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PATHO/PHARM II > Conditions Effecting the Nervous System and PharmacotherapyPart Three: Seizures > Flashcards

Conditions Effecting the Nervous System and PharmacotherapyPart Three: Seizures Flashcards

Exam 3

1
Q

Seizure Disorders & Epilepsy:

What are seizures?

A

Transient, sudden, uncontrolled discharge of neurons of the cerebral cortex interferes with normal function

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2
Q

Seizure Disorders & Epilepsy:

What changes occur with seizures?

What is something abnormal that occurs?

A

Physical or behavior △

Abnormal brain electrical activity

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3
Q

Seizure Disorders & Epilepsy:

What is a seizure disorder?

A

Epilepsy

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4
Q

Seizure Disorders & Epilepsy:

What is epilepsy? What are symptoms?

A

Recurrent unpredictable seizures

Sx: brief pds unconsciousness –> violent convulsions

Convulsions: jerking movements

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5
Q

Seizure Disorders & Epilepsy:

What are seizures initiated by?

A

Group of hyperexcitable neurons ~ focus

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6
Q

Seizure Disorders & Epilepsy:

What do neurons do in seizures?

How are neurons?

A

Neurons fire frequently with greater amplitude

Hypersensitive, easily activated by triggers

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7
Q

Seizure Disorders & Epilepsy:

Neurons are Hypersensitive, easily activated by triggers like what?

A

Hypoxia, hypoglycemia, hyponatremia, sensory stimulation

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8
Q

Seizure Disorders & Epilepsy:

Neurons are Hypersensitive, easily activated by triggers- why?

A

Results from hypoxia at birth, head trauma, brain infection, stroke, cancer, genetic disorders

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9
Q

Seizure Disorders & Epilepsy:

What kind of shift occurs?

A

Discharge from focus –> brain recruiting other neurons

Depolarization shift (Na+/K+/Ca+)

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10
Q

Seizure Disorders & Epilepsy:

Epilepsy patho: What can lead to this?

A

Genetic mutations & environmental effects

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11
Q

Seizure Disorders & Epilepsy:

Epilepsy patho: What are abnormalities?

A

Abnormalities in synaptic transmission, imbalance in brain’s excitatory & inhibitory NT

Development of abnormal nerve connections, loss of nerves after injury

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12
Q

Seizure Etiology

A

Idiopathic:

Acquired: secondary cause, cerebral damage (eg head trauma most common cause)

Prenatal causes: exposure to radiation, drugs in utero during 1st trimester, Pre-eclampsia, L&D, O2 deprivation

Congenital cerebral malformations/ genetic syndromes

Infants or young children with high fevers

Brain Infection

Space-occupying lesions/hemorrhage

Anoxia

Hypoglycemia

Cerebral edema

Degenerative brain disorders

CVAs

Ingesting toxic substances

Metabolic disturbances, electrolyte disorders

Drugs that lower seizure threshold/alcohol

NT: Glutamate vs γ-Aminobutyric acid (GABA)

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13
Q

Seizure Complications

A

Brain damage

TBI

Aspiration

Mood disorders

Status epilepticus

Risk of injury that may occur during violent shaking during a tonic-clonic grand mal seizure.

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14
Q

Precipitating Factors of Seizures:

Who can have a seizure?

A

Anyone can have a seizure

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15
Q

Precipitating Factors of Seizures:

A

Seizures can be triggered by environmental factors.

Loud noises and bright lights can bring on seizures, as well as biochemical stimuli and fluid retention.

Changes in medication, electrolytes or hypoventilation can bring on a seizure in an individual predisposed to seizures.

Hypoglycemia, lack of sleep, stress, drugs (withdrawal), women before menses

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16
Q

If someone is aware of precipitating factors that cause seizures what can they do?

A

A person with a seizure disorder, or who has a history of seizures, can avoid potential precipitating factors if they are aware of them.

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17
Q

Pathophysiology of Seizures:

A

When electrical impulses are discharged from different foci, or disorganized, abnormal motor and sensory activity result, along with a possible loss of consciousness.

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18
Q

Pathophysiology of Seizures:

How long do seizures last? What would effect them?

