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PT4024 > L1: Epilepsy > Flashcards

L1: Epilepsy Flashcards

1
Q

there is excessive __ in epilepsy

A

there is excessive firing in epilepsy

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2
Q

define epileptic seizures

A

episodic high frequency discharges by a localised group of neurons in the brain

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3
Q

what is the incidence of epilepsy?

A

0.5% of the population

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4
Q

what is primary epilepsy?

A

idiopathic (unknown cause): genetic & environment

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5
Q

what is secondary epilepsy?

A

epilepsy resulting from brain damage

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6
Q

what does a benzodiazepine pen do and where is it administered?

A

it reduces the duration of the seizure, it is administered in the buccal cavity

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7
Q

what are partial seizures?

A

local/focal, discharge localised to one brain region and one brain hemisphere.

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8
Q

what is a simple partial seizure?

A

consciousness unaffected

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9
Q

what is a complex partial seizures?

A

where consciousness is affected, can involve temporal lobe (hippocampus)

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10
Q

what do 30% of patients with partial seizures experience?

A

they sometimes can have generalized seizures, these are then known as secondary generalized seizures

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11
Q

what are generalized seizures?

A

discharge involving both hemispheres and reticular system, affecting consciousness

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12
Q

what are absense/petit mal seizures?

A

3 “spike and wave” discharges/second, oscillating feedback between cortex and thalamus. most common in children, presents as “staring spells”

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13
Q

what are tonic-clonic/grand-mal seizures?

A

tonic phase: muscle spasm, respiration stops, bowel/bladder discharge
clonic phase: release
physical signs include violent jerking, unable to stand.

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14
Q

what type of neurotransmission is increased and what type of neurotransmission is decreased in epilepsy?

A

excitatory neurotransmission via glutamate is increased and inhibitory neurotransmission via GABA is decreased

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15
Q

what does the altered neurotransmission often cause in epileptic patients?

A

excitotoxicity

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16
Q

what can BDNF do to neurons?

A

BDNF can increase membrane excitability

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17
Q

what is the chemical animal model of epilepsy?

A

IV Kainate injections (glutamate agonist)

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18
Q

what is the physical animal model of epilepsy?

A

Kindling, repeated low intensity brain stimulation via electrodes

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19
Q

what is the main aim of antiepileptic drugs?

A

to decrease excitatory (Glutamate) neurotransmission and increase inhibitory (GABA) neurotransmission

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20
Q

give examples of use-dependent Na+ channel block

A

phenytoin, carbemazepine, lamotrigine, valproate

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21
Q

give examples of Ca2+ channel inhibitors

A

ethosuximide, gabapentin, phenytoin, valproate

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22
Q

what antiepileptic drugs enhance GABAa activation

A

phenobarbital, benzodiazepines

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23
Q

what drugs inhibit GABA deaminase (inhibt GABA degradation)

A

valproate, vigabatrin

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24
Q

what drugs inhibit GABA reuptake

A

Tigabin

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25
Q

what drugs inhibit glutaminergic transmission

A

NMDA, AMPA, mGluR antagonists have shown efficacy in animal models.

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26
Q

name some other antiepileptic drug options

A

Carbonic anhydrase inhibitors, hormones, cannabidiol, ketogenic diet

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27
Q

what is cannabidiol (CBD) approved for?

A

Dravett’’s syndrome

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28
Q

what is the mutation in Dravett’s syndrome?

A

mutation in voltage-gated sodium channel (Na(V)1.1)

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29
Q

what are the three states that Na+ channels can exist in?

A

open, closed, inactivated

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30
Q

which state do use-dependent Na+ channel blockers act on Na+ channels?

A

in the inactivated state

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31
Q

describe the mechanism of use-dependent Na+ channel blockers?

A

enter when ion channel inactive, brings membrane potential to 0, stabilising the receptor

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32
Q

what does Na+ channel blockers preferentially inhibt?

A

Na+ channel blockers preferentially inhibit neurons that fire repetitively with high frequency, mainly affect neurons that have high-frequency discharge.

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33
Q

what is the most widely used antiepileptic?

A

Carbemazepine

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34
Q

describe CBZ metabolism (hint: phase 1)

A

epoxidation to CBZ-10, 11-epoxide, hydrolysis to CBZ-10,11-trans-dihydrodiol

35
Q

CBZ is a strong _ of P450 enzymes

A

CBZ is a strong inducer of P450 enzymes

36
Q

CBZ can _ _ its own _, decreasing its half life from 30 hours to 15 hours

A

CBZ can autoinduce its own metabolism, decreasing its half life from 30hrs to 15hrs

37
Q

side effects of CBZ?

A

ataxia, drowsiness, dizziness, cognitive and motor disturbances, hypersensitivity reactions

38
Q

difference between carbemazepine and oxcarbamazepine

A

ox is the prodrug analogue of CBZ

39
Q

when dos oxCBZ block Na+ channels?

