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Therapeutics 4 > Exam 3- Seizures > Flashcards

Exam 3- Seizures Flashcards

1
Q

Seizure

A

Characterized by excessive or hypersynchronous discharge of neurons in the cortex. Paroxysmal (sudden, rapid onset)

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2
Q

Epilepsy

A

Chronic disorder characterized by recurrent, spontaneous seizures

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3
Q

Potential causes for epilepsy

A

Head trauma, stroke, CNS lesion, metabolic disorder, genetic

70-80% of epilepsy has no known cause

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4
Q

Can drug withdrawal and overdose cause epilepsy?

A

No, they can precipitate a seizure but not epilepsy.

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5
Q

Ion channels and neuronal firing

A

Na channels opening leads to Na influx and depolarization/ action potential. K channels openings leads to K efflux and hyperpolarization.
Na and K impose limits on neuronal firing. They are targets for ASDs.

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6
Q

Neuronal networks and surround inhibition: Glutamate- GABA interactions

A

Excitatory neurons (glutamate) activates other excitatory neurons and inhibitory neurons (GABA), which prevent glutamate from activating surrounding circuits.

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7
Q

Biochemical properties of K and Na effects on seizures

A

Biochemical properties of K and Na channels limit frequency of neuronal firing, thereby preventing repetitive firing of neurons that characterize seizures.

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8
Q

What are brain circuits balanced by?

A

Excitatory (glutamate) and inhibitory (GABA) neurotransmitters

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9
Q

Two major categories of seizures

A

Focal onset and generalized onset

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10
Q

Focal seizures

A

Begin focally in one hemisphere, often preceded by aura.

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11
Q

Focal seizures without altered awareness

A

Motor seizures that cause change in muscle activity
Sensory seizures that cause changes in any one of the senses
Autonomic seizures cause changes in a part of the nervous system that automatically controls body functions.
Psychic seizures can cause changes in how people think, feel, or perceive

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12
Q

Focal seizure with altered awareness (complex partial)

A 
Usually lasts 1-2 minutes. 
Starts in an area of the temporal lobe
May be preceded by an aura (or warning)
Automatisms (involuntary, automatic behaviors) 
Unaware of surroundings or may wander.
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13
Q

Focal seizures with secondarily generalization: loss of consciousness

A

Starts in one area but then spreads to both sides of brain

Short-lasting but may take longer to recover

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14
Q

Generalized seizures

A 
Begins in central brain (thalamus) region and spreads to both hemispheres. 
Tonic-clonic
Absence (petit mal)
Myoclonic
Atonic
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15
Q

Tonic-clonic (grand mal) seizure

A

Tonic phase- all muscles stiffen. Patient often loses consciousness and falls, Tongue or cheek may be bitten
Clonic phase- arms and legs begin to jerk rapidly. Consciousness returns but patient may be drowsy, confused. May take 30 min for patient to return to normal.

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16
Q

Absence seizure

A

Brief lapse in awareness, blank stare, rapid recovery

Bursting activity of calcium channels give rise to abnormality in thalamo-cortical circuit.

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17
Q

Myoclonic seizure

A

Consciousness preserved, short muscle jerks

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18
Q

Atonic seizure

A

Consciousness preserved. Loss of muscle strength bilaterally, patient falls

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19
Q

Status epilepticus

A

An epileptic seizure of longer than 5 minutes or 2 or more seizures within a 5 min period without person returning to normal.
Seizure can be tonic-clonic, complex partial, or absence
Mortality 22%
Causes severe brain inflammation and injury, functional deficits and epilepsy

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20
Q

What was the first anti-seizure drug?

