L15 - Biological basis of Anxiety and Depression

Question 1

What is the monoamine theory of depression?

Answer 1

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

Question 2

What are monoamines?

Answer 2

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

Question 3

How does reserpine support the monoamine theory of depression?

Answer 3

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

Question 4

What role does serotonin play in depression?

Answer 4

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

Low levels of serotonin are associated with depression

Question 5

What role does noradrenaline play in depression?

Answer 5

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

Question 6

What are monoamine oxidase inhibitors?

Answer 6

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

Question 7

What is the “cheese effect” associated with MAOIs?

Answer 7

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

Question 8

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

Answer 8

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

Question 9

How do tricyclic antidepressants work?

Answer 9

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

Question 10

What are the common side effects of tricyclic antidepressants?

Answer 10

Hypotension

Dry mouth

Blurred vision

Sedation

Potentially fatal cardiac effects

Question 11

How do SSRIs differ from tricyclics?

Answer 11

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

Question 12

What are the side effects of SSRIs?

Answer 12

Nausea

Sexual dysfunction

Sleep disruption

Initial anxiety or panic attacks

Question 13

What are SSNRIs (selective serotonergic/noradrenergic reuptake inhibitors)

Answer 13

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

Question 14

What are the main limitations of current antidepressants?

Answer 14

Delay in clincal effect (4-6 weeks)

Side effects

Limited effectiveness in some patients

Question 15

How do antidepressants compare to placebos?

Answer 15

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

Question 16

What is a potential risk of antidepressants in some patients?

Answer 16

Increased rates of suicide in certain individuals

Question 17

How does normal anxiety differ from anxiety disorders?

Answer 17

Normal anxiety - psychological response to stress

Anxiety disorders - excessive, irrational fear and disress

Question 18

what are the main types of anxiety disorders?

Answer 18

Generalised anxiety disorder (GAD)

Panic disorder

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

Question 19

What brain regions are involved in the stress response?

Answer 19

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

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

Question 20

How is the septo-hippocampal system implicated in anxiety?

Answer 20

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

Question 21

What types of antidepressants are used to treat anxiety disorders?

Answer 21

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

Question 22

How do benzodiazepines treat anxiety?

Answer 22

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

Question 23

Why are BZs less commonly used today?

Answer 23

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

Question 24

How are stress and depression linked?

Answer 24

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

Question 25

What is the comorbitidy rate of depression and anxiety disorders?

Answer 25

50-60%

Question 26

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

Answer 26

Dysregulation of the stress response system may underlie both conditions

Question 27

What's a major challenge for antidepressant drug development?

Answer 27

Creating drugs with faster onset action and fewer side effects

Question 28

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

Answer 28

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

Question 29

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

Answer 29

To restore normal neurotransmitter function while minimising side effects

Question 30

Why is early intervention important for anxiety disorders?

Answer 30

To prevent maladaptive behaviours and improve long-term outcomes

Question 31

How do MAOIs affect neurotransmitter levels?

Answer 31

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

Question 32

How do tricylic antidperessants increase neurotransmitter levels

Answer 32

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

Question 33

What is the mechanism of action of SSRIS?

Answer 33

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

Question 34

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

Answer 34

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

Question 35

How might antidepressants increase suicide risk?

Answer 35

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

Question 36

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

Answer 36

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

Question 37

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

Answer 37

The hippocampus inhibits the HPA axis to regulate stress responses. The amygdala activates the HPA axis, increasing stress responses.

Question 38

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

Answer 38

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

Question 39

How do benzodiazepines act on the septo-hippocampal system?

Answer 39

They enhance GABAergic inhibition, reducing anxiety.

Question 40

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

Answer 40

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

Question 41

Why is understanding comorbidity important for clinical management?

Answer 41

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