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160 Cards in this Set

  • Front
  • Back
characteristics of epilepsy
1. recurring seizures
2. excessive, disorderly neuron discharge
3. instantaneous disturbance of sensation
4. loss conciousness
5. loss psychic function
epileptic Seizure classification
1. general seizures
2. partial seizures (local/focal)
3. other seizures
4 types of Generalized seizures
1. Tonic-clonic S.
2. Absence S.
3. Myo-clonic S.
4. A-tonic/A-kinetic S.
2 types of Partial Seizures
1. simple
2. complex
3 types of Micellaneous seizures
1. Symptomatic convulsions
2. Febrile seizures
3. Status Epilepticus
two most common types of seizures
1st most common:
Partial complex S.

2nd most common:
Generalized Tonic-Clonic S.
Tonic-clonic Seizures
1. 2nd most common
2. Two phases
a. Tonic Phase
b. Clonic Phase
Characteristics of Tonic Phase
1. ~1 minute long
2. loss conciousness
3. loss respiration
4. loss muscle rigidity
Characteristics of Clonic Phase
1. 2-3 minutes
2. Muslce jerking
3. lip/tongue biting
3. fecal/Urinary incontinence
4. post-ical depression
5. high voltage/frequency
6. cortical/bilateral/synchronous
Characteristics of Absence Seizures
1. Most common in children
2. Brief loss of conciousness
3. clonic movemts. eyelids, face, fingers
4. many attacks per day
5. S. may stop ~ age 20 y.o.
6. spike & dome waves
Seizures most common in children
Absence Seizures
Characteristics of Myo-clonic seizures
shock-like muscle contractions in one or more body areas
Characteristics of A-tonic/A-kinetic Seizures
1. loss muscle tone/strength
2. temporary paralysis
Tonic-Clonic seizures are also known as:
Grand Mal
Characteristics of Partial Simple Seizures:
1. Motor Dysfunction
2. Somato-sensory dysfunction
3. Visual dysfunction
4. Auditory dysfunction
5. Olfactory dysfunction
Partial Simple Seizures are also known as:
1. Cortico focal
2. Jacksonian
Characteristics of Partial Complex Seizures
1. Most common Seizures of all
2. Impared conciousness
3. Aura followed by mental confusion
4. Automatism followed by Amnesia
(inappropiate purposeful behaivior, oro-facial movmts., getting undressed)
5.Square waves
Do partial seizures evolve into generalized Seizures:
Yes, in 65% of patients
Characteristics of Symptomatic Convulsions
1. due to drug-overdose
2. disease-like (pre-clamsia, eclampsia)
3. No special classification of Seizure
Characteristics of Status Epilepticus
1. life-threatening emergency
2. due to abrupt withdrawal of anti-convulsant
3. charact. by succession of clonic-tonic convulsion without regaining conciousness between attacks
Causes of epileptics
1. genetic
2. developmental
3. infections
4. injury
5. tumors
6. degenerative disease
different MofA of anti-epileptic drugs:
1. Na+ Channel Inhibitor/blocker
2. GABA Enhacers
3. GABA transaminase inhibitors
4. Calcium channel blocker
5. K+ Channel permeability enhancers
6. Glutamate Receptor Blockers
7. NMDA Receptor Blockers
How do Na Channel Inhibitors work:
1. Block voltage-dependent Na Channels in neurons
2. Delay recovery of active Na channels
3. Inhibit generation of repetitive Action Potentials
4. Prolong inactivated state of Na Channels
How do GABA enhancers work:
Facilitate the inhibitory actions of GABA, which are excerpted through increased chloride ion conductance in brain.
The binding of the enhancer to the GABA/Benzodiazepine/Chloride ionophore complex results in increased hyperpolarization.
Increase duration of Chloride ion channel opening
How do GABA trans-aminase Inhibitors work:
Since GABA trans-aminase terminated the action of GABA, GABA trans-aminase inhibitors enhance/prolong the effects of GABA at the synapse.
How do Calcium Channel Blockers (CCB) work:
CCB inhibit low threshold (T-type) Calcium current, specially in the thalamic neurons that act as pacemakers to generate rhythmic cortical discharge.
How do K+ Channel Permeability Enhancers work:
Cause neuronal membrane hyper-polarization
How do Glutamate Receptor Blockers work:
Reduce excitatory effect of glutamate on brain. (Note: most neurons in brain are excited by Glutamic acid)
How do NMDA Receptor Blockers work:
NMDA is a sub-type of glutamate receptors also with excitatory effect on neurons. Thus, NMDA Receptor blokers reduce NMDA excitatoty effect on neurons.
List 8 "Na+ Channel Inhibitors/blockers"
1. phenytoin
2. carba-mazepine
3. primi-done
4. Valproic Acid
5. Lamo-trigine
6. Topiramate
7. Oxo-carbazine
8. Zoni-samide
List 9 GABA activity Enhancers
1. Phenobarbital
2. Primi-done
3. Valproic Acid
4. Benzo-diazepines
5. Gaba-pentine
6. Felba-mate
7. Topiramate
8. Tia-gabine
9. Viga-batrin
List 2 Calcium Channel blocker/Inhibitors
1. Etho-suximide
2. Phenytoin
List 2 Potassium permeability Enhacers
(increase hyperpolarization)
1. Valproic acid
2. Phenytoin
Glutamate inhibitor
NMDA Inhibitor
Unti-epileptics with unknown mechanism of action
1. Leve-tiracepam
2. MgSO4
Drug excerpting both Glutamate Receptor blocker & GABA activity enhancer
Gabapentin MofA
1. Glutamate Receptor Blocker
2. GABA activity enhancer
Drug acting both as NMDA inhibitor and GABA enhancer
Drugs acting as both Na Channel blocker and GABA activity enhancers
1. Valproic acid
2. Primidone
3. Topiramate
Phenytoin Mechanisms of action
1. Na Channel blocker/inhibitor
2. K+ channel permeability Enhancer
3. Calcium channel blocker
Valproic Acid Mechanisms of Action
1. Na Channel blocker/inhibitor
2. K+ channel permeability Enhancer
3. GABA activity enhancer
Gabapentin Mechanisms of Action
1. Glutamate Receptor blocker
2. GABA activity enhancer
Felbamate Mechanisms of Action
1. NMDA receptor inhibitor
2. GABA activity enhancer
Topiramate Mechanisms of Action
1. Na Channel blocker/inhibiitor
2. GABA activity enhancer
desired outcomes from anti-epileptic treatments: increase ___ and decrease___.
1. increase GABA activity
2. decrease NMDA activity
3. decrease Glutamate activity

