Week 1 - Mental health Flashcards
What is mental health?
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.
Depression definition
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.
What are the functions of dopamine?
Pleasure, motivation, reward, mood, motor control, sexual function.
What are the functions of serotonin?
Mood, appetite, emotion, arousal/wakefulness, body temperature and sleep.
What are the three things that can happen to serotonin in the synapse?
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)
What is the pathway of serotonin production and transportation?
- Tryptophan is converted to 5HT (serotonin)
- 5HT is packaged into vesicles
- 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.
Monoamine hypothesis of depression
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.
What are the three hypotheses of causes of depression?
Monoamine hypothesis
Neuroendocrine hypothesis
Neurotropic hypothesis
Neuroendocrine hypothesis of depression
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).
Neurotropic hypothesis
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.
What causes low BDNF in depressed patients?
Low serotonin.
Serotonin causes release of cyclic AMP –> protein kinase A –> CREB –> BDNF.. This process starts in the post-synaptic neuron.
How can depression be managed?
Antidepressants, cognitive behavioural therapy, electroconvulsive therapy, counselling and exercise.
What is a SSRI?
Selective Serotonin Reuptake Inhibitors.
What is the primary goal of pharmacological intervention for depression? How?
Alleviate symptoms and improve mood.
Increasing the function of serotonin and noradrenaline or inhibiting the reuptake of neurotransmitter or blocking MAOs.
Give two examples of SSRIs
Sertraline and Citalopram.
What are the side effects of SSRIs?
Feeling emotionally numb, experiencing sexual dysfunction.
Insomnia, GI disturbance, reduced platelet aggregation, increased suicidal ideation and withdrawal effects.
What is the effect of low BDNF on cortisol?
Increased cortisol through increased CRH and so activation of the HPA axis.
Why is sertraline more popular?
It has well tolerated, more favourable side effects
How long is the lag period for SSRIs?
2-3 weeks.
How effective are antidepressants?
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.
What are two consequences of increased cortisol?
Hyperactivity of the HPA axis through reduced receptor number and function.
How many patients respond well to their first dose of antidepressants?
1/3
How many patients then respond to their second dose of antidepressants?
20%
What is the primary goal of pharmacological intervention?
Increase the function of serotonin and noradrenaline
Inhibit reuptake of neurotransmitters
Block MAO from breaking serotonin down
