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Lecture week 4 > Pharmacological Mx of epilepsy > Flashcards

Pharmacological Mx of epilepsy Flashcards

1
Q

Epilepsy definition

A

Chronic neurological condition characterised by recurrent, unprovoked seizures

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2
Q

Types of epilepsy (onset) - two

A
  • Focal - particular area in the brain from which seizure originate (e.g. hypocampus sclerosis due to meningitis, injury)
  • Generalised - in all the areas of the brain
  • unknown onset
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3
Q

What’s symptomatic vs idiopathic epilepsy?

A

Symptomatic - arise from an identifiable brain lesion

*usually focal that +/- generalise

Idiopathic - when an identifiable cause or structural lesion cannot be found (normal EEG, normal brain scan)

*usually generalised

*80-90% will achieve complete freedom from seizures

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4
Q

What’s the disadvantage of Phenobarbital? Do we prescribe it in the UK?

A

Phenobarbital is highly sedating -> we therefore do not prescribe it in the UK

* it is one of the oldest anti-epileptics

* it is one of the cheapest as well - some countries in the world still prescribe them a lot

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5
Q

The most common anti-epileptic drugs used (8)

A
  • Lorazepam
  • diazepam
  • Phenytoin
  • Valproate
  • Clonazepam
  • Carbamazepine
  • Gabapentin
  • Lamotrigine
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6
Q

Main MoA of anti-epileptic drugs (easy explanation - two types)

A

Remember: anti-epileptics either affect electrical current or neurotransmitter release (or both)

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7
Q

What do anti-epileptics do in terms of neuronal excitability and how do they do that?

A

Detailed: Reduce neuronal excitability

( Na+ and Ca++ channels)

Aim: to decrease depolarisation-induced Ca++ influx and vesicular release of neurotransmitters

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8
Q

What happens to Na+ channel at resting state? (in neuronal membranes)

A

They are closed -> ions are outside

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9
Q

What ions do get out of the cell and which ones go in?

A

Na+ go in

K+ go out

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10
Q

What do most anti-epileptic drugs do to the sodium channel?

A

They keep the Na+ gate closed (by increasing the rate of inactivation gate) -> so less Na+ ions will get into the cell

Simply: sodium channel blocker -> they reset electro-chemical gradient -> so to stop electrical impulse from starting one after another (across the neurones)

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11
Q

Just have a look at the pictures - MoA of anti-epileptic drugs

A

Some will inhibit passing on the action potential at different points at the pre-synaptic/ synaptic and post-synaptic

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12
Q

What is the general MoA of the drugs that are alternatives to usual anti-epileptics?

A
  • usual anti-epileptics -> will reduce Glutamate (so reduce excitation of the neurones)
  • alternatives -> will increase GABA -> so increase inhibition
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13
Q

What is MoA of GABA inhibitors?

A

They are allosteric modulators (increase) of GABAa receptor -> via the increasing frequency of Cl- channel opening -> prevents depolarisation -> less electrical firing

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14
Q

Benzodiazepines properties (6):

A
  • sedatives
  • anxiolytics
  • muscle relaxants
  • hypnotics
  • anti- convulsant
  • amnesic (e.g. Midazolam)
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15
Q

Phenytoin use (3)

A

Phenytoin

  1. Acute control of tonic-clonic seizures
  2. Rx of status epilepticus
  3. Prevention of seizures following neurosurgery or brain injury
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16
Q

Steps in acute Rx of status epilepticus

A

rectal diazepam/ IV lorazepam -> Phenytoin -> general anaesthetic

17
Q

MoA of Phenytoin

A

Phenytoin

MoA: induces hyperpolarisation via sodium channels (blocks inactive Na+ channels) -> stabilises membranes -> prevents spread of seizure activity

18
Q

Where is Phenytoin metabolised

A

95% in the liver

19
Q

What’s meant by zero - order kinetics?

A

A constant amount of drug is eliminated (by enzymes) per unit time (so work in a predictable way) -> but that means that any increase in the dose will be not associated in an increase of the metabolism (therefore, an increase may lead to toxicity quickly)

20
Q

Why do we need to do therapeutic drug monitoring on people on Phenytoin?

A

Because Phenytoin is metabolised by zero-order kinetics (enzymatic activity at a constant rate, does not increase with increased dose) -> therefore may lead to toxicity

21
Q

What’s important to know about Phenytoin and COCP?

A

Phenytoin is CYP450 enzyme inducer -> so will cause more metabolism of combined oral contraceptive pill -> it will be less effective

22
Q

What’s the brand name for sodium valproate?

A

‘Epilim’

23
Q

What is Valproate used for? (2)

A
  1. Generalised or partial seizures
  2. Bipolar, anorexia, PTSD, migraine
24
Q

How does Sodium Valproate work?

A

It is a sodium channel blocker and GABA transaminase inhibitor

25
Q

What about women of reproductive age and Sodium Valproate?

A

They should never be given Valproate (as it is teratogenic) unless by an expert epileptologist

26
Q

Adverse effects of Valproate

A

weight gain, GI disturbance (settles), tremor, SIADH, hyponatremia

27
Q

What’s the brand name for Carbamazepine?

A

Tegretol

28
Q

Use of Carbamazepine

A

Carbamazepine

  • anti - epileptic
  • trigeminal neuralgia
29
Q

How is carbamazepine metabolised

A

almost completely by the liver

30
Q

Does Carbamazepine stay given at the same dose?

A

We need to increase the dose with a time, because Carbamazepine stimulates upregulation of the genes that are responsible for its own metabolism -> as body will become ‘toned’ to it

31
Q

What serious adverse drug reaction may happen with Carbamazepine? What populations are prone to it?

A

Steven Johnson Syndrome (SJS)

*more common in a Chinese population with HLA-B*1502 allele

32
Q

What’s the brand name for Levetiracetam?

A

‘Keppra’

33
Q

What is the advantage in use of Levetiracetam?

A

Levetiracetam = ‘ Koppra‘

It has a unique mechanism of action -> does not interact with other drugs

MoA: inhibits presynaptic Ca++ channels

34
Q

Adverse effects of the use of Levetiracetam?

A

Increased risk of suicidal intention

35
Q

Use of Vigabatrin

A
  • licensed for infantile spasm
  • add-on for refractory partial epilepsy where everything else has failed
36
Q

What potential side effect of Vigabatrin use?

A

Permanent development of tunnel vision (by bilateral visual field constriction)

37
Q

Lacosamide

  • use
  • MoA
  • side effects
A

Lacosamide

Use: adjunctive therapy for partial seizures

MoA: enhances slow inactivation of Na+ channels -> sodium channel blocker

Side effects: dizziness and ataxia

38
Q

Clobazam

  • use
  • class and its consequences
  • advantages of use
A

Clobazam

Use:

  • adjunctive therapy for seizures in those in whom monotherapy failed
  • refractory epilepsy

Class: benzodiazepine -> cannot be used in long- term Rx due to development of tolerance

Advantage: It enhances GABAA receptors (like benzodiazepines) but has different allosteric binding sites -> less sedation/sleepiness

39
Q

Why Lorazepam can be given only IV?

A

It is bound to protein = poor water and lipid solubility

Lecture week 4 (18 decks)

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