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
what are 2 common s/e of phenytoin that would indicated dose adjustment is needed?
diplopia and ataxia
26
carbmazepine peak absorption is around _______________
6-8 hours
27
carbamazepine 1/2 life
8-12 hours in tx patients; 36 h in normal subjects
28
what type of seizures does carbamazepine tx
1. generalized tonic clonic seizures 2. partial seizures
29
s/e carbamazepine
1. nausea 2. diplopia 3. ataxia 4. hyponatremia 5. HA
30
MOA of valproate
1. blocks high frequency firing of neurons 2. modified amino acid metabolism
31
1/2 life of valproate
9-16 hours
32
what types of seizures will valproate tx
1. generalized tonic clonic 2. partial 3. generalized 4. absence 5. myoclonic
33
s/e (toxicity) of valproate
1. nausea 2. tremor 3. weight gain 4. hair loss 5. hepatotoxic 6. teratogenic
34
MOA of lamotrigine
1. blocks VG sodium channels 2. acts on VG Ca channels (presynaptically) both actions decrease release of glutamate
35
1/2 life of lamotrigine
25-35 hours
36
what types of seizures can lamotrigine tx
1. generalized tonic clonic seizures 2. generalized seizures 3. partial seizures 4. absence seizures
37
s/e (toxicity) of lamotrigine
1. dizziness 2. HA 3. diplopia 4. rash
38
MOA of levetiracetam
binds to synaptic vesicle protein SV2A (prevents the expulsion of gluatmate into synapse)
39
levetiracetam is metabolized to _________ inactive metabolites
3
40
1/2 life of levetiracetam
6-11 hours
41
what types of seizures will levetiracetam tx
1. generalized Tonic clonic 2. partial 3. generalized
42
s/e (toxicity) of levetiracetam
1. nervousness 2. dizziness 3. depression 4. seizures
43
MOA of topiramate
multiple actions on synaptic fx probably via actions on phsophorylation
44
____________% of topiramate is excreted into the urine unchanged
40%
45
1/2 life of topiramate
20 h, but decreases with concomitant drugs
46
what types of seizures will topiramate tx
1. generalized tonic clonic 2. partial 3. generalized 4. absence 5. migraine
47
s/e of topiramate
1. somnolence 2. cognitive slowing 3. confusion 4. paresthesia
48
all neuro meds except which class are CYP450 inducers
anti-depressants
49
____________________ are anti-psychotic drugs that produce high incidence of extra-pyramidal s/e at clinically effective doses
neuroleptic ("typical")
50
what are examples of neuroleptic ("typical") anti-psychotics
1. phenothiazines: chlorpromazine 2. haloperiodl