Brainscape's Knowledge GenomeTM

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


See full index

2. Neuro exam 2 > Segars: Antiepileptic Agents > Flashcards

Segars: Antiepileptic Agents Flashcards

1
Q

List the 9 antiepileptic drugs which work as pre-synaptic voltage-gated Na+ channels blockers via enhanced fast inactivation.

A

1) Carbamazepine
2) Oxcarbazepine
3) Lamotrigine
4) Phenytoin
5) Rufinamide
6) Topiramate
7) Valproic acid
8) Zonisamide
9) Lacosamide

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

Which AED is unique in its ability to prolong fast inactivation of Nav ion channels and also enhance slow inactivation of Nav channels?

A

Lacosamide

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

Which 2 antiepileptic drugs are AMPA-receptor antagonists?

MOA?

A
  1. Topiramate
  2. Perampanel

MOA = bind AMPA receptor and block glutamate binding; channel doesn’t open –> AP does not propogate downstream

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

Which antiepileptic drug is an NMDA-receptor antagonist?

A

Felbamate

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

The pharmacological activity of AED Nav channel blockers is _______ and ________-dependent

A

State and Use-dependent

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

Which gate must be open for AED’s to access the pore of Nav channels?

Which states can this occur?

A
  • Activation gate
  • Open state and Fast-inactivated state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The probability of Nav blockade is proportional to what?

A

FREQUENCY of Nav channel opening and dose

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

Why do the AED’s that are Nav blockers act preferentially on the neurons involved in epileptic seizures?

A

The neurons involved will be firing at higher freqeuncy than normal, allowing more chances for these drugs to slip right in and bind

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

What is the water-soluble pro-drug of phenytoin which is given via IV and is an Nav channel blocker used as an antiepileptic?

A

Fosphenytoin

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

Which AED acts as a Nav channel blocker (fast inactivation), AMPA-receptor antagonist, and GABAA agonist?

A

Topiramate

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

What occurs when the post-synaptic GABAA receptor becomes occupied by GABA?

A
  • Cl- channel opens
  • Hyperpolarization occurs blunting AP propogation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the MOA of the AED, Tiagabine?

A
  • Blocks pre-synaptic reuptake of GABA by blocking the GABA transporter, GAT-1
  • Causes GABA to go post-synaptically, bind GABAA receptor leading to hyperpolarization and decreased AP propogation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 3 MOA’s of Valproic acid used as a AED at the pre-synaptic GABA terminal?

A

1) Increase activity of glutamic acid decarboxylase, leading to increased GABA presynaptically
2) Inhibit GABA-T, which typically metabolizes GABA
3) Inhibit Succinic Semialdehyde Decarboxylase (SSD), which typically metabolized GABA

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

Which 2 AED’s inhibit the metabolism of GABA through the inhibition of GABA-T?

A
  1. Vigabatrin
  2. Valproic acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which drug in the barbiturate family gets metabolized to phenobarbital in the body?

A

Primidone

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

Where do Benzodiazepines bind the GABAA receptor and what effects does this have?

A
  • Bind to a distinct site –> Allosteric change potentiate GABA binding
  • Cl- channel opens with greater frequency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where do Barbiturates bind the GABAA receptor and what is their effect?

A
  • Bind a distinct site
  • Increases the duration of Cl- channel opening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Of the GABAA receptor agonists used as AED’s which is more lethal at higher doses and why?

A
  • Barbituates are more lethal due to being GABA INdependent
  • Benzodiazepines are GABA-dependent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 7 AED’s which act post-synaptically to potentiate GABAA-receptor Cl- currents?

A

1) Phenobarbital
2) Primidone
3) Clonazepam
4) Lorazepam
5) Diazepam
6) Clobazam
7) Topiramate

20
Q

Which type of ion channel mediates the 3-Hz spike and wave activity in the thalamus which is the hallmark of absence (petit mal) seizures?

A

T-type Ca2+ channels

21
Q

Which narrow spectrum drug is only used for absence seizures and only limits excitation (Ca2+ channels)?

A

Ethosuximide

22
Q

Which 3 AED’s are antagonists of T-type Ca2+ channels?

A
  1. Ethosuximide (narrow spectrum)
  2. Valproic acid (also GABA-T inhibitor and prolongs fast inactivation of Nav channels)
  3. Zonisamide (also prolongs fast inactivation of Nav channels)
23
Q

Which 2 AED’s act as both antagonists of T-type Ca2+ channels and prolong fast inactivation of Nav channels?

A
  1. Valproic acid (also GABA-T inhibition)
  2. Zonisamide
24
Q

Which AED blocks synaptic vesicle 2A protein on the presynaptic terminal of glutamate neuron?

A

Levetiracetam

25
Q

Which 2 AED’s block the α2δ1 Ca2+ channel on the presynaptic terminal of the glutamate neuron?

