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LCRS Pharma > Anti-Convulsants > Flashcards

Anti-Convulsants Flashcards

1
Q

what is epilepsy?

A

the overactivity of the brain with a lack of synchronisation of the wave patterns

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2
Q

how is epilepsy activity and pathology detected ?

A

pathology can be seen on MRI

activity can be seen on EEG

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3
Q

what are the 2 main categories of seizures in epilepsy?

A

1) general seizures

2) partial/focal seizures

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4
Q

what are general seizures?

A

Begin simultaneously in both hemispheres

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5
Q

what are the causes of general seizures?

A

possible genetic link/disorder.

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6
Q

what are the types of general seizures?

A
  • tonic-clonic seizure
  • absence seizure
  • atonic
  • myoclonic
  • status epilepticus
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7
Q

what are partial/focal seizures?

A

start in a particular area and spread

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8
Q

what are the causes of partial seizures?

A

may be the result of an injury or insult.

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9
Q

what are the types of partial seizures?

A
  • simple
  • complex
  • temporal lobe epilepsy
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10
Q

what wave of brain activity is seen in aware- hyperactivity?

A

gamma

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11
Q

what wave of brain activity is seen in aware-thinking?

A

beta

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12
Q

what wave of brain activity is seen in aware-relaxed?

A

alpha

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13
Q

what wave of brain activity use seen in drowsy-meditation?

A

theta

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14
Q

what wave of brain activity is seen in deep sleep?

A

delta

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15
Q

what happens to the brain wave activity in seizure?

A

The wave patterns are irregular or asynchronous due to neuronal OVER-activity.

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16
Q

what are tonic-clonic seizures?

A

your classic movie seizure
general: loss of consciousness–> muscle stiffness–> jerking–> deep sleep

wake up after

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17
Q

what are absence seizures?

A

general: brief staring episodes with behavioural arrest; loss of muscle function

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18
Q

what are atonic seizures?

A

general: sudden muscle stiffness; sudden loss of muscle function

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19
Q

what are myoclonic seizures?

A

generalised: sudden brief muscle contraction

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20
Q

what is Status epilepticus?

A

seizure activity for greater than 5 minutes

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21
Q

what is a simple partial seizure?

A

there is retained awareness/conciousness

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22
Q

what is a complex partial seizure?

A

there is impaired awareness/conciousness

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23
Q

what is the significant of targetting glutamate-mediated neurotransmission in epileptics?

A

the aim is to reduce this excitatory neurotransmission in seizures

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24
Q

how does glutamate mediated neurotransmission occur?

