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PR3136 > ANTI-EPILEPTIC > Flashcards

ANTI-EPILEPTIC Flashcards

1
Q

Seizure definition

A

A paroxysmal event due to an abnormal, hypersynchronous discharge from a mass of CNS neurons

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2
Q

Potential reversible & corrective causes of seizures (4)

A
  • alcohol
  • hypoglycemia
  • pyrexia
  • sleep deprivation
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3
Q

Is epilepsy treatable?

A

Yes

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4
Q

Diagnosis of epilepsy (4)

A
  1. Accurate diagnosis from clinical history & examinations
  2. Blood tests (LFT, blood chemistry)
  3. Brain scan (CT/MRI)
  4. EEG (electro encephalogram)
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5
Q

How does seizures occur?

A

A seizure occurs when there is an excessive synchronous depolarisation, usually starting from defined regions (“foci”) and spreading to other regions.
Due to the unbalanced excitatory and inhibitory receptor / ion channel function which favour depolarisation.
excitatory > inhibitory

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6
Q

Causes of epilepsy (5)

A
  1. Congenital or hereditary
  2. Brain injury, scarring or tumor
  3. Infections (meningitis or encephalitis)
  4. Blood glucose alterations
  5. Metabolic disorders (eg adrenal insufficiency leading to hyponatremia)
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7
Q

Types of epilepsy (3)

A
  1. Generalised epilepsy (entire brain)
    - Tonic clonic (Grand mal)
    - Absence (Petit mal)
    - Myoclonic (muscle jerking)
    - Atonic (not happening)
  2. Partial seizures (parts of the brain)
    - Simple (consciousness not impaired)
    - Complex (consciousness impaired)
  3. Status epilepticus (emergency situation)
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8
Q

MOA of anti-epileptic drugs (2)

A
  1. Decrease membrane excitability by altering Na+ & Ca2+ conductance during action potentials
  2. Enhance effects of inhibitory GABA neurotransmitters
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9
Q

Anti-epileptic drugs (4)

A
  1. Phenytoin
  2. Carbamazepine
  3. Valproate
  4. Benzodiazepines (Clonazepam, Lorazepam, Diazepam)
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10
Q

Phenytoin

A

MOA : blockage of voltage-dependent Na+ channel

  • all types of seizures except absence seizures
  • narrow therapeutic range, saturation kinetics & consequent non-linear relationship between dose & plasma conc
  • inter-individual variability
  • req titration & monitoring
  • CI : pregnancy (teratogenic)
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11
Q

Carbamazepine

A

MOA : blockage of voltage-dependent Na+ channel

  • all types of seizures except absence seizures
  • hepatic CYP450 inducer (itself metabolised by CYP450, hence half life of carbamazepine shortens with repeated doses & require higher dose) & increase metabolism of other drugs
  • DDI : CYP450 metabolism
  • risk of aplastic anaemia
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12
Q

Valproate

A

MOA : blockage of voltage-dependent Na+ & Ca2+ channel

  • also inhibit GABA transaminase, increase GABA receptors (open Cl- channel & thus hyperpolarisation)
  • all types of seizures INCLUDING absence seizures
  • DDI : plasma protein bound drugs (eg TCAs - imipramine, amitriptyline, nortriptylline), displaces other plasma protein bound drugs
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13
Q

ADR of anti-epileptics (dose-related) (9)

A
  1. drowsiness
  2. confusion
  3. change in mental status
  4. abnormal behaviours
  5. nystagmus
  6. ataxia
  7. slurred speech
  8. nausea
  9. coma
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14
Q

ADR of anti-epileptics (non-dose related) (6)

A
  1. hirsutism
  2. acne
  3. gingival hyperplasia
  4. folate deficiency
  5. osteomalacia
  6. hypersensitivity
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15
Q

Benzodiazepines (3)

A

MOA : binds to benzodiazepines binding site of GABA receptors to potentiate the binding of GABA to GABA binding site. This opens the Cl- channel to allow the influx of Cl- ions into the cell, causing cell membrane potential to be hyperpolarised. Hence inhibiting depolarisation and excitation of CNS neurones
- high risk of dependence and tolerance

eg Clonazepam (tonic clonic), Lorazepam (status epilepticus) & Diazepam (seizures, refractory seizured & status epilepticus)

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16
Q

How to pick the 1st line drug for anti-epileptic? (6)

A
  1. seizure types
  2. epilepsy syndrome
  3. co-medication (DDI)
  4. co-morbidity
  5. lifestyle & preferences (dosing freq & side effect tolerance)
  6. physicians’ preferences
17
Q

What if the 1st line monotherapy causes ADR in patients?

A

Change the type of drug but maintain as monotherapy.

Do not add on another drug.

18
Q

Drug for partial and generalised tonic clonic seizures

A
  1. Phenytoin
  2. Carbamazepine
  3. Valproate
19
Q

Monitoring of anti-epileptic drug concentration (3)

A
  1. Assessment of compliance to drug treatment for patients with refractory epilepsy
  2. Assessment of symptoms due to possible anti-epileptic drug toxicity
  3. Titration of phenytoin dose (narrow therapeutic window, saturation kinetics, non-linear relationship between dose and plasma concentration)
20
Q

Why is monitoring of anti-epileptic drug concentration not done regularly?

A

It is not cost effective and there is no clear indication for monitoring.

21
Q

Increased risk for breakthrough seizures (5)

A
  1. non-compliance to anti-epileptic drug
  2. DDI with anti-epileptic drugs causing plasma conc to be lower
  3. alcohol abuse
  4. sleep deprivation
  5. concurrent illness
22
Q

Differential diagnosis of epilepsy (2)

A
  1. Loss of awareness
    - transient cardiac arrhyhthmia
    - transient ischemic attacks
    - heart attacks
    - panic attacks
  2. abnormal movements
    - movement disorders in sleep and wake
    - tremors or paroxysmal choreoathetosis dystonia (sudden involuntary movements)
    - drop attacks and cataplexy (sudden loss of muscle tone)
23
Q

Cataplexy

A

sudden loss of muscle tone

24
Q

Choreoathetosis dystonia

A

sudden involuntary movements

25
Q

Risk of recurrent seizures

A
  1. low risk (30-50%)
    - normal EEG
    - normal brain scan
    - single seizure episode
  2. high risk (80%)
    - epileptiform EEG
    - abnormal brain scan (CT/MRI)
    - previous undiagnosed seizures
26
Q

Seizure = epilepsy?

A

Seizure is the event

Epilepsy is several events of seizures

27
Q

Realtime EEG and seizure occurence

A

When seizures ending, EEG can still look epileptic

28
Q

Structural abnormalities of the brain

A

EEG can appear abnormal even without any episodes of seizures

PR3136 (19 decks)

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