A

1) Gabapentin
2) Pregabalin

26
Q

The abrupt withdrawl of any antiepileptic medication may precipitate?

May lead to what type of behavior?

A
  • Precipitate status epilepticus
  • Suicidal behavior and ideation
27
Q

Which AED follows zero-order (saturable) pharmacokinetics?

A

Phenytoin

***if you give more than the body can handle, it just builds up. thus, it is easy to give too much

28
Q

Phenytoin is a well-known inducer of?

A

CYP-450 enzymes

*Frequent drug-drug interactions

29
Q

What are 2 toxicities associated with the AED, Phenytoin?

A
  1. Gingival hyperplasia
  2. Hypocalcemia/Vit. D deficit/Osteoporosis
30
Q

Osteopenia/Osteoporosis is a side effect associated with chronic administration of which 4 AED’s?

What do these drugs induce?

A
  1. Carbamazepine
  2. Phenytoin
  3. Phenobarbital
  4. Valproic acid

*These drugs induce CYP450-dependent vitamin D catabolism

31
Q

What are some of the issues associated with the AED, Carbamazepine (i.e., serum drug level, inducer of, toxicities)?

A
  • Serum drug level monitoring (4-12 mcg/mL) = narrow window
  • Inducer of CYP-450 enzymes
  • Induces auto-induction (self-metabolism)
  • Hematological toxicities: leukopenia/neutropenia/thrombocytopenia
32
Q

Which AED induces its own metabolism?

Also occurs to a lesser extent with what other AED drug?

What may occur because of this?

A
  • Carbamazepine induces own metabolism
  • Also, to lesser extent (25%), with lamotrigine

*This may lead to a potential loss of efficacy and recurrence of seizures

33
Q

Before administering which AED is a CBC required as this drug has potential side effects including leukopenia, neutropenia, and thrombocytopenia?

A

Carbamazepine

34
Q

What analogue of carbamazepine was formulated which has fewer CNS/hematological SE’s and is a less-potent CYP450 inducer?

A

Oxcarbazepine

35
Q

What are some of the issues associated with the AED, Phenobarbital?

A
  • Need serum drug level monitoring (10-40 mcg/mL)
  • Well known inducer of CYP-450 enzymes (frequent drug-drug interactions)
  • Toxicities: hypocalcemia/Vit. D deficit/Osteoporosis
36
Q

Which AED is only prescribe-able via REMS program; why?

A
  • Vigabatrin
  • May cause progressive, permanent, bilateral, concentric vision loss
37
Q

Which 4 AED’s are associated with hepatic CYP450 induction?

A
  1. Carbamazepine
  2. Phenytoin
  3. Phenobarbital
  4. Valproate
38
Q

What are 3 major AED-drug interactions associated with the CYP450 inducers?

A
  1. Increased clearance of oral contraceptives –> 2-4 fold rise in OHC failure rate; risk for unplanned pregnancy
  2. Increase clearance of warfarin –> less anticoagulation; elevated risk for arterial/venous thrombosis
  3. Increase clearance of HIV meds –> elevated risk for HIV replication
39
Q

Which 2 AED’s inhibit conjugation of drugs by UGT causing accumulation of parent drug (esp. each other when used together)?

A

Valproic acid and Lamotrigine

40
Q

Which 3 AED’s induce conjugation of drugs by UGT causing a reduction of parent drug (i.e., when given with valproic acid will decrease levels of valproic acid)?

A

1) Phenytoin
2) Carbamazepine
3) Phenobarbital

41
Q

What are some of the example causes of Status Epilepticus?

A
  • Abrupt withdrawl of AED’s, BZD’s, Opioid’s, Alcohol
  • Brain mass/trauma
  • Infection
  • Fever
42
Q

What is the initial therapy for convulsive status epilepticus (i.e., the first IV, alternative drug, and if no IV access)?

A

- In first IV:

  • Lorazepam

- Alternative

  • Diazepam

*Wait 1 minute for response then additional lorazepam PRN

43
Q

Which AED opens pre/post-synaptic K channels to prevent seizures?

A

Ezogabine

44
Q

What are the 3 MOAs of Valproic acid?

Topiramate?

A

Valproic acid = Na channel blocker, GABA-T inh, Ca t-type blocker

Topiramate = Na channel blocker, AMPA blocker, post-syn GABA promotor

45
Q

What drug may be beneficial for the treatment of Dravet and Lennox-Gastaut syndrome?

A

Cannabidiol

46
Q

What are 3 options for 2nd therapy for status epilepticus?

A
  • Fosphenytoin
  • Intubation
  • Continuous BP and CV monitor
  • Continuous midazolam OR propofol infusion

2. Neuro exam 2 (16 decks)

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