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Neurology > Anxiety > Flashcards

Anxiety Flashcards

1
Q

What is anxiety?

A

A feeling of unease (worry / fear) which can range from mild to severe

anxiety can be a normal response: in some cases it is beneficial

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2
Q

When can anxiety become a problem?

A

It can become problematic due to:
Its intensity : could be intermittent
The source : certain events or situations
Chronic or irrational

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3
Q

What are the symptoms of anxiety?

A
  • Social disturbances
  • Avoidance behaviours
  • Incessant worry
  • Concentration / memory problems
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4
Q

What are the 2 categories of anxiety symptoms?

A

Psychological - stress, apprehension etc.

Physiology - headaches, palpitations, nausea, GI problems etc.

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5
Q

Outline some causes of anxiety

A 
Past childhood experiences 
Diet (e.g. sugar + caffeine)
Physical / mental health (e.g. chronic conditions)
Genetics?
Drugs and medication (alcohol)
Everyday life and habits
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6
Q

How does alcohol cause anxiety?

A

Alcohol is a depressant and has a sedative effect, however these benefits are short lived
Subsequent neurotransmitter imbalance (e.g. GABA, glutamate) can lead to anxiety symptoms

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7
Q

What role does genetics play in anxiety?

A

Research has linked genetic factors to a number of anxiety disorders (e.g. panic disorder)
Genetic risk however is believed to moderate

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8
Q

Which gene is responsible for onset of anxiety?

A

=> anxiety disorders aren’t based on a single gene but likely have a complex genetic basis which can be affected by environmental factors.

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9
Q

What are the 2 categories of anxiety disorders?

A

There are 2 types:

  • Anxiety disorders
  • OC and related disorders
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10
Q

What are the anxiety disorders?

A
  • Generalised anxiety disorder (GAD)
  • Specific phobias - (e.g. Agoraphobia)
  • Social phobias- (e.g. Selective mutism )
  • Panic disorder
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11
Q

What are the different OC and related disorders?

A

Obsessive compulsive disorder (OCD)

Post traumatic stress disorder (PTSD)

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12
Q

What is generalised anxiety disorder?

A

GAD is characterised by an ongoing state of excessive anxiety lacking clear reason or focus
Excessive anxiety and worry occurring for ~6 months
Difficult to control and impairs daily activities

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13
Q

What are the symptoms associated with GAD?

A

Associated with >3/6 symptoms

  • Fatigue
  • Restlessness
  • Increased muscle aches / soreness
  • Impaired concentration
  • Irritability
  • Difficulty sleeping
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14
Q

Why is GAD difficult to diagnose?

A

GAD sufferers symptoms likely to be different from another person’s experience with GAD

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15
Q

What are specific phobias?

A

These are extreme fears or anxieties provoked by exposure to a particular situation / object, often leading to avoidance behaviours

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16
Q

Name some phobias

A 
irrational 
- Ornithophobic - fear of birds
- Vertigo 
- Podophobia - fear of feet 
- Acrophobia - fear of heights 
- Agoraphobia - fear of an environment; No means of 
  escape
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17
Q

What are social phobias?

A

Social phobias are characterised by significant anxiety provoked by exposure to certain types of social (e.g. social gatherings) or performance (e.g. public speaking) situations

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18
Q

What is selective mutism?

A

> Form of social phobia
It is a severe anxiety disorder where a person is unable to speak in certain social situations, e,g, with classmates at school or to relatives they don’t see very often

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19
Q

What is Obsessive compulsive disorder?

A

Also known as OCD, characterised by compulsive, ritualistic behaviour driven by irrational anxiety

  • A problem when it becomes debilitating
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20
Q

What are obsessions?

A

recurrent, intrusive thoughts, images, ideas or impulses

e.g. checking windows are closed, gas is off

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21
Q

What are compulsions?

A

repetitive behaviours or mental acts that are performed to reduce anxiety associated with the obsessions
(e.g. avoiding cracks in pavements)

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22
Q

What is post traumatic stress disorder?

A

Also known as PTSD, characterised by distress triggered by the recall of past traumatic experiences - can lead to flashbacks and nightmares

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23
Q

What is panic disorder?

