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Neuropharmacology > Epilepsy 2 > Flashcards

Epilepsy 2 Flashcards

0
Q

what is an epileptic drug ?

A

a drug which decreases the frequency and/or severity of the seizures
- the drugs are able to treat the symptoms of seizures but not the underlying epileptic condition

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1
Q

what does the treatment of epilepsy require ?

A

it requires the form of epilepsy to be determined

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2
Q

what is the aim of anti epileptic treatment ?

A

to maximise the quality of life by minimizing seizures and adverse drug effects

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3
Q

what is the effectiveness of antiepileptic drugs on seizures ?

A

up to 80% of patients can expect partial or complete control of seizures

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4
Q

when are antiepileptic drugs implicated ?

A

when a patient has 2 or more seizures in a short interval- 6m to a year
- the initial therapy is to only use one drug (monotherapy)

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5
Q

what are the treatment goals in epilepsy ?

A 
no seizures
no side effects 
monotherapy
once daily dosing 
no blood tests 
- these are rarely all achieved
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6
Q

what are the advantages of monotherapy ?

A

fewer side effects
decreased drug-drug interactions
better compliance
lower costs

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7
Q

what is the percentage increase in taking a second drug?

A

it only causes a significant improvement in 10% of patients

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8
Q

what are the statistics for epileptic patients taking therapy ?

A

70% seizure free with one drug - still requires careful monitoring and adjustments
5-10% seizure free with 2 or more drugs
20% still have seizures (refractory epilepsy)

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9
Q

what are the common causes of failure of antiepileptics?

A

1) improper diagnosis of the type of seizures
2) incorrect choice of drug
3) inadequate or excessive dosage
4) poor compliance

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10
Q

what are the general features needed for appropriate clinical advice for treatment?

A
  • essential to have an accurate and comprehensive diagnosis
  • the underlying causes must be treated- hypoglycaemia, infection, tumour
  • adequate description of symptoms needs to be provided
  • EEG
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11
Q

what are the principals of pharmacological treatment 1 ?

A
  • use the appropriate drug for the type of seizure
  • use one drug and increase the dose till therapeutic result is gained or until toxicity appears
  • the treatment needs to be monitored by blood tests
  • if another drug is also required then it should be implemented however if the effect is beneficial, then the removal of the first drug should be considered
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12
Q

what are the principals of pharmacological treatment 2?

A

if monotherapy fails then 2 drugs can be used - the drugs used should be reviewed
add a 3rd drug if necessary
it may be necessary to accept that significant reduction in seizure frequency is the best that can be achieved

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13
Q

what factors contribute to compliance ?

A
  • actually taking the drug is required for it to be effective
    non-compliance is an important issue in poor control
    patients have to be fully involved in their treatment
    patients views have to be respected
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14
Q

why dont patients comply ?

A
  • poor communication
  • poor memory- seizures partly in temporal lobe can impact on cognition
  • poor understanding of instructions
  • misinformation
  • side effects
  • poor dose regimes
  • difficult to swallow or nasty tasting medication
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15
Q

what are the drugs of choice for partial simple and partial complex seizures ?

A

carbamezepine
phenytoin
valproic acid - this is the most widely used epileptic drug in the world

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16
Q

what are alternative drugs used to treat partial simple or partial complex seizures ?

A 
lamotrigine
gabapentin
levetiracetam
topiramate 
tiagabine 
oxcarbazepine
phenobarbital
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17
Q

what are the drugs of choice for generalised tonic clonic seizures ?

A

carbamazepine
phenytoin
valproic acid

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18
Q

what are alternative drug treatments for generalised tonic clonic seizures ?

A

lamotrigine
topirmate
phenobarbital

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19
Q

what are the drugs of choice for absence seizures ?

A

ethosuximide

valproic acid

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20
Q

what are alternative drugs for the treatment of absence seizures ?

A

lamotrigine

clonazepam

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21
Q

what is the drug of choice for the treatment of atypical absence atonic, myclonic seizures ?

A

valproic acid

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22
Q

what is an alternative drug for the treatment of atypical absence atonic, myclonic seizures ?

A

clonazepam

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23
Q

what is the drug of choice for febrile seizures ?

A

diazepam- take rectally

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24
Q

what are the alternative treatments for febrile seizures ?

A

diazepam taken intravenously

valproic acid

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25
Q

what are the 3 modes of actions of epileptic drugs ?

