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CPTP 3 > CPTP 3.5 Neuropharmacology 3 (Hypnotics and Anxiolytics) > Flashcards

CPTP 3.5 Neuropharmacology 3 (Hypnotics and Anxiolytics) Flashcards

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1
Q

What are the stages of sleep?

A

First 3 hours –> ‘slow wave’ sleep

After that –> REM sleep

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2
Q

What happens during each stage of sleep, and what brain region is responsible for the activity?

A

Slow wave sleep:
• Hippocampus and neocortex
• Reactivation of memories from the day

REM sleep:
• Cortex
• Consolidation of memory into long-term stores

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3
Q

Recall the mechanisms of arousal

A
  • Suprachiasmatic nucleus receives messages from the retina
    • This activates the dorsomedial hypothalamic nucleus
    • This activates the arousal pathways
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4
Q

Recall the ascending arousal pathways (which are activated by the dorsomedial hypothalamic nucleus)

What do they all do?

A
  • Raphe nucleus (5-HT)
    • Locus coeruleus (noradrenaline)
    • Tuberomammillary nucleus (histamine)

These project to the cortex and keep it alert by “washing over” the synapses

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5
Q

What structures inhibit the ascending arousal pathways?

A 
Ventrolateral preoptic nucleus
  •  GABA
  •  Galanine
Pineal gland
  •  Melatonin
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6
Q

What are the arousal and sleep-inducing neurotransmitters?

A 
Sleep inducing:
  •  GABA
  •  Galanine
  •  Melatonin
Arousal:
  •  Histamine
  •  Noradrenaline
  •  Serotonin
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7
Q

What happens to sleep as you age? Why?

A

Much reduced duration of sleep. You produce less melatonin as you age

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8
Q

What are the types of insomnia?

A
  • Initial (cant get to sleep)
    • Middle (wake up in the middle of the night)
    • Early waking
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9
Q

What are the causes of insomnia?

A 
>Stress
>Psychiatric disorders:
  •  Anxiety
  •  Depression
  •  Bipolar
  •  PTSD
>Illness
  •  Alzheimers
  •  Rheumatoid arthritis
  •  Asthma
>Medication
  •  Stimulants
  •  Antidepressants
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10
Q

Why does stress cause insomnia?

A

Increased HPA axis activity causes arousal pathways to be more active

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11
Q

What cause of insomnia gives rise to:

1) initial insomnia?
2) terminal insomnia?

A

1) Anxiety

2) Depression

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12
Q

What effect do bipolar disorder and PTSD have on sleep?

A

Bipolar disorder:
• Less SWS
PTSD:
• Less REM

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13
Q

What properties must a hypnotic have?

A
  • Short half-life
    • Inhibits ascending arousal pathways
    • Does not affect REM or SWS brain areas
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14
Q

What physiological effect does anxiety have?

A 
Sympathetic NS activation:
  •  CV
  •  Hyperventilation
  •  Sweating
  •  GI (butterflies)
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15
Q

What ‘theme’ of core symptoms fo anxiety disorders share?

A

Fear, escape, avoidance

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16
Q

Name the anxiety disorders

A
  • OCD
    • PTSD
    • GAD
    • Panic disorder
    • Agoraphobia
    • Social anxiety
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17
Q

What three main neurotransmitters are associated with anxiety disorders?

A

Serotonin and noradrenaline - Increased
• Increased release

GABA - Decreased
• Decreased amounts of GABA-A receptor function, so less binding

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18
Q

What effect do SSRIs have on 5-HT levels and anxiety?

A

Increases 5-HT in synaptic cleft, and increases anxiety

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19
Q

How are hypnotics and anxiolytics linked?

Study These Flashcards
A

They both are non-specific CNS depressants that reduce levels of arousal, the difference is the dose.

(To induce sleep, a higher dose is needed than for anxiolytic effects.)

20
Q

How should hypnotics and anxiolytics half lives differ?

Study These Flashcards
A

Anxiolytics - Long half life

Hypnotics - Short half life

21
Q

What are the classes of hypnotics and anxiolytics? What separates these?

Study These Flashcards
A
  • Barbituates
    • Benzodiazapines
    • (Alcohol)

HYPNOTIC ONLY:
• Z-hypnotics
• Antihistamines

Therapeutic windows and pharmacokinetics

22
Q

Why are barbituates not used any more?

Study These Flashcards
A
  • Interact with alcohol

* Very small therapeutic window

23
Q

Name the formulary benzodiazepines. What is the half-life and use of each?

Name the formulary Z-hypnotic

Study These Flashcards
A
  • Temazepam, 10hrs, hypnotic
    • Lorazepam, 15 hrs, anxiolytic
    • Chlorodiazepoxide, 20hrs, anxiolytic
    • Diazepam, 40hrs, anxiolytic

Z-hypnotic:
• Zopiclone, 6 hours

24
Q

What other use can hypnotics and anxiolytics have?

