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Class: Neuro > Anti-Seizure > Flashcards

Anti-Seizure Flashcards

1
Q

What is the mechanism of action of PHENYTOIN and CARBAMAZEPAM?

A

Binds to Na+ voltage gated channels -> Prolongs its INACTIVATION (Prolonging refractory period) -> INHIBITS high frequency neuronal firing and reduces neuronal excitability -> DECREASES PRE-SYNAPTIC RELEASE OF GLU

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2
Q

What is the mechanism of action of ETHOSUXIMIDE? (used for generalized ABSENCE seizures)

A

T-Type Ca2+ Channel Blocker - Reduces Ca2+ Influx -> Reduces PACEMAKER CURRENT underlying thalamic waves and spikes seen in Generalized absence seizures

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3
Q

Name the 3 mechanisms of anti-seizure drugs

A

1) REDUCE Glu-mediated excitatory transmission
2) ENHANCE GABA-mediated inhibitory transmission (either presynaptic or post-synaptic)
3) MODIFY Ionic Conductance - PROMOTE inactivated state of voltage-gated Na+ (Delay refractory period and inhibit sustained, repetitive neuronal firing) and INHIBIT voltage-gated Ca2+

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4
Q

What are the proposed mechanisms of action of PHENOBARBITOL (used for myoclonic seizures and status epilepticus)? (2)

A
  1. Blocks Na+ and Ca2+ conductance -> Decreasing pre-synaptic release of Glu
  2. Binds to GABA(A)R -> Enhances the opening of the Cl- channel -> Hyperpolarization -> Decreases neuronal excitability
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5
Q

What is the shared mechanism of action of BENZODIAZAPENES + BARBITURATES?

A

Binds and ENHANCES the activity of GABA(A)R [Cl- channel] -> Increased frequency of opening Cl- channel = GREATER Cl- Influx = Hyperpolarization = Lower neuronal excitability

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8
Q

What specific drug is used ONLY for ABSENCE SEIZURES?

A

ETHOSUXIMIDE

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9
Q

Which representative/conventional drugs are used to treat PARTIAL SEIZURES (Both simple, complex)?

A

PHENYTOIN
CARBAMAZEPINE
VALPROATE

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10
Q

Which representative/conventional drugs are used to treat GENERALIZED TONIC-CLONIC (Grand mal) SEIZURES?

A 
PHENYTOIN
CARBAMAZEPINE
VALPROATE
PRIMIDONE
PHENOBARBITAL
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11
Q

Which representative/conventional drugs are used to treat GENERALIZED ABSENCE (PETIT MAL) SEIZURES?

A

ETHOSUXIMIDE
VALPROATE
CLONAZEPAM

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12
Q

Which representative/conventional drugs are used to treat GENERALIZED MYOCLONIC SEIZURES?

A

PHENOBARBITOL
VALPROATE
CLONAZEPAM

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13
Q

Which representative/conventional drugs are used to treat GENERALIZED STATUS EPILEPTICUS?

A

PHENOBARBITOL
DIAZEPAM
FOSPHENYTOIN

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14
Q

Which representative/conventional drugs are used to treat PARTIAL seizures that evolved into GENERALIZED tonic-clonic seizure?

A

PHENYTOIN
CARBAMAZEPINE
VALPROATE
PRIMIDONE

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18
Q

What is the toxicity of NEW DRUG- FELBAMATE? (2)

A
  1. Aplastic Anemia

2. Hepatic failure

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19
Q

What is the toxicity of NEW DRUG GABAPENTIN? (4)

A

1-3. Nystagmus + Dizziness + Ataxia

4. Sedation

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20
Q

Which two drugs can have a chronic toxicity of Stevens-Johnson Syndrome?

A

CARBAMAZEPINE

LAMOTRIGINE

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21
Q

What is the prodrug of phenytoin designed for PARENTERAL (IV, or IM) routes? (used for status epilepticus)

A

FOSPHENYTOIN - Phosphate group attached to the N of phenytoin

22
Q

What is the toxicity of NEW DRUG - LAMOTRIGINE? (5)

A

1-3. Nausea + Dizziness + Ataxia

  1. Rash
  2. Rare Stevens-Johnson Syndrome
23
Q

PHARMACOKINETICS: Of the 3, which two drugs are highly bound to plasma proteins?