A

Panic disorder is characterised by recurring panic attacks with no apparent trigger

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24
Q

What are panic attacks?

A

Panic attacks are sudden feelings of overwhelming fear with marked somatic symptoms (e.g. sweating, chest pains etc.)

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25
When do panic attacks occur?
Panic disorder ≠ panic attacks Panic attacks can occur spontaneously or can be a feature of another anxiety disorder
26
What causes a panic cycle?
Panic attacks Can mean you feel constantly afraid of having another panic attack, to the point that this fear itself can trigger another panic attack → panic cycle
27
What is the physiological explanation of stress disorders?
Hallmark of anxiety disorders is an inappropriate stress response either when a stressor is not present, or not immediately threatening
28
What regulates the stress pathway?
The stress response is regulated by HPA (hypothalamic-pituitary-adrenal) axis.
29
How does the HPA axis lead to stress?
HPA leads to release of cortisol (glucocorticoid) | Cortisol contributes to the body’s physiological response to stress
30
What role does the amygdala play in the stress response?
Amygdala - role in emotion and fear response Stimulates HPA axis to promote cortisol release Amygdala hyperactivity linked to anxiety disorders
31
How does the hippocampus contribute to stress?
Hippocampus - role in learning and memory Suppresses HPA axis to prevent excessive cortisol release Hippocampus underactivity linked to anxiety disorders
32
Outline the physiological changes causing stress response
Amygdala hyperactivity , Hippocampus underactivity ⇒ increased Cortisol release into HPA ⇒ Increased stress and anxiety
33
How does hippocampal degeneration lead to anxiety?
Continuous exposure to cortisol (e.g. periods of chronic stress) can cause neuronal degeneration in the hippocampus Sets off a vicious cycle in which stress response becomes more pronounced, leading to greater cortisol release and more hippocampal damage E.g. there is a decrease in hippocampal volume in some people who suffer from PTSD
34
What are the different anxiolytic drugs?
``` GABAa Receptor Modulators - Benzodiazepines - Barbiturates 5-HT1A receptor agonists ꞵ-Adrenoceptor antagonists Antihistamines ```
35
What is the significance of the GABAa receptor in anxiety?
A key target of anxiolytics (and hypnotics) | Ligand gated cl- channel causes hyperpolarisation (membrane potential more -ve than resting potential)
36
Describe the structure of the GABAa receptor
GABAa is a pentameric structure | 2𝛼 2ꞵ γ configuration most common
37
Describe GABA neurotransmission
1. GABA released from presynaptic terminal via exocytosis | 2. Reuptake to presynaptic neuron via GAT
38
Where on the GABAa receptor do agonists/antagonists bind?
Agonists / antagonists e.g. GABA binds between the 𝛼 and ꞵ (alpha and beta)
39
Where on the GABAa receptor do benzodiazepines bind?
Senzodiazephine binding site between 𝛼 and γ subunits
40
Where do barbiturates bind on GABAa receptors?
Barbiturates bind between the ꞵ and γ subunits | Positive allosteric modulators (PAM) - binds a different site to the endogenous agonist (GABA)
41
What are barbiturates?
A class of GABAa allosteric modulators - no longer recommended as anxiolytics (or hypnotics) but may still be used for epilepsy, general anesthesia and capital punishment (e.g. phenobarbitoil)
42
What effect do barbiturates have on GABAa receptors?
Barbiturates increase activity of GABAa receptors - binding increases channel opening beyond that seen with GABA alone These have a severe depressant effect on the CNS
43
What is the drawback of using barbiturates?
Barbiturates have other actions on other receptors at high doses (‘dirty compounds’) Increased inhibition, decreased excitation
44
What other receptors do barbiturates induce effects on
- ↑↑↑[ ] direct GABAa agonist - Glycine receptor - also stabilises open channel - nAChR an 5-HT3 receptor blockade - AMPA/kainate receptor blockade - Blockade of Ca2+dependent neurotransmitter release
45
What are benzodiazepines?
``` A class of GABAa modulators - most widely used class of anxiolytics (and hypnotics) PAM - binds to a distinct regulatory site on GABAa receptors ```
46
What effect do benzodiazepines have on GABAa receptors?
