Anti Convuslants

Front 1

When is therapy not required?
When is tx required?

Back 1

- single sz and no risk factors
- risk factor and repeated sz

Front 2

What happens to recurrence risk if tx is deferred?

Back 2

- higher rates of repeated sz

Front 3

What is a partial sz?
What is a generalized sz?

Back 3

1. involves cortical site from 1 hemisphere-simple or complex (w/ consciousness impairment)
2. Generalized-- involves both hemispheres

Front 4

How should one generally start anti sz meds?

Back 4

1. initiate slowly w/ monotx and titrate slowly- recheck later and adjust to reduce adverse SE

Front 5

What are the baseline labs?
What labs should be used for continuing tx?

Back 5

1. LFTs, serum albumin, CBC, urinalysis, and serum electrolytes
2. all above PLUS vitamin D levels

Front 6

AED- general AE

Back 6

- neurotoxicity-- mental stat changes- sedation, nystagmus
- sim among all anticonvulsants--dose related
- biggest problem of AED is in 3-6 mos
- this is limiting factor for many pts

- skin rash that may progress to steven johnson syndrome

- aplastic anemia, agranulocytosis
- hepatotoxicity- resolves
- delayed hypersensitivity rxn- which leads to irreversible hepatic failure

Front 7

What is one factor that favors low risk of recurrence after therapy termination?

Back 7

- min 2 yr sz free period
- normal EEG, short epilepsy before control of sz, monotherapy controlled, age less than 16 yrs at sz onset

Front 8

What is the general difference b/w 1st and 2nd generation pharmacotx?

Back 8

- 2nd generation are generally adjunctive tx, have less serious adverse rxns

Front 9

which drugs block voltage dependent sodium channels thus increasing the refractory period?

Back 9

Phenytoin, carbamzepine, oxcarbazepine, lamotrigine, and zonisamide

Front 10

Phenytoin, fosphenytoin- MOA, Use

Back 10

MOA: block voltage dependent sodium channels to increase refractory period
Use: good for all sz except absence

Front 11

Phenytoin, fosphenytoin- PK

Back 11

- slow and variable
- HIGHLY protein bound and small changes in albumin levels can change the levels of phenytoin available significantly
- enzyme inducer
- NON LINEAR elimination

Front 12

Phenytoin, fosphenytoin- AE

Back 12

- CNS, gingival hyperplasia, hirsuitism, acne, hyperpigmentation, arrythmias

Front 13

Carbamazepine- Use, MOA

Back 13

Use: partial and tonic-clonic seizures, trigeminal neuralgia, bipolar affective disorders
MOA: block voltage dependent sodium channels which increases refractory period

Front 14

Carbamazepine- PK

Back 14

- slow and erratic absorption
- is an enzyme inducer-- EVEN its own metabolism-- auto induction

Front 15

Carbamazepine- AE

Back 15

- rash-- stevens johnson syndrome, liver injury, agranulocytosis
- CNS, electrolyte imbalance

Front 16

Oxcarbazepine- PK, SE

Back 16

- sim to carbamazepine but NOT an auto inducer of enzymes
- inducer for other enzymes
- lower risk of heptaotoxicity
- AE: higher incidence of hyponatremia

Front 17

Lamotrigine- MOA, PK

Back 17

MOA: inhibits release of excitatory NTs- glutamate and aspartate

PK: valproic acid will inhibit metabolism and increase serum concentrations, enzyme inducers will decrease serum level s

Front 18

Lamotrigine- AE

Back 18

AE: benign rash in first 2 mos of use
- may develop Steven johnson syndrome, children at highest risk so do not use under 16 y/o

Front 19

Zonisamide- MOA, PK

Back 19

MOA- precise mech is not known but blocks Ca channels
AE: self limited CNS se, kidney stones b/c carbonic anhydrase is inhibited, rash esp if pt has sulfonamide allergy

Front 20

Ethosuximide- MOA

Back 20

- blocks Ca+2 currents

Front 21

Ethosuximide- MOA, Use

Back 21

- diminishes T type calcium currents in thalamic neurons
- changes rate of reactivation and voltage dependancy of the calcium channel
Use: DOC for absence seizure, no activity against general tonic clonic sz, or partial sz

