CNS- Depression & Anxiety Flashcards Preview

BIOM*3090. UOG > CNS- Depression & Anxiety > Flashcards

Flashcards in CNS- Depression & Anxiety Deck (22)
Loading flashcards...

what is bipolar affective disorder?

mood swings not correlated to external environment.


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

ˇ monoamine activity -> depression
ˆmonoamine activity-> ˆMood


what is the single drug treatment for bipolarism?

lithium alone


what is the multiple medication treatment for bipolarism?

antipsychotic with antidepressant
lithium with antipsychotic
lithium with antidepressant


what is the lithium mechanism?

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


what is the adverse effect of lithium?

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


describe tricyclic antidepressants

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


describe bupropion

its unicyclic,
modest inhibitor of reuptake and stimulates release of DA and NE


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

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


what is serotonin syndrome?

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


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

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.


what is the danger/toxicity with MAO inhibitors?

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.


what is the clinical steps to prescribing antidepressants?

1. SSRIs first (low dose for 8-12 weeks)
the dosage = balance between clinical effectiveness and adverse effects. `


what are some long term effects of antidepressants?

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


List some anxiety disorders

panic disorder


what is anxiety?

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


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

1. benzodiazepines
2. barbiturates


what is the pharmacokinetics of the benzodiazepine Diazepam.

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


what is the method of action of the benzodiazepines?

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.


what are the pharmacokinetics of the barbiturates phenobarbital?

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


what is the method of action of barbiturates?

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


what is the toxicity of dose-dependent sedative hypnotics?

CNS depression ( impaired judgement/ motor skills) -> amnesia -> coma -> death)
prolonged: symptoms of withdrawal.
**barbituates= alter metabolism of self & other drugs