Epilepsy Flashcards

1
Q

What is the approach to a fallen patient.

A

History- Patient and eye witness before and after
Onset - environment and what they looked like
Event itself - movement, responsiveness awareness
Afterwards - Speed of recovery deficits

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2
Q

List some risk factors for epilepsy.

A

Difficult birth
Seizures in the past
Head injury
Drugs

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3
Q

Why is social history very important?

A

Driving is illegal whilst uncontrolled and un medicated need to alert the DVLA.

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4
Q

List some respiratory drugs which can trigger a fit.

A

Theophyline

Aminophyline

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5
Q

Give an example of an analgesic that can precipitate a fit.

A

Tramadol

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6
Q

Give an example of an anti emetic which can trigger a fit.

A

Prochlorperazine

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7
Q

Which opioid can trigger a fit?

A

Diamorphine

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8
Q

What investigations should someone who has presented with a new onset seizure/fall undergo?

A

ECG

CT/MRI

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9
Q

Why is an ECG so important for someone who has fallen?

A

To rule out syncope or Long QT syndrome all of which can present with falls.

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10
Q

When is a CT used instead of an MRI?

A

Residual focal signs
Trauma - e.g. skull fractures
Faling GCS
Suggestion of other pathology

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11
Q

List some differential diagnosis for epilepsy.

A
Syncope 
Panic attack
Sleep phenomena
TIA
MIgraine
Hypoglycaemia
MS - tonic spasms
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12
Q

What is epilepsy?

A

The tendency to have recurrent usually spontaneous epileptic seizures.

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13
Q

In counselling the patient what should be explained?

A

Seizures doesn’t mean epilepsy is certain
Risk of recurrence
Driving and the risks

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14
Q

What is the physiology behind an epileptic fit?

A

Abnormal synchronisation of neuronal activity. Causing focal or generalised cessation of normal activity.

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15
Q

What is the most common cause of lack of synchronisation behind epilepsy?

A

Too much excitatory AP

Too much inhibitory is rarer

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16
Q

Focal seizures can be divided into what?

A

Simple - no impairment of consciousness

Dicognative - impaired consciousness

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17
Q

Focal Motor seizure

A

Rhythmic jerking.
Head and eye deviation
Vocalisation

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18
Q

Focal Sensory Seizure

A

Auras - floating lights

Somatosensory changes

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19
Q

Conscious Focal Seizures

A

Deja Vu
Depersonalisation
Hallucination

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20
Q

What is the physiology behind focal seizures.

A

Due to structural abnormality i.e too many synaptic connection

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21
Q

How can focal seizures become generalised?

A

If the AP irritates enough tissue it can be propagated throughout the brain.

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22
Q

When do most people present with Primary Generalised Epilepsy?

A

Childhood early teens

23
Q

How do most people with Primary generalised epilepsy present?

A

Early morning jerks

Generalised Seizures

24
Q

What are risk factors for triggering a seizure in someone with Primary Generalised Epilepsy?

A

Sleep deprivation

Flashing Lights

25
Are EEGs useful in Primary Generalised Epilepsy?
Yes as they can help identify the subtype
26
What is the mainstay of treatment for someone with Primary Generalised Epilepsy?
Sodium Valproate
27
If someone with Primary Generalised Epilepsy is looking to conceive what must happen?
Sodium Valproate stopped before trying to conceive as it is teratogenic. Lamotrigine is used
28
A Focal seizure which has become a generalised seizure is classified as what?
Secondary Generalised
29
Focal seizures present themselves at what age?
Any age
30
How do Focal Seizures present?
Frequent complex seizures | Hippocampal Sclerosis
31
What is the treatment of choice for Focal Seizures?
Carbazemepine | Lamotrigine
32
Which drugs affect presynaptic excitability ?
Carbazemapine Lamotrigine | Retigabine
33
What is the action of Lamotrigine and Carbazemapine?
Block Voltage gated Na+ channels prevent depolarisation of the neurone.
34
What is the action of retigabine.
Increases activity of K+ Ion channels hyper polarising the neurone and therefore reducing propagation of the signals.
35
What drugs inhibit neurotransmitter release?
Levetiracetam | Pregablin Gabapentin
36
What is the mode of action of Levetiracetam?
Levetiracetam inhibits SV2A which is required for the exocytosis of neurotransmitter release
37
What is the mode of action of Pregablin and Gabapentin?
Ca2+ channel blocker . | Calcium influx drives neurotransmitter release.
38
Why should Sodium Valproate be taken alongside Lamotrigine ?
Sodium prevents the metabolism of lamotrigine thus increasing the efficacy of the drug.
39
How do Benzodiazapines help in epilepsy?
Increase GABA activity thus reducing the excitability of the neurones.
40
What is the mode of action of sodium Valproate?
Enhance GABA synthesis
41
Which drug targets the GABA transporter and how does that reduce excitability?
Tiagabine Reduce GABA reuptake Increased GABA in cleft Increased inhibitory action
42
What drugs are used for absence fits?
Sodium Valproate | Ethosuximate
43
What are absence fits?
Stop whatever they are doing | Look spaced out
44
What is the treatment for myoclonic muscle twitches?
Sodium Valproate | Clonazepam
45
What anticonvulsant drug is used acutely?
Phenytoin
46
Focal Onset seizures are generally treated with...
Carbazemapine
47
Women on lamotrigine should be aware of what?
Alters efficacy of the combined oral contraceptive pill | Shouldn't used progesterone morning after pill
48
What is Status Epilepticus?
Recurrent epileptic seizures without full recovery of consciousness between.
49
What are the different types of Status Epilepticus?
Generalised Convulsive Non Convulsive status Epilepsia Partialis Continua
50
Non Convulsive status
Conscious but in altered state
51
Epilepsia Partialis Continua
Focal seizures but consciousness is preserved
52
What are some causes of Status Epilepticus
``` Severe metabolic disorder Infection Head trauma Sub arachnoid haemorrhage Abrupt withdrawal of anti convulsants ```
53
How can Status Epilepticus be fatal?
Glutamate release and storm. Hypoxia Respiratory Insufficiency Hypotension