Anxiety disorders (done) Flashcards
What is anxiety?
A feeling of unease, such as worry or fear, that can be mild or severe
What conditions is anxiety the main symptom of?
- Generalised anxiety disorder (GAD)
- Panic disorder
- Obsessive compulsive disorder (OCD)
- Post-traumatic stress disorder (PTSD)
- Phobias
What are the psychological & physical symptoms of generalised anxiety disorder (GAD)?
- Feeling restless of worried
- Having trouble concentrating or sleeping
- Dizziness or heart palpitations
What are the 6 things that categorise GAD?
1 - Excessive worry, ocurring more days than not for at least 6 months
2 - Individual finds it difficult to control the worry
3 - 3 or more of 6 the key symptoms
4 - Anxiety, worry or physical symptoms cause significant distress
5 - Disturbance not attributed to drug abuse
6 - Disturbance is not better explained by anotehr disorder
What are the 6 key symptoms of GAD that 3 of are required to be diagnosed?
1 - Restlessness or feeling keyed up or on edge
2 - Being easily fatugued
3 - Difficult concentrating or mind going blank
4 - Irritability
5 - Muscle tension
6 - Sleep disturbance
What is the definition of panic disorder?
An anxiety disorder with regular panic attacks
What are the characteristics of a panic attack?
- Intense tymptoms that come on quickly, often for no apparent reason
- Some symptoms overlap other health conditions (e.g. low BP)
- Range from 1-2/month to multiple/week & usually last 5-20min
What are the characteristics of panic disorder?
1 - Palpitations
2 - Sweating
3 - Trembling or shaking
4 - Fear of dying
5 - Neausea
What are the 2 component of OCD?
Obsessions & compulsions
What are obsessions?
Unwanted/unpleasent thoughts that cause anxiety e.g. being burgled
What are compulsions?
Repetitive behaviour undertaken to supress -ive thoughts
What is the diagnosis for OCD?
Obsessions & compulsions must be time consuming & impact on day-to-day functioning
What are some examples of OCD obsessions?
- Aggressive
- Contamination
- Religion
- Self-control
- Sexual
- Cleanliness
Define PTSD:
An anxiety disorder caused by traumatic events
What are the charateristics of PTSD?
- Re-lived through nightmares or flashbacks
- Avoidance of linked memories
- Affects 1 in 3 exposed to trauma
Define a phobia:
Overwhelming & debilitating fear of something that is often little or no actual danger
What are the 2 types of phobias?
- Specific phobias
- Complex phobias
What are specific phobias?
Fear of something that is normally not harmful –> cna generally be avoided/worked around
e.g. Animals (spiders), environmental (heights), situational (flying/dentist), bodily (injections)
What are complex phobias?
They are life limiting as they cannot be avoided or worked around
e.g. Agoraphobia (open spaces), Social phobia (of social performance situations, from thoughts of negative judgement or humiliation –> dread or avoidance)
What are the 4 types of evidence that were used to understnad anxiety?
- Neuroimaging
- Genetics
- NTs - including treatment response
- Neuroendocrine
What are the 3 main brain areas that are involved in anxiety?
- PFC (prefrontal cortex)
- ACC (anterior cingulate cortex)
- Amygdala
What is the role of the PFC?
Involved in logical responses & reasoning to reduce anxiety
How does the PFC change in anxiety?
Anxiety can shut down the PFC –> hampers logical thinking & rationalising
What is the role of the anterior cingulate cortex?
Amplifies fear signals from the amygdala
How does the anterior cingulate cortex change in anxiety?
It malfunctions –> hyperactivating the amygdala
This amplifies -ive info, which increases anxiety
What is the role of the amygdala?
Responsible for responses to fearful stimuli
How does the amygdala change in anxiety?
In persistent anxiety, the amygdala increases in size - boosting response to scary stimuli
Inhibits the PFC & initiates fight-or-flight response
What are the key brain area malfunctions that result in anxiety?
PFC is underactive & amygdala is overactive
What did fMRI scans of GAD and healthy control brains show?
Patients w GAD showed weaker functional connectivity between the PFC & amygdala
(Dec PFC-amygdala connectivity in GAD)
What is the heratibility of GAD?
Family studies show ~30% heritability; parent –> child
Name 3 monoamines?
Dopamine, adrenaline & noradrenaline
What are the 4 risk genes that have been identified with GAD?
- 5-HT reuptake transporter
- 5-HT1A receptor C1019G polymorphism
- Monoamine oxidase A T941G polymorphism
- Brain-derived neurotrophic factor Val66Met polymorphism
What is the change caused by 5-HT1A receptor C1019G polymorphism in GAD?
