Session 11: Anxiety Flashcards

1
Q

Purpose of stress response.

A

Enables us to escape from potentially dangerous situations.

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2
Q

Which is the system primarily responsible for stress response?

A

Limbic system with neural and endocrine targets.

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3
Q

Explain the hippocampus involvment in stress response.

A

Inputs from many parts of the cortex to process the emotional content.

Will then project to the thalamus and back to the cortex, but also to the hypothalamus.

The circuit to hypothalamus causes the hypothalamus to send projections down through the cord to autonomic preganglionic neurones via the hypothalamospinal tract in response to the emotional response.

This will lead to sympathetic nervous system activation as well as release of adrenaline from the adrenal medulla leading to an acute stress response.

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4
Q

What is the papez circuit?

A

Thalamus projecting and communicating with the cortex.

It may be involved in memory consolidation.

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5
Q

Explain the involvment of amygdala in stress response.

A

Receives many inputs from the sensory system and have major outputs to the cortex, brainstem and hypothalamus.

It is involved, like the hippocampus in behavioural and autonomic emotional responses.

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6
Q

Where can the amygdala be found?

A

Sitting near the tip of the hippocampus and buried in the roof of lateral ventricle.

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7
Q

Where can the hippocampus be found?

A

Curved piece of cortex that is folded into medial surface of temporal lobe and occupies the floor of temporal horn of the lateral ventricle.

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8
Q

Three parts of hippocampus.

A

Subiculum

Hippocampus proper

Dentate gyrus

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9
Q

Explain the prefrontal cortex involvement in stress response.

A

Modulation of emotional responses like consciously suppressing features of anxiety.

Perception of emotion.

Not classically a part of the limbic system

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10
Q

Functions of the cingulate gyrus in stress response.

A

Involved in processing of emotions and memory.

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11
Q

Explain the endocrine involvement in stress response.

A

Limbic system is able to act on the hypothalamus to stimulate the secretion of stress hormones.

This is via the HPA-axis.

There is a realease of cortisole from the adrenal cortex as a part of the chronic stress response.

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12
Q

In general adaptation syndrome the body goes through three stages to the prolonged exposure to a stressor.

Which three stages?

A

Stage 1 - Alarm reaction

Stage 2 - Resistance

Stage 3 - Exhaustion

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13
Q

Explain stage 1 - alarm reaction.

A

Release of adrenaline and cortisol as well as sympathetic activation.

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14
Q

Explain stage 2 - resistance.

A

Resistance starts to build and the effect of adrenaline starts to wear off.

However there is still a prolonged release of cortisol

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15
Q

Explain stage 3 - exhaustion.

A

This comes into play when you can’t escape an ongoing stressor.

Cortisol levels are still high due to the chronic exposure and patient will start to experience side effects of prolonged elevated levels of cortisol.

Side effects such as muscle wasting, immunosuppression and hyperglycaemia.

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16
Q

When can the stress response become pathological?

A

When you cannot espace a stressor or when a ‘trivial’ stressor elicits a strong stress response.

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17
Q

Define anxiety.

A

A term used for a pathological stress response.

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18
Q

Symptoms of anxiety.

A

Palpitations

Sweating

Trembling or shaking

Dry mouth

Difficulty breathing

Chest pain or discomfort

Nausea or abdominal distress

Dizziness, unsteadiness, faint, light-headed.

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19
Q

Give examples of anxiety disorders.

A

Social phobia

Specific phobias such as spiders, heights, etc…

Generalised anxiety disorder (GAD)

Panic disorders

Obsessive compulsive disorder (OCD)

Post-traumatic stress disorder (PTSD)

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20
Q

Explain GAD.

A

Persistent anxiety about a variety of things.

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21
Q

Pathophysiology of anxiety disorders.

A

Unclear path but might be related to low levels of GABA.

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22
Q

Biological treatment of anxiety disorders.

A

Short term benzodiazepines

SSRIs

23
Q

Psychological treatment of anxiety disorders.

A

Cognitive behavioural therapy

24
Q

Social treatment of anxiety disorders.

A

Support groups

Charities

25
Q

Female to male ratio of OCD.

A

1:1

26
Q

Prevalence of OCD

A

1-5 will suffer from it at some point in their lives.

27
Q

Onset of OCD.