A

Phenobarbital in 1912

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21
Q

Anti-seizure agents

A

Suppress the rapid and excessive firing of neurons during seizures.
Prevent the spread of seizures within the brain
Only provide symptomatic treatment with many AE
Have not been demonstrated to alter the course of epilepsy

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22
Q

Mechanisms of anti-seizure agents

A

Ion channels- drugs that enhance Na channel inhibition, inhibit T-type and voltage-activated calcium channels, activates K channels.
Receptors- GABA, Glutamate
Actions on synaptic vesicle protein (SV2A) or special Ca channels

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23
Q

Drugs that enhance Na channel closure

A

Agents prolong refractory period of sodium channel, thereby preventing repetitive neuronal firing
Target sodium channels opening and closing rapidly
Phenytoin, carbamezapine, lamotrigine, valproate, zonisamide, ruflinamide
Strong specificity for focal and secondarily generalized seizures.

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24
Q

Drugs that inhibit T-type calcium channels

A

Include ethosuximide, valproic acid

Effective against absence seizures, which involve abnormal calcium currents originating in the thalamus

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25
Q

Calcium channel drugs

A

Pregabalin and Gabapentin inhibit high voltage activated calcium channels. They are structurally related to GABA but their main action is to inhibit calcium channels and glutamate release

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26
Q

Potassium channel drugs

A

Ezogabine (only drug in class)
Activates voltage gated K channels
Stabilizes membrane potential and reduces brain excitability

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27
Q

Drugs that facilitate GABA mediated inhibition moa

A

GABA-A receptor is a chloride channel. Opening this channel hyperpolarizes neuron, making is less likely to fire.

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28
Q

Drugs acting on the GABA/ benzodiazepine receptor MOA

A

Benzodiazepines (diazepam)- bind to receptor and facilitates GABA mediated Cl flux. Positive allosteric modulators.
Barbiturates- also bind to GABA/ Benzo receptor to facilitrate chloride flux. Limited by their sedative properties.

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29
Q

Receptor targeting anti-seizure drugs: glutamatergic inhibitors

A

Drugs that diminish glutamatergic excitation
Felbamate, topiramate
Secondary effects to block glutamate receptor function (less excitation)
Perampanel selectively blocks glutamate receptors. 1st drug in class for tx of epilepsy.

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30
Q

Problems with sodium channel drugs

A

Phenytoin- saturation kinetics. Small increase in dose may lead to large increase in plasma concentrations and AE (hirsutism, cardiac and CNS depression).
Carbamazepine- induces more P450 system thereby decreasing its own 1/2 life and requiring more frequent dosing.

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31
Q

Problems with benzos/barbiturates

A

Limited due to dizziness, sedation, and abuse
Withdrawal- increased seizure frequency w/ abrupt d/c
Diazepam useful for aborting seizure acutely (status epilepticus)

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32
Q

Anti-seizure drugs and pregnancy

A

Possible teratogenic effects of valproate, phenytoin, topiramate
Minimize exposure to pregnant women, but they still need to be treated.

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33
Q

Epidiolex

A

FDA approved for Dravet and Lenox-Gastaut syndromes

Purified, plant derived cannabidiol (CBD)

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34
Q

Abnormal neurophysiology in seizures

A

Surround inhibition may be overcome, leading to increased neuronal discharge.

  • Increased extracellular K, weakening hyperpolarization
  • Rapidly firing neurons may activate glutamate receptors
  • Decreased GABA inhibition is a major factor. (there is no longer GABA inhibiting glutamate from exciting surrounding neurons)
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35
Q

Valproic acid MOA

A

enhance sodium channel inhibition, inhibit T-type calcium channels, increase GABA synthesis, and inhibit GABA metabolism

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36
Q

Gabapentin MOA

A

Facilitates GABA release (minor) and blocks calcium channels inhibiting neurotransmitter release (major)

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37
Q

Vigabatrin MOA

A

Inhibits GABA metabolism

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38
Q

Tiagabine MOA

A

Inhibits GABA reuptake by neurons and glia

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39
Q

Felbamate and Topiramate GABA MOA

A

Facilitate actions of GABA on receptor site

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40
Q

Stiripentol MOA

A

Facilitates GABA action

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41
Q

1st generation ASDs

A 
Phenobarbital 
Primidone (metabolized into phenobarbital)
Phenytoin
Carbamazepine
Valproate
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42
Q

1st generation ASDs

A 
Phenobarbital 
Primidone (metabolized into phenobarbital)
Phenytoin
Carbamazepine
Valproate
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43
Q

Phenobarbital forms

A

PO and IV

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44
Q

Phenobarbital metabolism

A

Hepatic

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45
Q

Phenobarbital- enzyme induction?

