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6P > Psychopharmacology of mood/anxiety disorders > Flashcards

Psychopharmacology of mood/anxiety disorders Flashcards

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1
Q

Serotonin metabolism at synaptic cleft

A

Autoreceptors: 5HT1A, 1B/D
SERT: serotnonin transpoter
MAO-B: destroys 5HT at high concentrations in presynaptic membrane
MAO-A/B destroys 5HT at synaptic cleft

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2
Q

Norepinephrine metabolism at synaptic cleft

A

Autoreceptor: presynaptic alpha-2 autoreceptor
NET: norepinephrine transporter
VMAT on NT vesicles

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3
Q

Dopamine metabolism at synaptic cleft

A

Autoreceptor: presynaptic D2 autoreceptor
VMAT on vesicles
D1-5 receptors on postsynaptic membrane
DAT transporter

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4
Q

GABA metabolism at synaptic cleft

A

GABAA, B, C receptor complexes on postsynaptic membrane

GABA transporter: GAT

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5
Q

Glutamate metabolism ta synaptic cleft

A

Transporter: EAAT
vGluT on vesicles
Presynaptic metabotropic receptor (autoreceptor)
Post: NMDA, AMPA, kainate, postsynaptic metabotropic receptors

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6
Q

Neurochemistry of Mania

A

5HT, NE, DA hyperactivity: elevated/expansive or irritable mood, risk-taking/poor impulse control, decreased need for sleep
5HT/DA hyperactivity: grandiosity/flight of ideas, increased goal-directed activity or agitation
DA/NE hyperactivity: distractibility/concentration issues

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7
Q

Prefrontal cortex in manic symptoms

A 
racing thoughts
grandiosity
distractiliby
talkative/pressured speech
mood
risk
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8
Q

Thalamus in manic symptoms

A

decreased sleep/arousal

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9
Q

Nucleus accumbens in manic symptoms

A

racing thoughts
goal-directed
grandiosity

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10
Q

Time course of antidepressant effects

A

NT increases, receptor sensitivity decreases

clinical effect afterwards due to chronic adaptations in brain function, rather than increase in NT

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11
Q

SSRI examples

A 
fluoxetine
sertraline
paroxetine
citalopram
escitalopram
fluvoxamine
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12
Q

SSRI MOA

A

blocks SERT
interferes with recycling of serotonin back to presynaptic neurons
increases 5HT availability in synapse

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13
Q

SSRI side effects

A

GI
CNS:initial agitation/worsening of anxiety, tremors, insomnia, headache
Reproductive: sexual dysfunction
Hematologic: bleeding (decreased platelet aggregation)
Fatigue/apathy: longer term use –> serotonergic influence on NA/DA release

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14
Q

SNRI examples

A

venlafaxine
duloxetine
desvenlafaxine

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15
Q

SNRI MOA

A

blocks SERT and NET

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16
Q

SNRI side effects

A

similar to SSRIs

additional potential to affect blood pressure/pulse (peripheral NE effects)

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17
Q

NDRI examples

A

Buproprion (SR/XL)

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18
Q

NDRI MOA

A

blocks NET, DAT

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19
Q

NDRI MOA

A

No serotonergic involvement (less effect on sexual functioning)
may include insomnia if dosed too closely to bedtime

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20
Q

NaSSA example

A

Mirtazapine

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21
Q

NaSSA MOA

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A

noradrenergic serotonin specific antidepressant
Alpha-2 antagonism –> 5HT/NE disinhibition –> release of both
Blocks 5HT3: antiemetic
Blocks 5HT2A/2C: Sleep restoring, anxiolytic, antidepressant (increased NE/DA release in PFC)
Blocks histamine: hypnotic, anxiolytic effect, particularly at low doses

22
Q

SARI examples

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A

Trazodone

usually used as a sedative rather than a antidepressant

23
Q

SARI MOA

24
Q

SARI side effect

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A

histamine blockade
post-synaptic alpha-1 blockade: tiredness, dizziness/orthostasis
Post-synaptic alpha-2 blockade: priapism

