Anti-Epileptics Flashcards
Definitions
seizure
epilepsy
status epilepticus
Seizure
- abnormal neruonal firing in the cortex: physical or sensory manifestation
- an acute neurological event
- diferent types, severity, apperance based on location of firing
- a seizure does NOT = epiliepsy dx.
Epilepsy
- the occurance of 2+ seizures separated by at LEASE 24 hours
- a chronic, recurring disorder with an underlying process
Status Epilepticus
- any seziure last > 5 minutes : this is when neuronal damange can occur
- or any 2 seizures happening without complete recovery or consciousness/recovery of first seizure between
How do you select the proper drug for seizure management
- identify the underlying cause of the seizure: if its due to hypoglycemia: give dextrose!
- type of seizure (tonic-clonic, absence, etc.) guides
- MOA of drug: if on multiple: want different MOAs
- ADE: of the meds can guide therapy
what are some medications that can worsen seizure
the common ones
& ones to be aware of
Common meds to cause/worsen seizures
- meperidine (opioid)
- flumazemil (benzo reversal agent)
- contrast dyes!!
- vaccines
- phenothiazines (anti-psychotics)
Imipenem = can reduce seizure threshold
buproprion = can lower seizure threshold
withdrawl from benzos, alcohol and opioids can worsen seizures
MOA: Sodium channel antagonism
MOA
- these AED’s will antagonize the sodium channels: prolonging the inactivity and ability for the Na+ channels to open
- this then reduces the ability of a neuron to fire = decreasing excitabilty and propagation of APs
MOA: Calcium Channel Modulators
MOA
- these drugs antagonize the calcium channel (N-type)
- they prevent the channels from releasing Ca+
- if Ca+ cannot be releasd: then there is no ability for the vesicel full of glutamate to fuse to the cleft and release into the synapse
- without the release of glutamate: there can be no excitatory potentiation down the cleft: no depolarizaiton
MOA: drugs that act on GABA
GABA: an inhibitory NT
some drugs = enhance GABA: thus inhibiting the ability for an AP to occur, decrease excitability
some drugs = inhibit GABA-transaminase: thus inhibiting the breakdown of GABA: leading to more
what AED (anti-epileptic drugs) can be used for an Absence seizure
EL VZ!!
E: ethosuximide (can ONLY be used for absence seizures)
L: Lamotrigine
V: Valproate
Z: Zonisamide
what AED’s must be AVOIDED in myoclonic and absence seizures
AVOID the following for absence and myoclonic seizures
- carbamazepine
- oxcarbmazepine
- gabapentin
- tiagabine
- pregabalin
these will all exacerbate the seizure
role of benzodiazepines in seizure control
what is used for status epi. vs. what is used for add-on
Reserved for Status Epi.
- Lorazepam
- midazolam
- diazepam
Used for Add-on to gain control with AED
- clonazepam
- clobazam
Benzodiazepines
MOA
Indications (seizure and other)
Benzodiazepines: MOA
- bind to post-synaptic GABA A receptors: increase the inhibition that GABA gives
Indications
- Benzos are first line in status epilepticus (lorazepam, midazalam, diazepam)
- can be used for focal or general seizures (clonazepam, clobazam)
- can be used to control Lennox-Gastuat (a seizure syndrome)
Additional Indications
- anxiety, insomnia, ICU sedation, alcohol withdrawl, etc.
Benzodiazepines
side effects
monitoring
Drug interactions
Side Effects/ADR
- respiratory depression : in status epi. youll intubate because you’re giving in such high doses
- drowsiness
- ataxia
- hypotension: dose-related, propylene glycol can be given with lorazepam and diazepam to help decrease this effect
- watch for withdrawal symptoms upon abrupt discontinuation: taper off
Monitoring
- watch RR: work of breathing, O2 status
- mental stauts & neuro exam
- BP! wathc for hypotension
Drug Interactions
- no monitoring needed
- watch interactions with otehr CNS depressants (opioids, alcohol,etc.)
Carbamazepine
MOA
Uses
Adverse Effects /ADR
Carbamazepine: AED (Tegretol)
- fast sodium channel inactivator with active metabolite also inactiving the Na+ channel
Uses
- focal and general seizures (no absence)
- bipolar disorder
- trigeminal neuralgia
- neuropathic pain
ADR
- these are all concentration dependent
- diplopia, drowsiness and sedation
- slgnificant N/V
- leukopenia
- Aplastic anemia
- hyponatermia
- rash: SJS risk
- decreased BMD
- teratogenic
Carbamazepine
Contraindications to Use
Monitoring Parameters
what about metabolism
Contraindiciations
- bone mineral density suppression: depression
- use of MAO within 14 days
- using nefaxdone
- using NNRTI (HIV med)
- presence of the HLA-B 1502 gene: if you CANNOT TEST FOR THIS; you CANNOT USE this med
Monitoring
- drug level 4-12mcg/mL
- must screen for HLA-B1502 gene
- monitor CBC: WBC > 2,500 & ANC > 1,000
- Na: keep 135-145
Metabolism
Carbamazepine is an AUTOinducer:meaning it will metabolize itself quicky at 3A4 then over time level out
- increase dose every week until adequte concentration
- starts 3- 5days; ends 21-28 : check levels weekly for first 3-5 weeks
PT. MUST BE ON FOLIC ACID 1-4 MG DOSING IF THEY ARE ON CARBAMAZEPINE
Oxcarbazepine
MOA
Indications
MOA
- a prodrug: converted and then its metabolite inactivates fast sodium channels
Indications
- generalized and focal seizures
- can be usd in those not responding to carbamaizepine
Side Effects
- well tolerated
- diplopid, dizzty, somnelence
- rash: watch if they had it to carbamaz. they’ll probs have it here too
- hyponatremia: more likely
Oxcarbazepine
monitoring
metabolism
Monitoring
- no therapeudic monitoring needed
- watch neuro exam
- watch sodium levels
Metabolism
- no autoinduction
- this drug can decrease the bioavalibility of estrogen in OCP medications
Ethosuximide
MOA
Indications (specific)
Side Effects
Monitoring
Ethosuximide:MOA
- a calcium channel modulator
Indications
only used for absence seizures!!!!! : the first-line medication
Side Effects
- well tolerated
- N/V
- ataxia and sedation
- neutropenic: monitor CBC
- rash
- hepatoxicity
Monitoring
drug levels should be 40-100mcg/mL
