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CPTP 3 > CPTP 3.21 Neuropharmacology 6 Antiepileptics > Flashcards

CPTP 3.21 Neuropharmacology 6 Antiepileptics Flashcards

1
Q

Define epilepsy

A

Occasional, sudden, excessive local discharges of grey matter

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2
Q

What is a convulsion?

A

A ‘fit’: muscular contractions during a seizure

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3
Q

What is a seizure?

A

A period of synchronous discharge of neurones

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4
Q

What are anticonvulsants?

A

Drugs active against seizures

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5
Q

What are the potential causes of epilepsy?

A
  • Trauma, tumour or infection of the brain
    • Drug withdrawal
    • High fever
    • Metabolic imbalances
    • Heavy metal toxicity

Can also be idiopathic

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6
Q

What are the types of epilepsy?

A

Partial Seizures - where the epileptic focus is localised
• Jacksonian
• Temporal lobe epilepsy
• Psychomotor

Generalised
• Petit mal (absence)
• Grande mal (tonic-clonic)

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7
Q

How is brain electrical activity monitored?

What is normal and abnormal when using this?

A

EEG

Brain activity can be unsynchronised or synchronised when the activity of groups of neurones is summated. Unsynchronised is normal. (IMG 11 shows an example using six neurones). Synchronising suggests it is being caused by some underlying pathology

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8
Q

What do the symptoms of epilepsy depend on? Give examples

A

The location of the epileptic focus

Temporal lobe
• Hallucinations

Motor cortex
• Bizarre movements

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9
Q

Define a partial siezure

A

Synchronous activity with a localised epileptic focus (starting site)

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10
Q

Why is temporal lobe epilepsy associated with hallucinations?

A

It contains auditory and visual processing areas which are overstimulated during synchronous activity

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11
Q

Describe petit mal seizures

What causes them?

A
  • Generalised seizures
    • Synchronous discharge at all electrode sites at 3Hz
    • Short duration and random
    • ‘Absence’ (a brief loss and return of consciousness)
    • NO MOTOR SYMPTOMS
    • No post ictal coma

Dysfunction in thalamocortical circuits

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12
Q

What are grand mal seizures also known as?

A

Tonic-clonic seizures

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13
Q

Describe grand mal seizures, including where they start

Name the type of epilepsy characterised by a similar type of seizure but prolonged and continuous

A

• No focus at onset
• Involves synchronous discharge at all electrode sites
• Random with a LONG duration
• Post ictal coma occurs
• Two phases:
> ‘tonic’ (classic arched back away from floor)
> ‘clonic’ (looks like decerebrate posturing but with bent legs) (IMG 12)

Status epilepticus (prolonged tonic-clonic seizure)

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14
Q

What can precipitate and complicate status epilepticus?

A

Precipitated by:
• Fever and sweating
• Hypertension

Complicated by:
• Hypoxia

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15
Q

How are status epilepticus seizures stopped?

A

Induced coma

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16
Q

What are the main excitatory and inhibitory neurotransmitters in the brain?

A

Excitatory: Glutamate
Inhibitory: GABA

17
Q

which receptors and channels contribute to epileptic activity?

A
  • NMDA
    • AMPA
    • Subthreshold Na+ channels
    • Voltage-gated Ca2+ channels
18
Q

What terminates epileptic activity?

A
  • Glutamate depletion
    • Glutamate receptor desensitisation

Hyper-polarisation:
• Na+ channel inactivation
• K+ channel activation

19
Q

How do anticonvulsants work?

A

They target mediators of neuronal excitability (channels and receptors)
• Increasing GABA transmission
> Positively modulate receptors
> GABA reuptake inhibition
> GABA transaminase inhibition
• Block sodium channels
• Block calcium channels

20
Q

Name the formulary anticonvulsants

A
  • Diazepam (benzodiazepines)
    • Sodium Valproate
    • Phenytoin
    • Carbamazepine
    • Barbiturates
21
Q

What can barbiturates and benzodiazepines also be used to treat?

