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Medicine Year 1 > Case 13 SBA > Flashcards

Case 13 SBA Flashcards

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
Q

Lamotrigine side effects

A

Rash - Stevens-Johnson syndrome, toxic epidermal necrolysis, rash-related death

26
Q

Valproate side effects

A

Depression, ataxia, tremor, GI effects, hepatotoxicity and pancreatitis, prolonged actions of other drugs

27
Q

Topiramate side effects

A

Somnolence, weight loss, fatigue, nervousness, may precipitate kidney stones

28
Q

Tiagabine side effects

A

Dizziness, tremor, difficulty concentrating, depression, ataxia, somnolence, seizures

29
Q

Perampanel side effects

A

Somnolence, anxiety, confusion, imbalance, diplopia, dizziness, GI upset
Rarely: hostility, aggression, suicidal ideation

30
Q

Felbamate side effects

A

Both very rare
Aplastic anaemia with 30% fatality
Hepatic failure with 40% fatality

31
Q

Levetiracetam side effects seen in 13%

A

Agitation, hostility, apathy, anxiety, emotional liability, depression

32
Q

Levetiracetam side effects seen in 1%

A

Serious psychiatric effects: hallucinations, suicidal thoughts, psychosis

33
Q

Phenytoin mechanism of action

A

Voltage-dependent blockade of fast sodium current through prolongation of inactivated state which prevents repetitive firing

34
Q

Phenytoin anti-convulsant use

A

Licensed in tonic-clonic and focal
May exacerbate absence and myoclonic

35
Q

Phenytoin pharmacokinetics

A

Narrow therapeutic window, non-linear, complex drug-drug interactions

36
Q

Carbamazepine mechanism of action

A

Limits repetitive firing of action potentials evoked by a sustained depolarisation (sodium channels)

37
Q

Carbamazepine usage

A

Primary drug for generalised and focal seizures
Also used for trigeminal neuralgia

38
Q

Clinical implications of carbamazepine pharmacokinetics

A

Short half-life so requires dose three times daily

39
Q

Lacosamide mechanism of action

A

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
Q

Lamotrigine mechanism of action

A

Acts on both sodium and calcium channels. Suppresses sustained rapid firing of neurons via inactivated state

41
Q

Calcium channel effects of lamotrigine

A

May account for efficacy in childhood seizures and also leads to a decrease in synaptic release of glutamate

42
Q

Valproate mechanisms of action (5)

A

Prolongs inactivated state of sodium channels
Inhibits low-threshold t-type calcium channels
Inhibits GABA transaminase
Up-regulates glutamate decarboxylase
Inhibits histone deacetylase

43
Q

Zonisamide mechanism of action (4)

A

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
Q

Zonisamide usage

A

Focal seizures with or without secondary generalisation

45
Q

Topiramate mechanism of action

A

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
Q

Barbiturate and benzodiazepine mechanism of action

A

Positive allosteric modulators of GABA-A receptors

47
Q

Diazepam use as anti-convulsant

A

First choice for status epilepticus with phenytoin for longer relief

48
Q

Gabapentin mechanism of action

A

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
Q

Pregabalin use

A

Adjunctive for partial seizures with or without secondary generalisation
Neuropathic pain

50
Q

Tiagabine mechanism of action

A

Potent inhibitor GABA reuptake - preferentially GAT-1 in forebrain and hippocampus
Lipophilic modification of nipecotic acid

51
Q

Tiagabine usage

A

Adjunctive in partial
Dose as often as four times daily

52
Q

Perampanel mechanism of action

A

Non-competitive AMPA receptor antagonist

53
Q

Perampanel usage

A

Adjunct in focal seizures

54
Q

Felbamate mechanism of action

A

Positive allosteric modulator of GABA-A and use-dependent binding to glycine site at NMDA receptor reducing current amplitude

55
Q

Levetiracetam and brivaracetam mechanism of action

A

Binds to SV2 and reduces short-term plasticity at glutamatergic synapses
May alter protein-protein interactions at synapse

56
Q

Ethosuximide usage

A

Choice for absence seizures

57
Q

Ethosuximide mechanism of action

A

Reduces t-type calcium channel current without modifying voltage dependence of steady-state inactivation or time course of recovery from inactivation

58
Q

Why does ethosuximide work for absence seizures?

A

The t-type currents it blocks are thought to provide the pacemaker current responsible for generating the rhythmic cortical discharge of an absence attack

Medicine Year 1 (23 decks)

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