A

Seizures can last a few seconds or several minutes, depending on the extent of the neurons involved.

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19
Q

Pathophysiology of Seizures:

What can be used to determine the focus of activity and type of seizure?

A

EEG can determine the focus of the activity and the type of seizure.

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20
Q

Pathophysiology of Seizures:

During seizures, what is depleted?

A

During seizure, more O2 & glucose consumed & rapidly depleted

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21
Q

Pathophysiology of Seizures:

During seizures, what is accumulating?

What can this lead to?

A

Lactate accumulates in brain tissue

Can cause progressive brain injury/damage

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22
Q

Pathophysiology of Seizures:

What can clinical manifestations be used to determine?
What are clinical manifestations dependent on?

A

can also help determine the sz type.

Descriptions of onset of symptoms by witnesses can be beneficial in identifying the focus and type.

Sx depend on seizure focus & neuron connections to the focus

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23
Q

Classification: Partial Seizures

Where do they originate from?

A

Originating in one area of the brain (single or focal origin)

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24
Q

Classification: Partial Seizures

How do they spread?

A

Very limited spread to adjacent areas

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25
Q

What is a type of partial seizure?

A

Simple Partial (focal)

Complex partial (focal)

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26
Q

Simple Partial (focal): What can it be confused with?

A

Easily confused with other DX ~ migraines, syncope, psychiatric disorders

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27
Q

Simple Partial (focal): What is the focus of it?

A

Epileptogenic focus, related to a single area of damage in the cerebral cortex

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28
Q

Simple Partial (focal): What can occur before seizure happens? Epileptogenic focus, aka?

A

AKA an aura - Unusual sensation just before impending seizure when they precede more significant seizure activity

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29
Q

Classification: Partial Seizures

A

AKA an aura - Unusual sensation just before impending seizure when they precede more significant seizure activity

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30
Q

What does not occur with Simple Partial seizures?

A

⍉ loss of consciousness ~ persists for 20-60s

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31
Q

What are discrete symptoms of simple partial seizures?

A

Discrete symptoms:

Motor: twitching thumb, jerking movements in specific part of body

Sensory: numbness & visual, auditory, olfactory hallucinations

Autonomic: nausea, flushing, salivation, urinary incontinence

Psychoillusory: feelings of unreality, fear, depression, unexplained feelings of joy, sadness

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32
Q

Complex partial (focal)
What occurs during it?

A

Impaired consciousness & memory, lack of responsiveness ~ 45-90s

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33
Q

Complex partial (focal)
How do these seizures start? Then what happens?

A

Onset: motionless, fixed gaze then –> Automatism

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34
Q

Automatism:

A

repetitive, purposeless movements, lip smacking, blinking, hand wringing, circling, repeating phrases, clapping hands (multiple body parts affected)

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35
Q

Complex partial (focal)
What kind of experience is it?

A

Produces a dream-like experience

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36
Q

Complex partial (focal)
Where does it originate?

A

Originates in temporal lobe, frontal lobe, or limbic system

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37
Q

What may be present in Complex partial (focal) seizures?

What does it effect?

A

An aura or hallucination may be present, or sensation of déjà vu

Affects larger area of brain

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38
Q

Manifestations of focal seizures depend on ____

A

region of brain involved

Read slide 9

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39
Q

Classification: Generalized Seizures

What kind of activity occurs?
Are they convulsive or not?
What occurs immediately?

A

Abnormal activity on both sides of brain
May be convulsive or nonconvulsive
Immediate loss of consciousness

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40
Q

Classification: Generalized Seizures

What are the types?

A

Tonic-clonic (formerly grand mal)

Absence (petit mal)

Status epilepticus

Peds

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41
Q

Classification: Generalized Seizures

Tonic-clonic (formerly grand mal)
What are actions of patient?

A

Major convulsions –> loud cry –> forceful air expiration

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42
Q

Classification: Generalized Seizures

Tonic-clonic (formerly grand mal)
What happens to muscles?

A

Muscle rigidity (tonic phase) –> synchronous bilat jerks & shaking (clonic phase)

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43
Q

Classification: Generalized Seizures

Tonic-clonic (formerly grand mal)

How is consciousness? Urine continence?

