Case 13 SBA Flashcards

(58 cards)

1
Q

First line treatment for focal seizures with or without secondary generalisation

A

carbamazepine and lamotrigine

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2
Q

second choice treatments for focal seizures with or without secondary generalisation

A

oxcabazepine, sodium valproate, and levetiracetam

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3
Q

first line treatment for tonic-clonic seizures

A

sodium valproate

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4
Q

alternative treatment for tonic-clonic seizures and why is it not first line?

A

lamotrigine may exacerbate myoclonic seizures

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5
Q

treatment for absence seizures

A

ethosuximide or sodium valproate

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6
Q

treatment for newly diagnosed myoclonic seizures

A

sodium valproate

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7
Q

alternative treatments for myoclonic seizures

A

topiramate and levetiracetam

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8
Q

treatment for atonic and tonic seizures

A

sodium valproate with lamotrigine as adjunct if necessary

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9
Q

Sodium channel modulators that enhance fast activation

A

Phenytoin, carbamazepine, eslicarbazepine, lamotrigine

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10
Q

Sodium channel modulators that enhance slow inactivation

A

Lacosamide

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11
Q

Drugs that block t-type calcium channels

A

Ethosuximide and zonisamide

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12
Q

Calcium channel modulators - alpha-2-delta ligands

A

Gabapentin, pregabalin

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13
Q

GABA -A receptor allosteric modulators

A

Clonazepam, diazepam, phenobarbital (benzos ad barbiturates)

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14
Q

GABA uptake/GABA transaminase inhibitors

A

Tiagabine, vigabatrin

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15
Q

Synaptic vesicle 2A modulators with short-term plasticity

A

Levetiracetam

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16
Q

Anti-convulsants with mixed mechanisms of action

A

Topiramate and valproate

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17
Q

Which anti-convulsants can exacerbate absences and myoclonus?

A

Carbamazepine, oxcarbazepine, phenytoin

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18
Q

Which anti-convulsants are contraindicated in myoclonic epilepsies and can worsen seizures?

A

Gabapentin, pregabalin, tiagabine, vigabatrin

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19
Q

Which anti-convulsants can induce absence status epilepticus?

A

Tiagabine and vigabatrin

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20
Q

Which anti-convulsants have the lowest and highest risk of foetal malformations?

A

Valproate - 9.3%
Lamotrigine - 2.0%

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21
Q

Phenytoin effects on foetus

A

Craniofacial abnormalities and mild mental retardation

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22
Q

Side effects of phenytoin

A

Dose-dependent neurological, hirsutism, gingival hyperplasia, impaired insulin secretion, mild neuropathy, rash

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23
Q

Acute intoxication with carbamazepine effects

A

Stupor, coma, hyperirritability, convulsions, respiratory depression

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24
Q

Long-term side effects of carbamazepine

A

Drowsiness, vertigo, ataxia, diplopia, blurred vision, increased seizure frequency

25
Lamotrigine side effects
Rash - Stevens-Johnson syndrome, toxic epidermal necrolysis, rash-related death
26
Valproate side effects
Depression, ataxia, tremor, GI effects, hepatotoxicity and pancreatitis, prolonged actions of other drugs
27
Topiramate side effects
Somnolence, weight loss, fatigue, nervousness, may precipitate kidney stones
28
Tiagabine side effects
Dizziness, tremor, difficulty concentrating, depression, ataxia, somnolence, seizures
29
Perampanel side effects
Somnolence, anxiety, confusion, imbalance, diplopia, dizziness, GI upset Rarely: hostility, aggression, suicidal ideation
30
Felbamate side effects
Both very rare Aplastic anaemia with 30% fatality Hepatic failure with 40% fatality
31
Levetiracetam side effects seen in 13%
Agitation, hostility, apathy, anxiety, emotional liability, depression
32
Levetiracetam side effects seen in 1%
Serious psychiatric effects: hallucinations, suicidal thoughts, psychosis
33
Phenytoin mechanism of action
Voltage-dependent blockade of fast sodium current through prolongation of inactivated state which prevents repetitive firing
34
Phenytoin anti-convulsant use
Licensed in tonic-clonic and focal May exacerbate absence and myoclonic
35
Phenytoin pharmacokinetics
Narrow therapeutic window, non-linear, complex drug-drug interactions
36
Carbamazepine mechanism of action
Limits repetitive firing of action potentials evoked by a sustained depolarisation (sodium channels)
37
Carbamazepine usage
Primary drug for generalised and focal seizures Also used for trigeminal neuralgia
38
Clinical implications of carbamazepine pharmacokinetics
Short half-life so requires dose three times daily
39
Lacosamide mechanism of action
Selectively enhances sodium channel slow activation resulting in stabilisation of hyperexcitable neuronal membranes, inhibition of neuronal firing, and reduction in long-term channel availability without affecting psychological function
40
Lamotrigine mechanism of action
Acts on both sodium and calcium channels. Suppresses sustained rapid firing of neurons via inactivated state
41
Calcium channel effects of lamotrigine
May account for efficacy in childhood seizures and also leads to a decrease in synaptic release of glutamate
42
Valproate mechanisms of action (5)
Prolongs inactivated state of sodium channels Inhibits low-threshold t-type calcium channels Inhibits GABA transaminase Up-regulates glutamate decarboxylase Inhibits histone deacetylase
43
Zonisamide mechanism of action (4)
Slows activation of sodium channels Blocks t-type calcium channels Possible AMPA-R effects Enhances large-conductance calcium-activated potassium candles by decreasing mean closed time
44
Zonisamide usage
Focal seizures with or without secondary generalisation
45
Topiramate mechanism of action
Reduces sodium channels by inactivated state Activates hyperpolarising potassium current Enhances post-synaptic GABA-A receptor current Inhibits AMPA-kainate subtypes of glutamate receptors
46
Barbiturate and benzodiazepine mechanism of action
Positive allosteric modulators of GABA-A receptors
47
Diazepam use as anti-convulsant
First choice for status epilepticus with phenytoin for longer relief
48
Gabapentin mechanism of action
Elevates GABA synthesis via glutamate decarboxylase and branched chain aminotransferase Inhibits release through binding to alpha-2-delta subunit of voltage gated n-type calcium channels
49
Pregabalin use
Adjunctive for partial seizures with or without secondary generalisation Neuropathic pain
50
Tiagabine mechanism of action
Potent inhibitor GABA reuptake - preferentially GAT-1 in forebrain and hippocampus Lipophilic modification of nipecotic acid
51
Tiagabine usage
Adjunctive in partial Dose as often as four times daily
52
Perampanel mechanism of action
Non-competitive AMPA receptor antagonist
53
Perampanel usage
Adjunct in focal seizures
54
Felbamate mechanism of action
Positive allosteric modulator of GABA-A and use-dependent binding to glycine site at NMDA receptor reducing current amplitude
55
Levetiracetam and brivaracetam mechanism of action
Binds to SV2 and reduces short-term plasticity at glutamatergic synapses May alter protein-protein interactions at synapse
56
Ethosuximide usage
Choice for absence seizures
57
Ethosuximide mechanism of action
Reduces t-type calcium channel current without modifying voltage dependence of steady-state inactivation or time course of recovery from inactivation
58
Why does ethosuximide work for absence seizures?
The t-type currents it blocks are thought to provide the pacemaker current responsible for generating the rhythmic cortical discharge of an absence attack