A

Yes CYP2C9/19 enzyme inducer

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46
Q

Phenobarbital half life

A

Very long 1/2 life (2-5 days)

Needs loading dose

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47
Q

Phenobarbital AE

A

Drowsiness, sedation, ataxia, CNS depression
Cognitive and behavioral, altered bone metabolism
Respiratory and CV effects with IV use

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48
Q

Phenobarbital therapeutic concentrations

A

19-40mcg/ml

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49
Q

How do you increase phenobarbital doses?

A

Increase every 2-3 weeks by 30-60 mg

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50
Q

Phenytoin forms

A

PO and IV

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51
Q

Phenytoin metabolism

A

Hepatic (CYP2C19)

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52
Q

Phenytoin protein bounding

A

Highly protein bound!
Check free concentration (1-2mcg/mL) in patients with low albumin, on other highly PPB drugs (valproate), patients with decreased renal function

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53
Q

Is phenytoin an enzyme inducer?

A

Yes, STRONG 3a4/5

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54
Q

Phenytoin dose-concentration profile

A

Non-linear

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55
Q

Phenytoin AE

A

Dose related- drowsiness, sedation, ataxia, nystagmus

Idiosyncratic- gingival hyperplasia, hirsutism, anemia, lymphadenopathy, altered bone metabolism, rash

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56
Q

Phenytoin IV administration

A

Max rate 50 mg/min but slower is safer

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57
Q

Phenytoin BBW

A

CV risk with rapid infusion (hypotension)

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58
Q

What should you monitor for for Phenytoin IV LD?

A

Hypotension and bradycardia

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59
Q

Phenytoin therapeutic concentration

A

10-20 mcg/ml

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60
Q

Rules to adjust phenytoin doses to avoid toxicity

A

7/11 rule
SS plasma level <7 mcg/mL - increase dose by 100 mg/day
SS plasma level 7-11 mcg/mL- increase dose by 50 mg/day
SS plasma level >11 mcg/mL- increase dose by 30 mg/day

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61
Q

Phenytoin patient counseling

A

Need regular dentist visits
Need labs
Do not crush ER capsules
Keep seizure diary

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62
Q

Carbamazepine forms

A

PO and IV

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63
Q

Carbamazepine metabolism

A

Hepatic, auto inducer (induces own metabolism)

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64
Q

Carbamazepine enzyme inducer?

A

Yes, 3A3/4/5

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65
Q

Carbamazepine AE

A

Dose related- drowsiness, sedation, diplopia, N

Idiosyncratic- hyponatremia, leukopenia, aplastic anemia, rash, decreased calcium absorption

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66
Q

Carbamazepine BBW

A

CV risk w/ rapid infusion

Fatal skin reactions/ Stevens-Johnson syndrome (HLA-B*1502 predictive)

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67
Q

Valproate forms

A

PO and IV

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68
Q

Valproate metabolism

A

Hepatic

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69
Q

Valproate PPB

A

Highly protein bound (90%)

PPB is saturable at higher doses

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70
Q

Valproate indications

A

Absence, simple, complex, and complex partial

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71
Q

Valproate increasing dose

A

Doses may be increased weekly by 5-10 mg/kg/day until effective or toxicity occurs

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72
Q

Valproate therapeutic concentration

A

40-120 mcg/ml

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73
Q

Valproate AE

A

Dose related- tremor, drowsiness, sedation, N/V, hepatotoxicity
Idiosyncratic- weight gain, hair loss, pancreatitis, decreased ca absorption

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74
Q

Valproate in pregnancy

A

Teratogen

Birth defects- spina bifida

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75
Q

Valproate brand names

A

Depakene, Stavzor, Depakote, Depacon

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76
Q

Valproate counseling

A

Lab- liver function tests, CBC, drug levels

Monitor for weight gain, increased appetite

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77
Q

Valproate BBW

A

CV risk with rapid infusion

Hepatotoxicity

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78
Q

Limitations of first generation ASD

A

Limited dosage forms available
All are hepatically metabolized
DDI
Significant AE

