Brainscape's Knowledge GenomeTM

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


See full index

Pharm II Exam 3 > Antiepileptics > Flashcards

Antiepileptics Flashcards

1
Q

initiation of seizures involves 2 things

A

1) high frequency bursts of APs

2) hypersynchronization

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

3 mechanisms for the recruitment of surrounding neurons

A

1) more extracellular K depolarizes neighbors
2) Ca2+ accumulates in presynaptic neurons–> more NT release
3) activation of NMDA glutamate receptors –> Ca2+ influx

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

4 AED mechanisms

A

1) inactivate Na and Ca channels
2) target glutamate receptors
3) target GABA receptors
4) multiple mechanisms

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

Simple partial seizure

A
  • no impairment of consciousness

- usually confined to a limb or muscle group

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

Complex partial seizure

A
  • consciousness impaired

- brain origin is localized

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

Partial seizures secondarily generalized

A

partial seizure–> generalized tonic clonic seizure

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

Generalized tonic clonic seizure

A
  • tonic rigidity, followed by tremor

- massive jerking of the body

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

Absence seizure (petit mal)

A
  • 10-45 seconds
  • altered consciousness
  • childhood, assoc with mental retardation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Myoclonic

A

-isolated rhythmic clonic jerks

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

Atonic

A

sudden loss of posture–> collapse

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

infantile spasms

A
  • bilateral attacks of myoclonic jerks

- <1 yo, assoc with mental retardation

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

Glutamate receptors

A
  • EXCITATORY
  • found in all neurons
  • blocked by Mg2+ (or glycine, rarely)

types: NMDA, AMPA, KA

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

GABA receptors

A
  • INHIBITORY
  • only in neurons with glutamate decarboxylase

types: GABA-a, GABA-b

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

Barbituates vs. Benzos at GABA-a receptors

A

Barbituates: increase duration of Cl- channel opening

Benzos: increase frequency of Cl- channel opening

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

Phenytoin (diphenylhydantoin) MOA

A
  • blocks firing by inactivating Na+ channels

- reduces NT release

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

Phenytoin pharmacokinetics

A
  • Time to peak varies from pt to pt*
  • Gingival hyperplasia and hirsutism*
  • shifts from 1st order to zero-order kinetics
  • hard to predict serum conc–> need to monitor levels
17
Q

Carbamazepine (a TCA) MOA

A
  • blocks firing by inactivating Na+ channels
  • reduces NT release
  • potentiates GABA
18
Q

Carbamazepine pharmacokinetics

A
  • active metabolite
  • Toxicities: aplastic anemia, rash common
  • CNS effects: ataxia, diplopia, nystagmus, dizziness
  • some tolerance to SEs
  • many DDIs
19
Q

Primidone MOA

A
  • blocks firing by inactivating Na+ channels

- Phenobarbital is a metabolite–> enhances GABA

20
Q

Primidone pharmacokinetics

A
  • slow but complete absorption
  • not highly prot bound
  • induces hepatic enzymes
  • toxicities: nystagmus, ataxia
21
Q

Adjuvant therapies for partial seizures

A

Gabapentin
Lamotrigine
Vigabatrin

22
Q

Gabapentin MOA

A
  • does NOT interact with GABA-a (designed to though)
  • binds voltage-gated Ca2+ channels–> decreases glutamate release
  • inhibits GABA transaminase
23
Q

Gabapentin pharmacokinetics

A

-not prot bound or metabolized–> very few drug interactions**

24
Q

Lamotrigine MOA

A

-blocks firing by inactivating Na+ channels

  • lots of DDIs
  • rash common in children
25
Q

Vigabatrin

A
  • inhibits GABA-T

- rare SE: psychosis

26
Q

Topiramate

A
  • blocks firing by inactivating Na+ channels
  • inhibits KA and/or AMPA receptors
  • enhances GABA

-antimigraine and antiseizure

27
Q

Valproate MOA

A
  • blocks firing by inactivating Na+ channels
  • inhibits T-type Ca2+ channels (involved in ABSENCE seizures)
  • inhibits breakdown of GABA
28
Q

Valproate pharmacokinetics

A
  • well absorbed, 90% prot bound
  • little sedation
  • Hepatotoxicity– can be severe*
29
Q

Ethosuxamide

A
  • inhibits T-type Ca2+ channels
  • not prot bound
  • halflife=40 min
  • tox: gastric distress, but considered safe!
30
Q

Benzodiazepines

A
  • increases affinity of GABA for the GABA-a receptor
  • **sedative
  • tolerance leads to withdrawal–> limits usefulness in txting epilepsy LT

-good for status epilepticus

31
Q

Simple or complex partial seizure drugs

A

Conventional: carbamazepine, phenytoin

Adjuvent: gabapentin, lamotrigine

32
Q

Generalized tonic-clonic drugs

A

Conventional: carbamazepine, phenytoin, valproic acid*

Adjuvent: gabapentin, lamotrigine

33
Q

Absence seizure drugs

A

Ethosuximide, valproic acid

Adjuvent: lamotrigine

34
Q

Myoclonic seizure drugs

A

Valproic acid, clonazepam*

35
Q

Status epilepticus

A

Lorazepam or diazepam, henytoin, phenobarbitol, benzodiazepine

Pharm II Exam 3 (1 decks)

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