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PHS 931 > Block 2 Lecture 3 -- Anxiolytic and Hypnotic Drugs > Flashcards

Block 2 Lecture 3 -- Anxiolytic and Hypnotic Drugs Flashcards

1
Q

What is anxiety?

A

inappropriate worry in absence of a true threat that significantly impairs QoL.

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2
Q

Sxs of OCDs.

A

obsession
thoughts of murder + sex
hallucinations
fear to use public toilets

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3
Q

Sxs of social phobias.

A

fear of excessive humiliation
“ public speaking
“ public toilets

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4
Q

Sxs of mixed anxiety and depressive disorder.

A
    • anxiety
    • inner tension, depression
    • aggressiveness
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5
Q

Sxs of panic disorder.

A
    • fear of dying
    • fear of going
    • chest pain + SOB
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6
Q

How is GAD treated?

A

1st: CBT
2nd: anti-depressant
3rd: anti-depressant combos

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7
Q

What are the FDA-approved anti-depressants available for GAD treatment?

A

1st: SSRIs
– es/citalopram, paroxetine, fluoxetine
– +NET: duloxetine, venlafaxine
2nd: buspirone
also: hydroxyzine
also: combos, anti-convulsants
short-term: BZDs

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8
Q

What is hydroxyzine?

A

h1 antagonist

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9
Q

When is buspirone used in GAD?

A

2nd line as adjunct to SSRI or as monotherapy

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10
Q

Describe the onset of SSRIs

A

2-4 weeks

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11
Q

What happens if a GAD patient fails the 1st-line anti-depressant?

A

try another anti-depressant

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12
Q

What is agoraphobia?

A

avoidance of triggers evoking panic

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13
Q

How are agoraphobia and other anxiety disorders treated?

A

similar to GAD when chronic

    • anti-depressants (1+), buspar, combos
    • BZDs for exacerbations or agoraphobia
    • beta-blockers for acute panic
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14
Q

What drugs may cause secondary anxiety disorders?

A

1) NET/DAT-active anti-depressants
2) sympathomimetics
3) thyroid hormone
4) stimulants

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15
Q

What might anxiety disorders be secondary to?

A

1) medical conditions
2) drugs
3) drug withdrawal

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16
Q

For what conditions are barbs indicated?

A

1) induction of anesthesia
2) epilepsy
3) severe tension/migraine HA

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17
Q

MoA of barbs:

A

APLs of GABAa

    • increase duration of channel opening
    • synergistic with EtOH, BZDs, Z drugs, opioids
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18
Q

How does one become tolerant to barbs?

A

1) rapid PK (1a2, 2c9, 2c19, 3a4)

2) slow PD (decrease GABA # and change composition)

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19
Q

Why are barb withdrawals life-threatening?

A

convulsions

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20
Q

How are barbs categorized?

A

duration of action

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21
Q

ultra-short acting barbs:

A

methohexital

thiopental

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22
Q

What are ultra-short-acting barbs indicated for?

A

1) induction of anesthesia

2) terminal anesthesia

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23
Q

What are the intermediate-acting barbs?

A

1) pentobarbital

2) butalbital

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24
Q

What are the long-acting barbs?

A

phenobarbital

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25
Q

How is phenobarb used?

A

long-acting barb for anti-convulsant

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26
Q

How is butalbital used?

A

included with ASA/APAP and caffeine

– w/ codeine for tension HA

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27
Q

What is the old lethal injection cocktail?

A

sodium thiopental, pancuronium br, KCl

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28
Q

What is the newer lethal injection cocktail?

A

hi-dose Na thiopental or pentobarbital

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29
Q

Where are alpha-1 containing GABAa receptors located?

A

most abundant, most widely distributed
– also in VTA and HT
(hypnotic, anticonvulsant, amnestic, addiction)

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30
Q

Where are alpha-2 containing GABAa receptors located?

A

limbic, cortex, striatum (anxiolytic properties when agonized)

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31
Q

Where are alpha-3/5 containing GABAa receptors located?

A

spinal cord (muscle relaxant properties when agonized)

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32
Q

What is the MoA of BZDs?

A

non-selectively interact with a1/2/3/5 subunits of GABAa receptors

    • increase affinity for GABA
    • increase frequency of channel opening
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33
Q

Why don’t BZDs cause fatal respiratory depression?

A

do not directly open Cl channel

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34
Q

How long should BZDs be used?

A

DNE 2-4 weeks or past acute exacerbation

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35
Q

What co-morbidites can be problematic with BZD use especially if used w/ EtOH or opiates?

A

liver disease
respiratory issues (sleep apnea included)
child

36
Q

Describe metabolism of BZDs.

A
    • no enzyme induction
    • catabolized by 3a4 and c19
    • active metabolites may be GABAa APLs
37
Q

What enzyme does grapefruit juice inhibit?

A

3a4

38
Q

What factors of BZD selection should be selected for longer-acting effects?

A

active mets

lipid soluble

39
Q

What are sxs of BZD withdrawal?

A

due to downregulation of GABA…

– anxiety, muscle cramping/twitching, psychosis, panic, ANS sxs, convulsions

40
Q

What are the longer-acting BZDs?

A
    • clonazepam (longer t1/2)
    • chlordiazepoxie (active mets but low potency)
    • diazepam (long t1/2 + active mets)
41
Q

What are the ultra-rapid-acting BZDs?

