Anticonvulsants HR Flashcards

1
Q

What is the prevalence of epilepsy in the UK?

A

7-9% of the population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Recall the 5 types of GENERALISED seizure

A
  1. Tonic/clonic
  2. Absence
  3. Tonic/atonic
  4. Myoclonic
  5. Status epilepticus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the order of events of a tonic/clonic seizure

A
loss of consciousness
muscle stiffening (hence tonic)
jerking/twitching (hence clonic)
deep sleep 
wakes up (this seizure is what most people see in films etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most common type of generalised seizure?

A

Tonic/clonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the presentation of an absence seizure

A

brief staring episodes with behavioural arrest (NO JERKY MOVEMENTS etc. its essentially just someone going into a ‘quiet state’ staring at something)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the presentation of a tonic/atonic seizure

A
"Tonic" = sudden stiffening of muscles 
"Atonic" = loss of muscle control

basically tonic seizure but with just the muscle parts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the presentation of a myoclonic seizure

A

Sudden, brief muscle contractions

BTEC tonic seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How can tonic/atonic seizures and myoclonic seizures be differentiated

A

Presentations similar therefore use EEG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the presentation of a status epilepticus

A

More than 5 mins of chronic seizure activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a partial/ focal seizure?

A

Seizure that begins within a particular area of brain and may spread out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Recall the types of partial/ focal seizure

A

Retained awareness = simple

Impaired awareness = complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Briefly summarise the transmission events at glutaminergic synapses

A

VGSC and VGKC action –> AP
Glu stored in vesicle which is bound to presynaptic membrane via SV2A
Upon release, acts on excitatory receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Recall 4 approaches to inhibiting the excitatory effect of glutamate

A

Inhibit VGSCs
Inhibit VGCCs
inhibit SV2A docking protein
glutamate receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give 2 examples of drugs that inihibit VGSCs in glutaminerguc neurons

A

Carbamazepine

Lamotrigine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Recall the MOA of carbamazepine

A

Stabilises VGSC in its inactive state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
Pharmacokinetics of carbamazepine? 
-onset
- DOA
Selectivity of carbamazepine? 
Side effects?
A
Advantages:
1. Fast onset
2. Long DOA
Disadvantages:
1. Low selectivity
2. Enzyme inducer ie activates many enzymes--> many DDIs (drug drug interactions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Recall the indications for carbamazepine

A

Tonic/clonic seizures and partial/focal seizures

18
Q

What are the side effects associated with carbamazepine in individuals with a certain HLA haplotype, and what is this HLA allele?

A

HLA-B*1502
Severe skin conditions
Stephen Johnson syndrome
Toxic epidermal necrolysis

19
Q

Recall the MOA of lamotrigine

A

Pushes VGSCs into the inactive state

20
Q

Suggest an advantage of lamotrigine over carbamazepine as an anticonvulsant

A

Lamotrigine has higher specificity for Glu neurons

21
Q

Recall the indications for lamotrigine

A

Tonic/clonic seizures and absence seizures

22
Q

Recall an anticonvulsant that acts by inhibiting Glu vesicle docking

A

Levetiracetam

23
Q

Recall the MOA of levetirecetam

A

Binds SV2A to prevent Glu release

24
Q

Recall the MOA of topiramate

A

Inhibits NMDA and kainate Glu receptors

25
Q

Recall the indications for topiramate

A

Myoclonic seizures

26
Q

Recall the general PK of anticonvulsant drugs

A

Fast onset and long t1/2 (long DOA)

27
Q

Recall 2 anticonvulsant drugs that work by interacting with GABA transmission

A

Diazepam

Sodium valporate

28
Q

What is the MOA of valporate?

A

Inhibits GABA-T (NOT GAT) to increase synaptic GABA levels

29
Q

How is diazepam usually administered in a seizure?

A

Rectal gel

30
Q

Recall the indications for diazepam

A

Status epilepticus

31
Q

Recall the indications for valporate

A

All forms of epilepsy apart from SE

32
Q

Recall the drugs that are indicated for tonic/clonic seizure treatment

A

Carbamazepine
Lamotrigine
Valporate

33
Q

Recall the drugs that are indicated for absence seizure treatment

A

Ethosuximide
Lamotrigine
Valporate

34
Q

Recall an anticonvulsant that acts via VGCC interference

A

Ethosuximide

35
Q

What type of VGCC are found in the CNS?

A

T-type (transient)

36
Q

Recall the indications for ethosuximide

A

ONLY absence seizures

37
Q

Recall the drugs that are indicated for tonic/atonic seizure treatment

A

Valporate

38
Q

Recall the drugs that are indicated for myoclonic seizure treatment

A

Levetiracetam
Topiramate
Valporate

39
Q

Recall the drugs that are indicated for simple partial seizure treatment

A

Valporate
Carbamazepine
Lamotrigine
Levetiracetam

40
Q

What is a seizure?

What is epilepsy?

A

Seizures are sudden changes in behaviour caused by electrical hypersynchronization of neuronal networks in the cerebral cortex ie UNCOORDINATED rapid firing of neurones in the brain (caused by INCREASE in EXcitatory neurotransmission or DECREASE in INhibitory neurotransmission)

Epilepsy is the tendency to get recurrent unprovoked seizures

41
Q

When are the two peaks in incidence of epilepsy and what are they usually caused by?

A

Young adults – where genetic predispositions begin to manifest
Later years – when patients start getting brain injuries e.g. stroke can cause seizures after the stroke due to brain damage

42
Q

Summarise the main mechanisms of anti-convulsants

A

Inhibit Glutamate mediated excitation

  • VGSC inhibitor
  • VGCC inhibitor
  • SV2A inhibitor (synaptic vesicle protein)
  • glutamate receptor antagonist

Enhancing GABA mediated inhibition

  • benzodiazepines (Positive Allosteric Modulators)
  • GABA transaminase inhibitors (stop GABA breakdown)