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PMCOL 343 > antiseizure > Flashcards

antiseizure Flashcards

1
Q

is epilepsy just 1 disorder

A

no, it encompasses many disorders

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2
Q

what characterizes epilepsy

A

recurrent seizures (chronic disease) - heretogenous (several root causes) symptom complex

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3
Q

what is a seizure

A

finite period of brain dysfunction resulting from abnormal discharge of cerebral neurons

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4
Q

how do you figure out the degree of neural activity with electroencephalograms

A

you compare between pairs of electrodes (this allows a degree of localization of neuronal activity)

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5
Q

what are all seizures cause by

A

an imbalance between excitation and inhibition in brain

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6
Q

what are 2 types of partial seizures

A

simple and complex

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7
Q

what characterizes partial seizures

A

they have a localized onset

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8
Q

what are simple seizures like (3)

A

abnormal discharge with minimal spread - consciousness preserved

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9
Q

what are complex seizures like (4)

A

localized discharge with wide bilateral spread, usually limbic, loss of consciousness

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10
Q

is consciousness preserved in complex partial seizures

A

no

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11
Q

what is an aura

A

a sense that the seizure is starting

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12
Q

what are automatisms and when do they happen (which seizure type)

A

fragmented behaviours (like lip smacking, swallowing…) - complex partial seizures

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13
Q

can you have a partial seizure that then generalizes to a tonic clonic seizures

A

yes

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14
Q

what are 2 types of generalized seizures

A

generalized tonic clonic and absence (petit mal)

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15
Q

what do generalized tonic clonic seizures look like

A

full blown attack with rigidity (tonic), followed by alternating relaxation and rigidity, and jerking of body (clonic)

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16
Q

what do absence seizures look like

A

staring, altered consciousness, sometimes mild jerking of eyelids and extremeties

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17
Q

whats a heterogenous syndrome

A

where there are many diff symptoms possible, not just one thing

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18
Q

how do most of the anti-seizure drugs nowadays work (3)

A

reduce sympathetic excitation, enhance synaptic inhibition, block ion channels

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19
Q

what do anti-seizure drugs do to the sodium channel (2)

A

prolong inactivation to make repetitive firing more difficult

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20
Q

which kind of seizures do drugs that target Na+ channels work well for

A

partial seizures

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21
Q

which 4 drugs affect sodium channels

A

phenytoin, carbamazepine, lamotrigine, topiramate

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22
Q

how do drugs that target Ca2+ channels work

A

suppress activity of t-type Ca2+ channels, stopping oscillatory bursts

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23
Q

give 3 drugs that supress T-type Ca2+ channels

A

ethosuxamide, valproate, lamotrigine

24
Q

what does ethosuxamide do

A

block t type ca channel to stop oscillatory behaviour/ bursts

25
Q

what kind of seizure are ca2+ channel inhibitors good for

A

absence (eg. ethosuxamide)

26
Q

what do anti-seizure drugs want to do to GABA A receptors DIRECTLY

A

potentiate their action (GABA binds, channels open for longer)

27
Q

what do anti-seizure drugs want to do to GABA A receptors INDIRECTLY

A

reduce GABA uptake or metabolism

28
Q

which 2 drugs directly potential GABA A receptor action by either acting as an agonist/positive allosteric modulator

A

benzos and barbs

29
Q

which 3 drugs indirectly increase GABA levels by reducing the uptake/breakdown of GABA

A

gabapentin, tiagabine, vigabatrin

30
Q

which 2 drugs reduce glutamate action

A

phenobarbital and topiramate (they reduce excessive excitation)

31
Q

where does phenytoin act (which receptors)

A

Na+ K+ Ca++

32
Q

how does phenytoin do use dependent block of Na+ channel

A

it binds preferentially to inactive state of channel

33
Q

what does phenytoin do to Ca+ AND what does this cause

A

blocks influx so there is less ca-dependent secretory processes

34
Q

which kind of seizures in phenytoin best for

A

partial and generalized tonic clonic

35
Q

which 3 drugs are good for partial and generalized seizures

A

phenytoin, carbamazepine, phenobarbital

36
Q

what is the action of carbamazepine

A

similar to phenytoin (blocks K+ Ca+ Na+)

37
Q

what drug is used for trigeminal neuralgia

A

carbamazepine

38
Q

how does phenobarbital work (2)

A

suppresses (heavily) excitatory transmission, potentiates GABA A receptor activation (since it’s a barbituate)

39
Q

what are 3 main drugs just for generalized seizures

A

ethosuximide
valproid acid
benzos

40
Q

how does ethosuximide work

A

supresses T type Ca++ channels

41
Q

what is the type of seizure that ethosuximide is best for

A

absence seizures

42
Q

what is the mechanism of action for valproic acid

A

increase neuropeptide Y levels in brain (an antiseizure peptide)

43
Q

what kind of seizures is valproic acid good for (3)

A

absence, myoclonic, primary general tonic clonic

44
Q

when are benzos good for seizures

A

for acute seizure (status epilepticus), not for long term

45
Q

why dont you want to use benzos long term for seizures (2)

A

tolerance and sedation

46
Q

what is the mechanism of action of vigabatrin (2)

A

irreversible inhibitor of GABA-transaminase (breaks down GABA) AND inhibits GABA transporter

47
Q

what kind of seizures is vigabatrin good for

A

partial seizures

48
Q

what is the mechanism of action of tiagabine

A

GABA uptake inhibitor (GAT-1)

49
Q

what is the mechanism of action of lamotrigine

A

like phenytoin on Na+, also Ca+ (blocks)

50
Q

what kind of epilepsy is lamotrigine best used for

A

partial epilepsy and absence

51
Q

what is the main drawback for lamotrigine

A

rash can be life threatening especially for kids!!!

52
Q

what is the mechanism of action of felbamate

A

blocks NMDA on glycine sites (NR1 and NR2B)

53
Q

what kind of seizure is felbamate best for

A

focal/partial

54
Q

what are 2 really bad adverse effects for felbamate

A

aplastic anemia and severe hepatitis

55
Q

what is the mechnamism of action for topiramate

A

inhibits Na+ channels, potentiates GABA effects, inhibits AMPA receptors (Glu receptor)

56
Q

what is the unique structure like of topiramate

A

substituted monosaccharide

PMCOL 343 (31 decks)

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