Anxiety and Depression Flashcards

1
Q

Can mental health be defined?

A

Mental health is hard to define as human behaviour is highly variable, both within and between individuals

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2
Q

What influences human emotions?

A

Biological and cultural factors can influence human emotions and how they’re interpreted.

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3
Q

What is the DSM-5?

A

A group of mental health conditions that tries to describe a range of signs and symptoms to help diagnose.

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4
Q

What types of conditions are included in the DSM-5?

A

Anxiety Disorders, Major depressive disorder/Depression, Bipolar Disorder.

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5
Q

What is true about the neurological basis of these conditions?

A

It is incompletely understood and often inferred by understanding the mechanism of action of useful drug therapies.

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6
Q

Define anxiety disorder.

A

An inappropriate, or excessive, anticipatory manifestation of the fear response, often to a stressor.

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7
Q

What is the difference between a normal fear response and that in an anxiety disorder?

A

In an anxiety disorder, the fear response is anticipatory and can occur without the stressor actually being present.

“For understanding: The response is to the stressor but the stressor is not present.”

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8
Q

What may you expect in a fear response in an anxiety disorder?

A

Defensive behaviours, autonomic reflexes, corticosteroid secretions, and negative emotions.

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9
Q

What are the types of anxiety disorders?

A

Multiple types exist, including General anxiety disorder, Phobic anxiety, and Panic Disorder.

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10
Q

How do we move from normal to pathological anxiety?

A

Understanding normal anxiety and brain involvement is crucial, particularly the role of the hypothalamus.

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11
Q

What is the relationship of the hypothalamus to stress?

A

The hypothalamus is involved in the neuroendocrine response to stress via the HPA axis.

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12
Q

Describe the normal response to a stressor.

A

Activation of the Paraventricular nucleus in the hypothalamus leads to cortisol production, which negatively feedbacks to reduce its own production.

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13
Q

Describe the anxiety disorder response to a stressor.

A

The system can be activated without the presence of an external stressor, leading to increased cortisol and impaired negative feedback.

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14
Q

What triggers the hypothalamus in anxiety disorders?

A

Structures in the limbic system, such as the neocortex, amygdala, and hippocampus, can activate the hypothalamus in the absence of a stressor.

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15
Q

What are different methods to treat anxiety disorders?

A

Self-help, psychological methods (e.g., CBT), and pharmacological treatments.

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16
Q

What links the different methods of treating anxiety disorders?

A

Positive intervention across these methods often reverses the neuroplastic process that led to the anxiety disorder.

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17
Q

What are anxiolytic drugs?

A

Drugs used for pharmacological treatment of anxiety disorders.

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18
Q

What factors decide which drug to give for anxiety?

A

The nature of the predominant systems and the duration of treatment needed.

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19
Q

What are the three types of anxiolytic drugs?

A

B-adrenoreceptor antagonists (beta blockers), benzodiazepines, and monoaminergic drugs.

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20
Q

What are B-adrenoreceptor antagonists used for?

A

They reduce somatic symptoms due to elevated adrenaline and are used for situation phobias.

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21
Q

What drugs are often used in the short term for anxiety?

A

Benzodiazepines such as diazepam and nitrazepam, which have anxiolytic and hypnotic effects.

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22
Q

What is the mechanism of action of benzodiazepines?

A

They enhance GABAergic transmission by binding to an allosteric site on the GABA A receptor.

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23
Q

Where in the brain do benzodiazepines act?

A

Critical areas of the limbic system, such as the pre-frontal cortex and amygdala.

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24
Q

What are the side effects of benzodiazepines?

A

Sedation and acute overdose, which can lead to profound sedation and respiratory depression when combined with alcohol.