4. increase K influx
5. decrease Na influx
6. decrease Ca influx
Phenytoin net efffect
lower Action potentia (AP)
lower convulsions
Elimination of Phenytoin is ____ order
zero order
Penytoin is metabilized/inactivated by
Phenytoin goes through 1st Pass metabolism (true/false)
Phenytoin is hyghly protein bound (90%) therefore proteins that compete for protein binding increase free circulating levels of phenytoin and increase toxicity
Drugs that increase free phenytoin and its toxicity are____ &______ because they compete for binding to plasma proteins
1. Valproic acid
2. Sulfonamides
Drugs that induce expression/activity CYP 3A3 & 3A4
1. Phenytoin (+)
2. Phenobarbital (+)
3. Rifampin (+)
Drugs that inhibit expression/activity CYP 3A3 & 3A4
1. Grapefruit (-)
2. cimentidine (-)
3. Iso-niazid (-)
Phenytoin induces its own metabolism (true/false)
True, by inducing CYP 3A3/3A4
Phenytoin is used as 1st choice drug for
1. Generalized Tonic-clonic
2. Partial simple
3. Partial complex
Fos-phenytoin is:
1. Phenytoin pro-drug
2. water soluble
3. given para-enterally
Fos-phenytoin is prescribed for:
Status Epilepticus
Adverse effects of Phenytoin at any dose:
1. gingybal hyper-throphy
2. coarsening of facial features
3. hirsutism (hairyness)
Adverse effects of Phenytoin at high dose:
1. Eye rollong (Nystagmus)
2. low muscle coordination (ataxia)
3. Diplopia
4. Osteoporosis
5. higher metabolism of Vit. D, Warfaring, oral contraceptives
Phenytoin contraindications
1. Non-clonic-tonic generalized seisures
(Absence, Myoclonic S., Atonic/akinetic)
2. Sinus bradicardia (b/c lower HR)
3. SA/AV block
Phenytoin is effective against Absence Seizures (true/false)
false, it is contraindicated for all generalized S. (except for tonic-clonic S.) it can worsen this S. if given alone
Phenytoin is effective against Myo-clonic Seizures (true/false)
Phenytoin is effective against Atonic/Akinetic Seizures (true/false)
Carbamazepine m of A
1. Na channel blocker
2. acts presynaptically to decrease synaptice transmition
Carbamazepine 1st drug choice for
1. Generalized tonic-clonic S.
2. Partial simple S.
3. Partiall complex S.
4. trigeminal neuralgia (other use)
Adverse effects of Carbamazepine at any dose:
1. Aplastic anemia (rare but fatal)
2. Agranulocytosis (rare but fatal)
3. skin rash
Adverse effects of Carbamazepine at high dose:
1. Diplopia
2. ataxia
3. GI upset
4. Hyponatremia
5. cranio-facial abnormality (in offspring if pregnant))
6. spina bifida (offspring if pregnant)
Why is carbamazepin at high dose contraindicated in pregnant women;
high doses can cause
1. cranio-facial abnormalities in offsprig
2. spina-bifida in offsprig
Carbamazepine contraindications
use of carbamazepine alone for any non-tonic-clonic generalized seizures is contraindicated becaue it can worsen seizures. Can be given for this seizures only adjuvant to Valproic acid or Ethosuximide
Carbamazepine is the active compound (true/false)
False, carbamazepine-10-11-epoxide is the active metabolite
carbamazepine induces its own metabolism through CYPs (true/false)
Drugs that inhibit the matabolism of carbamazepine
1. Grapefruit
2. valproic acid
Drug used for trigeminal neuralgia
phenobarbital mechanism of action
1. GABA action enhancer (diff. binding site that Benzodiazepin)
2. directly increase Cl ion transport
Phenobarbital 1st drug use
none, eventhough it is very effective and relatively safe it is not 1st choice drug
Phenopbarbital is a CYP inducer (True/False)
true, induces its own and other drug metabolism
Phenobarbital prescribed for:
1. Generalized Tonic-clonic Seizures
2. Partial Simple s.
3. Partial complex s.

