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AC- CNS lectures > Anxiety disorder 1.2.1 (Anxiolytics & Hypnotics) > Flashcards

Anxiety disorder 1.2.1 (Anxiolytics & Hypnotics) Flashcards

1
Q

What are the type of anxiety disorders? What do you use to treat them?

A
  • generalised anxiety disorder
  • panic disorder
  • phobias (social phobia)
  • obsessive compulsive disorder
  • anxiolytics
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2
Q

Classify the anxiolytics & hypnotics please…

A

Benzodiazepine

  • diazepam, oxazepam, temaxepam

Newer non-benzodiazepine hypnotics

  • zolpidem, zoplicone, melatonin, suvorexant

5HT1A receptor agonist anxiolytics

  • buspirone
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3
Q

What are the causes of sleep disorders (insomnia)?

What is used to treat sleep disorders?

A
  • illness
  • alcohol or drugs
  • periodic limbic movement
  • sleep apnoea
  • psychiatric illness- depression, anxiety
  • shift work, flights
  • hypnotic drugs
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4
Q

How does serotonin affect anixety? What is there a overactivity of?

A
  • excessive serotonin in limbic region
  • overactivity of 5HT1A, 2A & 2C receptors
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5
Q

What is there a deficient inhibition of in many anixety disorders?

A
  • Deficient inhibition of limbic neurotransmission of GABA interneurons
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6
Q

Which are the long acting BZD?

>12 hours

A
  • diazepam
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7
Q

What are the short acting BZD?

1-6 hours

A
  • temazepam
  • midazolam
  • nitrazepam
  • flunitrazepam
  • triazolam
  • oxazepam
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8
Q

What other drugs are hypnotics?

A
  • melatonin
  • choral hydrate
  • sedative antidepressant-mirtazapine
  • sedative antihistamine- diphenhydramine, doxylamine
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9
Q

What other drugs are anxiolytics?

A
  • propanolol
  • antidepressants- venlafaxine, sertraline, paroxetine
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10
Q

What is GABA? What does it do?

A
  • calming neurontransmittor
  • Major inhibitory- sedation, insomnia, anxiety sx etc neurotransmitter in CNS
  • Widely distributed throughout the brain
  • Inhibits synaptic activity by mainly acting postsynaptically
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11
Q

What are GABA pathways & functions?

A
  • All regions
  • Motor control, memory, consciousness
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12
Q

What are the two types of GABA receptors? What do GABAA receptors do?

A
  • GABAA Postsynaptic Ligand-gated Clchannel
  • GABAB G-protein-coupled receptor, acts via Gi

GABAA receptors mediate most of the fast inhibitory neurotransmission (ligand gated) in the CNS

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13
Q

What are the most widely used anxiolytics & hypnotics?

A
  • benzodiazepines
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14
Q

What is the MOA of benzodiazepines?

A
  • potentiate the actions of GABA- inhibitoruy effects
  • act at site closely linked to the GABAA receptor
  • acts only in the presence of GABA, GABA needs to be bound to GABAA receptor before benzo can be effective
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15
Q

What does the potentiation of hyperpolarisation (postsynaptic membrane) produced by GABA result in?

A
  • Increased frequency of chloride channel opening –> more chloride enters the channel –> enhances inhibitory effect of GABA
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16
Q

The increase in inhibitory neurotransmission produced by BZDs has potentially useful effects. Explain how for the following:

a) anxiolytic
b) hypnotic

c) skeletal muscle relaxation
d) premedication

A

A) anxiolytic- actions on the limbic system and hypothalamus

B) hypnotics- reduced sensory input to the reticular activating system

C) skeletal muscle relaxtaion- reduction of muscle tone

D) Intravenous sedation (midazolam), anterograde amnesia produced is useful in this situation

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17
Q

What are the THREE pharmacological effects of BZDs?

A
  • sedation
  • amnesia
  • anxiolytics
  • muscle relaxation
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18
Q

Which BZDs are used as anxiolytics?

DOAC

A
  • diazepam
  • oxazepam
  • alprazolam
  • clobazam
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19
Q

What are the first choice drugs for treating anxiety? Where do they act and how do they work? What is a common precaution?

A
  • benzos
  • they rapidly relieve anxiety by potentiating GABA activity in the amygdala and other limbic regions of the brain
  • binds to omega 2 receptor subtype to enhance anxiolytic effect of GABA
  • avoid long term use
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20
Q

What are the anxiolytic effects of diazepam (long acting)? Include other effects…

A
  • Rapidly absorbed
  • Marked initial drowsiness
  • Accumulation and residual drowsiness because of its long half-life (30h) and active metabolite formed (60h)
  • significant muscle relaxant and anticonvulsant effects
21
Q

What are the anxiolytic effects of oxazepam (short -acting)? Why is it better than diazepam?

