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BB CC > Mood Disorders + Antidepressant Drugs > Flashcards

Mood Disorders + Antidepressant Drugs Flashcards

1
Q

DSM-IV

A

Major depression

Bipolar

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2
Q

DSM-V

A

Major depressive disorder

Disruptive mood dysregulation disorder

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3
Q

Depression Signs and Symptoms

A 
Psychomotor retardation
Fatigue/loss of energy
Diminished ability to concentrate
Diminished social activity interest
Insomnia
Guilt + worthlessness
Weight loss + decreased appetite
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4
Q

Bipolar chance

A

Increased if related to patient with bipolar

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5
Q

Depression chance

A

Increases if related to patient with bipolar

Increases even more if related to patient with major depression

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6
Q

Genes linked to depression

A

GRIK4
CRHR1
SLC6A4
MAOA

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7
Q

Pathophysiology of depression

A

Dysfunction of noradrenergic and serotonergic pathways

Key players, but not only players

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8
Q

Brain regions associated with depression

A 
Amygdala- fear and anxiety
Ventrolateral prefrontal cortex
Dorsolateral prefrontal cortex
Medial prefrontal cortex
Striatal regions (ventral striatum)
Hippocampus
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9
Q

Raphe

A

Place of origin of most of innervation of cortical structures
Neurones in raphe have slow activity in waking

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10
Q

Subgenual prefrontal cortex abnormalities- PET scan

A

Decreased metabolism- significant reduction in glucose consumption

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11
Q

Subgenual prefrontal cortex abnormalities- MRI scan

A

Mean grey matter volume of subgenual anterior cingulate cortex is REDUCED in patients with major depressive or bipolar disorder

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12
Q

Cortical Thickness

A

Depressed patients have significant cortical matter loss
12-15% change
–> structure abnormality/volume loss –> grey/white matter

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13
Q

Default mode network

A

Network of brain regions active when brain is at wakeful rest
Increased DMN connectivity in subjects with major depression

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14
Q

Gene-environment interactions

A

5HT transporter polymorphism is associated with a higher risk of major depression
Different alleles lead to different transcription of the transporter
Short allele, more at risk of depression
Long allele, more resistant

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15
Q

Genetic variations + CNS connectivity

A

Correlation between decreased connectivity amygdala-prefrontal cortex, certain MAOA isoforms (affect activity of enzyme) and state of clinical depression

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16
Q

Amygdala-prefrontal cortex

A

Connectivity is significantly reduced in depressed patients + carries of the higher active MAOA risk alleles (MAOA-H)
Reduced coupling in this circuit –> longer + more severe course of disease

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17
Q

MAOA gene genetic variation

A

Encodes enzyme which controls monoaminergic signalling

May affect the course of major depression by disrupting cortico-limbic connectivity

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18
Q

Higher active MAOA

A

Disrupts cortico-limbic connectivity

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19
Q

Rumination

A

Regions involved in persistent recurring thoughts in depression include amygdala + hippocampus
Hyperactivation in amygdala + hippocampus –> increased activity in subgenual cingulate cortex, region that integrates limbic feedback + relays to prefrontal cortex
–> increased subgenual activity increases activity in MPFC, region associated with internal representations of oneself
Activation decreased in DLPFC and VLPFC- areas associated with cognitive control

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20
Q

TCAs MOA

A

Inhibit reuptake of amines

Have affinity for H1, muscarinic, alpha-1 and alpha-2 adrenoreceptors

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21
Q

TCA examples

A

Clomipramine
Imipramine
Amitriptyline

22
Q

TCA Side effects

A 
Muscarinic- dry mouth, blurred vision, constipation, urinary retention
Adrenoreceptors- Postural hypotension
Fatigue
Sedation
Weight gain
Dizziness 
Loss of libido
23
Q

TCA overdose

A

Dangerous

Cardiotoxicity

24
Q

Monoamine oxidase inhibitors MOA

A

Irreversible inhibition of enzyme

Non-selective MAOa vs MAOb

25
Q

MAOIs examples

A

Phelzine
Iproniazid
Tranylcypromine

26
Q

MAOI - tyramine

A

Interactions with tyramine-containing foods –> mature cheese, pickled fish + meat, red wine, beer, yeast
With MAOIs, tyramine accumulates in brain –> will penetrate monoaminergic presynaptic terminals containing noradrenaline, pushing it out, leading to higher BP, headaches etc.