(note: not 1st choice drug for these s.)
Adverse effects of phenobarbital at high doses:
1. Drowsiness in adults
2. agitation/hyperactivity in kids
3. generalized Muscle pain
4. impotence/decreased libido
5. osteoporosis (b/c increase Vit. D. metabolism)
6. Birth deffects on offsprings
Penobarbital is prescribed at low doses during pregnancy, but high doses can cause birth defects on offsprings
True, low doses are recomended to avoid seizures because the fetus is at risk during seizures
It is ok to stop phenobarbital treatment during pregnancy (true/false)
False, low doses of phenobarbital are recomended during pregnancy, but should NOT STOP phenobarbital treatment because fetus is at risk during seizures
Penobarbital contraindications
1. non-tonic-clonic generalized seizures
2. Sudden withdrawal
sudden withdrawal of phenobarbital can result in:
1. exacerbated seizures
2. Status epilepticus (life threatening)
primidone mechanism of action
1. primidone: block Na channels
2. primidonne metabolite: GABA activity enhancer
primidone first choide drug for:
Nothing, it is effective and relatively safe, but not 1st drug choice
Primidone increases metabolism of itself and other anti-epileptic drugs (true/false)
Primidone drug uses
1. Generalized tonic-clonic seizures
2. Partial Simple s.
3. Partial Complex
4. other: febrile seizures
Febril seizures can be treated with
1. primidone
2. diazepam (benzodiazepine)
Adverse effects of Primidone
1. Drawsiness in adult
2. Agitation/hyperactivity in kids
3. Muscle pain
4. Impotence/low libido
5. osteoporosis

