37- Anxiety Flashcards

1
Q

what is anxiety?

A

a feeling of unease – e.g. worry or fear – which can range from mild to severe

it’s both a learned an innate adaptive response to fear-inducing stimuli

anxiety becomes a problem when it’s chronic and irrational as an inappropriate stress response to when a stressor is not present or not immediately threatening

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2
Q

symptoms of anxiety?

A

can be psychological and physiological

psychological symptoms - social disturbances, incessant worry

physiological symptoms - tachycardia, shortness of breath, trembling, headaches, dizziness, sweating, fatigue and insomnia

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3
Q

what are the causes of anxiety symptoms?

A

past experiences

issues in everyday life

diet

physical and mental health

alcohol and drugs, psychostimulants

has a genetic basis

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4
Q

how does alcohol contribute to causing anxiety symptoms?

A

alcohol is a CNS depressant - it increases GABAnergic transmission and blocks glutamatergic transmission, disrupting the excitatory-inhibitory neural activity in the brain, allowing the user to feel relaxed

brain has to adapt to counteract this imbalance, which causes low GABA levels and high excitatory glutamate levels

this can trigger anxiety symptoms

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5
Q

how do recreational drugs/ psychostimulants contribute to anxiety symptoms

A

psychostimulants such as cocaine and amphetamine increase CNS activity, causing tremors and shaking

each drug has a mechanism unique to it for causing anxiety-like symptoms

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6
Q

describe the genetic role in anxiety

A

genetic factors are linked to anxiety disorders but aren’t based on a single gene

the genetic basis for anxiety is complicated and likely an interplay between the environment and genetics

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7
Q

describe the pathophysiology of anxiety related to the CNS

A

hippocampus and amygdala regulate the HPA axis

hippocampus is involved in learning and memory - suppresses the HPA axis to prevent excessive cortisol release. underactivity underlies anxiety disorders.

amygdala is involved in emotion and the fear response. stimulates the HPA axis to promote cortisol release. hyperactivity is associated with anxiety disorders.

HPA hyperactivity from CRH over-expression is linked to anxiety-related symptoms as the stress response is regulated by the HPA axis and cortisol release

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8
Q

what are the three classifications of anxiety disorders? give examples

A

anxiety disorders - e.g. social phobias, specific phobias, generalised anxiety disorder

obsessive compulsive disorders - e.g. OCD, hoarding disorder, body dysmorphia disorder

trauma and stressor-related disorders - e.g. PTSD

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9
Q

describe generalised anxiety disorder - what is it? associated symptoms and criteria?

A

ongoing state of excessive anxiety lacking clear reason or focus

symptoms: restlessness, fatigue, irritability, increased muscle tension, difficulty concentrating, difficulty speaking

must have at least 3 of the 6 symptoms, persisting for at least 6 months which affect daily living and can’t be attributed to substance or medical conditions

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10
Q

describe specific phobias - what is it? associated symptoms and criteria?

A

out-of-proportion extreme fears/ anxieties provoked by exposure to a particular situation/ object which often leads to avoidance behaviours

specific phobias have specific triggers - a wide range of them exist

phobia must persist for at least 6 months and impair daily living

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11
Q

social phobia - what is it? associated symptoms and criteria?

A

significant anxiety provoked by exposure to certain types of social/ performance situations

immediate and out-of-proportion fear. anxiety in the face of social interactions, being observed or performing in front of others

phobia must persist for at least 6 months and impair daily living

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12
Q

panic disorder - what is it? associated symptoms and criteria?

A

recurring panic attacks without a seemingly clear cause/trigger

panic attacks are an abrupt surge of intense fear or discomfort, reaching a peak within minutes - can induce a panic cycle

symptoms: panic attacks, increased heart rate, sweating, trembling, shortness of breath, fear of dying

must have at least 4 of the 13 symptoms

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13
Q

PTSD - what is it? associated symptoms and criteria?

A

distress triggered by recalling past, traumatic experiences, triggered by exposure to certain situations

symptoms: recurrent intrusive memories, nightmares, dissociative reasons, psychological and physiological distress at exposure

disturbances must persist for at least 1 month, impair daily living

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14
Q

what are benzodiazepines?

A

a class of GABA-A receptor positive allosteric modulators, act as anxiolytics

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15
Q

mechanism of action of benzodiazepines?

A

benzodiazepine binds to the allosteric site between the alpha and gamma interface of the GABA-A receptor

stabilises the GABA-A receptor binding site in an open configuration

increases GABA affinity its binding site

increase GABA neuroinhibitory actions and helps resolve the imbalance between glutamate-GABA NTs/ excitatory-inhibitory imbalance associated with anxiety disorders

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16
Q

compare benzodiazepines to barbiturates

A

benzodiazepines - considered cleaner compounds, don’t activate other receptors and provide more selective anxiolytic effects
- provide more acute treatment, act quickly

both drug classes are associated with unwanted side-effects, tolerance and withdrawal symptoms

17
Q

effects of prolonged use of benzodiazepines

A

can lead to tolerance - will require a higher dosage of the drug for effect

additional glutamate receptors may be trafficked to the cell membrane, restoring the initial NT imbalance

sudden withdrawal can result in decreased GABA activity and withdrawal symptoms = individual must be gradually tapered off to help restore inhibitory-excitatory NT balance

18
Q

how does serotonin work as a neurotransmitter?

A

serotonin is an NT in the PNS and CNS – activates GCPR receptor subtypes and one LGIC subtype (5-HT3)

important in sleep and wakefulness, mood and emotional behaviours

19
Q

mechanism of action of buspirone as a 5-HT1A receptor agonist

A

buspirone as a 5-HT1A receptor agonist binds and activates 5-HT receptors

activates auto-inhibitory 5-HT1A receptors = initially inhibits 5-HT release

prolonged use (weeks) leads to desensitisation and downregulation of 5-HT1A receptors

leads to increased excitation of 5-HTergic neurons = increases 5-HT release

suppresses GAD symptoms

20
Q

why does buspirone initially lead to a decrease in serotonin?

A

initially activates 5-HT1A autoreceptors = leads to decrease in serotonin release

this contributes to the delay in its anxiolytic effects

21
Q

side effects of buspirone?

A

dizziness, nausea, headaches, decrease in arousal from inhibiting noradrenergic neuron activity

22
Q

compare buspirone as an anxiolytic with SSRIs as antidepressants

A

SSRIs are commonly used for long-term anxiety states = they block serotonin reuptake = increase serotonin availability in synapse

buspirone initially blocks serotonin release = induces desensitisation and downregulation of 5-HT1A receptors = increases serotonin release overtime

23
Q

how does noradrenaline work as a neurotransmitter?

A

noradrenaline is a major NT of the sympathetic NS for the peripheral and central NS

it activates GCPR receptor subtypes - alpha and beta noradrenergic receptors

affects cardiovascular tone, attention, arousal, sleep and wakefulness

24
Q

how does propranolol work as a beta-noradrenergic receptor antagonist for treating anxiety?

A

propranolol is non-selective – acts on B1 and B2 noradrenergic receptors

reduces some of the peripheral/physiological manifestations of anxiety - tachycardia, sweating, tremors, GI disturbances - by blocking peripheral sympathetic responses associated with the fight or flight response

its non-specificity for beta-1 and 2 adrenoreceptors means potential side effects on CV and respiratory function

25
Q

what are the three main classes of anxiolytics?

A

benzodiazepines

5-HT1A receptor agonists such as buspirone

beta-noradrenergic receptor antagonists such as propranolol