Seizure drugs Flashcards

1
Q

if patient has a normal brain scan, normal EEG, single seizure episode, what are the chances of it recurring?

A

low risk, 30-50%

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2
Q

if patient has eptileptiform EEG, previous seizures, abnormal brain scan, what are the chances of having a recurring seizure?

A

high chance 80%

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3
Q

what is the pathophysiology of seizure?

A

neuronal depolarisation depends on membrane potential.
seizure occurs when there is excessive synchronous depolarisation, usually starting from defined regions “foci”, spreading to other regions.
due to unbalanced excitatory and inhibitory receptors/ion channel function which favour depolarisation, it causes dysregulated discharge

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4
Q

causes of epilepsy?

A

hereditary
brain injury-scarring/ tumour
CSF infections- meningitis
blood glucose alterations ( hypoglycaemia)
metabolic disorders- adrenal insufficiency leading to hyponatremia

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5
Q

what is the difference between simple partial seizure and complex partial seizure?

A

simple alert
complex faints.

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6
Q

what is the MOA of antiepileptics? 2

A

1) decrease membrane excitability by altering NA+ and Ca2+ conductance during action potentials

2) enhance effects of inhibitory GABA neurotransmitters,

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7
Q

what is the indication of phenytoin?

A

suitable for all seizures except absence seizures

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8
Q

what is the adverse effect of phenytoin?

A

it is teratogenic

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9
Q

what is 1 impt thing to note about phenytoin regarding the toxicity level?

A

it has a narrow therapeutic level which requires close monitoring and titration plasma 40-100

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10
Q

what is the MOA of phenytoin and carbamazepine?

A

It blocks the Na+ channel thus blocking the sodium influx. This prevents neurons from firing rapidly and reduces brain excitability

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11
Q

examples of sodium channel blocker

A

phenytoin, carbamazepine

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12
Q

How does carbamazepine affect the half life of other drugs?

A

-It is a Hepatic enzyme (CYP450) inducer, T½ shortens with
repeated doses accelerates elimination of other
Drugs.
Thus the dosage of other drugs need to be higher.

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13
Q

adverse effect of carbamazepine

A

aplastic anemia- bone marrow is unable to produce enough RBC

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14
Q

MOA of sodium valproate?

A

it blocks sodium influx, calcium influx, inhibits GABA transaminase and enhance actions of GABA thus prevents neurons from firing rapidly and reduces brain excitability.

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15
Q

which medication is suitable for absence seizures?

A

sodium valproate

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16
Q

Dose related adverse effects of antiepileptics 9

A

drowsiness, confusion, nystagmus, ataxia, slurred speech, nausea, unusual behaviour, coma, mental changes

17
Q

Non dose related adverse effects: 6

A

hirsutism (excess hair), acne, gingival hyperplasia, folate deficiency, osteomalacia (softening of bones), hypersensitivity rxn: stevens johnson syndrome.

18
Q

MOA of benziodiazepine

A

Binding of GABA is enhanced by benzodiazepine, resulting in a greater entry of chloride ions.
entry of chloride ions hyperpolarize the cell, making it more difficult to depolarise (fire) and therefore reduce neural excitability

19
Q

do you give short acting benzodiazepine for seizure?

A

no

20
Q

examples of short acting benzodiazepine

A

midazolam, triazolam, oxazepam

21
Q

When are antiepileptic drug levels tested?

A

Antiepileptic drug levels may help clinical management
under the following clinical indications:
(1) Assessment of compliance to drug treatment for
patients with refractory epilepsy
(2) Assessment of symptoms due to possible
antiepileptic drug toxicity
(3)Titration of phenytoin dose.
Routine checking of antiepileptic drug levels without a
clear clinical indication is not required, and is not
cost effective.

22
Q

factors that increase risk for breakthrough seizures

A

– Non-compliance to antiepileptic
medication or drug
– Interactions with antiepileptic
medications lowering blood levels of
antiepileptic drugs.
– Alcohol abuse
– Sleep deprivation
– Concurrent illness