Study These Flashcards
A
  • Reduce muscle tone (i.e. in tension headaches)
    • Anticonvulsant
    • Surgical sedative
25
What drug is used as a surgical sedative, what is its half life and drug class?
Midazolam • t(1/2) = 1-4 hours • benzodiazapine
26
Why do chlorodiezepoxide and diezepam have such long half-lives?
Their metabolites are biologically active
27
What are the adverse effects associated with hypnotics and anxiolytics? What causes many of these?
* Interaction with alcohol * Poor motor co-ordination * Poor memory (this is why roofies, a benzo, causes the victim to not remember) * Decreased REM sleep * Tolerance, dependence and withdrawal syndrome Neurological side effects caused by non-selective CNS suppression
28
What are the modes of action of the hypnotics and anxiolytics classes?
Barbituates: • Non-selective depressant activity, reduces Na+ channels preventing action potentials • GABA-A receptor has barbiturate site which can activate it in absence of GABA, by opening the Cl- channel Alcohol: • Allosteric modulator of GABA-A receptor (enhance effect of GABA) Benzodiazepines: • Allosteric modulator of GABA-A receptor (enhance effect of GABA) Z-hypnotics: • Allosteric modulator of GABA-A receptor (enhance effect of GABA)
29
Why do barbiturates have a smaller therapeutic window and less safe in overdose?
They activate GABA-A, rather than modulate it, thus GABA does not need to be present, making it much more potent. (endogenous GABA cannot act as a rate-limiting step)
30
What is the nature of the interaction between alcohol and the hypnotic/anxiolytic drug classes?
They potentiate each other.
31
How many subunits are in each GABA-A receptor, and what types?
* Two alphas * Two betas * One 'other' --> USUALLY gamma-2 in the brain
32
Why are benzodiazepines described as 'non-selective'?
They are selective for GABA-A receptors whose fifth subunit is gamma-2, which accounts for most GABA-A receptors in the brain
33
Where are the targetted GABA-A receptors?
In the ascending arousal pathways | NB: endogenous GABA pathway terminating here is the ventrolateral preoptic nucleus
34
Why are benzodiazepenes not recommended for chronic use?
Rebound anxiety: * Patient with anxiety has reduced GABA function * Benzodiazepines are administered, and GABA function is increased, anxiety decreases * GABA receptors begin to adapt to the benzo therapy, slowly reducing the GABA function due to tolerance * When benzo therapy is removed, this adaptation remains, so brain GABA function is even lower than on day 0 * This causes even more severe anxiety after removal of therapy
35
How do Z-hypnotics compare to benzodiazepines?
They bind to the same site, but do not share the same structure. Z-hypnotics are more selective, as they are selective for a-1 subunit-containing pentamers (as the fifth subunit), rather than the gamma-2
36
Why should hypnotics have a shorter half life?
To reduce hangover
37
How do antihistamines work as hypnotics?
H1 antagonists, inhibit histamine excitatory pathways from the tuberomammillary nucleus Must be "drowsy" antihistamines (first generation)
38
What are the side effects of antihistamines used as hypnotics?
* Weight gain with long-term use | * Anticholinergic effects (dry mouth, constipation, etc.)
39
Do Z-hypnotics cause dependence?
Yes
40
What is NICE guidance on prescribing for insomnia?
If severe, prescribe benzos or Z-hypnotics for short periods
41
What should be prescribed for depression/anxiety co-morbid patients?
SSRIs, which are active on most anxiety disorders, therefore 2 birds with one stone
42
Which antidepressants can be used as anxiolytics, what neurotransmitter do these focus on?
Focuses on 5-HT neurotransmission: SSRIs • For comorbid depression and (any) anxiety disorder SNRIs • GAD TCAs • Panic disorder • GAD MAOs • Panic disorder • Agoraphobia • Social Phobia
43
What does each antidepressant class inhibit?
Serotonin reuptake transporter on presynaptic membrane • SSRIs • SNRIs • TCAs Monoamine oxidase underneath that membrane • MAOIs
44
But wait, antidepressants increase 5-HT, which is excitatory, but it still treats anxiety? What gives?
Initially, an increase in anxiety is seen (anxiogenesis stage) due to the increase in 5-HT. Eventually, tolerance occurs, and 5-HT2A receptors are downregulated, and 5-HT1A receptors are upregulated (anxiolysis) Takes time because changes in protein expression are needed
45
Should you use benzos or SSRIs for anxiolysis
SSRIs • Benzos cause withdrawal symptoms • Benzos do not treat depression Do not use benzos for anxiety disorders over a long period of time

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