(SAME A.E. as Phenobarbital)
Primidone contraindications
1. non-tonic-clonic generalized seizures
2. Sudden withdrawal

(same Contraindications as phenobarbital)
Adverse Effects include:
1. Drawsiness in adults
2. Agitation/hyperactivity in kids
3. osteoporosis
4. Impotence/decrease libido
5. Muscle pain
1. phenobarbital
2. Primidone
Etho-suxi-mide MofA
1. blocks T-type Ca channels in neurons
Ethosuximab is metabolized by CYP 3A4 (true/false)
Ethosuximide induces its own metabolism (true/false)
Ethoximide does not penetrate fat, therefore, its distribution is uniform
Ethoxumide is first choice drug for
Absence Seizures
Adverse effects of Ethosuximide
1. worsens/induce other seizures
2. headache/fatigue/lethargy
3. GI distress
Ethoxumide contraindications
1. Tonic-clonic Seizures
2. Partial (simple/complex) S.

(unless used adjuvant to appropiate anti-convulsant)
Valproic acid MofA
1. GABA enhancer
2. K+ permeability enhancer
3. Na+ channel blocker
Valproic acid is highly bound to protein (true/false)
true, VA is 90% bound to plasma protein. It can displace phenytoin from binding plasma protein and decrease its half-life.
Valproic acid is a CYP inducer
False, VA is a CYP INHIBITOR. It inhibits its own and other anti-epileptics metabolism, thus increasing half-life.
Valproic acid is recommended as monotherapy
Valproic metabolite is Fatal
true, VA metabolite is rare but fatal
Valproic Acid is used against:
1. All Generalized Seizures
2. All Partial (simple/complex) seizures
adverse effects of Valproic Acid at low dose:
1. Hepatotoxicity (rare)
2. weight gain
3. hair loss
adverse effects of Valproic Acid at high dose:
1. Tremor
2. GI distress
Valproate & Depakote cause less GI distress than Valproic Acid
True, because they are enteric coated and are taken with meals
MofA of Benzodiazepines
GABA activity enhancers
(useful b/c RAPID ONSET of action)
Benzodiazepin analogs
1. Di-azepam
2. Clon-azepam
3. Lor-azepam
Short acting benzodiazepin

onset: immediate (useful in emergency)
duration: 30 minutes
Long acting Benzodiazepines
1. Clon-azepam
2. Lor-azepam

