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Year 2 neuro exam 2 > Pharm anticonvulsants > Flashcards

Pharm anticonvulsants Flashcards

1
Q

definition of epilepsy

A

at least 2 unprovoked seizures separated by 24 hours

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2
Q

what single events can precipitate seizusres

A

withdrawal of CNS depressants
acute neuro illness or toxic systemic
fever

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3
Q

what is a simple partial seizure

A

minimal spread of abnormal discharge, normal consciousness, preserved awareness

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4
Q

what is a complex partial seizure

A

localized onset but discharge becomes widespread, almost always involves limbic system

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5
Q

characterstics of complex partial seizure

A

lip smacking, swallowing fubmling, scratching, memory loss or aberrant behavior

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6
Q

secondarily generalized seizure

A

partial that immediately precedes a generalized tonic clonic seizure

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7
Q

what is a generalized seixure

A

without evidence of localized onset, both brain hemispheres involved

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8
Q

what is a grand mal seizure

A

generalized tonic clonic
sudden, sharp tonic contraction followed by rigidity and clonic movements
patient may cry, moan, lose sphincter control, bite tongue or develop cyanosis

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9
Q

after grand mal seizure, patient may have

A

altered consciousness, drowsiness or confusion

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10
Q

postictal Sx of seizure

A

grand mal

generalized tonic clonic

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11
Q

what is an absence seizure

A

sudden onset and abrupt cessation, altered consciousness,
a blank stare
usually young children through adolescence

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12
Q

myoclonic jerking

A

brief shock like muscle contractions

occur in wide variety of seizures

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13
Q

atonic seizures

A

sudden loss of postural tone, head drop, fall to floor, slumping
many patients wear helmets to prevent head injury

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14
Q

AED treatments

A

suppress seizures but do not cure of prevent epilepsy

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15
Q

how do you switch AED Tx monotherapy

A

taper off initial AED after second AED is titrated to therapeutic level

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16
Q

MOA AED

A

affect ion channel kinetics
augmenting inhibitory neurotransmission
modulating excitatory neurotransmission

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17
Q

which AEDs are highly protein bound

A

phenytoin
tigabine
valproic acid

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18
Q

how are AEDs cleared

A

hepatic metabolism

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19
Q

Adverse effects AEDs

A

sedation, dizziness, blurred or double vision, difficulty concentrating and ataxia

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20
Q

MOA phenytoin

A

blocks sustained high frequency firing action potentials due to preferential binding to and prolongation of inactivated state of Na channel
also dec glutamate and enhances GABA release

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21
Q

PK phenytoin

A 
not IM
erratic absorption
highly protein bound
low dose first order kinetics
high dose disproprotionate elimination
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22
Q

use of phenytoin

A

partial seizures, generalized tonic-clonic seizures

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23
Q

adverse effects phenytoin

A

diplopia, ataxia, nystagmus, sedation, gingival hyperplasia, hirsutism

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24
Q

long term adverse effects phenytoin

A

worsening facial features, mild peripheral neuropathy

abnormalities in vit D metabolism causing osteomalacia

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25
Q

cardiac effects of phenytoin

A

hypotension, bradycardia, cardaic arrhythmia, CV collapse, venous irritation and pain, thrombophlebitis

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26
Q

DDI phenytoin

A

related to protein binding
sulfonamides by dispalce phenytoin from site increasing the amount of free drug!
CYP2C9, increased warfarin!!!
CYP3A4, increased risk pregnancy on oral contraceptives

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27
Q

MOA carbamazepine

A

acts on Na Ch resulting in inhibition of high frequency repetitive firing
also acts presynaptically to decrease synaptic release of glutamate

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28
Q

PK carbamezepine

A

autounduction, increased expression of CYPs and UGT

29
Q

use of carbamezapine

A

partial seizures, generalized tonic-clonic seizures, trigeminal neuralgia, mania in bipolar disorder

30
Q

adverse effects carbamazepine

A

diplopia, ataxia, mild GI upset, unsteadiness, drowsiness
hyponatremia and water intoxication
idiosyncratic blood dyscrasias
rash, sometimes stevens johnson

31
Q

what patients at higher risk stevens johnson syndrome reaction from carbamazepine

A

asians with HLA B*1502

32
Q

DDI carbamazepine

A

hepatic enzyme induction leading to increased metabolism of other drugs

33
Q

what drug inhibits carbamazepine clearance (increased levels)

