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Pharmacology > AEDs > Flashcards

AEDs Flashcards

1
Q

What happens during a seizure in the brain?

A

Large groups of neurones are activated repetitively, unrestrictedly and hyper-synchronously, with inhibitory neurones failing

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2
Q

What are the two main classifications of seizures?

A

Focal (partial) seizures

Generalised seizures

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3
Q

What is a focal seizure?

A

Where the discharges begin in a localised area of the cortex and symptoms reflect the area affected

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4
Q

What are the types of focal seizures?

A

Simple focal
Complex focal
Jacksonian (focal motor)
Temporal lobe (feeling of deja vu seizures)

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5
Q

What are the symptoms of a focal seizure?

A

Abnormal sensations or thoughts
Change in behaviour
An involuntary motor action

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6
Q

What happens in generalised seizures?

A

Generalised centrally and spread through the whole brain, including the reticular system - immediate loss of consciousness

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7
Q

What are the types of generalised seizures? Symptoms of each?

A

Absence
-patient stares, eyelids may twitch

Tonic-clonic

  • vague warning signs
  • body becomes rigid
  • tongue is bitten
  • incontinence can occur
  • clonic phase: generalised convulsion, frothing at mouth, rhythmic jerking of muscles

Myoclonic
-contraction and relaxation of a group of muscles, patient tends to be conscious

Atonic
-patient falls due to sudden loss of muscle tone

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8
Q

What is a seizure?

A

A convulsion or transient abnormal event from episodic discharge of high frequency electrical activity in the brain

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9
Q

What happens in a complex focal seizure?

A

The patient loses consciousness

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10
Q

What is status epilepticus defined as?

A

A single convulsion lasting more than 30 minutes or convulsions occurring back to back with no recovery between them

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11
Q

How can status epilepticus cause harm?

A

Physical injury relating to a fall/crash
Hypoxia
SUDEP (sudden depth in epilepsy)

Brain dysfunction
Cognitive impairment
Serious psychiatric disease

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12
Q

Difference between primary and secondary epilepsy?

A

Primary - no identifiable cause (idiopathic)

Secondary - underlying medical condition causes the seizures

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13
Q

Causes of secondary epilepsy?

A

Brain injury and hypoxia

Pyrexia (common in children, recurrence rare)

Brain tumours - partial focal or secondary generalised

Alcohol, drugs, drug withdrawal

Encephalitis and inflammatory conditions eg cerebral abscess, neurosyphilis

Metabolic abnormalities eg hypocalcaemia, hypoglycaemia, hyponatraemia

Provoked seizures eg photosensitivity

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14
Q

In general, what is epilepsy caused by?

A

Increased excitatory activity
Decreased inhibitory activity
Loss of homeostatic control
Spread of neuronal activity

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15
Q

How can untreated epilepsy lead to morbidity and mortality?

A 
Status epilepticus 
Physical injury through a seizure
SUDEP
Adverse reaction to medication
Higher risk of psychiatric disease
Cognitive impairment
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16
Q

What treatment is there for epilepsy if drugs are unsuccessful?

A

Temporal lobectomy

Corpus callosal section - prevents seizures spreading between hemispheres - useful for generalised seizures. Good for control but rarely become seizure-free

Hemispherectomy - for children who have irreversible damage to the whole hemisphere

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17
Q

How do voltage-gated sodium channel blockers prevent seizures?

A

Bind to internal face of sodium channel when in inactivated state
Act preferentially on neurones causing the high frequency discharge that happens in an epileptic fit whilst not interfering with low frequency neurones in their normal state

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18
Q

How do VGSC blockers act preferentially on high frequency neurones?

A

Because they depolarise more, so there are more of these neurones in the deactivated state, so the drug can bind to them more

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19
Q

Name some VGSC blockers

A

Carbamazepine
Phenytoin
Lamotrigine

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20
Q

Absorption, protein binding and half-life of carbamazepine?

A

Well absorbed
75% protein bound
Linear pharmacokinetics

Initially, half life is 30 hours, however is a strong inducer of CYP450 so increases its own metabolism - reduced to 15 hrs with repeated use

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21
Q

ADRs of carbamazepine?

A

CNS

  • dizziness
  • drowsiness
  • ataxia
  • motor disturbance
  • numbness
  • tingling

GI - vomiting

CVS

  • BP variation
  • contraindicated in AV conduction

Rash

Hyponatraemia

Severe bone marrow depression leading to neutropenia

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22
Q

Mnemonic to remember CYP450 enzyme inducers?

A 
PC BRAS
Phenytoin
Carbamazepine
Barbiturates 
Rifampicin 
Alcohol (chronic)
Sulphonylureas
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23
Q

DDIs of carbamazepine?

A

Reduces phenytoin, warfarin, corticosteroid and OCP levels

Antidepressants can interfere with its actions

Phenytoin can decrease its binding, increasing carbamazepine’s plasma concentration

24
Q

Epilepsy types treated with carbamazepine?

A

Generalised tonic-clonic

All types of partial

25
Q

Protein binding and half-life of phenytoin?

A

90% bound

Non-linear pharmacokinetics at therapeutic levels so has a variable half life: 6-24 hours

26
Q

ADRs of phenytoin?

