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Neurology Week 4 > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

1
Q

Note that fosphenytoin is a pro-drug for phenytoin

A
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2
Q

What are the types of partial seizures?

A

simple partial

complex partial

partial seizures secondarily generalized

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3
Q

What are the types of generalized seizures?

A

generalzed tonic-clonic (grand mal)

absence (petit mal)

tonic

atonic

clonic and myoclonic

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4
Q

How do seizures arise?

A

they begin discretely with depolarization of neurons via influx of Ca2+ and activation of voltage dependent Na+ channels, resulting in high-frequency bursts of action potentials

These APs are then carried forward through GABA and K+-mediated actions, where activation of NMDA excitatory neurons, cell swelling, and changes in tissue osmolarity prevent inactivation

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5
Q

How do AEDs work?

A
  • limit the sustained firing of neurons by promoting/prolonging the inactivated state of voltage-gated Na+ channels (partial and 2ndarily generalized tonic-clonic seizures)
  • pre- or post-synaptic enhancement of GABA-mediated synaptic inhbition, an effect mediated by either a presynaptic or postsynaptic action (partial and 2ndarily generalized tonic-clonic seizures)
  • Inhibition of voltage-gated Ca2+ channels responsible for T-type Ca2+ currents (absence seizures)
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6
Q

What AEDs work by limiting the sustained firing of neurons by promoting/prolonging the inactivated state of voltage-gated Na+ channels?

A

Carbamazepine

Phenytoin

Topiramate

Lamotrigine

Valproate

Zonisamide

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7
Q

Note that GABA works primarily via chloride gated channels, to inhibit transmission. How do benzodiapines and barbiturates promote this?

A

They bind seperately at sites on the multimeric ion channel complex to enhance the inhibitory effect of GABA

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8
Q

Note that GABA works primarily via chloride gated channels, to inhibit transmission. How does gabapentin promote this?

A

It acts presynaptically to promote GABA release

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9
Q
A
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10
Q

What drugs work via the blockade the T-type calcium channels, which reduce the activity of pacemaker currents (thus, both sodium and calcium blockers diminish the effects of glutamate)?

A

Valproate and Ethosuximide

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11
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A
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12
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13
Q

What are the main Na+ channel inhibitor AEDs?

A

Carbamazepine

Lacosamide

Lamotrigine

Oxcarbazepine (+ possible increased K+ and decreased Ca2+ effects)

Phenyotin

Zonisamide (and decreased T-type Ca2+ actions)

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14
Q

What are the main Ca2+ channel inhibitor AEDs?

A

Ethosuximide (t-type)

Pregabalin and Gabapentin (a2 delta-1 subunit of Ca channel)

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15
Q

What is the MOA of Felbamate?

A

decreased NMDA and increased GABA

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16
Q

What is the MOA of Clonazepam?

A

GABA allosteric agonist

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17
Q

What is the MOA of Topiramate?

A

decreased Na channels and glutamate activity

increased K+ current and GABA activity

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18
Q

Describe the ADME of AEDs

A
  • Most administered PO
  • limited plasma protein binding except phenyotin and valproate
  • long half lives
  • predominantly hepatic metabolism with urine output

slow release (facilitates adherence- fewer doses/day)

CYP interactions

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19
Q
A
20
Q

Routine monitoring of serum drug levels is required with what AEDs?

A

carbamazepine

Ethosuzimide

Gabpentin

Phenytoin

Valproate

21
Q

What is ano important thing to note about topiramate and zonisamide?

A

they are both weak carbonic anhydrase inhibitors, which cause of loss renal HCO3- and promote renal stones by reduing urinary citrate excretion and by icnreasing urinary pH

monitor serum HCO3-

22
Q

What can occur with abrupt termination of AED therapy?

A

It can precipitae the onset of status epilepticus, increase the frequency of seizures, and cause anxiety

Taper down termination over time

23
Q

Important points about Phenytoin

A
  • shows 0-order pharmacokinetic behavior (thus, the half-life varies with drug dose)
  • metabolism highly variable
  • CYP DDIs (confounding effects- age, cigs, and hepatic smoking all affect)
  • fosphenytoin pro-drug (dose adjustment needed when switching)
24
Q

What are the AEs of Phenytoin?

