Sweatman Antiepileptics Flashcards

1
Q

AED’s and pregnancy

A

teratogenic

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

name the types of partial seizures

aka focal seizures

A

simple partial

complex partial

partial seocndary to generalized

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

name the types of general seizures

A

grand mal-generalized tonic-clonic

absence-petit mal

tonic

myoclonic

clonic

atonic

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

initially a seizure begins with

A

depolarization of neurons through calcium channels and sodium channels

this insult carried forward through GABA and K mediated actions

meanwhile local supression is inhibited-abnormal neuronal activity is spread

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

two main pathophys processes of seizure activity at the membrane level

A

HIGH FREQUENCY BURSTS OF AP’S

  • -> CA2+ ENTRY-DEPOL
  • -> NA CHANNELS ACTIVATED -REPEITIVE AP’S GENERATED

HYPERSYNCHRONIZATIONS
-HYPERPOL AFTER POTENTIAL VIA GABA AND K RECEPTORS

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

3 MAIN MOA’S FOR AED

A
  1. PROMOTE THE INACTIVATED STATE OF VOLTAGE GATED NA CHANNELS, LIMITS SUSTAINED REPETITIVE FIRING OF NEURONS
  2. ENHANCEMENT OF GABA-INCREASED PRE AND POST SYNAPTIC INHIBITION
  3. INHIBITS VOLTAGE GATED CA2+CHANNELS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

CA2+ channels involved/blocked in AED’s treatment of ABSENCE SEIZURES

A

t type calcium channels

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

these drugs prolong the inactivation of Na channels, thereby reducing the ability to fire at high frequencies (prolong the absolute refractory period)

A
carbamazepine-tegretol
phenytoin/fosphenytoin
topiramate (topomax)
Lamotrigine
valproate
zonisamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

chloride gated channels respond to….signalling

A

GABA
*THEY ARE STIMULATED BY GABA, HYPERPOLARIZE THE CELL MEMBRANE AND BRING THE THRESHOLD DOWN WHEN A NEGATIVELY CHARGED ION ENTERS THE CELL

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

GABA ENHANCING AED drugs at the postsynaptic membrane

A

Benzos and Barbiturates

bind separately at sites in the mutlimeric ion channel to mudlate the activity of ENDOGENOUS GABA–lower membrane potential-IPSP

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

GABA ENHANCING DRUGS THAT WORK AT THE PRESYNAPTIC MEMBRANE AND THEIR MOA

A

Vigabatrin
Valproic acid
tiagabine
gabapentin?

enhance quantal yield of GABA release per neuron firing

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

type of EEG characterstic seen in absence seizures

A

3hz spike and wave rythm

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

type of Ca channel involved in generalized absence seizures

A

t type calcium channel

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

TYPES OF DRUGS THAT OVERALL DIMINISH THE EFFECTS OF GLUTAMATE

A

CALCIUM CHANNEL BLOCKERS AN SODIUM CHANNEL BLOCKERS

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

MOA accomplishes reduction in pacemaker current that underlise thalamic rhythm in spikes and waves in GASeizures

A

those that reduce flow of Ca2+ thru calcium channels

Valproate
ethosuximide

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

when administering anticonvulsants-what should you be worried about

A

suicidal ideation-2 fold increase

  • monitor for depression
  • monitor for behavioral changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when one anticonvulsant fails, what is the next course of action

A

replacement rather than additive

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

carbamazepine MOA

A

dec sodium channel conductance

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

Clonazepam MOA

A

gaba allosteric agonist

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

ethosuximide MOA

A

inhibition of T type calcium channels

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

felbamate MOA

A

decrease NMDA signalling of glutamate

increase GABA presence at the synapse

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

Lacosamide MOA

A

decrease Na channel activity

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

Lamotrigene MOA

A

sodium channel inhibition

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

levetiracetam MOA

A

unknown

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

Oxcarbazepine MOA

A

decrease NA channel activity, possibl increase K channel activity, decrease Ca2+ effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

phenytoin MOA

A

Na channel blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

pregabalin/gabapentin

A

inhibit alpha 2 delta 1 subunit of Ca2+ channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

topiramate MOA

A

inhibit NA channels, increase K current, enhance GABA, inhibit GLutamate activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Valproate MOA

A

enhance GABA release/activity, decrease NA channel activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

zonisamide MOA

A

dec Na channel activity, decrease T type calcoum channel acitvity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

works on Na K and CA

A

oxcarbezepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

limited protein binding in serum except for

A

phenytoin

valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

accumulates in RBC’s

A

zonisamide

34
Q

displacement causes significant acute drug toxicity

A

VALPROATE

PHENYTOIN

35
Q

very important ADME clinical issue with AED’s

A

hepatic processing by CYPS of UGT’s

36
Q

one example of a AED drug that induces its own metabolism-as tratmen progresses , half life decreases due to increased rate of hepatic metabolism

