Epilepsy and Status Epilepticus Flashcards
(46 cards)
1
Q
Drugs that cause seizures
A
- antimicrobials
- anesthetic and analgesics
- immunosuppressants
- psychotropics
- radiographic contrast agents
- theophylline
- sedative hypnotic drug withdrawal
- drugs of abuse
- flumazenil
2
Q
Classification of seizures - General
A
- Generalized: begin on both hemisphere, bilat motor
- Focal/partial: 80% of adult epilepsies; asymmetric
- simple vs complex depends on LOC
- *depends on where the activity started**
3
Q
Physiological consequence of seizure
A
- increased consumption of oxygen and glucose
- increased production of lactate and carbon dioxide
- increased cerebral blood flow is generally sufficient to compensate for changes
- brief seizures rarely cause long-term sequelae
- sympathetic discharge causes tachycardia, hypertension, hyperglycemia
- difficulty maintaining airway (hypoxia, hypercarbia, respiratory acidosis)
4
Q
Effects of prolonged consequences
A
- lactic acidosis
- rhabdomyolysis
- hyperkalemia
- hyperthermia
- hypoglycemia
5
Q
First Seizure consideration
A
- primary objective is to determine if it is a seizure
- provoked vs unprovoked
- antiseizure medications are not always indicated after a first seizure
6
Q
Seizure imitators
A
- syncope
- psychological disorders
- sleep disorders
- paroxysmal mvmt disorders
- migraine
- TIA
7
Q
Active seizure
A
- most seizures remit spontaneously within 2 minutes
- rapid admin of a benzo is not required unless lasting more than 2 min
- secure IV access
- ID and treat any metabolic/infectious etiologies
- if h/o epilepsy, measure level of antiepileptic and optimize therapy
8
Q
Goals of treatment for seizures
A
- accurate diagnosis - find the cause
- suppress seizure activities
- minimize ADRs
- optimize QOL
9
Q
General treatment approach of seizures
A
- dx seizure type (focal/generalized)
- ID pt specific treatment goals
- monotherapy is preferred
- if another drug is needed, pick one with different MOA
- pt education is vital (titration, compliance, ADRs)
10
Q
Ideal pharmacokinetics characteristics of anticonvulsants
A
- good oral bioavailability
- penetration through BBB
- long half life
- low binding to plasma proteins
- lack of metabolism
- renal elimination
- linear pharmacokinetics
- no drug interactions
11
Q
Choosing and AED
A
- no single AED is most effective or best tolerated
- must consider the pt, their other meds, comorbidities
12
Q
Treating focal epilepsy - first line
A
- Lamotrigine and oxcarbazepine
- showed longest treatment time to treatment failure
13
Q
Treating general epilepsy - first line
A
- Valproate and lamotrigine superior to topiramate for treatment failure
- topiramate superior to lamotrigine for 12 months seizure remission
14
Q
High priority considerations for treating seizures
A
Post stroke
- worry about interactions w/other meds for stroke
Brain tumors
- worry about interactions w/chemotherapeutics
15
Q
General pharmacokinetics of AEDs
A
Dosing frequency
- vary among choices
Drug interactions
- hepatic inducers and inhibitors have greatest potential for interactions
Aging - may need to adjust dose or med
16
Q
General ADRs of AEDs
A
- Adverse drug rxns vary among AED
- neurocog side effects vary
- hypersensitivity rxns
- -Stephens Johnson syndrome and toxic epidermal necrolysis are rare but are reported
- weight gain or loss
17
Q
Black Box warning on all AEDs
A
- Increased risk of suicidality (esp in children and adolescents)
18
Q
Meds with renal excretion - consideration if pt has renal disease
A
- gabapentin
- topiramate
- zonisamide
- lacosamide
- levetiracetam
- pregabalin
19
Q
Meds that may require supplemental doses if pt is on dialysis
A
- phenobarbital
- ethosuximide
- lacosamide
- levtiracetam
20
Q