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79
Q

Phenobarbital MOA

A

GABA receptor agonist

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80
Q

Phenytoin MOA

A

Prolongs Na channel inactivation, thereby preventing repetitive neuronal firing

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81
Q

Phenytoin birth defect

A

Fetal hydantoin syndrome

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82
Q

Phenytoin saturation kinetics

A

Small increase in dose can lead to large increases in concentration and toxicity

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83
Q

Carbamazepine MOA

A

Prolongs Na channel refractory period thereby preventing repetitive neuronal firing

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84
Q

Ethosuximide

A

Inhibits T-type calcium channels

1st line for absence seizures

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85
Q

Felbamate form

A

PO

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86
Q

Felbamate metabolism

A

Hepatic

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87
Q

Felbamate indication/ when is it used?

A

Lennox-Gastaut Syndrome (LGS)
and partial seizures (focal)
Only used when benefit outweighs the risk due to hepatotoxicity and aplastic anemia
Informed consent must be signed prior to use

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88
Q

Felbamate MOA

A

Facilitates actions of GABA at receptor site, decreases glutamate excitation

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89
Q

Gabapentin form

A

PO

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90
Q

Gabapentin indication

A

Partial seizures w/wo secondary generalized seizures (tonic-clonic)

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91
Q

Gabapentin metabolism

A

Renal 100%

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92
Q

Gabapentin AE

A

Dizziness, drowsiness, sedation, weight gain

93
Q

Lamotrigine form

A

PO

94
Q

Lamotrigine metabolism

A

hepatic

95
Q

Lamotrigine AE

A

drowsiness, but may be the least sedating

96
Q

Lamotrigine BBW

A

Rash, serious skin rxns

Factors associated with rash- age <16, VPA use, high doses

97
Q

Lamotrigine dosing

A

On EIASD’s (phenobarbital, phenytoin, carbamazepine) W/O valproate= 25 mg QD for two weeks, increase after

On EIASD’s WITH valproate- 25 mg every other day for 2 weeks, then increase

98
Q

Lamotrigine MOA

A

Enhances Na channel closure, thereby preventing repetitive neuronal firing.
Acts on high voltage Ca channels

99
Q

Lamotrigine indication

A

Myoclonic, tonic-clonic

May be helpful in LG

100
Q

Topiramate MOA

A

Facilitates actions of GABA at receptor site, decreases glutamate excitation

101
Q

Topiramate forms

A

PO

102
Q

Topiramate metabolism

A

Renal

103
Q

Topiramate AE

A

Mental slowing, drowsiness, ataxia, dizziness, renal calculi, acute glaucoma, weight loss, oligohidrosis, paresthesia`

104
Q

Topiramate indications

A

Tonic-clonic or partial (focal) seizures

Adjunct treatment for LGS

105
Q

Topiramate titration

A

Slower titration for patients with decreased renal function or not on EIASD

106
Q

Tiagabine MOA

A

Inhibits GABA reuptake

107
Q

Tiagabine forms

A

PO

108
Q

Tiagabine metabolism

A

Hepatic metabolism

109
Q

Tiagabine PPB

A

Highly protein bound (>96%)

110
Q

Tiagabine indications

A

Adjunct for partial (focal) seizures

111
Q

Tiagabine AE

A

Dizziness, asthenia/lack of energy, somnolence, Nausea, nervousness

112
Q

Levetiracetam forms

A

PO and IV

113
Q

Levetiracetam indications

A

Adjunctive therapy for partial, myoclonic, and generalized tonic-clonic seizures

114
Q

Levetiracetam metabolism

A

25% hydrolyzed

75% renal

115
Q

Levetiracetam AE

A

headache, dizziness, somnolence, depression

116
Q

Oxcarbazepine indications

A

monotherapy for adults with partial seizures

Adjunct therapy for partial seizures in adults and children >4

117
Q

Oxcarbazepine AE

A

Dizziness, fatigue,. HA, hyponatremia ( more common than with carbamazepine), rash, diplopia/double vision, somnolence

118
Q

Who has the greatest risk of hyponatremia on oxcarbazepine?

