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28 Cards in this Set

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mechanism of MAOi's
there are two types of MAO receptors: a which catabolized 5HT and NE and B which catabolizes primarily phenylethylamine. both break down dopamine.
Nonselective MAOI's: irreversible or psuedoirreversible because of extended binding or covalent bond.
selective MAOaI: RIMA's the selectivity prevents tyramine toxicity because it is reversible binding.
Selective MAObI
Adverse effects of MAO I's
-weight gain
-Food interactions: wine, beer, cheese etc
-drug interactions: opiates TCA's SSRI's etc. lead to Tyramine toxicity which is then converted into NE which leads to hypertensive crisis
-postural hypotension
TCA mechanism
non selective inhibition of NE and 5HT reuptake. blocks intracellular transporter.
3 amine: NE = 5HT
Clomipramine 5HT> NE
2 amine NE >5HT
Amitriptyline, nefazodone and maprotiline, mechanims
TCA
block post synaptic 5HT2 receptors
TCA adverse effects
sedation!! antihistamine, antimuscarinic
cardiovascular tox.! arrhytmias, HTn crisis. from symapthomimetic effects.
inactivation of p450 metabolization of other drugs
contraindicated for seizure disorder, or fam Hx of
suicide risk
orthostatic HypoTN
SSRI mechanism
selectively inhibit 5HT reuptake metabolized by p450
citalopram>sertaline>fluoxetine

metabolites Norfluoxetine, desmethylcitalopram, desmethylsertaline
SNRI mechanism
selectively inhibits 5HT reuptake and inhibits NE reuptake
low does: SSRI
high does: inhibits both pumps.
SNRI AE
same as SSRI's also sympathomimetic effects with high dose
SSRI AE
serotonin syndrome:
agitation, tremor, HTN hyperthermia cardio collapse. interaction with MAOI.. need washout period.
GIT effects initial.
sexual dysfx
benefits of SSRI's
sertaline: good for refractory response to other SSRI's
reduce thrombogenic actions good for post MI
Buproprion
moderate ability to block DA reuptake. DA> NE>>>5HT
phenytoin/fosphenytoin
use dependent inhibition of na channel
partial seizures, status epilepticus
gingival hyperplasia, hirsuitism, stim. CYP450, osteomalacia, teratogen
carbamazapine
ude dependent inhibition of na channel, high plasma protein binding.
first line for partial seizures agranulocytosis, aplastic anemia, transient luekopenia,
phenobarbital
sedative and hypnotic
seizures
allosteric modulator of GABA a Rskin rash, tolerance, dependence, stimulates cyt 450, possible hyperexcited.
benzodiazapine: diazepam, lorazepam, clonazapam
rectal suppository
allosteric modulator of gaba a R. IV initial tx of status epilepticus.
tolerance dependencd, hyperexcite
valproate
enhances GABA transmission, blocks Na, activates K high plasma binding,
IV don't use with phenytoin, #1 for generlized seizures.
inhibits 450, hepatotox. teratogen, weight gain
ethosuximide
blocks tca channels in thalamus
absence seizures
GI distress, N/V
oxycarbazepine
use dependent inhibition of na cheannel augment K
add on tx
induces cyp3 inhibits cyp2ac19
gabapentine
inhibits specific ca cheannel that leads to decreased glutamate release
excreted by kidney,
lamotrogine
skin rash, use dependent inhibition of Na channel inhibits glu
Felbamate
skin rash, use dependent inhibition of Na channel induces cyp3
BLACK BOX
levetiacetam
anti epileptic
binds synaptic vesicle proteins to regulate glu release
Zonisamide
blocks t type ca
add on
topiramate
cyp3a induces inhibits cyp2c19 can cause kidney stones
absence seizure
valproate, ethosuximide
partial seizure
CBM, phenytoin
Status epilepticus
diazepam or lorazepam followed by phenytoin or phenobarb.
tonic clonic
valproate