25
Why are benzodiazepines not used long-term?
Due to tolerance, dependence, and withdrawal symptoms.
26
What are monoaminergic drugs?
They can be antidepressant drugs, such as serotonin-selective reuptake inhibitors (SSRIs).
27
Is major depressive disorder (MDD) common?
Yes, 20% of individuals experience it during their lifetime.
28
What are the symptoms of MDD?
Misery, despair, loss of motivation, appetite changes, and suicidal thoughts.
29
What are the general causes of depression?
Reactive depression (75%) and endogenous depression (25%).
30
What is the monoamine theory of depression?
Depression is due to hypoactivity at monoaminergic synapses in the brain.
31
What evidence supports the monoamine theory of depression?
Antidepressants increase levels of monoamines in the brain rapidly.
32
What evidence contradicts the monoamine theory of depression?
Antidepressants take 1-3 weeks to work, suggesting a more complex neurobiology.
33
What are the treatments for MDD?
Psychotherapy, antidepressant drugs, and electroconvulsive therapy (ECT).
34
What are the classes of antidepressant drugs?
SSRIs, tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), and newer antidepressants.
35
What does drug choice for a patient depend on?
Efficacy and side effect profiles.
36
What are examples of SSRIs and their mechanism of action?
Examples include Fluoxetine, Paroxetine, and Sertraline. They elevate intrasynaptic levels of monoamines by reducing reuptake.
37
What are the unwanted side effects of SSRIs?
GI issues, weight changes, and suicidal thoughts.
38
What is the mechanism of action of tricyclic antidepressants?
They inhibit the reuptake of serotonin and norepinephrine.
39
What are the unwanted side effects of tricyclic antidepressants?
Anti-muscarinic effects and sedation.
40
What is the mechanism of action of newer antidepressant drugs?
They have various uptake/receptor mediated effects for 5-HT, NA, and dopamine.
41
Do antidepressant drugs actually work?
30% of patients may not respond at all, indicating the complexity of neurobiology in depression.
42
What is the new theory for depression: network hypothesis?
In MDD, there's an increase in CRF and cortisol, which is reversed by successful antidepressant treatment.
43
What is pharmacogenomics?
Pharmacogenomics is the study of how genes affect a person's response to drugs.
44
What does the neurobiology underpinning depression indicate?
The neurobiology underpinning depression is complex and variable.
45
What is the new theory for depression?
The new theory for depression is the network hypothesis.
46
What changes occur in MDD related to cortisol?
In MDD, there's an increase in [CR-F] and [Cortisol], which is reversed by successful antidepressants.
47
What does the increase in cortisol suggest about depression?
It suggests hyperactivity/sensitisation of the neuroendocrine stress response as a cause of depression.
48
What may happen with continued ongoing stress?
Continued ongoing stress may initially result in anxiety, but chronic stress may lead to depression.
49
How does high chronic stress affect cortisol regulation?
High chronic stress affects the negative feedback regulating cortisol.
50
What are the effects of continually elevated cortisol on the hippocampus?
Continually elevated cortisol negatively affects activity in the hippocampus.
51
What changes occur in neurons in the hippocampus due to stress?
Neurons show down regulation of glucocorticoid receptor expression and less BDNF, leading to decreased neurogenesis and neuroplasticity.
52
Why is neurogenesis important for the hippocampus?
Neurogenesis is important for normal hippocampal function, and its reduction due to elevated cortisol may affect emotional state.
53
How do antidepressants affect neurogenesis?
Antidepressants increase monoamine input to the hippocampus, resulting in increased neurogenesis and plasticity.
54
What is the significance of neurogenesis and plasticity in treating MDD?
Neurogenesis and plasticity are key for effective antidepressant treatment, restoring neuronal networks to their functioning prior to depression.
55
Why might there be a latency to clinical effect with antidepressants?
There may be a latency because it takes time for plastic effects and the birth of new neurons to integrate into circuits.
56
What future developments are required in depression treatment?
Linking monoamines and neuro-endocrine dysfunction is important for future developments.
57
What roles need increased understanding for better interventions?
Increased understanding of neuroplasticity, neurogenesis, and BDNF is required.
58
How might this understanding improve treatment?
It might lead to better pharmacological interventions and explain the effectiveness of non-pharmacological interventions like psychotherapy.