A
  • More slowly absorbed
  • Less initial drowsiness
  • Short half-life
  • Inactivated by glucuronidation
  • Short duration of action with minimal residual drowsiness
  • Better than diazepam in the eldery as it less likely to reduce alertness and phase II metabolism is less impaired in elderly.
22
Q

A) What are short acting/medium acting (DOA) benzodiazepines used for?

B) What are medium/long acting (DOA) benzodiazepines used for?

A

A) difficulty getting to sleep

B) problems waking up too early

23
Q

Which BZDs are used as hypnotics for insomnia? What do they do?

(TNFC)

A
  • tamazepem
  • nitrazepam
  • flunitrazepam
  • clobazam
  • Produce hypnotic effect with minimal residual drowsiness the following morning
  • Should not be used for longer than 1-2 weeks for insomnia.
24
Q

How do benzodizepines as hypnotics work? How do they alter the sleep cycle? What are the negatives to using this?

A
  • Reduce sleep onset, reduce awakening and increase sleep duration
  • Decrease the proportion of REM sleep and stages 3 & 4 of NREM sleep
  • Increase the proportion of stages 1&2 NREM sleep

Negatives

  • some tolerance may develop to these effects after 1-2 weeks
  • rebound insomnia can become a problem after prolonged use of benzodiazepines
25
Q

What happens to sleep in patients with insomnia?

A
  • time required to fall asleep (sleep latency) is usually prolonged
  • one or more awakenings during the night
  • total sleep time is decreased –> reduced amount of slow-wave sleep
26
Q

What are the ADV of BZDs?

A
  • CNS depression- drowsiness, lethargy, impaired coordination, muscle

weakness

  • Anterograde amnesia- impaired recall events that take place after dosing esp w triazolam
  • Paradoxial effects- insomnia, excitation, euphoria, heightened anxiety
  • Respiratory depression- weak depression, but to avoid combining with other CNS depressants
  • disinhibition- rage, violence, antisocial acts
  • others- vertigo, nausea, headache
27
Q

How do you get BZD tolerance?

A
  • with prolonged use
28
Q

What does the severity of BZD withdrawal depend on?

A
  • dose dependant
  • DOA
  • duration of treatment
29
Q

What are the symptoms of BZD withdrawal?

A
  • anxiety
  • tremor
  • insomnia
  • restlessness
  • sometimes paranoia
  • panic
  • delirium
  • convulsions
30
Q

Why are the withdrawal symptoms with diazepam less severe than those with oxazepam and other short acting BZDs?

A
  • because both it and its active metabolite, nordazepam have long half-lives
  • Oxazepam is directly converted to glucoronide metabolite via phase II –> shorter acting –> more severe withdrawal symptoms
31
Q

What are the CI for benzodiazepines?

A
  • History of drug abuse
  • Sleep apnoea
  • Respiratory depression, disease
  • Renal and hepatic impairment
  • Myasthenia gravis
  • Elderly with cognitive problems
32
Q

Can BZD be used in pregnancy & lactation?

A
  • it should be avoided
  • to minimise adverse effects on the foetus & newborn
33
Q

Is a BZD overdose serious? What happens in BZD OD? Can it be treated- with what?

A
  • no, rarely serious
  • symptoms include: drowsiness, lethargy, confusion
  • yes, with competitive BZD receptor antagonist, flumazenil
34
Q

How does flumazenil work in BZD OD?

A
  • reverse rapidly excessive respiratory depression produced by BZD
  • DOA is relatively brief
  • 1/2 life is 1h
  • repeated injc may be required
  • major adv is convulsion
35
Q

What are TWO examples of non-benzodiazepines (hypnotics)?

Hypnotic- insomnia

A
  • zolpidem
  • zoplicone
36
Q

How does zolpidem work?

A
  • Binds selectively to type-1a benzodiazepine receptors omega1 subtype to produce hypnotic effect
  • has minimal anxiolytic, muscle relaxant and anticonvulsant effects
  • A rapid and short-acting hypnotic. It has a duration of action of 4-6 h because it is rapidly inactivated by hepatic enzymes
37
Q

What is zolpidem used for?

A
  • short term treatment of insomnia
38
Q

What are the adverse effects of of zolpidem? What is the antidote?

