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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
Q

When do panic attacks occur?

A

Panic disorder ≠ panic attacks

Panic attacks can occur spontaneously or can be a feature of another anxiety disorder

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26
Q

What causes a panic cycle?

A

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
Q

What is the physiological explanation of stress disorders?

A

Hallmark of anxiety disorders is an inappropriate stress response either when a stressor is not present, or not immediately threatening

28
Q

What regulates the stress pathway?

A

The stress response is regulated by HPA (hypothalamic-pituitary-adrenal) axis.

29
Q

How does the HPA axis lead to stress?

A

HPA leads to release of cortisol (glucocorticoid)

Cortisol contributes to the body’s physiological response to stress

30
Q

What role does the amygdala play in the stress response?

A

Amygdala - role in emotion and fear response

Stimulates HPA axis to promote cortisol release
Amygdala hyperactivity linked to anxiety disorders

31
Q

How does the hippocampus contribute to stress?

A

Hippocampus - role in learning and memory

Suppresses HPA axis to prevent excessive cortisol release
Hippocampus underactivity linked to anxiety disorders

32
Q

Outline the physiological changes causing stress response

A

Amygdala hyperactivity , Hippocampus underactivity
⇒ increased Cortisol release into HPA
⇒ Increased stress and anxiety

33
Q

How does hippocampal degeneration lead to anxiety?

A

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
Q

What are the different anxiolytic drugs?

A 
GABAa Receptor Modulators  
- Benzodiazepines
- Barbiturates
5-HT1A receptor agonists 
ꞵ-Adrenoceptor antagonists 
Antihistamines
35
Q

What is the significance of the GABAa receptor in anxiety?

A

A key target of anxiolytics (and hypnotics)

Ligand gated cl- channel causes hyperpolarisation (membrane potential more -ve than resting potential)

36
Q

Describe the structure of the GABAa receptor

A

GABAa is a pentameric structure

2𝛼 2ꞵ γ configuration most common

37
Q

Describe GABA neurotransmission

A
  1. GABA released from presynaptic terminal via exocytosis

2. Reuptake to presynaptic neuron via GAT

38
Q

Where on the GABAa receptor do agonists/antagonists bind?

A

Agonists / antagonists e.g. GABA binds between the 𝛼 and ꞵ (alpha and beta)

39
Q

Where on the GABAa receptor do benzodiazepines bind?

A

Senzodiazephine binding site between 𝛼 and γ subunits

40
Q

Where do barbiturates bind on GABAa receptors?

A

Barbiturates bind between the ꞵ and γ subunits

Positive allosteric modulators (PAM) - binds a different site to the endogenous agonist (GABA)

41
Q

What are barbiturates?

A

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
Q

What effect do barbiturates have on GABAa receptors?

A

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
Q

What is the drawback of using barbiturates?

A

Barbiturates have other actions on other receptors at high doses (‘dirty compounds’)
Increased inhibition, decreased excitation

44
Q

What other receptors do barbiturates induce effects on

A
  • ↑↑↑[ ] 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
Q

What are benzodiazepines?

A 
A class of GABAa modulators - most widely used class of anxiolytics (and hypnotics)
PAM - binds to a distinct regulatory site on GABAa receptors
46
Q

What effect do benzodiazepines have on GABAa receptors?

A

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
Q

Why are benzodiazepines favoured over barbiturates?

A

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
Q

How are benzodiazepines chosen for patients?

A

benzodiazepine choice is made based upon duration of action (½ life of drug)

49
Q

Name short acting benzodiazepines

A

Midazolam, Temazepam and Lorazepam are short-action agents. These are prefered as hypnotics to avoid sedative actions throughout the day

50
Q

What is the down side of anxiolytics such as benzodiazepine and barbiturates?

A

Both drug classes are associated with tolerance and withdrawal symptoms

51
Q

Why are BZDs administered to combat anxiety?

A

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
Q

How is tolerance developed for BZDs?

A

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
Q

How do patients try to overcome tolerance of BZDs

A

Increased excitatory neurotransmission - patient requires larger dose of BZDs to combat this

54
Q

Outline why patients using BZDs for long periods experience withdrawal symptoms

A

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
Q

How are serotonin agonists used to treat anxiety?

A

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
Q

Which 5-HT1a agonist is used to treat GAD?

A

Buspirone most commonly administered 5-HT₁ₐ agonist for GAD

57
Q

How does the CNS initially respond to buspirone?

A

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
Q

What are the long term effects of buspirone?

A

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
Q

Outline how buspirone treats anxiety symptoms

A

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
Q

How do SSRIs affect 5-HT levels?

A

Selective serotonin reuptake inhibitors (SSRIs) inhibit reuptake of 5-HT via serotonin transporter (SERT)

61
Q

How do SSRIs treat anxiety?

A

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
Q

What is the net effect of 5-HT1A agonists?

A

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
Q

What effect do beta adrenoceptors antagonists have on anxiety patients?

A

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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