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PBL SEM 3 > 5 - generalised anxiety disorder > Flashcards

5 - generalised anxiety disorder Flashcards

1
Q

what does the Yerkes-Dodson Law describe?

A

how anxiety affects performance

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2
Q

when is anxiety abnormal?

A
  • excessively intense/disproportionate to the stimulus
  • triggered by harmless situations, or occurs without a cause
  • continues beyond exposure to danger
  • cant be controlled
  • causes severe distress
  • impairs functioning
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3
Q

what is GAD diagnosied in current systems (DSM5, ICD 11)?

A
  • a person must experience (a) a certain number of symptoms for (b) at least a minimum specific period
  • the symptoms must cause : significant stress, be associated with impairment in everyday function

—> persistent fear and worry plus at least 3 of:
- poor concentration
- restlessness
- fatigue
- muscle tension
- initial (ie difficulty getting to sleep) insomnia

—> symptoms for >6 months

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4
Q

what must be excluded when diagnosing GAD?

A
  • alcohol or street drug misuse
  • hyperthyroidism
  • phaeochromocytoma = benign tumour of the adrenal glands
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5
Q

what are psychological symtpoms of GAD?

A
  • constant worries, intrusive thoughts
  • feeling of apprehension and dread
  • poor concentration
  • if severe — depersonalisation, derealisation
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6
Q

what are physical symptoms of GAD?

A
  • tremor, sweatiness, “butterflies”, dry mouth, palpitations
  • muscular tension, tension headache
  • hyperventilation — difficulty taking a breath, “atypical chest pain”(doesnt radiate, not crushing, often on LHS), parasthesiae in hands, feet and lips (resp alkalosis)
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7
Q

what are some behavioural symptoms of GAD?

A
  • putting things off because of anxiety
  • avoidance of particular situations
  • “self-medication” — misuse of drugs or alcohol to relieve anxiety
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8
Q

who is GAD more common in?

A
  • more common in women (lifetime prevalence women:men = 5.3% : 2.8%)
  • onset commonly in young adult life (median age of onset = 30 years)
  • often not recognised partly because patients often present with physical symptoms
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9
Q

a first degree family history of GAD increases the risk how much?

A

x 2.5

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10
Q

what molecular genetics are associated with GAD?

A
  • several risk genes eg. chromosome 2p21, 2q12
  • eg. serotonin transporter gene
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11
Q

what do functional MR imaging studies show in people with GAD?

A

overactive amygdala (= in temporal lobe, important in fear and anxiety)

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12
Q

what is the main inhibitory neurotransmitter in the mammalian CNS, present in 1/3 synapses?

A

GABA = y-Aminobutyric acid

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13
Q

how is GABA synthesised?

A

decarboxylation of the amino acid glutamic acid

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14
Q

what does GABA play a major role in?

A

regulating neuronal excitability and muscle tone

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15
Q

GABA is the endogenous agonist at what 2 main receptors?

A
  • GABAA receptor - in brain (has multiple ligand binding sites_
  • GABAB receptor - in peripheral nervous system
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16
Q

what is a GABA analogue which acts as a selective agonist at GABAB receptors, used clinically as a muscle relaxant?

A

baclofen

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17
Q

describe the GABAA receptor

A
  • a transmembrane, ligand-gated ion channel receptor
  • 5 subunits arranged around a central chloride channel
  • 5 distinct types of subunit have been cloned to date = alpha, beta, gamma, delta, ro (p)
18
Q

where does GABA bind to on the GABAA receptor? effect?

A

to a binding pocket between the a and b subunits — causes Cl- ions to flow into the neuron, leading to a decreased chance of an AP (hyperpolarisation)

19
Q

what is the commonest mammalian structure of the GABAA receptor?

