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Yr 2 - Pharmacology > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What is epilepsy?

A

A group of neurological disorders marked by sudden and recurrent episodes of sensory disturbance, loss of conciousness or convulsions associated with abnormal electrical activity in the brain

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2
Q

On this pet scan which areas are coloured blue?(temporal lobe epilepsy)

A

The area of hypo-metabolism between seizures

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3
Q

How long between seizures in epilepsy?

A

It varies -> they are usually intermittent

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4
Q

What causes the seizures?

A

Excessive and abnormal cortical nerve cell activity

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5
Q

What 6 things can precipitate seizures?

A
  • altered blood glucose and pH
  • stress (going to dentist)
  • fatigue
  • flashing lights
  • noise
  • no apparent cause
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6
Q

How is epilepsy diagnosed (2)?

A
  • ruling out other conditions that might cause similar symptoms
  • confirmation with an electroencephalogram (EEG)
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7
Q

What are the major causes of epilepsy (10)?

A
  • birth and perinatal injuries
  • congenital malformations
  • genetic (ion channels)
  • idiopathic (unknown)
  • Vascular insults
  • Head trauma
  • Severe metabolic disturbances
  • drug/alcohol abuse
  • Neoplasia
  • Infection
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8
Q

What is the treatment when seizures are caused by something else i.e. tumours/infection?

A

Treat the underlying cause

NO ANTI-EPILEPTICS!!

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9
Q

What can epilepsy be confused with in children?

A

Febrile convulsion

(hyperthermia)

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10
Q

What are the NICE guidelines for epilepsy?

A

You must have 2 seizures and investigations prior to treatment

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11
Q

What are the two types of epilepsy?

A

Partial/focal/localised

Generalised/global

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12
Q

What are the different categories of localised seizures?

A

Simple (no loss of conciousness)

Complex (impairment of conciousness)

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13
Q

What are the different categories of Generalised seizures (6)?

A

Absence

Myclonic

Tonic clonic

Tonic

Atonic

Status epilepticus

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14
Q

What is a localised seizure?

A

It affects a specific region of a single hemisphere- includes psychomotor epilepsy

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15
Q

What % of seizures are accounted for by localised seizures?

A

60%

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16
Q

What can cause localised seizures?

A

Cortical lesions (tumours, developmental malformation, damage due to trauma or stroke)

Genetic

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17
Q

What are generalised seizures?

A

Discharges from both hemispheres

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18
Q

What % of seizures are accounted for by generalised seizures?

A

40%

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19
Q

What are generalised seizures often caused by?

A

Genetics

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20
Q

What are Absence seizures?

A

= look like daydreaming

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21
Q

What are Myclonic seizures?

A

= muscle twitch

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22
Q

What are Tonic clonic seizures?

A

= muscle convulsions

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23
Q

What are Tonic seizures?

A

= becoming stiff

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24
Q

What are Atonic seizures?

A

= drop seizures

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25
Q

What is Status epilepticus?

A

epileptic fits follow one another without recovery of conciousness between them

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26
Q

What are the two proposed mechanisms of epilepsy?

A
  1. Decreased inhibitory synaptic activity (insufficient GABA/ GABA-A receptor not working)
  2. increased excitatory synaptic activity (too much Glutamate (NMDA, Kainate or AMPA receptor)
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27
Q

What are the 3 proposed mechanisms for partial seizures?

A
  1. Selective loss of (inhibitory) interneurones = decreased feed forward/backward inhibiton of dendate gyrus cells
  2. Injury = synaptic reorganisation (axonal sprouting of remaining neurones) & recurrent excitatory connections
  3. Loss of excitatory neurones =usually inhibit dendate granule cells
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28
Q

What is an epileptic focus?

A

A high frequency burst of action potentials

(n.b. this is not a problem but its also not quite right)

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29
Q

How do epileptic foci develop into a seizure?

A

Hyper-synchronisation of neuronal populations = paroxysmal depolarising shift (PDS) = seizure

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30
Q

What is paroxysmal depolarising shift?

A

activation of AMPA (excitatory) receptors

-> e.g. by glutamate= NMDA receptor activation = increased intracellular K, accumulating Ca in pre-synaptic terminal (enhanced neurotransmitter release) & depolarisation induced NMDA receptor activation (increased Ca influx)

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31
Q

What follows the PDS and is used to help localise the brain region where seizures originate:

A

Interical spike

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32
Q

What is epileptigenesis?

A

The development of epilepsy (e.g. due to trauma)

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33
Q

What are the 3 stages of epileptigenesis?

A
  1. normal network becomes hyper-excitable = not working properly
  2. often a silent period after injury = gradual change of network
  3. full blown epilepsy
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34
Q

What is the kindling model?

