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Pharmacy Stage 3 - CNS > Anxiety and insomia: pathophysiology and pharmacology > Flashcards

Anxiety and insomia: pathophysiology and pharmacology Flashcards

1
Q

what is eustress?

A

acute stress

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2
Q

what is physiological stress?

A

the body’s response to an external pressure

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3
Q

what is anxiety?

A

Psychological response to a perceived threat

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4
Q

what is distress?

A

chronic stress

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5
Q

what is generalised anxiety disorder?

A

Excessive and persistent anxiety/worry for more than 6 months

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6
Q

what is obsessive compulsive disorders?

A
  • obsessive repetitive thoughts which are often negative

- accompanied with compulsive behaviours providing temporary relief

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7
Q

what is panic disorder?

A
  • Sudden unexpected panic attacks
  • Palpitations, tremor dizzy chest pains
  • fear of certain places can result in phobic avoidance = Agoraphobia
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8
Q

what are phobic disorders?

A

An excessive fear that is disproportionate to the specific situation
Generally predictable - thus phobic avoidance `

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9
Q

what is post traumatic stress disorder?

A

Onset delayed weeks to months following an intense traumatic experience
Re-experience of trauma

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10
Q

what three systems are involved in anxiety?

A
  1. CNS
  2. ANS
  3. Endocrine system
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11
Q

what is the role of the amygdala in the stress response?

A
  1. it integrates information about threat
  2. then appraises the new stimulus
  3. then coordinates the behavioural response, the autonomic response and the endocrine response
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12
Q

what happens to the 5-HT1A receptor binding in anxiety disorders?

A

there is decreased binding

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13
Q

what are the 2 core symptoms of anxiety disorders?

A
  • fear

- avoidance

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14
Q

what happens to the GABA receptor binding in anxiety disorders?

A

there is reduced binding

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15
Q

what pathway is active whilst awake?

A

The Ascending Arousal Pathway:

-the Locus coeruleus, Raphe and Tuberomammillary nucleus.

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16
Q

what pathway is inhibited for sleep?

A

the ascending arousal pathway

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17
Q

what impact does insomia have?

A
  • reduced quality of life

- increased risk of accidents

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18
Q

what can cause insomnia?

A
  • stress
  • psychiatric illness
  • medical illness
  • medications/drugs
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19
Q

what are the three main neurotransmitters in the ascending arousal pathway?

A
  • Histamine from the Tuberomammillary nucleus
  • Serotonin (5-HT) from Raphe
  • Noradrenaline from Locus coeruleus
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20
Q

first part of sleep is called what?

A

slow wave sleep

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21
Q

second part of sleep is called what?

A

rapid eye movement

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22
Q

what does the ventrolateral preoptic nucleus (VLPO) do?

A

releases GABA which inhibits the arousal pathway.

-however it is not active when awake.

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23
Q

what does the Suprachiasmatic Nucleus (SCN) do?

A

-active during the day and night to detect whether it is day or night and inhibits the VLPO during the day to prevent it from stopping the ascending arousal pathway.

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24
Q

What effect does adenosine have on the VLPO?

A
  • it builds up during the day in the basal ganglia so when it gets to a certain level, it activates the VLPO
  • this inhibits the arousal pathway
25
Q

what effect does the pineal gland have on the SCN?

A

-releases melatonin which is active on a night time therefore preventing SCN from inhibiting VLPO so GABA can be released to prevent the arousal pathway.

26
Q

what risk factor increases chances of insomnia?

A
  • increased age

- female

27
Q

what are the common side effects with acute use of hypnotics and anxiolytics?

A

-CNS depression e.g. poor memory and motor-co-ordination

28
Q

what are the common side effects with chronic use of hypnotics and anxiolytics?

A

-tolerance/dependence

29
Q

what is an example of a benzodiazepine?

A

diazepam

30
Q

what are the therapeutic uses of anxiolytics?

A
  1. short term sedation
  2. relieve muscle tension
  3. anxiolysis
  4. hypnosis (reduces time taken to fall asleep and increase how long you sleep for)
  5. anticonvulsants
31
Q

side effects of anxiolytics?

A
  1. unwanted sedation
  2. amnesia
  3. reduced cognition
  4. reduced motor-co-ordination
  5. interactions - barbituates and benzo’s with alcohol
  6. Decreased rapid eye movement
32
Q

what are the side effects associated with the chronic use of anxiolytics?