A

PHENYTOIN

VALPROATE

24
Q

PHARMACOKINETICS: CARBAMAZEPINE

Describe absorption, distribution (peak levels), metabolism, and elimination.

A

ABSORPTION - Slowly but well absorbed orally
DISTRIBUTION - Reaches peak levels from 6-8hrs
METABOLISM - 10,11- epoxide is the active metabolite
ELIMINATION - half life is 8-12hrs in TREATED pts and 36hrs in NORMAL pts

25
Q

PHARMACOKINETIS: VALPROATE

Describe absorption, metabolism, and elimination

A

ABSORPTION: Well absorbed from several formulations
METABOLISM: Extensively metabolized by UGT enzymes and beta-oxidation
ELIMINATION: Half-life is 9-16hrs

26
Q

DRUG INTERACTIONS: PHENYTOIN (3)

A
  1. Induces MICROSOMAL Enz -> Induces greater metabolism of other drugs such as ORAL CONTRACEPTIVES
  2. Induces CYP3A4 -> Induces greater metabolism of other anti-seizures (CARBAMAZEPINE/ PHENOBARBITOL/ VALPROATE)
  3. Competes with VALPROATE for protein binding sites -> Inhibits PHENYTOIN metabolism -> INCREASE in free phenytoin
27
Q

DRUG INTERACTIONS: CARBAMAZEPINE (1)

A
  1. Induces CYPs and UGT -> Enhances metabolism of other drugs (e.g. ORAL CONTRACEPTIVES + other Anti-seizures such as VALPROATE/ PHENYTOIN/ PHENOBARBITOL)
28
Q

DRUG INTERACTIONS: VALPROATE (2)

A
  1. **INHIBITS PHENYTOIN / PHENOBARBITOL/ LAMOTRIGINE/ LORAZEPAM Metabolism - unlike phenytoin and carbamazepine
  2. Competes with Phenytoin for protein binding sites (albumin) -> Inhibits Phenytoin metabolism -> INCREASE in free phenytoin
29
Q

PHARMACOKINETICS: PHENYTOIN

Describe absorption, metabolism, and elimination.

A

ABSORPTION - Formulation dependent
METABOLISM - No active metabolites
ELIMINATION - Dose-dependent (half-life = 12-36hrs)

35
Q

What is the toxicity of CARBAMAZEPINE?
(1-7. Mentioned in Class
8-12. Chronic Effects - Table)

A

1-4. Nausea + Diplopia + Dizziness + Ataxia
5-7. Headache + Hyponatremia + Rash
8-12. CHRONIC EFFECTS: Cognitive Dysfunction + Drowsiness + Rare occurrence of severe blood dyscrasis + Stevens-Johnson Syndrome (Han Chinese) + Potential Teratogenicity

36
Q

What is the toxicity of VALPROIC ACID?
(1-6. - pointed out in class)
(7-10. - in 2 tables)

A

1-6. Nausea (Transient)+ Anorexia (Transient) + Weight gain (Chronic) + Tremor + Acute Pancreatitis + Hyperammonia
7-10. Drowsiness + Hair loss + Teratogenicity (neural tube defects) + Hepatotoxicity (infants)/Inhibition of Hepatic Drug Metabolism

37
Q

What is the toxicity of PHENYTOIN?
(1-6. General Toxicity
7-11. Chronic Toxicity)

A

1-6. Nystagmus + Diplopia + Ataxia + Gingival Hyperplasia + Hirsutism + Neuropathy
7-11. COARSENING of facial features + OSTEOMALACIA (VitD metabolism abnormalities) + Peripheral neuropathy (hyporeflexia) + Induction of Hepatic Drug Metabolism + Sedation

Class: Neuro (10 decks)

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