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Neuropharmacology > Anti-epileptics & anti- convulsants > Flashcards

Anti-epileptics & anti- convulsants Flashcards

1
Q

State the manifestation of epilepsy

A
  1. loss/ disturbance of consciousness
  2. characteristic body movement
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1
Q

State the pathophysiology of epilepsy

A

excitation: glutamate
inhibition: GABA
-> imbalance => prone to excitation

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2
Q

Differentiate absence and non absence type epilepsy

A

absence type:
- focus in thalamus
- neurons fire abnormally and mediated by Ca2+ T type channels (slower)

non absence type:
- excessive neuronal discharge from rapid AP firing mediated by Na+ channels

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3
Q

Phenytoin MOA

A
  1. prolongs inactivated state of Na+ channel -> longer refractory period
  2. depress presynaptic glutamate release
  3. facilitate GABA release (reduce Ca2+ release)
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4
Q

State use of phenytoin

A
  1. used for status epilepticus when foephenytoin not available
  2. used to be for: GTCS and partial seizure
    - now only when better drugs cannot be used
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5
Q

State phenytoin relationship with CYP

A
  1. potent inducer of CYP2C8/9, CYP3A4/5
  2. competitively inhibits CYP2C9/19
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6
Q

State phenytoin metabolism due to interaction

A
  1. phenobarbitone inhibts
  2. carbamazepine induce
  3. valproate decrease
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7
Q

State how phenytoin affects other drugs

A
  1. inhibits warfarin metabolism
  2. induce enzyme
    -> degrade steroids
    -> failure of oral contraceptive
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8
Q

Carbamazepine MOA

A
  • actions resemble phenytoin:
    1. inhibit high frequency neuronal discharge
    2. decrease presynaptic transmitter release
  1. lithium like effect in mania and bipolar
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9
Q

Use of carbamazepine

A
  1. simple and complex partial seizure
  2. GTCS
    (same as phenobarbitone)

-> can exacerbate myoclonic and absence seizures

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10
Q

State carbamazepine interaction

A
  1. enzyme inducer
    -> reduce efficacy of haloperidol/ oral contraceptive/ lamotrigine/ valproate/ topiramate
  2. its own metabolism
    -> induced by phenobarbitone, phenytoin
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11
Q

Ethosuximide MOA and use

A
  • selectively suppress T type Ca2+ channels
  • selective action on absence seizures
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12
Q

Ethosuximide side effects

A
  • GI intolerance
  • headache
  • inability to concentrate
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13
Q

Phenobarbitone MOA

A

enhance GABAa receptor mediated synaptic inhibition

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14
Q

State phenobarbitone interaction

A
  • CYP450 inducer
  • valproate raise phenobarbitone level when given concurrently
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15
Q

Adverse effects of phenobarbitone

A
  1. sedation
  2. hepatotoxicity
  3. resp/ CV depression -> overdose can be fatal
  4. behavioural abnormalities
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16
Q

State use of phenobarbitone

A
  • effective in GTCS, simple partial, complex partial seizures （same as carbamazepine)
  • now infrequently used due to behavioural side effects
  • not effective in absence and atonic seizure
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17
Q

Clonazepam MOA

A
  • BZD with prominent anti-convulsant properties
  • potentiate GABA induced Cl- influx -> sedation & anticonvulsant
18
Q

Use of clonazepam

A
  1. primarily for absence seizure
  2. partial seizure
  3. myoclonic epilepsy
  4. suppress acute mania
19
Q

Clonazepam adverse effect

A
  1. sedation and dullness
  2. lack of concentration
  3. irritability/ temper
20
Q

Vigabatrin MOA

A
  1. increase overall levels of GABA in GABAnergic neurons
  2. Inhibits GABA transaminase (degradation of GABA into succinic semialdehyde)
  3. Inhibits glial/ astrocyte uptake of released GABA from synapse
21
Q

Use of vigabatrin

A
  1. refractory epilepsy
  2. adjuvants for partial and generalized seizure in infantile spasm
    - not effective in absence seizure
22
Q

Adverse effects of vigabatrin

A
  1. visual field contraction, alteration of colour vision
  2. behavourial changes, psychosis
23
Q

MOA of valproic acid (sodium valproate)

A
  • mutiple mechanism:
    1. frequency-dependent prolongation of Na+ channel inactivation (phenytoin like)
    2. weak attenuation of T type Ca2+ channel (ethosuximide like)
    3. enhanced release of GABA due to inhibition of GABA transaminase (vigabatrin like)
    4. blockade of excitatory NMDA receptor
24
Q

