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Seizures B&B Flashcards

1
Q

what are 4 electrolyte imbalances that can cause seizures, most often in children or elderly?

A
  1. hyponatremia
  2. hypernatremia
  3. hypoMg
  4. hypocalcemia
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2
Q

what are 5 components of seizure workup and the purpose of each?

A
  1. blood work - electrolyte imbalance can trigger seizure
  2. EKG - cardiac syncope can mimic seizure
  3. EEG - look for electrical abnormalities
  4. brain imaging (CT or MRI) - rule out tumor or stroke
  5. lumbar puncture - if infection is suspected
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3
Q

simple partial versus complex partial seizure

A

simple partial – no alteration in consciousness

Complex partial – altered consciousness

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4
Q

What are the four types of generalized seizures?

A
  1. absence/petite mal: staring off, blank stares
  2. Tonic clonic/grand mal: drop to the ground, writhing
  3. Atonic/drop seizure: drop, flaccid/ hypotonia
  4. Myotonic: rhythmic muscular contractions.
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5
Q

epigastric “rising” sensation is an autonomic symptom of seizures that is a common aura with ______ epilepsy

A

common aura with medial temporal lobe epilepsy

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6
Q

Jacksonian seizure

A

seizure aura of muscle jerking (simple partial seizure affecting motor cortex)

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7
Q

how do patients in the post-ictal state present?

A

transition period after a seizure in which brain recovers

patients show confusion and lack of alertness. Common focal neurological deficits may be present, variable time (mins-hours)

Helps differentiate seizure from cardiac cause - patients are immediately aware of their surroundings after regaining consciousness from cardiac problem

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8
Q

what is the most common site of partial seizures?

A

temporal lobe

many patients have mesial temporal sclerosis (hippocampal sclerosis) - lose neurons in hippocampus

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9
Q

mesial temporal sclerosis

A

aka hippocampal sclerosis - lose neurons in hippocampus

predisposes patients to temporal lobe seizures

often bilateral but one side more affected, can diagnose by MRI (looks like lesion in hippocampus)

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10
Q

how does juvenile myoclonic epilepsy present?

A

hallmark: myoclonic jerks on awakening from sleep, often presenting as shock-like irregular movements of both arms

absence seizures develop first (5yo) —> myoclonic seizures (15yo) —> grand mal seizures

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11
Q

child presenting with myoclonic jerks on awakening from sleep, often shock-like irregular movements of both arms =

A

juvenile myoclonic epilepsy

absence seizures develop first (5yo) —> myoclonic seizures (15yo) —> grand mal seizures

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12
Q

what is the prognosis of childhood absence epilepsy?

A

recurrent absence seizures (no change in body/motor tone) lasting a few seconds, NO post-ictal confusion

good prognosis, usually remits by puberty

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13
Q

A child is brought to the pediatrician by their parents, who are worried their child has an attention disorder. At parent teacher conferences, the child’s teacher said the child often stares off into space at class and is not paying attention. The teacher said they do this frequently, staring off for a few seconds before returning to focus. What could this be?

A

childhood absence epilepsy: recurrent absence seizures (no change in body/motor tone) lasting a few seconds, NO post-ictal confusion

good prognosis, usually remits by puberty

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14
Q

what is the classic EEG finding of childhood absence epilepsy?

A

2.5-5 Hertz spike wave activity superimposed on normal background EEG

recurrent absence seizures (no change in body/motor tone) lasting a few seconds, NO post-ictal confusion, usually remits by puberty

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15
Q

what does the following EEG finding indicate:

2.5-5 Hertz spike wave activity superimposed on normal background EEG

A

childhood absence epilepsy: recurrent absence seizures (no change in body/motor tone) lasting a few seconds, NO post-ictal confusion, usually remits by puberty

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16
Q

what is the treatment for childhood absence epilepsy?

A

recurrent absence seizures (no change in body/motor tone) lasting a few seconds, NO post-ictal confusion, usually remits by puberty

rx: ethosuximide is first line: blocks thalamic T-type Ca2+ channels

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17
Q

what is the mechanism and clinical use of ethosuximide?

A

first line tx for childhood absence epilepsy: blocks thalamic T-type Ca2+ channels

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18
Q

how do febrile seizures present in children? what is the prognosis?

A

common (2-4%) in children <5yo

Child loses consciousness, shakes – children at risk for more febrile seizures. However, overall prognosis is generally good (most kids outgrow them)

Not considered epilepsy

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19
Q

What is the treatment for seizures due to eclampsia?