A
  1. tolerance
  2. dependence
  3. withdrawal symptoms
33
Q

very short half life anxiolytics are used for what e.g. midazolam?

A

-conscious sedative, status epilepticus

34
Q

short half-life anxiolytics are used for what e.g. loprazolam?

A

hypnotics

35
Q

intermediate half-life anxiolytics are used for what e.g. alprazolam?

A

anxiolytic/panic disorders

36
Q

Long half-life anxiolytics are used for what e.g. lorazepam, diazepam, Chlordiazepoxide?

A

anxiolytic, acute alcohol withdrawal, panic disorder, anticonvulsants, status epilepticus, muscle spams

37
Q

why do some anxiolytics have a longer half-life?

A

because the long-half life ones are metabolised into active metabolites unlike the short half-lives ones

38
Q

How do Barbituates work?

A
  • Barbiturates act on GABA receptors (inhibitory receptors)
  • these receptors have Cl- channels around it which open to let Cl- in which hyperpolarises the cell and dampens down the cell activity.
  • the barbituates work in the absence of GABA so aren’t in competition with it.
  • GABA inhibits the ascending arousal pathway
39
Q

how do alcohol and benzodiazepines work?

A

-work to increase the effects of GABA which inhibits the arousal pathway

40
Q

why are anxiolytics non-selective?

A

because there are different GABA receptor subtypes in the brain (e.g. 6 alpha subtypes, 3beta, 3 gamma, 3 sigma etc) so you dampen other activities in the brain.

41
Q

what are alpha 1 subunits associated with?

A

sedation

42
Q

what are alpha 3 subunits associated with?

A

anxiolysis

43
Q

what are alpha 5 subunits associated with?

A

learning and memory

44
Q

what causes tolerance and dependence?

A

-long term use of the GABA receptor agonist causes the GABA function to increase but also the receptor to adapt making them ‘resistant’ to the anxiolytic

45
Q

what are the first line anxiolytics?

A

SSRIs (selective serotonin reuptake inhibitors)

  • SNRIs
  • TCAs
  • Monoamine oxidase inhibitors
  • 5-HT receptor agonist (for anxiety not depression!!)
46
Q

what is the initial risk of SSRIs?

A
  • increased anxiety
  • agitation
  • sleeping problems
47
Q

mechanism of serotonin action?

A
  • 5-HT released from presynaptic neurone and activates excitatory or inhibitory 5-HT receptors on postsynaptic neurone
  • autoreceptors on presynaptic neurone will turn off the further release 5HT
  • It is taken up by 5HT transporter and metabolised by monoamine oxidase
48
Q

what drugs inhibit the 5HT transporter?

A
  • SSRIs, TCAs and SNRIs

- this means 5HT remains in the synaptic cleft longer to activate 5HT receptors

49
Q

what do Monoamine Oxidase inhibitors do?

A

inhibit monoamine oxidase from metabolising 5HT therefore more 5HT neurotransmission

50
Q

how does buspirone work?

A

-as a 5HT receptor agonist (so basically binds to the 5HT receptor since there’s too little 5HT to bind to it)

51
Q

what do Z-hypnotics do?

A
  • they bind to GABA receptors like benzodiazepines
  • but they are more selective fir the GABA 1 receptor unlike benzos
  • this causes sedation (helping with insomnia) and may also help with anxiety
52
Q

how long do Z-hypnotics act?

A

very fast onset and short duration of action

53
Q

side effects of Z-hypnotics?

A

tolerance and dependence

54
Q

what do antihistamines do?

A
  • antagonise H1 receptors in the cortex inhibiting the histamine arousal pathway
  • can use for sedation
55
Q

what are the side effects to antihistamine use?

A
  • weight gain

- anticholinergic effects

56
Q

what does melatonin do?

A

-released at night and acts on melatonin receptors to inhibit the suprachiasmatic nucleus hence allowing the VLPO to release GABA and cause sedation.

57
Q

what is the only licenced melatonin drug for over 55yr olds in the UK?

A

circadin

58
Q

what is the theoretical mechanism underlying the initial increase in anxiety with SSRI administration?

A
  • inhibits 5HT transporter
  • causing increasing 5HT levels in synaptic cleft
  • that is associated with an increase in anxiety
  • this is from its acute use, with time, this becomes therapeutic as the 5HT receptors alter their expression over time

Pharmacy Stage 3 - CNS (13 decks)

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