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Anxiety Flashcards

1
Q

What is anxiety?

A

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

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2
Q

When does anxiety become a problems?

A

When the intensity changes from intermittent –> chronic

+ when source becomes irrational

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3
Q

What does anxiety lead to?

A

Social disturbances
Avoidance behaviours
Incessant worry
Concentration/memory problems

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4
Q

What can cause the symptoms of anxiety?

A

Difficult past/ childhood experiences

everyday life and habits - current issues or problems in every day can lead to anxiety

Diet - sugar and caffeine can trigger symptoms of anxiety

Physical and mental health can trigger or exacerbate anxiety

Drugs and medication - alcohol, recreational drugs and some prescribed medication can trigger anxiety

Genetics?

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5
Q

Expand on how alcohol can 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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6
Q

What does research show about genetics and anxiety?

A

Research has linked genetic factors to a number of anxiety disorders (e.g. panic disorder).

However, genetic risk is currently believed to be moderate.

Only clear result that can be derived from these studies is that anxiety disorders are not based on a single gene but likely have a complex genetic basis, which can be affected by environmental factors.

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7
Q

How are anxiety disorders classified?

A 
Anxiety disorders:
GAD 
Specific phobias (agoraphobia)
Social phobias (selective mutism)
Panic disorder

Obsessive- compulsive (and related disorders):
OCD
PTSD

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8
Q

What is GAD?

A

characterised by an ongoing state of excessive anxiety lacking clear reason or focus.

Excessive anxiety and worry occurring for at least six months, which is difficult to control and impairs activities of daily living.

Associated with three or more (of six) symptoms.

GAD sufferers symptoms likely to be different from another persons experience with GAD.

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9
Q

What are specific phobias?

A

Specific phobias are extreme fears or anxieties provoked by exposure to a particular situation or object – often leads to avoidance behaviours.

Agoraphobia
Acrophobia
Orthinophobia
Podophobia

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10
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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11
Q

What is selective mutism?

A

Selective mutism is a severe anxiety disorder where a person is unable to speak in certain social situations, such as with classmates at school or to relatives they do not see very often.

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12
Q

What is panic disorder?

A

Panic disorder is characterised by recurring panic attacks, without a seemingly clear cause or trigger.

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13
Q

What are panic attacks?

A

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

Panic attacks can occur spontaneously or be a feature of a number of anxiety disorders .

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14
Q

What is OCD?

A

Obsessive compulsive disorder (OCD) is characterised by compulsive, ritualistic behaviour driven by irrational anxiety.

Obsessions: Recurrent, intrusive thoughts, images, ideas or impulses.

Compulsions:
Repetitive behaviours or mental acts that are performed to reduce anxiety associated with the obsessions.

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15
Q

What is PTSD?

A

Post-traumatic stress disorder (PTSD) is characterised by distress triggered by the recall of past traumatic experiences – can lead to flashbacks and nightmares.

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16
Q

Expand on the pathophysiology of anxiety disorders.

A

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

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

HPA axis leads to the release of cortisol (a glucocorticoid).

Cortisol contributes to the body’s physiological response to stress.

17
Q

What is the role of the amygdala in the HPA axis?

A

Amygdala – role in emotion and fear response

Stimulates HPA axis (green) to promote cortisol release

Amygdala hyperactivity linked to anxiety disorders

18
Q

What is the role of the hippocampus in the HPA axis?

A

Hippocampus – role in learning and memory

Supresses HPA axis (red) to prevent excessive cortisol release

Hippocampus underactivity linked to anxiety disorders

19
Q

How does hippocampal degeneration link with anxiety?

A

e.g. PTSD

Continuous exposure to cortisol (e.g. during periods of chronic stress) can cause neuronal degeneration in the hippocampus.

Sets off a vicious cycle in which the stress response becomes more pronounced, leading to greater cortisol release and more hippocampal damage.

For example, there is a decrease in hippocampal volume in some people who suffer from PTSD.

20
Q

Give examples of anxiolytic drugs

A

GABA(A) receptor modulators:
Barbituates
benzodiazepines

5-HT(1A) receptor agonists

𝛽-Adrenoceptor antagonists

21
Q

Expand on the GABA(A) receptor as a key target for anxiolytics and hypnotics

A 
LGIC 
pentameric structure - 
Six α subtypes (α1 – α6)
Three β subtypes (β1-3)
Three γ subtypes (γ1-3)
Also δ ε π θ subunits
2α 2β γ most common configuration

Multiple binding sites:

  • Agonists/antagonists e.g. GABA
  • Benzodiazepine binding site
  • Channel blockers e.g. picrotoxin
  • Channel modulators e.g. GA
  • Allosteric modulators e.g. barbiturates
22
Q

How is GABA activity terminated?

A

Upon reuptake by GAT

23
Q

What are barbituates?

A

Barbiturates are a class of GABAA allosteric modulators – no longer recommended as anxiolytics (or hypnotics).

Barbiturates are positive allosteric modulators (PAMs).

Barbiturates increase the activity of GABAA receptors – binding increases channel opening beyond that seen with GABA alone.

