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54 Cards in this Set

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anxiolytics
minor tranquilizer: a tranquilizer used to relieve anxiety and reduce tension and irritability
-antipanic/antianxiety agents
sedatives
drugs that reduce anxiety, stress, irritability, & excitement
drugs that calm ,ease agitation, & permit sleep
hypnotics
drugs that induce sleep
GAD
abnormal anticipation of potential danger
Panic attack
fear of the physiological rxn that occurs in response to immediate danger
locus coeruleus
source of nonadrenegic neurons in CNS
involved in physiological response to stress & panic
brain circuits in OCD
increased activity in cortico-basalganglia-thalamic network
-nuerotransmitter circuits between the cortex, basal ganglia, and thalamus are hyperactive
dopaminergic inputs from substantia nigra have an excitatory effect on
basal ganglia

overactivity proudces excessive excitation implicated in OCD
sertonergic inputs from raphe nuclei have an inhbitory affect on
basal ganglia

hypofunction results in lack of inhibition implicated in OCD
few drugs are just
anxiolytics

hypnotic effects can be achieved with most anxiolytic drugs just by increasing the dose
MOA of most anxoolytics & hypnotics
agonists at GABA receptors
GABAa receptor
GPCR
Cl - channel
BZD binding site
barbituate binding site
steriod binding site
picrotoxin binding site
barbituates
all have 6-membered ring
indicated for seizure prophylaxis & tx, anxiety, insomnia, and anesthesia induction
ultra short acting barbituates
thiopental
high lipid solubility
used to induce anesthesia
short-intermediate acting barbituates
amobarbital/seobarbital/pentobarbital
moderate lipid solubility

insomnia(no hang over effect)
induction of anesthesia
Long acting barbituates
low lipid solubility
phenobarbital
mephobarbital
tx seizure control & prolonged sedation
phenobarbital indicated for
emergency treatment of seizures but may still take 15 minutes for onset of action
short-acting barbs do not have anticonvulsant activity
barbituates
cognitive AEs
10x therapuertic dose: respiratory depression, coma, & death
increased LFTs
rapid development of pharmacodynamic tolerance to anxiolytic and sedative/hypnotic effects
barbituates as hypnotics
readily induces sleep but not a restful sleep
reduces REM
rebound REM sleep upon D/C
barbituate tolerance
tolerance develops to hypnotic and anti-anxiety effects but not as much to respiratory depression
barbituates abuse
highly lipophillic/quick onset of action are most abused (thiopental)
fatal rebound hyperexcitability due to convulsions upon D/C
BZD
lower incidence of tolerance compared to barbs
less severe withdrawal syndrome
greater therapuetic index
anterograde amnesia
loss of memory for events immediately following a trauma; sometimes in effect for events during and for a long time following the trauma
BZD
anxiolytic at low doses
hypnotic
anticonvuslant
muscle relaxant at high
BZP MOA
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
BZD compared to Barbs
less tolerance
fewer DIs
little increase in LFTs
BZDs MOA
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
Barbituates MOA
can directly open GABAa receptors unlike BZD

barbs unlike BZDs block AMPA receptors which are normally activated by glutamate(excitatory neurotransmitter)
glutamate
major excitatory nuerotransmitter
3 ionotropic glutamate receptors
glutamate is most important nuerotransmitter for normal brain function
-NMDA
-AMPA
-kainate
long acting BZDs
undergoe phase I & II metabolism
phase I produces active metabolite
phase II conjugates w/glucuronide to form water soluble inactive metabolite
long acting BZDs
chlordiazepoxide
flurazepam
diazepam
chlorazepate
short acting BZDs
only undergo phase II metabolism - conjugated with glucuronide to form water soluble inactive metabolite
short acting BZDs
lorazepam
midazolam
temazepam
BZDs as hypnotics
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
BZDs AEs
impaired coordination
N/V
confusion
memory loss
muscle relaxation via presynaptic inhibition of motor
circuits in spinal cord
can develop tolerance
convulsions upon withdrawal
are more common with barbs than BZDs
Flumazenal
BDZ antagonist
tx BDZ overdose
selective for anxiety
busprione>BZD>meprobamate>barbs>alcohol
Buspirone
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
Buspirone MAO
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)
advantages of buspirone in elderly
less interfence than BZDs with motor functions
buspirone onset of action is delayed due to
down-regulation of presynaptic 5HT1A receptors
serotonin inhibits
locus cerulus firing of NE which mediate fight/flight response
increased firing during periods of anxiety or panic attacks
Zolpidem
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)
hypnotic effects of ambien
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
hypnotics are z-drugs
zolpidem/ambien
zaleplon/sonata
zopiclone/imovane
eszopiclone/lunesta
Clonidine MOA
alpha-2 receptor agonist
inhibition of central and peripheral adrenergic neurotransmission can be anxiolytic
selective for anxiety
busprione>BZD>meprobamate>barbs>alcohol
Buspirone
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
Buspirone MAO
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)
advantages of buspirone in elderly
less interfence than BZDs with motor functions
buspirone onset of action is delayed due to
down-regulation of presynaptic 5HT1A receptors
OCD pharmacotherapy
SSRIs + clomipramine(TCA)
BZD during latency period of antidepressants
adjuncts: atypical antipyschotics LOW DOSES [high doses can cause OCD symptoms]