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Ns And Neuropsychiatry > Anxiety > Flashcards

Anxiety Flashcards

1
Q

What are the syptoms o anxiety

A
  • Palpitations
  • Sweating
  • Trembling or shaking
  • Dry mouth
  • Difficulty breathing
  • Chest pain or discomfort
  • Nausea or abdominal distress (e.g. butterflies in stomach) • Feeling dizzy, unsteady, faint or light-headed
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2
Q

What are the systems involved in the street respons

A
  1. limbic system

2. limbic-hypothalamo-pituitary- adrenal axis

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3
Q

What is the limbic system

A

Ss Hippocampal formation (hippocampus, dentate gyrus, parts of parahippocampal gyrus)
Septal area Amygdala
+/-
Prefrontal cortex Cingulate gyrus

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4
Q

What is the hippocampus

A

Curved piece of cortex
Folded into medial surface of temporal lobe
Occupies floor of temporal horn of lateral ventricle
Three parts: subiculum, hippocampus proper, dentate gyrus
Involved in memory and expressions of emotion

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5
Q

How does the hippocampus fucntion?

A

o Receives inputs from many parts of the cortex and processes their emotional content
o Ultimately projects to the thalamus(and hence back to
the cortex – the Papez circuit) and also to the hypothalamus (causing autonomic features of emotional responses, since the hypothalamus send projections down through the cord to autonomic preganglionic neurones – the hypothalamospinal tract. This will lead to sympathetic nervous system activation, as well as release of adrenaline from the adrenal medulla – the acute stress response)
o Role in memory – already discussed
 Papez circuit may be involved in memory consolidation

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6
Q

What is the amygdala

A

Almond shaped structure sitting near to tip of hippocampus, Buried in the roof of lateral ventricle
Collection of nuclei
Inputs of sensory information, brainstem, thalamus, cortex
Outputs to cortex, brainstem and hypothalamus
Drive related behaviours and processing of associated autonomic emotional responses

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7
Q

What is the role of the prefrontal cortex in aniety

A

• Prefrontal cortex (classically not part of the limbic system but
definite roles in emotion)
o Modulation of emotional responses (e.g. consciously
suppressing features of anxiety) o ‘Perception’ of emotion?

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8
Q

What are the endocrine elements of the stress response

A

Endocrine elements of the stress response
• The limbic system is able to act on the hypothalamus to
stimulate the secretion of stress hormones
o Via the familiar hypothalamo-pituitary-adrenal axis

o Release of cortisol from the adrenal cortex is part of the ‘chronic’ stress response

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9
Q

What is the general adaptation syndrome

A

The general adaptation syndrome refers to three stages that the body goes through during prolonged exposure to stressors
o Stage 1: The alarm reaction
 Release of adrenaline and cortisol as well as sympathetic activation
(described above)
o Stage 2: Resistance (effect of adrenaline starts to wear off)
 Chronic stress response, prolonged release of cortisol
o Stage 3: Exhaustion (when you cannot escape an ongoing stressor)
 Chronic side effects of prolonged cortisol secretion start to occur o The stress response can become pathological when you cannot escape a
stressor(s), or when ‘trivial’ stressors elicit a strong stress response. However, patients with anxiety disorders may go through all of the stages above

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10
Q

What is the classification of anxiety disorders

A 
Anxiety disorders
o Classification
 Social phobia
• Anxiety about being in social situations
 Specific phobias
• Spiders, heights etc
 Generalised anxiety disorder
• Persistent anxiety about a variety of things
 Panic disorder
• Recurrent, unexpected panic attacks (severe episodes of acute
stress response)
 Obsessive compulsive disorder (OCD)
 Post-traumatic stress disorder (PTSD)
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11
Q

Describe the pathophysiology of anxiety

A

Pathophysiology
 Unclear
 Equivocal findings in studies of brain activation patterns
 GABA levels appear to be low in some anxiety disorders (maybe
explaining action of benzodiazepines)
 Increasing serotonin levels can help treat anxiety disorders
(mechanism unclear, but hippocampus may be involved)

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12
Q

What are the treatment options for anxiety

A 
Treatment
 Biological
• Short term benzodiazepines
• SSRIs 
 Psychological
• Cognitive behavioural therapy
o Getting patients to reflect on their
feelings/thoughts/behaviours
• Support groups, charities etc
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13
Q

What os GABA

A
  • GABA is the main inhibitory neurotransmitter
  • GABA levels are decreased in cortex in patients with panic disorder • Benzodiazepines increase GABA transmission so reduce anxiety
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14
Q

What are benzodiazepines

A

• Benzodiazepines increase GABA transmission so reduce anxiety
But very addictive - instantly feel better. Or can build up tolerance over time. Dont withdraw suddenly bc withdrawal symptoms

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15
Q

Describe Ssris in aniety

A
  • Increased levels of serotonin (due to SSRIs) may stimulate serotonin receptors in hippocampus
  • Leads to neuroprotection, neurogenesis and reduction of anxiety
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16
Q

How are aniety disorders treated

A

• Mainstay of treatment is SSRIs
• Cognitive behavioural therapy
• Can use pregabalin – a GABA analogue
Don’t use benzodiazepines long term!