A

Urine incontinence

Impaired consciousness –> CNS depression (postictal)

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44
Q

Classification: Generalized Seizures

Absence (petit mal)
Who does it occur in primarily? When does it stop?

A

Primarily peds, cessation typical by early teens

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45
Q

Classification: Generalized Seizures

Absence (petit mal)
What kind of activity occurs?

A

Brief LOC ~ 10-30s, hundreds/day

Mild, symmetric motor activity ~ eye blinking

Or ⍉ motor activity at all

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46
Q

Classification: Generalized Seizures

Status epilepticus: How long does it last?

A

≥ 15-30min

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47
Q

Classification: Generalized Seizures

Status epilepticus: What is it a series of?

How is consciousness?

A

Series of recurrent sz
No regain of consciousness

Generalized convulsive SE ~ life threatening

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48
Q

Classification: Generalized Seizures

When do seizures occur in Peds? What age is it common?
What occurs at that time?
What occurs for short periods?

A

Febrile
Common in peds 6m – 5yo
Short periods of generalized tonic-clonic

Atonic

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49
Q

Classification: Generalized Seizures

Peds: Atonic- What occurs?

A

Sudden loss of muscle tone
“Head drop” collapse

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50
Q

Myoclonic: what happens and when does it occur?

A

Jerking of arms, shoulder and head

Episodes typically occur soon after awakening?

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51
Q

Tonic-Clonic: What happens?

A

Look at picture

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52
Q

Three main phases of seizures:

Clinical Manifestations

A

Preictal Phase

Ictal

Postictal Phase

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53
Q

Three main phases of seizures:

Clinical Manifestations

What is part of the preictal phase?

A

Prodroma

Aura

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54
Q

Three main phases of seizures:

Clinical Manifestations

Preictal Phase: What are Clinical Manifestations during prodroma?

A

Early clinical manifestations:

Malaise

HA

Depression,

alterations in smell, taste, vision, hearing

can occur days to hours before seizure

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55
Q

Three main phases of seizures:

Clinical Manifestations

Preictal Phase: When do symptoms of prodroma phase occur?

A

Sx occur hours –> days prior to sz

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56
Q

Three main phases of seizures:

Clinical Manifestations

Preictal Phase: What occurs during aura?

A

A funny feeling

peculiar sensations

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57
Q

Three main phases of seizures:

Clinical Manifestations

Ictal Phase: What is it?

A

The event of the seizure

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58
Q

Three main phases of seizures:

Clinical Manifestations

Ictal Phase: What are the parts to the ictal phase?

A

Tonic phase

Clonic phase

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59
Q

Three main phases of seizures:

Clinical Manifestations

Ictal Phase: What occurs during Tonic phase?

A

A state of muscle contraction in which there is excessive muscle tone

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60
Q

Three main phases of seizures:

Clinical Manifestations

Ictal Phase: What occurs during Clonic phase?

A

A state of alternating contraction and relaxation of muscles

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61
Q

Three main phases of seizures:

Clinical Manifestations

Ictal Phase: How do symptoms range in ictal phase?

A

sx range from amnesia, pupils dilate, diaphoresis, cyanosis, frightened, crying, laughing, violent, angry behavior, incontinence

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62
Q

Three main phases of seizures:

Clinical Manifestations

Postictal Phase: How do symptoms range in ictal phase?

A

Sx: h/a, confusion, post seizure CNS depression, confusion, fatigue, deep sleep, memory loss

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63
Q

Three main phases of seizures:

Clinical Manifestations

Postictal Phase: When it is?

A

Time period immediately following cessation of seizure activity

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64
Q

DX of seizures how?

A

PMH
PE
Head CT, MRI, PET
Electroencephalogram
Lumbar puncture –
Labs
EKG

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65
Q

Dx seizure: What may Scans reveal?

What may Electroencephalogram reveal?

What does lumbar puncture reveal?

What does labs and EKG reveal?

A

Head CT, MRI, PET ~ may reveal trauma

Electroencephalogram ~ essential for DX & to localize focus

Lumbar puncture – infection

Labs – r/o metabolic disturbances

EKG – r/o cardiac dysrhythmias

66
Q

Classification: Generalized Seizures

What is treatment done before a seizure?