Benzodiazepines stabilise the GABAa receptor binding site for GABA in the open configuration - increases GABA affinity for its binding site and produces a general enhancement of its neuro-inhibitory actions
47
Why are benzodiazepines favoured over barbiturates?
Increasing inhibitory drive alleviates anxiety symptoms Benzodiazepines are ‘cleaner’ compounds - much more specific to the GABAa receptors, compared to barbiturates which act on a variety of different receptors
48
How are benzodiazepines chosen for patients?
benzodiazepine choice is made based upon duration of action (½ life of drug)
49
Name short acting benzodiazepines
Midazolam, Temazepam and Lorazepam are short-action agents. These are prefered as hypnotics to avoid sedative actions throughout the day
50
What is the down side of anxiolytics such as benzodiazepine and barbiturates?
Both drug classes are associated with tolerance and withdrawal symptoms
51
Why are BZDs administered to combat anxiety?
Anxiety patients show an imbalance in excitatory (glutamate) and inhibitory neurotransmitter (GABA) Therefore patients may be administered BZDs/ barbiturates - increasing GABA inhibitory drive ⇒ balance is restored
52
How is tolerance developed for BZDs?
However overtime patients can develop tolerance to BZDs - extra glutamate receptors are trafficked to plasma membrane to restore symptomatic balance seen prior to BZD administration - body isn’t used to balance
53
How do patients try to overcome tolerance of BZDs
Increased excitatory neurotransmission - patient requires larger dose of BZDs to combat this
54
Outline why patients using BZDs for long periods experience withdrawal symptoms
Excessive excitatory neurotransmission Unpleasant withdrawal > lack of pleasurable effect Previous symptoms are exacerbated due to neuroadaptations Long term anxiety states should not be treated with BZDs - SSRIs first choice for GAD
55
How are serotonin agonists used to treat anxiety?
5-HT₁ₐ receptor agonists (e.g. buspirone) are a class of drugs primarily used to treat anxiety - less tolerance and withdrawal symptoms compared to BZDs
56
Which 5-HT1a agonist is used to treat GAD?
Buspirone most commonly administered 5-HT₁ₐ agonist for GAD
57
How does the CNS initially respond to buspirone?
Activates presynaptic 5-HT₁ₐ autoinhibitory receptors - inhibiting 5-HT₁ₐ serotonin release - can worsen anxiety symptoms Also reduces the activity of noradrenergic neurons and decreases arousal - doesn’t induce sleep Delay of several days before clinical effects are seen
58
What are the long term effects of buspirone?
However, if buspirone is taken over a period of time (e.g. weeks), it can induce desensitisation of autoinhibitory 5-HT1A receptors - leads to downregulation of 5-HT1A receptors on the presynaptic plasma membrane.
59
Outline how buspirone treats anxiety symptoms
Desensitisation and downregulation of 5-HT1A receptors ⇒heightened excitation of serotonergic neurons and enhanced 5-HT release, which can suppress the symptoms of anxiety in some patients.
60
How do SSRIs affect 5-HT levels?
Selective serotonin reuptake inhibitors (SSRIs) inhibit reuptake of 5-HT via serotonin transporter (SERT)
61
How do SSRIs treat anxiety?
SSRIs use leads to increased 5-HT availability If SSRIs are taken over a period of time (e.g. weeks), SSRIs can induce desensitisation of autoinhibitory 5-HT1A receptors - this can lead to downregulation of 5-HT1A receptors on the pre-synaptic plasma membrane. SSRIs can also lead to downregulation of 5-HT receptors on the postsynaptic plasma membrane
62
What is the net effect of 5-HT1A agonists?
Overall, there is an increase in 5-HT neurotransmission (via fewer autoinhibitory 5-HT1A receptors and inhibiting the re-uptake of 5-HT) decrease in 5-HT neurotransmission (via fewer post-synaptic 5-HT receptors). On the balance of these changes, there is an overall increase in 5-HT neurotransmission, which can suppress the symptoms of anxiety in some patients.
63
What effect do beta adrenoceptors antagonists have on anxiety patients?
𝝱-Adrenoceptors Antagonists reduce some peripheral manifestations of anxiety (e.g. tremor, sweating, tachycardia, diarrhoea etc.) However there is no effect on the central CNS affective component

Neurology (20 decks)

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