Anti Epileptics Flashcards

0
Q

Carbamazepine

A

VGSC blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Voltage gated sodium channel blockers in epilepsy mechanism

A

Bind in the refractory period
Keep channels inactive for longer
Reduces probability of high abnormal spiking activity
Only active when there is heavy depolarisation in the neurone - normal potentials still fire
Detach once the membrane potential returns to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Carbamazepine pharmacokinetics

A
Well absorbed
75% protein bound
Linear pharmacokinetics
Initial T1/2~30 hours
CYP450 inducer - induces own metabolism
T1/2 ~ 15 hrs in repeated use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Carbamazepine ADRs

A
CNS- dizziness, drowsiness, ataxia, motor disturbance, numbness, tingling
Gi upset, vomiting
Rash
Can alter BP
Hyponatraemia 
Rarely bone marrow depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Carbamazepine contraindications

A

AVN conductance problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Carbamazepine DDIs

A

CYP450 induction - reduces phenytoin, warfarin, OCP, systemic corticosteroids
Protein binding displacement
Antidepressants interfere with action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Carbamazepine uses

A

Generalised tonic clonic
All types of partial
NOT ABSENCE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Phenytoin

A

VGSC blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Phenytoin pharmacokinetics

A

Well absorbed
90% protein bound
Linear PK at sub therapeutic doses, but non linear at therapeutic concentrations
T1/2 6-24 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Phenytoin ADRs

A

CNS- dizziness, ataxia, headache, nystagmus, nervousness
Gingival hyperplasia
Rashes- hypersensitivity, Stevens Johnson in 2-5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phenytoin DDRs

A

Competitive binding - valproate, NSAIDS
Reduces OCP
Cimetidine increases phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Phenytoin monitoring

A

Plasma levels

Salivary levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Phenytoin uses

A

Generalised tonic clonic
All types of partial
NOT ABSENCE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lamotrigine

A

Blocks VGSC

May also block Ca channels and reduce glutamate release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lamotrigine pharmacokinetics

A
Well absorbed 
Linear PK
T1/2 24 hours
No CYP450 effects
Enters phase 2 metabolism directly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lamotrigine ADRs

A

CNS-dizziness, ataxia, somnolence
Nausea
Skin rashes of varying severity
Overall fewer ADRs than other VGSC blockers

16
Q

Lamotrigine DDIs

A

OCP reduces Lamotrigine level in plasma

Valproate increases Lamotrigine levels in plasma

17
Q

Uses of Lamotrigine

A

Partial
Generalised including absence
Safer in pregnancy
Not first line in paediatrics as more ADRs

18
Q

GABA agonists in epilepsy

A

GABA has a major role in post synaptic inhibition (natural anticonvulsant)
GABA exhibits benzodiazepine and barbituate binding sites - binding enhances GABA action
Increases inward Cl current, hyperpolarising neurones

19
Q

Valproate mechanism

A
Mixed sites
Weak GABA inactivating enzyme inhibitor
Weak GABA synthesising enzyme stimulator
VGSC blocker
Weak Ca channel blocker
20
Q

Valproate pharmacokinetics

A

Well absorbed
90% protein bound
Linear PK
T1/2 - 15 hrs

21
Q

Valproate ADRs

A

Generally less severe
CNS- sedation, ataxia, tremor
Weight gain
Reduces transaminases in 40% but rarely leads to hepatic failure

22
Q

Valproate DDIs

A

Care with other AEDs
Antidepressants - SSRIs, MAOIs, TCAs- all inhibit action
Antipsychotics- lower convulsive threshold
Aspirin - competitive binding

23
Q

Valproate monitoring

A

Free concentration in plasma (not closely associated with efficacy)
Salivary levels

24
Q

Valproate uses

A

Partial

Generalised tonic clonic and absence

25
Q

Benzodiazepines pharmacology

A

Act on receptor site on GABA chloride channel

Allosteric binding

26
Q

Benzodiazepines pharmacokinetics

A
90-100% protein bound
Well absorbed
Linear PK
T1/2 15-45 hrs
Lipid soluble
27
Q

Benzodiazepines ADRs

A
CNS-sedation, confusion, impaired coordination, aggression
Tolerance, dependence, withdrawal
Abrupt withdrawal triggers seizures
Respiratory and CNS depression
Dry mouth, blurred vision, GI upset
28
Q

Benzodiazepines reversal

A

Flumazenil

29
Q

Benzodiazepine uses

A

Lorazepam, diazepam - status epilepticus

Clonazepam - absence seizures, short term use

30
Q

Management of status epilepticus

A

ABC
Exclude hypoglycaemia
Benzodiazepines (IV or rectal)
Phenytoin