A

Elderly patients on diuretics

119
Q

Zonisamide MOA

A

Enhance Na channel closure

T-type calcium channels

120
Q

Zonisamide forms

A

PO

121
Q

Zonisamide indication

A

Adjunct for partial seizures

122
Q

Zonisamide PK profile

A

Extensively bound to erythrocytes
Hepatic metabolism
Very long t1/2 (50-69 hours)
Up to two weeks to reach SS

123
Q

Zonisamide AE

A

Sulfonamide compound; possible skin reactions, Stevens-Johnson syndroms
Drowsiness, N/V, ataxia, kidney stones, anorexia, paresthesia

124
Q

Fosphenytoin

A

Phenytoin prodrug
Rapidly converted into PHT
Water soluble, not dissolve din propylene glycol, ethanol

125
Q

Fosphenytoin form

A

Only IV

126
Q

Fosphenytoin BBW

A

CV risk with rapid infusion

127
Q

Pregabalin MOA

A

Inhibit voltage gated calcium channels, inhibiting glutamate release

128
Q

Pregabalin forms

A

PO

129
Q

Pregabalin PK

A

Renal metabolism

>90% bioavailable

130
Q

Pregabalin indication

A

Adjunctive treatment for partial onset seizures

131
Q

Pregabalin AE

A

Dizziness, weight gain, edema, somnolence, ataxia, dry mouth, blurred vision

132
Q

Lacosamide (Vimpat) forms

A

PO and IV

133
Q

Lacosamide PK

A

Renal

134
Q

Lacosamide indication

A

Adjunct in partial onset seizures w/ epilepsy

Adjunct of primary GTC seizures >4 yo

135
Q

Lacosamide AE

A

Diplopia, HA, dizziness, N, ataxia, syncope, hypersensitivity rxns

136
Q

Lacosamide caution

A

Caution in patients with cardiac conduction problems (increases PR interval)

137
Q

Ruflinamide MOA

A

Na channel closure

138
Q

Ruflinamide form

A

PO

139
Q

Ruflinamide PK

A

Hydrolysis, not CYP dependent

140
Q

Ruflinamide AE

A

Somnolence, loss of coordination, dizziness, gait disturbances, QT shortening, ataxia`

141
Q

Ruflinamide indications

A

Adjunctive for LGS >4 years old

142
Q

Vigabatrin MOA

A

Inhibit GABA metabolism

143
Q

Vigabatrin form

A

PO

144
Q

Vigabatrin indications

A

Adjunct for adults with refractory complex partial seizures who have inadequately responded to other medications
Monotherapy for peds 1 month- 2 years with infantile spasms

145
Q

Vigabatrin PK

A

Renal excretion

146
Q

Vigabatrin AE

A

Permanent vision loss, anemia, somnolence, peripheral neuropathy, weight gain, edema

147
Q

Vigabatrin and vision loss

A

Permanent bilateral concentric visual field loss in 30% or more of patients
Need vision testing at baseline and every 3 months
SHARE rems progam

148
Q

Clobazam form

A

PO

149
Q

What makes clobazam unique?

A

It is the only 1,5 benzo available (the rest are 1,4)

150
Q

Clobazam indication

A

Adjunct for LGS in >2 years old

151
Q

Clobazam PK

A

Hepatic

152
Q

Clobazam AE

A

Somnolence, lethargy, dizziness, mood changes, irritability, more behavioral effects in children
Tolerance less likely than with other benzos

153
Q

Perampanel MOA

A

Selective AMPA type glutamate receptor noncompetitive antagonist

154
Q

Perampanel formn

A

PO

155
Q

Perampanel Use

A

Adjunct for partial onset > 12 yo

156
Q

When should you avoid perampanel?