25
TCA exapmles
Amitriptyline (SNRI) - Pain Desipramine (NRI) Clomipramine (SRI) - OCD
26
TCA MOA
``` classification based more on chemical structure Antihistaminergic Anticholinergic Post-synaptic alpha-1 blockade Na channel blockade ```
27
TCA side effects
Anti-histamine Anticholinergic: constipation, blurry vision, dry mouth, drowsiness Post-synaptic alpha1 block: tiredness, dizziness, orthostasis Na channel block in brain: coma, seizures Na channel block in heart: arrhythmia, death
28
MAOI examples
Phenelzine Tranylcypromine - both nonselective, irreversible Moclobemide (MAOI-A selective)
29
MAOI MOAs
MAO-A: metabolizes NE, 5HT, tyramine MAO-B> preferentially metabolizes dopamine enhance monoamine function by interfering with metabolism
30
Mood stabilizer examples
``` Valproic acid Carbamazepine Lamotrigine Oxcarbazepine Less commonly used adjuncts: gabapentin, topiramate ```
31
Lithium MOA
inhibits 2nd messenger enzyme systems (inositol monophosphatase) modulates G proteins interacts with various sites within downstream signal cascades (regulation of gene expression for GFs, neuronal plasticity)
32
Valproic acid salt MOA
Inhibits NaV channels (non-specific sites), boosts GABA actions regulates downstream signal transduction cascades
33
Carbamazepine/oxcarbazepine MOAs
inhibits alpha unit of VSSC, CaV channel, nonspecific K channel, can enhance GABA
34
Lamotrigine MOA
inhibits alpha unit of VSSC diminishes glutamate release additional synaptic effects on glutamate
35
NaV/CaV channels in mania
too much Na/Ca flow in mania leading to excessive glutamate release binding to channels helps reduce Na/Ca influx, lowering glutamate transmission
36
GABA/glutamate imbalance
restored in pharmacologic treatment | decrease glutamate/increase GABA
37
Agents that increase GABA
``` benzodiazepines Zolpidem Valproate Carbamazepine Topiramate ```
38
Agents that decrease glutamate
memantine amantadine topiramate clozapine
39
Atypical antipsychotics in bipolar mania
5-HT2a antagonism --> reduces glutamate hyperactivity can be beneficial for either mania or depression D2 blockade useful for psychotic states
40
Atypical antipsychotics in bipolar/unipolar depression
5HT2/5HTc antagonism useful for reducing apathy/fatigue --> in combo with SSRIs, releases brake that chronic 5HT effects hae on NE/DA release Alpha-adrenergic blockade may improve mood via NE/5HT disinhibition Dopamine partial agonism - useful for mood/cognition 5HT1A partial agonism - mood/anxiety positive impacts on neurogenesis, sleep, cognition
41
Side effects of atypical antipsychotics
anticholinergic antihistaminergic alpha-1 antagonism (orthostasis), EPS due to excessive D2 blockade
42
Pertinent NTs in anxiolytics
Serotonin NE GABA
43
Anxiety disorder initiation of treatment
SSRI/SNRIs both 1st line, but initiating dose is lower than depression May use benzodiazepine to manage short-term when starting therapy
44
SNRI usefulness in anxiety
NE may contribute to some of the related symptoms of anxiety, but could be useful due to: Phasic reactivity - anxiety: increase in phasic noradrenergic firing - stress or threatening stimuli: extracellular NE very high Tonic activity - at rest, basal noradrenergic firing rate lower than would be expected in non-anxious individuals --> low levels of NE in synaptic cleft and at somatodendritic end of neuron After several weeks of therapy: Rest: basal NE firing rate low, extracellular NE levels increased --> blockade of reuptake/desensitization of alpha-2 autoreceptors In response to stress: NE firing rate attenuated: likely due to somatodendritic alpha-2 autoreceptors failing to desensitize --> inhibition of dramatic increase in NE usually observed with stress
45
SSRI usefulness in anxiety
enhances 5HT neurotransmission | 5HT has little phasic reactivity (unlike NE)
46
Buspirone
primarily functions as partial 5HT-1A agonist No GABA effects not useful for as needed treatment of anxiety useful for GAD
47
Benzodiazepine MOA
all bind to gamma subunit of GABAA receptors --> increase in receptor activity due to structural modification do not substitute for GABA ( bind at alpha subunit), but increase freq of channel opening events --> increased chloride conductance --> hyperpolarization/inhibition of AP Sedative/hypnotic, amnestic, anxiolytic, myorelaxant, anticonvulsant Available benzodiazepines are non-selective; multiple benzos are additive rather than distinct Clinically important differences due to PK properties do not affect GABA-B on presynaptic mem (no effect on GABA release)
48
Benzodiazepine examples
``` lorazepam clonazepam diazepam alprazolam triazolam oxazepam ```
49
Benzodiazepine indication
as needed/routine management of anxiety symptoms | management of insomnia
50
Anticonvulsants and anxiety
activation of fear circuits (amygdala) --> anxiety Gabapentin/pregabalin - not Health Canada indicated for anxiety possible adjuncts for managing anxiety symptoms Directly blocks alpha2delta subunits of CaV --> decrease Ca flow --> reduction in presynaptic NT release of glutamate

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