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OD2 Semester 1 - Applied Clinical Training > P: Antiepileptic Drugs - Week 10 > Flashcards

P: Antiepileptic Drugs - Week 10 Flashcards

1
Q

What proportion of the world’s population have epilepsy?

A

1%

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2
Q

Name 4 genes linked to epilepsy and state what type of receptor they are

A 
KCNQ2 = K+ channel
KCNQ3 = K+ channel
CHRNA4 = Nicotinic ACh receptor
SCN1B = Na+ channel subunit
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3
Q

What is the result of KCNQ2 activation? What about KCNQ3 activation?

A

both cause repolarization

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4
Q

What is the result of CHRNA4 activation?

A

reduced GABA release

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5
Q

What is the result of SCN1B activation?

A

slower inactivation

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6
Q

List 7 causes of seizures

A 
Fever
Brain tumour
Trauma
Abnormalities in CNS development
Infection
Stroke
Hereditary
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7
Q

What does the term “precipitating factor” mean in regards to seizures?

A

A precipitating factor is one that lowers the overall threshold for excitation, therefore increasing the frequency of Action Potentials and therefore increase the likelihood of seizures

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8
Q

List 7 precipitating factors for seizures

A 
Stress, anxiety
Sleep deprivation/fatigue
Hormonal changes associated with the menstrual cycle
Certain medications
Diabetes, blood sugar imbalances
Neon or Xenon strobe-flashes
Rapid motion
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9
Q

What instrument can you use to measure seizures?

A

Electroencephalograph (EEG)

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10
Q

What is the function of an EEG?

A

Measures potential difference between pairs of electrodes (electrical activity)

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11
Q

Does EEG measure the activity of singular neurons?

A

No, it instead measures groups of neurons in the cerebral cortex

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12
Q

How does the EEG differ between someone having a seizure and someone not having a seizure? (2)

A

The normal EEG is chaotic. During a seizure, the neurons become hyper-excitable and hyper-synchronised, so you see patterns emerge in the EEG

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13
Q

How can you classify seizures? (2)

A
  1. Focal (partial) seizures

2. Generalised seizures

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14
Q

How can you further classify focal seizures? (2) What is the main distinguishing factor between these 2 classifications? (1)

A

1a. Simple (no loss of consciousness)

1b. Complex (loss of conzciousness)

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15
Q

What sort of changes occur during a simple seizure? (5)

A

motor, sensory, autonomic, psychic, auras (e.g. feeling of deja-vu)

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16
Q

Describe how the neurons are affected in a focal seizure?

A

a focal seizure is a seizure that occurs in a discrete population of cortex neurons

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17
Q

Where do most of the changes in a complex seizure occur?

A

most changes arise from the temporal lobe (part of the brain that controls emotion, behavior, memory)

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18
Q

How can you further classify generalized seizures? (2)

A

Tonic-clonic (grand mal)

Absence (petit mal)

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19
Q

How is an absence seizure characterized on an EEG?

A

a 3Hz spike and wave EEG. The wave pattern is widespread.

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20
Q

To an outside observer, what is the difference in the appearance of a Tonic-clonic seizure vs an Absence siezure?

A

Tonic-clonic seizure: I’m pickle rick!!!! Reeee Reeee. Starts convulsing on floor demanding for szechuan sauce

Absence: Just kind of goes blank. Much more subtle. If in the middle of conversation will pick back up where they left off

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21
Q

How is a tonic-clonic seizure characterized on an EEG?

A

various phases with widespread excitation and syncrhony to them

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22
Q

How is a partial seizure characterized on an EEG?

A

Excitation happens only in specific cortical regions (2 in this example)

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23
Q

What are the treatment options for epilepsy? (4)

A
  1. Identify the underlying cause
  2. Avoid precepitants (behavioral modification)
  3. Antiepileptic drugs
  4. Surgery
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24
Q

What factor should you consider when trying to identify the underlying cause of epilepsy? (1)

A

Age

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25
Q

What factors should you consider when thinking about using anti-epileptic drugs? (4)

A

Does impact of seizure outweigh risk of treatment?
It is palliative rather than curative
It is effective in around 75% of patients, but there are measurable side effects
Consider polytherapy: 1/3rd of patients do not respond to a single antiepileptic

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26
Q

Why might side-effects be an issue when prescribing antiepileptic drugs? (1)

A

May cause issues with patient compliance

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27
Q

Name 1 way we can modify behavior to help treat epilepsy?

A

limit stress

28
Q

Define palliative

A

relieving pain without dealing with the cause of the condition.

29
Q

Why is drug treatment for epilepsy only considered a palliative treatment?

A

Because it does not modify the underlying brain structures underlying the epilepsy

30
Q

When should we consider surgery for epilepsy?

A

When medication is not working (i.e. refractory to medication)

31
Q

Where is the most common surgical resection for epilepsy?

A

the temporal lobe

32
Q

What is the aim for antiepileptic drugs?

A

to inhibit abnormal neuronal discharge

33
Q

Can a synapse be both excitatory and inhibitory?

A

No. It can be either but not both

34
Q

Can a neurotransmitter be both excitatory and inhibitory?

A

Yes. Serotonin for instance is both excitatory and inhibitory

35
Q

How does Phenytoin affect epilepsy?

A

limits excitatory nerve activation – which reduces excitatory input

36
Q

How do Benzodiazepines affect epilepsy?

