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Neuro-Psych Exam II > Anti epileptic Drugs > Flashcards

Anti epileptic Drugs Flashcards

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1
Q

Define status epilepticus**

A

Generalized tonic-clonic seizures w/ ^^^ frequency (recur before patient returns to normal consciousness from the postictal state)
***MEDICAL EMERGENCY W/ HIGH MORTALITY RATE
(HYPOXIC BRAIN DAMAGE)

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2
Q

Describe treatment for status epilepticus:
First line–> Refractory–> Secondary Refractory

What is important to remember about secondary refractory treatment?

A

1st: IV BDZ, then IV Phenytonin/Fosphenytoin
(*Admin. to prevent seizure reoccurrence even if seizure has stopped)
Refractory: ^^^Phentonin, ^^^ BDZ
Secondary Refractory: Barbs or Propofol
*Note: secondary refractory treatment may require respiratory support

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3
Q

3 stages of seizure

A
  1. Aura (convulsive + partial seizures only)
  2. Itcus (“seizing”)
  3. Postictus (hypoglycemic state–not present in absence seizure)
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4
Q

What percentage of patients with uncomplicated tonic/clonic seizures can achieve complete seizure control with treatment?

A

85%

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5
Q

What are three important things we generally try to avoid when administering anti-convulsive agents?

A

Alteration in:

  1. Intellect/alertness
  2. Physical abilities
  3. Reproductive ability due to therapy
    * Patients generally on tx for life
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6
Q

What are four important issues with compliance to consider when choosing anti convulsive therapy?

A
  1. Potential effectiveness
  2. Adverse problems (i.e. hirsutism in women…)
  3. Convenience (daily pill)
  4. $$
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7
Q

Describe two reasons why serum drug levels are important in anti convulsive therapy:

A
  1. avoid drug toxicity/ ensure proper dosage

3. check patient compliance

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8
Q

Phenytoin:
MOA (3)
(means = likely to be tested!)

A

Inhibits seizure spread + Suppresses epileptic foci

  1. Blocks Ca++ influx
  2. ^ Cl- influx (GABA tranmission, IPSPs)
  3. ^ affinity for inactivated Na+ channels
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9
Q

Phenytoin:

Therapeutic Use

A

**DOC for all seizures EXCEPT absence epilepsy/ atonic seizures

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10
Q

Phenytoin:
ROA (2)
Transport/ Metabolism*

A
  • PO; IV for status epilepticus
  • 90% protein bound in plasma
  • Metabolized in the liver by saturable enzymes: small dose = ^ in plasma & toxicity
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11
Q

5 most important phenytoin ADRs:

A
  1. Gingival hyperplasia (20% kiddos)
  2. Hirsutism (compliance*)
  3. vestibular disturbance: nystagmus, ataxia
  4. Allergic rxn: SJS* rash, hematological
  5. Cardiotox with ^ IV bolus
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12
Q

CI populations for phenytoin therapy

A

ALL women of childbearing age; teratogenic

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13
Q

Which vitamin should be supplemented in patients on phenytoin therapy? Why?

A

Vitamin K; phenytoin = CYP3A4 inducer

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14
Q

**Carbamazepine:
Therapeutic Uses (3)
When should it NOT be used (2)

A
  1. Gen tonic-clonic seizures (2nd line)
  2. Complex partial seizures (2nd line)
  3. Trigeminal neuraligia (2nd line)
  • Not effective for absence seizures
  • Makes myoclonic seizures WORSE
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15
Q

Which 2 populations should not take Carbamazepine?

A 
Elderly patients (hepatotoxic) 
Patients with myoclonic seizures ** ACTUALLY MAKES THESE WORSE**
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16
Q

Describe the unique nature of carbamazepine metabolism

A

Auto induces its own metabolism via CYP1A2/2C/3A

*Metabolic rate will ^^ within first 4-6 weeks and stabilize within 1mos

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17
Q

**Valparoic Acid:
MOA (3)
Which is a target for treatment of absence epilepsy?

A
  1. potentiates GABA
  2. blocks Na+/K+ channels
  3. inhibits T-type Ca+ channels (**Tx. absence epilepsy)
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18
Q

2 Important therapeutic uses for Valparoic acid

A
  1. Absence seizures refractory to ethosuximide (often 1st line)
  2. Bipolar disorder
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19
Q

How is it valparoic acid absorbed?
Special method of administration?
Which 4 groups is it CI?

A

-gut
- can give to kiddos as sprinkles!!! (makes it easy to use)
DO NOT give:
1. kiddos younger than 2
2. elderly
(1 + 2 because hepatotoxic)
3. bleeding disorders
4. Preggos: teratogenic

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20
Q

Most common ADR associated with valparoic acid

A

1 alopecia- problem with compliance

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21
Q

2 important DD interactions with valproic acid:

A
  1. Lamotrigine (^ conc by inhibiting P450)

2. Phenytoin (Displaces from plasma proteins, decreases elimination)

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22
Q

Ethosuximide:
MOA
Therapeutic use

A

Blocks T type Ca++ channels

Tx: absence seizures only

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23
Q

**Lorazepam and other BDZs:
MOA (3)
Most important use

A
  1. Potentiate GABA
  2. inhibit VGNa++ channels
  3. block Ca++ channels @ sedating doses
    * *IV admin for status epilepticus
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24
Q

Gabapentin:
MOA
Therapeutic use (2)
Advantages to use

A
  • ^ GABA release from central neurons
  • Tx: Diabetic neuropathy, occasional adjunct anti epileptic (not very effective for this use)
  • *Does not change conc. of other anticonvulsants
25
Q

**Which antiepileptic drug has the HIGHEST probability of causing SJS

A

**Lamotrigine

26
Q

**Lamotrigine: MOA- inhibits what four things?

A
  1. Ca Channels
  2. Na Channels
  3. Glutamate release
  4. aspartate release
27
Q

**Lamotrigine:

Therapeutic use + stipulations*

A

Used to treat most all seizure disorders in patients >16yo**

28
Q

Topiramate is abroad spectrum anti epileptic.

