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NSB > Anxiety and Stress Treatment > Flashcards

Anxiety and Stress Treatment Flashcards

1
Q

What is the amygdala and functions?

A
  • series of nuclei
  • involved in integrating the fear
    response
  • limbic system
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2
Q

What happens when an amygdala is removed from the brain?

A
  • loss of phobia of spiders
  • loss of fear/inhibitions
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3
Q

Key Inputs to the Amygdala:

A
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4
Q

What is the role of the hippocampus in the regulation of anxiety?

A

by relating fearful memories to the current context

if abnormal function may generate fear in response to non-threatening stimuli

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5
Q

Key Neurobiological Stress Responses:

A
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6
Q

Activation of HPA Axis in Fear:

A
  • amygdala activates the
    hypothalamus
  • hypothalamus releases
    corticotrophin releasing hormone,
    (CRH) which acts on the pituitary
    gland
  • pituitary releases
    adrenocorticotropic hormone
    (ACTH) which acts upon adrenal
    glands
  • adrenal cortex releases cortisol
  • cortisol is a glucocorticosteroid
    which will ultimately release
    glucose into the bloodstream in
    response to the fear
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7
Q

HPA Axis:

A
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8
Q

Regulation of the HPA Axis:

A

negative feedback loop

cortisol directly feedback to hypothalamus and pituitary

cortisol acts on the hypothalamus also feedback to control cortisol levels

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9
Q

Activation of the Locus Coeruleus:

A
  • amygdala activates locus coeruleus
  • locus ceoruleus activation releases
    noradrenaline
  • fight or flight response
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10
Q

Noradrenaline Pathways:

A
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11
Q

Amygdala and hippocampus respond to which neurotransmitter systems (3):

A
  • noradrenergic
  • serotonergic
  • GABA
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12
Q

Noradrenergic Systems that affect that Hippocampus and Amygdala:

  • origin
  • effect
A
  • originate in locus coeruleus
  • increase arousal and anxiety
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13
Q

Serotonergic (5-HT) Systems that affect the Hippocampus and Amygdala:

  • origin
  • effect
A
  • raphe nuclei
  • signals presence of threat
  • restrain associated behaviours
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14
Q

GABA System that affects the Hippocampus and Amygdala:

  • origin
  • effect
A
  • distributed widely through the
    brain
  • reduce anxiety
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15
Q

Noradrenaline involvement in Anxiety:

A
  • increased noradrenaline in
    prefrontal cortex found in anxiety
    and PTSD
  • impaired cognitive function
  • some adrenergic receptor
    antagonists improve stress induced
    cognitive impairment
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16
Q

Serotonin and Anxiety:

A
  • arise from raphe nuclei
  • drugs increasing serotonin levels
    effective in treating both anxiety
    and depression (SSRIs)
17
Q

Serotonin and Anxiety:

A
18
Q

Why SSRIs help with balancing pathways?

A
  • noradrenaline increased in stress
  • serotonin decreased in stress
  • SSRIs increase serotonin in
    synapses, hence push the shifted
    balance back to normal
19
Q

Some antidepressant that are effective in depression and anxiety increase reuptake both serotonin and noradrenaline.

Why do they not make people with depression more anxious?

A
  • actions of SSRIs and SNRIs are
    complex; delayed onset of action
    suggests neuroadaptive changes
    eg complicates
  • baseline activity vs reactivity of
    noradrenergic systems
  • complex array of adrenoreceptors
    and actions of these receptors
20
Q

GABA and Anxiety:

A
  • drugs increasing GABA activity
    decrease anxiety
  • partial agonist: alcohol
  • indirect agonist: barbiturates,
    benzodiazepines
  • drugs decreasing GABA activity
    increase anxiety
  • antagonist: flumazenil
  • could anxiety be associated with
    fewer GABA (A) receptors
  • endogenous neuromodulator
    blocking benzo site at GABA (A)
    receptor
21
Q

GABA and Panic:

