Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology - Exam 2 > anti-epileptics > Flashcards

anti-epileptics Flashcards

1
Q

mechanisms of anti-epileptics (5)

A

inactivate Na channels

inactivate Ca channels

reduce synaptic vesicle fusion

modulate glutamate receptors

modulate gaba receptors

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

pathophysiology of epilepsy

A

too much excitation or too little inhibition

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

are there increased or decreased levels of glutamate during seizures

A

increased

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

what is the ionotropic receptor type for GABA?

A

GABAA

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

what is the metabotropic receptor type for GABA

A

GABAB

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

targets of anti-epileptic drugs

A

glutamate- decrease activity at receptors

increase activity of GABA at receptors

Increase release of GABA

Inhibit breakdown of GABA

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

first line for treating status epilepticus

A

benzodiazepines: diazepam (valium), lorazepam (ativan)

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

first line of drug for absence seizures

A

ethosuximide

valproic acid

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

mechanism of benzodiazepines

A

increase affinity of GABA for the GABAA receptor

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

where are benzodiazepines metabolized

A

liver

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

side effects of benzodiazepines

A

sedative

withdrawal symptoms due to tolerance

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

mechanism of vigabatrin

A

inhibit GABA-T to reduce GABA breakdown

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

indication for vigabatrin (sabril)

A

complex partial seizures that are refractory to several others AEDs

infantile spasms

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

drug interaction of vigabatrin

A

reduces plasma concentration of primidone

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

side effects of vigabatrin

A

concentric visual field deficit (can be irreversible)

drowsiness

dizzinesss

weight gain

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

what is carbamazepine indicated for

A

focal seizures and GTCSs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

mechanism of carbamazepine

A

block tetanic firing

increases Na channel inactivation, reduces transmitter release

potentiates GABA response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is carbamazepine used for other than seizures

A

bipolar disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

carbamazepine toxicities

A

ataxia, diplopia, nystagmus, dizziness

tolerance to side effects

aplastic anemia

rash- Stevens Johnson Syndrome, Toxic Epidermal Necrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what drugs should never be used with carbamazepine

A

drugs that inhibit hepatic metabolism- increases toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

mechanism of phenytoin (dilantin)

A

blocks tetanic firing

increases Na channel inactivation

releases neurotransmitter release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

indication for phenytoin

A

focal seizures and GTCSs

status epilepticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

notable phamacokinetic aspect of phenytoin

A

oral absorption peak time variable from patient to patient, difficult to get dosing within therapeutic range

functions at 1st order kinetic at low doses and zero order kinetics at high doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

side effects of phenytoin

A

cardiac arrhythmias

dizziness

nystagmus

headaches

rash

gingival hyperplasia and hirsutism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

mechanism of primidone (mysoline)

A

similiar to phenytoin- increase Na channel inactivation

notable mention- phenobarbital is a metabolite (enhances GABAA receptor activity) but this is not thought to be part of the mechanism of action

26
Q

what disorder is treated with primidone

A

focal dyscognitive seizures (not used much now in favor of carbamazepine and phenytoin)

27
Q

primidone pharmacokinetics

A

slow, complete absorption

half life 8-12 hours

induces hepatic enzymes

28
Q

primidone toxicities

A

drowsiness

nystagmus and ataxia only at excessive doses

29
Q

in what diagnoses would you prescribe topiramate

A

partial seizures and GTCSs

anti-migraine/migraine prophylaxis

30
Q

mechanism of action of topiramate

A

increase Na channel inactivation

inhibits kainate/AMPA receptors

Enhances GABA

31
Q

side effects of topiramate (topamax)

A

somnolence

fatigue

weight loss

nervousness

congnitive impairment

32
Q

indication for use of lamotrigine (lamictal)

A

partial seizures

GTCSs

33
Q

mechanism of action of lamotrigine

A

increase Na channel inactivation

inhibit release of amino acids by acting on voltage gated Ca channels

(decrease Na and decrease Ca)