A

Prevention
Medical-alert bracelet
Avoid precipitating factors
Sleep deprivation, EtOH, illicit drugs, Excessive stimuli
Pharm: AEDs/anticonvulsants

67
Q

Classification: Generalized Seizures

What is drug treatment done before a seizure?

A

Pharm: AEDs/anticonvulsants

68
Q

Classification: Generalized Seizures

What is treatment done during a seizure?

A

position the individual on their side

protect head

⍉ forcing items b/w teeth

⍉ restrain(ts)

Manage airway, O2

Time the event & describe nature of event (eg – aura, muscle twitching, LOC, incontinence)

Ensure all pts with seizures/epilepsy have
IV access

69
Q

Generalized seizure: Treatment- what drug class for during a seizure?

A

Pharm: Benzodiazepines

70
Q

Classification: Generalized Seizures

What is treatment done after a seizure?

A

Allow them to rest

AEDs (anti-epileptics)

71
Q

Antiepileptic Drug (AED) Classification

AKA anticonvulsants

What are traditional AEDs?

A

Phenytoin
Carbamazepine
Valproic acid VPA
Phenobarbital

72
Q

Antiepileptic Drug (AED) Classification

AKA anticonvulsants

What are newer AEDs?

A

Gabapentin
Levetiracetam
Topiramate
Lamotrigine

73
Q

Antiepileptic Drug (AED) Classification

AKA anticonvulsants

What is a third group of drugs?

A

Benzodiazepines

ending in “pam”

74
Q

Antiepileptic Drugs AEDs:

What effects do they have (what do they suppress)?

A

Suppress discharge of neurons within seizure focus

Suppress spread of seizure activity from the focus to other areas of the brain

75
Q

Antiepileptic Drugs AEDs:

AEDs act through 4 basic mechanisms:

(But list 5 things)

A

Blockade of sodium channels

Blockade of calcium channels

Blockade of receptors for glutamate (an excitatory neurotransmitter)

Potentiation of GABA (an inhibitory neurotransmitter).

Suppression of K influx

76
Q

Antiepileptic Drugs AEDs:

AEDs act through 4 basic mechanisms:

Suppress Na influx/Promote K+ efflux:

A

Na entry thru gated pores cell membrane –> Action Potentials
Channel must be in activated state for sodium influx
Binding to inactivated Na channels
Prolong inactivation ~ ↓ firing @ high frequency
Na in  depolarization
K out repolarization (some drugs work here – promote K efflux – prolong repolarization)

77
Q

Antiepileptic Drugs AEDs:

AEDs act through 4 basic mechanisms:

Ca:

A

Influx of Ca –> transmitter release

Certain drugs block channels, transmission suppress

78
Q

Antiepileptic Drugs AEDs:

AEDs act through 4 basic mechanisms:

Glutamate: What is it? What does it do?

A

Glutamate ~ excitatory NT
Glu –> X –> NMDA receptors (works here)
Suppress neuronal excitation

79
Q

Antiepileptic Drugs AEDs:

AEDs act through 4 basic mechanisms:

GABA: What is it?

A

GABA ~ inhibitory NT in brain

80
Q

Antiepileptic Drugs AEDs:

AEDs act through 4 basic mechanisms:

GABA: What does it do?

A

↓ neuronal excitability & suppress seizure activity

81
Q

Antiepileptic Drugs AEDs:

AEDs act through 4 basic mechanisms:

GABA: ????????

A

Direct binding to receptors to GABA receptors

Benzodiazepines & barbiturates

82
Q

Antiepileptic Drugs AEDs:

AEDs act through 4 basic mechanisms:

GABA: Promotion of GABA release is by?

A

Promotion of GABA release
Gabapentin

83
Q

Antiepileptic Drugs AEDs: What are the goals of these drugs?

A

Reduce seizures to restore QOL

Balance b/w control & ADEs

84
Q

Antiepileptic Drugs AEDs cont: How is drug treatment?

A

Drug TX is highly individualized

85
Q

Antiepileptic Drugs AEDs cont: What is done to determine AED that should be used?