A

when metabolized by the liver

40
Q

ox-CBZ has less drug interactions, but still interacts with?

A

oral contraceptive pill

41
Q

what receptor does both CBZ and oxcarbemazepine act on?

A

they are both GABA agonists and have been used for schizophrenia and neuropathic pain

42
Q

what dos phenytoin inhibit?

A

Calcium and sodium channels

43
Q

what % of phenytoin binds to albumin

A

80-90% of phenytoin binds to plasma albumin

44
Q

what other AED can displace phenytoin from albumin?

A

valproate

45
Q

phenytoin is metabolised by and increases the enzyme expression and activity of?

A

phenytoin is metabolized by and increases the enzyme expression and activity of CYP450.

46
Q

what effect might phenytoin have of CBZ, barbiturates, and valproate?

A

it can increase the metabolism of CBZ, Valproate and barbiturates

47
Q

phenytoin adverse effects?

A

gum hyperplasia, vitamin D deficiency, teratogenesis

48
Q

what is the therapeutic range of phenytoin?

A

40-100 microM

49
Q

What is associated with a plasma conc. of more than 100 microM of phenytoin?

A

vertigo, ataxia, headache

50
Q

what is associated with a plasma conc. of more than 150 microM of phenytoin?

A

confusion, intellectual deterioration.

51
Q

what is the name of the safer, prodrug of phenytoin

A

fosphenytoin

52
Q

what type of AED is Lamotrigine?

A

a Na+ channel blocker

53
Q

what other effect does the Na+ channel blocker Lamotrigine have?

A

inhibits presynaptic depolarisation of glutaminergic neurons to decrease glutamate release

54
Q

what is lamotrigine usually combined with?

A

valproate

55
Q

what Na+ channel AED is suitable for pregnancy and why?

A

Lamotrigine, non-teraogenic

56
Q

what does Zoisamide inhibit?

A

Na+ and Ca2+ channels

57
Q

describe Zonisamide metabolism

A

CYP450 and then glucuronidation

58
Q

what is Zonisamide half-life and why is this beneficial?

A

60 hour half-life, useful for drug compliance as only needs to be taken once a day or once every two days

59
Q

why do AEDs target Calcium channels?

A

because calcium channels release the calcium that activates proteases needed for vesicle fusion

60
Q

ethosuximide mechanism

A

ehtosuximide is a calcium channel inhibing AED that blocks T-type calcium channels (pre and post-synaptic)

61
Q

other effects of ethosuximide

A

inhibits Na+/K+ATPase and inhibit GABA deaminase

62
Q

side effects of ethosuximide

A

nausea, anorexia, lethargy, dizziness, sometimes hypersensitivity

63
Q

what is GABApentin?

A

a presynaptic L-type calcium channel inhibitor

64
Q

what does GABApentin bind

A

GABApentin binds the alpha-2-delta subunit of calcium channels in cerebral neocortex, hippocampus, and spinal cord

65
Q

effect of GABApentin

A

decreased release of glutamate, increases GABA due to mild stimulation of glutamic acid decarboxylase

66
Q

what is the more potent version of GABApentin

A

pregabalin

67
Q

valproate mechanism

A

increases GABA

68
Q

how does valproate increase GABA in the brain

A

it stimulate glutamate decarboxylase, inhibits gaba deaminase

69
Q

side effects of valproate

A

teratogenesis and hepatotoxicity

70
Q

vigabatrin mechanism

A

increases GABA, irreversibly inhibits GABA deaminase

71
Q

side effects of vigabatrin

A

depression, psychotic disturbances

72
Q

what is Tigabine

A

a lipophillic GABA analogue, penetrates BBB, irreversibly inhibits GABA transporter 1 (GAT-1), preventing GABA reuptake and prolongs GABA effect at inhibitory synapses

73
Q

phenobarbital is a strong P450 __

A

Phenobarbital is a strong P450 inducer,

74
Q

what is the main effect of phenobarbital

A

to increase GABAa receptor response

75
Q

what is there a high risk of with phenobarbital

A

overdose due to sedative effect

76
Q

what are some examples of benzodiazepines

A

diazepam, lorazepam, clonazepam

77
Q

what develops over time with benzos

A

tolerance

78
Q

what is felbamate

A

an NMDA glutamate receptor antagonist

79
Q

what is topiramate

A

an AMPA glutamate receptor antagonist, D-Fructose analogue

80
Q

carbonic anhydrase inhibitor example and effect

A

acetazolamide, inhibits carbonic anhydrase, increasing carbonic acid and decreasing cellular pH.

81
Q

what effect does a decrease in pH have on the cell

A

causes a K+ efflux, hyperpolarisation.

82
Q

effect of pregesterone on seizures

A

anticonvulsant, increases GABAa conductance, reduces glutaminergic excitation, alters GAD and GABAa expression

83
Q

effect of oestrogen on seizures

A

proconvulsant, reduces GABAa conductance, NMDA agonist in hipppocampus

PT4024 (6 decks)

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