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Pharmacology Test #6 > Sedative Hypnotics and Anxiolytics > Flashcards

Sedative Hypnotics and Anxiolytics Flashcards

1
Q

Stress versus anxiety

A

stress is something that happens to you and anxiety is a reaction to stress that the brain produces

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2
Q

Amygdala

A

part of the limbic system; ancient, primitive structure; conditioned fear in rodents; anxiety in humans

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3
Q

Anxiety disorders

A

GAD; phobias; OCD; eating disorders; panic attacks; mixed anxiety-depression; PTSC

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4
Q

Sedation

A

reduced responsiveness, calming effect

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5
Q

hypnosis

A

drug-induced sleep

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6
Q

Anesthesia

A

drug-induced amnesia, analgesia, unconsciousness, lsot muscle tone

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7
Q

Coma

A

unconsciousness for 6+ hours, no sleep cycles, non-responsive to pain, light/sound

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8
Q

Major inhibitor neurotransmitter in the CNS

A

GABA

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9
Q

What is GABA produced from

A

glutamate

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10
Q

GABA activates

A

GABAA type ligand gated Cl- channels, and GABAB and GABAC receptors which are GPCRs

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11
Q

Most sedative/hypnotics act at which receptors

A

act at the GABA-A receptor complex (ligand-gated chloride channel) through via different pharmacological mechanisms

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12
Q

How many GABA molecules are required to bind and activate a GABA-A receptor?

A

2 GABA molecules

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13
Q

Cl- influx through the GABA receptor does what to the cell membrane?

A

hyperpolarizes the cell membrane

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14
Q

Where do benzodiazepines bind?

A

at a site distinct from the GABA binding site

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15
Q

What does binding of a BZD molecule enhance?

A

enhances the activity of GABA in activating the receptor, but binding of BZD has no activity on its own

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16
Q

What type of binding does BZDs exhibit?

A

allosteric

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17
Q

How does the addition of a BZD or barbiturate when GABA is present enhance the action of GABA?

A

BZD largely increases the frequency of channel openings whereas barbiturates increase the duration of openings

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18
Q

What do molecules with inverse agonist action at the BZD site do when they bind to the BZD site?

A

they make it harder for GABA to open the channel (negative allosteric modulation), which is the opposite of what BZDs do

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19
Q

What is a GABA(A) receptor agonist

A

an agonist at the GABA binding site

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20
Q

What does a BZD site agonist do?

A

facilitates the action of GABA

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21
Q

What does a BZD site antagonist do?

A

antagonizes the action of BZD agonists without antagonizing the action of barbiturates

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22
Q

What is a BZD site inverse agonist

A

negative allosteric modulator of GABAAR function

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23
Q

Benzodiazepines

A
  1. Alprazolam
  2. Flurazepam
  3. Midozolam
  4. Flumazenil
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24
Q

How do benzodiazepines work?

A

potentiate GABA throughout the CNS

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25
Q

Metabolism of benzodiazepines

A

extensively metabolized with many active metabolites

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26
Q

What are benzodiazepines potentiated by?

A

potentiated by other CNS depressants as well as alcohol

27
Q

What is the potential risk associated with benzodiazepines?

A

significant potential for psychological and physical dependence - people can become addicted to drugs such as Xanax and sleep pills

28
Q

Clinical use of Midazolam

A

for acute seizure control, pre-surgery anxiolysis, amnesia and sedation;
rapid onset, fast recovery

29
Q

Clinical use of Alprazolam

A

mainly for panic, GAD;

rapid acting, moderate duration

30
Q

Clinical use of Flurazepam

A

long duration, next-day sedation is possible;

for insomnia and those who need help maintaining sleep

31
Q

Metabolism of Benzodiazepines

A

CYP3A4 and CYP2C19

32
Q

Adverse effects of benzodiazepines (largely apply to barbiturates as well)

A
  1. Amnesia (short-acting benzos)
  2. Daytime sedation (long-acting benzos)
  3. Respiratory/CV depression (esp in pts with pulmonary disease)
  4. Withdrawal (anxiety, insomnia, CNS stimulation, convulsions)
  5. Dependence
  6. Potentiated by P-450 inhibitors
33
Q

MOA of Flumazenil

A

Simple antagonist at the allosteric site (neither negative or positive modulator); can compete for binding at the BZD site with a positive allosteric modulator and therefore antagonist its own action

34
Q

Psychologic dependence

A

compulsive use

35
Q

Physiologic dependence

A

continued drug use to prevent withdrawal

36
Q

Tolerance

A

decreased responsiveness to fixed dose; increase dose to maintain effect

37
Q

Barbiturates induce

A

P450s

38
Q

Why is overdose easier to achieve with barbiturates than with benzos?