A

magnesium sulfate (MgSO4) - only used for seizures due to eclampsia

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20
Q

status epilepticus

A

continuous seizure lasting more than 30 mins OR seizures that recur less than every 30 mins

medical emergency, can cause arrhythmias, lactic acidosis, HTN

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21
Q

what is the first line treatment for breaking seizures in status epilepticus? give drug class and DOC name

A

benzodiazepines - rapid acting, Lorazepam is DOC

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22
Q

Lorazepam is a _______ and is the DOC for ______

A

Lorazepam is a benzodiazepine and is the DOC for status epilepticus

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23
Q

Lorazepam (benzodiazepine) is DOC for breaking status epilepticus. If that is not working, _____ or _____ will be administered to prevent recurrent seizures. If patients are still seizing, ______ can be tried. If that doesn’t work, general anesthesia + intubate.

A

Lorazepam (benzodiazepine) is DOC for breaking status epilepticus. If that is not working, phenytoin (PO) or fosphenytoin (IV) will be administered to prevent recurrent seizures.

If patients are still seizing, phenobarbital can be tried. If that doesn’t work, general anesthesia + intubate.

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24
Q

what are the 2 categories of drugs used to prevent seizures?

A
  1. sodium inactivators: block channels —> less neuron activity
    (ex: phenytoin, carbamazepine, lamotrigine, valproic acid)
  2. GABA activators: inhibitory NT
    (phenobarbital, tiagabine, vigabatrin, also valproic acid)

[and of course there are drugs that work by other mechanisms not in these categories]

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25
Q

status epilepticus is always treated with _____

absence seizures are always treated with ______

A

status epilepticus is always treated with benzodiazepines

absence seizures are always treated with ethosuximide

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26
Q

what is the most teratogenic anti-epileptic drug?

A

valproic acid: 1-3% chance of neural tube defects (spina bifida)

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27
Q

what type of anti-epileptic drug is carbamazepine, and which types of seizures is it used for?

A

Na+ channel inactivator - used for partial and generalized seizures, also used for bipolar disorder and trigeminal neuralgia

MANY side effects
[A very PALE (anemic) man FELL OVER (ataxia) after DRINKING too much (liver toxicity) eating too many CARBS (carbamazepine) and was awoken by his friend STEVE (Stevens-Johnsons) who gave him a big bottle of WATER (SIADH)]

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28
Q

what are the clinical uses of carbamazepine? (4)

A

Na+ channel inactivator

  1. partial seizures
  2. generalized seizures
  3. bipolar disorder
  4. trigeminal neuralgia

MANY side effects!

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29
Q

what are the side effects of carbamazepine (used to treat seizures, bipolar disorder, and trigeminal neuralgia)? (6)

A
  1. diplopia, ataxia
  2. low blood counts/ bone marrow suppression - agranulocytosis, aplastic anemia, low WBC, low platelets (must monitor CBC)
  3. liver toxicity (must monitor LFTs)
  4. SIADH
  5. Stevens-Johnson syndrome (rash)
  6. hyponatremia

[A very PALE (anemic) man FELL OVER (ataxia) after DRINKING too much (liver toxicity) eating too many CARBS (carbamazepine) and was awoken by his friend STEVE (Stevens-Johnsons) who gave him a big bottle of WATER (SIADH)]

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30
Q

what side effects are associated with ethosuximide? (4) What is this DOC for?

A

blocks thalamic T-type Ca2+ channels, DOC for childhood absence seizures

adverse effects:
1. Stevens-Johnson syndrome
2. N/V
3. sleep disruption
4. fatigue, hyperactivity

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31
Q

what is the MOA of phenobarbital? what are the associated adverse effects (2 symptoms, 1 contraindication, 1 drug-drug interaction)?

A

barbiturate: GABA activator (holds Cl- channel open), anti-epileptic

adverse effects:
1. myocardial/respiratory depression
2. CNS depression (esp. w/ alcohol!!)
3. contraindicated in porphyria (heme disorder) - causes attacks of abdominal pain
4. induces P450

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32
Q

which 3 anti-epileptic drugs induce CYP450?

A
  1. carbamazepine
  2. phenobarbital
  3. phenytoin

recall induction of CYP450 causes drug levels to fall

33
Q

which 2 drugs that are metabolized by P450 are still used sustainably today, and must be monitored for interaction with drugs which inhibit P450?

