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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
Q

what effect does the pineal gland have on the SCN

A
  • 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
Q

what risk factor increases chances of insomnia

A

increased age

female

27
Q

common side effecs with chronic use of hypnotics and anxiolytics

A

tolerance

dependence

28
Q

what is an example of benzodiazepine

A

diazepam

29
Q

therapeutic uses of anxiolytics

A
  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
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 alchol
  6. decreased rapid eye movement
31
Q

side effects associated with chronic use of anxiolytics

A

tolerance
dependence
withdrawel symtpoms

32
Q

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

A

conscious sedative, status epilepticus

33
Q

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

A

hypnotics

34
Q

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

A

anxiolytic/ panic disorders

35
Q

long half-life anxiolytics are used for what e.g. lorazepam, diazepam, chloradiazepoxide

A

anxiolyic, acute alcohol withdrawel, panic disorder, anticonvulsants, status epilepticus, muscle spams

36
Q

why do some anxiolytics have a longer half-life

A

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

37
Q

how do barbituates work

A

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
Q

how do alcohol and benzodiazepines work

A

work to increase the effects of GABA which inhibit the arousal pathway

39
Q

why are anxiolytics non-selective

A

because there are different GABA receptor subtypes in the brain so you dampen other activities in the brain

40
Q

what are alpha 1 subunits associated with

A

sedation

41
Q

what are alpha 3 subunits associated with

A

anxiolysis

42
Q

what are alpha 5 subunits associated with

A

learning and memory

43
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 ‘receptor’ to the anxiolytic

44
Q

what are the first line anxiolytics

A

SSRIs (selective serotonin reuptake inhibitors)
SNRIs
TCAs
Monoamine oxidase inhivitors
5-T receptor agonist ( anxiety not depression)

45
Q

inital risk of SSRI’s

A

increases anxiety
agitiation
sleeping problems

46
Q

mechanism of serotoin action

A

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
Q

what drugs inhibit the 5HT transporter

A

SSRIs, TCAs and SNRIs

this means 5HT remains in the synpatic cleft longer to actvate 5HT receptors

48
Q

what do monoamine oxidase inhibitors do

A

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

49
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 )

50
Q

what do Z-hypnotics do

A

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
Q

how long do Z-hypnotics act

A

very fast onset and short duration of action

52
Q

side effects of Z-hypnotics

A

tolerance and depndence

53
Q

what do antihistamines do

A
  • antagonise H1 receptors in the cortex inhibiting the histaine arousal pathway
  • can use for sedation
54
Q

what are the side effects to antihistamine use

A
  • weight gain

- antichlinergic effects

55
Q

what does melatonin do

A
  • released at night and acts on melatonin receptors to inhibit the suprachiasmatic nucelues hence allowing the VLPO to release GABA and cause sedation
56
Q

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

A

circadin

57
Q

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

A
  • 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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