Anxiety Flashcards

1
Q

What is the physiological role of anxiety?

A

Stress response - which results in anxious feeling - enables us to escape from potentially dangerous situations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the anxiety response mediated by?

A

Majority the limbic system - hippocampus, amygdala

Also pre-frontal cortex
These systems have neural and endocrine targets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Role of hippocampus in anxiety

A
  • Receives inputs from many parts of cortex and processes their emotional content
  • Then projects to thalamus (and then back to cortex = Papez circuit) and also the hypothalamus
  • Hypothalamus causes emotional response sending projections down autonimic preganglionic neurones
  • = sympathetic nervous system activation
  • and adrenaline release from adrenal medulla
  • Hippocampus also has role in memory - Papez circuit may be involved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the amygdala?

A

Almond shaped structure sitting near tip of hippocampus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Amygdala role in anxiety

A

Recieves many inputs from sensory system
Outputs to cortex and hypothalamus
Involved in behavioural and autonomic emotional responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Prefrontal cortex role in anxiety

A

Modulation of emotional responses - conciously supressing features of anxiety
May be your ‘perception of emotion?’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens when HPA axis is stimulated by stress?

A

Hypothalamus paraventricular nucleus releases CRH
Anterior pituitary releases ACTH
Adrenal cortex (zona fasciciulata) to releases cortisol and medulla to release adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the endocrine elements of the stress response?

A
  • Limbic system (hippocampus and amygdala) is able to act on hypothalamus to stimulate secretion of stress hormones via HPA axis (adrenal)
  • Release of cortisol from adrenal cortex is part of the chronic stress response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the general adaptation syndrome?

A

Three stages the body goes through during prolonged exposure to stressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3 stages of general adaptation syndrome

A
  1. Alarm reaction - adrenaline and cortisol are released as well as sympathetic activation
  2. Resistance - adrenaline wears off, chronic stress response and prolonged release of cortisol
  3. Exhaustion - cannot escape ongoing stressor, chronic side effects of prolonged cortisol exposure start
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What overall happens in chronic stress?

A

Less negative feedback on cortisol release = levels continue to rise
Increased activity of amygdala and hypothalamus
= increased acitivty of sympathetic ANS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is stress habituation?

A

Repeated mild stress exposure leads to a reduced response to HPA axis
Mild stress reduces activity seen in sympathetic ANS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When is anxiety a problem?

A

When response is to a perceieved threat, not an actual one
Difficult to manage
Cannot cope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When can chronic stress response/general adaptation syndrome become pathological?

A

If you cannot escape stressors or when trivial (‘minor’) stressors elicit a strong stress response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is anxiety?

A

Pathological stress response - anticipatory, future focused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Symptoms of anxiety

A

Primarily due to sympathetic activation:
* Palpitations
* Sweating
* Tembling/shaking
* Dry mouth
* Difficulty breathing
* Chest pain/discomfort
* Nausea or abdominal distress - butterflies
* Dizzy, unsteady, faint or light headed

17
Q

Classification of 6 anxiety disroders

A
  • Social phobia - anxiety about social situations
  • Specific phobia - eg spiders
  • Generalised anxiety disorder - peristent anxiety about many things
  • Panic disorder - recurrent unexpected panic attacks
  • Obsessive compulsive disorder
  • Post-traumatic stress disorder (PTSD)
18
Q

Pathophysiology of anxiety disorders

A

Unclear
GABA can be low in some anxiety disorders
Increasing serotonin can help treat anxiety disorders

19
Q

Treatment for anxiety disorders - broad

A

Biological:
* short term benzodiazepines
* SSRIs

Physiological:
* Cognitive behavioural therpay - reflect on thoughts, feelings and behaviours

Social:
* Support groups, charities

20
Q

OCD epidemiology

A
  • Common - 1 in 50 at some point
  • 1/3 cases start between 10-15 years old
  • 3/4 started by 30
  • Equal male:female
21
Q

What is OCD characterised by?

A

Obsessions:
* Thoughts that persist and dominate individuals thinking despite their awareness that the thought are without purpose or have persisted beyond the point of relevance or usefulness
* Unpleasant, repugnant often causing anxiety

Compulsions:
* Motor act (sometimes a thought) resulting from obsession
* Acting out compulsion may relieve anxiety caused by obsession but frequently carring out compulsions is unpleasant

22
Q

How long are obsessions and compulsions present in OCD?

A

Must be present most days for at least 2 weeks

23
Q

Common features of obsessions and compulsions in OCD?

A
  • Originate from the mind of the patient
  • Repetitive and unpleasant
  • Acknowledged to be unreasonable and excessive
  • Patient tries to resist but at least one obesession/compulsion is unsuccessfully resisted
24
Q

Pathophysiology of OCD

A

Unclear, some theories:
Basal ganglia rentrant circuits:
* Cortex projects to BG, these then project via thalamus back to cortex
* = re-entrant loop may be caused by overactivity of direct pathway
* Treatments inhibit thalamic activity (then cortical) by reducing direct pathway or increasing indirect pathway may help?

Reduced serotonin levels
* SSRIs help

Altered activity in a range of cortical areas

Autoimmune - streptococcal antigens and basal ganglia cross reaction?

25
Q

Treatment for OCD

A

Bio:
* SSRIs +/- antipsychotics
* Deep brain stimulation?

Psychological and social:
* Cognitive behavioural therapy
* Family support, groups etc

26
Q

PTSD features

A
  • Can occur within 6 months following an exceptionally severe traumatic event (eg rape, war trauma)
  • Causes repetitive intrusive recollection or re-enactment of event in memories, daytime imagery or dreams
  • = emotional detachment, numbing of feeling and avoidance of stimuli that may arouse recollection of trauma
27
Q

Pathophysiology of PTSD

A

Unclear
Amygdala hyperactivity causing exaggerated beahvioural response?
But low levels of cortisol

28
Q

Treatment for PTSD

A

Bio:
* SSRIs
* Short term benzodiazepines

Psychological
* CBT
* Eye movement desensitization reprocessing therpay - follow pendulum with eyes and talk through trauma

Social:
* Charities - eg help for heroes

29
Q

Good thing about anxiety

A

Moderate levels improve performance - allow for focus and tunnel vision for goal

30
Q

Treatments for phobias

A

Systematic desensitisation - expose them little at a time to the phobia

31
Q

Whats agoraphobia?

A

Fear of crowds, open spaces, difficulty to get home

32
Q

Triggers of agoraphobia

A

Distance from home
Crowding
Open space
Social situations

33
Q

Social phobia - what is it?

A

Anxiety in social situations due to fear of scrutiny by other people
Feel inferior

34
Q

Psychological symptoms of anxiety

A
  • Fearful anticipation
  • Irritability
  • Sensitivuty
  • Restless
  • Poor concentration
  • Anxious thoughs
35
Q

What is the basal ganglia re-entrant loop in OCD?

A

Increased activity in caudate nucleus
= activation of orbitofrontal cortex
= increased activity thalamus via cingulate gyrus
= increased stimulation cortex which projects back to BG