A

Several AEDs may be tried before

AEDs are selective for certain seizure d/o

Must match sz type with drug

Good history taking/EEG

Trial period

86
Q

Antiepileptic Drugs AEDs cont.

What is the order in which drugs are used?

A

Initial TX ~ one AED
Failure of initial TX
D/C 1st agent & start 2nd agent

2nd failure
3rd AED alone (not used prior) as mono-TX
Or- AED combo

87
Q

Antiepileptic Drugs AEDs cont.

Drug evaluation & adherence

A

Antiepileptic drug (AED) trial period
No guarantee seizure will be controlled

88
Q

Antiepileptic Drugs AEDs cont.

Patient & family ed

A

Avoid hazardous activities until control achieved

Chronic nature of disease

Importance of adhering to regimen

Seizure frequency chart/record events

89
Q

Antiepileptic Drugs AEDs cont.:

What should be monitored? Why?

A

Monitoring plasma levels

Evaluate adherence

Determine cause of lost seizure control
Identify cause of toxicity in pts taking > 1 drug

90
Q

Antiepileptic Drugs AEDs cont.

Withdrawal: How should meds be withdrawn?

A

May go into remission

⍉ guidelines indicating appropriate time to D/C

Slow taper ~ 6w to several months
D/C sequentially, ⍉ simultaneously

Failure to gradually reduce –> freq cause of SE

91
Q

Antiepileptic Drugs AEDs cont.

What effect do these drugs have on oral contraceptives?

So what must you have?

A

↓ Oral Contraceptive efficacy

Backup birth control

92
Q

Antiepileptic Drugs AEDs cont.

What are oral contraceptives considered?

A

Oral contraceptives are inducers= the med is metabolized quickly

93
Q

Antiepileptic Drugs AEDs cont.

What do they do to CNS? So what should you do?

A

CNS depression

Avoid hazardous activities until control achieved
Risk ↑ w/ concurrent depressants
⍉ EtOH consumption

94
Q

Antiepileptic Drugs AEDs cont.

How do these drugs effect fetus? What should be done?

What should be done to avoid problems for fetus?

A

Teratogenic

Benefit > risk

Avoid all traditional (some newer AEDs)

Folic acid for prevention

95
Q

Antiepileptic Drugs AEDs cont.

Suicide risk: How common?

A

May be lower than previously believed

Rare, ONLY certain AEDs NOT all

Higher risk when taken for epilepsy vs other conditions

Potential relation of psyc illness from epilepsy > medication

Pt & family ed to report warning sx

Screen all pts

96
Q

Use of AEDs in Select DX:

What traditional AED can be used in all types of seizures? What newer AED can be used in all seizures?

A

Traditional AEDs: Valproic acid

Newer AEDs: Lamotrigine

97
Q

Nsg Implications that apply to all AEDS

A

Know type of seizure

Educate pts to take med as rx’d

Teach pt/family to maintain seizure frequency chart, indicating date, time, nature of event

Advise pts to avoid potentially hazardous activities until seizure control achieved & to carry some form of ID b/c seizures may reoccur even after they’re under control

Be aware of ones that cause fetal harm/caution in breast-feeding

98
Q

Nsg Implications that apply to all AEDS:

ADRs:

A

Most AEDs cause CNS depression – warn pts against etoh & CNS depressant use

Abrupt discontinuation –> SE (must be over 6wks –> several months)

Take lowest effective dose during pregnancy & to reduce risk of neural tube deficits; advise women to take folic acid supplements before & throughout pregnancy

Educate pt/family about sx that might precede suicide: increased anxiety, agitation, mania, hostility

D/c use if severe skin reactions develop (more common in genetic mutation, which mostly occurs in Asian descent)

99
Q

Classification of Antiepileptic Drugs:

What are the two major categories?

A

Traditional AEDs

Newer AEDs

100
Q

Notable AEDs: Phenytoin(Dilantin)

What is the mode of action?

A

MOA: inhibition/blockade of Na+ channels so action potentials suppressed

101
Q

Notable AEDs: Phenytoin(Dilantin)

What is it used for?

