CNS- Depression & Anxiety Flashcards

1
Q

what is bipolar affective disorder?

A

mood swings not correlated to external environment.

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2
Q

what is the monoamine theory (NE, dopamine, 5-HT)

A

ˇ monoamine activity -> depression

ˆmonoamine activity-> ˆMood

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3
Q

what is the single drug treatment for bipolarism?

A

lithium alone

antipsychotics

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4
Q

what is the multiple medication treatment for bipolarism?

A

antipsychotic with antidepressant
lithium with antipsychotic
lithium with antidepressant

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5
Q

what is the lithium mechanism?

A

ˇ in precursors for IP3 and DAG synthesis therefore ˇIP3 and DAG when receptors linked to there secondary mesengers are activated

*it may ˆ serotonin neurotransmission and ˇ NE and dopamine neurotransmission

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6
Q

what is the adverse effect of lithium?

A

it has a narrow therapeutic index thus blood levels need to be monitored.

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7
Q

describe tricyclic antidepressants

A

primarily affect NE and serotonin,
not first chosen to use
side effects: block cardiac sodium channels
antagonist at: muscarinic, histaminic and alpha1 receptors.

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8
Q

describe bupropion

A

its unicyclic,

modest inhibitor of reuptake and stimulates release of DA and NE

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9
Q

describe the selective serotonin reuptake inhibitor (SSRI) fluoxetine (PROZAC)

A

side effects: insomnia, sexual dysfunction, ^ suicide rates
inhibits CYP2D6
overdose generally not dangerous unless combined with other antidepressants

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10
Q

what is serotonin syndrome?

A

when CYP2D6 metabolizes tricyclic antidepressants it combines with MAO inhibitors and causes serotonin syndrome.

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11
Q

what are monoamine oxidace inhibitors? (MAO) and in what case would you use them?

A

not selective for MAO-A, or MAO-B, therefore NE, serotonin, and dopamine pathways are all affected via their metabolites.
There are only used if tricyclic antidepressants are not effective.

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12
Q

what is the danger/toxicity with MAO inhibitors?

A

hypertensive crises can occur if thyramine-containing foods are ingested or if taking CNS stimulant like cocaine.
mix with SSRIS or SNRIS, or trycyclic antidepressants can cause serotonin-syndrome.

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13
Q

what is the clinical steps to prescribing antidepressants?

A
  1. SSRIs first (low dose for 8-12 weeks)

the dosage = balance between clinical effectiveness and adverse effects. `

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14
Q

what are some long term effects of antidepressants?

A

long-term treatments reported to alter sensitivity or levels of a verity of CNS receptor and neuronal growth factors

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15
Q

List some anxiety disorders

A

panic disorder
phobias
OCD
general

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16
Q

what is anxiety?

A

feelings of apprehension, tension, uncertainty and fear, its usually a secondary to other disorders. usually best treated with acting on primary illness

17
Q

what two kinds of sedative hypnotics are used to treat anxiety?

A
  1. benzodiazepines

2. barbiturates

18
Q

what is the pharmacokinetics of the benzodiazepine Diazepam.

A

phase 1: (oxidation by cytochrome p450; all metabolites active)
phase 2: (oxazepam conjugation with glucuronide)
oxidation—> active metabolite

19
Q

what is the method of action of the benzodiazepines?

A

it binds to subset of GABAa receptors distint from GABA, causes an opening of Cl- channels, and therefore ^ inhibition of many neurons. This enhances GABA neurotransmission, but it requires GABA for effect.

20
Q

what are the pharmacokinetics of the barbiturates phenobarbital?

A
Phase 1 (oxidation by cytochrome p450) 
phase 2 (conjugation with glucuronide)
21
Q

what is the method of action of barbiturates?

A

enhance GABA neurotransmission, by binding to all GABAa receptors at site distict from GABA and benzodiazepines.
high doses can directly activate GABAa receptors + inhibit glutamate receptors and high-frequency sodium channels

22
Q

what is the toxicity of dose-dependent sedative hypnotics?

A

CNS depression ( impaired judgement/ motor skills) -> amnesia -> coma -> death)

prolonged: symptoms of withdrawal.
* *barbituates= alter metabolism of self & other drugs