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Neuro II > Pharm For Seizures And Epilepsy > Flashcards

Pharm For Seizures And Epilepsy Flashcards

1
Q

What drug is used for Generalized Onset Absence seizures?

A

Ethosuximide

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2
Q

What drug is used for generalized onset myotonic, atonic, or clinic seizures?

A

Benzodiazepines (clonizapam has multiple forms of administration)

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3
Q

What drugs are used to treat generalized onset tonic/clinic (grand mal) seizures?

A

Phenytoin, phenobarbital, carbamazepine (must start with partial onset)

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4
Q

What drugs can be used for partial onset simple complex seizures?

A

Carbamazepine, gabapentin, lecosamide, oxcarbazepine, tigabine, vigabatrin, ezogabin.

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5
Q

What are the broad spectrum drugs used to treat seizure activity?

A

Valproate, lemotrigine, topirmate, levetiracetam, zonisamide.

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6
Q

What two structures do AED’s antagonize to decrease excitation?

A

1) Voltage-gated Na+ channels

2) Low-Threshold (t type) Ca2+ channels

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7
Q

What drugs antagonize the voltage-gated Na+ channels on pre-synaptic neurons?

A

Phenytoin, carbamazepine, lamotrigine, oxcarbazepine, zonisamide.

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8
Q

What drugs prolong the fast inactivation state of the Na+ channel?

A

Phenytoin, Carbamazepine, lamotrigine, oxcarbazepine

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9
Q

What drug enhances the slow inactivation of voltage gated Na+ channels?

A

Lacosamide

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10
Q

At what state can AED’s bind to the interior of the Na+ channel?

A

Activation gate must be open

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11
Q

How does phenytoin and carbamazepine differ with their actions at the Na+ channel?

A

Phenytoin- most effective at depolarized potentials and high-frequency AP firing.

Carbamazepine- binds less effectively, but with much faster rate then phenytoin. More effective in blocking high-frequency AP firing.

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12
Q

What is the MOA of Lamotrigine?

A

Similar to phenytoin and carbamazepine with the addition of N and P type voltage gated Ca2+ channels in cortical neurons.

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13
Q

What is the MOA of Lacosamide?

A
  • Stabilizes the slow-inactivated state.

- Used in the treatment of partial seizures.

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14
Q

What are the defining features of absence seizures (petit mal)?

A
  • 3Hz spike and wave activity of EEG.
  • T-type Ca2+ channels are affected.
  • Target cortex-thalamus oscillation.
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15
Q

What is the drug off choice in treating absence petit mal seizures?

A
  • Ethosuximide-> only used to treat this type!

- Non-Sedating

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16
Q

If your patient does not respond to Ethosuximide in the treatment of their petit mal seizure, what is the next best drug to use?

A

Broad spectrum AED such as Valproate or lamotrigine. By definition they will affect the dysregulated channels.

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17
Q

What is unique about the AED zonisamide?

A

Blocks voltage dependent Na+ channels and T-type calcium channels.

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18
Q

What two mechanisms do AED’s use to augment Inhibition?

A

1) Block GABA re-uptake or metabolism

2) Potentiate GABAa receptor Cl- currents

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19
Q

What drug inhibits GABA re-uptake?

A

Tiagabine

20
Q

What drug inhibits GABA metabolism, doesn’t allow the conversion of GABA-> glutamate to occur?

A

Vigabatrin

21
Q

What is the MOA of benzodiazepines?

A

Bind to GABAa causing an allosteric change that potentiates GABA binding allowing Cl- to enter the cell.

22
Q

What is the MOA of barbiturates?

A

Bind to a distinct and increase the duration of the Cl- channel opening

23
Q

What is the main difference between benzodiazepines and barbiturates?

A

Benzodiazepines are GABA dependent. At high concentrations barbiturates are not!

24
Q

What are some causes of status epilepticus?

A

Abrupt discontinuation of AED medication, ETOH withdrawal, cocaine abuse, poisons.

25
Q

What are the first line treatment for status epilepticus?

A

1) benzodiazepines (diazepam and lorazepam)

2) if no response–> Fosphentoin IV (water soluble Na+ channel antagonist)

26
Q

What are two drug-drug interactions that must be accounted for in starting a patient on carbamazepine?

A

1) starting carbamazepine can INCREASE clearance of oral contraceptives.
2) starting carbamazepine can INCREASE clearance of warfarin-> increased risk of arterial/venous thrombosis.

27
Q

What is a unique feature of the newer AED’s?

A

Mixed clearance, renal and liver each at 50%.

28
Q

What is the name of the drug that is an analogue of carbamazepine that has fewer side effects and what is this due to?

A

Oxcarbazepine–> less side effects due to its lack of formation of an active metabolite.

29
Q

What ion disturbance can be seen with carbamazepine and oxcarbazepine?

A

Hyponatremia due to increaed responsiveness of collecting tubules to ADH.

30
Q

What is the mode of clearance of Gabapentin and pregablin?

A

100% renal clearance. Renal ionsufficieny requires dose adjustment.

31
Q

What are the two serious boxed warning complications of Carbamazepine use?

A

1) Life threatening allergic reaction (Steven-Johnson syndrome)
2) Aplastic anemia

32
Q

What is the boxed warning complication of Lamotrigine?

A

Life threatening allergic reaction (Steven-Johnson syndrome).

33
Q

What is the potential complication of valproate and lamotrigine being administered together?

A

Together they inhibit conjugation of drugs by UGT enzymes causing accumulation of parent drug.

34
Q

What are the potential serious side effects of Levettiracetam?

A

None

35
Q

What are the potential serious side effects of Oxcarbazepine?

A

Hyponatremia

36
Q

What are the potential serious side effects of Tiagabine?

A

Stupor

37
Q

What are the potential serious side effects of Topiramate?

A

Nephrolithiasis, open angle glaucoma, hypohidrosis.

38
Q

What are the potential serious side effects of Zonisamide?

A

Rash, renal calculi, hypohidrosis.

39
Q

What 3 AEDs are class D Teratogens?

A

Valproate, carbamazepine, phenytoin

40
Q

What 4 AEDs are CYP450 inducers?

A

Carbamazepine, Phenobarbital, Phenytoin, Valproic acid.

41
Q

What are the complications associated with Carbamazepine?

A
  • aplastic anemia
  • Leukopenia, neutropenia, thrombocytopenia,
  • Hypocalcemia, osteoporosis
  • P450 inducer
42
Q

What are the complications associated with Phenytoin?

A
  • Zero-Order kinetics!
  • Gingival hyperplasia
  • Hirsuitism
  • hypocalcemia and osteoporosis
  • P450 inducer
43
Q

What is the MOA of Gabapentin?

A
  • Binds to voltage-dependent Ca2+ channels.

- No significant drug interactions

44
Q

What is the MOA of Leviteracetam?

A
  • Binds to synaptic vesicle protein SV2A- blunts glutamate release
  • Well tolerated
45
Q

What is the MOA of Pregabalin

A
  • multiple MOA

- 100% renal clearance

46
Q

What is the MOA of Ezogabine?

A
  • Opens voltage-gated K+ channels

- Causes urinary retention

Neuro II (6 decks)

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