A

Animal model of epilepsy produced by electrical stimulation= alters glutamate channel properties, increase neuron loss

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35
Q

What is the general seizure mechanism?

A

Widespread cortical areas

  • genetic (e.g. juvenile myoclonic epilepsy = JME)
  • idiopathic gene mutations/change in ion channels (Ca, Na, K, Cl) & GABA/ACh gated channels
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36
Q

What is the seizure mechanism for absence seizures?

A
  • spike wave complexes on EEG
  • GABA-B receptors, Ca & K channels within thalamus = oscillations
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37
Q

In which % of patients is the current epilepsy therapy are effective?

A

75%

38
Q

Which specific type of epilepsy is not well controlled?

A

Psychomotor epilepsy

39
Q

How do anti epilepsy drugs work?

A

They target the symptoms (they do NOT cure epilepsy!)

40
Q

The ideal anti-epileptic drug should be able to…(4):

A
  • orally active
  • allow normal function (not sedative) so can still work
  • non-toxic
  • low incidence of interactions with other drugs e.g. NSAIDs
41
Q

What are the two aims of pharmacological intervention in epilepsy?

A
  • Block activity in the focus
  • Block spread of activity (no synchronisation)
42
Q

What are the actions of pharmacological intervention in epilepsy?

A
  • increase inhibitory influences (decrease neuronal firing rates (Na channels) & increase neurotransmitter release (Ca channels))
  • decrease excitatory synaptic transmission (decrease glutamate release & decrease glutamate’s actions)
43
Q

What does AED stand for?

A

Anti-epileptic drugs

44
Q

How many generations of AED are there?

A

3 (the first generation was the first discovered etc. etc.)

45
Q

Name 3 first generation AEDs:

A

Phenytoin

Phenobarbitone

Ethosuximide

46
Q

What is the mechanism of action for Phenytoin?

A

Inhibits voltage gated Na & Ca channels

47
Q

What is the mechanism of action for Phenobarbitone?

A

Potentiates GABA at GABA-A receptors

48
Q

What is the mechanism of Ethosuximide?

A

Inhibits Ca channels (T-type)

49
Q

Name 3 second generation AEDs:

A

Carbamazepine

Valproate

Diazepam

50
Q

What is the mechanism of action of Carbamazepine?

A

Inhibits Na channels

51
Q

What is the mechanism of action for Valproate?

A
  • Potentiates GABA at GABA-A receptors
  • Inhibits GABA-T, SSA dehydrogenase & Na channels
52
Q

What is the mechanism of action of Diazepam?

A

Potentiates GABA at GABA-A receptors

53
Q

Name 4 third generation AEDs:

A

Lamotrigine

Gabapentin

Vigabatrin

Tiagabine

54
Q

What is the mechanism of action of Lamotrigine?

A

Inhibits Na channel

Inhibits Ca channels

55
Q

What is the mechanism of action of gabapentin?

A

Initially synthesised to be a GABA-mimetic

Inhibits voltage-gated Ca channels

Modulates action of GAD

56
Q

What is the mechanism of action of Vigabatrin?

A

Inhibition of GABA-T

57
Q

What is the mechanism of action of Tiagabine?

A

Inhibits GABA reuptake by blocking the GABA transporter

58
Q

What is the mechanism of action of Talampenel and Tezampanel?

A

AMPA antagonist

59
Q

Which anti-epileptic drug is not used for epilepsy as it does not work in the way expected?

A

Gabapentin

  • instead it binds Ca channel subunit = used for neuropathic pain and other disorders= INCREASE INHIBITORY INFLUENCES
60
Q

Which drugs potentiate GABA at GABA-A receptors (3)?

A

Benzodiazepines (Diazepam)

Phenobarbitone

Valproate

= INCREASE INHIBITORY INFLUENCES

61
Q

Which drugs inhibit GABA break down (2)?

& which enzymes do they inhibit?

A

Inhibit GABA-T

= vigabatrin & valproate

Inhibit SSA dehydrogenase

= valproate

= INCREASE INHIBITORY INFLUENCES

62
Q

Which drugs inhibit GABA reuptake (in both neurones & glial cells)?

A

Tagabine= INCREASE INHIBITORY INFLUENCES

63
Q

Which 4 antiepileptic drugs work by blocking volatge-activated sodium channels?

A

Carbamazepine

Phenytoin

Valproate

Lamotrigine

= INCREASE INHIBITORY INFLUENCES

64
Q

What are the three main conformations of sodium channels?

A

Resting

Open

Inactivated

65
Q

Which conformation of sodium channels does phenytoin preferentially bind?

A

Inactive form (once bound it holds the channel in the inactivated form)

66
Q

How does blocking voltage gated sodium channels are used to treat epilepsy?