Adverse effects of valproic acid

A
  1. avoid in pregnancy: produce spina bifida & neural tube defects in baby
  2. fluminant hepatitis -> rare but serious adverse effect
  3. anorexia, heart burn, loose motion (diarrhoea)
25
Q

Interaction of valproic acid

A
  1. concurrent administration with clonazepam contraindicated - may precipitate absence status epilepticus may precipitate
  2. increase plasma level of phenobarbitone and lamotrigine
  3. may cause phenytoin toxicity (displace from protein)
  4. inhibit hydrolysis of active epoxide metabolite of carbamazepine
26
Q

State MOA of lamotrigine

A
  • multiple action
    1. prolongs Na+ channel inactivation + suppress high frequency firing
    2. inhibits voltage gated Ca2+ channels
    3. directly block voltage Na+ channel
27
Q

Use of lamotrigine

A
  1. refractory cases of partial seizure and GTCS
  2. absence and myoclonic epilepsy
  3. neuralgic pain
28
Q

MOA of gabapentin

A
  • multiple action
    1. lipophilic GABA derivative cross brain -> enhance GABA release
    (but NOT a agonist at GABAa receptor)
    2. modulate voltage Ca2+ channels -> reduce glutamate release -> lower neuronal excitability
    *congener: pregabalin
29
Q

Use of gabapentin

A
  1. reduce seizure frequency in refractory partial seizure
  2. add on in SPS and CPS
  3. first line drug for neuralgic pain
30
Q

MOA of topiramate

A
  1. prolongation of Na+ channel inactivation
  2. GABA potentiation
  3. antagonism of glutamate receptors
  4. neuronal hyperpolarization through K+ channels
31
Q

Use of topiramate

A
  1. refractory SPS, CPS and GTCS
  2. myoclonic epilepsy
  3. add on inabsence seizure
32
Q

State anticonvulsants that act by enhancing GABA actions

A
  1. Phenobarbitone
  2. Vigabatrin
  3. Clonazepam
33
Q

Name anticonvulsants that inhibit Na+ channels

A
  1. Phenytoin
  2. Carbamazepine
34
Q

Name anticonvulsant that inhibit T type Ca2+ channels

A
  • Ethosuximide
35
Q

Name anticonvulsants that act by multiple mechanism

A
  1. Valproic acid
  2. Lamotrigine
  3. Topiramate
  4. Gabapentin
36
Q

Which two drugs induce each other’s metabolism

A
  • phenytoin and carbamazepine
37
Q

Which two drugs primarily used for absence seizure

A
  1. ethosuximide
  2. clonazepam
38
Q

Summary of use

A

(G1) - phenytoin: status epilepticus

(G2)
- carbamazepine/ phenobarbitone/ topiramate: GTSC, SPS, CPS
- gabapentin: SPS and CPS

(G3)
- ethosuximide/ clonazepam: absence seizure
- valproic acid/ lamotrigine: myoclonic, absence seizure

(G4)
- vigabatrin: refractory epilepsy

39
Q

Use of valproic acid

A
  • absence seizure
  • myoclonic seizure
40
Q

Summary of side effects

A
  1. phenytoin: (+) warfarin, (-) oral contraceptive
  2. carbamazepine: (-) efficacy of halo, oral contraceptive, LVT
  3. ethosuximide: GI intolerance
  4. phenobarbitone: overdose fatality (resp and CVS depression)
  5. clonazepam: sedation (BZD) + lack of concentration
  6. vigabatrin: eyes - visual field contraction & colour vision altering
  7. Valproic acid: avoid in pregnancy + contraindicated with clonazepam (prepcipitate absence epilepsy) and phenytoin
    8-10: not mentioned
41
Q

Past paper:

  1. gum hyperplasia
  2. Steven Johnson/ HLA-B*1502 allele
  3. oxidation of other drugs in liver
  4. status epilepticus
  5. irreversible block on GABA transaminase
A
  1. gum hyperplasia: phenytoin
  2. Steven Johnson/ HLA-B*1502 allele : carbamazepine
  3. oxidation of other drugs in liver : carbamazepine
  4. status epilepticus: lorazepam (BZD)
  5. irreversible block on GABA transaminase: vigabatrin
42
Q

Which two drug can inhibit GABA transaminase

A
  • vigabatrin
  • valproic acid
    -> two Vs

Neuropharmacology (6 decks)

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