Front 22

Ethosuximide- AE

Back 22

- CNS, GI, and behavioral changes-- hyperactivity and parkinsonian movements

Front 23

Phenobarbital- MOA, PK

Back 23

MOA: binds to GABA receptor and improves and extends the effect of GABA
PK: enzyme inducer, half life 2-6 days

Front 24

Phenobarbital- AE

Back 24

AE: use limiting sedation, irritability and hyperactivity in children and confusion in elderly ppl, sexual dysfx

Front 25

Gabapentin- MOA, PK

Back 25

MOA: increases Gaba through unknown mech
Pk: no liver metabolism-- 100% renal clearance-- must change for renally compromised pts

Front 26

Gabapentin- Use, AE

Back 26

Use: management of post herpes neuralgia, chronic pain, bipolar disorder. LESS COGNITIVE effects than other anticonvulsants
AE: sedation, wt gain, goes into breast milk

Front 27

Tiagabine- MOA, PK, Use

Back 27

MOA: inhibits GABA uptake into presyn neurons-- more availabe to post synaptic neurons
PK: protein bound
Use: add on for partial or generalized sz that are not well controlled

Front 28

Tiagabine- AE

Back 28

- seizures in pts w/o epilepsy and may aggravate myoclonic sz

Front 29

Pregabalin- MOA, PK, AE

Back 29

MOA: chem and struc sim to gabapentin which binds to calcium channel-- NTs reduction
PK: renal elimination-- 98% unchanged
AE: CNS and wt gain

Front 30

Valproic Acid- Use, MOA

Back 30

Use: partial and generalized sz, absence, bipolar disorder, and migraine prophylaxis
MOA: enhanced sodium channel inactivation sim to carbamazebine and phenytoin
- increased GABA by inhibiting its degradation

Front 31

VAlproic Acid- PK, AE

Back 31

PK- highly protein bound, liver enzyme inhibitor
AE: weight gain by stimulating appetite, LFTs increase, alopecia, teratogenic effects, hyperammonia

Front 32

Felbamate- MOA, PK

Back 32

MOA: blocks NMDA excitatory aa receptor
- augments GABA fx
PK: inhibits the cyp2c19, and induces cyp3A4

Front 33

Felbamate: Use, AE

Back 33

Use: effective, but recommended rt now fro refractory sz
AE: wt loss, CNS, aplastic anemia, acute liver failure ( acouple mos after tx)

Front 34

Topiramate- MOA, PK

Back 34

MOA: Blocks voltage dep socium channels, potentiates GABA receptors and antagonizes excitatory NMDA glutamate receptor
PK: renal excretion, at high doses is an enzyme inducer (>200 mg.day)

Front 35

Topiramate- AE

Back 35

- sedation, slow thinking, wt LOSS, kidney stones, hyperthermia

Front 36

Levetiracetam- MOA, PK, AE, Use

Back 36

MOA: may prevent hypersynchronization and propagation of sz activity
PK: renal elimination
AE: fatigue, URI, PERSONALITY changes
Use: broad spectrum of sz

Front 37

What drugs enhance the AED neurotoxicity?

Back 37

- alcohol, antidepressants, antihistaminees, antipsychotics, BZD, narcotic, and hypnotics

Front 38

Which AEDs are enzyme inducers?
Which AEDs are enzyme inhibitors?

Back 38

1. enzyme inducers- pheobarbital, carbamzepine, phenytoin, topiramate, oxcarbazepine
2. enzyme inhibitor- valproic acid

Front 39

Which drug was found to be worst teratogen? What are secondarily not recommended for pregnant pts?
Was polytherapy or monotherapy worse?

Back 39

- valproic acid
- phenytoin and phenobarb
- polytherapy

Front 40

How prevent NTDs due to lower levels of folate w/ AEDs?

Back 40

- folic acid supplement and monitoring serum levels of folate

Front 41

If drug is enzyme inducer than it will enhance metabolism of __________, so should also supplement pregnant pts w/ __

Back 41

1. vitamin K dep clotting factors
2. vitamin K

Front 42

Which drugs have high levels of crossing into breast milk?

Back 42

- those that are lipophillic and small-- ethosuximide, gabapentin, pregabalin, levetiracetam

Front 43

Epileptic pts are at a much higher risk to ___

Back 43

1. commit suicide