A

midazolam

lorazepam

42
Q

How is midazolam used?

A

anesthetic

43
Q

How is clonazepam used?

A

anxiolytic, anti-convulsant

44
Q

How is alprazolam used?

A

anxiolytic, agoraphobia

45
Q

What BZDs are used for sleep?

A

1) flurazepam
2) temazepam
3) triazolam

46
Q

What other drugs act on the BZD-binding site?

A

1) flumazenil

2) flunitrazepam

47
Q

What is flumazenil?

A

BZD-binding site antagonist

– IV admin for BZD overdose

48
Q

What is flunitrazepam?

A

rapid-onset APL of GABAa via the BZD-binding site

– date-rape

49
Q

What are non-barb, non-BZD anxiolytic sedatives?

A

1) buspirone!

50
Q

What is the MoA for buspar?

A

5ht1a partial agonist

51
Q

Where is 5HT1a dense?

A

amygdala and limbic regions

52
Q

What is the main use for buspar?

A

GAD

    • no efficacy for acute panic
    • not as efficacious as SSRIs for other anxiety-related disorders
53
Q

Describe metabolism of buspar.

A

3a4

– caution MAOI or SSRI

54
Q

What are the advantages of buspar?

A

fewer ADRs and less sedation

55
Q

Describe the ADRs of buspar.

A

n/v, dizziness, ha

56
Q

What are the disadvantages of buspar?

A

– 2-4 week onset

57
Q

How is non-rem sleep regulated?

A

raphe (5-HT) and NTS (NE and autonomics)

58
Q

How is REM sleep regulated?

A

cholinergic regions of forebrain and midbrain

59
Q

What are the primary complaints of primary sleep disorder?

A

1) getting to sleep
2) staying asleep
3) waking up too early
4) sleeping at wrong time

60
Q

What are dyssomnias?

A

primary insomnia, primary hypersomnia, narcolepsy, jet lag, shift-work disorder, sleep apnea, non-24

61
Q

What are parasomnias?

A

nightmares, night terrors, sleepwalking, bruxism

62
Q

What sedative drugs are used for primary sleep disorders?

A

1) trazodone
2) TCAs
3) clonidine
4) CNS-acting muscle relaxants

63
Q

MoA of trazodone.

A

5ht1a partial agonist; 5ht2a antagonist; SSRI

64
Q

What are the general categories of drugs used for sleep disorders?

A

1) sedatives
2) BZDs
3) Z-drugs
4) melatonin and MTr agonists
5) OXr antagonists

65
Q

What effects do BZDs have on sleep?

A

1) quicker induction
2) quicker time to REM
3) decreased awakenings
4) more sleep (greatest increase in stage 2 non-rem)

5) decreased total REM

66
Q

What are ADRs of BZDs used for sleep?

A
    • risk for hangover
    • rapid-onset = abuse
    • rebound insomnia
    • rebound REM sleep
67
Q

What is the MoA of Z-drugs?

A

a1-selective-GABAa (HT sleep center); bind BZD site

68
Q

What are Z-drugs used for?

A

effective for sleep induction and maintenance only

69
Q

How do Z-drugs differ?

A

half-life

70
Q

What is the shorter-acting Z drug?

A

zalepon (sonata) shorter –1hr– than zolpidem (ambien)–2hr–

71
Q

What are the MTr agonists?

A

ramelteon

tasimelteon

72
Q

What is the MoA for ramelteon?

A

Mt1/Mt2 receptor agonist

73
Q

Which MTr is thought to be more important for sleep?

A

MT2

74
Q

Describe the MTr.

A

Gi coupled, dense in circadian regions of HT

75
Q

What are the advantages of ramelteon?

A

1) non-scheduled
2) does not disturb REM
3) 30-min onset with 2 hr t1/2

76
Q

Describe metabolism of ramelteon.

A

30 min onset
2 hour half-life
1a2 metabolism

77
Q

What are ADRs of MTr agonists?

A

HA, sedation, fatigue, N/V

78
Q

How does tasimelteon differ from ramelteon?

A

1) $$
2) more M2-selective
3) 1a2 and 3a4

79
Q

What are OXr antagonists?

A

suvorexant

80
Q

What are orexins?

A

wake-promoting peptides synthesized by orexin neurons

81
Q

Describe OX1/OX2 receptors.

A

Gs GPCRs on wake-active neurons; localized to lateral and posterior HT

82
Q

Why is suvorexant scheduled?

A

anorectic (abuse potential)

83
Q

What concentration of EtOH is the legal limit?

A

17 mM

84
Q

How does EtOH work at 1mM?

A

potentiation of delta-subunit GABAa receptors

85
Q

How does EtOH work at 10 mM?

A

GlyR potentiation

inhibition of a7 nAChR, NMDAr, vgCA channels

86
Q

How does EtOH work at 50 mM?

A

1) potentiation of GABAa, a4-nAChR, NMDAr, 5ht3

2) inhibition of AMPA and kainate

87
Q

EtoH MoA:

A

1) indirect intx with target proteins
- - membrane fluidization
- - lateral membrane pressures
- - replaces H2O at lipid-protein surfaces
2) direct interaction with allosteric/orthosteric receptor sites
- - low affinity

PHS 931 (29 decks)

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