A

(a1)2(B2)2(y2)

20
Q

describe the clinical assessment in GAD

A
  • full psychiatric Hx from patient
  • collateral history
  • exclude physical causes or complicating factors (eg. hyperthyroidism, angina, asthma, excess caffeine intake)
  • check whether using alcohol and/or drugs to self-medicate (anxiety also may be part of a withdrawal state, “rebound anxiety” can be part of a hangover)
  • assess for underlying depression. assess life events
21
Q

what are the main treatment modalities for GAD?

A
  • psychological therapy
  • medication
  • if GAD not severe enough a doctor may suggest simple lifestyle changes before adopting ‘formal’ treatment using drugs or therapy eg. exercise, work/life balance, avoid excess caffeine and other stimulant drugs, avoid excess alcohol
22
Q

describe the NICE guidelines stepped care approach 1

A

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

  • psychological therapy eg. CBT
  • pharmacological therapy — an SSRI licensed for GAD
  • self-help (online education)
  • shared-decision making
23
Q

what should not be used for > 2 weeks?

A

benzodiazepines

24
Q

describe 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 (thorough reassessment)

25
Q

what psychological treatments are available for GAD?

A
26
Q

what are the core elements of CBT?

A
  • it identifies unhelpful patterns of thinking (such as catastrophisation) 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 most effective whe there are specific environmental triggers eg crowded places : “graded exposure”
27
Q

NICE recommends how much CBT?

A

12 to 15 one-hour long sessions of CBT over 4 months

28
Q

what % of people who have GAD respond to CBT?

A

60%

29
Q

psychological vs pharmacological treatment

A
30
Q

pharmacological management

A
  • SSRIs = first line
  • tricyclic antidepressants
  • other antidepressants eg. mirtazapine
  • pregabalin
  • benzodiazepines eg. diazepam
31
Q

how do benzodiazepines work?

A

bind at a separate site between the a and y subunits on GABAAR — this potentiates the action of GABA and increases Cl- influx

ie. it is a positive allosteric modulator (POM) at the GABAA receptor

32
Q

how do SSRIs work?

A
  • block serotonin reuptake from synapse — increase 5-HT in synaptic clefts
  • first line pharmacological treatment
33
Q

name some SSRIs shown to be effective in GAD

A
  • sertraline
  • escitalopram
  • paroxetine
34
Q

SSRIs vs older drugs such as tricyclic antidepressants

A
  • fewer side effects
  • safer in overdose
35
Q

what do you tell a patient before they start SSRIs?

A
  • may take 1-2 weeks to start working (unlike BDZ which start in ab 20 mins)
  • not addictive
  • effective in 70% of cases. continue for at least 6 moths if effective
  • side effects include: GI disturbance (nausea, diarrhoea) (most common - usually transient) , sexual dysfunction, dizziness, dry mouth, loss of appetite, sweating, feeling agitated, insomnia)
  • mild withdrawal effects occasionally, tail off
36
Q

name some dual acting antidepressants that are effective in GAD and what they do

A
  • mirtazapine — blocks presynaptic alpha-2 autoreceptors
  • duloxetine (SNRI)
  • venlafaxine (SNRI)
  • imipramine (tricyclic)
  • side effects differ to SSRIs
    (SNRI = serotonin, NA reuptake inhibitors)
37
Q

describe pregabalin

A
  • 3rd line drug
  • anticonvulsant used in epilepsy and neuropathic pain
  • now licensed to treat GAD
  • structurally similar to GAD
  • binds to a2d subunit of the Ca++ channel, decreasing neurotransmitter release inc Glu, NA, and substance P
38
Q

what do benzodiazepines differ mainly in?

A

their half life eg. diazepam (valium) 30 hrs vs triazolam 2 hrs

39
Q

symptoms of anxiety reduce within how long of taking a benzodiazepine?

A

30 to 60 mins

40
Q

what are some side effects of benzodiazepines

A
41
Q

describe beta blockers

A
  • antagonists at adrenergic B receptors in heart muscle, smooth muscle, and other tissues of the SNS
  • effective in treating physical but not psychological symptoms of anxiety —> tremor, palpitations
  • contraindicated in asthma

PBL SEM 3 (49 decks)

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