5 - generalised anxiety disorder Flashcards
what does the Yerkes-Dodson Law describe?
how anxiety affects performance
when is anxiety abnormal?
- 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
what is GAD diagnosied in current systems (DSM5, ICD 11)?
- 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
what must be excluded when diagnosing GAD?
- alcohol or street drug misuse
- hyperthyroidism
- phaeochromocytoma = benign tumour of the adrenal glands
what are psychological symtpoms of GAD?
- constant worries, intrusive thoughts
- feeling of apprehension and dread
- poor concentration
- if severe — depersonalisation, derealisation
what are physical symptoms of GAD?
- 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)
what are some behavioural symptoms of GAD?
- putting things off because of anxiety
- avoidance of particular situations
- “self-medication” — misuse of drugs or alcohol to relieve anxiety
who is GAD more common in?
- 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
a first degree family history of GAD increases the risk how much?
x 2.5
what molecular genetics are associated with GAD?
- several risk genes eg. chromosome 2p21, 2q12
- eg. serotonin transporter gene
what do functional MR imaging studies show in people with GAD?
overactive amygdala (= in temporal lobe, important in fear and anxiety)
what is the main inhibitory neurotransmitter in the mammalian CNS, present in 1/3 synapses?
GABA = y-Aminobutyric acid
how is GABA synthesised?
decarboxylation of the amino acid glutamic acid
what does GABA play a major role in?
regulating neuronal excitability and muscle tone
GABA is the endogenous agonist at what 2 main receptors?
- GABAA receptor - in brain (has multiple ligand binding sites_
- GABAB receptor - in peripheral nervous system
what is a GABA analogue which acts as a selective agonist at GABAB receptors, used clinically as a muscle relaxant?
baclofen
describe the GABAA receptor
- 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)
where does GABA bind to on the GABAA receptor? effect?
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)
what is the commonest mammalian structure of the GABAA receptor?
(a1)2(B2)2(y2)
describe the clinical assessment in GAD
- 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
what are the main treatment modalities for GAD?
- 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
describe the NICE guidelines stepped care approach 1
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
what should not be used for > 2 weeks?
benzodiazepines
describe the NICE guidance stepped care approach 2
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)
what psychological treatments are available for GAD?
what are the core elements of CBT?
- 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”
NICE recommends how much CBT?
12 to 15 one-hour long sessions of CBT over 4 months
what % of people who have GAD respond to CBT?
60%
psychological vs pharmacological treatment
pharmacological management
- SSRIs = first line
- tricyclic antidepressants
- other antidepressants eg. mirtazapine
- pregabalin
- benzodiazepines eg. diazepam
how do benzodiazepines work?
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
how do SSRIs work?
- block serotonin reuptake from synapse — increase 5-HT in synaptic clefts
- first line pharmacological treatment
name some SSRIs shown to be effective in GAD
- sertraline
- escitalopram
- paroxetine
SSRIs vs older drugs such as tricyclic antidepressants
- fewer side effects
- safer in overdose
what do you tell a patient before they start SSRIs?
- 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
name some dual acting antidepressants that are effective in GAD and what they do
- mirtazapine — blocks presynaptic alpha-2 autoreceptors
- duloxetine (SNRI)
- venlafaxine (SNRI)
- imipramine (tricyclic)
- side effects differ to SSRIs
(SNRI = serotonin, NA reuptake inhibitors)
describe pregabalin
- 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
what do benzodiazepines differ mainly in?
their half life eg. diazepam (valium) 30 hrs vs triazolam 2 hrs
symptoms of anxiety reduce within how long of taking a benzodiazepine?
30 to 60 mins
what are some side effects of benzodiazepines
describe beta blockers
- 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