Barbiturates are responsible for severe depressant effect on the CNS…

24
Q

What other actions do barbiturates have at high doses?

A

Increase[ ] direct GABAA agonist
Glycine receptor – also stabilises open channel
nAChR & 5-HT3 receptor blockade
AMPA/kainate receptor blockade
Blockade of Ca2+-dependent neurotransmitter release

increase inhibition, decrease excitation

25
Q

What may barbiturates still be used for?

A

Epilepsy
General Anaesthesia
Capital punishment

26
Q

Expand on benzodiazepines.

A

Benzodiazepines are a class of GABAA modulators – most widely used class of anxiolytics (and hypnotics).

Benzodiazepines bind to a distinct regulatory site 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 neuroinhibitory actions.

‘cleaner’ compounds compared to barbiturates

27
Q

How do you choose which benzodiazepine to use?

A

Benzodiazepine choice made based on duration of action (e.g. short-acting preferred as hypnotics to avoid sedation throughout day).

28
Q

What are barbiturates and benzodiazepines associated with?

A

Barbiturates and benzodiazepines are associated with tolerance and withdrawal symptoms.

29
Q

How do barbiturates and benzodiazepines induce withdrawal symptoms?

A

Symptomatic:
it’s been proposed that there’s an imbalance between GABA (inhibitory) and glutamate (excitatory) in anxiety disorders - GABA usuall low

In order to address this imbalance, a patient can be prescribed benzodiazepines (BZDs).
BZDs act as PAM (at the BZD binding site on the GABAA receptor) –> stabilise the GABAA receptor binding site for GABA in the open configuration–> increases GABA affinity for its binding site –> produces enhancement of GABA’s neuroinhibitory actions –> supress symptoms of anxiety in some patients.

Tolerance:
Over time, a patient can develop tolerance to BZDs. It has been proposed that this is due to trafficking of additional glutamate receptors to the cell membrane. This serves to restore the initial imbalance seen in the ”symptomatic” stage.

Patients therefore need to take a higher dose of BZDs to address this new imbalance between inhibitory and excitatory neurotransmission.

Withdrawal:
If a patient suddenly withdraws from taking these high doses of BZDs, there is a sudden decrease in inhibitory GABA neurotransmission. Coupled with increased excitatory glutamate neurotransmission, this can lead to the development of seizures.

30
Q

Expand on 5-HT receptor agonists

A

Metabotropic - GPCRs

Receptor 1A-F: Gi/o to inhibit AC
Receptor 2A-C: Gq to stimulate IP3 and DAG formation
Receptor 3: LGIC
Receptor 4: Gs to stimulate AC
Receptor 5A, 5B, 6, 7: Gs to stimulate AC by 6 & 7, 5 not established

31
Q

Expand on 5-HT1A receptors

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 the benzodiazepines.

Buspirone is the most commonly prescribed 5-HT1A agonist for generalised anxiety disorder (GAD).

Activates pre-synaptic 5-HT1A autoreceptors – this inhibits 5-HT release.

Also reduces activity of noradrenergic neurons and decreases arousal (but does not induce sleep).

Delay of several days before clinical effects are seen…

32
Q

How does buspirone work compared to SSRIs?

A

Buspirone is a 5-HT1A receptor agonist. Receptors are autoinhibitory therefore, buspirone initially inhibits 5-HT release.

However, if buspirone is taken over a period of time (e.g. weeks), buspirone can induce desensitisation of autoinhibitory 5-HT1A receptors –> downregulation of 5-HT1A receptors on the pre-synaptic plasma membrane –> heightened excitation of serotonergic neurons and enhanced 5-HT release –> suppress the symptoms of anxiety in some patients.

Selective serotonin re-uptake inhibitors (SSRIs) inhibit the re-uptake of 5-HT via the serotonin transporter (SERT) - this leads to an increase in 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. However, in addition, SSRIs can also lead to the downregulation of 5-HT receptors on the post-synaptic plasma membrane.

Overall, there is an increase in 5-HT neurotransmission (via fewer autoinhibitory 5-HT1A receptors and inhibiting the re-uptake of 5-HT) and a 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.

33
Q

Expand on the structure of adrenoceptors

A

Metabotropic - GPCR

Subtypes:
α1 couples to Gq proteins to activate phospholipase C
α2 couples to Gi/o and inhibits adenylate cyclase

β1 and β2 couple to Gs and activate adenylate cyclase

Signalling: NA
NERT
MAO

34
Q

What are the functions of beta-adrenoceptors?

A

β1
The heart: increases heart rate, impulse conduction, contraction and ejection fraction
Increases renin release by Juxtaglomerular cells

β2
Increases renin release by juxtaglomerular cells

35
Q

What are 𝛽-adrenoceptor antagonists?

A

𝛽-adrenoceptor antagonists (e.g. propranolol) are a class of drugs used to treat some symptoms of anxiety.

𝛽-adrenoceptor antagonists reduce some of the peripheral manifestations of anxiety (notably tremor, sweating, tachycardia and diarrhoea).
However, there is no effect on the central CNS affective component.

Accordingly, they find abuse in some sports (reduce tremor) and the performing arts (reduce stage fright).

Neuro (10 decks)

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