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MD4001 Week 5 > 10. Anti-epileptic drugs > Flashcards

10. Anti-epileptic drugs Flashcards

1
Q

Epilepsy epidemiology?

A

0.5% of population

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2
Q

What is epilepsy?

A

Epilepsy is a continuing tendency to have seizures

Seizures are sudden discharges of abnormal electrical activity

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3
Q

Epileptic attack can be confused with…

A

Syncope attack (fainting)

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4
Q

Points to consider in the initial diagnosis of epilepsy before examination?

A
  • History is most important, both from patient and witness.
  • ? Aura/warning
  • Abnormal movements
  • Colour
  • Position
  • When?
  • After effects?
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5
Q

What investigations are used in epilepsy diagnosis?

A

ECG
EEG
MRI

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6
Q

Difference epileptic classificaitons.

A

Partial, simple, complex

Generalised, primary or secondary

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7
Q

Presentation of a generalised seizures?

A 
Absence
Myoclonic
Clonic
Tonic
Tonic-clonic
Atonic
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8
Q

Features of simple partial seizure?

A
  • Focal with minimal spread of abnormal discharge

* normal consciousness and awareness are maintained

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9
Q

Features of complex partial seizures?

A 
 Local onset, then spreads
 Impaired consciousness
 Clinical manifestations vary with site of origin and degree of spread
– Presence and nature of aura
– Automatisms
– Other motor activity
 Temporal lobe epilepsy
most commonq
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10
Q

Features of secondarily generalised seizures?

A

 Begins focally, with or without focal neurological symptoms
 Variable symmetry, intensity, and duration of tonic (stiffening)
and clonic (jerking) phases
 Typical duration up to 1-2 minutes
 Postictal confusion and somnolence

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11
Q

Which hemispheres are involved in generalised seizures>

A

Both

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12
Q

Success of epilepsy medications?

A
  • Just under 60% of all people with epilepsy can become seizure free with drug therapy
  • In another 20% the seizures can be drastically reduced
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13
Q

Deciding factors for when choosing an anti-epileptic drug?

**exam **

A 
§ Seizure type
 Epilepsy syndrome
 Pharmacokinetic profile
 Interactions/other medical conditions 
 Efficacy
 Expected adverse effects
 Cost
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14
Q

AED?

A

Anti-epileptic durg

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15
Q

What are the targets for AED?

A
  • Increase inhibitory neurotransmitter system— GABA
  • Decrease excitatory neurotransmitter system—glutamate
  • Block voltage-gated inward positive currents— Na+ or Ca++
  • Increase outward positive current—K+

Many AEDs pleiotropic—act via multiple mechanisms

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16
Q

The brain’s major excitatory neurotransmitter, which NT?

A

Glutamate

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17
Q

What are the two groups of glutamate receptor?

A

– Ionotropic—fast synaptic transmission • NMDA, AMPA, kainate
• Gated Ca++ and Gated Na+ channels
– Metabotropic—slow synaptic transmission
• Regulation of second messengers (cAMP and Inositol)
• Modulation of synaptic activity

18
Q

Modulators of glutamate receptors by…

A

Glycine, polyamine sites, Zinc, redox site

19
Q

What are the two groups of glutamate receptor?

A
  1. Ionotropic—fast synaptic transmission
    • NMDA, AMPA, kainate
    • Gated Ca++ and Gated Na+ channels
  2. Metabotropic—slow synaptic transmission
    • Regulation of second messengers (cAMP and Inositol)
    • Modulation of synaptic activity
20
Q

Which AEDs act primarily on Na+ channels

A
  1. Phenytoin, carbamazepine: Block voltage-dependent sodium channels at high firing frequences. Use dependent
  2. Oxcarbazepine: Block voltage-dependent sodium channels at high firing frequencies. Also effects K_ channels
  3. Zonisamide: Blocks voltage-dependent Na channels and T-type calcium channel
  4. Lamotrigine
21
Q

What are the currently commonly used anti-epileptic drugs?

A
  • Lamotrigine,
  • Sodium Valproate,
  • Carbamazepine,
  • Oxcarbazepine,
  • Levetiracetam,
  • Topiramate.
22
Q

Lamotrigine:
MoA?
Side effects?

A

MoA:
Na+ inhibiting channels

Side effects:
Hypersensitivity reactions (esp skin rashes)
23
Q

Sodium valproate:
MoA?
side effects?