A

1) suppress action potentials
2) enhance GABA transmission
3) suppression of excitatory transmission

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26
Q

how are action potentials suppressed?

A

sodium channel blocker or modulator

potassium channel opener

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27
Q

how is GABA transmission enhanced?

A

GABA uptake inhibitor

GABA mimetics

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28
Q

how is excitatory transmission suppressed?

A

glutamate receptor antagonist

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29
Q

what are the mechanisms of action for anticonvulsant activity ?

A

enhancement of GABAergic transmission
inhibition of sodium channels
mixed actions- combination of above and also inhibiting neurotrnsmitter release

30
Q

what drugs can be used to enhance GABA transmission ?

A

PHENOBARBITAL- enhance action of GABAa receptors with barbituates - this has issues with dependency
CLONAZEPAM- enhance action of GABAa receptors with benzodiazepams
VIGABATRIN- inhibits GABA transaminase
TIGABINE- inhibit GABA uptake

31
Q

what is the mode of action of phenobarbital ?

A

binds to allosteric barbiturate binding site- low to moderate doses
it potentiates the actions of endogenous GABA - increasing chlorine influx

32
Q

what is phenobarbital effective/ineffective against ?

A

effective- partial and tonic clonic seizures

ineffective- absence seizures

33
Q

what is the main unwanted effect of phenobarbital?

A

sedation

overdose causes coma due to direct activation of GABAa receptors

34
Q

what is clonazepam effective against?

A

generalised tonic clonic, absence and partial seizures

35
Q

what is clorazepate effects against ?

A

partial seizures - often used in conjunction with other drugs

36
Q

what is diazepam and lorazepam effective against ?

A

statsus epilepticus when give by iv

37
Q

describe the structure of GABAa receptors ?

A

multiple subunits- 19 subunit genes
pentameric- combination of alpha, beta, and gamma subunits eg 2 alpha, 2 beta and one gamma
the combinations of different subunits varies throughout different brain regions
different receptor subtypes have different functions
benzodiazepams binds between alpha and gamma subunits

38
Q

what are the actions caused by benzodiazepams ?

A 
sedative - calming 
hyponotic
anxiolytic 
anticonvulsant 
muscle relaxant 
amnesic - anterograde after admin
39
Q

what is the mechanism of benzodiazepines ?

A

increase affinity of GABA for its receptor

  • increases chloride influx
  • suppresses seizures by raising action potential threshold
  • strengthens surround inhibition which prevents spread
40
Q

what are the side effects of benzodiazepines ?

A

sedation= main one
also has problems with tolerance and dependence therefore long term use is avoided
can cause respiratory depression if taken intravenously
confusion, amnesia and poor coordination

41
Q

when can benzodiazepines potenitally be lethal ?

A

if they are taken with other CNS depression

if they are taken with ethanol it could cause respiratory depression

42
Q

what drug is used in a benzodiazepine overdose ?

A

flumazenil- antagonist

43
Q

what effects become tolerant during benzodiazepine admin?

A

anticonvulsant activity and sedative/hyponotic effects

44
Q

what are the marked withdrawal symptoms of BZs?

A

symptoms include anxiety, tremor and dizziness
they are difficult to wean patients off if they have been used for a long time - therefore they are used only for short term treatment

45
Q

describe vigabatrin

A

its an analogue of GABA
GABA is metabolised by GABA transaminase
forms covalent bonding with GABA transaminase and inhibits the enzyme
short half life yet has long lasting effects

46
Q

what is vigabatrin useful to treat ?

A

generalised tonic clonic

partial seizures

47
Q

what are the main unwanted effects of vigabatrin ?

A

depression and psychotic disturbances

48
Q

describe tagabine

A

newer analogue of GABA
crosses BBB
blocks the uptake of GABA into presynaptic neurones

49
Q

what is tiagabine used to treat ?

A

generalised tonic clonic

partial seizures

50
Q

what are the main unwanted effects of tiagabine ?

A

tiredness
dizziness
GIT upsets

51
Q

which antiepileptic drugs causes sodium channel inhibition ?

A

phenytoin
carbamazepine and oxcarbamazepine
lamotrigine

52
Q

describe phenytoin

A

non sedative analogue of phenobarbital

has narrow therapeutic range and non-linear pharmacokinetics

53
Q

what is phenytoin useful to treat ?

A

effective for partial and secondary generalised seizures and status epilepticus
little effect on absence seizure

54
Q

what is phenytoins mechanism of action ?