A

In severe renal or hepatic disease

157
Q

Perampanel PK

A

70% urine elimination

Extensively metabolized by CYP then glucuronidation

158
Q

Perampanel AE

A

Dizziness, somnolence, HA, fatigue

159
Q

Perampanel DDI

A

Using with EIASDs significantly reduces T1/2. May need to start at higher doses and titrate up faster

160
Q

Eslicarbazepine MOA

A

Voltage gated sodium channel blocker

161
Q

Eslicarbazepine PK

A

Hydrolysis

90% urine excretion

162
Q

Eslicarbazepine indications

A

Adjunct for partial onset

163
Q

Brivaracetam MOA

A

Unknown, displays high affinity for sv2A in brain

164
Q

Brivaracetam uses

A

Adjunct for partial onset > 16 yo

165
Q

Brivaracetam form

A

PO, IV

166
Q

Brivaracetam PK

A

Hepatic metabolism

167
Q

Epidiolex indications

A

Seizures in LGS or Dravet syndrome >2 years old

168
Q

Epidiolex AE

A

Somnolence, decreased appetite, diarrhea, transaminase elevations, fatigue, malaise, asthenia, rash, insomnia, infections

169
Q

Stiripentol indications

A

Pts >2 yo who are taking clobazam for Dravet

170
Q

Stiripentol form

A

po

171
Q

Stiripentol PK

A

Hepatic

Highly PPB

172
Q

Stiripentol admin

A

Capsules must be swallowed whole with water during a meal

173
Q

Cenobamate moa

A

modulation of GABA channels and decrease excitatory currents by inhibiting sodium currents

174
Q

Cenobamate indication

A

partial onset seizures in adults

175
Q

cenobamate form

A

PO

176
Q

Cenobamate PK

A

metabolism by glucuronidation and oxidation

very long t1/2

177
Q

Cenobamate contraindication

A

Contraindicated in familal short QT syndrome

178
Q

Cenobamate ae

A

diplopia, N, somnolence, dizzinesss, fatigue, HA

179
Q

Fenfluramine indication

A

tx of seizures with Dravet syndrome >2 yo

180
Q

Fenfluramine BBW

A

Valvular HD

FINTEPLA REMS program

181
Q

Fenfluramine PK

A

hepatic metabolism

182
Q

Fenlfluramine AE

A

Decreased appetite, somnolence, sedation, lethargy, diarrhea, constipation, abnormal ECG, fatigue, malaise, asthenia, ataxia, balance disorder, gait disturbances, drooling, HTN, salivary hypersecretion, pyrexia, upper RTI, vomiting, weight loss, fall, status epilepticus

183
Q

Patient counseling: Oxcarbazepine

A

Dizziness, sedation, N/V

184
Q

Patient counseling: Levetiracetam

A

Behavioral changes, N/V

185
Q

Patient counseling: Topiramate

A

dizziness, paresthesias, weight loss, drink fluids

186
Q

Patient counseling: Lamotrigine

A

Dizziness, rash, N/V

187
Q

Patient counseling: Pregabalin

A

Peripheral edema, dizziness, weight gain

188
Q

Patient counseling: Lacosamide

A

Dizziness, HA, irregular heart beat

189
Q

Patient counseling: Ruflinamide

A

Somnolence, dizziness

190
Q

Patient counseling: Vigabatrin

A

Permanent vision loss

191
Q

Patient counseling: Clobazam

A

Sedation

192
Q

What are the default DOC for seizures?

A

Carbamazepine, phenytoin, oxcarbazepine

193
Q

What ASD do you avoid in bleeding?

A

Valproate

194
Q

What ASDs do you avoid in a history of a rash, hypersensitivity reaction, S-J syndrome?

A

Phenytoin, carbamazepine, lamotrigine, oxcarbazepine

195
Q

What ASDs do you use in a patient with hepatic impairment or if DDI are a concern?

A

Gabapentin, levetiracetam, pregabalin, topiramate, tiagabine, lacosamide

196
Q

What drugs do you use if you use for rapid titration?

A

Phenytoin, valproate, gabapentin, levetiracetam

197
Q

What is DOC ASD for the elderly?

