Depression Flashcards

1
Q

What pathways are affected by noradrenaline?

A

Alertness
Arousal
Sensory perception
Motor tone

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2
Q

What pathways are affected by serotonin?

A
Sleep
Food intake
Thermoregulation
Sexual behaviour
Pain
Motor tone
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3
Q

Give 4 types of unipolar depression.

A

Major depressive disorder
Dysthymia
Seasonal affective disorder
Postnatal depression

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4
Q

What is often the main focus of treatment?

A

CBT in order to change mindset and promote positive behaviour

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5
Q

What areas of the brain and neurotransmitters are responsible for loss of pleasure/motivation?

A

Dorso-lateral and pre-frontal cortex

Dopamine

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6
Q

What areas of the brain and neurotransmitters are responsible for sadness and suicide?

A

Ventro-medial and pre-frontal cortex

Serotonin, noradrenaline and dopamine

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7
Q

What areas of the brain and neurotransmitters are responsible for fatigue/loss of energy?

A

Dopamine
Noradrenaline
Serotonin

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8
Q

What areas of the brain and neurotransmitters are responsible for sleep, appetite and libido?

A

Nucleus accumbent and hypothalamus

Serotonin, noradrenaline and dopamine

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9
Q

What areas of the brain and neurotransmitters are responsible for attention, concentration and problem solving?

A

Dorso-lateral and pre-frontal cortex

Dopamine, ACh, serotonin, noradrenaline, GABA, histamine

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10
Q

Give examples of emotional symptoms of depression.

A

Loss of pleasure and motivation
Sadness
Suicidal thoughts

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11
Q

Give examples of somatic symptoms of depression.

A
Fatigue
Loss of energy
Sleep changes
Appetite changes
Loss of libido
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12
Q

Give examples of cognitive symptoms of depression.

A

Attention
Concentration
Problem solving

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13
Q

What are the 4 physical interventions that may be used in depression?

A

Electroconvulsive therapy
Electromagnetic therapy
Deep brain stimulation
Vagal stimulation

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14
Q

Describe the features of the serotonergic synapse?

A

Serotonin is returned from synapse to pre-synaptic terminal via re-uptake transporter
Auto-receptors on presynaptic membrane can be used to back synthesis and release of serotonin, activated by serotonin in the synapse

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15
Q

What is the major problem with MAOI antidepressants?

A

Dietary tyramine is a precursor for monoamine synthesis
Inhibition of MAO enzyme increases transmitter levels when these foods are eaten
Large hypertensive response, can cause haemorrhage

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16
Q

Describe the acute effect of antidepressants on serotonin levels.

A

Acute use of antidepressants causes blockage of transporters, increasing serotonin around the cell body
Increased activation of auto-receptors, reducing firing and release

17
Q

Describe the chronic effect of antidepressants on serotonin levels.

A

Re-uptake blockade causes serotonin to remain in the synapse for longer allowing it to exert an effect and cell firing is restored

18
Q

How is depression diagnosed?

A

Patient must meet 5 out of 9 DSM-5 criteria with at least one core symptom.

19
Q

What are the DSM-5 core symptoms?

A

Low mood

Loss of pleasure

20
Q

What are the DSM-5 symptoms?

A

Fatigue/loss of energy
Worthlessness, guilt
Recurrent thoughts of death, suicidal thoughts/attempts
Reduced ability to think or concentrate, indecisiveness
Psychomotor agitation or retardation
Insomnia/hypersomnia
Weight loss or gain

21
Q

When is pharmacological treatment for depression considered?

A

Moderate/severe depression
Past history of moderate/severe depression
Sub-threshold symptoms for 2 years
Sub-threshold symptoms or persistent mild depression after other interventions

22
Q

Give examples of SSRIs.

A
Sertraline
Citalopram
Escitalopram
Fluoxetine
Paroxetine
23
Q

What is first line pharmacological treatment for depression?

24
Q

What are the adverse effects and dangers of SSRIs?

A

Hyponatraemia
Bleeding risk
QT prolongation with citalopram and escitalopram

25
Give examples of SNRIs.
Venlafaxine | Duloxetine
26
When is venlafaxine contraindicated?
Uncontrolled hypertension
27
What are the adverse effects and dangers of mirtazipine?
Sedation Weight gain Blood disorders
28
Give examples of TCAs.
Amitriptyline Clomipramine Lofepramine Dosulepin
29
Describe the action of TCAs.
Inhibit serotonin and noradrenaline uptake
30
What are the adverse effects and dangers of TCAs?
Sedating Anti-muscarinic side effects Cardiotoxicity, fatal in overdose
31
Give examples of MAOIs.
Phenelzine Isocarboxazid Moclobemide (reversible)
32
What are the adverse effects and dangers of MAOIs?
Strict diet required | Potential for interactions
33
What is reboxetine?
NARI
34
What is agomelatine?
Melatonergic agonist
35
What is the main danger agomelatine?
Liver injury and hepatoxicity
36
What is vortioxetine?
Serotonin based | Newest available antidepressant
37
When is vortioxetine used?
Recommended by NICE where no response is seen from use of 2 antidepressants in the current episode
38
What should be done when there is little/no improvement with antidepressant use?
4 weeks to full effect Check compliance Increase dose Switch mono therapies before considering combination If slight improvement, continue for 2-4 week further
39
How should treatment be stopped?
Continue for 6 months after remission Continue for 2 years at treatment dose if needed Gradual reduction to prevent discontinuation symptoms