C to G change at position 1019 in this gene = mutation
Increases -ive feedback, dec serotonergic signalling
What is the change caused by Monoamine oxidase A T941G polymorphism in GAD?
(Something about long allele)
Increases monoamine metabolism, decreases monoamine signalling
What is the change caused Brain-derived neurotrophic factor Val66Met polymorphism in GAD?
Decreases BDNF activity
What % of GAD is environmental?
If ~30% is inherited then ~70% is environmental
What are some environmental risk factors for anxiety?
- Childhood trauma
- Stressful family circumstances
- Natural disasters
What are some examples of gene-environment interactions causing GAD?
- Childhood trauma X 5-HT transporter, COMT & MAOA variants
- Hurricane victim X neuropeptide Y variants
- Daily life stress X 5-HT transporter variants
- Family relationship scale X nueropeptide S receptor 1 variants
How does GABA act in ppl with GAD & how can we use this to treat GAD?
- GABA dysregulated in GAD
- GABA A receptor downregulated in patients
- Symptoms treated w GABA A agonists
What are the 4 NT that can be targeted to treat GAD?
- GABA
- 5-HT
- Corticotrophin releasing factor
- Neuropeptides
How can we treat GAD symptoms using 5-HT receptors?
SSRIs can be used to treat issues with them & inhibit serotonin reuptake
Have treatments been found for GAD with corticotrophin releasing factor & neuropeptides?
Cortico –> clinical trials were unsuccessful
Neuropeptides –> patients are hypesensitive to cholecystokinin (CCK) agonists
–> unsuccessful trials investigating CCK-antagonists
What does the HPA axis include?
- Hypothalamus (in forebrain)
- Pituitary gland (below hypothalamus)
- Adrenal glands (above kidneys)
What is the role of the HPA axis?
Work together to regulate stress reponses, mood, immune function, metabolism
What hormones are released in the HPA axis?
Hypothalamus
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Corticotrophin releasing hormone - CRH
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Pituitary gland
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Adrenocorticotropic hormone (ACTH)
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Adrenal glands
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Cortisol, adrenaline & noradrenaline
how can the HPA axis cause symptoms of GAD?
- Cortisol activates fight-or-flight response & inhibits CRH & ACTH release
- This -ive feedback reduces cortisol & noradrenaline release
- Chronic stress & GAD associated w HPA-axis dysfunction
What needs to be considered udirng assessment for GAD?
- Mental health history
- Environemental stressors
- Medical & drug history
- Degree of distress & functional impairment
- Risk of suicide
What are the non-pharmacaological treatments of GAD?
- Self help
- Meditation & relaxation techniques (e.g. mindfulness)
- Exercise
- Lifestyle changes
What are the 2 types of symptoms that are treated in GAD?
- Autonomic symptoms
- Anxiety symptoms
What pharmacological treatments are used for the autonomic symptoms of GAD?
Beta-adrenoceptor antagonists –> e.g. propranolol
Can be given for experiencing inc HR that is affecting psychological symptoms
What pharmacological treatments are used for the anxiety symptoms of GAD?
- SSRIs (selective serotonin reuptake inhibitors)
- SNRIs (serotonin & noradrenaline reuptake inhibitors
- Atypical antidepressants
- Benzodiazepines
Give an example of an SNRI:
Venlafaxine
Give an example of an SSRI:
Sertraline
(Meachanisms covered in depression lecture)
Give examples of atypical antidepressants:
Vilazodone or mirtazapine
When are benzodiazepines (BZs) used?
Short term use in a crisis - as they work immediately
What are BZs used for?
Widely used for insomnia, epilepsy & surgical pre-medication
What action do BZs have?
They enhance the effects of GABA (main inhibitory NT)
How do BZs enhance the effects of GABA?
- Bind to GABA A recpetor between the alpha & gamma subunit
- Causes a conformational change that enhances GABA binding –> i.e. GABA A receptor positive allosteric modulator (PAM)
- Channel opening –> Cl- influx, hyperpolarisation, red neuronal activity
What are some problems that can occur from use of BZs?
Include non-responsiveness in patients
Also impair daily function as they make u DROWSY –> can’t drive or operate hearvy machinery
List the novel treatments that are being explored:
- Glutamatergics –> e.g. ketamine, riluzole, xenon
- Neurosteroids –> e.g. aloradine
- Cannabinoids
- MDMA
- L-Dopa
What do existing treatments for GAD generally target vs novel treatments?
Existing –> 5-HT & GABA
Novel –> Glutamate, neurosteroids & cannabinoids
What are some negative effects of SSRIs?
Can cause sexual dysfunction & weight gain