A 
Dizziness
Ataxia
Headache 
Nystagmus
Nervousness

Gingival hyperplasia

Hypersensitivity rashes including Stevens-Johnson syndrome

27
Q

DDIs of phenytoin?

A

Enzyme inducer

Competitive binding with valproate, NSAIDs, salicyclate to increase its plasma levels, exacerbating non-linear pharmacokinetics

Decreases levels of OCP

Cimetidine increases phenytoin levels

28
Q

How is phenytoin level monitored?

A

Use salivary levels as indicator of free plasma levels

29
Q

When is phenytoin used?

A

Generalised tonic-clonic
All types of partial

IV in status epilepticus

30
Q

How does lamotrigine work?

A

Prolongs VGSC inactivation state (like carbamazepine and phenytoin)
Also is a possible calcium channel blocker, and decrease glutamate release

31
Q

Half-life of lamotrigine?

A

24 hours, phase II metabolism

32
Q

ADRs of lamotrigine

A

Less marked CNS symptoms but

  • dizziness
  • ataxia
  • somnolence
  • nausea

Mild and severe skin rashes

33
Q

DDIs of lamotrigine?

A

Can be used as an adjunct therapy with other AEDs

OCP reduces plasma LTG levels

Valproate increases plasma LTG levels due to competitive binding

34
Q

When is lamotrigine used?

A

Partial seizures

Generalised

  • tonic clonic
  • absence

First line AED in epilepsy
Safer in pregnancy
Not in paeds due to increased risk of ADRs

35
Q

How do drugs causing GABA-mediated inhibition help epilepsy?

A

Enhance activation of GABA receptors by facilitating GABA-mediated opening of chloride ion channels

Causes an inhibitory effect on neurones by increasing threshold for action potential due to Cl

Makes membrane potential more negative, reducing likelihood of epileptic neuronal hyper-activity

36
Q

Name some drugs which enhance GABA-mediated inhibition

A

Valproate sodium

Benzodiazepines

37
Q

Mechanism of action of valproate sodium?

A

Increases GABA content of brain by stimulating GABA-synthesising enzymes
Inhibit GABA inactivating enzymes

38
Q

Is valproate sodium protein bound?

Half-life?

A

Yes

Half-life of 15 hours with linear PK

39
Q

ADRs of valproate sodium?

A 
Less severe than other AEDs 
CNS
-ataxia
-tremor
-weight gain

Hepatic

  • increases transaminase effects
  • hepatic failure (rarely)
40
Q

DDIs of valproate sodium?

A

Antidepressants inhibit its action

Antipsychotics antagonise it by lowering convulsive threshold

Aspirin competitively binds in plasma, increasing free valproate

41
Q

What monitoring is required with valproate sodium?

A

Free plasma concentration using salivary levels

Monitor for blood, metabolic and hepatic disorder

42
Q

When is valproate sodium used?

A

Partial seizures
Generalised
-tonic-clonic
-absence

43
Q

Mechanism of action of benzodiazepines?

A

Act at a distinct receptor site on GABA chloride binding channel

Binding if GABA or BZD enhances eachother’s binding, act as positive allosteric effectors

Increases the chloride current into the neurone, increasing threshold for action potential generation

44
Q

How much are benzodiazepines absorbed and how much are they protein bound in plasma?

Half-life?

A

Well absorbed - 90-100%

85-100% plasma protein bound

Linear PK - half-life varies from 15-45 hours

45
Q

ADRs of benzodiazepines?

A 
Sedation
Tolerance with chronic use
Confusion and impaired coordination 
Aggression
Dependence and withdrawal with chronic use
Abrupt withdrawal seizure trigger
Respiratory and CNS depression
46
Q

How to treat an overdose of benzodiazepines?

A

IV flumazenil however this may precipitate an arrhythmia or seizure

47
Q

When and which benzodiazepines are used?

A

Lorazepam/diazepam - status epilepticus

Clonazepam - absence seizure, short-term use

Side effects limit first line use

48
Q

What is the first line treatment for generalised seizures?

A

Valproate sodium

49
Q

What is the first line treatment for partial seizures?

A

Carbamazepine

50
Q

What is the first line treatment for generalised and partial seizures in women of child-bearing age?

A

Lamotrigine

  • less effect on OCP
  • fewer teratogenic effects
51
Q

First line of treatment for status epilepticus?

A

Basic ABCS

Benzodiazepines (lorazepam)
IV Phenytoin - zero order kinetics means therapeutic levels can be reached more quickly

Also paralysis, sedation, intubation

52
Q

How can AEDs be teratogenic?

A

Valproate can cause neural tube defects
Congenital malformations
Facial and digital hypoplasia
Learning difficulties

53
Q

What can be given with AEDs to reduce the risk of neural tube defects?

A

Folate supplements

54
Q

Why is vitamin k given in pregnancy with AEDs?

A

They can cause vitamin K deficiency so reduces risk of cerebral haemorrhage and coagulopathy

55
Q

What tests should be done in emergency management of status epilepticus?

A 
Blood glucose
U&Es 
Plasma calcium 
Blood gases
Imaging

Pharmacology (23 decks)

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