A

Used as anxiolytics and hypnotics (lowers activity)

22
Q

Describe GABAergic neurotransmission

A

GABA neurones are found all over the brain, in the form of short interneurones which make up 20% of neurones and are involved in 30% of synapses

23
Q

Describe the GABA receptors receptor types

A

GABA-A
• Ligand gated ion channel

GABA-B
• G-protein linked receptor

24
Q

Recall how barbiturates and benzodiazepines work

A

Enhances GABAergic neurotransmission:

Barbiturates
• Inhibits Na+ channels thus preventing action potentials. Also a GABA-A agonist.

Benzodiazepines
• Allosteric modulators of GABA-A receptor
• IMG 12

25
Q

Recall why barbiturates have a small therapeutic window.

A

They activate GABA-A receptors without the need for endogenous GABA.

Also targets Na+ channels

26
Q

Describe the effect of benzodiazepine agonists on:
• Maximum effect of GABA
• Minimum effect of GABA
• EC50 of GABA

A

IMG 12

No change in minimum or maximum effect, but lowers EC50 of GABA on receptor

27
Q

Describe GABA synthesis

A
  • Glutamine is taken up
    • This is converted into glutamate
    • Glutamic acid decarboxylase converts this into GABA
28
Q

How is GABA broken down?

A

It is broken down by GABA transaminase into succinic semialdehyde

29
Q

What potential do voltage-gated sodium channels open at?

A

-55mV (threshold)

30
Q

What states do sodium channels exist in?

A
  • Open
    • Inactivated
    • Resting
31
Q

What can cause an epileptic focus to become overactive?

A

Paroxysmal depolarising shift:
• A rapid depolarising of the membrane which provokes repetitive firing
• This is caused by the premature transition of the receptor from the resting state, ready to be activated again by the cell potential which hasn’t had enough time to restore to normal yet
• IMG 14 - rapid depolarisation, then rapid action potentials within this depolarised state

32
Q

How can you identify a paroxysmal depolarising shift in an EEG to identify an epileptic focus?

A

IMG 15

• Spike followed by a slow wave

33
Q

What are the three brain ‘states’ which can be seen on an EEG?

A

IMG 16
• Normal - no pattern seen as all potentials balance out
• Interictal - occassional spikes and slow waves caused by paroxysmal depolarising shifts
• Ictal - seizure state whereby epileptic focus initiates long periods of activity and depolarisation

34
Q

What is the rationale of using voltage gated sodium channel inhibitors to selectively treat epilepsy?

A

Blocks repetitive firing in a use-dependent and voltage-dependent manner so that they only act on the pathological region of the brain which is rapidly firing (i.e. the epileptic focus)

It does this by binding to resting receptors, preventing their premature transition back to open/closed state

35
Q

Which anticonvulsants target sodium channels?

A
  • Phenytoin
    • Carbamazepine
    • Sodium Valproate
    • Lamotrigine
36
Q

What is each of the following treated by:

1) Generalised tonic clonic
2) Partial epilepsy
3) Status epilepticus

A

1) Carbamazepine, phenytoin, sodium valproate, lamotrigine
2) As in generalised tonic clonic
3) Diazepam, lorazepam, phenytoin

37
Q

Why are benzodiazepines or barbiturates used for Status epilepticus?

A

Status epilepticus does not end, and must be treated by using these hypnotics to pharmacologically induce a coma

38
Q

Which anticonvulsant drugs induce metabolism of other medications including themselves?

What other pharmacological property of these properties is of note?

A
  • Phenytoin
    • Carbemazepine

These have a narrow therapeutic window

39
Q

What non-drug treatments are available for epilepsy?

A
  • Surgery
    • Vagus nerve stimulation
    • Deep brain stimulation

CPTP 3 (21 decks)

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