A

enhance GABA receptor activity – i.e. enhances inhibitory input

37
Q

How can antiepileptic drugs inhibit neuronal discharge? (4)

A
  1. inhibit voltage-dependent Na+ channels
  2. inhibit voltage-dependent Ca2+ channels
  3. Enhance GABA action

Note: May have more than one mechanism

38
Q

What is the first line treatment for focal seizures?

A

Carbamazepine

39
Q

What is the first line treatment for tonic-clonic seizures?

A

Valproate

40
Q

What is the first line treatment for absence seizures? (2)

A

ethosuximide, valproate

41
Q

Describe the activation of voltage-gated Na+ channels (8)

A
  1. Resting state = channels closed
  2. Action potential initiated and propagated along axon
  3. A.P increases positivity, increasing m.p
  4. Na+ ion channels undergo conformational change when m.p increases over threshold
  5. Pore opens, allowing a massive influx of Na+ ions
  6. increased polarity of our membrane and A.P continues
  7. Na+ ion channel undergoes another conformational change and enters “inactive state”
  8. Membrane re-polarizes while channel is in inactive state
42
Q

Name 2 drugs for the treatment of epilepsy that inhibit the voltage-dependent Na+ channel and describe how they do this

A

Carbamazepine and Phenytoin block the channel in the ‘inactive state’, keeping it in this ‘inactive state’ for a longer period of time such that the ion channel is no longer available to be opened

43
Q

In what way are the drugs carbamazepine and phenytoin considered “use-dependent” in the treatment of epilepsy?

A

they only affect high frequency action potentials and not what occurs normally

44
Q

Name 3 inhibitors of voltage-dependent Na+ channels for the treatment of epilepsy.

A

Carbamazepine
Lamotrigine
Phenytoin

45
Q

What form of epilepsy does not respond effectively to voltage-gated Na+ channel inhibitors? (1)

A

Absence seizures

46
Q

When treating a patient for epilepsy with phenytoin, in what circumstance can the plasma concentration of phenytoin change drastically? (1)

A

Can change drastically when the patient is given another drug which displaces phenytoin from the plasma binding proteins

47
Q

How large is the therapeutic range for phenytoin?

A

is narrow

48
Q

How do different patients respond to treatment with phenytoin? (2)

A

Different patients respond differently. Different doses may be required.

49
Q

What is the role of T-type Ca2+ channels?

A

Thalamic relay neuronal firing (i.e. neuronal firing from the thalamus to the cortex)

50
Q

What form of seizure is associated with abnormalities in T-type Ca2+ channels? (1) What type of EEG pattern does the T-type Ca2+ channel produce in this case? (1)

A

Absence seizures. The T-type Ca2+ channel generates the characteristic 3 Hz spike and wave pattern

51
Q

When are T-type Ca2+ channels commonly active?

A

during sleep

52
Q

Name 1 T-type Ca2+ channel antagonist

A

Ethosuximide

53
Q

What is the effect of enhancing GABA activity on our likelihood to produce seizures? Explain

A

Enhanced GABA reduce our overall membrane potential, making it harder to reach the threshold for an action potential (thus less likely to have seizures)

54
Q

What is the receptor for GABA that confers allosteric modulation in epilepsy treatment? Explain (2)

A

GABA-A receptor: It has multiple binding sites for other substances. These binding sites modulate the ability of this ion channel to open

55
Q

Name 5 binding sites for the GABA-A receptor

A 
Benzodiazepine site
Barbiturate site
GABA site
Steroid site
Picrotoxin site
56
Q

What must be present for Benzodiazepines and Barbiturates to have any effect on the GABA-A receptor?

A

GABA

57
Q

How does Tiagabine enhance GABA action?

A

Inhibits reuptake of GABA into the neuron by inhibiting the GAT-1 transporter

58
Q

How does valproate enhance GABA action?

A

Inhibits (GABA-T and SSADH) the enzymes that breaks down GABA into succinic semialdehyde and then metabolites respectively

59
Q

What does GABA-T stand for?

A

GABA transaminase

60
Q

What does SSADH stand for?

A

Succinic semialdehyde dehydrogenase

61
Q

How do Tiagabine and Vigbatrin effect the action of GABA? (2)

A

Tiagabine: enhances by inhibiting GABA reuptake
Vigabatrin: enhances by irreversibly inhibiting GABA transaminase

62
Q

For what type of epilepsy are Tiagabine and Vigbatrin used for?

A

Only used for refractory epilepsy

63
Q

List 3 effects of valproate

A

enhance GABA action
inhibit voltage gated sodium channels
inhibit t-type Ca2+ channels

64
Q

List 4 effects of topiramate

A

enhance GABA action
inhibit voltage gated sodium channel
activates a hyperpolarizing potassium current
blocks AMPA receptors (glutamate receptors)

65
Q

Name 5 general side effects of anti-epileptic drugs

A 
sedation
unsteadiness
diplopia
nausea
increased fracture risk (phenytoin, carbamazepine, barbiturates, valproate)
66
Q

What are 3 factors to consider when thinking about using anti-epileptic drugs in women

A

risk of congenital malformations (pregnancy)
enhanced metabolism of oral contraceptive
consider withdrawal if planned pregnancy (balance risk)

OD2 Semester 1 - Applied Clinical Training (47 decks)

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