17
Q

What are obsessions

A

‘a thought that persists and dominates an individual’s thinking despite their awareness that the thought is either entirely without purpose, or has persisted and dominated their thinking beyond the point of relevance or usefulness’
Often causes great anxiety and guilt Particularly repugnant to individual Reflect changes in society

18
Q

What are compulsions

A

obsessional motor acts. May result from an obsessional impulse that leads directly to the action, or they may be mediated by an obsessional mental image or fear’
e.g. ‘I need to turn the light switch on and off ten times or my family will die’
Can lead to patients wasting a lot of time!
Can also have mental compulsions e.g. repeating phrases

19
Q

What are the diagnostic criteria for ocd

A

• Obsessions/compulsions/both present on most days for a period of at least 2 weeks
• Obsessions and compulsions share all of the following features
• Originate in the mind of the patient
• Repetitive and unpleasant
• Acknowledged as excessive or unreasonable
• Patient tries to resist, but at least one obsession/compulsion is unsuccessfully resisted
• Carrying out the obsessive thought or act is not in itself pleasurable
• Obsessions/compulsions must causes distress or interfere with the
patient’s social or individual functioning

20
Q

Describe teh epidemiology of ocd

A
  • Usually begins in adolescence or early adulthood
  • 33% start between 10 and 15 years old • 75% started by age 30
  • Lifetime prevalence of around 2%
  • M : F 1 : 1 (but childhood OCD more common in boys)
  • Lots of doctors show traits
21
Q

What are suggestions for pathophysiology of ocd

A

Suggested theories:
• Re-entry circuits in basal ganglia
• Reduced serotonin
• Reduced activity in dorsolateral prefrontal cortex
• Reduced activity in orbitofrontal cortex
• Increased activity in cingulate cortex
Cortical area changes - cause ro effect??
• PANDAS - There may be cross-reactivity with certain streptococcal antigens and the basal ganglia

22
Q

Describe re entry circuits in basal ganglia in ocd

A

Basal ganglia re-entrant circuits
o The cortex projects to the basal ganglia, and these then project back up to the cortex via the thalamus
o This is an example of a ‘re-entrant’ loop, where obsessional thoughts can re-enter the cortex having entered the basal ganglia
o This may be due to overactivity in the direct pathway
o Treatments that inhibit thalamic (and hence cortical) activity by reducing the direct pathway or increasing
the indirect pathway may hold promise (e.g. subthalamic nucleus stimulation)

23
Q

What is pandas

A

Paediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal Infection
• Sudden onset of OCD symptoms or tics after infection with Group-A beta-haemolytic strep. Usually 3-12 years
• Usually dramatic onset of psychiatric or behavioural problems • Antibodies ‘cross-react’ with neurons in basal ganglia, causing
symptoms
• Responds to treatment with antibiotics and usual OCD managment

24
Q

Describe treatment of ocd

A

o Treatment
 Biological
• SSRIs +/- antipsychotics Eg lomiphene
High dose SSRIs (need higher dose and longer treatment course than in depression)
• Deep brain stimulation?
 Psychological
• CBT and variety of other interventions
Even if hands feel dirty but not, don’t wash then -> aniety in short term but better in long term
Cognitive behavioural therapy Exposure response prevention
 Social
• Family support
• Groups etc.

25
Q

What is ptsd

A
  • Within 6 months of a traumatic event of exceptional severity
  • Evidence of trauma
  • Repetitive, intrusive recollection or re-enactment of the event in memories, daytime imagery, or dreams
  • Conspicuous emotional detachment, numbing of feeling, and avoidance of stimuli that might arouse recollection of the trauma
26
Q

What is comple ptsd-

A

-

27
Q

Descrbe the pathophysiology of ptsd

A

Hyperactivity of amygdala, causing exaggerated response to perceived threat
Cortisol inhibits
traumatic memory retrieval and controls sympathetic response
In PTSD, lower than normal levels of cortisol
However evidence is conflicting!

28
Q

Descrbe the treatment for ptsd

A 
Treatment
 Biological
• SSRIs
• Maybe short term benzodiazepines 
 Psychological
• CBT
• Eye movement desensitization reprocessing therapy 
 Social
• Charities are particularly active, such as ‘Help for Heroes’

Ns And Neuropsychiatry (19 decks)

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