A

Gabapentin

198
Q

What is the least sedating ASD

A

Lamotrigine

199
Q

Non-pharm seizure treatment

A

Surgery
Vagal nerve stimulation
Ketogenic diet

200
Q

Switching ASD

A

Start new ASD at a low dose and gradually increase dose. The previous drug should be tapered gradually.

201
Q

Stopping ASDs

A

Five criteria must be met:

  • No seizures for 2-5 years
  • Normal neurological examination
  • Normal intelligence
  • Single type of partial or generalized seizure
  • Normal EEG with treatment
202
Q

Methods of contraception and ASDs

A

Those with 1st pass hepatic metabolism most affected (morning after pill, oral contraceptive)
If choosing to take combined OCP, must contain 50mcg of estrogen at a minimum

203
Q

Levonorgestrol impants and ASDs

A

Contraindicated with enzyme inducers due to VERY strong failure rate

204
Q

Mirena coil and ASD

A

Releases progestin and is not affected by hepatic metabolism

205
Q

Depo-provera and ASD

A

Injections may need more frequent dosing

206
Q

ASDs that do not affect OCPs

A 
Gabapentin
Lacosamide
Levetiracetam
Pregabalin
Zonisamide
Valproate
Lamotrigine
207
Q

ASDs that affect OCPs

A 
Carbamezapine
Oxcarbemazepine
Phenobarbital
Phenytoin
Primidone
Topiramate
Felbamate
208
Q

Oral contraceptives decrease the concentrations of which ASDs?

A

Lamotrigine and valproate

209
Q

ASD use during pregnancy

A

Use one ASD if possible at the lowest possible dose. Use the most effective ASD.
Administer at least 4-5 mg/day folic acid

210
Q

Breastfeeding and ASD

A

Depends on protein binding property of ASD
Risk of sedation, irritability, failure to gain weight
Recommend baby nurse prior to taking ASD
Consider monitoring levels, especially for lamotrigine
No effect on cognitive outcomes

211
Q

Phenobarbital and valproate combo AE

A

Sedation and weight gain

212
Q

Phenytoin and carbamazepine AE

A

Dizziness and diplopia

Maintaining therapeutic doses can be difficult

213
Q

Valproate and lamotrigine combo

A

Requires adjustment of lamotrigine dose because of increased lamotrigine levels

214
Q

Topiramate, Lamotrigine, or zonisamide and enzyme-inducing drugs (carbamazepine, phenytoin)

A

Doses of the additive drugs to enzyme-inducers will need to be substantially higher because of increased clearance

215
Q

Benozodiazapines AE

A

Hypotension, CNS depression

216
Q

Emergency therapies for SE

A

Diazepam, Lorazepam, Midazolam

217
Q

Urgent therapies for SE

A

Brivaracetam, Fosphenytoin, Lacosamide, Levetiracetam, Phenobarbital, Phenytoin, Topiramate, Valproate

218
Q

Refractory therapies for SE

A

Ketamine, Midazolam, Pentobarbital, propofol

219
Q

Divalproex ER brand and dose

A

Depakote 500-750 TID

220
Q

Valproic acid brand and dose

A

Depakene, Stavzor

500-750 BID

221
Q

Phenytoin brand and dose

A

Dilantin 100-500 mg QD

222
Q

Levetiracetam brand and dose

A

Keppra, 500-1000mg BID

223
Q

Lamotrigine brand and dose

A

Lamictal 100-200 BID

224
Q

Pregabalin brand and dose

A

Lyrica, 100-200 bid

225
Q

Gabapentin brand and dose

A

Neurontin 300-600 TID

226
Q

Topiramate brand and dose

A

Topamax 50-100 mg BID

227
Q

Carbamazepine brand and dose

A

Tegretol XR, Carbatrol/Equestrol

200-600 BID

228
Q

Which drugs have renal elimination?

A

Gabapentin, Topiramate, Levetiracetam, Pregabalin, Lacosamide, Vigabatrin, eslicarbazepine, ezogabine, ruflinamide

Therapeutics 4 (8 decks)

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