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6P > Psychopharmacology of mood/anxiety disorders > Flashcards

Psychopharmacology of mood/anxiety disorders Flashcards

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

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

A

Trazodone

usually used as a sedative rather than a antidepressant

23
Q

SARI MOA

A

low doses (

24
Q

SARI side effect

A

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

25
Q

TCA exapmles

A

Amitriptyline (SNRI) - Pain
Desipramine (NRI)
Clomipramine (SRI) - OCD

26
Q

TCA MOA

A 
classification based more on chemical structure
Antihistaminergic
Anticholinergic
Post-synaptic alpha-1 blockade
Na channel blockade
27
Q

TCA side effects

A

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
Q

MAOI examples

A

Phenelzine
Tranylcypromine - both nonselective, irreversible
Moclobemide (MAOI-A selective)

29
Q

MAOI MOAs

A

MAO-A: metabolizes NE, 5HT, tyramine
MAO-B> preferentially metabolizes dopamine
enhance monoamine function by interfering with metabolism

30
Q

Mood stabilizer examples

A 
Valproic acid
Carbamazepine
Lamotrigine
Oxcarbazepine
Less commonly used adjuncts: gabapentin, topiramate
31
Q

Lithium MOA

A

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
Q

Valproic acid salt MOA

A

Inhibits NaV channels (non-specific sites), boosts GABA actions
regulates downstream signal transduction cascades

33
Q

Carbamazepine/oxcarbazepine MOAs

A

inhibits alpha unit of VSSC, CaV channel, nonspecific K channel, can enhance GABA

34
Q

Lamotrigine MOA

A

inhibits alpha unit of VSSC
diminishes glutamate release
additional synaptic effects on glutamate

35
Q

NaV/CaV channels in mania

A

too much Na/Ca flow in mania leading to excessive glutamate release
binding to channels helps reduce Na/Ca influx, lowering glutamate transmission

36
Q

GABA/glutamate imbalance

A

restored in pharmacologic treatment

decrease glutamate/increase GABA

37
Q

Agents that increase GABA

A 
benzodiazepines
Zolpidem
Valproate
Carbamazepine
Topiramate
38
Q

Agents that decrease glutamate

A

memantine
amantadine
topiramate
clozapine

39
Q

Atypical antipsychotics in bipolar mania

A

5-HT2a antagonism –> reduces glutamate hyperactivity
can be beneficial for either mania or depression
D2 blockade useful for psychotic states

40
Q

Atypical antipsychotics in bipolar/unipolar depression

A

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
Q

Side effects of atypical antipsychotics

A

anticholinergic
antihistaminergic
alpha-1 antagonism (orthostasis), EPS due to excessive D2 blockade

42
Q

Pertinent NTs in anxiolytics

A

Serotonin
NE
GABA

43
Q

Anxiety disorder initiation of treatment

A

SSRI/SNRIs both 1st line, but initiating dose is lower than depression
May use benzodiazepine to manage short-term when starting therapy

44
Q

SNRI usefulness in anxiety

A

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
Q

SSRI usefulness in anxiety

A

enhances 5HT neurotransmission

5HT has little phasic reactivity (unlike NE)

46
Q

Buspirone

A

primarily functions as partial 5HT-1A agonist
No GABA effects
not useful for as needed treatment of anxiety
useful for GAD

47
Q

Benzodiazepine MOA

A

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
Q

Benzodiazepine examples

A 
lorazepam
clonazepam
diazepam
alprazolam
triazolam
oxazepam
49
Q

Benzodiazepine indication

A

as needed/routine management of anxiety symptoms

management of insomnia

50
Q

Anticonvulsants and anxiety

A

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

6P (13 decks)

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