032415 anti-anxiety agents Flashcards

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1
Q

slow wave sleep has what neurotransmitter involved

A

serotonin

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2
Q

REM sleep has what neurotransmitter involved

A

NE

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3
Q

tx of anxiety and insomnia

A
  • benzodiazepines and related drugs (most commonly used)
  • SSRIs (commonly used for anxiety)
  • buspirone
  • classical antihistamines
  • alcohol, cannabis, opiates
  • barbiturates
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4
Q

GABA localization

A
substantia nigra
globus pallidus
hippocampus
limbic structures-amygdala
hypothalamus
spinal cord
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5
Q

GABA receptor

A

Cl ion channel that when Cl enters, hyperpolarizes neuron and makes it less likely to fire

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6
Q

benzodiazepines’ MOA

A

binds alpha subunit of the Cl channel. enhances GABA’s actions at the GABA receptor (causes more hyperpolarization per amt of GABA)

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7
Q

flumazenil

A

blocks action of benzodiazepines at the GABA receptor

used for overdoses of benzos, or for waking up from surgery

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8
Q

buspirone’s MOA

A

partial agonist of 5HT1A-inhibits adenylate cyclase and opens K channel

also binds dopamine receptors

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9
Q

alprazolam vs diazepam vs buspirone

A

alprazolam and diazepam depress the CNS and create dependence. they are both BDZ. alprazolam is short duration. diazepam is long duration.

buspirone produces little sedation and has no dependence. it has delayed onset

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10
Q

role of lipophilicity of benzodiazepines

A

diazepam has high lipid solubility-so rapid absorption into brain–has FAST onset of action.

lorazepam is less lipid soluble than diazepam, so absorption is slower. it has a longer duration of action after a single dose.

lipophilicity determines quick vs slow onset

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11
Q

metabolism of benzodiazepines

A

chlordizepoxide, DIAZEPAM, prazepam, chlorzepate get converted to desmethyldiazepam, which is an active metabolite and has LONG HALF LIFE.

OXAZEPAM, LORAZEPAM, alprazolam and triazolam don’t have active metabolites

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12
Q

CNS effects of BDZ

A
decreased anxiety
sedation
hypnosis
muscle relaxation
anterograde amnesia (IV)-dental work, colonoscopy
anticonvulsant
minimal CV and respiratory actions
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13
Q

drug interactions of BDZ

A

additive CNS depressionw most other depressant drugs (alcohol, etc)

drugs that affect hepatic metabolism like cimetidine

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14
Q

drug of choice for sleep disorders

A

BDZ

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15
Q

BDZ used for alcohol withdrawal

A

chlordiazepoxide

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16
Q

BDZ used for manic episodes

A

clonazepam (no EPS)

17
Q

benzodiazepine withdrawal

A

(when BDZ used at high doses for long period, creates tolerance and dependence)

anxiety, insomnia, irritability, headache, hyperacusis, hallucianations, seizures

18
Q

how to tx BDZ abuse

A

gradual dose reduction, or switch to longer acting drugs

19
Q

buspirone does not potentiate other sedative-hypnotics and depressants: true or false

A

true

20
Q

performance anxiety-what can you tx with?

A

beta blockers

21
Q

effects of BDZ on sleep

A
decreased latency to sleep (good for insomnia)
increased stage 1, 2 sleep
decreased stage 3, 4 sleep
decreased REM sleep
rebound insomnia upon withdrawal
22
Q

adverse effects of BDZ

A
daytime sedation
ataxia
rebound insomnia
tolerance and dependence
occasional excitement and stimulation
increased death rate?
23
Q

zolpidem and zaleplon MOA

A

NON-benzodiazepines chemically

bind to benzodiazepine receptor on GABA receptor complex

24
Q

eszopiclone MOA

A

similar to zolpidem and zaleplon

25
Q

ramelteon

A

melatonin MT1 and MT2 receptor agonist

26
Q

barbiturates’ MOA

A

act also on GABA receptor

27
Q

barbiturates’ side effects

A

respiratory depression

CV effects-if high doses, can produce sustained decreased in MAP and pulse pressure

28
Q

chloral hydrate

A

aldehyde hydrate with pungent taste
pharm is similar to barbiturates
less effects on stages of sleep than BDZ and barbiturates

29
Q

baclofen MOA

A

GABA mimetic agent that works at GABA B receptors, resulting in hyperpolarization and causing presynaptic inhibition. can result in decreased release of glutamate

30
Q

tizanidine

A

alpha2 adrenergic agonist related to clonidine

may enhance both presynpatic and postynpatic inhibition