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Pharmacology II > Antiepileptics > Flashcards

Antiepileptics Flashcards

1
Q

_____ people experience a seizure during their lifetime

A

11%

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2
Q

_____ of people that have a seizure are diagnosed with epilepsy

A

3%

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3
Q

seizure activity reports ___ of emergency department visits

A

1%

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4
Q

recurrent seizures are associated with a ____ fold increased risk of sudden death

A

2.5

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5
Q

what are the impacts of epilepsy on quality of life

A
  • education: inadequate schooling
  • employment: unemployment levels are higher
  • independence: physical disability, fear of future seizures, cognitive consequences of disease and treatment, ineffective treatments, inability to obtain a drivers license
  • social isolation: depression
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6
Q

what is a seizure

A

a discrete clinical event that results in the abnormal discharge of a set of neurons in the brain

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7
Q

epilepsy is at least:

A

2 unprovoked seizures

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8
Q

what are acute repetitive seizures

A

seizure clusters over 1-2 days, usually less than 5 minutes, differs from normal pattern, recover consciousness between seizures

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9
Q

what is convulsive status epilepticus

A

failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms which lead to abnormally prolonged seizures
- length of seizures beyond 5 minutes
- second seizure without recovery from the first
- repeated seizures lasting 30 mins or longer

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10
Q

what is the pathophysiology of seizures

A

excessive excitation of cortical neurons (hyperexcitable/hypersynchronization)
- neuronal hyperexcitability
- alterations in the properties of ion channels in the neuronal membrane
- defects in ion transport across neuronal membranes
- abnormal synaptic vesicle protein 2-A
- biochemical modification of receptors
- modulation of second messaging systems and gene expression
- changes in extracellular ion concentrations
- alterations in neuroransmitter uptake and metabolism in glial cells
- modifications in the ratio and function of inhibitory circuits
- transitory imbalance in NTs

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11
Q

what is neuronal hyperexcitability

A

enhanced predisposition of neuronal depolarization and discharge when stimulated

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12
Q

what ion channels in the neuronal membrane are altered

A

Na+, Ca2+ and Cl-

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13
Q

what is synaptic vesicle protein 2-A responsible for

A

fusion of vesicles to membrane but get upregulated in some epilepsies

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14
Q

what are the imbalances in NTs

A

ehanced excitatory neurotransmission
- glutamate/aspartate
- NMDA/AMPA receptors

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15
Q

what are the epilepsy etiologies

A
  • genetic
  • structural
  • infectious
  • metabolic
  • immune
  • unknown
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16
Q

describe the genetic epilepsy etiology

A
  • usually present at a young age
  • dravet syndrome: mutations in sodium channel, type I alpha subunit
  • childhood absence epilepsy- mutations in T-type Ca2+ channels and GABA receptor subunits
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17
Q

what are the structural epilepsy etiologies

A
  • abnormalities found with neuronal imaging- cortical dysplasia, post traumatic epilepsy
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18
Q

what are the infectious etiologies of epilepsy

A

neurocysticercosis (parasite), meningitis, encephalitis

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19
Q

what are the metabolic epilepsy etiologies

A

abnormal glycogen metabolism (LaFora Disease)

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20
Q

what is the immune etiology of epilepsy

A

anti_NMDA receptor encephalitis (autoimmune)

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21
Q

what are the additional seizure etiological considerations

A
  • cerebrovascular abnormality
  • tumors
  • head trauma
  • infection
  • hypoxia
  • fever
  • medications and seizure meds: clozapine (dose), bupropion (dose), carbamazepine (SIADH), TCAs, phenothiazines
  • drug intoxication: cocaine, ephedrine
  • metabolic distrurbance: high or low
  • electrolyte disturbance: calcium, sodium, magnesium
  • alcohol withdrawal
  • sleep deprivation
  • hormonal changes
  • stress
  • prenatal or birth injury
  • congenital malformation
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22
Q

what are the seizure recurrence risk factors

A
  • abnormal EEG
  • seizure occurs during sleep
  • positive fam history (sibling)
  • prior acute seizure
  • downs syndrome and cerebral palsy
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23
Q

with downs syndrome and cerebral palsy:

A

there is no clear associate with seizure type, seizure length or age of onset

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24
Q

what are the seizure types

A
  • focal onset
  • generalized onset
  • unknown onset
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25
describe generalized seizures
- originate at some point within and rapidly engage bilaterally distributed networks - can include cortical and subcortical structures but not necessarily the entire cortex
26
describe focal seizures
- originate within networks limited to one hemisphere - may be discretely localized or more widely distributed
27
when a seizure type begins with "focal, generalized or absence" then the word ____ can be presumed
onset
28
what are the classifications of focal onset
- aware - impaired awareness - focal to bilateral tonic clonic - motor onset: - automatisms - atonic - clonic - epileptic spasms - hyperkinetic - myoclonic - tonic - Nonmotor onset: - autonomic - behavior arrest - cognitive - emotional - sensory
29
what are the classifications for generalized onset
- motor: - tonic-clonic - clonic - tonic - myoclonic - myoclonic-tonic-clonic - myoclonic- atonic - atonic - epileptic spasms - nonmotor (absence): -typical - atypical - myoclonic - eyelid myoclonia
30
what are the classifications for unknown onset
- motor: - tonic-clonic - epileptic spasms - nonmotor: - behavior arrest
31
focal seizures occur in:
one hemisphere
32
what are the types of focal seizures
- focal aware - focal impaired awareness - focal to bilateral tonic-clonic
33
what are the focal seizure subgroups
motor onset: - automatisms: lip smacking, rubbing hands, clothes picking - atonic - clonic - spasms - myoclonic - tonic nonmotor onset - autonomic - behavioral - cognitive - emotional - sensory
34
what are the types of generalized seizures
- absence (5-20 seconds) - myoclonic - clonic - tonic - tonic-clonic - atonic - infantile spasms
35
what does tonic mean
muscles in the body become stiff
36
what are the words used to describe generalized seizures
- tonic - atonic - myoclonic - clonic
37
what is atonic
muscle in the body relax
38
what is myoclonic
short jerking in parts of the body
39
what is clonic
periods of shaking or jerking parts on the body
40
describe childhood epilepsy
- many children become seizure free - most seizures are brief - rarely do seizures cause long term brain damage without neurologic insult- hypoxia in first 24-48 hours increases risk - medications may cause long term side effects - children with idiopathic first seizure and normal EEG have favorable prognosis
41
rule out_______ in childhood epilepsy
fever, infection, trauma
42
what do EEGs tell us
- graphical representation of cortical electrical activity - provides high temporal resolution, poor spatial resolution or cortical disorder - most important neuropsychological assessment tool for dx and tx
43
what is taken in a seizure disorder history
- identifiable source - precipitating event (stress) - age of onset/frequency - EEG patterns - severity - family hx - current meds - observe and note the before, during and after
44
what can be the sources in a seizure hx
- phenothiazines, TCAs, clozapine, bupropion - unmasking: CBZ, phenytoin, phnobarbital (absence)
45
what might labs show in precipitating event
- strss - hypoglycemia - hyponatremia - infection
46
what are the medications associated with lowering the seizure threshold
- theopylline - carbapenems - flouroquinolones - isoniazid - antidepressants - lithium - chlorpromazine - clozapine - cyclosporine
47
what is phase 1 of physiologic effects of continued seizure activity
- continued seizure activity - increased autonomic hyperactivity - hypertension - hyperglycemia - hyperpyrexia - sweating - salivation
48
what is phase 2 of seizure activity
- minor twitching - failure of cerebral circulation - decreased cerebral blood flow - increased intracranial hypertension - systemic hypotension
49
what are the considerations for starting therapy
- what is the risk for recurrent seizures - what is the expected benefit - tolerability of medications - patient values and preferences - unprovoked 1st seizure recurrence risk is 21-45% in following 2 years - after two or more unprovoked seizures
50
consider treating after first seizure if:
- idiopathic and abnormal EEG - symptomatic and abnormal EEG - prior neurologic or brain imaging abnormality - positive family history - nocturnal seizures
51
what are the treatment goals
- prevent occurrence of seizure: decrease frequency and severity - prevent or reduce drug side effects and drug interactions (no side effects) - prevent the development of neurologic changes - improve the patients quality of life
52
longer or repeated seizures =
more ischemia, increased risk of cognitive decline secondary to neuronal damage
53
how does treatment improve patients quality of life
- provide cost effective care - ensure patient satisfaction - prevent toxicity
54
what are the targets for treatment and the effect
- sodium channels: decrease AP frequency - calcium T type channel: decrease thalamocortical reverbs - calcium L type channel: decrease cortical excitation - calcium N type channel: decrease NT release - enhanced GABA transmission: increased inhibition - decreased glutamate transmission: decreased excitation
55
how is GABA transmission enhanced
- increased GABAa receptor activity - increased GABA synthesis - decreased GABA reuptake - increased serotonin release
56
how is glutamate transmission decreased
inhibit receptor/decrease release
57
what are the reasons treatments dont work
- inappropriate treatment: choose wrong drug - inappropriate dose - poor compliance/lack of education - drug storage issues - CBZ - drug administration issues - phenytoin suspension - drug interactions: cytochrome P450 and p-glycoprotein - seizure refractoriness
58
when can you consider trying to stop AED medications
- seizure free for 2-4 years - 2 years for absence - 4 years for focal and generalized tonic-clonic - normal neuro exam/ normal IQ - normal EEG with treatment - epilepsy of single seizure type - history of control within one year - no juvenile or myoclonic epilepsy
59
what are the seizure disorder meds
- dilantin (phenytoin) - luminal (phenobarbital) - tegretol (carbamazepine) - depakote (divalproex) - keppra (levetiracetam) - zonegran (zonidamide) - gabitril (tiagabine) - banzel (rufinamide) - briviact (brivaracetam) - onfi (clobazam) - cenobamate (Xcopri) - fenfluramine (Fintepla) - topamax (topiramate) - trileptal (felbamate) - lamictal (lamotrigine) - neurotonin (gabapentin) - lyrica (pregabalin) - zarontim (ethosuximide) - vimpat (lacosamide) - fyocompa (perampanel) - aptiom (aslicarbazepine) - epidiolex (cannabidiol) - valtoco (diazepam NS) - diacomit (stiripentol)
60
what are the FDA approved treatments for focal onset new dx
- carbamazepine - lacosamide - phenobarbital - phenytoin - topiramate - valproic acid - brivaracetam - cenmobamate
61
what are the FDA approved treatments for focal onset refractory adjunct
- carbamazepine - gabapentin - lamotrigine - levetiracetam - oxcarbazepine - phenobarbital - phenytoin - pregabalin - tiagabine - valproic acid - vigabatrin - zonisamide
62
what are the treatments for generalized absene
- lamotrigine - ethosuzimide - valproic acid
63
what are the FDA approved treatments for generalized tonic clonic
- lamotrigine - levetiracetam - topiramate - perampanel
64

Pharmacology II (13 decks)

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