A
  1. statins - combo with P450 inhibitor causes rhabdomyolysis
  2. warfarin

ex of P450 inhibitors: isoniazid, erythromycin, cimetidine, cyclosporin, azole antifungals, grapefruit juice, ritonavir (HIV)

[many P450 drugs are rarely used anymore - theophylline, cisapride, terfenadine, etc]

34
Q

which of the following is NOT a P450 inhibitor?
a. isoniazid
b. erythromycin
c. phenobarbital
d. azole antifungals
e. grapefruit juice
f. ritonavir (HIV)

A

c. phenobarbital

many anti-epileptic drugs are P450 inducers - cause there to be more metabolism of drugs

other inducers include: chronic EtOH, rifampin, carbamazepine, phenytoin

35
Q

for which type of seizures is phenytoin very useful?

A

Na+ channel inactivator, very useful for tonic-clonic seizures

36
Q

what adverse effects are associated with phenytoin (Na+ channel inactivator, treats tonic-clonic seizures)? (7)

A
  1. gingival hyperplasia
  2. rash
  3. folic acid depletion
  4. decreased bone density
  5. long term: nystagmus, diplopia, ataxia
  6. teratogenic
  7. hirsutism, facial coarsening

[PENNY (phenytoin) was a very WEAK (decreased bone density) girl trying to lift a heavy weight so hard that she got RED IN THE FACE (rash), BORE HER TEETH (gingival hyperplasia), and CROSSED HER EYES (diplopia)]

37
Q

describe the special metabolism of phenytoin (anti-epileptic)

A

dose-dependent hepatic metabolism - at low dose, there is a small increase in blood levels (first-order kinetics); at high dose, enzymes are saturated and there is a rapid increase in blood levels —> dose increments of equal size produce disproportional rise in steady-state plasma concentration (zero-order kinetics)

phenytoin induces but is also metabolized by P450! must monitor drug levels (oral contraceptives, warfarin, carbamazepine - caution with combination therapy!)

38
Q

describe the MOA (3) and clinical use of valproic acid (2)

A

MOA:
1. Na+ channel inactivator
2. GABA activator
3. inhibits T-type Ca2+ channels

clinical uses: anti-epileptic + mood stabilizer (bipolar, acute mania)

adverse effects: TERATOGENIC (spina bifida!), N/V, hepatotoxic, tremor, weight gain

39
Q

what kind of drug is levetiracetum, and what is its brand name?

A

aka Keppra: VERY effective anti-epileptic drug

exact mechanism unknown, useful for many types of seizures, drug titrated to clinical effect, well tolerated

40
Q

Lamotrigine

A

Na+ channel inactivator, broad-spectrum anti-seizure

caution: can cause Stevens-Johnson syndrome

41
Q

MOA and clinical use of Gabapentin

A

aka Neurontin

affects calcium channels (NOT GABA! they were wrong oh well)

used for seizures and neuropathies

can cause sedation and ataxia

42
Q

MOA, clinical use (2), and adverse effects (4) of topiramate

A

MOA: Na+ channel inactivator AND GABA activator

clinical use: seizures AND migraines

adverse effects: sedation, weight loss, kidney stones (weak carbonic anhydrase inhibitor)

43
Q

clinical uses of primidone (2)?

A

mechanism unclear, but metabolized to phenobarbital

  1. seizures
  2. essential tremor
44
Q

what are the 3 stages/degrees of focal onset seizures?

A
  1. focal aware
  2. focal with impaired awareness
  3. focal onset to bilateral tonic-clonic
45
Q

what are the 4 phases of generalized seizures?

A
  1. aura - peculiar sensation, dizziness, strange smell, numbness
  2. tonic phase - rigid muscle contraction, open eyes with dilated pupils (30-60s)
  3. clonic phase - rhythmic, jerking contraction and relaxation of all muscles (generalized convulsion), frothing at mouth, tongue biting, incontinence (several minutes)
  4. post-ictal state - drowsiness, confusion, or coma due to neural depression (several hours)
46
Q

contrast presentation of childhood absence epilepsy with juvenile myoclonic epilepsy

A

childhood absence epilepsy: ages 4-10, staring spells and arrested activity lasting ~10 seconds, EEG shows 2.5-3 Hz spike and wave discharges, tx = ethosuximide

juvenile myoclonic epilepsy: ages 12-18, myoclonus when awakening, exacerbated by sleep deprivation and alcohol, EEG shows 4-6 Hz irregular spike-waves and poly-spike waves (PSW)

47
Q

Benign Rolandic Epilepsy

A

aka childhood epilepsy with centrotemporal spikes

ages 4-15, infrequent seizures occurring during sleep

present with sensorimotor phenomena of face —> hyper-salivation, jaw contraction, speech arrest, etc

most kids outgrow it

48
Q

what is the triad of West Syndrome?