What two other conditions are treated with Topiramate?

A
  1. migraine

2. IICH

29
Q

Three important ADRS with Topiramate?

A
  1. **Renal stone formation (Its hard “TO” pee”)
  2. paresthesia (CA inhibitor)
  3. Loss of mental acuity (“TOPI makes you dopey”)
30
Q 
**Levetiracetam (Keppra): 
Therapeutic use (2)
Most important advantage to use; in which population is it highly indicated?
A

Unknown MOA

  1. Adjunct therapy for partial seizures; increasingly used for others
  2. Migraines
    * *Not appreciably metabolized in body; great for patients with hepatic insufficiency (Keppra keeps the liver safe)
31
Q

Oxcarbazepine:
MOA
Therapeutic use
ADR

A

Blocks VG Ca++ channels
Tx partial seizures
Causes hyponatremia in first 3 mos

32
Q

Pregabalin:

Most Common Therapeutic Use

A

neuropathic pain (esp. diabetics)

33
Q

Broad Spectrum Antiepileptics (4)

A

Lamotrigine (>16yo)
Levetiracetam (Keppra keeps the liver safe)
topiramate (“TOPI makes you dopey”)
valproate (No child bearing age ladies!)

34
Q

Narrow Spectrum anti epileptics (4)

A

Carbamazepine- makes myoclonics worse; not absence
Oxcarbazepine- partial seizures
Phenobarbital- febrile/ status epilepticus
Phenytoin- not absence/atonic

35
Q

Drug only for absence seizure (DOC)

A

Ethosuximide

36
Q

Why should anticonvulsants be avoided in women of child bearing age despite OCP use?

A

Anticonvulsants alter hepatic metabolism and plasma protein binding of OCPs–this can lead to unplanned preggos + possible birth defects

37
Q

Measures to be taken with female on anticonvulsant therapy in planned preggos?
What is the ideal therapy for these patients?

A
  • Best choice: Keep on same drug if possible. Start ladies of this age/in general on safe drug even before desire for pregnancy!!!
  • Have to stop barbs, phenytoin, and valproate though if they were taken!!! Switch drug

GOAL: mono therapy with lowest possible dose to

38
Q

Describe Fetal Hydantoin Syndrome:

Which drug causes this?

A

Caused by phenytoin:

  1. Cleft lip/palate
  2. Congenital heart disease
  3. slowed growth
  4. mental deficiency
39
Q

Describe epilepsy in pregnant patient: does it get better or worse? why? how do we monitor these patients?

A

Will ^ # seizures during preggos despite medication use

  1. ^ drug clearance
  2. ^ maternal volume
    * monitor by ^ frequency of labs
40
Q

What should be avoided in unplanned pregnancy of woman on anticonvulsant therapy (2)

A
  1. DON’T COMPLETELY REMOVE ANTICONVULSANT
  2. DON’T SWITCH ANTICONVULSANT IF PREGNANCY WAS UNPLANNED

**Risk of meds is safer than altering therapy

41
Q

What happens if a woman with seizure disorder discontinues anti epileptic therapy during preggos?

A

^ seizure frequency–> anoxic conditions–> birth defects

42
Q

2 non-pharm therapies for epileptic conditions

A
  1. vagal n. stimulation (pulse generator implant )

2. surgical removal of epileptic focus

43
Q

What seizures generally lack auras?

A

1) absence
2) myoclonic
3) seizures in kids, because kids may not recognize them
(a true Melissa statement- hahaha)

44
Q

Post ictus state is caused by?

A

hypoglycemia

45
Q

General mechanisms for seizure drugs:

If you forget MOA, guess these:

A

decrease Na/ Ca/ glutamate/ aspartate

increase Cl-/ GABA

46
Q

Serious risk assc with all antiepileptics

A

Steven Johnsons

47
Q

Role of phenobarbital in anticonvulsive therapy:

A

-IV administration to stop status epilepticus (2nd refractory)
-severe febrile seizure
(Emergencies, not maintenance)

48
Q

Two treatments for absence seizures:

A

valproic acid
ethosuximide

**via T-type Ca+ channels

49
Q

Felbamate treats?

A

Lennox Gastaut

50
Q

Age group Lennox Gastaut is seen in?

A

under 4 yoa

51
Q

Infantile spasms:
Age of onset
% idiopathic

A

under 6 months

15% idiopathic; 85% have identifiable cause

52
Q

Drugs that are absolutely pregnancy X/ not good for managing seizures in child bearing age women?

A
  • barbs
  • phenytoin
  • valproate
53
Q

Drug that requires vitamin K supplementation?

A

phenytoin- induces CYP3A4

54
Q

Which seizure drug is safe in hepatic failure patients?

A

leviteracetam (Keppra)

-no metabolism in the body (“Keppra keeps the liver safe”)

55
Q

Drug that causes hyponatremia in the first three months?

A

oxcarbazepine

56
Q

Drug that auto-induces its own metabolism/ requires dose release during initial 4-6 weeks of treatment?

A

carbamazepine

57
Q

Drug that is metabolized by saturable enzymes? What is the consequence?

A
  • phenytoin
  • can go rapidly from therapeutic –> toxic levels
  • must monitor patient plasma
58
Q

Drug w/ zero order kinetics?

A

Phenytoin

Neuro-Psych Exam II (11 decks)

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