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Pharmacology > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

1
Q

What is epilepsy?

A

A neurological condition causing frequent seizures.

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2
Q

What are seizures?

A

Seizures are ‘sudden changes in behaviour caused by electrical hypersynchronisation of neuronal networks in the cerebral cortex’.

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3
Q

What is the prevalence and incidence of epilepsy?

A

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) or MRI.

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5
Q

What are the different types of epileptic seizures?

A

General seizures: tonic-clonic, absence, tonic/atonic, myoclonic, status epilepticus.
Partial focal seizures: simple, complex.

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6
Q

What feature is common to all general seizures?

A

Begin simultaneously in both hemispheres of the brain.

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7
Q

What are tonic-clonic seizures?

A

General seizures.

Loss of consciousness, muscle stiffening, jerking/twitching, deep sleep then wake up.

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8
Q

What are absence seizures?

A

General seizures.

Brief starting episodes with behavioural arrest.

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9
Q

What are tonic/atonic seizures?

A

General seizures.

Sudden muscle stiffening/ sudden loss of muscle control.

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10
Q

What are myoclonic seizures?

A

General seizures.

Sudden, brief muscle contractions.

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11
Q

What is status epilepticus?

A

> 5 minutes of continuous seizure activity.

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12
Q

What feature is common to partial focal seizures?

A

Begin with a particular area of brain and may spread out.

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13
Q

What is the difference between simple and complex partial focal seizures?

A

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

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14
Q

Explain the process of neurotransmission at a glutamatergic synapse.

A

Voltage gated Na+ channel (VGSC) opens leading to membrane depolarisation.
Voltage gated K+ channel (VGKC) opens leading to membrane repolarisation.
Ca2+ influx through voltage gated calcium channels (VGCCs) leading to vesicle exocytosis- synaptic vesicle associated (SV2A) protein allows vesicle attachment to presynaptic membrane.
Glutamate activates excitatory postsynaptic receptors (e.g. NMDA, AMPA and kainate receptors).

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15
Q

Give examples of voltage gated sodium channel blockers.

A

Carbamazepine.

Lamotrigine.

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16
Q

What are the pharmacodynamics of carbamazepine?

A

Stabilises inactive site of sodium channel, reducing neural activity.

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17
Q

Discuss the pharmacokinetics of carbamazepine.

A

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

18
Q

What are the indications for treatment with carbamazepine?

A

Tonic-clonic seizures, partial seizures.

19
Q

What is a problem with carbamazepine?

A

Potential severe side effects (SJS and TEN) in individuals with HLA-B*1502 allele.

20
Q

What are the pharmacodynamics of lamotrigine?

A

Inactivates sodium channels, reducing glutamate neuronal activity.

21
Q

Discuss the pharmacokinetics of lamotrigine.

A

Onset of activity within 1 hour.

24-34 hour half-life.

22
Q

What are the indications for treatment with lamotrigine?

A

Tonic-clonic seizures, absence seizures.

23
Q

Give an example of a voltage gated calcium channel blocker.

A

Ethosuximide.

24
Q

Discuss the pharmacodynamics of ethosuximide.

A

T-type calcium channel antagonist, reduces activity in relay thalamic neurons.

25
Q

Discuss the pharmacokinetics of ethosuximide.

A

Long half-life (50 hours).

26
Q

What are the indications for treatment with ethosuximide?

A

Absence seizures.

27
Q

Give examples of drugs that interfere with glutamate exocytosis and receptors.

A

Levetiracetam.

Topiramate.

28
Q

Discuss the pharmacodynamics of levetiracetam.

A

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

29
Q

Discuss the pharmacokinetics of levetiracetam.

A

Fast onset (1 hour), half-life of 10 hours.

30
Q

What are the indications for treatment with levetiracetam?

A

Myoclonic seizures.

31
Q

Discuss the pharmacodynamics of topiramate.

A

Inhibits NMDA and kainate receptors, also affects voltage gated sodium channels and GABA receptors.

32
Q

Discuss the pharmacokinetics of topiramate.

A

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

33
Q

What are the indications for treatment with topiramate?

A

Myoclonic seizures.

34
Q

How does neurotransmission occur at a glutamatergic synapse?

A

VGSC → depolarisation → VGKC → repolarisation.
Ca2+ influx through VGCCs → vesicle exocytosis.
SVA2 allows vesicle attachment to membrane.
Glutamate activates excitatory postsynaptic receptor.

35
Q

Give examples of pharmacological uses of the glutamatergic synapse.

A

VGSC antagonist, e.g. carbamazepine.
VGCC antagonist, e.g. ethosuximide (T-type antagonist).
SV2A inhibitor, e.g. levetiracetam.
Glutamate receptor antagonist, e.g. topiramate.

36
Q

How does neurotransmission occur at a GABAergic synapse?

A

GABA can be released tonically and also following neuronal stimulation.
GABA activates inhibitory postsynaptic GABA-A receptors.
GABA-A receptors are chloride (Cl-) channels → membrane hyperpolarisation.
GABA is taken up by GAT and metabolised by GABA transaminase (GABA-T).

37
Q

Discuss the pharmacodynamics of diazepam.

A

GABA receptor, PAM - increases GABA-mediated inhibition.

38
Q

Discuss the pharmacokinetics of diazepam.

A

Rectal gel- fast onset (within 15 minutes), half-life of 2 hours.

39
Q

What are the indications for treatment with diazepam?

A

Status epilepticus.

40
Q

Discuss the pharmacodynamics of sodium valproate.

A

Inhibits GABA transaminase, increasing GABA-mediated inhibition.

41
Q

Discuss the pharmacokinetics of sodium valproate.

A

Fast onset (1 hour), half-life of 12 hours.

42
Q

What are the indications for treatment with sodium valproate?

A

All forms of epilepsy.

Pharmacology (21 decks)

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