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PS2101 - Psychopathology > L15 - Biological basis of Anxiety and Depression > Flashcards

L15 - Biological basis of Anxiety and Depression Flashcards

1
Q

What is the monoamine theory of depression?

A

Depression is caused by a reduction in monoamine function, particularly serotonin and noradrenaline, in the brain

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2
Q

What are monoamines?

A

Monoamines include catecholamines (dopamine, noradrenaline) and indoleamines (serotonin)

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3
Q

How does reserpine support the monoamine theory of depression?

A

Reserpine depletes monoamine transmitters by preventing their storage, causing depression in some patients

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4
Q

What role does serotonin play in depression?

A

Involved in pain sensitivity, emotional regulation and response to negative events.

Low levels of serotonin are associated with depression

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5
Q

What role does noradrenaline play in depression?

A

May be involved in depression, but evidence for its reduction in depressed patients is inconsistent

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6
Q

What are monoamine oxidase inhibitors?

A

Drugs that block the enzyme monoamine oxidase increasing levels of monoamines like serotonin and noradrenaline

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7
Q

What is the “cheese effect” associated with MAOIs?

A

MAOIs can cause dangerous increases in blood pressure when foods containing tyramine (e.g., cheese, wine) are consumed

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8
Q

How do reversible inhibitors of MAO-A ( Reversible inhibitors of MAO-A) improve safety)

A

Reversible inhibitors of MAO-A (RIMAs) reduce the risk of the cheese effect by allowing tyramine to compete for enzyme binding

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9
Q

How do tricyclic antidepressants work?

A

They block the reuptake of serotonin and noradrenaline, increasing the levels in the synaptic cleft

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10
Q

What are the common side effects of tricyclic antidepressants?

A

Hypotension

Dry mouth

Blurred vision

Sedation

Potentially fatal cardiac effects

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11
Q

How do SSRIs differ from tricyclics?

A

SSRIs selectively block serotonin reuptake with fewer side effects and lower overdoes risl

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12
Q

What are the side effects of SSRIs?

A

Nausea

Sexual dysfunction

Sleep disruption

Initial anxiety or panic attacks

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13
Q

What are SSNRIs (selective serotonergic/noradrenergic reuptake inhibitors)

A

Drugs that block the reuptake of both serotonin and noradrenaline –> offering dual-action treatment

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14
Q

What are the main limitations of current antidepressants?

A

Delay in clincal effect (4-6 weeks)

Side effects

Limited effectiveness in some patients

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15
Q

How do antidepressants compare to placebos?

A

Some studies show antidepressants aren’t significantly more effective than placebos in mild to moderate depression

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16
Q

What is a potential risk of antidepressants in some patients?

A

Increased rates of suicide in certain individuals

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17
Q

How does normal anxiety differ from anxiety disorders?

A

Normal anxiety - psychological response to stress

Anxiety disorders - excessive, irrational fear and disress

18
Q

what are the main types of anxiety disorders?

A

Generalised anxiety disorder (GAD)

Panic disorder

Phobias (social, agoraphobia specific object, OCD and PTSD)

19
Q

What brain regions are involved in the stress response?

A

The hypothalamus, pituitary gland and adrenal glands (HPA axis)

Modulated by the hippocampus (inhibitory) and amygdala (excitatory)

20
Q

How is the septo-hippocampal system implicated in anxiety?

A

It involves high-density benzodiazepine binding and major serotonergic and noradrenergic inputs, playing in role in the regulation of anxiety

21
Q

What types of antidepressants are used to treat anxiety disorders?

A

SSRIs and SSNRIs –> used at higher doses than for depression

22
Q

How do benzodiazepines treat anxiety?

A

By enhancing GABAergic inhibition, reducing neural excitability and breaking the cycle of anxiety

23
Q

Why are BZs less commonly used today?

A

Due to risks of dependence and sedation, and because antidepressants offer a more targeted treatment for anxiety disorders

24
Q

How are stress and depression linked?

A

Through abnormal brain responses e.g., stress-diathesis model

25
Q

What is the comorbitidy rate of depression and anxiety disorders?

A

50-60%

26
Q

How does abnormal HPA axis function relate to depression and anxiety?

A

Dysregulation of the stress response system may underlie both conditions

27
Q

What’s a major challenge for antidepressant drug development?

A

Creating drugs with faster onset action and fewer side effects

28
Q

What’s the potential advantage of combining antidepressants with anxiolytics?

A

It may address both the emotional and physiological symptoms of comorbid conditions

29
Q

What is the primary goal of treatment for depression and anxiety?

A

To restore normal neurotransmitter function while minimising side effects

30
Q

Why is early intervention important for anxiety disorders?

A

To prevent maladaptive behaviours and improve long-term outcomes

31
Q

How do MAOIs affect neurotransmitter levels?

A

MAOIs block monoamine oxidase, preventing the breakdown of monoamines like serotonin and noradrenaline, increasing their levels

32
Q

How do tricylic antidperessants increase neurotransmitter levels

A

They block the reuptake of serotonin and noradrenaline –> prolonging their presence in the synaptic cleft

33
Q

What is the mechanism of action of SSRIS?

A

SSRIS selectively block serotonin reuptake, increasing its avaliability in the synaptic cleft

34
Q

How do reversible inhibitors of MAO-A (RIMAs) differ from traditional MAOIs?

A

RIMAs temporarily inhibit MAO-A and allow tyramine to compete for binding, reducing the risk of the “cheese effect.”

35
Q

How might antidepressants increase suicide risk?

A

By increasing energy and motivation before mood improves, they may lead to increased impulsivity in some patients.

36
Q

What is the role of the HPA axis in stress response?

A

The HPA axis coordinates the release of cortisol from the adrenal glands in response to stress.

37
Q

How does the hippocampus and the amygdala influence the HPA axis?

A

The hippocampus inhibits the HPA axis to regulate stress responses.

The amygdala activates the HPA axis, increasing stress responses.

38
Q

What role does the septo-hippocampal system play in anxiety?

A

It integrates noradrenergic and serotonergic inputs, modulating anxiety through GABAergic inhibition

39
Q

How do benzodiazepines act on the septo-hippocampal system?

A

They enhance GABAergic inhibition, reducing anxiety.

40
Q

What does the high comorbidity of depression and anxiety suggest about their treatment?

A

Treatments targeting both conditions, such as SSRIs, may be more effective.

41
Q

Why is understanding comorbidity important for clinical management?

A

It helps clinicians address overlapping symptoms and choose appropriate treatment strategies.

PS2101 - Psychopathology (22 decks)

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