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Neuro 2 Exam 2 > Anticonvulsant drugs > Flashcards

Anticonvulsant drugs Flashcards

1
Q

Barbiturate drugs

A

Phenobarbital

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2
Q

Benzodiazepine drugs

A

lorazepam

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3
Q

Seizure

A

episode of neurologic dysfunction (abnormal neuronal firing) manifest by changes in motor control, sensory perception, behavior, and/or autonomic dysfunction

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4
Q

Epilepsy

A

recurrent spontaneous seizures arising from aberrant electrical activity in the brain

Occurrence of unprovoked seizures separated by 24 hours

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5
Q

Seizure types

A

Focal- seizure activity starts in one area of the brain

Generalised- seizure activity involves both hemispheres of the brain (absence, tonic clonic, myoclonic, clonic, tonic, atonic)

and Unknown (epileptic spasm, others)

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6
Q

Focal (Partial) Seizures

A

Aware (simple partial)
Impaired awareness (complex partial)
Secondarily generalized

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7
Q

Generalized

A

Tonic-clonic (grand mal)
Absence (petit mal)
Myoclonic
Atonic

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8
Q

Pathophysiology: Excessive excitation or disordered inhibition:

A

Small number of neurons fire abnormally
Membrane conductance and inhibitory currents break down
Excess excitability spreads
Locally (focal) or more widely (generalized)

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9
Q

Pathophysiology: Multiple mechanisms:

A

Altered ion channels
Receptor modification
Alteration in 2nd messaging
Changes in extracellular ion concentrations
Abnormal neurotransmitter uptake & metabolism
Shift in ratio/function of inhibitory circuits

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10
Q

Antiepileptic Drug (AED) Mechanisms of Action

A

Limit sustained, repetitive firing of neurons, mediated by promoting the inactivated state of voltage-gated Na+ channels

Enhanced γ-aminobutyric acid (GABA) mediated synaptic inhibition, mediated by presynaptic or postsynaptic actions

Inhibition of voltage-gated Ca2+ channels

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11
Q

drugs that enhance Na+ channel inactivation

A

carbamazepine, phenytoin, topiramate

lamotrigine, valproate, zonisamide

(anti-focal seizures)

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12
Q

drugs that enhance GABA synaptic transmission

A

vigabatrin, valproate, tiagabine (pre-synaptic)

benzodiazepines, barbiturates (post-synaptic)

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13
Q

drugs thatt reduce Ca2+ channel current

A

valproate, ethosuximide

anti-absence drugs

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14
Q

Basic Pharmacology of AEDs- Pharmacokinetics:

A

Absorption 80-100%

Most not highly protein bound
- Exception: phenytoin, tiagabine, valproic acid

Hepatic metabolism

Slow plasma clearance

Some have long t1/2 > 12 hours

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15
Q

Common Adverse Drug Reactions

A 
Neurotoxic Effects:
Sedation
Dizziness
Blurred or double vision
Difficulty concentrating
Ataxia
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16
Q

Phenytoin MOA, PK, uses, ADRs

A

MOA: * prolongs inactivated state of Na+ channel
– Decreases synaptic release of glutamate and enhances release of GABA

PK: * highly protein bound

  • Dose-dependent elimination
  • CYP2C9 and CYP2C19 metabolism
  • Fosphenytoin (phosphate ester prodrug)

Focal seizures, generalized tonic-clonic

Unique ADRs: * gingival hyperplasia, hirsutism
– Cardiac effects: hypotension, bradycardia, arrhythmia

17
Q

Carbamazepine

A

MOA: * prolongs inactivated state of Na+ channel
– Decrease presynaptic release of glutamate

PK: * potent CYP inducer
– Autoinduction t1/2 36 hours –> 8-12 hours after cont. therapy

Focal seizures, generalized tonic-clonic, trigeminal neuralgia, mania in bipolar disorder

Unique ADRs: * hyponatremia, blood dyscrasias (agranulocytosis), * leukopenia, SJS (Asian descent esp.)

18
Q

Lamotrigine

A

MOA: * prolongs inactivated state of Na+ channel
– Also inhibits voltage-gated Ca2+ channels

Focal seizures, generalized tonic-clonic, bipolar disorder

Unique ADRs: *skin rash

19
Q

Valproic Acid

A

MOA: * prolongs inactivated state of Na+ channel, may block NMDA receptor mediated excitation, may increase levels of GABA

PK: * highly protein bound

Absence seizures, myoclonic seizures, generalized tonic-clonic, focal seizures, status epilepticus, bipolar disorder, migraine prophylaxis

Unique ADRs: GI distress, * fine tremor, weight gain, hair loss
– Hepatotoxicity, thrombocytopenia

20
Q

Topiramate

A

MOA: actions on * Na+ channels, * GABAA receptors, high-voltage * Ca2+ currents, may act on *glutamate/NMDA receptors

Focal, generalized tonic-clonic, Lennox-Gastaut, infantile spasms, absence seizures, migraine

Unique ADRs: *paresthesias, nervousness, *weight loss

21
Q

Benzodiazepines and Barbiturates

A

Diazepam:
MOA: enhance * GABA-mediated Cl- influx and enhance the generation of inhibitory membrane potentials
PK: * extremely lipophilic
Status epilepticus, myoclonic, focal, generalized tonic-clonic seizures

Phenobarbital
MOA: * enhances GABA mediated current and can also decrease excitatory responses (glutamate release)
PK: * hepatic enzyme inducer
Focal seizures, generalized tonic-clonic

22
Q

Gabapentin

A

MOA: bind α2δ subunit of voltage-gated N-type Ca2+ channels, *decrease Ca2+ entry, decrease synaptic release of glutamate

PK: * not metabolized

Focal seizures, generalized tonic-clonic, neuropathic pain, post-herpetic neuralgia

Unique ADRs: headache, tremor

23
Q

Levetiracetam

A

MOA: binds * synaptic vesicular protein SV2A. Modifies synaptic release of glutamate and GABA.

