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Brain and Behaviour Year 2 > Anxiety > Flashcards

Anxiety Flashcards

1
Q

name some of the clinical uses of hypnotics and anxiolytics

A
  • Relief of anxiety states
  • Induction of sleep (relief of insomnia)
  • Sedation and amnesia before medical procedures
  • Control of withdrawal states in addiction such as delirium tremens
  • Muscle relaxation
  • Severe behaviour disturbance
  • Benzodiazepines ca also be used for the treatment of epilepsy
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2
Q

what controls the sleep wake cycle (circadian rhythm)

A
  • SCN = suprachiasmatic nucleus in the hypothalamus

- The SCN controls 24 hour circadian rhythm

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3
Q

what happens to the SCN in the light phase of the sleep wake cycle

A

the SCN has increased activity in the light phase and decreased activity in the dark phase

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4
Q

what happens to melatonin in the dark phase of the sleep wake cycle

A

there is an increase in melatonin in the dark phase and decrease in the light phase

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5
Q

what are the neurone projections that cause wakefulness

A

o Cholinergic Systems:
 Pedunculopontine (acetylcholine)
 Laterodorsal tegmental nuclei (acetylcholine).

o Monoaminergic Projections:
 Locus Coeruleus (noradrenaline)
 Raphe nuclei (serotonin)
 Tuberomamillary nucleus (histamine).

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6
Q

what are the neurones that promote sleep

A

o GABA and Galanin Neurons

 Ventrolateral preoptic nucleus.

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7
Q

what are the neurotransmitters that maintain wakefulness

A
  • noradrenaline,
  • dopamine
  • histamine
  • acetylcholine
  • orexin.
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8
Q

what are the neurotransmitters that promote sleep

A
  • GABA
  • Galanin
  • melatonin
  • adenosine (caffeine is an adenosine blocker).
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9
Q

what can block adenosine

A

caffeine

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10
Q

what controls nocturnal/diurnal rhythms

A

superchiasmatic nucleus of the hypothalamus

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11
Q

How long does each sleep cycle last

A

90 minutes

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12
Q

what are the different types of sleep

A
  • REM = rapid eye movement phase
  • NREM = no rapid eye movement phase
  • SWS – slow wave deep sleep (NREM-3 and NREM-4)
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13
Q

what two sleep phases make up slow wave sleep

A

– slow wave deep sleep (NREM-3 and NREM-4)

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14
Q

what phase of sleep is lose to waking us up

A
  • REM phase sleep is close to waking up

- as we get closer to the morning we have more dreams and sleep more lightly

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15
Q

what waves are used in normal wakefulness

A

beta waves (13-30hz)

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16
Q

what waves are used when you are awake and relaxed

A

alpha waves (8-12hz)

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17
Q 
name the waves used in 
- stage 1 
- stage 2 
- stage 3
- stage 4
of sleep
A
  • stage 1 = theta waves (35-75hz)
  • stage 2 = theta waves with sleep spindles and K complex
  • stage 3 = delta waves (less than 35hz) less than 50%
  • stage 4= delta waves (less than 35hz) more than 50%
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18
Q

what does hz mean

A

this is the number of waves per second

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19
Q

what happens during sleep to memory

A
  • The brain is active and sleep may consolidate memories through gene expression changes
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20
Q

what are the types of insomnia

A
  • Transient (e.g. jet lag)
  • Short-Term (associated with illness/bereavement stress)
  • Chronic (lasts longer than 3 weeks).
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21
Q

what can be the cause of a sleep disorder

A
  • can be trivial e.g. due to stress or it can be due to something more serious such as a psychiatric disorder or early stage of neurodegeneration
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22
Q

what is currently used to treat insomnia

A

Benzodiazepines (short acting) and Z drugs are used to treat insomnia

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23
Q

what is used for short term use in insomnia

A

lorazepam

temazepam

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24
Q

what do benzodiazepines end in

A

pam

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25
Q

what drugs are used long term in insomnia treatment

A
  • Eszopiclone (z-drugs)

* Zolpidem (extended release).

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26
Q

what are the targets of Z drugs

A

alpha subunits
• Alpha-1: hypnotic role
o Zaleplon/zolpidem.

• Alpha-2 subunits: anxiolytic effects

27
Q

what are the side effects that benzodiazepines can give you

A
  • Change in sleep patterns (suppress deep sleep and REM sleep)
  • Daytime sedation
  • Rebound insomnia – start becoming tolerant and need them all the time to induce sleep and if you stop then you wont be able to sleep, can lead to hyperanxiety
  • Tolerance
  • Dependence (withdrawal syndrome characterised by anxiety, nausea, muscle cramps, seizures)
28
Q

what is the withdrawal symptoms of benzodiazepines characterised by

A

withdrawal syndrome characterised by anxiety, nausea, muscle cramps, seizures

29
Q

what has been recently used for insomnia and why

A
  • pregabalin
    positive effects;
  • no disruption of sleep architecture
  • no tolerance
30
Q

what can pregabalin also be used as

A

anxiolytic

31
Q

what can excessive use of hypnotics such as benzodiazepines and Z drugs lead to

A
  • creates a spiral of dependence
32
Q

how can you avoid the spiral of dependence

A
  • avoid prolonged prescription of hypnotics

- non pharmacological intervention for the control of chronic insomnia such as CBT

