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Sweatman Antiepileptics Flashcards

1
Q

AED’s and pregnancy

A

teratogenic

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2
Q

name the types of partial seizures

aka focal seizures

A

simple partial

complex partial

partial seocndary to generalized

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3
Q

name the types of general seizures

A

grand mal-generalized tonic-clonic

absence-petit mal

tonic

myoclonic

clonic

atonic

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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

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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

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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
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7
Q

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

A

t type calcium channels

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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
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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

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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

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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

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12
Q

type of EEG characterstic seen in absence seizures

A

3hz spike and wave rythm

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13
Q

type of Ca channel involved in generalized absence seizures

A

t type calcium channel

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14
Q

TYPES OF DRUGS THAT OVERALL DIMINISH THE EFFECTS OF GLUTAMATE

A

CALCIUM CHANNEL BLOCKERS AN SODIUM CHANNEL BLOCKERS

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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

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16
Q

when administering anticonvulsants-what should you be worried about

A

suicidal ideation-2 fold increase

  • monitor for depression
  • monitor for behavioral changes
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17
Q

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

A

replacement rather than additive

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18
Q

carbamazepine MOA

A

dec sodium channel conductance

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19
Q

Clonazepam MOA

A

gaba allosteric agonist

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20
Q

ethosuximide MOA

A

inhibition of T type calcium channels

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21
Q

felbamate MOA

A

decrease NMDA signalling of glutamate

increase GABA presence at the synapse

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22
Q

Lacosamide MOA

A

decrease Na channel activity

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23
Q

Lamotrigene MOA

A

sodium channel inhibition

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24
Q

levetiracetam MOA

A

unknown

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25
Oxcarbazepine MOA
decrease NA channel activity, possibl increase K channel activity, decrease Ca2+ effects
26
phenytoin MOA
Na channel blockade
27
pregabalin/gabapentin
inhibit alpha 2 delta 1 subunit of Ca2+ channel
28
topiramate MOA
inhibit NA channels, increase K current, enhance GABA, inhibit GLutamate activity
29
Valproate MOA
enhance GABA release/activity, decrease NA channel activity
30
zonisamide MOA
dec Na channel activity, decrease T type calcoum channel acitvity
31
works on Na K and CA
oxcarbezepine
32
limited protein binding in serum except for
phenytoin valproate
33
accumulates in RBC's
zonisamide
34
displacement causes significant acute drug toxicity
VALPROATE PHENYTOIN
35
very important ADME clinical issue with AED's
hepatic processing by CYPS of UGT's
36
one example of a AED drug that induces its own metabolism-as tratmen progresses , half life decreases due to increased rate of hepatic metabolism
Carbemazepine-Na channel blocker
37
ultimate elimination of AED's
urine thus in renal dysfunction, drug accumulation can occur over time
38
AED not metabolism
Gabapentin pregabalin also topiramate is very minorly
39
not metabolized by CYPS
gabapentin, pregabalin lamotrigine levetiracetam tpoiramate
40
comes out in stoool
phenytoin
41
no induction, no inhibition
``` clonazepam ethosuximide gabapentin pregabalin levetiracetam topiramate zonisamide ```
42
capable of inducing its own metabolism via CYPS or UGT's thus the half life lessens with continued administration
Carbemazepine-induces CYPS and UGT Felbamate-induces cyps Lamotrigine phenytoin
43
metabolized through conjugation
oxcarbazepine
44
can prolong perseistence in the plasma by inhibiting the CYP that breaks it down, thus increasing half life potentially with long term dosing
Lacosamide Valproate
45
routine monitoring of these drugs is required due to their own abilit to alter their own persistence in the plasma
``` carbamzepine ethosuximide gabapenting phenytoin valoproate ```
46
cause renal stones
Topiramate and zonisamide
47
carbonic anhydrase ibhibitords
topiramate zonisamide
48
cause loss of bicarbonate from renal
topiramate zonisamide
49
requires periodic monitoring of blood gases (HCO3)
topiramate zonisamid
50
ABRUPT DISCONTINUATION OF AED CAN PRECIPITATE THUS TAPER GRADUALLY
STATUS EPILEPTICUS ICREASED SEIZURE FREQUENCY ANXIETY
51
ZERO ORDER KINETICS MEANS
HALF LIFE VARIES WITH DRUG DOSE
52
ZERO ORDER KINETIC AED
PHENYTOIN
53
CNS EFFECTS OF PHENYTOIN
NYSTAGMUS HA ATAXIA DROWSINESS
54
WEIRD SIDE EFFECT OF PHENYTOIN
GINGIVAL HYPERPLASIA
55
DERM SIDE EFECTS OF PHENYTOIN
``` SJS TEN DRESS HYPERTRICHOSIS HIRSUTISM ```
56
HEME CHANGES WITH PHENYTOIN
UNCOMMON BUT MAY OCCURE
57
HYPERTRICHOSIS SHOULD BE ONLY ASSOCIATED WITH
PHENYTOIN
58
HEMATOLOGIC CHANGES IN CARBEMAZEPINE
AGRANULOCYTOSIS OR APLASTIC ANEMIA ALSO CAUSES XEROSTOMIA NV, ATAXIA, DIZZINESS
59
UNIQUE TO CARBEMAZEPINE
BUT THE MAIN ONE TO REMEMBER IS APLASTIC ANEMIA
60
certain HLA b1502 genotypes (asians mostly) should avoid which AED's
carbamazepine phenytoin fopshenytoin lamotrigine
61
valproic acid side effects
CNS effects related to infusion rate thrombocytopenia prolonged INR SJS, DRESS, TEN NAusea, Diarrhea hepatotoxicity
62
BBW for felbamate
aplastic anemia bone marrow suppression hepatic disease
63
B for Lamotrigine
TEN or SJS
64
valproic acid preg category
X
65
Carbemazepine and phenytoin category
D
66
Lamotrigine category
C
67
PARTIAL SEIZURE , INCULDING SECONDARY GENERALIZED SEIZURE DOC'S
Lamo Carba Leve Oxc
68
DOC for primary generalized tonic clonic seizures
Valproate Lamo Levet
69
DOC for absence seizures
Ethosixumide | Valproate
70
atypical absence seizures
Valproate LAMO Levat
71
Status epilepticus brought on by
changes in AED's-mostly in young folks in the older cohort-mostly due to stroke
72
TX guidelines of SE
IV benzo (lorazepam, midal, diaze) ``` IV AED valproate or (pheny, midazolam continuout, leve,pheno) ```
73
prolong the openinh of the CL channel after exposure to endogenous GABA
barbiturates
74
shift dose-response curve to the left making the effect of GABA more pronounced
benzo's
75
only which GABA enhancer will induce CYPS
barbiturates-phenobarbital
76
advantage of benzos and barbs tover phenytoin and valproate
can be given by rapid IV administration
77
SJS not reported with
CLonazepam Lacosamide
78
which AED;s have blood toxicity
Carbamazepine felbamate valproate
79
which ones are teratogens
Lamo carba phenytoin valproate
80
first drug for status epilepticus
IV lorazepam
81
lorazepam AKA
ativan

Neuro (19 decks)

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