A

Use: Partial & tonic-clonic seizures

IV for generalized convulsive SE

102
Q

Notable AEDs: Phenytoin(Dilantin)

What is the difficulty with this drug?

A

Absorption varies, hard to establish effective dose, standardize, with meals

Difficult to maintain plasma levels within the therapeutic range

103
Q

Notable AEDs: Phenytoin(Dilantin)

How is this drug taken? What happens?

A

Oral – chewable, ext Release
IV – hypotension (give slow), tissue damage if infiltrates

104
Q

Notable AEDs: Phenytoin(Dilantin)

How is this drug taken fast or slow? What happens?

A

Small increments in dosage produce sharp increases in plasma drug levels. HD = prolonged ½ life

Difficult to maintain plasma levels within the therapeutic range

105
Q

Notable AEDs: Phenytoin(Dilantin)

How is therapeutic index?

A

Narrow TI ~ CNS toxicity when above therapeutic levels, otherwise CNS effects mild

106
Q

Notable AEDs: Phenytoin(Dilantin)

Narrow TI ~ CNS toxicity when above therapeutic levels, otherwise CNS effects mild= how is this evident?

A

Nystagmus, sedation, ataxia, diplopia, cognitive impairment

107
Q

Notable AEDs: Phenytoin(Dilantin)

Drug Interactions (there are many – that ↑&↓ levels)

A

CYP-450 pathway inducer
Can decrease effects of OCs, warfarin, GCs
Etoh – may increase/decrease serum levels whether taken acutely/chronically

108
Q

Notable AEDs: Phenytoin(Dilantin)

ADRs?

A

Gingival hyperplasia

Dermatologic Reactions

CV effects:

Teratogenic

109
Q

Notable AEDs: Phenytoin(Dilantin)

ADRs: Gingival hyperplasia

What should be done to avoid?

A

Oral hygiene & supplement w/folic acid

110
Q

Notable AEDs: Phenytoin(Dilantin)

ADRs: Dermatologic Reactions

A

Measles-like rash, SJS or toxic epidermal necrolysis

If have genetic variant HLA-B* (Asian descent)

Notify prescriber

111
Q

Notable AEDs: Phenytoin(Dilantin)

ADRs: CV effects: Because of effects, how should meds be given?

A

Hypotension & cardiac dysrhythmias when adm by IV injection

Administer slowly

112
Q

Notable AEDs: Phenytoin(Dilantin)

ADRs: Teratogenic- WHat should be done?

A

Only use if safer ALTs ineffective

113
Q

Notable AEDs: Carbamazepine (Tegretol)

Mode of action?

A

delayed recovery of Na+ channels from inactive state

Suppresses high-frequency neuronal discharge in and around seizure foci

114
Q

Notable AEDs: Carbamazepine (Tegretol)

PO

A

Take IR & chewable with food

ER Capsules may be adm whole with food, opened & sprinkled on food, but contents shouldn’t be chewed or crushed

Shake suspensions well

115
Q

Notable AEDs: Carbamazepine (Tegretol)

What are the uses for this drug?

A

Partial & tonic-clonic seizures

116
Q

Notable AEDs: Carbamazepine (Tegretol)

What are ADRs?

A

CNS effects (nystagmus, blurry vision, diplopia, ataxia))

Derm
SJS & TEN, photosensitivity, measles-like rash
If have genetic variant HLA-B* (Asian descent)

Hematological

Hyponatremia/hypo-osmolality

Hepatic metabolism & inducer of enzymes

Teratogenic

117
Q

Notable AEDs: Carbamazepine (Tegretol)

What are Hematological effects?

A

Bone marrow suppression
Leukopenia, anemia, thrombocytopenia

CBC @ baseline & periodically

Report fever, sore throat, pallor, weakness, infection, bruising, petechiae

D/C if WBC < 3000/mm3

118
Q

Notable AEDs: Carbamazepine (Tegretol)

Hyponatremia/hypo-osmolality: Why does this occur?

A

ADH secreted
Water retention
Periodic monitoring of serum Na+ recommended
Monitor I&O

119
Q

Notable AEDs: Carbamazepine (Tegretol)

Hepatic metabolism & inducer of enzymes include? and what do they do?

