epilepsy Flashcards

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1
Q

what counts as status epilepticus

A

Seizures which last more than 5 minutes (or more than one seizure in 5 min, without regain of consciousness)

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2
Q

other name for grand mal seizure

A

tonic-clonic seizure

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3
Q

what is tonic, what is clonic

A

tonic is tightening of muslces, eyes drifting upwards. clonic is jerking mvts and possible sphincter opening

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4
Q

what are the 5 stages of a tonic-clonic seizure

A

Premonition (‘aura’ - a vague sense that a seizure is imminent; changes in sensation, intense emotion, mood change)
Pre-tonic-clonic phase (a few myoclonic jerks or brief clonic seizures)
Tonic phase (tonic contraction of the axial musculature; upward eye deviation and pupillary dilatation; tonic contraction of the limbs; cyanosis; respiratory muscle contraction - “epileptic cry”; tonic contraction of jaw muscles)
Clonic phase - jerks of increasing amplitude followed by relaxation (sphincter opening may occur)
Postictal period (generalized lethargy; decreased muscle tone, headaches, muscle soreness)

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5
Q

epilepsy diagnosis

A

2 or more seizures more than 24h apart

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6
Q

EEG between seizures looks

A

normal

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7
Q

2 examples of structural changes in epilepsy

A

mossy fibres sprouting leads to aberrant pathways
loss of chandelier cells (GABAergic) leads to loss of inhibition

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8
Q

where do chandelier cells have their effect

A

axon initial segmnet

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9
Q

which receptors are involved in burst firing neurones in epilepsy

A

NMDA

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10
Q

why would astrocyte deficiency/malfunction cause epilepsy

A

astrocytes clear up glutamate from synapse after action potential through EAAT1 and 2. Too much glutamate left hanging about can lead to aberrant action potentials

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11
Q

which neurones are most involved in epilepsy

A

interneurones

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12
Q

what is mTOR pathway

A

regulattor of growth and homeostasis - protein synthesis

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13
Q

what is REST pathway- what conditions

A

leads to negative regulation
of the expression of many genes in the CNS

global ischemia, stroke, epilepsy, Alzheimer’s and Huntington’s disease.

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14
Q

what do you need to think about re pharmacokinetics phenytoin, carbemazepine

A

CYP450 enhancer, so other drugs pt is on will be eliminated faster - less effective

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15
Q

sodium channel antiepileptics

A

Phenytoin
Leads - lamotrigine
To - Topiramate
Less - lacosamide
Sodium - sodium valproate
Channel - carbemazapine
Zoom - zonisamide

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16
Q

valproate age restric

A

no under 55 women unless 2 consultants agree no other effective option

17
Q

which antiepileptics target Ca channel. which sub-unit

A

Ethosuximide (used in absence seizures, targets T-type calcium channels)
Gabapentin and pregabalin (alpha2delta subunit of calcium channels; also enhanced GABA synthesis)

18
Q

benzo ending and mia

A

zepam GABA A receptor allosteric agonist

19
Q

What ion is transported in GABA channel

A

Cl-

20
Q

epileptic neuro transmitter drugs

A

Neurotransmitter release
Levetiracetam (protein SV2A; modulates neurotransmitter release)
Neurotransmitter uptake
Tiagabine (GAT-1 transporter)
Neurotransmitter metabolism
Vigabatrin (inhibition of GABA transaminase)
Neurotransmitter receptors
Perampanel (selective non-competitive antagonist of AMPA receptors)
Felbamate (NMDA receptors; also GABAA receptors?)

21
Q

tx status epilepticus

A

Benzodiazepines (buccal midazolam or rectal diazepam) are recommended by NICE as the first-line treatment for patients without intravenous access. If intravenous access were available, lorazepam would be the drug of choice.