Week 1 - Mental health Flashcards

1
Q

What is mental health?

A

A person’s condition with regard to their psychological and emotional well-being.

A state of wellbeing in which an individual realises his or her own abilities, can cope with the normal stresses of life, can work productively and is able to make a contribution to his or her own community, more than just the absence of mental disorders or disabilities.

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2
Q

Depression definition

A

A mood disorder characterised by a persistently low mood, feelings of sadness and loss of interest… that can affect a person’s thoughts, behaviours, feelings and sense of wellbeing.

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3
Q

What are the functions of dopamine?

A

Pleasure, motivation, reward, mood, motor control, sexual function.

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4
Q

What are the functions of serotonin?

A

Mood, appetite, emotion, arousal/wakefulness, body temperature and sleep.

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5
Q

What are the three things that can happen to serotonin in the synapse?

A

Binds to 5-HTR (serotonin receptor) on the post-synaptic neuron.
Broken down by MAO (monoamine oxidase) enzymes - reduced availability within the synaptic cleft.
Taken back up into the pre-synaptic neuron by SERT (serotonin reuptake transporter)

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6
Q

What is the pathway of serotonin production and transportation?

A
  1. Tryptophan is converted to 5HT (serotonin)
  2. 5HT is packaged into vesicles
  3. Released into the synaptic cleft

Presynaptic receptors are inhibitory to form a negative feedback loop so there is not overstimulation of the system - keeps the mood stable.

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7
Q

Monoamine hypothesis of depression

A

Deficiency in the amount or function of neurotransmitters in the CNS.
Overactive MAO enzyme - increased degradation.
Depression is due to a deficit in monoamine transmission - either from reduced production or increased degradation.

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8
Q

What are the three hypotheses of causes of depression?

A

Monoamine hypothesis
Neuroendocrine hypothesis
Neurotropic hypothesis

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9
Q

Neuroendocrine hypothesis of depression

A

HHyperactivity in the HPA axis (hypothalamus, anterior pituitary gland, adrenal cortex).

Higher HPA hormone levels (CRH, ACTH, Cortisol).
Enlarged adrenal gland = increased cortisol secretion.
Cortisol is not diurnal - elevated all day/night.
If monoamine levels are low, more CRF is produced.
Feedback is inhibited due to reduced glucocorticoid receptors or sensitivity (particularly on the hypothalamus and pituitary).

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10
Q

Neurotropic hypothesis

A

BDNF promotes growth and development of neurons by binding to tyrosine kinase receptor B - enhancing neurogenesis.

Low BDNF may be responsible for loss of monoaminergic neurons, loss of function or atrophy of the hippocampus - impacts emotion control.
Hippocampus loses its ability to inhibit CRH release from the hypothalamus –> increased glucocorticoids.

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11
Q

What causes low BDNF in depressed patients?

A

Low serotonin.
Serotonin causes release of cyclic AMP –> protein kinase A –> CREB –> BDNF.. This process starts in the post-synaptic neuron.

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12
Q

How can depression be managed?

A

Antidepressants, cognitive behavioural therapy, electroconvulsive therapy, counselling and exercise.

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13
Q

What is a SSRI?

A

Selective Serotonin Reuptake Inhibitors.

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14
Q

What is the primary goal of pharmacological intervention for depression? How?

A

Alleviate symptoms and improve mood.
Increasing the function of serotonin and noradrenaline or inhibiting the reuptake of neurotransmitter or blocking MAOs.

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15
Q

Give two examples of SSRIs

A

Sertraline and Citalopram.

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16
Q

What are the side effects of SSRIs?

A

Feeling emotionally numb, experiencing sexual dysfunction.
Insomnia, GI disturbance, reduced platelet aggregation, increased suicidal ideation and withdrawal effects.

17
Q

What is the effect of low BDNF on cortisol?

A

Increased cortisol through increased CRH and so activation of the HPA axis.

18
Q

Why is sertraline more popular?

A

It has well tolerated, more favourable side effects

19
Q

How long is the lag period for SSRIs?

A

2-3 weeks.

20
Q

How effective are antidepressants?

A

They are effective for about 1/3 of patients respond to the first antidepressant they try, 20% to the second dose and then fewer after that.

21
Q

What are two consequences of increased cortisol?

A

Hyperactivity of the HPA axis through reduced receptor number and function.

22
Q

How many patients respond well to their first dose of antidepressants?

A

1/3

23
Q

How many patients then respond to their second dose of antidepressants?

A

20%

24
Q

What is the primary goal of pharmacological intervention?

A

Increase the function of serotonin and noradrenaline
Inhibit reuptake of neurotransmitters
Block MAO from breaking serotonin down

25
Q
A