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Year 2 LCRS Pharmacology > 33: Anti-Convulsants > Flashcards

33: Anti-Convulsants Flashcards

1
Q

What is Epilepsy?

A

•A neurological condition causing frequent seizures

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2
Q

What is a seizure?

A

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

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3
Q

How can Epilepsy be diagnosed?

A

•Brain activity can be measured using:

  • Electroencephalography (EEG)
    • during seizures
  • Magnetic resonance imaging (MRI)
    • to see form underlying cuase of Epilepsy
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4
Q

What are the two main categories of seizures in regards to affected brain area?

A
  1. General Seizure
    • Begins simultaneously in both hemispheres of brain
  2. Partial Seizure
    • Begins within a particular area of brain and may spread out
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5
Q

What is a partial seizure?

A

Begins within a particular area of brain and may spread out

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6
Q

What is a general seizure?

A

Begins simultaneously in both hemispheres of brain

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7
Q

What are the different types of general seizures?

A
  1. Tonic Clonic
  2. Absence
  3. Tonic/atonic seizure
  4. Myolclonic
  5. Status epilepticus
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8
Q

What are the different types of partial or focal seizures?

A
  1. Simple: retained awareness/consciousness
  2. Complex: impaired awareness/consciousness
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9
Q

What are the characteristics of a tonic-clonic seizure?

A

Normally relatively clear pattern

  • loss of consciousness
  • muscle stiffening
  • jerking/twitching
  • deep sleep
  • wakes upp
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10
Q

What are the characteristics of an absence seizure?

A

brief staring episodes with behavioural arrest

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11
Q

What are the characteristics of a tonic/atonic seizure?

A
  1. Tonic/atonic seizures
    * sudden muscle stiffening/sudden loss of muscle control
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12
Q

What are the characteristics of a Myoclonic Seizure?

A

sudden, brief muscle contractions

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13
Q

What is a Status Epilepticus?

A

> 5 min of continuous seizure activity

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14
Q

Explain the release of Glutamate from a Glutaminergic Neuron

A
  1. AP–> Na+ influx
  2. K+ efflux
  3. Ca2+ influx
    1. vesicle exocitosis
    2. SV2A neeeded! (Synaptic Vesicle Associsated Protein)
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15
Q

Explain how Na+ channels can be a target in the treatment of Epilepsy and Name examples

A

If Na+ channels of glutamate signaling blocked–> Less exitory glutamate signals

E.g.

  1. Carbamazepine
  2. Lamotrigine
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16
Q

What is the MOA of Carbamazepine?

What is its indication?

A

Stabilises inactive state of Na+ channel –> reducing neuronal activity

  • Used in
    • Tonic-clonic seizures
    • partial seizures
17
Q

What are the Pharmacokinetic properties of Carbamazepine?

A
  • Enzyme inducer
  • Onset of activity within 1 hour
  • 16-30 hour half-life
18
Q

What are the pharmacokinetic propterties of anti-convulsants?

A

Overally: almost all have a relatively fast onset of action (about 1 h) and a lont duration of action

19
Q

What is the MOA and indication of Lamotrigine?

A

It Inactivates Na+ channels –> reducing glutamate neuronal activity

Used in

  • Tonic-clonic seizures; absence seizures
20
Q

Which anti-convulsant drug targets the Voltage gated calcium channels of a glutaminergic neuron?

A

Ethosuximide

21
Q

What is the MOA and indiction for the use of Ethosuximide?

A

It is a

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

  • used in absence seizures
22
Q

What is the MOA and indication of Levetiracetam?

A

•Binds to synaptic vesicle associated protein (SV2A) –> preventing glutamate release

  • Used in Myoclonic Seizures
23
Q

What is the MOA and indication of use of Topiramate?

A

•Inhibits NMDA & kainate receptors

•Also affects VGSCs & GABA receptors

  • Used in Myoclonic Seizures
24
Q

When is GABA released?

A

1.GABA can be released tonically & also following neuronal stimulation

25
Q

How is GABA removed from the Synapse?

A

GABA is taken up by

  • GAT
  • & metabolised by GABA transaminase (GABA-T) (to glutamate)
26
Q

What is the MOA of Diazepam

A

GABA receptor PAM (=positive allosteric modulator) –> ® increases GABA-mediated inhibition (by increasing the affinitiy/efficycy of GABA on the GABA receptor

27
Q

What ist the ROA and indication of the use of Diazepam in Epilepsy?

A

Used as rectal gel in status epilepticus

–> fast onset of action

28
Q

What ist the MOA of Sodium Valproate?

A

Inhibits GABA transaminase –> increases GABA-mediated inhibition

29
Q

What is the Indication of Sodium Valproate?

A

All forms of epilepsy

  • fast onset, t1/2 12h
30
Q

Which Drugs can be used in the treatment of a tonic-clonic seizure?

What are their MOA?

A

Sodium channels + Valporate

  • Carbamazepine = stabelises inactive VGSC
  • Lamotirgine = inactivates VGSC

Sodium Valproate = inhibition of GABAtransaminase

31
Q

Which drugs can be used in treatement of an absence seizure?

What is their MOA?

A

Ethosuximide = T-type Ca2+ channel antagonist

Lamotrigine = inactivates VGSC

Valproate= GABA transaminase inhibitor

32
Q

Which drug can be used in the treatment of Tonic/atonic seizures?

A

Valproate

33
Q

Which drugs can be used in the treatment of Myoclonic Seizures?

A

Glutamate Binding + Release

  • Levetiracetam = binds to SV2A and inhibits Glutamate release
  • Topiramate= inhibits NMDA+ Kainate receptors

Valproate = GABA transaminase inhibior

34
Q

Which drugs can be used in the treatment of Status epilepticus?

A

Diazepam

35
Q

Which drugs can be used in the treatment of partial seizures?

A

Carbamazepine = stabelises inactive Na+ channels

Levetiracetam= Binds to SV2A –> inhibition of Glutamate release

Lamotrigine= inactivates VGSC

Valproate = GABA transaminase inhibitor

Year 2 LCRS Pharmacology (38 decks)

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