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A: PnT- for the rest(du(c)) > Anticonvulsants COPY > Flashcards

Anticonvulsants COPY Flashcards

1
Q

Define epilepsy

A

A neurological condition causing frequent seizures

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2
Q

Define seizure

A

Seizures are “sudden changes in behaviour caused by electrical hypersynchronization of neuronal networks in the cerebral cortex”

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3
Q

Prevalence and incidence of epilspesy

A

Prevalence between 2-7% of the population Incidence increased over the last 30-40 years

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4
Q

How is epilepsy diagnosed

A

Brain activity can be measured using: -Electroencephalography (EEG) -Magnetic resonance imaging (MRI)… more specific

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5
Q

Two Main Seizure types

A

General Partial/focal

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6
Q

Distinguish types of general seizures

A

Tonic-clonic Absence Tonic/atonic Myoclonic Status epilepticus

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7
Q

Distingish partial/focal seizures

A

Simple Complex

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8
Q

What are general seizures

A

Begins simultaneously in both hemispheres of brain

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9
Q

Outline tonic-clonic seizure

A

loss of consciousness –> muscle stiffening (=tonic part) –> rhythmic jerking/twitching (=clonic part) –> deep sleep –> wakes up

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10
Q

Outlin absence seizures

A

brief staring episodes with behavioural arrest

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11
Q

Tonic/atonic seizure

A

sudden muscle stiffening/sudden loss of muscle control (similar but doesn’t have the phases in tonic-clonic)

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12
Q

Outline myoclonic seizure

A

sudden, brief muscle contractions

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13
Q

Outline status epilepticus

A

> 5 min of continuous seizure activity

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14
Q

What are partial/focus seizues

A

Begins within a particular area of brain and may spread out

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15
Q

Simple vs complex partial/focus seizure

A

Simple: retained awareness/consciousness Complex: impaired awareness/consciousness

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16
Q

Activity at the glutamaterig synapse

A
  1. VGSC open –> depolarization 2. VGKC opens –> repolarisation 3. Ca2+ influx through VGCC –> vesicle exocytosis 4. Glutatmate activates post synaptic receptors
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17
Q

How are synpatic vesicles attached to presynaptic membrane for glutamate

A

Synaptic vesicle associated (SV2A) protein allows vesicle attachment to presynaptic membrane (a docking protein)

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18
Q

Which receptors fores glutatmate bind to on the post-synaptic receptors

A

Glutamate activates excitatory post-synaptic receptors (e.g. NMDA, AMPA & kainate receptors)

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19
Q

Outline the morphooy of the Na+ channel

A

Closed, open then inactive

20
Q

Outline mechanism of carbamezapine

A

Pharmacodynamics: Stabilises inactive state of Na+ channel –> reducing neuronal activity

21
Q

PK of carbamazapine

A

Enzyme inducer Onset of activity within 1 hour 16-30 hour half-life Basically all have fast onset, and long duration of action

22
Q

Indication of carbamazapine

A

Tonic-clonic seizures; partial seizures

23
Q

What are the very dangerous side effects of the carbamazepine

A

NB: potential severe side-effects (SJS (stephen-johnson syndrome) & TEN) in individuals with HLA-B*1502 allele Especially Han chinese

24
Q

What is the mechanism of lamotrigine action

A

Inactivates Na+ channels  reducing glutamate neuronal activity

25
Q

What is the PK of lamotrigine

A

Onset of activity within 1 hour 24-34 hour half-life (again, fast onset, long duration of action)

26
Q

Indication of lamotrigine

A

Tonic-clonic seizures; absence seizures

27
Q

Which drug blocks calcium channel

A

Ethosuximide

28
Q

Mechanism of Ethasuximide action

A

T-type Ca2+ channel antagonist –> reduces activity in relay thalamic neurones (as opposed to dihydropyridines, which are used in treatment of HTN)

29
Q

Half life of ethasuximide

A

Long half life (50 hrs)

30
Q

What is the infication of ethosuximide

A

Absence seizures

31
Q

What drug inhibits SV2A

A

Levetiracetam

32
Q

What is the mechanism of levetiracetam

A

Binds to synaptic vesicle associated protein (SV2A)  preventing glutamate release

33
Q

PK of levetiracetam

A

Fast onset, half life 10hrs

34
Q

Infications of levetiracetam

A

Myoclonic

35
Q

What drugs block postsynaptic membane receptors

A

Topiramate

36
Q

What is the mechanism of topiramate action

A

Inhibits NMDA & kainate receptors Also affects VGSCs & GABA receptors

37
Q

What is the PK of topiramate

A

Fast-onset (1 hour); long half-life (20 hours)

38
Q

Indication of topiramate

A

Myoclonic seizures and neuropathic pain (more)

39
Q

Action at GABA receptor

A

DIFFERENCE TO OTHERS: there is always a small amount of GABA released as the brain is always in an inhibitory mode GABA can be released tonically & also following neuronal stimulation

40
Q

How does GABA get released and work on receptor

A

GABA activates inhibitory post-synaptic GABAA receptors GABAA receptors are chloride (Cl-) channels–> membrane hyperpolarisation GABA is taken up by GAT & metabolised by GABA transaminase (GABA-T)

41
Q

What is the acton of diazepam

A

GABA receptor, PAM –> increases GABA-mediated inhibition POSITIVE ALLOSTERIC MODULATOR I.e. BDZs cannot activate the GABA-A receptor without the normal GABA ligand bindin

42
Q

What is the indication of diazepam in epilepsy + how it is administered in this case

A

Rectal gel - Fast-onset (within 15 min); half-life (2 hours) for Status epilepticus

43
Q

Function of sodium valproate

A

Inhibits GABA transaminase –> increases GABA-mediated inhibition

44
Q

What does GABA transaminase do

A

Converts GABA-A to glutamate So with sodium valproate, a GAT inhibitor, you will have less Glu and more GABA :)

45
Q

What is the infication for sodium valproate

A

Indicated for ALL forms of epilepsy

A: PnT- for the rest(du(c)) (23 decks)

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