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Neuro > Anxiety > Flashcards

Anxiety Flashcards

1
Q

What is anxiety?

A

Feeling of unease such as worry or fear which can range from mild to severe

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2
Q

What are the 2 symptoms of anxiety?

A
  • Psychological - feelings

- Physiological - tachycardia, hyperventilation

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3
Q

When does anxiety intensity become a problem?

A
  • When it becomes very intense
  • Source - certain events or situations will trigger anxiety
  • When it becomes chronic and irrational
  • The person starts to develop social disturbance, avoidance behaviours, incessant worry and concentration or memory problems
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4
Q

What can cause anxiety?

A
  • Past or childhood experience
  • Everyday life and habits, for example money and exams
  • Diet, some food can trigger anxeity for example sugar can heighten the feeling
  • Physical and mental health can have a knock on effect (cormorbidity)
  • Drugs and medication, alcohol is a depressant and therefore has a sedative effect but the effects are short lasting
  • Neurotransmitter balance can lead to anxiety
  • Cannabis and cocaine have been linked to anxiety
  • Genetics has also be linked however, not to a single gene, but instead a complex of genetic basis that have a direct effect on environmental factors.
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5
Q

Anxiety disorders

A

Generalised anxiety disorder
Specific phobias
Social phobias
Panic phobias

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6
Q

OC and related disorders

A

Obsessive compulsive disorder

Post-traumatic stress disorder

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7
Q

Cause of Generalised anxiety disorder

A
  • No real stimulus
  • On-going-chronic
  • Cause of anxiety cannot be pinpointed.
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8
Q

Symptoms of generalised anxiety disorder

A
  • Symptoms include insomnia, restlessness, fatigue, excessive worry, increased muscle soreness and impaired concentration
  • Difference in symptoms between individuals
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9
Q

What is a specific phobia?

A

Extreme fear for anxieties provoked by exposure to specific situations or objects which often leads to avoidance behaviours

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10
Q

Example of a specific phobia

A

Agoraphobia - fear of an environment - no means of escape

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11
Q

What is social phobias?

A

Significant anxiety provoked by exposure to certain types of social or performed situations

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12
Q

What is generalised anxiety disorder?

A
  • Excessive worry occuring for at least 6 months - difficult to control and impacts daily activity
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13
Q

Example of social phobia

A

Selective mutism - a severe anxiety disorder where a person is unable to speak in certain situations such as with classmates at school or to relatives they don’t see often.

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14
Q

What is a panic disorder?

A
  • Recurring panic attacks without clear cause or trigger
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15
Q

Symptoms of panic disorder

A

Sudden feeling of overwhelming with marked somatic symptoms such as sweating or chest pain.

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16
Q

When do panic attacks occur?

A
  • Can occur spontaneously or can be a feature of anxiety disorders.
  • Constantly scared of having another panic attack, to the point that fear itself can trigger another panic attack.
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17
Q

Obsessions in Obsessive Compulsive Disorder

A

Recurrent, intrusive thoughts, images and ideas or impulses/checking e.g. that windows are closed, gas is off.

18
Q

Compulsions in Obsessive Compulsive Disorder

A

Repetitive behaviours or mental acts that are performed to reduce anxiety associated with obsession e.g. avoiding cracks in pavements

19
Q

What is post-traumatic stress disorder (PTSD)?

A
  • Re-living unpleasant memories
  • Flashbacks and nightmares
  • Suspicious
  • No apparent trigger
20
Q

Pathophysiology of anxiety in the brain

A
  • Hallmark of anxiety disorders is inappropriate stress response either with a stressor not present or when it is not threatening
  • This is involved in the HPA axis.
  • Increase in cortisol is linked to stress
21
Q

Role of the amygdala in anxiety

A
  • Amygdala activates HPA axis which leads to increased cortisol and therefore anxiety disorders.
  • It is connected to fear, depression and emotion.
22
Q

Role of hippocampus in anxiety

A
  • The hippocampus is responsible for inhibiting the HPA axis to prevent cortisol secretion and therefore inhibit anxiety disorders.
  • Therefore, hippocampus underactivity is linked with anxiety disorders
23
Q

Link between hippocampal degeneration and anxiety - PTSD

A
  • Continuous exposure to cortisol leads to neuronal degeneration in the hippocampus
  • This sets off a vicious cycle where the stress response becomes more pronounced due to less inhibition on the HPA axis.
  • This leads to increased cortisol production and therefore more hippocampal damage.
  • In PTSD, there is decreased hippocampal mass.
24
Q

Examples of Anxiolytic drugs

A
  • GABA(A) receptor modulators - Barbiturates and Benzodiazepines
  • 5HT receptor agonists
  • B-adrenoceptor antagonists
25
Q

GABA(A) receptor mechanisms

A

A ligand gated inhibitory receptor. It is a ligand gated Cl- channel which causes hyperpolarisation and therefore inhibtion. It has multiple binding site for different compounds.