A
  • diarrhoea, impaired alertness, drowsiness headache, sleep walking
  • Tolerance and dependence can develop to zolpidem, but to a lesser extent than with
  • Zolpidem should not be used for more than 1-2 weeks
  • An overdose of zolpidem can be dangerous if combined with other CNS depressants
  • Flumazenil can be used to reverse excessive respiratory depression produced by zolpidem (OD)
39
Q

What are the mechanisms of action of non-BZDs on GABAA receptor:

A) Omega 1 receptor sybtype

B) Omega 2 receptor subtype

C) Omegae 3 receptor subtype

A

A) Omega 1 receptor sybtype- sedation, amnesia

B) Omega 2 receptor subtype- anxiolysis

C) Omegae 3 receptor subtype- no effect

Non selective benzodiazepines= A, B, C

Zolpidem= A

Zoplicone= A, B

40
Q

What is the MOA of Buspirone as anxiolytic?

A
  • 5-HT 1A Agonist
  • affects serotonin (5-HT) activity in the brain by acting as a partial agonist on 5-HT1A receptors
  • unsuitable for acute anxiety because its anxiolytic effect requires about 1-3 weeks to develop
  • effective for generalised anxiety disorder
  • ineffective for panis disorder
  • may also have antidepressant activity
41
Q

What does stimulation of postsynaptic 5-HT1A receptors in limbic and corticalregions do?

A
  • reduces anxiety
42
Q

Why does buspirone take 1-3 weeks to develop?

A
  • Anxiolytic action of buspirone on postsynaptic 5‐HT1A receptors is less than expected
  • This is because increased activation of 5‐HT1A autoreceptors on the soma and dendrites which reduces 5‐HT release
43
Q

What are the ADV E of buspirone?

A
  • Buspirone does not cause excessive drowsiness, impaired coordination
  • Its use is NOT associated with dependence, withdrawal & abuse
  • The main adverse effects include: tachycardia, palpitations, nausea, dizziness, headaches & restlessness
  • Is relatively safe if an overdose is taken
  • Safety in pregnancy not established
44
Q

What is the long term effect of buspirone?

A
  • After 1‐3 weeks, buspirone produces desensitisation of presynaptic but NOT postsynaptic HT1A receptors
  • Desensitisation of the autoreceptors reduces inhibitory effect on 5‐HT release from the nerve terminals = elevation of serotonin cell body and dendrites
  • The need to desensitise somato‐dendritic 5‐HT1A receptors could thus explain in part the slow onset of buspirone
45
Q

Why is the non-selective beta blocker (propanolol) used in social phobia’s when there is sympathetic over activity?

A
  • treats the prominent sympathetic symptoms of acute

anxiety disorder and social phobia

  • disabling symptoms include tremors, palpitations, sweating
  • does not directly relieve the mental aspects of SP
  • avoid in patients with asthma or severe peripheral vascular disease and heart failure
  • use with caution in patients with diabetes
46
Q

What are the TWO other hypnotics used?

A
  • melatonin
  • suvorexant
47
Q

Indication for melatonin?

What is the MOA of melatonin?

Common ADV?

Drug interactions?

A
  • Indication
    • 55 y0 and above
    • for short term insomnia
  • MOA
    • acts at melatonin MT1 & MT2 receptors
    • melatonin secretion is high at night & low by day
    • given PO, well absorbed
    • 1/2 life is around a few mins, hence circadin used
  • ADV
    • back pain, arthralgia
  • Drug interactions
    • drowsiness, increased with others that cause drowsiness
    • fluvoxamine–> inhibits melatonin metabolism- more melatonin in body- increase drowsiness
48
Q

What is the indication of suvorexant?

What is the MOA?

Common adverse effects?

Drug interactions?

A
  • Indicated for chronic insomnia
  • MOA- orexin receptor antagonist that blocks binding of wake- promoting orexin A and B neuropeptides
  • ADV
    • somnolence, headache (common)
    • abnormal dreams, fatigue, dizziness, hallucination during sleep
  • Drug Interactions
    • avoid using with drugs that are moderate or strong inhibitors of CYP3A4 and with drugs that are strong inducers of CYP3A4
49
Q

How can BZD improve sleep?

A
  • reduces sleep onset, reduce awakening & increase sleep duration
  • decrease the proportion of REM sleep & stages 3 & 4 of NREM sleep
  • increase the proportion of stages 1 & 2 NREM sleep
  • stage 3- deep sleep, difficult to wake person up

AC- CNS lectures (28 decks)

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