33
Q

where is orexin produced

A
  • it is a peptide that is produced in the hypothalamus
34
Q

what are the two forms of orexin

A

• Two forms: orexin A and orexin B (also known as hypocretin 1 and hypocretin 2)

35
Q

what receptors does orexin bind to

A

• orexin OX1 and OX2 receptors

36
Q

what does orexin do

A

• Regulates arousal, appetite, wakefulness

37
Q

what results if you have a deficiency in orexin

A

narcolepsy

38
Q

what is narcolepsy

A

this is a condition characterised by excessive sleepiness, increased frequency of falling alsleep in daytime

39
Q

what does an orexin antagonist do

A

decrease wakefulness

- therefore it can be used in the treatment of insomnia

40
Q

name an orexin antagonist

A

Suvroextant - this is an orexin receptor antagonist that an be used for insomnia treatment

41
Q

what does suvroextant result in

A

o Morning sedation
o Sleep paralysis
o Decreased amnesia
o Decreased confusion

42
Q

name some anxiety disorders

A
  • Panic disorder
  • Agoraphobia – fear of open spaces
  • Social phobia (social anxiety disorder) – e.g. fear of speaking in public
  • Simple phobia
  • Obsessive compulsive disorder
  • Post-traumatic stress disorder
  • Generalized anxiety disorder
43
Q

are anxiety disorders more common in males or females

A

females

44
Q

what are the structures and neurotransmitters that are involved in anxiety disorders

A
  • Limbic structures: amygdala, insula, anterior cingulate, prefrontal cortex, thalamus.
  • abnormalities of the HPA axis.
  • Monoaminergic systems.
  • GABAergic systems.
45
Q

is the amygdala hypoactive ir hyperactive in anxiety disorder

A
  • hyperactive and part of the anxiety disorder results from the inability of higher cortical structures to control this hyperactivity
46
Q

describe what each part of the amygdala results in which symptom of fear and panic

  • lateral hypothalamus
  • dorsal vagus nerve
  • parabrachial nerve
  • basal forebrain
  • reticules ponis caudales
  • central grey area
  • paraventricular nucleus
A
  • lateral hypothalamus - hear rate and blood pressure
  • dorsal vagus nerve - bradycardia and ulcers
  • parabrachial nerve - panting and respiratory distress
  • basal forebrain - aroual, vigilance and attention
  • reticules ponis caudales- increase startle response
  • central grey area - freezings and social interaction
  • paraventricular nucleus - corticosteroid release
47
Q

what genes are linked to anxiety

A
  • Catechol-O-methyl transferase (COMT)
  • Cholecystokinin (CCK)
  • CCKB receptor
  • Adenosine A2 receptor
  • Monoamine oxidase A (MAOA)
  • 5-HT2 receptor
48
Q

what are the types of anxiolytics used to treat anxiety

A
  • Benzodiazepines
  • 5-HT1A agonists
  • SSRIs
  • SNRIs
  • β-adrenoceptor antagonists
  • Barbiturates
49
Q

name examples of benzodiazepines

A
  • Clonazepam
  • Alprazolam
  • Lorazepam
  • Diazepam
50
Q

name examples of 5HT1A agonist

A
  • buspirone

- ipsapirone

51
Q

name examples of SSRIs

A
  • Fluoxetine
  • Escitalopram
  • Paroxetine
52
Q

name examples of SNRIs

A
  • Venlafaxine

* Duloxetine

53
Q

Name an example of a beta adrenoreceptor antagonists

A

• Propranolol.

54
Q

what are there risks of using barbiturates

A

• Major risk of drug dependence
• Development of tolerance
• Induction of liver microsomal enzymes (risk of drug interactions).
• Fatal toxicity in overdose (respiratory depression).
• Withdrawal symptoms: agitation, insomnia, depression, tension.
- Accumulation causes drowsiness, disorientation, ataxia, slurred speech

55
Q

What are the withdrawal symptoms of barbiturates

A

: agitation, insomnia, depression, tension.

56
Q

What does the GABAa receptor do

A

 Expressed post-synaptically, lead to fast inhibitory transmission (hyperpolarization) through influx of Cl-
- therefore this stops the transmission of electrical activity in the cerebral cortex

57
Q

what part of the GABAa receptor does benzodipaeine binds to

A

alpha1 gamma 2 part of the channel

58
Q

describe what benzodiazepines do to the GABA channel versus barbiturates

A

benzodiazepines increase frequency of opening whereas barbiturates increase the duration of opening

59
Q

wha does diazepam do the GABAa channel

A

g. Diazepam potentiates GABA-induced hyperpolarization.

60
Q

What is Flumazenil

A
  • Flumazenil acts as an antagonist at the benzodiazepine binding sites but has a short half-life
61
Q

name an antagonist of the benzodiazepine binding site

A

flumazenil

62
Q

what is the treatment of generalised anxiety disorder

A
  • buspirone
  • venlafaxine, duloxetine (SNRI)
  • fluoxetine, escitalopram (SSRI)
  • risperidone, quetiapine, olanzapine (APD)
63
Q

what are complications of benzodiazepine use in the elderly

A
  • Psychomotor impairment
  • Risk of falls
  • Daytime drowsiness
  • Intoxication
  • Amnesia
  • Depression
  • Respiratory problems
  • Abuse and dependence

Brain and Behaviour Year 2 (36 decks)

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