A

barbiturates have stronger action at GABA-A, the ability to directly open GABA receptors, and actions at other NT systems

39
Q

Use of barbiturates

A

rarely for seizures, anesthesia; commonly for severely brain injured patients to induce coma in order to bring down ICP following an injury

40
Q

Which barbiturate is used for the death penalty

A

pentobarbital

41
Q

Barbiturate overdose

A

coma, respiratory depression, death

42
Q

Buspirone

A

5-HT1A receptor partial agonist; less sedation; little or no withdrawal syndrome; low abuse potential

43
Q

Clinical uses of Buspirone

A

GAD, not panic disorders

44
Q

Types of insomnia

A
  1. Transient (~3 days)
  2. Short-term (3-21 days)
  3. Long-term (>21 days)
  4. Rebound
45
Q

What is rebound insomnia?

A

withdrawal insomnia due to drug discontinuation, possibly worse than original insomnia, occurs most with short-acting agents, avoid by titrating down

46
Q

How do you treat transient insomnia with sedatives?

A

smallest efficacious dose for the shortest time possible (2-4 days)

47
Q

How do you treat short term insomnia with sedatives?

A

due to personal stress (grief, illness), only use drugs for 7-10 days

48
Q

Why do you use BZD and Z compounds instead of barbiturates for insomnia?

A

efficacy is the same with less adverse effects/risk; Z compounds associated with less day-after sedation; better formulation options

49
Q

Why is rebound insomnia more common in drugs with a short half life?

A

they wear off quicker, making it more likely that you will be in a state of withdrawal the next day; more likely to be exposing the state where there is increased excitability due to adjustment of GABA-A receptor levels

50
Q

Who is more likely to be at a risk for liver issues that can disturb the metabolism of hypnosedatives?

A

elderly people - can lead to overdose or adverse effects

51
Q

Non-Benzodiazepine “Z” compounds act where

A

at the BZD site like BZDs

52
Q

What are Z compounds more selective for

A

alpha1-containing receptors

53
Q

Why are the effects of Z compounds more mild and not as sedating as BZDs?

A

because Z compounds are more selective for alpha1-containing receptors

54
Q

What is possible with high doses and prolonged use of Zolpidem?

A

dependence

55
Q

Non-benzodiazepine “Z” compounds

A
  1. Zolpidem
  2. Zaleplon
  3. Eszopiclone
56
Q

Ramelteon is selective for

A

MT1 and MT2 receptors, not MT3 receptors

57
Q

What is Ramelteon?

A

melatonin mimetic; acts in suprachiasmatic nucleus to promote sleep; no action at GABAa

58
Q

The suprachiasmatic nucleus is involved in regulating

A

circadian rhythms

59
Q

Stages of sleep

A

Stage 1: somnolence, drowsy, transition
Stage 2: sleep spindles, K complexes, unconsciousness
Stage 3/4: “deep” sleep
REM: “paradoxical” sleep

60
Q

What happens in Stage 1 sleep?

A

transition stage from wakefullness to sleep

61
Q

What happens in Stage 2 sleep?

A

electrophysiological characteristics define stage 2 as spindles and K complexes

62
Q

What happens in REM sleep?

A

dreams, rapid eye movements, paralysis (probably beneficial)

63
Q

BZD/Barbs effect on sleep stages

A

increase Stage 2; decrease REM; decrease stage 3/4

64
Q

Z compounds effect on sleep stages

A

increase or maintain stage 2; decrease or maintain REM

Pharmacology Test #6 (12 decks)

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