A
  1. infantile spasms
  2. delay in development
  3. hypsarrhythmia on EEG
49
Q

how do infantile spams present? how are they treated?

A

3-12 months old, idiopathic

spasms occur in clusters of briefly sustained movements of axial musculature (most commonly flexors), commonly upon awakening (sleep-wake transition), EEG shows chaotic high-amplitude and multi-focal spikes

tx: ACTH or prednisone

50
Q

Sandifer Syndrome

A

occurs in early childhood with intermittent spells of stiffening associated with feedings - pediatric manifestation of gastro-esophageal reflux

seen in neuro-developmentally normal children, normal EEG

treat with anti-reflux medications

51
Q

what are stereotypies?

A

Nonpurposeful, intermittent, and repetitive movements or
behaviors, usually seen in neurologically impaired children

Head shaking, head nodding, rocking movements, jumping,
tongue thrusting, chewing, hyperventilation, hand shaking and
tonic postures, etc

generally improve over time

52
Q

what does EEG of syncope vs seizures show?

A

syncope - high voltage delta flattening of EEG

seizures - spike waves on EEG

53
Q

what is a more soluble form of phenytoin (Dilantin) which can be administered IV?

A

phenytoin = Na+ channel inhibitor, anti-seizure drug

fosphenytoin: prodrug of phenytoin, designed for parenteral use

54
Q

for which types of seizures is phenytoin (Dilantin) contraindicated? (2)

A

may exacerbate
1. myoclonic seizures
2. absence seizures

55
Q

how does phenytoin (Dilantin) travel through the body?

A

Na+ channel inhibitor, anti-seizure

90% bound to plasma protein, but only free phenytoin can penetrate BBB

therefore, hypoalbuminemia can impact plasma levels (increased proportion of active drug)

56
Q

what are the contraindications (3) of carbamazepine (Tegretol, Carbatrol)?

A

Na+ channel inhibitor, anti-seizure

  1. exacerbates absence or myoclonic seizures
  2. blood disorders
  3. liver disorders
57
Q

describe the pharmacokinetics of carbamazepine (Tegretol, Carbatrol) - what is the clinical significance of this?

A

75% protein-bound, t1/2 falls significantly over first few weeks of therapy due to induction of hepatic enzymes (CYP) that metabolize itself - ”autoinduction”

patients who respond well to initial therapy may be mistakenly considered refractory if auto-induction phenomena is not taken into account

58
Q

which patients are at most risk of developing carbamazepine-induced Stevens-Johnson syndrome? What is the specific allele that causes the predisposition?

A

carbamazepine = anti-seizure Na+ channel inhibitor

incidence of Stevens-Johnson highest in Asian patients due to HLA allele B1502

patients with Asian ancestry should be screened for HLA B1502 before initiating tx w/ carbamazepine

59
Q

name 2 newer derivatives of carbamazepine (Tegretol, Carbatrol) with fewer adverse effects and NO auto-induction of CYP enzymes

A
  1. OXcarbazepine
  2. ESLIcarbazepine
60
Q

what are the indications of valproic acid/ valproate (Depakote)?

A

broad spectrum anti-seizure drug

  1. focal and generalized seizures
  2. absence, myoclonic, and atonic seizures
  3. photosensitive epilepsy, juvenile myoclonic epilepsy

ok so like everything got it

61
Q

describe the pharmacokinetics of valproate (depakote) - looking for 3 points here

A

90% protein bound and can displace other drugs from albumin

crosses the placenta —> highly teratogenic! (spina bifida!)

hepatic elimination and inhibits hepatic enzymes - caution with combination therapy of other anti-seizure drugs! (INCREASES plasma concentration)

62
Q

what are the adverse effects of valproate (Depakote)? (6)

A
  1. N/V, tremor, sedation, ataxia - transient symptoms
  2. alopecia
  3. weight gain
  4. thrombocytopenia
  5. hepatotoxicity - monitor LFTs
  6. teratogenic NEURAL TUBE DEFECTS - esp. spina bifida
63
Q

what are 2 other clinical uses of valproate besides seizures?

