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Module 202 Theme 3 > Affective disorders: Neurobiology and treatment > Flashcards

Affective disorders: Neurobiology and treatment Flashcards

1
Q

Describe the neurobiology of major depression

A

Adverse childhood experience, current stress, genetic factors- decreased 5HT and NA function
Current stress and genetic factors - HPA Axis function - cortisol - Decreased 5HT and NA function

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2
Q

Give the aetiology of depression

A

Multifactorial
Incompletely understood
Interactions of genetic factors, childhood adversities, past hx of mood disorders, psychological predisposition (neuroticism)
Often precipitated by stressful life events

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3
Q

What do all traditional antidepressants affect?

A

5HT/NA systems

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4
Q

Describe antidepressants in 1950

A

Monoamine oxidase inhibitors (MAOIs) - Anti-TBC drug having euphorigenic effect

Tricyclics (TCAs) - anti-histaminic having antidepressant effect

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5
Q

List some antidepressants

A 
Monoamine oxidase inhibitors (MAOIs)
Tricyclics (TCAs)	
Trazodone 
Fluoxetine (Prozac)
Bupropion 
Venlafaxine 
Mirtazapine
Duloxetine
Agomelatine
Vortioxetine
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6
Q

What do all traditional antidepressants cause

A

5-HT concentrations (acute tryptohan depletion) studies
Decreased reduced 5-HT Transporter in post-mortem suicide studies
Reduced 5-HT Transporter in DepressionPET/SPECT studies

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7
Q

Describe monoamine oxidase inhibitors

A

Nonselectively inhibit enzymes involved in the breakdown of monoamines, including serotonin, dopamine, and norepinephrine

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8
Q

Name some monoamine oxidase inhibitors

A

Phenelzine, Tranylcypromine

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9
Q

Name some tricyclic antidepressants

A

Amytryptiline, Clomipramine

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10
Q

Describe the action of tricyclic antidepressants

A

Nonselectively inhibit the reuptake of monoamines, including serotonin, dopamine, and norepinephrine

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11
Q

List some second generation antidepressants

A

SSRI: Selective serotonin reuptake inhibitors
SNRI: Serotonin-noradrenaline reuptake inhibitors
alpha2 and 5-HT2Cantagonist [modulate serotonin and NA release]
Dopamine-noradrenaline reuptake inhibitor

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12
Q

Name some SSRI: Selective serotonin reuptake inhibitors

A

Sertraline, Citalopram, Escitalopram, Fluoxetine

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13
Q

Name some SNRI: Serotonin-noradrenaline reuptake inhibitors

A

Venlafaxine, Duloxetine

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14
Q

Name some alpha2 and 5-HT2Cantagonist [modulate serotonin and NA release]

A

Mirtazapine

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15
Q

Name some Dopamine-noradrenaline reuptake inhibitor

A

Bupropion (not approved as antidepressant in UK)

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16
Q

Describe SSRIs

A

Efficacy equal to tryciclics in outpatients
Large spectrum of action (OCD, PTSD, Panic, GAD, social anxiety)
Low toxicity and safe in overdose

The initial treatment phase is the most delicate, due to prevalence of side effects over benefits – slow titration

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17
Q

What are the side effects of SSRIs?

A

gastro-intestinal symptoms (nausea, diarrhea)
headache, Irritability, Anxiety
reduction of libido and sexual dysfunction

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18
Q

What are the side effects of monoamine oxidases inhibitors?

A

Dry mouth, GI side effects, headache, drowsiness, insomnia, dizziness, food interactions (hypertension crises)

19
Q

What are the side effects of tricyclic antidepressants?

A

Constipation, orthostatic hypotension, dry mouth, drowsiness, cardiac toxicity in overdose

20
Q

Give the side effects of Venlafexine

A

nausea,vertigo, headache, insomnia

21
Q

Give the side effects of Mirtazapine

A

drowsiness, sedation, hypotension, increased appetite and weight gain

22
Q

Describe HPA dysfunction in mood disorders

A

Lack of dexamethasone suppression
Glucocorticoid receptor alterations
Depression in Cushing’s syndrome

23
Q

Describe the relationship between depression and inflammation

A

Raised plasma cytokine levels and inflammatory markers
High comorbidity between chronic inflammation and depression
Administration of cytokines promotes depressive symptoms
Microglial activation in brain of depressed patients (PET studies)

24
Q

What happens to the size of the hippocampus in depression?