onset: 20-30 minutes
duration: 6-8 hours
Benzodiazepines are used for:
1. Abscence Seizures
2. Myo-clonic S.
3. other: Status Epilepticus
4. other: febrile Seizure
Lorazepam is specially useful for the treatment of febrile seizures
False, diazepam is used to treat febrile seizures due to its immediate action
Adverse effects/limitations of benzodiazepines (-azepams)
1. sedation in adults
2. hyperactivity in kids
3. Develop TOLERANCE (w/in months)
Mechanisms of action of Gabapentin
1. Glutamate Receptor Inhibitor (lower excitatory effect of glutamic acid)
2. GABA activity enhancer (does not appear to act on GABA receptors)
Gabapentin is an amino acid
true, gabapentine is an AA with similar structure to GABA
Gabapentin is liver metabolized
Gabapentin uses
1. Neuropathic pain
2. Diabetic nephro-pathic pain
3. Partial Seizures (as adjuvnt therapy)
Adverse Effects of Gabapentine at high dose
1. Drowsiness
2. Dizziness
3. Ataxia
Amino acid with structure similarity to GABA used as anti-epileptic
Lamo-trigine MofA
block Na channels and as a result decrease glutamate and aspartate release.
Lamo-trigine uses
Partial (simple/complex) seizures
(monotherapy or adjunct)
Lamotrigine adverse effects
1. Dizziness (CNS complaint)
2. Headache (CNS complaint)
3. Ataxia
4. Rash
Felbomate MofA
1. NMDA receptors inhibitor
2. GABA activity enhancer
NMDA receptor inhibiitor
Felbamate uses
1. Partial (simple/complex) seizures
2. Multiple Seizure conditions
Dose-related adverse effect of Felbamate
1. Aplastic Anemia
2. Liver Failure
3. GI distress
4. CNS complaints
Topiramate MofA
1. Na channel blocker
2. GABA activity enhancer
3. AMPA receptor inhibitor (inhibit Gluutamate excitatory response)
Topiramate used against___ & ____ seizures:
1. Tonic-clonic Seizures
2. Partial (simple/complex) seizure
In addition to epilepsy, Topiramate is also used for:
1. Essential tremor
2. Migrane
3. cocaine addiction
Topiramate adverse effects:
1. Fatigue/dizzy/nervous/confused
2. tingling
3. teratorgenic in animals
anti-epilectic used to treat essential tremor, migrane, and cocaine addiction:
anti-epileptic teratogenic in animals
Tia-gabine Mofa
GABA reuptake transporter inhibitor in neurons and glial cells, thus increase GABA activity
Tia-gabine is highly protein bound
Tia-gabine uses
Partial (simple/complex) seizures
(monotherapy or adjunct)
Adverse effects of Tiagabine
1. Depresion
2. difficult concentrating
3. tremor
4. CNS complaints
Viga-trin MofA
GABA trans-aminase Inhibitor. Inhibits GABA metabolism, thus increaseing GABA activity at synapse
GABA trans-aminase inhiibiitor
Vigratrim is used as adjunct treatment in
Partial (simple/complex) seizures
Vigatrim adverse effects
(mira la viga en tu ojo)
1. Eye problems
-eye pain
-eye rolling
-blurred vision
-decreased vision
2. weight gain
3. mood/mental changes
Oxycarbazine MofA
Na channel blocker
Oxy-carbazine is metabolized to hydroxy-carbazyme active metabolite
Oxycarbazine is used against ____seizures
partial (simple/complex) seizures
Oxycarbazine adverse effects
not listed!
Zoni-samide MofA
Na channel blocker
Zonizamide used agains ____ & ____ seizures
1. tonic-clonic Seizures
2. Partial (simple/complex) s.
Levetiracetam Mofa & use
MofA: unknown
use: Partial (simple/complex) Seizures
MgSO4 MofA & use
MofA: unknown
-pre-eclampsia: (hypertension @ pregancy)
-eclampsia: convulsion after pregnancy
(NOT for prophylactic use)
Drugs effective against both
Tonic-clonic & partial Seizures
1. Phenytoin
2. carbamazepine
3. Phenobarbital
4. Primidone
5. Valproic acid
6. Topiramate
7. Zoni-samide
(7 out of 17 drugs)
Drug effective only against partial seizures:
1. Gaba-pentin (adjunct only)
2. Lamo-trigine (mono-/adjunct)
3. Tia-gabine (mono-/adjunct)
4. Vigatrin (adjunt only)
5. Oxy-carbazine
6. Leve-tira-cetam
anti-epileptic used for ALL generalized and ALL partial Seizures:
Valproic Acid
Treatments for Status Epilepticus:
1. Phenytoin (Fos-phenytoin)
2. Benzodiazepines (-azepam)
Treatment for Trigeminal Neuralgia:
treatments for Febrile Seizures:
1. Primidone
2. Benzodiazepine (Diazepine)
Treatment for Absence Seizures:
1. Ethosuximide (1st drug choice)
2. Banzodiazepines (-azepam)
Treatment for Myoclonic Seizures:
Benzodiazepines (-azepam)
treatment for Neuro-pathic and diabetes nephro-pathic pain:
Effective against multiple seizure conditions
treatment for pre-eclampsia & eclampsia