A

valproic acid

34
Q

what drug has fewer DDI than carbamazepine

A

oxcarbazepine

35
Q

MOA phenobarbital

A

binds GABA and enhances GABA mediated current by prolonging Cl Ch

36
Q

MOA gabapentin

A

analogs of GABA

bind 2alphadelta on vNtype Ca Ch decreasing Ca, decreasing release of glutamate

37
Q

use of gabapentin

A

partial seizures, generalized tonic-clonic seizures, neuropathic pain
post herpetic neuralgia

38
Q

adverse to gabapentin

A

somnolence, dizziness, ataxia, HA, tremor

39
Q

MOA lamotrigine

A

like pheytoin suprres neurons through inactivation Na Ch

inhibits vCa Ch

40
Q

uses of lamotrigine

A

> 2y.o with partial seizures or generalized
also used for monotherpay partial seizures
adjunct in primary generalized tonic clonic
absence
bipolar

41
Q

adverse effects lamotrigine

A

dizziness, HA, diplopia, ataxia, nausea, somnolence, skin rash

42
Q

DDI lamotrigine

A

concentrations decrease with use oral contraceptives (E component)
may lead to contraceptive failure in P only pill

43
Q

MOA levetiracetam

A

binds to synaptic vesicular protein SV2A modifies synaptic release of glutamate and GABA through action on vesicular function

44
Q

use of levetiracetam

A

adjunct for partial seizures in adults and children
primary generalized tonic clonix
myoclonic seizures of jevenile epilipsy

45
Q

adverse effects levetiracetam

A

somnolence, asthenia, ataxia dizziness

46
Q

adverse effect tigabine

A

cause seizures in some patients who take tiagabine for bipolar disorder, anxiety and neuropathic pain

47
Q

MOA ethosuximide

A

reduce threshold Ca T type which are pacemaker for thalamic neurons

48
Q

use of ethosuximide

A

absence seizures

49
Q

adverse effects ethosuximide

A

gastric distress, pain , nausea and vomiting

50
Q

DDI ethosuximide

A

valproic acid can inhibit metabolism of ethosuximide

51
Q

MOA valproic acid and Na valporate

A

blocks firing of neurons through Na currents
blocks NMDA R mediated excitation
increased levels GABA in brain

52
Q

use of valproic acid

A 
absence seizures
myoclonic seizures
generalized tonic clonic seizures
partial seizures
status epilepticus (IV
bipolar disorder
migraine prophylaxis
53
Q

adverse effects valproic acid

A

nausea, vomiting, abdominal pain, heartburn
fine tremor
weight gain, hair loss
hepatotoxicity and thrombocytopenia

54
Q

what must you monitor if put patient on valproic acid

A

liver function because of hepatotoxicity

55
Q

MOA diazepam

A

bind GABAa R

increase GABA Cl Ch to increase inhibitory membrane potentials

56
Q

PK diazepam

A

lipophilic, goes to CNS in sec when IV

redistributes to fat quickly

57
Q

why do you give a longer acting AED after giving diazepam

A

prevent seizure recurrence

58
Q

therapeutic use diazepam

A

status epilepticus, adjunct, myoclonic, partial, and generalized tonic clonic seizures

59
Q

adverse effects to diazepam

A

sedative
drowsiness
ataxia
behavior disorders

60
Q

first DOC for partial seizures and secondarily generalized

A

carbamazepine
or lamotrigrine
or oxcarbazepine
or levetiracetam

61
Q

second line of drugs for partial seizures or secondarily generalized

A

topiramate, gabapentin, pheytoin

62
Q

first DOC for primary generalized tonic clonic or grand mal

A

valporate
lamotrigine
levetiracetam

63
Q

second line for grand mal seizure

A

carbamazepine, phenytoin

64
Q

first DOC for absence seizures

A

ethosuximide

or valproate

65
Q

second DOC for absence seizures

A

lamotrigine

levetiracetam

66
Q

first DOC for atypical absence of myoclonic or atonic seizures

A

valproate
lamotrigine
levetiracetam

67
Q

teratogenicity of AED

A

increased risk congenital malformations

68
Q

phenytoin teratogenicity

A

fetal hydantoin syndrome (abnormal skull, facial features, growth deficiency, underdeveloped nails or mild developmental delays)

69
Q

what AED indicated in spina bifida

A

valproate

Year 2 neuro exam 2 (23 decks)

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