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Year 2 - LCRS - Pharmacology > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

1
Q

What is epilepsy?

A
  • A neurological condition causing frequent seizures
  • Seizures are “sudden changes in behaviour caused by electrical hypersynchronization of neuronal networks in the cerebral cortex”
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2
Q

Prevelance and Incidence of Epilepsy

A
  • Prevalence between 2-7% of the population

- Incidence increased over the last 30-40 years

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3
Q

Diagnosis of Epilepsy

A
  • Brain activity can be measured using:
    • Electroencephalography (EEG)
    • Magnetic resonance imaging (MRI)
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4
Q

Seizure types & Symptoms

A

General

  1. Tonic-clonic seizures: loss of consciousness -> muscle stiffening -> jerking/twitching -> deep sleep -> wakes up
  2. Absence seizures: brief staring episodes with behavioural arrest
  3. Tonic/atonic seizures: sudden muscle stiffening/sudden loss of muscle control
  4. Myoclonic seizures: sudden, brief muscle contractions
  5. Status epilepticus: > 5 min of continuous seizure activity

Focal/Partial

a) Simple: retained awareness/consciousness
b) Complex: impaired awareness/consciousness

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5
Q

General seizures

A

Begins simultaneously in both hemispheres of brain

-> 5 types

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6
Q

Epilepsy for more than 5 minutes

A
  • Status epilepticus
  • most dangerous type of seizure
  • can be any type of seizure
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7
Q

Partial/focal seizures

A

Begins within a particular area of brain and may spread out

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8
Q

Glutaminergic synapse: Neurotransmission

A
  1. Voltage-gated Na+ channel (VGSC) opens  membrane depolarisation
  2. Voltage-gated K+ channel (VGKC) opens  membrane repolarisation
  3. Ca2+ influx through voltage-gated calcium channels (VGCCs) -> vesicle exocytosis
    a) Synaptic vesicle associated (SV2A) protein allows vesicle attachment to presynaptic membrane
  4. Glutamate activates excitatory post-synaptic receptors (e.g. NMDA, AMPA & kainate receptors)
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9
Q

Name voltage gated Na+ channel blockers

A

Carbamazepine

Lamotrigine

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10
Q

Carbamazepine

A

Pharmacodynamics

  • Stabilises inactive state of Na+ channel -> reducing neuronal activity
  • doensn’t close the pore itself, just stabilises inactive state.

Pharmacokinetics

  • Enzyme inducer
  • lots of drug-drug interactions
  • Onset of activity within 1 hour
  • 16-30 hour half-life

Indications
- Tonic-clonic seizures; partial seizures

NB: potential severe side-effects (Steven Johnson Syndrome and TEN -> skin complications in individuals with HLA-B*1502 allele

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11
Q

Lamotrigine

A

Pharmacodynamics
- Inactivates Na+ channels -> reducing glutamate neuronal activity

Pharmacokinetics

  • Onset of activity within 1 hour
  • 24-34 hour half-life

Indications
- Tonic-clonic seizures; absence seizures

tends to be a better drug than carbamazepine, but also more expesive

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12
Q

Voltage-gated ion channels blockers

A

e.g. Ethosuximide

Pharmacodynamics
- T-type Ca2+ channel antagonist -> reduces activity in relay thalamic neurones

Pharmacokinetics
- Long half-life (50 hours)

Indications
- Absence seizures

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13
Q

Ethosuximide

A

Pharmacodynamics
- T-type Ca2+ channel antagonist -> reduces activity in relay thalamic neurones

Pharmacokinetics

  • Long half-life (50 hours)
  • reasonably fast onset of action

Indications
- Absence seizures

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14
Q

Name drugs targeting glutamate exocytosis and receptors

A

Levetiracetam

Topiramate

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15
Q

Name drugs targeting glutamate exocytosis and receptors

A

Levetiracetam

Topiramate

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16
Q

Levetiracetam

A

Pharmacodynamics
- Binds to synaptic vesicle associated protein (SV2A) -> preventing glutamate release

Pharmacokinetics

  • Fast-onset (1 hour)
  • half-life (10 hours)

Indications
- Myoclonic seizures

17
Q

Topiramate

A

Pharmacodynamics

  • Inhibits NMDA & kainate receptors
  • Also affects VGSCs & GABA receptors
  • > multiple targets

