Test 3 - anticonvulsants (10/21) Flashcards
principle MOA of anti-seizure meds. (3)
1.modification of ion conductance (Na, K, Ca)
- enhancing inhibition (GABA)
- inhibiting excitation (glutamate)
Historical treatments of seizures
- Trephining (drilling into brain)
- cupping
- herbal remedies
- animal extracts
What causes seizures
Uncontrolled firing of CNS neurons
How much of the worlds population has seizures?
~1%
What are some of the causes of seizures?
variable
1. infection
2. neoplasm
3. head injury
4. heredity
5. toxic effects
6. metabolic disorder
Classification of seizures. what is the difference?
- focal - starts in small area of brain
- generalized - starts all over brain
What are the different focal seizures?
- simple focal
- complex focal
- Secondarily generalized
What do we see with simple focal seizures
- minimal spread of discharge
- don’t lose consciousness or awareness
- EEG may show normal discharge
What do we see with complex focal seizure. where do they arise from?
- affect level of consciousness
- may be unresponsive
- automatisms
-most arise from temporal lobes
What are the most common atiomatisms (5)
- lip smacking
- swallowing
- fumbling
- scratching
- walking about
what do we see with focal seizures secondarily generalized?
- begin as simple, but then spreads to rest of brain
- looks like generalized tonic-clonic
differentiate tonic and clonic
tonic- increased muscle tone all over body
clonic- rapid movement back and forth
What are the five generalized seizures?
- tonic clonic
- absence
- monoclonic
- atonic/tonic
- infantile spasms
What do we see with generalized tonic clonic seizures? what are the 3 phases?
-begin over entire surface of brain
- aura
- generalized tonic-clonic
- post-ictal
What do we see with absence (3)
- stare into space
- wake up, no notice of seizure
- some automatisms
What do we see with tonic seizures
- muscles contract and stiffen
- often falls down
Drop attack
what do we see with atonic seizures
- sudden loss of muscle tone
- fall without warning
- drop attack
What do we see with clonic and myoclonic
jerky mvmts
what do we see with infantile spasms (2)
- muscle spasms that affect childs head torso and limbs
- usually before age of 6 mo
Infantile seizures are indicative of ____
underlying pathology
Phenytoin is used for what seizures
- focal
- generalized tonic clonic
carbamazepine is used for what seizure type? What is it also used for? What kind of med is it?
Used for focal seizures.
Its a TCA (tricyclic antidepressant)
also used for trigeminal neuralgia and bipolar disorder
Pharmacokinetics for carbamazepine
D: increased protein binding (70% bound to plasma proteings)
M: induces hepatic enzymes
True/false. Carbamazepine enhances metabolism of most other AEDs.
True
Adverse effects with carbamazepine
diplopia and ataxia
Lacosamide is used for what seizure
focal
Phenobarbital is used for what kind of seizure
focal
generalized tonic clonic
Lamotrigine is used for what seizure
focal and absence
Ethosuximide is the drug of choice for what? what form does it come in?
absence.
can come in syrup form so good for kids
valrpoic acid is used for what seizure
broad spectrum. Absence, bipolar, migraine
What treatments can we use for infantile seizures
Often palliative. prednisone
GABA analog (keeps gaba around for longer period of time.)
MOA for phenytoin
alters Na, K and Ca conductance.
MOA for carbamazepine
blocks Na channel
MOA for lacosamide
blocks Na channel
MOA for phenobarbital
sedative-hypnotic
MOA for lamotrigine (lamictal)
ion channel blocker
uses for GABA analogs (vigabatrin)
adjunct, partial, neuralgia
MOA for ethosuxamide
Ca channel inhibition
MOA for valproic acid
Unknown but likely all.
-blocks high frequency firing
-effects on Na currents
-increase GABA
-increase K conductance
MOA for benzo
increase GABA
What do we worry about with phenytoin in regards to free form
it is highly protein bound so if we give a drug that completes for the binding site we can have more in the free form and it can be toxic in higher amounts
Toxicity for phenytoin
- nystagmus
- Diplopia (double vision)
- Sedation
- gingival hyperplasia
- hirsuitism
Pharmacokinetics of phenytoin
approaches zero order kinetics (see dosing, toxic levels)
half life for carbamazepine
half life after one dose is 36hrs
half life after continuous therapy is 20hrs
considerations for carbamazepine
inducer of cp450 (drug interactions)
compete for binding sites
Lacosamide (vimpat) toxicity
dizziness, nausea, HA, diplopia
phenobarbital toxicity
-sedation
-increase hepatic enzymes
Overdose
-respiratory depression
What is the drug of choice for infant seizures?
Phenobarb
What drug can actually worsen absence, drop, or infantile spasms
Phenobarb
ethosuximide toxicity
-gastric distress
-lethragy
valproic acid toxicity
-GI (N/V and heartburn)
-displaces phenytoin from proteins
-inhibits metabolism of other AEDs
Phenytoin and valproic acid interactions
Phenytoin is highly protein bound and valproic acid can compete for that binding site and kick phenytoin off and we can have high levels of free phenytoin (no bueno)
major considerations for status epilepticus
-life threatening emergency
-lasts at least 30min
-IV Benzo or fosphenytoin
describe the half life and duration for diazepam
long half life (20-100hrs)
short duration (30min)
Alternative therapies for seizures
craniotomy.
vagus nerve stimulation
keto diet
What do we need before starting treatment for seizures
firm diagnosis to tell what kind of seizure. EEG or imaging
anesthesia considerations during surgery of an epileptic patient
- adequate control during surgery
- phenytoin blocks NMB, higher levels can enhance.
- avoid methohexital, sevo, and demerol