A

Decreases

25
Q

Describe the neural systems involved in depression

A 
Increased activity (Amy; VST, PFC) to negative emotional stimuli (fearful faces)
Decreased activity (VST) to positive emotional stimuli, and during receipt and anticipation of reward

bias of attention towards negative emotional stimuli, and away from positive emotional and reward- related stimuli

Neural systems that are important to understand major depressive disorder include those that support emotion processing, reward seeking, and regulate emotion, all of which are dysfunctional in the disorder. These systems include subcortical systems involved in emotion and reward processing

26
Q

List some factors which contribute to the cause of bipolar disorder

A 
Catecholamines
Oxidative stress
Neutrophins 
Inflammation 
Stress hormones, glucocorticoids
27
Q

What is the purpose of short term treatment?

A

To reduce the severity and shorten the duration of the acute episode and achieve remission of symptoms

28
Q

What is the purpose of long term treatment?

A

prevention of new episodes and to achieve adequate inter-episode control of residual or chronic mood symptoms

29
Q

List some categories of drug treatments of bipolar

A

Antipsychotics

Lithium

Anticonvulsants

Antidepressants

30
Q

List the receptors targeted in antipsychotics

A

D2/D3 antagonist
1st generation: Haloperidol
D2/D3 antagonists (also targeting 5-HT)
(2nd generation: Olanzapine, Risperidone, Quetiapine, Lurasidone, Asenapine, Amisulpride, Clozapine)
DA partial agonist (Aripiprazole)

31
Q

What do antipsychotics cause?

A

Rapid anti-manic effect
Often used long-term to maintain same treatment effective in acute episode
Long-term adverse effects on weight, glucose regulation and lipids [except for Aripiprazole, Amisulpride, and Lurasidone]
Full D2 antagonism (Haloperidol) may cause EPSEs

32
Q

What is lithium and what is it used to treat?

A

Element, present in food and drinking water
Treatment of bipolar disorder
Anti-suicidal effects
Possible efficacy on impulsive and violent behaviours
Strongest evidence for prevention of relapses of any polarity

33
Q

Describe the mechanism of action of lithium

A

Multiple neurotransmitters (including DA)
Cellular signalling
Neurotrophic factors

34
Q

Describe the adverse effects of lithium

A

Narrow therapeutic index
blood tests every 3 months for the 1st year
Adverse long-term effects on Kidney function with excessive levels
Risk of Lithium toxicity

35
Q

List some anticonvulsants

A

Valproate
Lamotrigine
Carbamazepine

36
Q

Describe valproate

A

Actions via GABA, intracellular signalling, sodium channel blockade, epigenetic modulation, etc.
Anti-manic and effective in prevention of mania
Useful in combination, but potential pharmacokinetic interactions

37
Q

When should valproate not be used?

A

not be used for women of child bearing potential because of its unacceptable risk to the foetus of teratogenesis and impaired intellectual development

38
Q

Describe Lamotrigine

A

actions via GABA, Glutamate and sodium channel blockade
Mostly effective in prevention of depressive relapses
Ineffective as anti-manic agent

39
Q

Describe carbamazepine

A

less effective in maintenance treatment than lithium but may be used as monotherapy if lithium ineffective
especially in patients who do not show the classical pattern of episodic euphoric mania
almost exclusively effective against manic relapse
pharmacokinetic interactions

40
Q

Describe the treatment of depressive episodes

A

Antipsychotics (Quetiapine, lurasidone)

Fluoxetine/Olanzapine combinations

Antidepressants to be co-prescribed with an anti-manic drug

Consider Lamotrigine (usually with antimanic drug)

41
Q

Describe the treatment of acute manic episodes

A

Dopamine antagonists (haloperidol, olanzapine, risperidone and quetiapine)

Valproate

Discontinue any antidepressant treatment

42
Q

Describe the long term treatment of bipolar disorder and the prevention of new episodes

A

Consider long-term treatment following a single severe manic episode

Lithium as initial monotherapy (target serum level range: 0.6-0.8 mmol/l)

Alternatives (if Lithium ineffective, poorly tolerated or unlikely adherence to treatment):
Valproate
Dopamine antagonists/partial agonists
Carbamazepine

43
Q

State the adverse effects of long term preventative treatment

A 
Weight gain (most medications, particularly Olanzapine and Quetiapine)
Metabolic syndrome (Olanzapine, Quetiapine, Risperidone)
Hyperprolactinemia (Dopamine antagonists)
Tardive dyskinesia (much reduced risk with newer agents)

Liver damage (e.g. Valproate)

Kidney and Thyroid dysfunction (poorly regulated Lithium)

Module 202 Theme 3 (11 decks)

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