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Y2 Pharmacology and Therapeutics > Anti-convulsants > Flashcards

Anti-convulsants Flashcards

1
Q

Define epilepsy

A

A neurological condition causing frequent seizures

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2
Q

Define seizures

A

sudden changes in behaviour caused by electrical hypersynchronization of neuronal networks in the cerebral cortex

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3
Q

What is the prevalence and incidence of epilepsy

A

Prevalence between 2-7% of the population

Incidence increased over the last 30-40 years

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4
Q

How is epilepsy diagnosed

A

Brain activity can be measured using:
Electroencephalography (EEG)
Magnetic resonance imaging (MRI)

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5
Q

What is the difference between general seizures and partial/focal seizures

A

General - Begins simultaneously in both hemispheres of brain

Partial - Begins within a particular area of brain and may spread out

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6
Q

What are the types of general seizures

A 
Tonic-clonic seizures
Absence seizures
Tonic/atonic seizures
Myoclonic seizures
Status epilepticus
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7
Q

Describe tonic clonic seizures

A

loss of consciousness - muscle stiffening - jerking/twitching - deep sleep - wakes up

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8
Q

Describe absence seizures

A

brief staring episodes with behavioural arrest

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9
Q

Describe tonic/atonic seizures

A

sudden muscle stiffening/sudden loss of muscle control

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10
Q

Describe myoclonic seizures

A

sudden, brief muscle contractions

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11
Q

What is status epilpeticus

A

> 5 min of continuous seizure activity

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12
Q

What are the types of partial/focal seizures

A

Simple: retained awareness/consciousness
Complex: impaired awareness/consciousness

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13
Q

Explain what occurs at the glutamatergic synapse on action potential

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
  4. Synaptic vesicle associated (SV2A) protein allows vesicle attachment to presynaptic membrane
  5. Glutamate activates excitatory post-synaptic receptors
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14
Q

Give 2 examples of voltage gated ion channel blockers

A

Na + = Carbamazepine, Lamotrigine

Ca2+ = ethosuximide

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15
Q

Describe the pharmacokinetics (onset, half life, interaction) and pharmacodynamics of carbamazepine

A

Enzyme inducer
Onset of activity within 1 hour
16-30 hour half-life

Stabilises inactive state of Na+ channel - reducing neuronal activity

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16
Q

What are the indications for carbamazepine

A

Tonic-clonic seizures; partial seizures

17
Q

Describe the pharmacokinetics (onset, half life) and pharmacodynamics of lamotrigine

A

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

Pharmacodynamics
Inactivates Na+ channels - reducing glutamate neuronal activity

18
Q

What are the indications of lamotrigine

A

Tonic-clonic seizures; absence seizures

19
Q

Describe the pharmacokinetics (half-life) and pharmacodynamics of ethosuximide (VGCC blocker)

A

Long half-life (50 hours)

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

20
Q

What are the indications for ethosuximide

A

Absence seizures

21
Q

Give 2 examples of drugs that target glutamate exocytosis and receptors and what are their indications

A

Levetiracetam - Myoclonic seizures

Topiramate - Myoclonic seizures

22
Q

Describe the pharmacokinetics (onset, half-life) and pharmacodynamics of levetiracetam

A

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

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

23
Q

Describe the pharmacokinetics (onset, half-life) and pharmacodynamics of topiramate

A

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

Inhibits NMDA + kainate receptors
Also affects VGSCs + GABA receptors
Pharmacokinetics

24
Q

Describe the process of GABAergic synapse transmission

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)
25
Q

Describe the pharmacokinetics (admin,onset, half-life) and pharmacodynamics of diazepam

A

Rectal gel - Fast-onset (within 15 min); half-life (2 hours)

GABA receptor, PAM -> increases GABA-mediated inhibition

26
Q

What are the indications for diazepam

A

Status epilepticus

27
Q

Describe the pharmacokinetics (onset, half-life) and pharmacodynamics of sodium valproate

A

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

Inhibits GABA transaminase -> increases GABA-mediated inhibition

28
Q

Give examples of glutamatergic post-synaptic receptors

A

NMDA-R
AMPA
kainate receptors

29
Q

When may carbamazepine contra-indicated

A

potential severe side-effects (SJS + TEN) in individuals with HLA-B*1502 allele

30
Q

Describe the onset of action and half life for anti-convulsants

A

Short onset of action with a long half life

Y2 Pharmacology and Therapeutics (34 decks)

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