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Pharmacy Stage 3 > anxiety and insomnia: pathophysiology and pharmacology > Flashcards

anxiety and insomnia: 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.

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
what effect does the pineal gland have on the SCN
- release melatonin which is active on a night time therefore preveting SCN from inhbiting VLPO so GABA can be released to prevent arousal pathway
26
what risk factor increases chances of insomnia
increased age | female
27
common side effecs with chronic use of hypnotics and anxiolytics
tolerance | dependence
28
what is an example of benzodiazepine
diazepam
29
therapeutic uses of anxiolytics
1. short term sedation 2. relieve muscle tension 3. anxiolysis 4. hypnosis ( reduces time taken to sleep and increases how long you sleep for) 5. anticonvuslants
30
side effects of anxiolytics
1. unwanted sedation 2. amnesia 3. reduced cognition 4. reduced motor co-ordination 5. interactions barbituates and benzo's with alchol 6. decreased rapid eye movement
31
side effects associated with chronic use of anxiolytics
tolerance dependence withdrawel symtpoms
32
very hort half life anxiolytics are used for what e.g. midazolam
conscious sedative, status epilepticus
33
short half-life anxiolytics are used for what e.g. loprazolam
hypnotics
34
intermediate half-life anxiolytics are used for what e.g. alprazolam
anxiolytic/ panic disorders
35
long half-life anxiolytics are used for what e.g. lorazepam, diazepam, chloradiazepoxide
anxiolyic, acute alcohol withdrawel, panic disorder, anticonvulsants, status epilepticus, muscle spams
36
why do some anxiolytics have a longer half-life
because long half-life ones are metabolised into active metabolites unlike the short half-lives ones
37
how do barbituates work
GABA receptors(inhibitory receptors) these receptors have CI-channels around it which open to let CI- in which hyperpolarises the cell and dampens down the cell activity barbituates work in the absence of GABA so aren't in competition with it GABA inhibits the ascending arousal pathway
38
how do alcohol and benzodiazepines work
work to increase the effects of GABA which inhibit the arousal pathway
39
why are anxiolytics non-selective
because there are different GABA receptor subtypes in the brain so you dampen other activities in the brain
40
what are alpha 1 subunits associated with
sedation
41
what are alpha 3 subunits associated with
anxiolysis
42
what are alpha 5 subunits associated with
learning and memory
43
what causes tolerance and dependence
long term use of the GABA receptor agonist causes the GABA function to increase but also the receptor to adapt making them 'receptor' to the anxiolytic
44
what are the first line anxiolytics
SSRIs (selective serotonin reuptake inhibitors) SNRIs TCAs Monoamine oxidase inhivitors 5-T receptor agonist ( anxiety not depression)
45
inital risk of SSRI's
increases anxiety agitiation sleeping problems
46
mechanism of serotoin action
5-HT released from presynaptic neurone and activates excitatory or inhibitory 5-HT recepors on postsynaptic neurone autoreceptors on presynpatic neurone will turn off the further release 5HT it is taken up by 5HT transporter and metabolised by monoamine oxidase
47
what drugs inhibit the 5HT transporter
SSRIs, TCAs and SNRIs | this means 5HT remains in the synpatic cleft longer to actvate 5HT receptors
48
what do monoamine oxidase inhibitors do
inhibit monoamine oxidase from metabolising 5HT therefore more 5HT neurotransmission
49
how does buspirone work
as a 5HT receptor agonist ( so basically binds to the 5HT receptor since there's too little 5HT to bind to it )
50
what do Z-hypnotics do
they bind to GABA receptors like benzodiazepines but they are more selective for the GABA 1 receptor unlike benzos this causes sedation (helping with insomnia) and may also help with anxiety
51
how long do Z-hypnotics act
very fast onset and short duration of action
52
side effects of Z-hypnotics
tolerance and depndence
53
what do antihistamines do
- antagonise H1 receptors in the cortex inhibiting the histaine arousal pathway - can use for sedation
54
what are the side effects to antihistamine use
- weight gain | - antichlinergic effects
55
what does melatonin do
- released at night and acts on melatonin receptors to inhibit the suprachiasmatic nucelues hence allowing the VLPO to release GABA and cause sedation
56
what is the only licenced melatonin drug for over 55yr olds in the UK
circadin
57
what is the theoretical mechanism underlying the inital increase in anxiety with SSRI administration
- inhibits 5HT transporter - causing increasing 5HT levels in synpatic cleft - that is associated with increased 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 (51 decks)

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