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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
status epilepticus is always treated with _____ absence seizures are always treated with ______
status epilepticus is always treated with *benzodiazepines* absence seizures are always treated with *ethosuximide*
26
what is the most teratogenic anti-epileptic drug?
*valproic acid*: 1-3% chance of neural tube defects (*spina bifida*)
27
what type of anti-epileptic drug is carbamazepine, and which types of seizures is it used for?
*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)]
28
what are the clinical uses of carbamazepine? (4)
Na+ channel inactivator 1. partial seizures 2. generalized seizures 3. bipolar disorder 4. trigeminal neuralgia MANY side effects!
29
what are the side effects of carbamazepine (used to treat seizures, bipolar disorder, and trigeminal neuralgia)? (6)
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)]
30
what side effects are associated with ethosuximide? (4) What is this DOC for?
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
31
what is the MOA of phenobarbital? what are the associated adverse effects (2 symptoms, 1 contraindication, 1 drug-drug interaction)?
*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
32
which 3 anti-epileptic drugs *induce* CYP450?
1. carbamazepine 2. phenobarbital 3. phenytoin recall induction of CYP450 causes drug levels to fall
33
which 2 drugs that are metabolized by P450 are still used sustainably today, and must be monitored for interaction with drugs which inhibit P450?
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
which of the following is NOT a P450 inhibitor? a. isoniazid b. erythromycin c. phenobarbital d. azole antifungals e. grapefruit juice f. ritonavir (HIV)
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
for which type of seizures is phenytoin very useful?
Na+ channel inactivator, very useful for *tonic-clonic seizures*
36
what adverse effects are associated with phenytoin (Na+ channel inactivator, treats tonic-clonic seizures)? (7)
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
describe the special metabolism of phenytoin (anti-epileptic)
*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
describe the MOA (3) and clinical use of valproic acid (2)
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
what kind of drug is levetiracetum, and what is its brand name?
aka *Keppra*: VERY effective anti-epileptic drug exact mechanism unknown, useful for many types of seizures, drug titrated to clinical effect, well tolerated
40
Lamotrigine
Na+ channel inactivator, broad-spectrum anti-seizure caution: can cause Stevens-Johnson syndrome
41
MOA and clinical use of Gabapentin
aka Neurontin affects *calcium channels* (NOT GABA! they were wrong oh well) used for *seizures* and neuropathies can cause sedation and ataxia
42
MOA, clinical use (2), and adverse effects (4) of topiramate
MOA: Na+ channel inactivator AND GABA activator clinical use: seizures AND migraines adverse effects: sedation, weight loss, kidney stones (weak carbonic anhydrase inhibitor)
43
clinical uses of primidone (2)?
mechanism unclear, but metabolized to phenobarbital 1. seizures 2. essential tremor
44
what are the 3 stages/degrees of focal onset seizures?
1. focal aware 2. focal with impaired awareness 3. focal onset to bilateral tonic-clonic
45
what are the 4 phases of generalized seizures?
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
contrast presentation of childhood absence epilepsy with juvenile myoclonic epilepsy
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
Benign Rolandic Epilepsy
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
what is the triad of West Syndrome?
1. infantile spasms 2. delay in development 3. hypsarrhythmia on EEG
49
how do infantile spams present? how are they treated?
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
Sandifer Syndrome
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
what are stereotypies?
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
what does EEG of syncope vs seizures show?
syncope - high voltage delta flattening of EEG seizures - spike waves on EEG
53
what is a more soluble form of phenytoin (Dilantin) which can be administered IV?
phenytoin = Na+ channel inhibitor, anti-seizure drug *fosphenytoin*: prodrug of phenytoin, designed for parenteral use
54
for which types of seizures is phenytoin (Dilantin) contraindicated? (2)
may exacerbate 1. myoclonic seizures 2. absence seizures
55
how does phenytoin (Dilantin) travel through the body?
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
what are the contraindications (3) of carbamazepine (Tegretol, Carbatrol)?
Na+ channel inhibitor, anti-seizure 1. exacerbates absence or myoclonic seizures 2. blood disorders 3. liver disorders
57
describe the pharmacokinetics of carbamazepine (Tegretol, Carbatrol) - what is the clinical significance of this?
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
which patients are at most risk of developing carbamazepine-induced Stevens-Johnson syndrome? What is the specific allele that causes the predisposition?
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
name 2 newer derivatives of carbamazepine (Tegretol, Carbatrol) with fewer adverse effects and NO auto-induction of CYP enzymes
1. OXcarbazepine 2. ESLIcarbazepine
60
what are the indications of valproic acid/ valproate (Depakote)?
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
describe the pharmacokinetics of valproate (depakote) - looking for 3 points here
*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
what are the adverse effects of valproate (Depakote)? (6)
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
what are 2 other clinical uses of valproate besides seizures?
broad spectrum anti-seizure + *migraine prophylaxis* and *bipolar disorder*
64
what are the mechanisms of action of lamotrigine (Lamictal)? (3)
broad spectrum anti-seizure 1. Na+ channel inhibition - prolongs inactive state 2. inhibits synaptic release of glutamate 3. inhibits voltage-gated Ca2+ channels
65
what are the adverse effects of ethosuximide (Zarontin)? (3)
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
what is the mechanism of benzodiazepines and barbiturates?
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
what is the MOA and clinical use of phenobarbital (Luminal)?
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
describe the pharmacokinetics of phenobarbital (Luminal)
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
_____ is a prodrug that is metabolized to phenobarbital in the body
*primidone* is a prodrug that is metabolized to phenobarbital in the body
70
what is the mechanism of action of diazepam (Valium), lorazepam (Ativan), clonazepam (Klonopin), and clobazam (Onfi)? what are the adverse effects?
*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
diazepam (Valium) and lorazepam (Ativan) are first line for… what kind of drugs are these?
*benzodiazepines*: bind to GABA(A) receptor and increase *frequency* of chloride channel opening first line for *status epilepticus*
72
name 2 drugs which are first line for status epilepticus
diazepam (Valium) and lorazepam *benzodiazepines*: bind to GABA(A) receptor and increase *frequency* of chloride channel opening
73
what is the MOA and clinical use of *tiagabine* (Gabitril)?
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
what is the MOA and clinical use of *vigabatrin* (Sabril)? which adverse effect should be monitored?
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
what is the MOA and clinal use of *gabapentin* (Neurontin) and *pregabalin* (Lyrica)?
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
what is the MOA and clinical use of *levetiracetam (Keppra)*?
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
what is the MOA and clinical use of perampanel (Fycompa)?
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
what is the treatment protocol for status epilepticus?
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

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