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Neuro Week 7 > Mood disorder > Flashcards

Mood disorder Flashcards

1
Q

Mechanism TCAs

A

block reuptake of NE and/or 5HT by nerve terminals –> results in higher concentrations at receptors

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2
Q

NE selective TCA

A

Desipramine (Norpramin)

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3
Q

NE/5HT mixed action TCA

A

Imipramine (Tofranil)

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4
Q

Adverse effects of TCAs

A 
Orthostatic hypotension
blockade of α adrenoceptors
Antimuscarinic effects - may be severe in elderly patients
Acute confusional state
Constipation
Glaucoma
Weight gain
Tachycardia and increased tendency for arrhythmias with high doses
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5
Q

SSRIs examples

A 
Fluoxetine (Prozac) *
Sertraline (Zoloft)*
Paroxetine (Paxil) 
Fluvoxamine (Luvox)
Citalopram (Celexa)
Escitalopram (Lexapro)
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6
Q

SSRIs mechanism

A

Selective inhibition of serotonin reuptake by CNS neurons

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7
Q

amine hypothesis of mood disorders

A

Certain levels of amine neurotransmitters and receptor sensitivity are necessary for normal mood
Norepinephrine
Serotonin
Dopamine
Depression occurs if receptors are insensitive or if amine synthesis, storage or release is deficient
Mania occurs if there is an excess

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8
Q

problems with amine hypothesis

A

mismatch between time course, no evidence in decrease of brain levels of NE or 5HT, most AD cause downregulation of amine receptors, some AD don’t affect NE or 5HT

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9
Q

neurotrophic hypothesis of mood disorders

A

Nerve growth factors such as brain-derived neurotrophic factor (BDNF) are critical in the regulation of neural plasticity, resilience, and neurogenesis.
Depression is associated with the loss of neurotrophic support

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10
Q

TCAs metabolized by ______ and interact with ________

A

CYP2D6, inhibited by fluoxetine - do not give together –> TCA toxicity

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11
Q

glutamine hypothesis for depression, drug associated

A

elevated glutamine –> depression

Ketamine - NMDA receptor antagonist

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12
Q

MAOI

A

phenelzine

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13
Q

mechanism phenelzine

A

Irreversibly blocks the oxidative deamination of monoamines

Nonselectively inhibit both MAO-A and MAO-B ( A - NE and 5HT)

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14
Q

Why SSRIs not starts until at least 14 days after MAOI

A

irreversibly block MAO - need to wait for protein synthesis

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15
Q

Serotonin syndrome

A

MAOIs
hyperthermia, muscle rigidity, tremors, autonomic instability, confusion, irritability, and agitation
Overactivation of subset of 5-HT receptors
Can progress toward coma and death
Administer nonselective serotonin antagonists (Cyproheptadine, etc.)
Also caused by MDMA (Ecstasy)

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16
Q

MAOIs drug interactions

A

Potentiate sympathomimetic amines - such as tyramine, completely metabolized by hepatic MAO –> tyramine enters systemic circulation –> Accumulation of tyramine in adrenergic nerve endings and neurotransmitter vesicles and induces norepinephrine and epinephrine release –> stimulate postsynaptic receptors in the periphery, increasing blood pressure to dangerous levels.

17
Q

SSRIs

A

Fluoxetine (Prozac)

Sertraline (Zoloft)

18
Q

SSRIs mechanism

A

Selective inhibition of serotonin reuptake by CNS neurons

19
Q

Adverse effects SSRIs

A

Nausea, diarrhea and weight loss
Stimulation - anxiety, nervousness, insomnia, sufficient to discontinue treatment
Sexual dysfunction
Suicidal ideation

20
Q

atypical antidepressants

A

venlafaxine

mirtazapine

21
Q

venlafaxine mechanism

A

Serotonin-norepinephrine reuptake inhibitor (SNRI)
Blocks serotonin reuptake like SSRIs
Also blocks NE reuptake

22
Q

how venlafaxine differ from tcas

A 
Venlafaxine does NOT affect 
Adrenergic receptors
Histaminergic receptors 
Cholinergic receptors
Action of the TCAs on these receptors trigger majority of adverse effects
23
Q

venlafaxine contraindicated in patients on

A

MAOIs (and vice versa)

24
Q

Raising dose of ________ changes efficacy

A

Raising the dose of venlafaxine can improve efficacy, likely due to secondary mechanisms of action

25
Q

Mirtazapine mechanism

A

Blocking a2 receptors increases NE and 5-HT levels
On presynaptic adrenergic neurons (autoreceptors)
On serotonergic neurons (inhibiting additional 5HT release)(heteroceptors)
Also antagonizes postsynaptic 5-HT2 receptors –> antidepressant activity

26
Q

Ketamine mechanism

A

Potent, N-methyl-D-aspartate (NMDA) receptor antagonist

Growing evidence for elevated glutamate in depression

27
Q

Lithium carbonate mechanism

A

Unknown
involves effect on postsynaptic rather than presynaptic neuron
Interferes with the production and release of IP3 (phosphatdylinositol-4,5-bisphosphate) and DAG (diacyl glycerol)
Effects downstream from neurotransmission
alters gene expression implicated in long-term neuroplastic events that could underlie long-term mood stabilization

Neuro Week 7 (6 decks)

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