Focal seizures, generalized tonic-clonic, myoclonic seizures

Unique ADRs: * serious mood and behavioral changes (less common)

24
Q

Ethosuximide

A

MOA: reduces low threshold * Ca2+ (T-type) current
PK: long t1/2 40 hours
* Absence seizures
Unique ADRs: * gastric distress

25
Q

General Treatment Approach

A

AEDs suppress seizures but do not cure
Accurate seizure diagnosis essential
Monotherapy preferred (50-70% can be maintained on single agent)
Increase dose gradually
Monitor treatment regularly
If further dose increase inadvisable, consider prescribing another drug as monotherapy
Compliance is essential

26
Q

Focal seizures

drugs of choice

A

Carbamazepine –or– lamotrigine –or– levetiracetam –or– oxcarbazepine –or– valproate

27
Q

Primary generalized tonic-clonic

drugs of choice

A

Carbamazepine –or– lamotrigine –or– oxcarbazepine –or– valproate

28
Q

drugs of choice Absence

A

Ethosuximide –or– lamotrigine –or– valproate

29
Q

drugs of choice Atypical absence, myoclonic, atonic

A

Levetiracetam –or– lamotrigine –or– valproate

30
Q

AED Drug Interactions

A

Phenytoin

  • Protein binding (sulfonamides)
  • Metabolism
  • —– Competes for metabolism CYP2C9 (warfarin) & 2C19
  • —– Also results in enzyme induction (oral contraceptives)

Carbamazepine
- Enzyme induction (phenytoin, oral contraceptives)

Valproic acid
- Enzyme inhibition (carbamazepine)

Lamotrigine
- Oral contraceptives may decrease lamotrigine concentrations

31
Q

AEDs and Pregnancy

A

Interactions with oral contraceptives
- Effectiveness of OCs reduced (likely due to induction of CYP3A4) by : carbamazepine, oxcarbazepine, phenobarbital, phenytoin, primidone, rufinamide

Potential teratogenic effects
- Increased risk of congenital malformations: phenytoin, valproate, topiramate

32
Q

Treatment of Status Epilepticus

A

A medical emergency – continuous seizures lasting at least 5 minutes or ≥ 2 seizures with incomplete recovery of consciousness, mortality 20%. Goal is rapid termination of behavioral and electrical seizure activity.

Steps: assessment –> initial therapy –> long-term control

IV benzodiazepines – enhance GABAA Cl- flux

  • Lorazepam (Ativan) longer duration of action than diazepam
  • Diazepam (Valium)

IV phenytoin or fosphenytoin – enhances inactivated state of voltage-dependent Na+ channels.

IV phenobarbital – enhances GABAA Cl- flux

Anesthesia

33
Q

A 25 y/o male is referred to a neurologist after experiencing a motor vehicle accident in which there were no injuries. He has always had episodes of “zoning out”; but unfortunately, his most recent episode occurred while driving home from work. His neurologist will most likely recommend an agent with which mechanism of action to treat these episodes?

A. Binds an allosteric site on GABA receptor
B. Blocks voltage-gated Na+ channels
C. Enhances GABA-mediated Cl- influx
D. Modifies release of glutamate and GABA through action on SV2A protein
E. Reduces the low threshold Ca2+ (T-type) current

A

These are absence seizures.

Reduces the low threshold Ca2+ (T-type) current

34
Q

A 16 y/o female with complex partial seizures is instructed to begin taking lamotrigine. Her neurologist recommends initiating low doses with dose increases every two weeks. It is important to titrate lamotrigine slowly, as it may cause dose-related:

A. gingival hyperplasia.
B. leukopenia.
C. paresthesias.
D. skin rash.
E. tremor.
A

D. skin rash.

35
Q

A 15 y/o male with juvenile myoclonic epilepsy presents to his neurologist for follow-up. He has been receiving appropriate drug therapy, but is concerned about recent hair loss. Which drug is this patient most likely receiving?

A. Gabapentin
B. Lamotrigine
C. Levetiracetam
D. Phenytoin
E. Valproic acid
A

Valproic acid

36
Q

A 60 y/o female has a history of complex partial seizures and a mechanical valve replacement. She has been receiving carbamazepine and warfarin (INR therapeutic) concomitantly for several years. She recently began experiencing an increased incidence of seizures; therefore, during a non-related hospital stay, her carbamazepine is switched to levetiracetam. 12 days later, she presents to the ED with an uncontrolled bloody nose, ecchymosis across her back and legs, and an INR = 10.4. What is the best explanation as to the cause of this drug-drug interaction?

A. CYP450 inducer added; increased warfarin metabolism
B. CYP450 inducer removed; decreased warfarin metabolism
C. CYP450 inhibitor added; decreased warfarin metabolism
D. CYP450 inhibitor removed; increased warfarin metabolism

A

CYP450 inducer removed; decreased warfarin metabolism

37
Q

A 28 y/o female with a history of complex partial seizures presents to her PCP for follow-up. Her only medication is carbamazepine which she began six months ago; she has since been seizure free. At this routine visit, her provider discovers she is six weeks pregnant. What is the best strategy for antiepileptic drug therapy in this patient?

A. Continue carbamazepine
B. Continue carbamazepine and add diazepam
C. Convert carbamazepine to valproic acid
D. Immediately discontinue carbamazepine
E. Immediately discontinue carbamazepine and begin folic acid

A

Continue carbamazepine

Neuro 2 Exam 2 (19 decks)

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