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Flashcards in Anxiety and Depression Deck (37)
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1
Q

Define anxiety disorder.

A

An anxiety disorder is an inappropriate or excessive anticipatory manifestation of the fear response.

2
Q

List 4 responses typical of anxiety disorders.

A

Responses of anxiety disorders include:

1 - Defensive behaviours.

2 - Autonomic reflexes.

3 - Corticosteroid secretions.

4 - Negative emotions.

3
Q

List 3 types of anxiety disorder.

A

Types of anxiety disorder include:

1 - General anxiety disorder.

2 - Phobic anxiety.

3 - Panic disorder.

4
Q

Which endocrine axis is involved in the stress response?

Describe this axis.

List 2 conditions in which this axis is impaired.

A
  • The hypothalamic-pituitary-adrenal axis is involved in the stress response:

1 - The paraventricular nucleus of the hypothalamus releases corticotropin-releasing factor (CRF) to stimulate the anterior pituitary.

2 - The anterior pituitary releases adrenocorticotropic hormone (ACTH) to stimulate the adrenal gland.

3 - The adrenal gland produces cortisol, which has an inhibitory effect (negative feedback) on the hypothalamus.

  • This axis is impaired in anxiety and depression (it’s in the name of the deck duh).
5
Q

What is the source of input to the hypothalamus to trigger the hypothalamic-pituitary-adrenal axis in response to stress?

A

The limbic system triggers the HPA axis in response to stress:

  • The cortex sends information to the amygdala and hippocampus.
  • The amygdala has an excitatory effect on the hypothalamus (triggers the stress response).
  • The hippocampus has an inhibitory effect on the hypothalamus (prevents the stress response).
  • Remember this circuit is known as the Papez circuit.
6
Q

List 2 physiological abnormalities in the stress response in individuals suffering from anxiety disorders and major depressive disorder.

A

1 - Cortisol loses its inhibitory effect at the hypothalamus.

2 - Neuroplastic changes in the Papez circuit that precedes the hypothalamus, resulting in a loss of inhibition or increased excitation.

7
Q

List 3 treatments of anxiety disorders.

A

1 - Psychological, e.g. CBT.

2 - Prescribed medications.

3 - Self-medication (alcohol, cannabis etc.).

8
Q

Give an example of a potential mechanism for psychological treatments for anxiety disorders.

A

Psychological treatments might reverse neuroplastic changes in the Papez circuit.

9
Q

List 2 factors that determine the choice of anxiolytic drugs (drugs for treating anxiety disorders).

A

1 - Nature of predominant symptoms.

2 - Duration of treatment needed.

10
Q

List 3 anxiolytic drug classes.

A

1 - Beta antagonists.

2 - Benzodiazepines.

3 - Monoaminergic drugs.

11
Q

Describe the mechanism of action of beta antagonists for the treatment of anxiety disorders.

For which type of anxiety disorder are they most useful?

A
  • Beta antagonists reduce somatic symptoms, e.g. by reducing heart rate.
  • They are most useful for phobic anxiety disorders, as they can be taken in preparation or in response to a particular stressor in the medium-short term.
12
Q

Give an example of an effect of benzodiazepines other than anxiolysis.

A

Benzodiazepines are hypnotic (sleep-inducing) as well as anxiolytic.

13
Q

Briefly describe the mechanism of action of benzodiazepines.

A

Benzodiazepines bind to benzodiazepine allosteric sites on GABA receptors to enhance the action of GABA, increasing Cl- influx upon GABA binding.

14
Q

List 2 structures of the limbic system that are affected by benzodiazepines.

A

1 - Prefrontal cortex.

2 - Amygdala.

*GABA receptors are ubiquitous in the brain so benzodiazepines aren’t specific to the limbic system.

15
Q

What is the combined effect of benzodiazepines and alcohol?

A

The combined effect of benzodiazepines and alcohol is respiratory depression.

16
Q

What is the recommended duration of benzodiazepine use?

A

The recommended duration of benzodiazepine use is <4 weeks.

17
Q

List 5 effects of benzodiazepine withdrawal.

A

Effects of benzodiazepine withdrawal include:

1 - Anxiety.

2 - Tremor.

3 - Seizure.

4 - insomnia.

5 - Depression.

18
Q

List 3 benzodiazepines.

A

Examples of benzodiazepines:

1 - Diazepam.

2 - Nitrazepam.

3 - Midazolam.

19
Q

Give an example of a monoaminergic drug class.

List 4 drugs within this class.

A
  • Serotonin-selective reuptake inhibitors (SSRIs) are an example of a monoaminergic drug class. They include:

1 - Fluoxetine.

2 - Paroxetine.

3 - Sertraline.