34
Q

side effects of lamotrigine

A

rash- usually only in children

35
Q

indication for zonisamide

A

broad spectrum

absence, myoclonic, infantile spasms

36
Q

mechanism of zonisamide

A

Na channel (decrease Na)

acts on T-type voltage gated Ca channels (decrease Ca)

37
Q

side effects of zonisamide

A

drowsiness, cognitive impairment, skin rashes

no interaction with other AEDs

38
Q

indication for gabapentin

A

adjunct therapy: focal seizures

chronic pain management

39
Q

mechanism of gabapentin

A

decreases Ca- binds to voltage gated Ca channels, decreases glutamate release

(does not interact with GABAA as designed)

(inhibits GABA-T but not at physiologic concentrations)

40
Q

drug interaction of gabapentin

A

very few!

cimetidine and aluminum/magnesium antacids

41
Q

which drugs are the most effective anti-epileptics (think mechanism of action)

A

drugs that block transmitter release

(drugs that affect Ca channels, Na channels, or vesicle fusion blocking)

42
Q

indication for levetiracetam

A

partial seizures and GTCSs

43
Q

mechanism of action of levetiracetam (keppra)

A

targets synaptic vesicle protein 2A (SV2A) protein ligand

inhibit calcium dependednt amino acid transmitters by interfering with vesicle fusion

44
Q

side effects of levetriacetam

A

dizziness

somnolence

weakness

dermatologic conditions

behavioral changes in psych patients

45
Q

drugs that enhance GABA transmission

A

vigabatrin

benzodiazepines

barbiturates

46
Q

drugs that cause Na channel inactivation (6)

A

phenytoin

carbamazepine

lamotrigine

primidone

topiramate

zonisamide

47
Q

what type of drugs should you choose for absence seizures

A

ones that affect Ca channels

they are associated with T-type Ca channels

48
Q

Drugs that affect T-type Ca channels

A

valproate

ethosuximide

49
Q

indication for ethosuximide

A

absence seizures and myoclonic seizures

50
Q

mechanism of ethosuximide

A

inhibits T-type Ca channel activity in thalamic neurons

51
Q

pharmacokinetics of ethosuximide (zarontin)

A

not protein bound

metabolized by microsomal enzymes

52
Q

side effects of ethosuximide

A

gastric distress- pain, nausea, vomiting

53
Q

indication of valproic acid (depakote)

A

absence, generalized, and complex partial seizures

54
Q

mechanism of valproic acid

A

decrease Na and Ca

increase GABA

similar to phenytoin- blocks tetanic firing by increasing Na inactivation, reduce transmitter release

reduce T-type Ca channel activity

inhibits breakdown of GABA

55
Q

pharmacokinetics of valproic acid

A

90% protein bound

well absorbed

half life 9-18 hours

56
Q

side effects of valproic acid

A

nausea, vomiting, GI distress

sedation

hepatotoxicity

57
Q

what should you give during pregnancy

A

lowest effective dose of a monotherapy

drug withdrawal dangerous for fetus

58
Q

what drugs should you consider in simple/complex PARTIAL seizures?

A

conventional: carbamazepine or phenytoin

recently developed: gabapentin, topiramate, lamotrigine, levetiracetam

59
Q

drugs to consider for generalized tonic-clonic

A

conventional agents: carbamzepine, phenytoin and valproic acid

recently developed: gabapentin, topiramate, lamotrigine, lacosamide

60
Q

what drugs to consider for absence seizures

A

conventional agents- ethosuximide and valproic acid

recently developed- lamotrigine

61
Q

what drugs to consider for myoclonic seizures

A

conventional: valproic acid or clonazepam

recently developed: levetiracetam

62
Q

what drugs to consider for status epilepticus

A

lorazepam, diazepam, fosphenytoin, phenytoin, or phenobarbital

Pharmacology - Exam 2 (14 decks)

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