27
Q

MAOI side effect

A

Hepatotoxicity

Massive hypotensive activities

28
Q

MAO enzymes

A

Breakdown of noradrenaline, dopamine and serotonin

29
Q

SSRI MOA

A

Increased selectivity for serotonin reuptake

–> leave serotonin in synapse

30
Q

SSRI examples

A

Citalopram- most effective
Fluoxetine
Paroxetine

31
Q

SSRI side effects

A 
Nausea
Headaches
GI problems
Increased aggression
Insomnia
Anxiety
Sexual dysfunction
32
Q

S-isomer of citalopram

A

Escitalopram

33
Q

Reversible MAOIs

A

Moclobemide
Increased selectivity for MAOa
Safer than irreversible MAOIs
Adverse effects- nausea, agitation, confusion

34
Q

Venlafaxine

A

Serotonin noradrenaline reuptake inhibitors (SNRIs)

35
Q

Reboxetine

A

Noradrenaline reuptake inhibitors (NARIs)

36
Q

Mirtazapine

A

Noradrenergic and specific serotonergic antidepressants (NaSSAs)
Antagonism at 5HT2 and alpha-2 adrenergic receptors

37
Q

Trazodone

A

Serotonin antagonist and reuptake inhibitor (SARI)

Mainly antagonist at 5HT2 receptors + serotonin reuptake inhibition

38
Q

Agomelatine

A

Agonist at melatonin MT1 + 2 receptors and antagonist at 5HT2c receptors
Noradrenaline/dopamine disinhibitor

39
Q

Antidepressant drug Discontinuation Syndrome

A

Can occur after decrease in dose of drug taken, after interruption of treatment, or abrupt cessation of treatment
Dependant on medication

40
Q

Discontinuation syndrome symptoms

A 
Insomnia
Anxiety
Nausea
Headaches
Electric shock sensations
Agitations
41
Q

Delay of action of antidepressant drugs

A

Changes in autoreceptors (5HT1a)
Autoreceptors activated due to immediate increase in synaptic amine concentration
–> decrease firing of neurones
They then become desensitised –> neurones back to normal firing rate
–> effect no longer inhibited

42
Q

Bipolar- Lithium

A

Narrow therapeutic margin
Renal + thyroid function must me checked
Adverse effects- thirst, nausea, fine tremor, polyuria, weight gain, oedema, acne

43
Q

Bipolar- carbamazepine, sodium valproate

A

Mood stabilisers

44
Q

Risk order for mania switch

A

TCAs> SNRIs> MAOIs> SSRIs

45
Q

Principals Depression management

A 
Ensure optimum thyroid function
Treat co-morbidity (substance misuse) 
Ensure full symptom control
Monitor course of illness (mood chart)
Adapt and review treatment
Prevent recurrence
46
Q

Phases of treatment

A

Acute
Continuation
Maintenance

47
Q

Acute treatment

A

First 6-12 weeks

Aims at remission (control of symptoms)

48
Q

Continuation treatments

A

For 6 months after full symptom control
Maintain remission status
Prevent relapse

49
Q

Maintenance treatment

A

Prevention of recurrence of further episode

50
Q

Non-pharmacological approaches

A

Electroconvulsive therapy- treatment for refractory depression with suicide risk, treatment-resistant depression
CBT
Vagal nerve stimulation
DBS- subcallosal cingulate white mater, subgenual cingulate cortex

51
Q

Hippocampus

A

Neuronal loss + neurogenesis in hippocampus affects whole spectrum of symptoms associated with depression
Increases in cortisol + pro-inflammatory cytokines –> neuronal loss + structural changes in hippocambus

BB CC (29 decks)

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