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Epilepsy Flashcards

(59 cards)

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1
Q

Focal Seizure

A

Unilateral with local onset usually originates from cortical tissue

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2
Q

Generalized Seizure

A

Bilateral and originates from subortical or deeper brain focus.

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3
Q

Prodroma

A

early clinical manifestations of malaise, headache, and sense of depression
hours-few days before seizure onset

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4
Q

Aura

A

peculiar sensation preceding onset of focal seizure; gustatory (taste), visual or auditory experience; feeling of dizziness or numbness

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5
Q

Absence Seizure

A

sudden onset of interruption of activities, blank stare that lasts 20-30 seconds. No aura, prodroma, or postictal state

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6
Q

Myoclonic jerks

A

brief shock-like muscular contractions; single jerk or series of jerks. Synchronous and bilateral of the whole body. No alteration in concsiousness.

electric shock

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7
Q

Clonic

A

state of alternating contraction and relaxation of muscles; bilateral and more sustained/rhythmic than myoclonic

contract + relax

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8
Q

Tonic phase

A

state of muscle contraction with excessive tone (stiffening)

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9
Q

Tonic-clonic

A

initial tonic phase followed by clonic phase

stiff, contract, relax

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10
Q

Atonic

A

sudden loss of muscle tone

head drop, limb drop, or slumping

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11
Q

Post-ictal state

A

time period immediately following cessation of a seizure

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12
Q

Epilepsy

A

condition in which a person has recurrent seizures due to a chronic, underlying process

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13
Q

Seizures

Genetic causes

A

Juvenile Myoclonic Epilepsy (JME), Dravet Syndrome, Childhood Absence Epilepsy (CAE)
most common in childhood

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14
Q

Dravet Syndrome

A

mutations of voltage-gated Na+ channel type 1 alpha subunit (SCN1A)

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15
Q

Childhood Absence Epilepsy (CAE)

A

mutations in T-type Ca2+ channels and GABA receptor subunits

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16
Q

Seizures

Structural Causes

A
  • Mesial temporal lobe form occurs with sclerosis/glial scarring in hippocampus
  • Traumatic brain injury from blunt force or stroke
  • common in older adults
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17
Q

seizures

Infectious causes

A

the most common cause worldwide
development of epilepsy as sequele of infection
common in children

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18
Q

seizures

Metabolic and Immune forms

A
  • less common
  • metabolic: altered glycogen metabolism causes insoluble glycogen inclusion bodies
  • immune: anti-NMDA receptor encephalitis
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19
Q

Epilepsy risk factors

A

premature birth/low birth weight, family history, sleep deprivation, sensory stimuli, stress, hormonal changes can be associated with frequency

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20
Q

Drugs that Cause Seizures

A

theophylline, alcohol, phenothiazines, antidepressants, street drugs, or antiseizure drugs at toxic levels

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21
Q

Glutamate causes

A

excitation!

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22
Q

GABA causes

A

inhibition!

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23
Q

Status Epilepticus (SE)

A

a seizure lasting longer than 30 minnutes (now worry at 5 min) with/without impairment of consciousness or, occurence of recurrent seizures without intervening periods of consciousness

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24
Q

Status Epilepticus Causes

Study These Flashcards
A

results from initiation mechanism or failure of termination mechanisms leading to abnormally prolonged seizures
high incidence in children < 1 and elderly >60