A

↑ dose for warfarin & Oral Contraceptives
⍉ GFJ – may ↑ levels

120
Q

Notable AEDs: Valproic Acid VPA (Depakote):

How can it be taken?

A

PO ~ ER tabs with meals to avoid GI upset
Can be sprinkled on soft food, but not crushed

121
Q

Notable AEDs: Valproic Acid VPA (Depakote)

MOA: What does it block / suppress?

A

Blocks Na+ channels

Suppresses Ca+ influx thru channels

121
Q

Notable AEDs: Valproic Acid VPA (Depakote)

MOA: What does it augment?

A

May augment the inhibitory influence of GABA

122
Q

Notable AEDs: Valproic Acid VPA (Depakote):

What are its uses?

A

Partial & generalized, very broad-spectrum

123
Q

Notable AEDs: Valproic Acid VPA (Depakote):

What is the dangerous thing with this drug?

A

Highly Teratogenic, pregnancy is contraindicated

124
Q

Notable AEDs: Valproic Acid VPA (Depakote):

What should be done with pregnancy?

A

Advise woman use effective birth control

Take 5mg of folic acid to reduce risk of neural tube deficits if pregnancy occurs

125
Q

Notable AEDs: Valproic Acid VPA (Depakote):

ADEs

A

Liver injury (rare)

Fatal pancreatitis

Hyperammonemia

126
Q

Notable AEDs: Valproic Acid VPA (Depakote):

ADEs: Liver injury (rare)

A

High risk – younger than 2 yrs old receiving multidrug tx

Baseline & periodic LFTs, bleeding time

Report reduced appetite, malaise, nausea, abdominal pain, jaundice

127
Q

Notable AEDs: Valproic Acid VPA (Depakote):

ADEs: Fatal pancreatitis?

A

Report abdominal pain, distension, nausea, vomiting, anorexia, fever, malaise
D/C stat if (+)

Idiosyncratic reaction

? Reduces enzymes that remove free radical –> tissue damage

128
Q

Notable AEDs: Phenobarbital

What is the mode of action?

A

Potentiating effects of GABA

Binds to GABA receptors

Anticonvulsant barbiturate

129
Q

Notable AEDs: Phenobarbital

What are uses for this drug?

A

Partial seizures (simple & complex)

Tonic-clonic seizures

130
Q

Notable AEDs: Phenobarbital

What are Adverse Drugs Events?

A

CNS depression (lethargy, depression, learning impairment

Peds – paradoxical effect

131
Q

Notable AEDs: Phenobarbital

How is this drug administered?

A

PO

IV
Reserved for convulsive SE

132
Q

Notable AEDs: Phenobarbital

How is this drug with Pregnancy?

A

Risky in pregnancy
major fetal malformations

133
Q

Notable AEDs: Phenobarbital

What can this drug do differently from other barbiturates?

A

In contrast to other barbiturates, phenobarbital can suppress seizures without causing generalized CNS depression.

134
Q

Notable AEDs: Phenobarbital

How are effects?

A

Effects are modest.

Can reduce seizures without causing sedation

135
Q

Newer AEDS: What are benefits of them?

A

Better tolerated

Less fetal risk

Some are used for monotherapy, others as adjuncts

136
Q

Newer AEDS: Lamotrigine (Lamictal)

What is the mode of action?

A

Blocks Na & Ca channels
Both actions ↓ glutamate release, an excitatory NT

137
Q

Newer AEDS: Lamotrigine (Lamictal)

MOA: When Na and Ca channels are blocked, what does it cause?

A

Both actions ↓ glutamate release, an excitatory NT

138
Q

Newer AEDS: Lamotrigine (Lamictal)

What is the use?

A

Partial & generalized

Adjunct tx in peds & adults

Monotherapy in partial > 16y converting from another AED

139
Q

Newer AEDS: Lamotrigine (Lamictal)

What is the drug interactions?

A

CYP-450 inducers/inhibitors

Other AEDs, estrogens & progesterone can lower lamotrigine levels (concern with OCs)

140
Q

Newer AEDS: Lamotrigine (Lamictal):

ADRs and how is pregnancy?

