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PHAR324 > Anticonvulsants and BZDs > Flashcards

Anticonvulsants and BZDs Flashcards

1
Q

Differentiate seizures and epilepsy.

A

seizure:
-sudden, uncontrolled burst of electrical activity in the brain
-changes in behavior, movements, feelings, consciousness
-most last 30s-2min (>5min=emergency)
epilepsy:
-two or more seizures at least 24 h apart that dont have a known cause

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2
Q

Differentiate generalized and focal seizures.

A

generalized:
-happen in both sides (hemispheres) of the brain
-more severe effects and symptoms
focal:
-only happen in one hemisphere
-symptoms only happen on one side or specific part of the body
-can spread and become generalized seizures

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3
Q

What are the types of generalized seizures?

A

absence seizures
myoclonic seizures
tonic seizures
tonic-clonic seizures
atonic seizures

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4
Q

Which class of medications is used to treat epilepsy and other seizure disorders?

A

anticonvulsants

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5
Q

Provide a recap of seizure mechanism.

A

imbalance of inhibitory and excitatory activity
-more excitatory activity
-glutamate > GABA

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6
Q

What is the MOA of carbamazepine and phenytoin?

A

block voltage gated Na+ channel
-stop glutamate release/binding

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7
Q

What is the MOA of barbiturates and BZDs?

A

behave like GABA
-enhancement of inhibitory transmission

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8
Q

Describe the absorption of CBZ.

A

slow, unpredictable
tmax: 4-8 hours
delay owing to anticholinergic effects
some evidence of enterohepatic recirculation

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9
Q

Describe the distribution of CBZ.

A

Vd = 0.8-2 L/kg
plasma protein binding: 76%
-not suitable for dialysis

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10
Q

Describe the metabolism of CBZ.

A

CBZ –> CBZ 10,11 epoxide (via 3A4)
-CBZ 10,11 epoxide is active and toxic
CBZ 10,11 epoxide –> trans-CBZ-diol (via epoxide hydrolase)

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11
Q

Describe the elimination of CBZ.

A

autoinduction
-t1/2 initial: 25-65h
-t1/2 after multiple doses: 12-17h
-t1/2 CBZ 10,11 epoxide: 5-10h
*drug as well as toxic metabolite induce CYPs

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12
Q

What is the therapeutic range of CBZ?

A

20-50 umol/L (narrow therapeutic window)
-toxicity develops within TR

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13
Q

What are the systems affected by CBZ toxicity?

A

neurologic (nystagmus, ataxia)
respiratory
cardiovascular

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14
Q

What are symptoms of toxicity from chronic use of CBZ?

A

headache
diplopia
ataxia
ECG abnormalities
hyponatremia due to SIADH

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15
Q

What kind of impacts can VPA and lamotrigine have on CBZ?

A

enzyme inhibitors of epoxide hydrolase
-therefore accumulation of the 10,11 epoxide active metabolite

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16
Q

What is the antidote to CBZ?

A

no antidote

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17
Q

How is CBZ toxicity managed?

A

supportive/symptomatic care
-hydration, airway, electrolytes, ABCs
-BZDs for refractory seizures due to CBZ

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18
Q

What is the decontamination method for CBZ?

A

SDAC
-binds
-1 to 2 hr window

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19
Q

What are the elimination methods for CBZ?

A

MDAC
-if severe
hemodialysis
-if theres lots of drug in the body, free proportion increases

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20
Q

Is death common due to phenytoin toxicity?

A

rare if good supportive care

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21
Q

What is the problem if IV phenytoin is released too quickly?

A

local tissue damage
cardiotoxicity

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22
Q

Describe absorption of phenytoin.

A

erratic absorption following PO administration
tmax: 3-12h after a single oral dose
-bezoar would increase time to tmax

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23
Q

Describe distribution of phenytoin.

A

rapidly distributed to all tissues
extensive PPB (88-93%)
-serum levels may not represent total drug
-TR but patient may exhibit signs of toxicity

24
Q

Describe metabolism of phenytoin.

A

95% hepatically metabolized to inactive metabolite
polymorphism
-2C9, 2C19 poor metabolizers may experience toxicity at therapeutic levels

25
Q

What happens to elimination of phenytoin as the concentration increases?

A

1st to zero order kinetics

26
Q

What are therapeutic levels of phenytoin?

A

40-80 umol/L

27
Q

What level do toxic effects of phenytoin start showing up?

A

after 80 umol/L

28
Q

What is nystagmus?

A

rapid eye movement

29
Q

Which systems are impacted by phenytoin toxicity?

A

neurologic
CV
GI/hepatic

30
Q

What is the antidote for phenytoin?

A

no antidote

31
Q

What is the management of phenytoin toxicity?

A

ABCs
supportive/symptomatic care
mainstay:
-if hypotension from IV = reduce infusion rate, IV fluids, vasopressors
-airway protection

32
Q

What is a decontamination method for phenytoin?

A

SDAC
-binds; consider but no evidence of any change in clinical course

33
Q

What are the elimination methods for phenytoin?

A

MDAC
-generally not necessary
hemodialyis
-current toxicology resources do not recommend hemodialysis for phenytoin toxicity

34
Q

What are examples of barbiturates?

A

phenobarbitone
butobarbitone
pentobarbitone
thiopentone
methohexitone

35
Q

What do most BZDs end in?

A

pam
-except chloradiazepoxide

36
Q

Why did BZDs replace barbiturates?

A

safer profile in terms of respiratory depression
-however they can still cause some respiratory depression

37
Q

What is the MOA of BZDs?

A

stimulating GABA-a receptor
-thereby opening Cl channel
lower the potential difference between the interior and exterior of the cell, blocking ability of cell to conduct nerve impulses

38
Q

What is the antidote to BZDs?

A

flumazenil

39
Q

Describe absorption of BZDs.

A

rapid and complete orally
tmax: 1-3h
relative lipophilic
-more lipophilic means faster onset and longer duration
half-life ranges from 2-50h

40
Q

Describe distribution of BZDs.

A

Vd 0.75-1.5 L/kg
highly protein bound

41
Q

How are BZDs eliminated?

A

hepatically metabolized
metabolites excreted renally

42
Q

Describe BZD toxicity.

A

mortality from pure BZD overdose is rare
toxicity depends on:
-coingestants especially CNS depressants
-shorter acting BZD = more toxicity
-IV more likely to cause significant toxicity
-tolerance skews the course

43
Q

What is a very important piece of information to gather when someone presents with BZD toxicity?

A

co-ingestants

44
Q

What happens with chronic use of BZDs?

A

tolerance

45
Q

What do urine levels test for in regards to BZDs?

A

substances metabolized to oxazepam and nordiazepam
false-negative if not metabolized to oxazepam/nordiazepam

46
Q

What are decontamination methods for BZD toxicity?

A

SDAC (maybe)
-if within 1h of ingestion
gastric lavage (no)

47
Q

What are elimination methods for BZD toxicity?

A

MDAC (no)
hemodialysis (ineffective)

48
Q

What is the MOA of flumazenil?

A

selective competitive antagonist of GABA receptor
out competes BZD at recognition site on receptor complex thereby reversing BZD effect on CNS

49
Q

What is the onset of flumazenil?

A

1-2 min
effect is short lived

50
Q

What are safety concerns with flumazenil?

A

seizures
dysrhythmias possible when mixed overdose
re-sedation

51
Q

What are the pros and cons of flumazenil?

A

pros:
-adverse effects minimal
cons:
-seizure risk
-withdrawal risk

52
Q

Is flumazenil effective at reversing respiratory depression?

A

effective at reversing CNS depression but not respiratory depression

53
Q

Which patients is it ideal to use flumazenil in?

A

BZD-naive and single BZD-ingested patients

54
Q

When is flumazenil a poor option?

A

unknown overdoses because of life threatening seizures and dysrhythmias
can also precipitate seizure and withdrawal in BZD-dependent patients
safer to prioritize ABC in unknown overdose

55
Q

What are the indications for flumazenil?

A

pure BZD OD
non-tolerant AND CNS depression, normal vital signs, normal ECG, normal neurological exam

56
Q

Differentiate the MOA of barbiturates and BZDs.

A

barbiturates:
-enhance binding of GABA to GABA-a receptor
-prolong duration of channel opening
-narrow therapeutic index
BZD:
-enhance binding of GABA to GABA-a receptor
-increase frequency of channel opening
-wider therapeutic index than barbiturates

PHAR324 (10 decks)

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