A

broad spectrum anti-seizure + migraine prophylaxis and bipolar disorder

64
Q

what are the mechanisms of action of lamotrigine (Lamictal)? (3)

A

broad spectrum anti-seizure

  1. Na+ channel inhibition - prolongs inactive state
  2. inhibits synaptic release of glutamate
  3. inhibits voltage-gated Ca2+ channels
65
Q

what are the adverse effects of ethosuximide (Zarontin)? (3)

A

DOC for absence seizures (inhibit thalamic T-type Ca2+ channels)

  1. GI distress (N/V, pain)
  2. urticaria, possible Stevens-Johnson syndrome
  3. leukopenia, thrombocytopenia, pancytopenia, aplastic anemia
66
Q

what is the mechanism of benzodiazepines and barbiturates?

A

enhance GABA(A) receptor-mediated inhibition of action potentials by enhancing influx of Cl-

benzodiazepines - increase frequency of receptor opening

barbiturates - prolong receptor opening

67
Q

what is the MOA and clinical use of phenobarbital (Luminal)?

A

binds GABA(A) receptor, prolonging chloride influx

indicated for all seizure types, especially those difficult to control (status epilepticus)

relatively low toxicity and low cost

68
Q

describe the pharmacokinetics of phenobarbital (Luminal)

A

indicated for all seizure types, esp. difficult to control (status epilepticus) - binds GABA(A) receptor to prolong chloride influx

metabolized by hepatic enzymes (CYP), also induces hepatic enzymes (CYP and UGT isozymes) —> drugs metabolized by these (oral contraceptives) will be more rapidly degraded

69
Q

_____ is a prodrug that is metabolized to phenobarbital in the body

A

primidone is a prodrug that is metabolized to phenobarbital in the body

70
Q

what is the mechanism of action of diazepam (Valium), lorazepam (Ativan), clonazepam (Klonopin), and clobazam (Onfi)?

what are the adverse effects?

A

benzodiazepines: bind to GABA(A) receptor and increase frequency of chloride channel opening

adverse effects: sedation, dependence, CNS depression (risk of cardio-respiratory depression), behavioral disturbances

limited by sedation, tolerance, and dependence

treat seizures, anxiety disorders, insomnia, NMJ disorders

71
Q

diazepam (Valium) and lorazepam (Ativan) are first line for…

what kind of drugs are these?

A

benzodiazepines: bind to GABA(A) receptor and increase frequency of chloride channel opening

first line for status epilepticus

72
Q

name 2 drugs which are first line for status epilepticus

A

diazepam (Valium) and lorazepam

benzodiazepines: bind to GABA(A) receptor and increase frequency of chloride channel opening

73
Q

what is the MOA and clinical use of tiagabine (Gabitril)?

A

GABA analog which inhibits GAT-1 GABA transporter —> reduces reuptake of GABA

used as adjunct therapy for focal seizures, off-label use for bipolar disorder, anxiety, neuropathic pain

74
Q

what is the MOA and clinical use of vigabatrin (Sabril)? which adverse effect should be monitored?

A

GABA analog which inhibits breakdown of GABA by targeting GABA transaminase

used as adjunct therapy for refractory complex focal seizures and monotherapy for infantile spasms

watch for renal toxicity!

75
Q

what is the MOA and clinal use of gabapentin (Neurontin) and pregabalin (Lyrica)?

A

designed to be GABA analogs BUT ACTUALLY INHIBIT VOLTAGE-GATED CA2+ CHANNELS containing alpha2delta1 subunit

used as adjunct therapy for focal and secondarily generalized seizures, also prescribed for neuropathic pain (fibromyalgia)

76
Q

what is the MOA and clinical use of levetiracetam (Keppra)?

A

binds synaptic vesicle protein 2A (SVP2A) protein and inhibits NT release

treats focal seizures (monotherapy), Lennox-Gastaut syndrome, primary generalized tonic-clonic seizures

renal clearance - contraindication with renal dysfunction

77
Q

what is the MOA and clinical use of perampanel (Fycompa)?

A

non-competitive antagonist of glutamate - binds AMPA receptor

new drug, adjunct therapy for adults with focal seizures and generalized tonic-clonic seizures

black box warning of serious psychiatric/behavioral adverse reactions — reserve for use after failure of other drugs

78
Q

what is the treatment protocol for status epilepticus?

A
  1. treat initially with benzodiazepine — lorazepam or diazepam via IV preferential
  2. followed fosphenytoin or phenobarbital

this treatment is done for any seizure lasting >5 minutes

Neuro (50 decks)

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