Anxiety Flashcards

1
Q

When is anxiety pathological?

A

When there is a bias to interpret non-threatening situations as life threatening.
Concern about stressor is out of proportion to the realistic threat and can occur without exposure to an external stressor

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2
Q

Core elements of anxiety disorders

A

Negative cognition
Physiological symptoms - autonomic activation
Defence/Avoidance behaviours

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3
Q

Negative cognition

A

Bias to interpret unthreatening situations are threatening
Context/memory/reinforcement

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4
Q

Physiological symptoms of anxiety

A

Racing heart/palpitations
Restlessness
Sweating
Increased blood pressure
etc

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5
Q

Defence/Avoidance behaviours

A

Activation of aminergic pathways

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6
Q

Neuroanatomy involved in anxiety

A

Cortex
Hippocampus
Amygdala
Hypothalamus
Basal ganglia/cerebellum

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7
Q

Cortex and anxiety

A

Negative cognition

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8
Q

Hippocampus and anxiety

A

Memory and context
Uses input from prefrontal cortex

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9
Q

Amygdala and anxiety

A

Fear perception
Thalamus relays sensory information to prefrontal cortex and amygdala

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10
Q

Hypothalamus and anxiety

A

Stress responsiveness
Maintained through release of ACTH and cortisol
Responds to sensory amygdala and hippocampal outputs to adjust output

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11
Q

Basal ganglia/cerebellum and anxiety

A

Movement control

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12
Q

5HT pathways in anxiety

A

Hypothalamus –> Temporal lobe –> Raphe nuclei
Neocortex –> Basal ganglia –> thalamus –> cerebellum
If these are affected, mood and wellbeing may be depressed

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13
Q

Noradrenaline pathways in anxiety

A

Hypothalamus –> temporal lobe –> locus coeruleus
Neocortex –> thalamus –> cerebellum
These can increase alertness and attention - hypervigilance

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14
Q

GABA and anxiety

A

Reduced expression of GABAA-receptors
Reduced function/regulation of GABAA-receptors by benzodiazepines
Reduced function/regulation of GABAA-receptors by neurosteroids

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15
Q

Pharmacotherapy for anxiety

A

b-blockers: target autonomic symptoms
Benzodiazepines
Antidepressants: SSRIs
Buspirone: partial agonist at 5HT 1A receptors

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16
Q

β-adrenoreceptor blockers

A

Treat the symptoms of anxiety
Reduce the sympathetic manifestations of the stress/fear responses
Treatment, not cure
Effects on memory consolidation

17
Q

Antidepressants for anxiety

A

SSRIs - fluoxetine, citalopram
Combined NA and 5HT uptake blockers - venflaxanine, duloxetine
SSRIs now preferred choice for GAD, panic disorders and PTSD
SSRIs have a delayed clinical response (3-4 weeks)

18
Q

Main treatment for anxiety

A

Benzodiazepines

19
Q

Structure of benzodiazepines

A

Benzene ring fused to a seven membered diazepine ring.

20
Q

Method of Action of Benzodiazepines

A

Binds with specific modulatory site on GABA A receptor
Enhances GABA activity
Opening of Cl- channels
Hyperpolarisation of cells
Depression of CNS

21
Q

R side groups influence the _ of benzodiazepines

A

Affinity of the BZ to bind the GABA receptor
Intrinsic efficacy of BZ to produce a functional effect

22
Q

BZ inverse agonists

A

Bind to the BZ site but produce the opposite effect.
Said to have negative intrinsic efficacy

23
Q

BZ antagonists

A

Bind to the BZ site but are unable to activate the receptor
Intrinsic efficacy = 0

24
Q

Intrinsic efficacy of BZ agonists

A

100%

25
Q

Benzodiazepine is a CNS _

A

Depressant

26
Q

Effects of Benzodiazepines on the CNS

A

Anxiolytic
Sedation and induction of sleep
Muscle relaxation
Anticonvulsant
Anterograde amnesia
Decrease dose of anaesthetic

27
Q

Effect of Benzodiazepines on PNS

A

Neuromuscular blockade (paralysis) in high doses
Coronary vasodilation at lower doses

28
Q

Adverse effects of normal dose of benzodiazepines

A

Dry mouth, Light headache, Confusion, Ataxia, Impair driving skill

29
Q

Adverse effects of acute overdose of benzodiazepine

A

Prolonged sleep

30
Q

Other adverse effects of benzodiazepines

A

Tolerance and dependency
Decrease libido
Abuse potential

31
Q

Benzodiazepines as hypnotics

A

Can be used, but there are problems with tolerance and dependence
Rebound insomnia also a concern