A

Dizziness, diplopia, blurred vision, nausea, vomiting, ataxia and headache

Life-threatening severe skin reactions
-Concurrent use of valproic acid increase risk

Risk for suicide

Safer in pregnancy but small risk of cleft palate/lip

141
Q

Newer AEDS: Gabapentin (Neurontin)

What is the mode of action?

A

MOA: GABA analog, enhances GABA release, increases GABA-mediated inhibition of neuronal firing by pushing up GABA

142
Q

Newer AEDS: Gabapentin (Neurontin)

Use:

A

Use: adjunct tx of partial

143
Q

Newer AEDS: Gabapentin (Neurontin)

Off-label use:

A

Neuropathic pain, prophylaxis of migraine, treatment of fibromyalgia.

144
Q

Newer AEDS: Gabapentin (Neurontin)

For seizures, how much is given?

A

For seizures, higher dose is given

145
Q

Newer AEDS: Gabapentin (Neurontin)

What does it do to liver metabolizing enzymes?

A

Doesn’t inhibit/induce liver metabolizing enzymes

146
Q

Newer AEDS: Gabapentin (Neurontin)

How is it eliminated?

A

Eliminated mostly unchanged in urine

147
Q

Gabapentin (Neurontin):

ADRs:

A

Very well tolerated

Most common side effects: Somnolence, dizziness, ataxia, fatigue, nystagmus, increased appetite, irritability and peripheral edema

Monitor weight & behavioral changes

148
Q

Unique agent that is chemically and pharmacologically different from all other AEDs.

A

Levetiracetam (Keppra)

149
Q

Levetiracetam (Keppra):

What does it inhibit? What does it NOT do?

A

Inhibits excessive firing

Does not bind to receptors, GABA, or other NTs

150
Q

Levetiracetam (Keppra):

What are uses for it?

A

Use: adjunct treatment for general, monotherapy for partial, preventative

151
Q

Levetiracetam (Keppra)

How is it tolerated? Pregnancy and otherwise?

A

Better tolerated, less risk to fetus

152
Q

Levetiracetam (Keppra):

How does it interact with other drugs?

A

Less interactions w/other drugs as opposed to traditional ones

Started as adjuncts

153
Q

Levetiracetam (Keppra)

A

Mechanism of action: Unknown, binds to synaptic vesicle protein (SV2A), which is involved in the regulation of neurotransmitter release.

This helps stabilize neuronal activity and prevents seizure propagation.

154
Q

Levetiracetam (Keppra):

Adverse effects?

A

Adverse effects: Mild to moderate
Most common are drowsiness & lack of strength, weakness

155
Q

Levetiracetam (Keppra):
Drug interaction:

A

Drug interaction: Does not interact with other AEDs

156
Q

Levetiracetam (Keppra):

How is it given?

A

Can be given PO, IV
Adm with or w/o meals
Swallow whole
Infuse over 15 min

157
Q

Management of Generalized Convulsive Status Epilepticus SE

When should treatment be started? Why?

A

TX STAT ~ Give 5 min of onset
TX resistance with time progression

158
Q

Management of Generalized Convulsive Status Epilepticus SE

What occurs with the first line management?

A

Strong binding to the GABA-benzodiazepine receptor complex

Binding enhances the affinity for GABA (gamma-aminobutyric acid), a NT that plays a crucial role in inhibiting nerve impulses within the brain.

Calming Effect: By enhancing GABA’s inhibitory action, lorazepam helps reduce excessive neuronal activity, calming the brain.

159
Q

Management of Generalized Convulsive Status Epilepticus SE

What is first line management?

A

1st line management: Benzodiazepam (lorazepam/Ativan), diazepam (valium)

160
Q

Management of Generalized Convulsive Status Epilepticus SE:

Goals of treatment

A

Establish IV line ~ blood analysis: glucose, electrolyte, drug levels

Maintain ventilation

Correct hypoglycemia

Terminate seizures ~ initial BDZ -»drowsiness, dizziness, confusion, resp depression

Initiate or continue long-term suppression ~ phenytoin or fosphenytoin, levetiracetam

PATHO/PHARM II (27 decks)

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