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Pharm Y3S2 > Depression > Flashcards

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?

A

SSRI

24
Q

What are the adverse effects and dangers of SSRIs?

A

Hyponatraemia
Bleeding risk
QT prolongation with citalopram and escitalopram

25
Q

Give examples of SNRIs.

A

Venlafaxine

Duloxetine

26
Q

When is venlafaxine contraindicated?

A

Uncontrolled hypertension

27
Q

What are the adverse effects and dangers of mirtazipine?

A

Sedation
Weight gain
Blood disorders

28
Q

Give examples of TCAs.

A

Amitriptyline
Clomipramine
Lofepramine
Dosulepin

29
Q

Describe the action of TCAs.

A

Inhibit serotonin and noradrenaline uptake

30
Q

What are the adverse effects and dangers of TCAs?

A

Sedating
Anti-muscarinic side effects
Cardiotoxicity, fatal in overdose

31
Q

Give examples of MAOIs.

A

Phenelzine
Isocarboxazid
Moclobemide (reversible)

32
Q

What are the adverse effects and dangers of MAOIs?

A

Strict diet required

Potential for interactions

33
Q

What is reboxetine?

A

NARI

34
Q

What is agomelatine?

A

Melatonergic agonist

35
Q

What is the main danger agomelatine?

A

Liver injury and hepatoxicity

36
Q

What is vortioxetine?

A

Serotonin based

Newest available antidepressant

37
Q

When is vortioxetine used?

A

Recommended by NICE where no response is seen from use of 2 antidepressants in the current episode

38
Q

What should be done when there is little/no improvement with antidepressant use?

A

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
Q

How should treatment be stopped?

A

Continue for 6 months after remission
Continue for 2 years at treatment dose if needed
Gradual reduction to prevent discontinuation symptoms

Pharm Y3S2 (29 decks)

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