A

CNS effects (nystagmus, HA, atacia; drowsiness not common)

  • Gingival hyperplasia
  • Derm effects are rare (rash to SJS, TEN, and DRESS; hypertrichosis or hirsutism)
  • Heme changes
25
Q

What are the AEs of Carbamazepine?

A

-CNS effects during initial tx phase (Dizziness, drowsiness, ataxia)

Heme changes- agranulocytosis or aplastic anemia

Derm effects are rare (rash to SJS, TEN, etc.)

-Constipation or dry mouth, N/V

26
Q

Who is at a higher risk of developing SJS and TEN when using AEDs?

A

Asians with a SNP mutation in their human leukocyte antigen-B 1502 allele (most common with carbamazepine, phenytoin, and fosphenytoin). Whole blood EDTA testing is available

27
Q

What are the AEs of Valproic Acid?

A

-CNS effects related to infusion rate (somnolence, dizziness, asthenia, HA)

Heme changes- thrombocytopenia, prlonged bleeding time

Derm effects are rare (rash to SJS, TEN)

Nausea, diarrhea

Hepatotoxicity in children rarely

28
Q

What are the main AEs of Felbamate?

A

asplastic anemia, bone marrow suppression, hepatic disease

29
Q

What are the main AEs of Lamotrigine?

A

serious rash (TEN/SJS)

dizziness, diplopia, ataxia

30
Q
A
31
Q

What AEDs are contraindicated in pregnancy (teratogenic)?

A

Valproate (worst)- Cat X

Lamotrigine- C

Carbamazepine- D

Phenytoin- D

Phenobarbital- D

32
Q

How does fetal hydrantoin syndrome present (similar effects seen with phenobarbital and carbamazepine)?

A

upper facial features including upturned nose, mild midface hypoplasia, and long upper lip with thin vermillion vorder

lower distal digital hypoplasia

33
Q

What drugs should be used to tx partial, including 2ndarily generalized seizures?

A

lamotrigine

carbamazepine

levetiracetam

oxcarbazapine

34
Q

What drugs should be used to tx primary, generalized tonic-clonic seizures?

A

Valproate

Lamotrigine

Levetriacetam

35
Q

What drugs should be used to tx absence seizures?

A

ethosuximide

valproate

These are equally effective (50-75% of pts experience complete control)

36
Q

What drugs should be used to tx atypical absence, myoclonic, and atonic seizures?

A

valproate

lamotrigine

levatiracetam

37
Q

What is status epilepticus?

A

A prolonged seizure, or cluster, without a return to baseline, lasting 30+ minutes

These seizures can be generalzied tonic-clonic, complex or simplex partial, absence, or subclinical

38
Q

Up to 50% of cases of SE occur in pts with epilepsy due to what?

A

recent changes in AEDs or non-adherence

The remainder of cases in adults are most often due to strokes

39
Q

T or F. SE is a medical emergency

A

T. With a 7-40% mortality rate. predictors of mortality include generalized seizure, increased pt age, anoxic brain injury, stroke, CNS infection or tumor, and long duration of SE.

Successful outcomes require early and aggressive tx

40
Q

How should SE be handled?

A

Benzodiazepines are the DOA

Backups: IV lorazapam, IM midazolam, or rectal diazepam, followed by:

IV valproate, phenytoin, midazolam, levetiracetam, or phenobarbital

41
Q

Compare and contrast Phenobarbital and Benzodiazepine

A

Both work on GABA receptors, but at different site

Barburates prolong the opening time of Cl- channels

Benzodiazepines shift the dose-response curve of GABA

BOTH have issues of dependence and withdrawal, develop tolerance, will produce dose-related sedation, and can be given rapid IV, unlike phenyotin or valproate

Only phenobarbital will induce CYP2B6 and 3A4 levels

42
Q

Why are benzodiazepines first line for tx of SE?

A

They can be given rapidly IV, where the admin of other drugs is limited. Thus, the benzodiazepine can rapidly terminate the SE< but short BNZ half-lives mean that additional drugs must be given to provide more drug control

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Neurology Week 4 (26 decks)

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