hepatotoxic meds - consideration if pt has hepatic disease
A
- valproate
- felbamate
21
Q
Considerations if pt has psychiatric disorders
A
- some AEDs have mood stabilizing effects
- some exacerbate depression (GABA potentiation mechanism)
22
Q
What AED should be avoided for pts with diabetes
A
- Valproate
- due to weight gain and insulin resistance
23
Q
AED and osteoporosis
A
Chronic AED use is associated with bone loss
24
Q
Which drugs act by prolonging inactivation of the voltage-sensitive sodium channel
A
- phenytoin
- carbamazepine
- lamotrigine
25
Which drugs enhance GABA mediated inhibition
- Direct
- -Benzodiazepine (BDZP)
- -barbiturates
- -topiramate
- Indirect
- -gabapentin
- -tiagabine
- -vigabatrine
26
Which drugs reduce glutaminergic excitation
AMPA
- topiramate
- phenobarbitol (PB)
27
Describe GABAergic Neuro transmission
- GABA receptors are expressed on most cell membranes of CNS neurons and astrocytes
- Affect
- -arousal/attention
- -memory formation
- -anxiety
- -sleep
- -muscle tone
28
AEDs that affect voltage gated Na+ channels
- carbamazepine
- oxcarbazepine
- phenytoin
- lamotrigine
- zonisamide
- lacosamide
- rufinamide
- elsicarbazepine
29
Indications of carbamazepine (tegretol)
- blocks Na+ channels
- Indicated for:
- -focal seizures
- -generalized seizures
- -also used in bipolar disorder and chronic pain
30
Pharmacokinetics and monitoring of carbamazepine
- 70% protein bound
- metabolism through auto induction (induces its own metabolism)
- -through first 20-30 days of treatment
- -autoinduction is dose dependent
- -after autoinduction is complete, steady state cxns after 3 days
31
Carbamazepine monitoring
- monitoring of serum concentration required for effective dosing
- monitor at 3, 6, 9 weeks and then bimonthly
32
Carbamazepine drug interactions
- potent inhibitor of may drug metabolizing enzymes and transporters
33
Dose Related ADRs of Carbamazepine
Dose related:
- vertigo
- ataxia
- diplopia
- drowsiness
- nausea
34
CNS ADRs of Carbamezepine - Not Dose related
CNS (not dose related): - HA
- paresthesias
- confusion
- psychosis
35
Non-specific ADRs of carbamazepine
- SIADH
- leukopenia
- thrombocytopenia
- stevens Johnson syndrome
36
What do you have to screen for regarding carbamazepine and Stevens-Johnson Syndrome
- need to screen for HLA-B*1502
| - Especially recommended in those with Asian descent
37
MOA and metabolism of Oxcarbazepine
- active metabolite blocks Na+ channels
| - analog of carbamazepine - minimal P450 interactions
38
Efficacy of oxcarbazepine compared to carbmazepine and phenytoin
- oxcarbazepine has equal efficacy compared to carbamazepine and phenytoin
- less side effects of carbamazepine and phenytoin
39
AEDs of oxcarbazepine
- Dizziness
- HA
- ataxia
- fatigue
- GI
- hyponatremia (2.5%)
- rash (and 30% cross reactivity for rash with carmabezepine
40
Monitoring of oxcarbazepine
NONE!!!!
| - and no autoinduction
41
MOA of phenytoin (dilantin)
- blocks Na+ channels
| - affects second messenger sxs
42
When is phenytoin indicated
- focal seizures
- generalized seizures
- status epiepticus
43
Pharmacokinetics of phenytoin
- metabolism by P450 system
- potent and non-specific inducer of many drug metabolizing enzymes including P450
- Highly protein bound
- non-linear kinetics
44
Monitoring of phenytoin
Close therapeutic monitoring
- therapeutic range 10-20 mg/L
- Check blood levels 2-3 weeks after first dose
- Low serum albumin or other protein bound drugs
- measure free levels vs total levels
45
Phenytoin considerations for Enteral feeding
- reduces oral absorption
| - oral suspension must be shaken vigorously
46
Phenytoin considerations for IV formulation
- basic pH
- concern with phlebitis and estravasation
- max infusion rate of 50mg/min
- no IM injections
