anticonvulsant drugs Flashcards
epilepsy
occurrence of at least 2 unprovoked seizures separated by 24 hours
partial/focal seizures
localized onset, ascertained either by observation or EEG 3 subcategories: -simple partial -complex partial -secondarily generalized seizure
simple partial seizure
minimal spread of abnormal discharge
normal consciousness
perserved awareness
complex partial seizure
localized onset, but discharge becomes widespread, almost always involves limbic system
pt may have automatisims, memory loss, aberrant behavior
secondarily generalized seizure
partial seizure immediately precedes a generalized tonic-clonic seizure
generalized seizures
those w/o evidence of localized onset clinical manifestation indicate involvement of both brain hemispheres 4 subcategories: -generalized tonic-clonic/grand mal -absence/ petit mal -myoclonic jerking -atonic
generalized tonic-clonic/grand mal
sudden sharp tonic contraction followed by rigidity and clonic mvmts
pt may cry/moan, lose sphincter control, bite tongue, cyanotic
after seizure pt may have altered consciousness, drowsiness, or confusion
absence/petit mal
sudden onset and abrupt cessation, altered consciousness, blank stare
young kids-adolescence
myoclonic jerking
brief, shock-like mm contraction’
occur in wide variety of seizures
atonic seizures
sudden loss of postural tone, head drop, fall to floor, slumping
many pts wear helmet
generalization of Rx seizure Tx
suppress do not cure
should try different monotherapies before combining drugs
compliance is VERY important
generics may not be a good idea
MOA of AEDs in general
- affect ion Ch kinetics (delay NaCh recovery)
- augmenting inhibitory neurotransmission
- modulating excitatory neurotransmission
PK of AEDs in general
cleared chiefly by hepatic metabolism
many are potent CYP inducers
general ADRs of AEDs
common neurotoxic effects- sedation, dizziness, blurred or double vision, difficulty concentrating, and ataxia
phenytoin MOA
- blocks sustained high frequency firing of APs d/t preferential binding and prolongation of inactivated NaCh
- decrease synaptic release of glutamate and enhances release of GABA
phenytoin PK
cannot be given IM- fosphenytoin can be injected highly protein bound elimination dose-dependent CYP meta narrow therapeutic index
phenytoin uses
partial seizures
generalized tonic-clonic seizures
phenytoin ADRs
gingival hyperplasia, hirsutism
in early use can present w/rash, fever, hepatits, and lymphadenopathy,
rarely causes dermatits and stevents-johnson syndrome
phenytoin long term ADRs
worsening facial features
mild peripheral neuropathy
vit D meta abnormalities -> osteomalacia
phenytoin cardiac ADRs
hypotension, bradycardia, cardiac arrythmia, CV collapse, venous irritation, pin, thrombophlebitis
Phenytoin DDIs
related to protein binding- sulfonamides
related to meta- warfarin (increased INR), OBC (increased risk of prego)
carbamazepine and oxcarbazepine MOA
NaCh -> inhibit high frequency repetitive firing
also acts presynaptically to decrease release of glutamate
carbamazepine and oxcarbazepine PK
hepatic meta
potent CYP inducer (including its own meta)
carbamazepine and oxcarbazepine uses
partial seizures, generalized tonic-clonic seizures, trigeminal neuralgia, mania in bipolar disorder
carbamazepine and oxcarbazepine ADRs
hyponatremia and water intoxication blood dyscrasias (fatal aplastic anemia and agranulocytosis, leukopenia)- monitor mild rash to stevens-johnson syndrome