Pharmacology Of Anxiolytics, Sedatives, & Hypnotics

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anxiolytics

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minor tranquilizer: a tranquilizer used to relieve anxiety and reduce tension and irritability
-antipanic/antianxiety agents

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sedatives

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drugs that reduce anxiety, stress, irritability, & excitement
drugs that calm ,ease agitation, & permit sleep

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hypnotics

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drugs that induce sleep

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GAD

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abnormal anticipation of potential danger

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Panic attack

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fear of the physiological rxn that occurs in response to immediate danger

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locus coeruleus

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source of nonadrenegic neurons in CNS
involved in physiological response to stress & panic

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brain circuits in OCD

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increased activity in cortico-basalganglia-thalamic network
-nuerotransmitter circuits between the cortex, basal ganglia, and thalamus are hyperactive

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dopaminergic inputs from substantia nigra have an excitatory effect on

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basal ganglia

overactivity proudces excessive excitation implicated in OCD

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sertonergic inputs from raphe nuclei have an inhbitory affect on

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basal ganglia

hypofunction results in lack of inhibition implicated in OCD

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few drugs are just

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anxiolytics

hypnotic effects can be achieved with most anxiolytic drugs just by increasing the dose

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MOA of most anxoolytics & hypnotics

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agonists at GABA receptors

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GABAa receptor

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GPCR
Cl - channel
BZD binding site
barbituate binding site
steriod binding site
picrotoxin binding site

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barbituates

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all have 6-membered ring
indicated for seizure prophylaxis & tx, anxiety, insomnia, and anesthesia induction

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ultra short acting barbituates

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thiopental
high lipid solubility
used to induce anesthesia

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short-intermediate acting barbituates

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amobarbital/seobarbital/pentobarbital
moderate lipid solubility

insomnia(no hang over effect)
induction of anesthesia

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Long acting barbituates

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low lipid solubility
phenobarbital
mephobarbital
tx seizure control & prolonged sedation

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phenobarbital indicated for

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emergency treatment of seizures but may still take 15 minutes for onset of action
short-acting barbs do not have anticonvulsant activity

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barbituates

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cognitive AEs
10x therapuertic dose: respiratory depression, coma, & death
increased LFTs
rapid development of pharmacodynamic tolerance to anxiolytic and sedative/hypnotic effects

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barbituates as hypnotics

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readily induces sleep but not a restful sleep
reduces REM
rebound REM sleep upon D/C

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barbituate tolerance

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tolerance develops to hypnotic and anti-anxiety effects but not as much to respiratory depression

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barbituates abuse

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highly lipophillic/quick onset of action are most abused (thiopental)
fatal rebound hyperexcitability due to convulsions upon D/C

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BZD

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lower incidence of tolerance compared to barbs
less severe withdrawal syndrome
greater therapuetic index

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anterograde amnesia

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loss of memory for events immediately following a trauma; sometimes in effect for events during and for a long time following the trauma

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BZD

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anxiolytic at low doses
hypnotic
anticonvuslant
muscle relaxant at high

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BZP MOA

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enhances binding of GABA and results in greater entry of Cl- which hyperpolarizes the cell making it more difficult to depolarize & therefore reduces neuronal excitability

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BZD compared to Barbs

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less tolerance
fewer DIs
little increase in LFTs

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BZDs MOA

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allosteric enhancers of GABAa receptors
activate GABAa only in the presence of GABA
maximum level of CNS depression is limited by release of endogenous GABA

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Barbituates MOA

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can directly open GABAa receptors unlike BZD

barbs unlike BZDs block AMPA receptors which are normally activated by glutamate(excitatory neurotransmitter)

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glutamate

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major excitatory nuerotransmitter

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3 ionotropic glutamate receptors

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glutamate is most important nuerotransmitter for normal brain function
-NMDA
-AMPA
-kainate

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long acting BZDs

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undergoe phase I & II metabolism
phase I produces active metabolite
phase II conjugates w/glucuronide to form water soluble inactive metabolite

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long acting BZDs

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chlordiazepoxide
flurazepam
diazepam
chlorazepate

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short acting BZDs

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only undergo phase II metabolism - conjugated with glucuronide to form water soluble inactive metabolite

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short acting BZDs

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lorazepam
midazolam
temazepam

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BZDs as hypnotics

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reduces the amount of REM
causes rebound REM after withdrawal
deep refreshing sleep
unlike barbs, effectiveness as a sedative is largely determined by PK parameters rather than PD

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BZDs AEs

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impaired coordination
N/V
confusion
memory loss
muscle relaxation via presynaptic inhibition of motor
circuits in spinal cord
can develop tolerance

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convulsions upon withdrawal

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are more common with barbs than BZDs

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Flumazenal

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BDZ antagonist
tx BDZ overdose

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selective for anxiety

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busprione>BZD>meprobamate>barbs>alcohol

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Buspirone

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most selective anxiolytic
tx depression that often accompanies anxiety
does not enhance of CNS depressants
no associated w/drug dependence
no rebound anxiety/signs of withdrawal

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Buspirone MAO

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5HT1A presynaptic receptor agonist
-Gi/Go couples
-inhibit voltage activated Ca2+ channels which decreases serotonin release
-once all receptors are blocked they are internalized and sertonin secretion will increase(why takes several weeks for effect to take place)

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advantages of buspirone in elderly

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less interfence than BZDs with motor functions

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buspirone onset of action is delayed due to

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down-regulation of presynaptic 5HT1A receptors

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serotonin inhibits

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locus cerulus firing of NE which mediate fight/flight response
increased firing during periods of anxiety or panic attacks

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Zolpidem

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ambien
not BZD but binds to BZD receptor to enhance GABA binding to GABAa receptor
specific for GABAa receptors in sleep circuits which explains why its only a hypnotic and not anxiolytic or sedative

actions blocked by flumazenal (BZD antagonist)

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hypnotic effects of ambien

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last 1wk-6 months after D/C
safer than BZDs due to fewer AEs (more specific hypnotic action)
result in dependence but is not addictive

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hypnotics are z-drugs

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zolpidem/ambien
zaleplon/sonata
zopiclone/imovane
eszopiclone/lunesta

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Clonidine MOA

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alpha-2 receptor agonist
inhibition of central and peripheral adrenergic neurotransmission can be anxiolytic

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selective for anxiety

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busprione>BZD>meprobamate>barbs>alcohol

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Buspirone

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most selective anxiolytic
tx depression that often accompanies anxiety
does not enhance of CNS depressants
no associated w/drug dependence
no rebound anxiety/signs of withdrawal

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Buspirone MAO

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5HT1A presynaptic receptor agonist
-Gi/Go couples
-inhibit voltage activated Ca2+ channels which decreases serotonin release
-once all receptors are blocked they are internalized and sertonin secretion will increase(why takes several weeks for effect to take place)

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advantages of buspirone in elderly

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less interfence than BZDs with motor functions

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buspirone onset of action is delayed due to

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down-regulation of presynaptic 5HT1A receptors

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OCD pharmacotherapy

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SSRIs + clomipramine(TCA)
BZD during latency period of antidepressants
adjuncts: atypical antipyschotics LOW DOSES [high doses can cause OCD symptoms]