A

1/3 cases start between 10 and 15 yo

3/4 will have started by 30 yo

28
Q

Define obsessions.

A

Thoughts that persist and dominate an individuals thinking despite their awareness that the thoughts are entirely purposeless.

The thoughts have persisted and dominated their thinking beyond a point of relevance of that thought.

They are often unpleasant and repugnant and can therefore cause anxiety.

29
Q

Define compulsion.

A

A motor act resulting from the obsession.

You act out a compulsion to relieve yourself of the anxiety that is provoked by its associated obsession.

However the motor act might be unpleasant in itself and exacerbate the anxiety.

30
Q

Give examples of intrusive thoughts.

A

I might harm my baby

I might be a paedophile

I might kill my family

etc…

31
Q

Give a common OCD behaviour.

A

Flicking a switch on and off multiples of times because if they don’t do it their family will die.

The person is aware that their thoughts make no sense but still can’t help it.

32
Q

Diagnostic criteria of OCD.

A

Obsessions and/or compulsions must be present on most days for at least 2 weeks.

They must originate in their mind

Be repetitive and unpleasant.

Acknowledged as excessive or unreasonable.

The patient will resist the obsessions/compulsions but one is unsuccessfully resisted.

33
Q

Give proposed hypotheses of OCD.

A

Basal ganglia re-entrant circuits

Reduced serotonin levels

Altered activity in cortical areas.

PANDAS

34
Q

What is PANDAS.

A

Paediatric autoimmune neuropsychiatric disorder associated streptococcal infection.

35
Q

Explain PANDAS.

A

Onset of OCD symptoms and tics after an infection of Group-A betahaemolytic streptococcus usually around 3-12 yo.

This is by antibodies cross-reacting with neurones in the basal ganglia and cause symptoms.

36
Q

Tx of PANDAS.

A

Antibiotics and OCD management.

37
Q

Explain basal ganglia re-entrant circuits.

A

Cortex -> basal ganglia -> back into cortex via thalamus.

Obsessional thought can re-enter the cortex having entered the basal ganglia and loop.

38
Q

Why might basal ganglia re-entrant circuits happen?

A

Overactivity of the direct pathway.

39
Q

Biological Tx of OCD.

A

SSRIs +/- antipsychotics

Deep brain stimulation

40
Q

Why might deep brain stimulation help in OCD?

A

Because of stimulation of the subthalamic nucleus in order to increase the indirect pathway to inhibit re-entrant.

41
Q

Psychological tx of OCD.

A

CBT

Other interventions

42
Q

Social tx of OCD.

A

Family support

Groups

43
Q

Features of PTSD.

A

Within six months following an exceptionally severe traumatic event.

Repetitive and intrusive recollection of the event or even re-enactment.

This is in memories, daytime imagery or in dreams

There is also emotional detachment and emotional numbing.

Avoidance of stimule that might arouse recollection of the trauma as well.

44
Q

Pathophysiology of PTSD.

A

Amygdala hyperactivity causing behavioural responses.

Cortisol levels are however low and cortisol is supposed to inhibit the traumatic memory retrieval and also control sympathetic response.

45
Q

Biological tx of PTSD.

A

SSRIs

Maybe short term benzodiazepines

46
Q

Psychological tx of PTSD.

A

CBT

Eye movement desensitisation reprocessing therapy.

47
Q

Social tx of PTSD.

A

Charities such as help for heroes, or for rape victims.

48
Q

Definition of anxiety.

A

A feeling of worry, nervousness, or unease about something with an uncertain outcome.

49
Q

Give an example of classification of psychiatric disorders.

A

DImensional classification

50
Q

Explain dimensional classification.

A

Various axes or dimension which gives an average of a personality.

Based on

Extraversion, neuroticism, conscientiousness, agreeableness, and openness.

51
Q

Study designs of psychiatric disorders.

A

Family study (sharing genes and environment)

Twin study (MZ or DZ). If there isn’t a 100% concordance in MZ then we assumen that there is another factor causing psychiatric disorder. (sharing genes and environment)

Adoption studies (sharing genes but not environment)

52
Q

Risk of schizophrenia in siblings vs MZ twins.

A

8-10% in siblings

MZ twins around 45%.

This means that there is environmental factors that have a place as well.

Epigenetics??

53
Q
A