Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Pharmacology > Antiepileptic Drugs > Flashcards

Antiepileptic Drugs Flashcards

1
Q

What is the goal of antiepileptic therapy?

A

To reduce the frequency and intensity of seizures; they are most effective at treating epileptic seizures.

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

What are the other indications of antiepileptic drugs?

A

Neuropathic pain; mood stabilization; migraine headache.

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

What is a seizure?

A

An excess of neuronal excitation (depolarization); the outcome depends on the location and focus of the activity.

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

How do AEDs impede the transmission of neuronal impulses?

A

(1) Sodium-channel blockade; (2) calcium-channel blockade; (3) glutamate (excitatory) antagonism; (4) GABA (inhibitory) enhancement.

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

How are AEDs typically used?

A

They are often used in combination to treat a specific type of seizure disorder; drugs used in combination are always chsen from different classes.

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

Describe the absorption of AEDs:

A

They undergo complete absorption; absorption is slowed by the presence of food in the stomach; absorption usually takes several hours (important when ordering labs).

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

Which drug is an exception in terms of absorption?

A

Gabapentin – it is absorbed via an amino acid transporter; high-protein meals will limit the absorption of Gabapentin.

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

Describe the auto-induction property of carbamazepine:

A

Carbemazepine is an auto-inducer (it stimulates its own metabolism); auto-induction dissipates in 3-4 weeks.

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

How is lamotrigine metabolized?

A

Phase II (glucuronidation).

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

How is valproic acid metabolized?

A

Through a combination of phase I and phase II.

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

What are the principle phase I enzymes involved with AEDs?

A

CYP2C19, 2C19, and 3A4; this is the source of many drug interactions, and the narrow therapeutic index of these drugs.

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

How do you characterize the phase I interactions of the older AEDs?

A

They tend to be CYP-450 inducers; this increases metabolism through the system, and decreases blood levels of other drugs.

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

How do you characterize the phase I interactions of phenytoin and carbamazepine?

A

They are broad-spectrum inducers; must monitor closely for DDIs.

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

How do you characterize the phase I interactions of newer AEDs (oxcarbazepine/topiramate)?

A

Thy tend to be a bit cleaner, but still induce the 3A4 system at higher doses.

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

How do you characterize the metabolic interactions of valproic acid?

A

It inhibits phase II metabolism, and is a 2C19 inhibitor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the therapeutic index of AEDs:

A

Older AEDs have a narrow TI (phenytoin/carbamazepine); the newer AEDs have a much wider TI; but data is less established for newer drugs.

17
Q

When are AED serum concentrations useful, and when should labs be drawn?

A

They are useful fr optimizing therapy, monitoring adherence, or looking for possible DDIs; labs should be drawn after 4-5 half-lives have elapsed.

18
Q

What is the caveat with newer AEDs?

A

Many of them are lousy AEDs in monotherapy.

19
Q

How is AED metabolism altered in geriatrics?

A

Decreased albumin (higher free-drug); decreased hepatic enzymes; decreased renal clearance.

20
Q

How is AED metabolism altered in children?

A

Metabolism is faster; may require higher, more frequent dosing.

21
Q

Describe the use of AEDs during pregnancy:

A

Most are teratogenic; if they are used it will require higher, more frequent dosing.

22
Q

How is AED metabolism altered in febrile illness?

A

Metabolism increases; AED serum levels are decreased.

23
Q

How is AED metabolism altered in chronic renal disease?

A

Altered protein binding to albumin results in higher free drug; the patient will appear toxic at therapeutic levels (seen most often with valproic acid).

24
Q

What is a concern when using AEDs with OCP therapy?

A

AEDs are 3A4 inducers, they decrease the efficacy of OCPs – this is especially concerning because AEDs are teratogenic.

25
Q

What are the acute, dose-related ADRs of AEDs?

A

Sedation, fatigue, incoordination, cognitive impairment, tremor, parasthesia, diplopia, mood/libido changes.

26
Q

Which AED has the highest incidence of cognitive impairment?

A

Topiramate.

27
Q

Which drugs can cause hyponatremia, SIADH?

A

Carbamazepine and oxcarbazepine.

28
Q

What is Stevens-Johnson syndrome?

A

An idiosyncratic ADR: exfoliative rash, hepatic damage, abdominal pain; appears in the first several months of treatment.

29
Q

Which AEDs have the highest incidence of Stevens-Johnson syndrome?

A

Valproic acid and lamotrigine; may also occur with rapid titration of dose.

30
Q

What are the other idiosyncratic ADRs that can occur with AEDs?

A

Hematologic damage (lamotrigine); gingival hyperplasia (phenytoin); and hypersensitivity syndrome (demonstrates cross-re-activity).

Clinical Pharmacology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions