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Clinical Neuro > Sweatman - Epilepsy Drugs > Flashcards

Sweatman - Epilepsy Drugs Flashcards

1
Q

Which anti-convulsant should NOT be used in pregnant women?

A
  • Valproic acid
  • With women of child-bearing age, should be concerned about whether or not they are pregnant when you initiate therapy
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2
Q

What is fetal hydantoin syndrome?

A
  • Gp of defects to fetus via teratogenic effects of Phenytoin or Carbamazepine
  • Intrauterine growth restriction w/small head (microcephaly) and minor dysmorphic craniofacial features + limb defects (skeletal malformations particular to fingers/hands, incl. hypoplastic nails of fingers and/or toes)
  • May have developmental delay, intellectual disability
  • Heart defects and cleft lip may also be seen
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3
Q

What is the 1st-line drug for acute, prolonged epileptic crisis?

A
  • Lorazepam
  • NOTE: while you control epilepsy with subsequent drugs, their physico-chemical characteristics are that they cannot be given as a bolus, and you want to terminate the epileptic rxn now
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4
Q

7-y/o child w/o any hx of brain damage, but who had mild speech delay and hyperkinesia started having brief episodes of fixed gaze and falls. In sleep, the parents observed tonic fits. Which of the following is most appropriate to tx this pt?

A
  • Valproate
  • He said this is absence?
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5
Q

What drug can elicit gingival hyperplasia as a symptom?

A
  • Phenytoin
  • NOTE: Cyclosporine, dihydropyridine Ca-channel blockers can also cause this (i.e., Nifedipine)
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6
Q

What drug is used in tx of epilepsy that works by INH Ca channels?

A
  • Gabapentin (alpha-2-delta-1 subunit)
  • NOTE: Pregabalin (alpha-2-delta-1 subunit), Oxcarbazepine (possibly), and Zonisamide (Type-T) also do this
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7
Q

What is the MOA of Valproate?

A
  • INH the breakdown of GABA, INC its time in the synaptic cleft —> slightly unusual MOA
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8
Q

What drug gets dose adjusted over time to maintain appropriate serum levels?

A
  • Carbamezepine bc it induces its own metabolis via CYP -> activity reaches a pt where it’s maximally induced, so you don’t keep INC dose
  • Phenytoin also a self-inducer, but may not be as much as Carbamezepine
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9
Q

Metabolic acidosis secondary to AED tx is most likely to occur with which drug?

A
  • Topiramate: INH carbonic anhydrase, so bicarb retained in urine flow
  • Can also get formation of kidney stones
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10
Q

Which drug exhibits zero-order kinetics?

A
  • Phenytoin
  • Linear elimination: constant amt eliminated per unit time, so half-life changes as you INC dose
  • NOTE: high-dose ASA also exhibits zero-order kinetics
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11
Q

Routine CBC reveals neutrophil count of <0.5 x 10^9/L; what is the most likely causative agent?

A

Carbamazepine

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12
Q

57-y/o woman being tx’d for epilepsy has petechiae on lower legs and a number of recent bruises. What drug is she on?

A
  • Valproic acid: can cause thrombocytopenia
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13
Q

For which pt would HLA-B genotyping be prudent if considering Carbamazepine therapy?

A

Asian

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14
Q

56-y/o man with epilepsy complains of weakness, SOB on exertion. He is tachycardic, with pale skin. What AED is he on?

A
  • He is anemic
  • He is taking Felbamate
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15
Q

What is the pro-drug for Phenytoin?

A

Fosphenytoin

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16
Q

What 2 drugs share the same pharmacology as Valproate?

A
  • Divalproex
  • Valproic acid
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17
Q

What is the drug list for anti-convulsants (table)?

A
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18
Q

What are the seizure classifications (table)?

A
  • Many of the drugs have specific indications in regards to types of seizures they are used to treat
  • This relates underlying pathophys of seizure and MOA of respective drug
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19
Q

What is the pathophys of seizures?

A
  • Start discretely, then spread to neighboring regions
  • High-frequency bursts of AP’s: influx of EC Ca, then depolarization = activation of voltage-dependent Na channels, generating repetitive AP’s
  • Hypersynchronization: hyperpolarizing after-potential via GABA receptors or K+ channels
  • Surrounding (normally) INH neurons opposed by:
    1. INC in EC K+
    2. Ca in presynaptic terminals -> INC NT release
    3. Activation of NMDA excitatory neurons
    4. Cell swelling, and changes in tissue osmolarity
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20
Q

What are the 3 MOA’s of the anti-convulsants? How do these vary by seizure type?

A
  • PARTIAL and SECONDARILY GENERALIZED tonic-clonic seizures:
    1. Limit sustained, repetitive firing of neurons by promoting inactivated state of voltage-gated Na channels (MOA of local anesthetics)
    2. Pre- or post-synaptic enhancement of GABA-mediated synaptic INH via pre- or post-synaptic action
  • ABSENCE seizures: INH of voltage-activated Ca channels responsible for T-type Ca currents
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21
Q

Which drugs target voltage-gated Na+ channels? How does this MOA work?

A
  • Prolong inactivation of Na+ channels, reducing ability of neurons to fire at high frequencies (LVZ - PCT)
    1. Bind to specific components of Na channel, preventing action, even in presence of membrane depolarization
  • Multimeric transmembrane-spanning channel complex normally exists in closed state -> when the membrane is depolarized, various subunits rapidly reconfigure to open ion channel to free mvmt of Na+
    1. Almost immediately, inactivation gate swings across open pore to rapidly terminate ion passage
    2. Normally, various components reconfigure into closed, but activatable state
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22
Q

Which anti-convulsants enhance GABA action? How?

A
  • Several mechanisms, but all produce greater quantum yield of GABA release w/e/neuronal impulse:
    1. Benzodiazepines/barbiturates bind separately at sites on multimeric ion channel complex to modulate activity of endogenous GABA (post-syn)
    2. Gabapentin acts pre-syn to promote GABA release
    3. Vigabatrin and Valproate reduce metabolism of GABA
  • NOTE: GABA is principle INH NT in the brain
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23
Q

Which drugs act via Ca-channel blockade? How?

A
  • Reduce flow of Ca through T-type Ca channels
  • Reduce pacemaker current underlying thalamic rhythm in spikes and waves seen in generalized ABSENCE seizures
  • Both Na- and Ca-channel blockers diminish effects of glutamate, the principal stimulatory NT in the brain
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24
Q

How do AED’s affect the high-frequency firing characteristic of seizures?

A
  • Phenytoin, Carbamazepine, and sodium valproate all markedly reduced number of AP’s elicited by current pulses -> diminish atypical neuronal activity, reducing seizure activity, as seen on an EEG
  • NOTE: in absence of drug, a series of high-frequency AP’s filled entire duration of current pulse
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25
Q

What psych concern should you be conscious of with all of the anti-convulsants? How can you monitor this?

A
  • Suicidal ideation: INC incidence, according to FDA
  • According to clinical trials, behavioral effect observed 1-24 weeks after starting drug
  • MONITOR all pts for emerging or worsening depression or suicidial thoughts/behavior
    1. Educate pts/caregivers about risks, and advise to immediately report emergence of worsening of depression, suicidal, or self-harm thoughts/beh
  • Minimally effective drug levels should be used
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26
Q

How effective are current anti-convulsants?

A
  • Current drugs control seizures in ONLY 50% of pts, with another 25% helped somewhat
  • AE’s vary from minimal impairment to death from aplastic anemia or hepatic failure
    1. Can limit pt adherence, and be responsible for tx discontinuation
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27
Q

What are 2 clinical guidelines for anti-convulsant therapy?

A
  • 1) Use single-agent therapy; substitution preferred with Rx failure, rather than additive tx
  • 2) # of these drugs require monitoring of serum drug level, but these levels provide only guidance; clinical assessment of effect vs. toxicity is paramount
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28
Q

What is the MOA of Carbamazepine?

A

INH Na+ channels

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29
Q

What is the MOA of Clonazepam?

A

GABA allosteric agonist

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30
Q

What is the MOA of Ethosuximide?

A

INH T-type Ca channels

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31
Q

What is the MOA of Felbamate?

A

INH NMDA; enhance GABA

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32
Q

What is the MOA of Gabapentin?

A

INH alpha-2-delta-1 subunit of Ca channel

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33
Q

What is the MOA of Lacosamide?

A

INH Na+ channels

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34
Q

What is the MOA of Lamotrigine?

A

INH Na+ channels

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35
Q

What is the MOA of Levetiracetam?

A

Unknown

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36
Q

What is the MOA of Oxcarbazepine?

A

INH Na+; possible INC K+ and DEC Ca effects

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37
Q

What is the MOA of Phenytoin?

A

INH Na+ channels

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38
Q

What is the MOA of Pregabalin?

A

INH alpha-2-delta-1 subunit of Ca channel

39
Q

What is the MOA of Topiramate?

A
  • INH N+ channels
  • INC K+ current
  • INC GABA
  • DEC glutamate activity
40
Q

What is the MOA of Valproate?

A

INC GABA activity; INH Na+ channels

41
Q

What is the MOA of Zonisamide?

A

INH Na+ and INH T-type Ca channels

42
Q

Describe the ADME of the anti-convulsants?

A
  • Most administered ORALLY, but some available for IV dosing
  • Limited protein binding, except Phenytoin and Valproate -> issues of protein binding displacement may be significant in producing acute drug toxicity
  • Zonisamide accumulates in erythrocytes
  • Predominantly hepatic metabolism w/urinary elim of parent drug and/or metabolites -> some have active metabolites
  • Some induce CYPs (Carbamazepine); others INH CYPs -> 1/2 lives may change for drug and/or concurrent agents
  • Long half-lives
  • Slow release products facilitate adherence: fewer doses/day
43
Q

Which anti-convulsant accumulates in erythrocytes?

A

Zonisamide

44
Q

Which anti-epileptic drugs exhibit extensive protein binding?

A
  • Phenytoin
  • Valproate
45
Q

What are the key points for metabolism, CYPs, and elimination of antiepileptic drugs (table)?

A
  • HEPATIC METABOLISM: involving CYP’s (phase 1) and uridine glucuronosyl transferase (phase 2)
    1. Concurrent agents impacting activity of these metabolic processes can alter serum drug level of concurrent AED, changing clinical effectiveness -> potential drug-drug interaxns
    2. Several AED’s modulate enzyme activity and can alter serum levels of o/drugs, incl. inducing their own metabolism (i.e., Carbamazepine)
  • For all AED’s, elim of drug and/or metabolites in urine, so renal dysfunction may be significant in regards to potential for drug accumulation over time
46
Q

How is the metabolism of Carbamazepine unique? Implications?

A
  • As tx progresses, 1/2-life of drug DEC due to INC rate of hepatic metabolism
47
Q

Which anti-convulsants can be given IV?

A
  • Lacosamide
  • Levetiracetam
  • Phenytoin
  • Valproate Na
48
Q

Which antiepileptic drugs have NO CYP interactions?

A
  • Gabapentin, Pregabalin: NOT metabolized in liver (or at all)
  • Lamotrigine (metabolized by UGT and induces UGT, however)
  • Topiramate
  • Levetiracetam
49
Q

Which antiepileptics influence their own metabolism?

A
  • Carbamazepine: CYP3A4 inducer
  • Felbamate: 2C19 INH and 3A4 inducer
  • Lacosamide: 2C19 INH
  • Lamotrigene: UGT inducer
  • Phenytoin: 3A4 and 2C19 inducer
  • Valproate: 2C9 INH
50
Q

Which antiepileptic is eliminated in the stool?

A

Phenytoin

51
Q

Which antiepileptic drugs are metabolized by UGT?

A
  • Lamotrigene
  • Valproate Na (+2C9, 2C19)
  • Zonisamide (+ 3A4)
52
Q

For which AED’s is routine monitoring of serum drug levels required?

A
  • Carbamazepine, Ethosuximide, Gabapentin
  • Phenytoin, Valproate
  • NOTE: this is for guidance and to see trends, rather than as an absolute
    1. High serum drug levels + good control of seizures + absence of toxicity does not necessarily warrant reduction in drug dosing -> use clinical presentation to guide tx
53
Q

What are some things you should be concerned about regarding metabolism of the AED’s (3)?

A
  • Inducers of CYP or (UGT) uridine 5’-diphospho-glucuronosyl-transgerase can change 1/2-life of concurrent substrate AED’s (and any other drugs)
  • May INH concurrent parenteral drug, but INC levels of active metabolites
  • Some drugs may self-induce (Carbamazepine) and changing their own 1/2-life, requiring dose-adjustment over time to compensate
54
Q

What are some of the issues with Topiramate and Zonisamide?

A
  • Weak carbonic anhydrase INH: renal bicarb loss (<68% and 43%, respectively)
    1. R​outine MONITORING of serum bicarb required
    1. Promote stone formation by reducing urinary citrate excretion and INC urinary pH
55
Q

Should you abruptly terminate AED’s? Why or why not?

A
  • No: caution in adjustment of drug doses
  • Discontinuation can precipitate status epilepticus, INC freq of seizures, and various neuro issues, like anxiety
  • Clinicians must BE WARY of this if they elect to terminate tx due to severe AE’s
    1. Where possible, termination should involve tapering of drug over period of time
56
Q

What are some of the metabolic issues with Phenytoin?

A
  • Metabolism highly variable
  • Zero-order elimination: 1/2-life varies w/drug dose, making clinical use of this agent problematic
  • Issues of protein binding displacement and CYP-mediated drug-drug interactions
    1. Highly variable induction of CYP’s 3A4, 2C9, and 2C19
    2. Age, cigarette smoking, and hepatic status are confounding factors
57
Q

What are some of the AE’s with Phenytoin?

A
  • CNS effects: most commonly nystagmus, but also headache, ataxia, incoordination
    1. Drowsiness NOT common at therapeutic levels
  • GINGIVAL HYPERPLASIA: >15% of long-term pts
  • DERM EFFECTS (rare; <5%): range from measles-like rash to SJS, TEN, DRESS (possible with most AED’s)
    1. Hypertrichosis, hirsutism: generally confined to extremities, but can affect trunk/face (may be irreversible; rarely with Carb, Lamo, Zonis)
  • HEME CHANGES: may occur, but uncommon for pt taking phenytoin to devo severe blood dyscrasia (potentially life-threatening)
58
Q

What are some of the issues with Carbamazepine?

A
  • CNS effects (esp. during initial tx phase): dizziness, drowsiness, ataxia, blurred vision; sedation upon initiation and dose escalation
  • HEME CHANGES: routine monitoring required due to 5-8 fold INC risk of agranulocytosis (BBW; life-threatening) or aplastic anemia
  • DERM EFFECTS (rare; <5%): measles-like rash to SJS, TEN, DRESS
  • Miscellaneous: dry mouth, constipation, N/V (common to many AED’s)
59
Q

How is HLA-B 1502 genotyping relevant to AED tx? For which drugs?

A
  • Whole blood EDTA testing to ID Asian pts at-risk of SJS and TEN (SNP change in HLA-B 1502 allele, placing carrier at INC risk of immune system-mediated AE’s)
    1. Carbamazepine, Phenytoin, Fosphenytoin, Lamotrigine
  • May be prudent to advise carriers to avoid Carb and structurally related anticonvulsants like Phenytoin, Oxcarbazepine, and possibly Lamotrigine
60
Q

What are some of the issues with Valproic acid?

A
  • CNS effects: related to infusion rate -> somnolence, dizziness, paresthesias, asthenia, headache
  • HEME CHANGES: thrombocytopenia, prolonged bleeding time
  • DERM EFFECTS (rare): measles-like rash to SJS, TEN, DRESS
  • Miscellaneous: N, diarrhea, hepatotoxicity (rare, but occurs most commonly in KIDS)
61
Q

What are the side effects of Clonazepam?

A
  • Somnolence (37%)
  • Ataxia, dizziness, fatigue (about 10% each)
62
Q

What are the side effects of Ethosuximide?

A
  • Somnolence
  • Dizziness
  • Headache
  • N/V
  • Diarrhea
  • GI upset
63
Q

What are the side effects of Felbamate?

A
  • BBW: aplastic anemia, bone marrow suppression, hepatic disease
  • N/V (25%)
  • Constipation (12%)
64
Q

What are the side effects of Gabapentin?

A
  • Somnolence (20%)
  • Dizziness, ataxia, fatigue (15% each)
65
Q

What are the side effects of Lacosamide?

A
  • Dizziness
  • Headache
  • Diplopia
  • N/V
66
Q

What are the side effects of Lamotrigine?

A
  • BBW: serious rash (TEN/SJS)
  • Dizziness (38%)
  • Diplopia
  • Ataxia
  • Blurred vision
  • Rhinitis
67
Q

What are the side effects of Levetiracetam?

A
  • Headache
  • URTI
  • Somnolence
68
Q

What are the side effects of Oxcarbazepine?

A
  • Dizziness/diplopia (50% each)
  • Headache
  • N/V
  • Nystagmus, somnolence, ataxia
69
Q

What are the side effects of Pregabalin?

A
  • Dizziness
  • Somnolence
  • Peripheral edema
70
Q

What are the side effects of Topiramate?

A
  • Dizziness, fatigue
  • Ataxia, paresthesias, abnormal vision/psychomotor slowing
71
Q

What are the side effects of Zonisamide?

A
  • Somnolence
  • Anorexia
  • Dizziness
72
Q

What is Fosphenytoin?

A
  • Pro-drug dosed in phenytoin equivalents
    1. 150mg fosphenytoin = 100mg phenytoin: DOSE ADJUSTMENT important when transitioning b/t these products
  • Process unaffected by concurrent drug therapy
73
Q

What are the pregnancy categories for the potentially teratogenic AED’s? Abnormalities described?

A
  • Lamotrigine: CAT C
  • Carbamazepine, Phenytoin, Topiramate, Phenobarbitol: CAT D
  • Valproate: CAT X -> greatest risk of AE’s
74
Q

Which AED’s can cause fetal hydantoin syndrome? What is this?

A
  • Carbamazepine, Phenytoin
  • FEATURES: upturned nose, mild mid-facial hypoplasia, long upper lip with thin vermilion border, and digital hypoplasia
  • NOTE: not all investigators are convinced of the existence of this syndrome, and similar effects have also been attributed to both Phenobarbitol
75
Q

What abnormalities can Valproate cause in the developing fetus?

A
  • Neural tube defects
  • Clefts
  • Skeletal abnormalities
  • Developmental delay
  • NOTE: greatest risk during pregnancy with this drug
76
Q

What abnormalities can be seen in fetus exposed to Phenobarbitol in utero?

A
  • Clefts
  • Cardiac abnormalities
  • Urinary tract malformations
77
Q

What abnormalities can be seen in fetus exposed to Lamotrigine in utero?

A
  • INH dihydrofolate reductase, lowering fetal folate levels
  • Registry data suggest INC risk for clefts
78
Q

What AE’s can be seen in fetus exposed to Topiramate in utero?

A
  • Cleft lip
  • Cleft palate
79
Q

What abnormalities can be seen in fetuses exposed to Carbamazepine?

A
  • Fetal hydantoin syndrome
  • Spina bifida
80
Q

What are the DOC for partial, incl secondarily generalized seizures (table)?

A
81
Q

What are the DOC for primary generalized tonic-clonic seizures (table)?

A
82
Q

What are the DOC for absence seizures (table)?

A
  • These 2 drugs are considered equally effective
  • 50-75% of pts experience complete control
83
Q

What are the DOC for atypical absence, myoclonic, atonic seizures (table)?

A
84
Q

What is status epilepticus? Causes? Tx?

A
  • Status epilepticus = prolonged seizure, or cluster of seizures, w/o return to baseline, lasting >30 mins
    1. Can be generalized tonic-clonic, complex or simple partial, absence, or subclinical
    2. Up to 50% occur in pts w/epilepsy due to recent changes in AED’s or non-adherence
    3. Remainder of cases in adults most often secondary to a stroke
  • MEDICAL EMERGENCY: mortality from 7-40%
85
Q

What are some of the predictors of mortality in status epilepticus?

A
  • Generalized seizure
  • INC patient age
  • Anoxic brain injury
  • Stroke
  • CNS infection or tumor
  • Long duration of SE
  • NOTE: successful outcomes require early, aggressive tx and collaboration b/t EM doc, hospitalist, neurologist
86
Q

What are the important similarities/differences b/t benzos and Phenobarbitol?

A
  • BOTH work on GABA receptor, but at different sites: barbs prolong opening time of Cl- channel and benzos shift dose-response curve for GABA
  • BOTH have issues of dependence/withdrawal + devo of tolerance
  • BOTH will produce dose-related sedation
  • ONLY Phenobarbitol will induce CYP2B6, 3A4 levels
  • BOTH can be given by rapid IV admin, unlike Phenyton or Valproate (these can be given IV, but apparently not rapidly)
87
Q

Why is a benzo first-line tx for SE? Why are they followed up with another drug?

A
  • Significant reinforcement of INH effects of GABA
  • Can be given rapidly IV, whereas o/agents have limitations in rate at which they can be administered by this route due to physico-chemical issues (i.e., Phenytoin, Valproate)
  • NOTE: can rapidly terminate SE, but short 1/2-lives for these agents mean add’l drugs must be administered to provide for more sustained drug control
88
Q

What are the 3 main MOA’s of the AED’s

A

Work on Na+, Ca2+ (T-type) channels, or reinforce GABA’s action

89
Q

What are common side effects of all AED’s?

A
  • CNS effects like sedation, dizziness, ataxia
90
Q

What is a serious side effect assoc with MOST AED’s? For which 2 drugs is this effect NOT reported?

A
  • RASH possible with most AED’s; rarely SJS
    1. Asian predisposition with HLA-B 1502 allele
    2. SJS NOT reported w/Clonazepam, Lacosamide
91
Q

Which AED’s have blood toxicities?

A
  • Carbamazepine: agranulocytosis
  • Felbamate: aplastic anemia, bone marrow suppression, hepatic toxicity (BBW)
  • Valproate: thrombocytopenia, prolonged bleeding time
92
Q

Which AED’s are teratogens?

A
  • Lamotrigine
  • Carbamazepine
  • Phenytoin
  • Valproate
  • Topiramate
  • Phenobarbitol
93
Q

What is the first drug for SE?

A

Lorazepam IV

Clinical Neuro (15 decks)

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