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Year 2 BB > 16. Epilepsy and AEDs > Flashcards

16. Epilepsy and AEDs Flashcards

1
Q

Define epilepsy

A

A neurological disorder that represents a brain state that supports recurrent, unprovoked seizures
Has neurobiological, cognitive, psychological and social consequences

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2
Q

What are seizures?

A

Abnormal, paroxysmal changes in the electrical activity of the brain - they reflect large scale synchronous discharge of neuronal networks

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3
Q

What is epileptogenesis?

A

The process by which normal brain function progresses towards generation of abnormal electrical activity

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4
Q

Give the classification of the different epileptic seizures (done in more detail in PBL)

A

Focal seizures:
Simple focal seizures
Complex focal seizures

Generalised seizures:
Tonic-clonic
Absence
Clonic
Tonic
Atonic 
Myoclonic
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5
Q

What is meant by ‘status epilepticus’?

A

This is a (life threatening) medical emergency
This is a form of epilepsy in which seizures last more than 5 minutes - can be 15, 20 minutes and there is no resolution OR might be that there is more than one seizure in 5 minutes

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6
Q

State the general features of a tonic-clonic seizure aka. grand mal seizure

A

Premonition - vague sense that a seizure is imminent e.g. funny smell, feel sick
Pre-tonic clonic phase - a few myoclonic jerks i.e. few very short jerky movements
Tonic phase - massive contraction, often an epileptic cry is heard as the muscles of the throat becomes strangulated, contraction of the jaw muscles, cyanosis
Clonic phase - Jerks of increasing amplitude followed by relaxation, sphincter opening may occur
Postictal period - generalised lethargy, decreased muscle tone, headaches, muscle soreness, drowsiness, confusion, nausea

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7
Q

What are the outlines for an epilepsy diagnosis?

A

The patient must have an occurrence of two or more seizures in the past - the patient will generally not recall this and so a witness account of the seizure is essential

Investigations may also be used - EEG, MRI, PET, ECG

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8
Q

What are the cellular mechanisms linked to the the development of epilepsy and causing seizures?

A

Abnormal neuronal excitability - ion channels
Decreased inhibition of neurones (GABA-dependent)
Increased excitation of neurones (glutamate dependent)

Glial cell abnormalities may also play a role - these have an important role in glutamate transport

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9
Q

What structural changes can the brain undergo due to epilepsy?

A

Reorganisation of the tissue i.e. the hippocampus in temporal lobe epilepsy - loss of cells and receptors for neurotransmitters

Abnormal sprouting of fibres - when some cells are lost, some of the remaining neurones then sprout and there is the development of abnormal circuits and an abnormal excitation of neurones occurs

Loss of chandelier cells - these are GABAergic - express high levels of GABA transporter GAT-1 - interneurones which control the activity of cortical pyramidal cells - synapse on the AIS (axon initial segment) of pyramidal cells

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10
Q

What is secondary epilepsy?

A

Where epilepsy is secondary to another event e.g. stroke, brain tumours, infections

This occurs via the process of epileptogenesis - gradual process of development

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11
Q

What is a channelopathy?

A

This is where voltage gated or ligand gated ion channels undergo structural change due to mutations
This alters their activity and excitability in the brain
Results in changes in e.g. potassium, sodium and calcium channels - alters the potential difference of the neurone

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12
Q

What are the different targets for antiepileptic drugs?

A 
Sodium channels (major target)
Calcium channels
GABAa receptor
Neurotransmitter release
Neurotransmitter uptake
Neurotransmitter synthesis
Neurotransmitter receptors
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13
Q

GO THROUGH THE INDIVIDUAL DRUGS AND THEIR MECHANISM OF ACTION AND THEIR TARGETS - THESE ARE ON THE COLOURED SQUARED PAPERS AS FLASHCARDS - NEED TO KNOW FOR SAQS!!!!

A

GO THROUGH THE INDIVIDUAL DRUGS AND THEIR MECHANISM OF ACTION AND THEIR TARGETS - THESE ARE ON THE COLOURED SQUARED PAPERS AS FLASHCARDS - NEED TO KNOW FOR SAQS!!!!

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14
Q

Which drugs have an action on hepatic enzymes and what is the consequence of this on their dosage?

A

Phenytoin and carbamazepine increase the hepatic enzymes

This means that they increase their own metabolism and so you need to up the dosage slightly to compensate for this

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15
Q

What is the imperative treatment for status epilepticus?

A

Intravenous benzodiazepine

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16
Q

What other non-pharmacological treatment methods are their for epilepsy?

A

Vagal nerve stimulation
Deep brain stimulation
Surgical - lobe resection, corpus callostomy, functional hemispherectomy
Ketogenic diet

17
Q

What is an abnormal paroxysmal shift?

A

This is a wave of depolarisation occurring at the start of a seizure

Neuronal membrane depolarises by about 30-40mV and remains depolarised for a few seconds before returning to normal
This depolarisation results in a burst of action potentials - these are stimulated via the activation of NMDA glutamate receptors

18
Q

What are the general aims of AEDs?

A

To increase the neural inhibition or to decrease the neural excitation

19
Q

What is the action of AEDs at sodium channels?

A

Na+ channels are normally inactivated - AEDs bind to them to keep them inactive for longer to reduce the excitability of the neurone - do this by causing them to close at a lower membrane potential than normal - an increased refractory period

20
Q

What is the action of AEDs at GABAa receptors?

A

Expressed post-synaptically
AEDs causes them to remain open for longer e.g. benzodiazepines and leads to hyperpolarisation of the neurone - reduced excitability

21
Q

What is the action of AEDs at GABAb receptors?

A

Activation of these leads to inhibition of adenyl cyclase, VGCA2+ channels and an activation of K+ channels
Presynaptic activation inhibits the release of glutamate at excitatory synapses

22
Q

What is the action of AEDs at potassium channels?

A

Influences the resting potential

AEDs have poor effect on these channels

23
Q

What is the effect of AED usage on pregnancy?

A

All AEDs are potentially teratogenic but carbamazepine and lamotrigine are perceived to be the safest

BUT coming off of the medication and suffering seizures can also be potentially harmful to the baby

24
Q

What is the inheritance/genetic basis of epilepsy

A

Inheritance is polygenic - poorly understood

30% of patients with epilepsy have a patient who also suffered

25
Q

What is the standard anti-convulsant prescribed or epilepsy?

A

Carbamazepine

26
Q

What is the kinetic order of phenytoin?

A

Zero-order kinetics

27
Q

Receptor involved in absence seizures

A

T type calcium channel receptors

28
Q

Action of pregabalin and gabapentin on epilepsy and mechanism of action

A

Act to increase extracellular levels of GABA

Bind to the A2O receptors on VG calcium channels
This acts to increase the GABA transporter proteins
Hence, acts to increase extracellular levels of GABA

Year 2 BB (36 decks)

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