4 - Citalopram.

*These drugs are also used to treat depression.

20
Q

Give an example of a monoaminergic drug that is not a serotonin-selective reuptake inhibitor (SSRI).

What is the mechanism of action for this drug?

A
  • Buspirone is a monoaminergic drug that is not classed as an SSRI.
  • The mechanism of action is unknown.
21
Q

List 4 symptoms of major depressive disorder.

A

1 - Misery.

2 - Loss of motivation.

3 - Loss of appetite.

4 - Suicidal thoughts.

22
Q

What proportion of cases of major depressive order is reactive (to some stimulus) and what proportion is endogenous?

A
  • 75% of cases of major depressive disorder are reactive.

- 25% are endogenous.

23
Q

What is the monoamine theory of depression?

A

The monoamine theory of depression suggests that depression is due to hypoactivity at monoaminergic synapses in the brain.

24
Q

List 3 treatments for depression.

A

1 - Antidepressant drugs (monoaminergic drugs).

2 - Psychotherapy (as with anxiety).

3 - Electroconvulsive therapy (inducing currents in the brain to induce a brief seizure).

25
Q

What is the physiological effect of antidepressant drugs?

How long do antidepressant drugs take to work?

A
  • Antidepressant drugs rapidly increase monoamines in the brain.
  • Despite this, the drugs take 1-3 weeks to have an effect on symptoms.
26
Q

List the classes of antidepressant drugs.

List the classes in order of side effect intensity from strongest to weakest.

A

1 - Selective serotonin reuptake inhibitors (SSRIs).

2 - Tricyclic antidepressants (TCAs).

3 - Monoamine oxidase inhibitors (MAOIs).

27
Q

List 3 side effects of selective serotonin reuptake inhibitors (SSRIs).

A

1 - GI symptoms (nausea / vomiting).

2 - Weight changes.

3 - Suicidal thoughts.

28
Q

Give an example of a monoamine oxidase inhibitor (MAOI).

A

Moclobemide.

29
Q

Which type of monoamine oxidase enzyme is targeted by moclobemide?

Why is this advantageous?

How strongly does moclobemide bind to monoamine oxidase?

A
  • Moclobemide selectively binds to monoamine oxidase-A.
  • This is advantageous because MAO-A handles serotonin in particular.
  • Moclobemide binds reversibly to the enzyme.
30
Q

List 3 side effects of monoamine oxidase inhibitors (MAOIs).

A

1 - Cheese reaction, e.g. increased blood pressure (due to unmetabolised tyramine from cheese, red wine and yeast extracts displaces noradrenaline out of sympathetic neurones as a result of monoamine buildup).

2 - Antimuscarinic effects.

3 - Alpha 1 receptor antagonism.

31
Q

Give an example of a tricyclic antidepressant.

A

Amitriptyline.

32
Q

Briefly describe the mechanism of action of tricyclic antidepressants.

A

Tricyclic antidepressants inhibit the reuptake of both serotonin and noradrenaline.

33
Q

List 2 side effects of tricyclic antidepressants.

A

1 - Antimuscarinic effects.

2 - Sedation (due to H1 receptor antagonism - remember histamine has a role in sleep).

34
Q

Give an example of a newer antidepressant drug.

Briefly describe the mechanism of action of this drug.

A
  • Agomelatine is a new antidepressant drug.

- It is a melatonin receptor agonist which adjusts the circadian rhythm.

35
Q

Describe the network hypothesis of depression.

A
  • The network hypothesis of depression suggests that hyperactivity and sensitisation of the neuroendocrine stress response (HPA axis) due to chronic stress is the cause of depression.
  • It also suggests that depression is an exacerbated form of the impaired neuroendocrine stress response seen in anxiety.
36
Q

How is the network hypothesis of depression explained by changes in the neuroendocrine stress response (HPA axis)?

A

1 - Chronically high levels of cortisol act on the hippocampus (rather than on the hypothalamus directly) to exert an inhibitory effect on the hypothalamus, where there are many cortisol receptors.

2 - Chronic stimulation of cortisol receptors reduces the number of the receptors in the hippocampus.

3 - Chronic stimulation of cortisol receptors also reduces brain-derived neurotrophic factor, which is important for synapse maintenance.

4 - Chronic stimulation of cortisol decreases potential for neurogenesis and neuroplasticity.

37
Q

How might the network hypothesis of depression explain the 1-3 week latency for antidepressant drugs?

A
  • The reduction in neurogenesis and neuroplasticity at the hippocampus is antagonised by the increase in monoamines caused by antidepressant drugs.
  • This means that antidepressant drugs restore neuronal networks by restoring neurogenesis and neuroplasticity, which takes 1-3 weeks.