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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
Q

what enables the glutamate vesicle to be exocytosed after calcium influx occurs?

A

docking proteins like SV2a
(Synaptic Vesicle Associated) allows vesicle attachment to the presynaptic membrane

therapeutic target

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26
Q

what are the receptors that glutamate can bind to post-synaptically to have an excitatory effect?

A

NMDA
AMPA
Kainate receptors

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27
Q

what are the targets within the glutamate neuronal system for treating seizure?

A
  • VGSC
  • VCKC
  • VGCC
  • exocytosis of glutamate vesicles
  • post synaptic glutamate receptors
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28
Q

what drugs target VGSCs to prevent Na+ influx?

A

Carbamazine
– VGSC antagonist

Lamotrigine
– VGSC antagonist

Phenytoin
– VGSC antagonist

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29
Q

what types of seizures can be treated with carbamazine?

A

partial seizures
and
tonic-clonic seizures (general)

30
Q

how does carbamazine act as a VGSC antagonist?

A

stabilises the sodium channel in the inactive state so to prevent excitation

31
Q

describe the pharmacokinetics of carbamazepine (VGSCant)

A
  • Induces hepatic enzymes.
  • T1/2 = 16-30 hours.
  • Dangerous in people with HLA-B*1502 alleles–> e.g. Stevens–Johnson syndrome
32
Q

what type of seizures can be treated with lamotrigine?

A 
sodium channel blocker: 
tonic-clonic (general) 
absence seizures (general)
33
Q

how does lamotrigine act as a VGSC antagonist?

A

inactivates the sodium channel

34
Q

describe the pharmacokinects of lamotrigine

A
  • Onset of activity within 1 hour

- 24-34 hour half-life

35
Q

which drugs target VGCC to prevent calcium influx?

A

o Ethosuximide
– T-type Ca2+-channel antagonist

o Gabapentin
- alpha2 delta subunit inhibitor.

36
Q

what kind of seizures are treated by ethosuximide?

A

absent seizures (general)

37
Q

what kind of seizures are treated by phenytoin?

A

most forms of epilepsy (bar absent)

38
Q

describe the pharmacokinetics of phenytoin

A

Onset = 10 minutes (FAST), T1/2 = 10-20 hours (LONG).

39
Q

how does ethosuximide act as a VGCC antagonist?

A

T-type Ca2+ channel antagonist –> reduces activity in relay thalamic neurones

40
Q

describe the pharmacokinetics of ethosuximide?

A

T1/2 = 50 hours (LONG).

41
Q

what kind of seizures does gabapentin (VGCCant) treat?

A

partial seizures

42
Q

what drugs target VGKCs to increase K+ efflux?

A

Retigabine – K+-channel opener

 Adjunctive treatment.
 Onset = 30 mins (FAST), T1/2 = 10 hours (SHORT).

43
Q

what drug targets glutamate exocytosis?

A

Levetiracetam

– SV2A inhibitor (of vesicle exocytosis)

44
Q

how does Levetiracetam act as a exocytosis blocking drug?

A

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

45
Q

what kind of seizures does levetiracetam treat?

A
  • Myoclonic seizures (general)
  • tonic-clonic (general)
  • partial
46
Q

describe the pharmacokinetics of levetiracetam

A

VGCC blocker
Onset = 1 hour (FAST)
T1/2 = 10 hours (SHORT)

47
Q

what drugs target the post-synaptic receptors that glutamate can bind to prevent excitation?

A

Topiramate
– Kainate-R GluK5 subunit inhibitor

Perampanel
– AMPA-selective inhibitor

48
Q

what kind of seizures can topiramate be used for?

A

most types (focal and general)

bit of dirty drug tho

49
Q

describe the pharmacokinetics of topiramate

A 
Onset = 1 hour (FAST)
T1/2 = 20 hours (LONG).
50
Q

what kind of seizures does perampanel treat?

A

AMPA selective
partial seizures as an adjuvant.

Onset = 1 hour (FAST)
T1/2 = 24 hours (LONG).
51
Q

what else, apart from glutamate neurotransmission, can be targetted in treating epilepsy?

A

GABAergic neurotransmission

this can be enhanced to have an increased inhibitory effect

52
Q

how does GABA mediated neurotransmission normally occur?

A
  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
Q

what are the targets in the GABAergic neurotransmission pathway for treatment of seizures?

A
  • GABAa receptors
  • GABA metabolism
  • GABA reuptake transporter
54
Q

what types of drugs are used in increasing GABAergic neurotransmission?

A
  • GABAa receptor agonists
  • GABA metabolism inhibitors (GABA-T)
  • GABA reuptake transporter inhibition (GAT-1)
55
Q

what types of drugs are used in decreasing glutamate-mediated neurotransmission?

A
  • VGSC antagonists
  • VGCC antagonists
  • VGKCs antagonists
  • exocytosis inhibitors (SV2A)
  • post-synaptic receptor blockers (Kainate R, AMPA)
56
Q

what drugs are used to agonise post-synaptic GABAa receptors to enhance transmissions?

A

Diazepam (benzodiazepine)
– GABA-R agonist
also Clonazepam

Phenobarbital (barbiturate)
– GABA-R agonist

57
Q

how does Clonazepam enhance GABA action?

A

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
Q

what particular seizure are treated by diazepam (BZD)?

A

Status epilepticus

59
Q

describe the pharmacokinetics of diazepam

A

Rectal gel

  • Fast-onset (within 15 min)
  • half-life (2 hours)
60
Q

what kinds of seizures can be treated by phenobarbital (Barbs)?

A

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
Q

describe the pharmacokinetics of phenobarbital

A

barb

Onset = 20 mins (FAST), T1/2 = 60 hours (LONG).

62
Q

what drugs target
- GABA metabolism
- GABA reuptake
to enhance GABAergic transmission?

A

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
Q

what kind of seizures are treated with sodium valproate?

A

Indicated for ALL forms of epilepsy

64
Q

describe the pharmacokinetics of sodium valproate

A

Onset = 1 hour (FAST)

T1/2 = 12 hours

65
Q

which drug can be used for all types of seizure?

A

sodium valproate

66
Q

which drug can be used for status epilepticus?

A

diazepam (bzd)

clonazepam used for all forms

67
Q

name drugs used for tonic-clonic seizures

A

Valproate
Carbamazepine (VGSC)
Lamotrigine (VGSC)

68
Q

name drugs used for myoclonic seizures

A

Valproate (GABA-T)
Levetiracetam (SV2A)
Topiramate (Kainate R)

69
Q

name drugs used for atonic seizures

A

Valproate

70
Q

name drugs used for absence seizures

A

Ethosuximide
Lamotrigine
Valproate

71
Q

name drugs used for partial seizures

A

Carbamazepine
Levetiracetam
Lamotrigine
Valproate

LCRS Pharma (32 decks)

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