26
Q

What are barbiturates?

A
  • They are allosteric modulators that bind anywhere but the binding site of the enogenous molecule (GABA binds to the alpha and beta site).
  • Positive allosteric modulators because they increase the activity of the receptor.
27
Q

Effect of barbituates

A
  • Used for epilepsy, general anaesthesia no longer for anxiety
28
Q

Side effects of barbituates

A
  • Responsible for severe depressant effect on the CNS
  • Considered dirty drugs because they can bind to multiple other receptors and cause major side effects
  • As well as binding to the GABA receptors, they bind to glycine receptors and cause further inhibtion.
  • Also bind to nAcHR and 5HT receptors and block them causing reduced excitation.
  • They block AMPA/Kainate receptors and inhibit Ca2+ release.
  • All of these effects cause more inhibition and less excitation
29
Q

Effect of benzodiazepines

A
  • Bind between the gamma and alpha subunit
  • Increase the GABA affinity for its binding site, therefore same functional response is achieved at lower GABA
  • Stabilise the GABA receptor therefore causing inhibition
  • Cleaner than barbiturates
30
Q

Action of benzodiazepines

A
  • Short acting are used for hypnotics (insomnia) to avoid sedation throughout the day. Whereas, ones used for anxiety have a long half life.
31
Q

What symptoms are barbiturates and benzodiazepines associated with?

A

Associated with tolerance and withdrawal symptoms

32
Q

What imbalance is linked to anxiety disorders?

A

The imbalance between Glutamate and GABA

33
Q

Which receptors are activated more in anxiety?

A

In an anxiety patient (symptomatic), they have more activation of the glutamate receptors compared with GABA receptors.

34
Q

Effects of barbiturates and benzodiazepines on the receptors

A

When a patient is given these drugs, they work on the GABA receptor and increase stabilisation of the receptor and therefore more inhibition occur leading to decreased anxiety.

35
Q

How does withdrawal symptoms to barbiturates and BZDs occur?

A

Overtime tolerance builds up due to the trafficking of more glutamate receptors and therefore, the initial imbalance of receptors is seen again. This means patients then need to take more dosage of the BZN drugs to address the new imbalance.
If a patient was to stop taking the drug, they would have high withdrawal symptoms due to the reduction in GABA receptor activation and an increase in glutamate receptors and therefore more excitation. This leads to development of seizures.

36
Q

What other neurotransmitter is anxiety associated with?

A

Low serotonin levels like depression

37
Q

Which drugs are used to treat generalised anxiety disorder?

A

5HT1a agonist such as Buspirone is used to treat GAD because they have less side effect than the ones above.

38
Q

What are SSRIs used to treat?

A

Used to treat long-term anxiety by increasing serotonergic neurotransmission

39
Q

How does buspirone work?

A
  • It works by activation of the pre-synaptic 5HT auto-receptors that leads to the inhibition of serotonin release from the presynaptic neuron.
  • It does this by inhibiting the release of serotonin, even if it takes weeks, it causes desensitisation of the 5HT1A receptors which leads to the downregulation of the receptors on the pre-synaptic membrane.
  • This results in the heightened excitation of serotonergic neurons due to less autoinhibition and therefore the symptoms of anxiety are treated.
40
Q

How do SSRIs work?

A

SSRIs work in a similar way, they inhibit the uptake of serotonin via SERT and therefore more serotonin in the synaptic cleft.

  • If they are taken over a period of time, they also induce the densensitisation of the 5HT1A receptors.
  • They can also lead to the down regulation of the 5HT receptor on the postsynaptic membrane which means a decrease in the 5HT neurotransmission.
  • However, even though there is some degree of decrease in the serotonergic transmission, the overall effect is an increase in the neurotransmission due to 5HT1a densisitisation and the blocking of SERT.
  • Symptoms of anxiety are supressed in patients.
41
Q

Effects of adrenoceptors antagonists

A
  • GPCR
  • B1 and B2 overall increase arousal and awareness
  • B-adrenoceptor antagonists reduce the peripheral manifestation of anxiety such as tremor, tachycardia and diarrhoea.
  • They have no effect on the central CNS

Neuro (20 decks)

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