A

Carbemazepine-Na channel blocker

37
Q

ultimate elimination of AED’s

A

urine

thus in renal dysfunction, drug accumulation can occur over time

38
Q

AED not metabolism

A

Gabapentin
pregabalin

also topiramate is very minorly

39
Q

not metabolized by CYPS

A

gabapentin, pregabalin

lamotrigine

levetiracetam

tpoiramate

40
Q

comes out in stoool

A

phenytoin

41
Q

no induction, no inhibition

A
clonazepam
ethosuximide
gabapentin
pregabalin
levetiracetam
topiramate
zonisamide
42
Q

capable of inducing its own metabolism via CYPS or UGT’s thus the half life lessens with continued administration

A

Carbemazepine-induces CYPS and UGT
Felbamate-induces cyps
Lamotrigine
phenytoin

43
Q

metabolized through conjugation

A

oxcarbazepine

44
Q

can prolong perseistence in the plasma by inhibiting the CYP that breaks it down, thus increasing half life potentially with long term dosing

A

Lacosamide

Valproate

45
Q

routine monitoring of these drugs is required due to their own abilit to alter their own persistence in the plasma

A
carbamzepine
ethosuximide
gabapenting
phenytoin
valoproate
46
Q

cause renal stones

A

Topiramate and zonisamide

47
Q

carbonic anhydrase ibhibitords

A

topiramate

zonisamide

48
Q

cause loss of bicarbonate from renal

A

topiramate

zonisamide

49
Q

requires periodic monitoring of blood gases (HCO3)

A

topiramate

zonisamid

50
Q

ABRUPT DISCONTINUATION OF AED CAN PRECIPITATE

THUS TAPER GRADUALLY

A

STATUS EPILEPTICUS
ICREASED SEIZURE FREQUENCY
ANXIETY

51
Q

ZERO ORDER KINETICS MEANS

A

HALF LIFE VARIES WITH DRUG DOSE

52
Q

ZERO ORDER KINETIC AED

A

PHENYTOIN

53
Q

CNS EFFECTS OF PHENYTOIN

A

NYSTAGMUS
HA
ATAXIA
DROWSINESS

54
Q

WEIRD SIDE EFFECT OF PHENYTOIN

A

GINGIVAL HYPERPLASIA

55
Q

DERM SIDE EFECTS OF PHENYTOIN

A
SJS
TEN
DRESS
HYPERTRICHOSIS
HIRSUTISM
56
Q

HEME CHANGES WITH PHENYTOIN

A

UNCOMMON BUT MAY OCCURE

57
Q

HYPERTRICHOSIS SHOULD BE ONLY ASSOCIATED WITH

A

PHENYTOIN

58
Q

HEMATOLOGIC CHANGES IN CARBEMAZEPINE

A

AGRANULOCYTOSIS

OR APLASTIC ANEMIA

ALSO CAUSES XEROSTOMIA
NV, ATAXIA, DIZZINESS

59
Q

UNIQUE TO CARBEMAZEPINE

A

BUT THE MAIN ONE TO REMEMBER IS APLASTIC ANEMIA

60
Q

certain HLA b1502 genotypes (asians mostly) should avoid which AED’s

A

carbamazepine
phenytoin
fopshenytoin
lamotrigine

61
Q

valproic acid side effects

A

CNS effects related to infusion rate

thrombocytopenia

prolonged INR

SJS, DRESS, TEN

NAusea, Diarrhea

hepatotoxicity

62
Q

BBW for felbamate

A

aplastic anemia
bone marrow suppression
hepatic disease

63
Q

B for Lamotrigine

A

TEN or SJS

64
Q

valproic acid preg category

A

X

65
Q

Carbemazepine and phenytoin category

A

D

66
Q

Lamotrigine category

A

C

67
Q

PARTIAL SEIZURE , INCULDING SECONDARY GENERALIZED SEIZURE DOC’S

A

Lamo
Carba
Leve
Oxc

68
Q

DOC for primary generalized tonic clonic seizures

A

Valproate
Lamo
Levet

69
Q

DOC for absence seizures

A

Ethosixumide

Valproate

70
Q

atypical absence seizures

A

Valproate
LAMO
Levat

71
Q

Status epilepticus brought on by

A

changes in AED’s-mostly in young folks

in the older cohort-mostly due to stroke

72
Q

TX guidelines of SE

A

IV benzo (lorazepam, midal, diaze)

IV AED
valproate or (pheny, midazolam continuout, leve,pheno)
73
Q

prolong the openinh of the CL channel after exposure to endogenous GABA

A

barbiturates

74
Q

shift dose-response curve to the left making the effect of GABA more pronounced

A

benzo’s

75
Q

only which GABA enhancer will induce CYPS

A

barbiturates-phenobarbital

76
Q

advantage of benzos and barbs tover phenytoin and valproate

A

can be given by rapid IV administration

77
Q

SJS not reported with

A

CLonazepam

Lacosamide

78
Q

which AED;s have blood toxicity

A

Carbamazepine
felbamate
valproate

79
Q

which ones are teratogens

A

Lamo
carba
phenytoin
valproate

80
Q

first drug for status epilepticus

A

IV lorazepam

81
Q

lorazepam AKA

A

ativan