A
  • patients with panic disorder have
    fewer benzopdiazepine binding
    sites
  • indicates a lack of sufficient
    inhibitory control via GABA in
    cortical and limbic regions to
    suppress inappropriate fear
    response and then panic attack
22
Q

Functional Neuroanatomical Changes in Anxiety:

A
  • amygdala: reduced volume,
    hyperactivity
  • hyperactivity of thalamus
  • overactivity of insular cortex in
    response to threat
  • reduced volumes in anterior
    cingulate cortex and prefrontal
    cortex: areas important for
    conscious threat appraisal and loss
    of frontal-limbic regulation
    processes
  • hippocampal changes
23
Q

Chronic Stress and the Hippocampus:

A
  • chronic activation by cortisol
    • increases Ca2+ into neurons
    • excitotoxicity results in cell
      death
  • damage to the hippocampus
    means it cant feedback to limit
    cortisol production
  • some anxiety disorders may result
    from:
    - diminished activity of the
    hippocampus
    - loss of feedback to amygdala
    - inappropriate fear response

**reduced hippocampal volume in PTSD and in chronic stress in animals

Microscopically: fewer large pyramidal cells

24
Q

Neurobiology of PTSD:

A
25
Q

Neuroanatomy of PTSD:

A
26
Q

Neurobiology of Phobia:

A
  • hyperactivity of amygdala on
    presentation of feared stimulus:
    decreases with successful
    treatment
  • anticipation of phobic stimulus:
    activates the anterior cingulate
    cortex
  • failure to activate cortical regions
    that regulate limbic system:
    ventromedial prefrontal cortex
27
Q

Neurobiology of OCD:

A
  • associated with conditions
    affecting basal ganglia: Tourette’
    syndrome, encephalitis lethargica,
    sydenhams chorea
  • functional changes in neural
    networks:
    • cortico-striatal-thalamo-cortical:
      involves dopaminergic pathways
    • hyperactivity in head of caudate
      nucleus, which can be reduced
      by SSRIs and psychological
      therapy
28
Q

Anxiety: Management: General Principles:

A
29
Q

CBT:

A
  • strong evidence across range os
    psych disorders
  • involves talking about thoughts,
    feelings and behaviour
  • focus is on maladaptive thinking
    and behaviour
30
Q

Anxiety Disorders: Phrmacotherapy:

A
  • antidepressants: SSRIs; 6 months
    for full effect
  • benzodiazepines: short term, avoid
    when possible, high risk of
    dependance, tolerance

not prescribed in primary care:

  • buspirone: acts on 5-HT receptors,
    not first line
  • pregablin: anticonvulsant,
    controlled drug
  • combinations of antidepressants
    or augmentation with other
    medications; evidence less solid
31
Q

GAD Diagnosis Timeline and Effect on Symptoms:

A
  • only diagnosed at symptoms have
    been present for 6 months
  • symptoms are already chronic at
    the time of diagnosis
32
Q

Panic disorder: Management:

A
  • relies on general principle of
    anxiety disorder management
  • psychoeducation re
    hyperventilation
  • CBT will focus on cognition and
    behaviours related to panic attacks
33
Q

Specific phobia: Management:

A
  • CBT based on graded exposure
  • benzo short term used for
    situational anxiety, till CBT
34
Q

Social Anxiety Disorder: Management:

A
  • ideally specialist CBT
  • Some evidence for weekly
    psychodynamic psychotherapy (6
    months)
  • SSRIs may be effective
35
Q

OCD: Management:

A
  • CBT focused on obsessions and
    compulsions
  • medication: SSRI, clomipramine
    (tricyclic antidepressant) (not first
    line)
  • no response to treatment -> mdt
    review of all biopsychosocial
    interventions -> consider
    antipsychotic medication
36
Q

PTSD: Management:

A
  • general support if symptoms last
    <4 weeks and not severe
  • consider screening for PTSD 4
    weeks after major disorder
  • First line: specialist psychological
    therapy: CBT, EMDR (eye
    movement densitisation therapy)
  • Second Line: antidepressants
  • Specialist: combinations of
    medication including an
    antipsychotic

NSB (50 decks)

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