Pharmacokinetics

  • Fast-onset (1 hour)
  • long half-life (20 hours)

Indications

  • Myoclonic seizures
  • also used in treatment of some types of neuropathic pain
18
Q

Glutaminergic synapse neurotransmission

A
  1. VGSC -> depolarisation
  2. VGKC -> repolarisation
  3. Ca2+ influx through VGCCs -> vesicle exocytosis
  4. SVA2 allows vesicle attachment to membrane
  5. Glutamate activates excitatory post synaptic receptor
19
Q

Drugs acting on the glutaminergic synapse

A
  1. VGSC antagonist: e.g Carbamazepine, Phenytoin, Lamotrigine
  2. VGCC antagonist: Ethosuximide (T-type antagonist);
  3. SV2A inhibitor: Levetiracetam
  4. Glutamate receptor antagonist: Topiramate

=> correlates to transmission at. the glutaminergic synapse

=> prevent too much excitation

20
Q

GABAergic Synapse neurotransmission

A
  1. GABA can be released tonically & also following neuronal stimulation
  2. GABA activates inhibitory post-synaptic GABAA receptors
  3. GABAA receptors are chloride (Cl-) channels  membrane hyperpolarisation
  4. GABA is taken up by GAT & metabolised by GABA transaminase (GABA-T)
21
Q

NT secreted most is the brain?

A

GABA

22
Q

Diazepam

A

Pharmacodynamics
- GABA receptor, PAM  increases GABA-mediated inhibition

Pharmacokinetics

  • Rectal gel - Fast-onset (within 15 min) -> this is very important
  • half-life (2 hours)

Indications
- Status epilepticus

23
Q

What is he only drug that is effective in status epilepticus?

A

Diazepam

24
Q

Sodium Valproate

A

Pharmacodynamics
- Inhibits GABA transaminase -> increases GABA-mediated inhibition

Pharmacokinetics

  • Fast onset (1h)
  • half-life (12h)

Indications
- Indicated for ALL forms of epilepsy

25
Q

Which drugs are licensed for tonic-clonic seizures?

A

Carbamazepine
Lamotrigine
Valproate

26
Q

Tonic/Atonic seizures - which drug?

A

Valproate

27
Q

Which drugs are licensed/used for status epilepticus?

A

Diazepam

28
Q

Characteristics of anti-convulsants

A
  • fast onset of action

- long duration of action

29
Q

What is valproate used for?

A

Every type of seizure

30
Q

Which drug can be used for any type of seizure?

A

valproate

31
Q

Which drug is used for absence seizures?

A

Ethosuximide
Lamotrigine
Sodium Valproate

32
Q

Which drugs are used for partial seizures?

A

Carbamazepine
Lamotrigine
Levetiracetam
Valproate

33
Q

Which drugs are used for myoclonic seizures?

A

Levetiracetam
Topiramate
Valproate

34
Q

LO2: Anti-convulsants: recognise that anti-convulsant therapy is determined by the seizure type coupled with pharmacodynamics/pharmacokinetic properties of specific anti-convulsant drugs

A
  • Inhibition of VGSCs (e.g. Carbamazepine, lamotrigine) – Tonic-clonic, partial
  • Inhibition of VGCCs (e.g. Ethosuximide) – Absence
  • Inhibit vesicular release (e.g. Levetiracetam) – Myoclonic
  • Inhibit glutamate receptors (e.g. Topiramate) – Myoclonic
  • Enhance GABA channel activity (e.g. Diazepam) – status epilepticus
  • Inhibit GABA metabolism (e.g. Valproate) – all types
35
Q

LO1: Seizures

A
  • Tonic-clonic seizures: loss of consciousness -> muscle stiffening -> jerking/twitching -> deep sleep -> wakes up
  • Absence seizures: brief staring episodes with behavioural arrest
  • Tonic/atonic seizures: sudden muscle stiffening/sudden loss of muscle control
  • Myoclonic seizures: sudden, brief muscle contractions
  • Status epilepticus: > 5 min of continuous seizure activity
  • Simple partial: retained awareness/consciousness
  • Complex partial: impaired awareness/consciousness

Year 2 - LCRS - Pharmacology (34 decks)

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