A

Reduces the amplitude of sodium-dependent action potentials

-> has a greater block of rapidly firing neurons (e.g. high frequency firing = stops synchronicity)

= works along side GABA= INCREASE INHIBITORY INFLUENCES

67
Q

Name three drugs used to treat epilepsy that block voltage gated calcium channels:

A

Ethosuximide

Lamotrigine

Gabapentin

68
Q

How does Ethosuximide work?

A

Binds T-Type voltage gated Ca channel = low threshold Ca currents = modulates firing patterns of neurons= INCREASE INHIBITORY INFLUENCES

69
Q

How does Lamotrigine work?

A

Inhibits voltage sensitive Na and/or Ca channels = modulates glutamate release= INCREASE INHIBITORY INFLUENCES

70
Q

How does Gabapentin work?

A

Binds α2δ subunit of Ca channel (prevents trafficking to plasma membrane)= increases synaptic GABA = enhanced GABA response at non-synaptic sites of neuronal tissue & reduces release of mono amine neurotransmitters)= INCREASE INHIBITORY INFLUENCES

71
Q

Which antiepileptic drugs are used to increase inhibitory influences (10)?

A
  • Gabapentine
  • Benzodiazepines (Diazepam)
  • Phenobarbitone
  • Valproate
  • Vigabatrin
  • Tigabine
  • Carbamazepine
  • Phenytoin
  • Valproate
  • Lamotrigine
72
Q

Which anti-epileptic drugs are used to reduce Glutamate actions?

A

AMPA antagonists (talampanel & tezamapanel)

Kainate or NMDA receptor antagonist

73
Q

What is Glutamate?

A

Major fast excitatory neurotransmitter

74
Q

Which neurones does Glutamate act at?

A

AMPA, kainate & NMDA receptors

Metabotropic glutamate receptors

75
Q

Which 5 drug treatments are preferred in Partial seizures?

A

Carbamazepine/ Lamotrigine

Sodium valproate (often not used as teratogenic)

Phenytoin

Phenobarbitone

Ritagabine (adjunct)

76
Q

Which type of epilepsy is poorly treated with current drugs?

A

Psychomotor epilepsy

77
Q

Which 5 drug treatments are preferred in General seizures?

A
  • Carbamazepine,
  • valproate,
  • Phenytoin,
  • Phenobarbitone,
  • Lamotrigene (not in myclonic)
78
Q

Which 7 drugs can NOT be used in myoclonic or absence seizures?

A
  • Carbamazepine
  • gabapentine
  • oxcarbazepine
  • phenytoin
  • Pregabalin
  • tiagabine
  • Vigabatrin
79
Q

Which 2 drug treaments are used to treat status epilepticus/ seixures in children?

A

Buccal midazolam

Rectal diazepam

80
Q

Which 3 drug treatments are used to treat absence seizures?

A

Ethosuximide

Valproate

Lamotrigine

81
Q

Which 3 drug treatments are used to treat myclonic seizures?

A

Sodium valproate

Levetiracetam

topiramate

82
Q

Which 3 antiepileptic drugs can also be used to for migraines and neuropathic pain?

A

Topiramate

gabapentin

Levetiracetam

83
Q

Which antiepileptic drug can also be used for trigeminal neuralgia?

A

Carbamazepine

84
Q

Which 3 antiepileptic drugs can also be used to treat bipolar disorders and anxiety?

A

Clonazepam

Lamotrigine

Divalproex

85
Q

2 Key things that should be taken into account with an epileptic patient:

A
  • falls increase risk of dental injuries, soft tissue damage and misalignment of TMJ
  • fixed dental replacements (e.g. tooth implants) are recommended to reduce the risk of aspiration
86
Q

Which dental side effects does Phenytoin have?

A

Causes gingival hyperplasia in 50% -60% of patients

87
Q

Which 4 dental side effects does carbamazepine have?

A

Xerostomia

Ulcer

Glossitis

Stomatitis

88
Q

Which dental side effects does sodium valproate have?

A

reduce blood clotting mechanism

89
Q

Which dental side effects does phenytoin and phenobarbital have?

A

Accelerates the excretion and metabolism of Vitamin D = increased risk of fractures (recommend vitamin D + Ca supplements)

90
Q

Which other drugs affect the metabolism of Carbamazepine, sodium valproate and phenytoin negatively?

A

NSAIDs and some antifungals (metronidiazole, fluconazole & miconazole)

91
Q

Which types of local anaesthetic should be used in an epileptic patient?

A

NO ADDED ADRENALINE!!

e.g. Mepivacain & Articain

92
Q

Which local anaesthetic possess both proconvulsant & anticonvulsant properties (3)?

A

Enflurane

High dose opioids

Lidocane

Yr 2 - Pharmacology (18 decks)

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