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Justin Lyle Cards > Neuro 5 > Flashcards

Neuro 5 Flashcards

1
Q

drugs used to tx generalized seizures are determined by ________________

A

the seizure subtype

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2
Q

therapeutic strategy for tx of seizures (/ recommendation)

A
  1. use of single drug preferred 2. multiple drugs can be used simultaneously for pts with hard to control seizures 3. thepaeutic index for most anti-seizure meds is low 4. avoid abrupt withdrawal 5. newer drugs (after 1990) have broader spectrum of activity and many are well tolerated
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3
Q

T/F: increased seizure frequency and/or severity can occur with accidental or purposeful withdrawal of anti-seziure meds

A

TRUE

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4
Q

when is a trial of gradual discontinuation of anti-seizure medications appropriate

A

when seizure free x3-4 years

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5
Q

in general, anti-seizure medications are well absorbed with about ____________% reaching circulation

A

80-100%

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6
Q

general anti-seizure drug kinetics

A
  1. well absorbed 2. not highly protein bound 3. cleared via hepatic mechanisms 4. converted to active metabolites (CYP450 inducers) 5. plasma clearance is slow
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7
Q

which anti-seizure drugs are highly protein bound?

A
  1. phenytoin (dilantin) 2. tiagabine (gabatril) 3. valproic acid
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8
Q

phenytoin is used for what types of seizures

A

partial and generalized tonic-clonic

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9
Q

what is the IV form of phenytoin

A

fostphenytoin

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10
Q

what is the prodrug of phenytoin

A

fosphenytoin

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11
Q

phenytoin will decrease the synaptic release of _______________, while increasing the synaptic release of ___________________

A

gluatmate; GABA

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12
Q

at therapeutic levels the major action of phenytoin is to ?

A

block Na channels (pre-synaptic glutamate) and inhibit the generation of rapidly repetitive AP

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13
Q

fosphenytoin is a _____________________ compound that is rapidly converted to phenytoin in the plasma

A

phosphate ester

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14
Q

oral absorption of phenytoin

A

100%

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15
Q

___________________ is highly protein bound anti-seizure medication, and accumulates in the brain, liver, muscle, and fat

A

phenytoin

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16
Q

phenytoin is excreted via ____________________

A

urine

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17
Q

elimination of phenytoin is ___________________, via ______________ order kinetics

A

dose dependent; first

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18
Q

what is the 1/2 life of phenytoin

A

12-36 hours; with 24 hours being average for most pts

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19
Q

how long does it take for phenytoin levels to reach a steady state after each dose change

A

5-7 days (4 half-lives)

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20
Q

a dose change, at high level doses of phenytoin, could take up to ______________ before med reaches a steady state

A

4-6 wks

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21
Q

s/sx of phenytoin toxicity

A
  1. nystagmus 2. diplopia 3. ataxia 4. gingival hyperplasia 5. sedation 6. hirsutism
22
Q

what are early sx of phenytoin toxicity

A
  1. nystagmus 2. loss of smooth extra-ocular movements
23
Q

T/F: if pt on phenytoin starts showing nystagmus and loss of smooth extraocular movments you should decrease the dose

A

false; these are early signs of toxicity, but not indicators that dose needs to be decreased

24
Q

long term use of phenytoin can lead to

A
  1. coarsening of facial features 2. mild peripheral neuropathy 3. osteomalacia 4. vitamin D deficiencies 5. low folate levels 6. megoblasic anemia
25
Q

what are 2 common s/e of phenytoin that would indicated dose adjustment is needed?

A

diplopia and ataxia

26
Q

carbmazepine peak absorption is around _______________

A

6-8 hours

27
Q

carbamazepine 1/2 life

A

8-12 hours in tx patients; 36 h in normal subjects

28
Q

what type of seizures does carbamazepine tx

A
  1. generalized tonic clonic seizures 2. partial seizures
29
Q

s/e carbamazepine

A
  1. nausea 2. diplopia 3. ataxia 4. hyponatremia 5. HA
30
Q

MOA of valproate

A
  1. blocks high frequency firing of neurons 2. modified amino acid metabolism
31
Q

1/2 life of valproate

A

9-16 hours

32
Q

what types of seizures will valproate tx

A
  1. generalized tonic clonic 2. partial 3. generalized 4. absence 5. myoclonic
33
Q

s/e (toxicity) of valproate

A
  1. nausea 2. tremor 3. weight gain 4. hair loss 5. hepatotoxic 6. teratogenic
34
Q

MOA of lamotrigine

A
  1. blocks VG sodium channels 2. acts on VG Ca channels (presynaptically) both actions decrease release of glutamate
35
Q

1/2 life of lamotrigine

A

25-35 hours

36
Q

what types of seizures can lamotrigine tx

A
  1. generalized tonic clonic seizures 2. generalized seizures 3. partial seizures 4. absence seizures
37
Q

s/e (toxicity) of lamotrigine

A
  1. dizziness 2. HA 3. diplopia 4. rash
38
Q

MOA of levetiracetam

A

binds to synaptic vesicle protein SV2A (prevents the expulsion of gluatmate into synapse)

39
Q

levetiracetam is metabolized to _________ inactive metabolites

A

3

40
Q

1/2 life of levetiracetam

A

6-11 hours

41
Q

what types of seizures will levetiracetam tx

A
  1. generalized Tonic clonic 2. partial 3. generalized
42
Q

s/e (toxicity) of levetiracetam

A
  1. nervousness 2. dizziness 3. depression 4. seizures
43
Q

MOA of topiramate

A

multiple actions on synaptic fx probably via actions on phsophorylation

44
Q

____________% of topiramate is excreted into the urine unchanged

A

40%

45
Q

1/2 life of topiramate

A

20 h, but decreases with concomitant drugs

46
Q

what types of seizures will topiramate tx

A
  1. generalized tonic clonic 2. partial 3. generalized 4. absence 5. migraine
47
Q

s/e of topiramate

A
  1. somnolence 2. cognitive slowing 3. confusion 4. paresthesia
48
Q

all neuro meds except which class are CYP450 inducers

A

anti-depressants

49
Q

____________________ are anti-psychotic drugs that produce high incidence of extra-pyramidal s/e at clinically effective doses

A

neuroleptic (“typical”)

50
Q

what are examples of neuroleptic (“typical”) anti-psychotics

A
  1. phenothiazines: chlorpromazine 2. haloperiodl

Justin Lyle Cards (27 decks)

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