SEIZURES Flashcards

(72 cards)

1
Q

myoclonic seizure

A

shock like contraction of muscles
isolated jerking

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2
Q

tonic seizure

A

in children
rigididy as a result of increased tone in extensor muscles

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3
Q

clonic seizure

A

babies and young children
rapid and repetitive movement

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4
Q

atonic seizure

A

sudden loss of muscle tone
patients fall if standing

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5
Q

tonic clonic

A

tonic phase - rigidity followed by clonic rapid motion

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6
Q

seizure definition

A

paroxysmal disorder of CNS by abnormal cerebral discharges with or without loss of consciousness

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7
Q

convulsion

A

attack manifested by involuntary muscle movements

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8
Q

epilepsy

A

repeated seizures due to damage, irritation, chemical imbalance in brain
- sudden electrical discharge

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9
Q

what kind of firing is in seizures

A

disordered, synchronus, rhythmic
synchronized hyperexcitability

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10
Q

seizure classifications

A

focal onset
generalized onset
unknown onset

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11
Q

focal onset location

A

comes from one place in the brain
being in temporal lobe

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12
Q

generalized onset location

A

all over the brain

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13
Q

focal seizures usually due to

A

lesion, head trauma, infection

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14
Q

generalized seizures description

A

loss of consciousness, both brain hemispheres, idiopathic, usually genetic

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15
Q

how do primary generalized seizures propagate

A

diffuse via interconnections between thalamus and cortex

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16
Q

difference in EEG for focal vs. generalized seizure

A

focal has different waves
generalized all has the same

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16
Q

aware focal seizures

A

no loss of consciousness
auras can occur
limited jerking of single part of body

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17
Q

impaired awareness focal seizures

A

most common
clouding of consciousness
repetitive motor behaviors
POSITICTAL STATE
aura common

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18
Q

generalized absence seizure typical

A

no convulsions, aura, postictal period, brief loss of consciousness
staring or eye flickering

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19
Q

generalized absence seizure atypical

A

slower onset than typical

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20
Q

do generalized tonic clonic have aura

A

no

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21
Q

do focal to bilateral have aura

A

brief aura

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22
Q

status epileptics definition and goal

A

seizure lasting > 30 mins
want to bring seizures within 60 minutes

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23
Q

does one seizure make an epilepsy

A

no

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24
when should we stop drug therapy in seizures
gradually stopped who havent had seizures in 2-5 years
25
depolarization involves what
activation AMPA and NMDA by glutamate and Ca channels influx of Ca
26
hyperpolarization involves what
activation GABA receptors and K+ channels influx Cl and efflux K+
27
can we stop epilepsy drugs suddenly
no, higher risk for status epilepticus
28
drugs that increase risk of seizure
alcohol bupriopion theophylline CNS stimulants oral contraceptives depressant withdrawal clozapine
29
MOA anticonvulsants
stabilize and reduce neuronal excitability
30
drugs that decrease sodium influx, prolong inactivation of Na+ channels
carbemazepine oxcarbazepine phenytoin lacosamide lamotrigine valproate
31
drugs that decrease Ca influx
lamotrigine ethosuximide valproate
32
drugs that increase GABA inhibition
barbituates benzodiazepines valproate gabapentin vigabatrin tiagabine
33
excitatory antagonists
felbamate topiramate
34
why are there few drugs targeting K channels
hERG target, bad side effects like arrythmias
35
excitatory pre synaptic targets
Na channels Ca channels
36
excitatory post synaptic targets
NMDA AMPA
37
inhibitory pre synaptic targets
GABA transporter (GAT-1) GABA transaminase (GABA-T)
38
inhibitory post synaptic targets
GABA A and B receptors
39
phenytoin MOA
binds inactive state Na channel not isoform selective- other targets
40
what is fosphenytoin
prodrug phenytoin IV
41
phenytoin kinetics are
non linear, dose dependent
42
phenytoin interactions
displaced from plasma proteins (increase blood level conc) induces P450s (inc. conc of other drugs)
43
side effects phenytoin
arrythmia visual ataxia - loss coordination GI sx hirsutism rash
44
carbemazepine and oxcarbazepine structure
tricyclic
45
carbemazepine and oxcarbazepine MOA
binds and stabilizes inactivated state of Na channels
46
carbemazepine and oxcarbazepine interactions
cyp450, increase its metabolism
47
carbamazepine side effects
blurry vision, ataxia, GI, sedation, rash (Stevens Johnson sydrome),eosinophillia / DRESS
48
lacosamide MOA
enhances inactivation of Na+ channels
49
lacosamide toxicity
dermatological reactions, cardiac risk (PR interval), visual disturbances
50
barbituates drugs
phenobarbitol primidone
51
who is phenobarbital drug of choice in
infants up to 2 months
52
phenobarbital MOA
binds to allosteric site on GABA a a increases DURATION Cl- channel opening
53
phenobarbital toxicities
sedation, dependance (abuse)
54
benzodiazepine drugs
diazepam clonazepam
55
diazepam use
tonic-clonic status epilepticus, rectal gel
56
diazepine MOA
binds allosteric regulatory site on GABA - A receptor, increases FREQUENCY of Cl- channel opening events
57
diazepam toxicity
sedation, physcial dependance, not useful for chronic treatment
58
clonazepam use
acute treatment of epilepsy and absence seizures
59
gabapentin and pregabalin MOA
increase GABA release, decrease Ca influx, reduce glutamate release
60
vigabatrin MOA
irreversible inhibitor of GABA-T, which degrades GABA
61
tigabine MOA
inhibits GAT-1, gaba transporter
62
felbamate MOA
NMDA receptor antagonist
63
felbamate toxicity
severe hepatitis
64
topiramate MOA
AMPA and kainate antagonist
65
ethosuximide MOA
blocks T type Ca channels in thalmic neurons
66
lamotrigine MOA
inhibits Na and Ca channels
67
lamotrigine side effect
skin rash, stevens johnson syndrome
68
valproate MOA
inhibits Na and Ca chanels increases GABA
69
levitiracetam MOA
binds synaptic protein vessel SV2A, interferes with synaptic vessel release and neurotransmission also interferes with Ca entry
70
encephalopathy < 3 mo tx
phenytoin
71
encephalopathy > 3 mo tx
levitracetam