A

MoA:
Increase in GABA content of the brain
Weak inhibition of GABA transaminase

Side effects:
Hair loss
Teratogenicity (embryo malaborption causative factor)
Foetal syndrome
Liver damage
24
Q 
Carbamazepine:
relation to anti-depressants?
Therapeutic use?
Strong enzyme inducting agent, leads to... 
Side effects?
A

Relation to anti-depressants?
Tricyclic derivative

Therapeutic use?
Partial seizures
Trigeminal neuralgia

Strong enzyme inducting agent, leads to… drug interactions e.g. Contraceptive pill

Side effects?
Sedation
Ataxia
Mental disturbances
Water retention
25
Q

Oxcarbazepine

  • Use?
  • MoA?
  • Side effects?
A

Use:
Monotherapy
Add-on therapy in partial seizures

MoA:

  • Augments K+ channels
  • P450 induction

Side effects: Sedations

Note: Related to carbamazepine but less P450 induction and less toxic

26
Q

Name 4 newer AEDs?

A

Levetiracetam
Topiramate
Tiagabine
Zonisamide

27
Q

Action of levetiracetam?
Use?
Side effects?

A

Newer AED

MoA:
Inhibit precsynaptic Ca+ channels

Use:

  1. Analogue of piracetam, a drug used to improve cognitive function
  2. Used in partial and generalised seizures
  3. 2nd line in children

Psychiatric side effects

28
Q

Action of topiramate?

Side effects?

A

Newer AED, unknown MoA

Side effects:

  • Risk of teratogenesis
  • Needs slow titration to avoid cognitive side effects (dizziness and confusion)
29
Q

Which 3 older AED’s should be made aware of as they are still in use?

A

Phenytoin: Na+ blocker, requires close monitoring as 1st order kinetics, lots of drug interactions and side effects

Ethosuximide: Treated absence seizures in chidlren but may exacerbate other forms

Phenobarbitone: Side effect os osteoporosis

30
Q

What is the NMDA receptor?

A

The NMDA receptor is very important for controlling synaptic plasticity and memory function.

The NMDAR is a specific type of ionotropic GLUTAMATE receptor.

NMDA receptor: “N-methyl-D-aspartate (NMDA)” binds selectively to it, and not to other glutamate receptors.

31
Q

What is the role of benzodiapepines in epilepsy treatment?

A

E.g. Lorazapam and Diazepam
• Benzodiazepines used as first-line treatment for status epilepticus (delivered IV – fast acting)
• Sedating

32
Q

Why is felbamate rarely used to treat epilepsy?

A

Risk of severe hypersensitivity reactions and aplastic anaemia

33
Q

Why is vagabatrin rarely used to treat epilepsy?

A

Inhibiting GABA transaminase

Side effects: Drowsiness, behavioural/mood changes, retinal loss

34
Q

Role of Gabapentin and Pregabalin (2nd generation derivative of gabapentin) as AEDs:
Act specifically…….
Use?
Bonus?

A

Act specifically on calcium channel subunits called a2d1.

Use: Add-on therapy for partial seizures and tonic-clonic seizures. Neuropathic pain

Bonus: Less sedating

35
Q

Role of Gabapentin and Pregabalin (2nd generation derivative of gabapentin) as AEDs:
Act specifically…….
Use?
Bonus?

A

Act specifically on calcium channel subunits called a2d1.

Use: Add-on therapy for partial seizures and tonic-clonic seizures. Neuropathic pain

Bonus: Less sedating

36
Q

1st and 2nd line treatment for Simple, Complex and Seconary generalised partial seizures?

A

1st line: Carbamazepine, Lamotrigine oxcarbazepine, Sodium valproate,
levetiracetam

2nd line: Valproic acid, lamotrigine, topiramate, (levetiracetam, zonisamide)

37
Q

1st line treatment for primary generalised seizures (tonic-clonic, tonic, myoclonic, atonic)?

A

Valproic acid, lamotrigine, topiramate, (levetiracetam, zonisamide)

38
Q

treatment for absence seizures (primary generalised)?

A

Ethosuximide

39
Q

AEDs in children?

A

Little RCT evidence

VALPROATE still first line, consider foetal
abnormalities
• Lamotrigine, Levetiracetam increasingly being used
• Ethosuxamide for Primary generalised

40
Q

What is status epilepticus?

A

More than 30 minutes of continuous seizure activity
Two or more sequential seizures spanning this period without full recovery between seizures
* Is a medical emergency*

41
Q

Treatment of status epilepticus?

A

– Diazepam, lorazapam IV (fast, short acting)

– Followed by phenytoin, fosphenytoin, or phenobarbital (longer acting) when control is established

42
Q 
Baclofen:
MoA?
Administration?
Use?
Side effects?
Epilepsy?
A

MoA: Selective agonist on GABA-receptors
Administration: Oral
Use: Spasticity associated with MS or spinal injury
Side effects: Drowsiness, motor inco-ordination, nausea
Epilepsy: NOT USED IN TREATMENT

MD4001 Week 5 (11 decks)

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