A
  1. VGSC opens –> membrane depolarisation.
  2. VGKC opens —> membrane repolarisation (efflux)
  3. VGCC-mediated Ca2+ influx –> glutamate vesicle exocytosis into the cleft
  4. Glutamate binds to post-synaptic receptors
    – e.g. NMDA, AMPA, Kainate receptors
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25
what enables the glutamate vesicle to be exocytosed after calcium influx occurs?
docking proteins like SV2a (Synaptic Vesicle Associated) allows vesicle attachment to the presynaptic membrane therapeutic target
26
what are the receptors that glutamate can bind to post-synaptically to have an excitatory effect?
NMDA AMPA Kainate receptors
27
what are the targets within the glutamate neuronal system for treating seizure?
- VGSC - VCKC - VGCC - exocytosis of glutamate vesicles - post synaptic glutamate receptors
28
what drugs target VGSCs to prevent Na+ influx?
Carbamazine – VGSC antagonist Lamotrigine – VGSC antagonist Phenytoin – VGSC antagonist
29
what types of seizures can be treated with carbamazine?
partial seizures and tonic-clonic seizures (general)
30
how does carbamazine act as a VGSC antagonist?
stabilises the sodium channel in the inactive state so to prevent excitation
31
describe the pharmacokinetics of carbamazepine (VGSCant)
- Induces hepatic enzymes. - T1/2 = 16-30 hours. - Dangerous in people with HLA-B*1502 alleles--> e.g. Stevens–Johnson syndrome
32
what type of seizures can be treated with lamotrigine?
``` sodium channel blocker: tonic-clonic (general) absence seizures (general) ```
33
how does lamotrigine act as a VGSC antagonist?
inactivates the sodium channel
34
describe the pharmacokinects of lamotrigine
- Onset of activity within 1 hour | - 24-34 hour half-life
35
which drugs target VGCC to prevent calcium influx?
o Ethosuximide – T-type Ca2+-channel antagonist o Gabapentin - alpha2 delta subunit inhibitor.
36
what kind of seizures are treated by ethosuximide?
absent seizures (general)
37
what kind of seizures are treated by phenytoin?
most forms of epilepsy (bar absent)
38
describe the pharmacokinetics of phenytoin
Onset = 10 minutes (FAST), T1/2 = 10-20 hours (LONG).
39
how does ethosuximide act as a VGCC antagonist?
T-type Ca2+ channel antagonist --> reduces activity in relay thalamic neurones
40
describe the pharmacokinetics of ethosuximide?
T1/2 = 50 hours (LONG).
41
what kind of seizures does gabapentin (VGCCant) treat?
partial seizures
42
what drugs target VGKCs to increase K+ efflux?
Retigabine – K+-channel opener  Adjunctive treatment.  Onset = 30 mins (FAST), T1/2 = 10 hours (SHORT).
43
what drug targets glutamate exocytosis?
Levetiracetam | – SV2A inhibitor (of vesicle exocytosis)
44
how does Levetiracetam act as a exocytosis blocking drug?
Binds to synaptic vesicle associated protein (SV2A) to preventing glutamate release
45
what kind of seizures does levetiracetam treat?
- Myoclonic seizures (general) - tonic-clonic (general) - partial
46
describe the pharmacokinetics of levetiracetam
VGCC blocker Onset = 1 hour (FAST) T1/2 = 10 hours (SHORT)
47
what drugs target the post-synaptic receptors that glutamate can bind to prevent excitation?
Topiramate – Kainate-R GluK5 subunit inhibitor Perampanel – AMPA-selective inhibitor
48
what kind of seizures can topiramate be used for?
most types (focal and general) bit of dirty drug tho
49
describe the pharmacokinetics of topiramate
``` Onset = 1 hour (FAST) T1/2 = 20 hours (LONG). ```
50
what kind of seizures does perampanel treat?
AMPA selective partial seizures as an adjuvant. ``` Onset = 1 hour (FAST) T1/2 = 24 hours (LONG). ```
51
what else, apart from glutamate neurotransmission, can be targetted in treating epilepsy?
GABAergic neurotransmission this can be enhanced to have an increased inhibitory effect
52
how does GABA mediated neurotransmission normally occur?
1. GABA is released tonically (basally) and/or via neuronal stimulation. 2. GABA activates post-synaptic inhibitory GABAa receptors. 3. GABAa receptors are Cl—channels --> lead to membrane hyperpolarisation (products are succinic semialdehyde and L-glutamate) 4. GABA is taken up by GAT (GABA Transporter). 5. GABA is metabolised by GABA-T (GABA Transaminase).
53
what are the targets in the GABAergic neurotransmission pathway for treatment of seizures?
- GABAa receptors - GABA metabolism - GABA reuptake transporter
54
what types of drugs are used in increasing GABAergic neurotransmission?
- GABAa receptor agonists - GABA metabolism inhibitors (GABA-T) - GABA reuptake transporter inhibition (GAT-1)
55
what types of drugs are used in decreasing glutamate-mediated neurotransmission?
- VGSC antagonists - VGCC antagonists - VGKCs antagonists - exocytosis inhibitors (SV2A) - post-synaptic receptor blockers (Kainate R, AMPA)
56
what drugs are used to agonise post-synaptic GABAa receptors to enhance transmissions?
Diazepam (benzodiazepine) – GABA-R agonist also Clonazepam Phenobarbital (barbiturate) – GABA-R agonist
57
how does Clonazepam enhance GABA action?
as it is a BDZ it binds to BZD-receptor protein on GABAaR it is important that GABA is also present (dependent). It will enhance GABAs affinity and so will GABA (increased BDZ affinity for receptor)
58
what particular seizure are treated by diazepam (BZD)?
Status epilepticus
59
describe the pharmacokinetics of diazepam
Rectal gel - Fast-onset (within 15 min) - half-life (2 hours)
60
what kinds of seizures can be treated by phenobarbital (Barbs)?
most forms of epilepsy (bar absent) Acts as a sedative in adults (may cause behavioural disturbances in children) but a dirty drug with a large number of drug interactions however GABA does not need to be present unlike with BZD
61
describe the pharmacokinetics of phenobarbital
barb | Onset = 20 mins (FAST), T1/2 = 60 hours (LONG).
62
what drugs target - GABA metabolism - GABA reuptake to enhance GABAergic transmission?
1) metabolism: - Sodium Valproate – GABA-T inhibitor (Treats all forms of seizure) - Vigabatrin – GABA-T irreversible inhibitor (Treats – infantile spasm, adjuvant for partial seizures) 2) re-uptake: - Tiagabine – GAT-1 inhibitor (Treats – partial seizures as adjuvant)
63
what kind of seizures are treated with sodium valproate?
Indicated for ALL forms of epilepsy
64
describe the pharmacokinetics of sodium valproate
Onset = 1 hour (FAST) | T1/2 = 12 hours
65
which drug can be used for all types of seizure?
sodium valproate
66
which drug can be used for status epilepticus?
diazepam (bzd) clonazepam used for all forms
67
name drugs used for tonic-clonic seizures
Valproate Carbamazepine (VGSC) Lamotrigine (VGSC)
68
name drugs used for myoclonic seizures
Valproate (GABA-T) Levetiracetam (SV2A) Topiramate (Kainate R)
69
name drugs used for atonic seizures
Valproate
70
name drugs used for absence seizures
Ethosuximide Lamotrigine Valproate
71
name drugs used for partial seizures
Carbamazepine Levetiracetam Lamotrigine Valproate

LCRS Pharma (32 decks)

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