Case 5 - Anxiety lecture Flashcards

1
Q

what is the Yerkes-dodson law

A

how anxiety affects performance

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2
Q

when does anxiety become abnormal

A

excessively intense / disproportionate to the stimulus
Triggered by harmless situations, or occurs without a cause
Continues beyond exposure to danger
Can’t be controlled
Causes severe distress
Impairs functioning

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3
Q

what is the operational diagnosis

A

to meet a psychiatric diagnosis in current systems (DSM5, ICD11)
- a person must experience (a) a certain number of symptoms for (b) at least a minimum specified period of time

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4
Q

what must the symptoms cause

A
  • significant stress
  • be associated with impairment of everyday function
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5
Q

what is classification for GAD

A
  • persistent fear and worry
  • plus at least three of:
    poor concentration
    restlessness
    fatigue
    muscle tension
    initial (start of sleep) insomnia
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6
Q

how long must you have had these symptoms for

A

more than 6 months

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7
Q

what do u exclude while diagnosing

A

alcohol or street drug missuse
hyperthyroidism
pheochromocytoma

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8
Q

what is pheochromocytoma

A

benign tumour on the puituatiry gland

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9
Q

what is the median onset age

A

30

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10
Q

what are the molecular genetic aetiology

A

GWAS: several risk genes egg chromosome 2p21, 2q12

candidate gene studies e.g serotonin transporter gene

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11
Q

what is GABA

A

the main inhibitory neurotransmitter in the CNS

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12
Q

what is GABA synthesised by

A

decarboxylation of the amino acid glutamic acid

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13
Q

what is GABA’s major roles

A

regulating neuronal excitability and muscle tone

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14
Q

what are the GABA receptor

A

GABAa - multiple ligand binding sites
GABAb - baclofen is a GABA analogue which acts as a selective agonist for GABAb receptors. used clinically as a muscle relaxant

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15
Q

features of the GABAa receptor

A
  • transmembrane ligand gates ion channel receptor
  • 5 subunits arranged around a central chloride channel
  • 5 distinct types of subunit have been cloned to date; alpha, beta, gamma, sigma and p
  • GABA binds to the binding pocket between the alpha and beta subunits. this causes CL- ions to flow into the neurone leading to decrease chance of action potential
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16
Q

what is the NICE guidance stepped care approach 1

A

Step 1: recognition and diagnosis of GAD
Step 2: offer treatment in primary care

interventions with positive evidence base:
Psychological therapy (CBT)
Pharmacological therapy - SSRI or benzodiazepines
Self help (online self education)
shared decision making

17
Q

what is the NICE guidance stepped care approach 2

A

Step 3: non-response: review and offer alternative treatment

Step 4: review and offer referral to secondary care
if 2 interventions have been provided and the person still has significant symptoms, then referral to specialist mental health services should be offered

Step 5: care in specialist mental health services
through reassessment

18
Q

what are the core elements of CBT

A
  • identifies unhelpful patterns of things and how these cause feelings of anxiety
  • aims to replace these unhelpful beliefs with more realistic and balanced ones. it mainly focuses on current problems rather than events from the past
  • ## the B part is most effective when there are specific environmental triggers
19
Q

how many sessions of CBT does NICE recommend

A

12 to 15 one hour long sessions over 4 months

20
Q

what is first line treatment for anxiety

A

SSRI’s

21
Q

benzodiazepines mode of action

A

bind at a separate site between the alpha and gamma units

this potentiates the action od GABA and increase CL- influx

diazepam is a positive allosteric modulator at the GABAa receptor

22
Q

how do SSRI’s work

A

block serotonin re uptake from the synapse

23
Q

what are the other antidepressants used in GAD

A

Mirtazapine (blocks pre synaptic alpha-2 auto receptors)
Duloxetine (SNRI)
Venlafaxine (SNRI)
Imipramine (tricyclic)
side effects differ to SSRIs

24
Q

what is the action of pregabalin

A

precise action unknown: molecule is structurally similar to GABA. it can bind to the alpha2delta subunit of the calcium channel, decreasing the release of neurotransmitters including glutamate, noradrenaline and substance P

25
Q

how do benzodiazepines differ

A

mainly in their half life
- diazepam (valium) 30 hours vs triazolam 2 hours

26
Q

where do benzos act

A

at the GABAa receptor