25
Generalized Convulsive Status Epilepticus
most common and severe - repeated generalized seizures involving both hemispheres
26
Nonconvulsive Status Epilepticus
"epileptic twilight" altered consciousness and/or behavior
27
4 stages of generalized convulsive status epilepticus
1. impending (0-20 min) 2. established (20-40 min) 3. refractory (greater than 40-60) 4. super refractory (greater than 24h)
28
Status Epilepticus Phase 1
First 30 minutes - increase in NE, Epi, steroids (HTN, tachycardia) - increased insulin and glucagon due to initial hyperglycemia, then glucose decrease - muscle contractions/hypoxia lead to lactic acid release - muscle breakdown leads to secondary hyperkalemia
29
Status Epilepticus Phase 2
decompensation: hypotension, decrease in cerebral blood flow, excess oxygen, and glucose consumption **not sustainable so respiratory and metabolic acidosis**
30
# Pharmacology MOA Modulation of cation channels (Na+, K+, Ca2+)
1. prolongation of inactivated state of voltage gated Na+ channels 2. positive modulation of K+ channels 3. inhibition of Ca2+ channels
31
# Pharmacology MOA Modulation of GABA A and it's receptor
1. stimulation of GABA A receptors to enhance GABA neurotransmitters 2. modulation of GABA metabolism 3. inhibition of GABA reuptake
32
# Pharmacology MOA Acting on ________ to modulate synaptic release of neurotransmitter or on Ca2+ channels with the ____ subunit
SV2A protein, alpha2delta
33
# Pharmacology MOA ________ (decreasing, increasing) activation of ionotropic glutamate receptors: ____ and ____
decreasing, AMPA and NMDA
34
Benzodiazepine MOA
Clobazam, Clonazepam, Diazepam, Lorazepam **enhance GABA-mediated synaptic inhibition** BZD receptor is integral part of GABA A, it increases the **frequency** of the opening of GABA activated Cl- channels and leads to hyperpolarization/increased seizure threshold
35
What benzodiazepines used for status epilepticus?
Diazepam and Lorazepam at higher doses
36
Barbiturates MOA
phenobarbital and primidone **increases synaptic inhibition via GABA A receptor** increases **duration** of bursts of the Cl- current
37
Which barbiturate is a prodrug?
Primidone is rapidly metabolized to phenobarbital
38
Hydrantoins MOA
Phenytoin and Fosphenytoin (prodrug) **decreases repetitive firing of APs -- selectively slows rate of recovery of voltage-activated Na+ channels from inactivation** narrow therapeutic index, and 20% of patients develop Gingival hyperplasia
39
Iminostilbenes MOA
carbamazepine, oxcarbazepine, eslicarbazepine **slows rate of recovery of Na+ channels from inactivation**
40
What is carbamazepines black box warning?
hepatotoxicity and aplastic anemia
41
Oxcarbazepine is converted to
Eslicarbazepine which is then further converted to S-licarbazepine (faster than oxcarbazepine)
42
Oxcarbazepine/Carbamazepine HLA variant
HLA-B15:02 variant is associated with SJS, TEN ADRS -start low go slow-
43
Succinimides: Ethosuximide MOA
** inhibition of (post-synaptic) T-type Ca2+ channels to reduce Ca2+ current** significant effects in the thalamus, which exhibits large-amplitude T-type currents that underlie the APs
44
Gabapentin and Pregabalin MOA
**involves binding to a protein in cortical cell membranes that has an amino acid sequence identical to the Ca2+ channel subunit alpha2delta-1 and also binds to voltage-gated K+ channels** (inhibit Ca2+ and activate K+)
45
Lacosamide MOA
**first agent to prolong the slow inactivation of voltage-gated Na+ channels and limit sustained repetitive firing** also binds the phosphoprotein collapsin response mediator protein
46
Topiramate MOA
**reduces voltage-gated Na+ current with MOA similar to phenytoin** also activates hyperpolarizing K+ currents, enhances postsynaptic GABA A receptor currents, and decreases activation of AMPA-kainate glutamate receptors
47
Valproate MOA
**slows rate of recovery of Na+ channels from inactivation** also produces small reductions in T-type Ca2+ currents
48
Ezogabine MOA
**K+ channel opener - enhances outward K+ current mediated by KCNQ ion channel family - stabilizing resting membrane potential - reducing excitability** may also enhance GABA-mediated currents A/E: blue skin and lips
49
Felbamate MOA
**MIGHT: inhibit NMDA-evoked responses and potentiates GABA-evoked responses** no longer uses - life threatening adverse effects
50
Lamotrigine MOA
**slows rate of recovery of Na+ channels from inactivation** may inhibit synaptic release of glutamate
51
Perampel MOA
**first in class selective noncompetitive antagonist of AMPA-type ionotropic glutamate receptor** prevents repetitive firing and reduces excitory signaling needed for seizures
52
Levetiracetam and Brivaracetam MOA
**involves SV2A (blocks and blocks release of glutamate) mutation in SV2A associated with disruption in action potential invoked GABA release** - Levetiracetam: also inhibits N-type Ca2+ channels and release of Ca2+ - Brivaracetam: binds with high affinity to SV2A and inhibits voltage-gated Na channels
53
Rufinamide MOA
**prolongs slow inactivation of voltage-gated Na+ channels limiting sustained repetitive firing**
54
Tiagabine MOA
**Inhibits GAT-1 GABA transporter, reducing GABA uptake into neurons and glia, prolonging time GABA in the synapse** - can induce seizures in patients without epilepsy
55
Vigabatran MOA
**irreversible inhibitor of GABA transaminase resulting in increase GABA at receptor to enhance neurotransmission** transaminase breaks down GABA
56
Zonisamide MOA
**slows rate of recovery of Na+ channels from inactivation** also inhibits T-type Ca2+ currents
57
Cannabidiol MOA
**not mediated via cannabinoid receptors: 1. activation of the vanilloid receptor TRPV1 2. anatgonism of the orpha GPR55 and GPR55-mediated elevation of presynaptic Ca2+ 3. activation of 5HT1A receptors 4. competitive inhibition of the equilibrative nucleoside transporter 1 (ENT-1) to regulate adenosine tone** for Dravet, Lennox-Gastaut and drug resistant epilepsy
58
Cenobamate MOA
**Na+ channel inhibitor and non-BZD-type positive modulator of GABA A receptor (enhances GABA current)**
59
Fenfluramine (amphetamine derivative) MOA
**increase EC serotonin levels by inhibiting reuptake transporter SERT. Acts as agonists at 5HT2, 5HT1D, and 5HT2C receptors** dravet, lennox-gastaut, and drug-resistance epilepsy

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