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PR3153 Midterms > IC4 > Flashcards

IC4 Flashcards

1
Q

phenytoin MOA

A

block voltage-dependent Na+ channels to reduce the membrane excitability

not suitable for absence seizures

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2
Q

CBZ MOA

A

block voltage-dependent Na+ channels

not suitable for absence seizures

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3
Q

VAL MOA

A

block voltage dependent Na+ and Ca2+ channels

suitable for all types of seizures

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4
Q

what are the general dose-related side effects of ASMs

A

drowsiness
confusion
nystagmus (eyes move rapidly, uncontrollably)
ataxia (no coordination)
slurred speech
nausea
unusual behavior/mental changes
coma

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5
Q

what are non-dose related side effects of ASMs

A

hirsutism
acne
gingival hyperplasia
folate deficiency
osteomalaica
hypersx SJS/TEN

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6
Q

benzodiazepines MOA

A

potentiates influx of cl- ions entering the GABA receptors cl- channels leading to hyperpolarisation = decreased excitability
(enhance effect of inhibitory GABA neurotransmitters)

GABA-A receptors.
GABA is the inhibitory neurotransmitter.

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7
Q

DOA of benzodiazepines

A

varying DOA

midazolam is the shortest acting with appx 3h t1/2. rarely used for epilepsy but general anaesthetic procedures

clonazepam, lorazepam
intermediate acting appx 12-30h t1/2

diazepam
long acting appx 43h t1/2
more suitable for status epilepticus

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8
Q

ADR benzodiazepines

A

acute toxicity/overdose
- severe respiratory depression (esp with alcohol use) = slow shallow breathing rate
- treat with flumazenil (benzo antagonist)

during use
- drowsy, confusion, amnesia
- impaired muscle coordination (impair manual skills)

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9
Q

how to treat respiratory depression from benzodiazepines

A

flumazenil

binds to benzodiazepines but does not activate it = gets displaced

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10
Q

management AND PROBLEM of benzodiazepine ADRs.

A

tolerance develops with increased frequency of use.

HOWEVER, may also cause dependence with overuse. = withdrawal effects like disturbed sleep, rebound anxiety, tremor, convulsions.

IF WITHDRAW = DO IT GRADUALLY

RISK OF ABUSE.

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11
Q

phenobarbital MOA?

A

also potentiates GABA-A mediated CL- currents
BUT at a different site

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12
Q

what is the other indication of phenobarbital and benzodiazepines

A

sedative hypnotic

although benzodiazepines replaced them due to increased tendency of barbiturates to cause tolerance and dependence

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13
Q

common indication of phenobarbital?

A

ASM
for pediatric or neonatal patients
(IV loading > IV/oral maintenance)

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14
Q

DOA of phenobarbital

A

long acting (1-2days) = anticonvulsant = phenobarbital

short (3-8h) = sedative hypnotic = pentobarbital, amobarbital

ultrashort (20min) = IV induction of anaesthesia = thiopental

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15
Q

pk of phenobarbital vs benzodiazepines

A

dose dependent depression
increasing dose of benzodiazepines will eventually reach a peak in how much it can cause CNS effects (max medullary depression)

however, phenobarbitals has no peak effect and may induce coma at high doses.

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16
Q

PK of levetiracetam

A

highly soluble and permeable

similar linear profile like phenytoin

low intra and inter subject variability

ORAL AND IV

17
Q

common and rare ADR levetiracetam

A

common: headache, vertigo, cough, depression, insomnia

rare: agranulocytosis, suicide, delirium, dyskinesia (abnormal invol movement)

18
Q

MOA of lamotrigine

A

blocks voltage gated Na+ channels
inhibit release of glutamate
impedes sustained repetitive neuronal depolarisation

19
Q

what special ASM indication for lamotrigine?

A

use as initial or adjunct to lennox gastaut syndrome

20
Q

PK of lamotrigine (t1/2)

A

oral (chewable)
t1/2 short for children
t1/2 reduced with co-admin of CBZ, PH
t1/2 increased with co-admin of VAL

21
Q

common and rare ADR lamotrigine

A

common: headache, irritable/aggression, tiredness

rare: agranulocytosis, hallucination, movement disorder (worsen PD), SJSTEN, hepatic failure

22
Q

topiramate MOA

A

UNCLEAR
increase gaba activation of gaba-a receptor to enhance induction of cl-?
but does not increase channel opening time
may act on benzodiazepine insensitive subtype of GABA-A receptors

23
Q

what special ASM indication for topiramate?

A

lennox-gastaut
ADJUNCT therapy

24
Q

other indications for topiramate

A

prophylaxis of migraine in ADULTS

25
Q

PK of topiramate

A

oral long plasma half life
renal clearance
not a potent inducer of drug-metabolising enzymes

26
Q

common and rare ADR of topiramate

A

common: depression, drowsy, fatigue, nausea, weight change

rare: neutropenia, mania, tremor, transient blindness, SJS/TEN, hepatic failure

26
Q

implication of serotonin in migraine

A

Serotonin may be an important mediator of migraine headache:

Agonists of vascular and neuronal 5-
HT1 receptor subtypes = 1) vasoconstriction of meningeal blood vessels and
2) inhibition of vasoactive neuropeptide release and pain signal transmission.

27
Q

PK of cafergot
tmax
BA
metabolism

A

oral and rectal
rapidly absorbed with max plasma conc reached in 1.5-2hours

high plasma protein binding, low absolute BA (2-5%)

inhibits cyp3a4 = risk of elevated toxicity and vasospasm/tissue ischemia

28
Q

ADR common and rare of cafergot

A

common: N/V
rare: hypersx, myocardial infarction, vascular ischemia (ergotism)

29
Q

PK of sumatriptan

A

oral. nasal. iv

rapidly absorbed
low plasma protein binding
eliminated by MAO

30
Q

C/I sumatriptan

A

hypersx to triptans
concurrent admin with MAOi
myocardial infarction

31
Q

common and rare ADR of sumatriptan

A

common: dysgeusia (unpleasant taste), transient BP increase, flushing, sensation of cold, pressure, tightness

rare: minor disturbances in LFT

32
Q

PK of erenumab and how long for effect

A

SQ injection monthly
benefit in 3 months

linear kinetics = saturable binding of cgrp receptor

33
Q

ADR erenumab

A

hypersx
injection site reactions
constipation
pruritis

PR3153 Midterms (9 decks)

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