazepine BZD receptor agonists are structurally distinct from BZDs and are allosteric agonists at a distinct region on the GABA-A receptor.

A

False- allosteric agonists are the BZD receptor on GABA-A

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28
Q

Selectivity of non-BZ BZD receptor agonists

A

Selective for GABAa receptors containing A1 subunits

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29
Q

What are non-BZ BZD receptor agonists actions limited to?

A

Hypnotic and amnestic effects (NO anti-anxiety, anti-seizure, muscle relaxation, affect on learning/memory NONE)

30
Q

What are 3 similarities between zolpidem, eszopiclone, and zaleplon?

A

Considered ultra-short acting (half-lives 1.5-7 H), schedule IV, do not suppress REM or N3 sleep at therapeutic doses

31
Q

Has no limitation of how long it can be used

A

Eszopiclone

32
Q

How do non-BZ BZD agonists’ ADEs compared to BZDs’?

A

Similar but frequency and severity may be less (actions limited to hypnotic and amnestic…)

33
Q

Function: orexin A and orexin B - antagonist?

A

Hypothalamic neuropeptides that promote wakefulness and regulate the sleep-wake cycle - suvorexant

34
Q

MOA of suvorexant

A

Block OX1R and OX2R receptors to prevent binding of orexins A and B

35
Q

What DOA does suvorexant have?

A

Short acting (half-life 12 h)

36
Q

ADE of suvorexant

A

Similar to other hypnotics, mild cataplexy (leg weakness/paralysis)

37
Q

Use and schedule of suvorexant

A

New drug with unclear role in insomnia; CIV

38
Q

Melatonin is a hormone involved in circadian rhythms and the sleep-awake cycle. How/where does it act?

A

Stimulates melatonin MT1 and MT2 GPCRs in the suprachiasmatic nucleus of the hypothalamus

39
Q

MOA= agonist at MT1 receptors

A

Ramelteon

40
Q

DOA of ramelteon

A

Ultra-short acting (half-life 1.5-5 H)

41
Q

Use and schedule of ramelteon

A

Improves some sleep parameters but effect size is small, not controlled (melatonin for jet lag?)

42
Q

ADE of ramelteon

A

Generally milder than BZDs (somnolence, dizziness)

43
Q

When to use lower doses: (3)

A
  • Patient is likely to use alcohol
  • elderly patients (avoid use if possible)
  • patients with hepatic or renal disease
44
Q

How long should hypnotics be used for?

A

Used temporarily, avoid successive nightly therapy

45
Q

When do you taper hypnotics off?

A

After chronic use (to avoid/deal with withdrawal)

46
Q

Contraindications for hypnotics (4)

A
  • Sleep apnea (heavy snoring)
  • history of alcohol or drug abuse
  • pregnancy
  • suicidal risk
47
Q

Non-REM is what % of sleep?

A

50-60%

48
Q

How is Non-REM sleep distinguished

A

increasing arousal threshold and slowing or cortical EEG

49
Q

REM is what % of sleep?

A

20-25%

50
Q

What occurs in REM?

A

rapid eye movements
dreaming
sleep muscle paralysis

51
Q

The ascending arousal system is located where?

A

pons/hypothalamus

52
Q

What does the ascending arousal system use?

A

NE, DA, 5-HT, H1, glutamate, Ach

also peptide orexin

53
Q

Orexin is used for what?

A

reinforce and maintain wakefulness

54
Q

sleep-promoting system is located where?

A

pre optic area/pons/hypothalamus

55
Q

What does the sleep-promoting system use?

A

GABA to inhibit arousal system

56
Q

Hormone involved in circadian rhythms and sleep-awake cycle

A

melatonin

57
Q

definition of insomnia

A

inability to fall asleep
difficulty remaining asleep
waking too early
happens despite adequate opportunity

58
Q

Short term insomnia

A

lasts <3 weeks

related to identifiable stressor

59
Q

Chronic insomnia

A

occurring >3 times per week, >3 months
specific stressor not identifiable likely
usually requires combo of behavioral therapy and hypnotics

60
Q

Common causes of insomnia

A
  • increase with age
  • poor sleep hygiene
  • meds/drugs
  • pain and other medical conditions
  • psychological stress
61
Q

Medical conditions that could cause insomnia

A

sleep apnea

parkinsons

62
Q

General approach to treating insomnia

A
  • treat underlying disorder
  • counsel on sleep hygiene and stimulus control
  • behavioral therapy
63
Q

Types of behavioral therapy for insomnia

A

relaxation
sleep restriction
cognitive therapy

64
Q

Rationale for hypnotic therapy

A
  • shorten sleep onset
  • prolong duration of sleep
  • reduce nocturnal wakefulness
  • improve daytime function
65
Q

Effect of hypnotics on first night

A
  • decrease sleep latency, lengthen duration
  • decrease awake time after sleep onset
  • decrease N3 and REM time
  • increase N2 sleep time
66
Q

Effect of hypnotics with chronic use

A
  • tolerance to hypnotic effect
  • REM returns to previous point
  • rebound insomnia upon discontinuation
67
Q

Side effects common to all hypnotics

A
  • residual daytime sleepiness, drowsiness, dizzy
  • cognitive impairment
  • sleeping while driving, cooking, sex, phone calls
  • suppress respiration that worsen in apnea
  • habit forming & rebound
68
Q

Pregnancy and hypnotics

A

teratogenicity

neonatal dependency

69
Q

Alcohol consumption and hypnotics

A

excessive sedation

respiratory depression

70
Q

Geriatric patients and hypnotics

A

decreased renal/hepatic Cl a
increased susceptibility to sedative effects
risk of falls greatly increases

Pharmacology II Exam 1 (9 decks)

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