A

it binds to the inactivated state of sodium channels and slows down its recovery back to closed state

55
Q

what does it mean by phenytoins inhibition is use dependent ?

A

phenytoin only binds to sodium channels that have been opened so therefore known as use dependent block
- only blocks rapidly firing neurons, doesnt interfere with normally firing neurons

56
Q

what are the pharmacokinetics of phenytoin ?

A

taken orally- well absorbed
very highly protein bound - plasma proteins, especially albumin (80-90%)- same binding site as many other drugs - therefore if taken together it produces more free phenytoin
incrase hepatic clearance of the drug so effects can be unpredictable

57
Q

what part of phenytoin interacts with sodium channels ?

A

free phenytoin is the active moiety that interacts with sodium channels

58
Q

what is the metabolism of phenytoin like ?

A

it is highly metabolised by the liver 95% to an inactive metabolite
metabolism is saturable
half life increases with concentration to about 20 hours
the steady state plasma concentration is not proportionate to the dose- a small increase in dose can cause large increase in plasma concentration because elimination becomes saturated

59
Q

due to phenytoins kinetics what does this mean for dosing ?

A

minor dosage changes can have highly variable changes in concentration

60
Q

what are the mild unwanted effects of phenytoin ?

A

at 100 micromol/litre

  • vertigo
  • ataxia
  • headache
  • nystagmus
61
Q

what are the severe side effects of phenytoin ?

A 
at 150 micromole/litre
confusion
intellectual deterioation
hyperplasia of the gums, hirsutism 
megaloblastic anaemia
hypersensitivity and rashes 
foetal malformation- cleft palate
hepatitis
62
Q

what is carbamazepine used to treat ?

A

effective against complex partial seizures

also useful against various forms of neuropathic pain

63
Q

what does carbamazepine do ?

A

binds to the same site on sodium channels as phenytoin

- taken orally and its effects are inhibited by a number of drugs

64
Q

what are the unwanted effects of carbamazepine ?

A

induces cytochrome p450 enzymes - increases metabolism of other drugs therefore best not to mix with other antiepileptics
it is the metabolite carbamazepine expoxide thought to cause unwanted effects
- mild to moderate= dizziness, drowsiness, ataxia, water retention and GIT effects
- severe= mental and motor disturbances

65
Q

what are the different metabolic properties of oxcarbamazepine compared to carbamazepine ?

A

less induction of liver enzymes
MHD is a metabolite which is thought to cause much of the antiepileptic effects
fewer side effects due to lack of production of carbamazepine epoxide

66
Q

what is gabapentin and what is its mechanism of action ?

A

analogue of GABA - was intended as a GABA antagonist but doesnt act on GABA receptor

  • inhibits L-type calcium channels
  • decreases GABA turnover
67
Q

what is valporate, what is it used to treat?

A

its effective against both tonic clonic and absence which is unusual
can also be useful in bipolar disorder
taken orally

68
Q

what is the mechanism of action of valporate ?

A

inhibits sodium channels but less than phenytoin
decreases GABA turnover - inhibits succinic semialdehyde dehydrogenase and thereby directly inhibits GABA transaminase and this may lead to increase synaptic GABA levels
blcoks NT release by blocking T-type calcium channels

69
Q

what is the mechanism of action of levetiracetam ?

A

inhibit NT release
- binds to synpatic vesicle protein (SVA2) involved in vescicle NT exocytosis
- binding affinity is directly proportional to seizure protection
inhibits calcium mediated synaptic vesicle release
may also inhibit calcium channel function directly

70
Q

what is levetiracetam effective in ?

A

partial seizures and possibly other seizure types

usually used in conjunction with other drugs

71
Q

what are the unwanted effects of levetiracetam ?

A

well tolerated overall

somnolence, dizziness, asthenia and irritability are the most common but they are generally transient

72
Q

what is the association with antiepileptics and pregnancy ?

A

seizures are very harmful for pregnant women

  • monotherapy is usually better
  • folic acid is recommended for every pregnant woman with epilepsy
  • phenytoin, valproic acid are absolutely contraindicated
  • oxcarbamazepine is better than carbamazepine
73
Q

what is foetal valproate syndrome ?

A

6-9% risk of congenital malformation in infants exposed to valproic acid prenatally compared to normally only 2-3%
valproic acid has teratogenic effects - the mechanism of action of these effects are unknown

Neuropharmacology (15 decks)

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