Medication Therapy to Control Seizure Activity

The flashcards below were created by user Prittyrick on FreezingBlue Flashcards.

  1. Seizures
    Uncontrolled Physiologic response to abnormal electrical discharges in the CNS

    usually indicative of neuronal hyperexcitability 

    • seizures are a symptom rather than a disease
    • tells us something is going on in the brain
  2. Factos influence the occurence of a seizure
    • seizure are generated/initiated by synchronous high frequency discharge from a group of abnormal hyperexcitable neurons (focus), spread to adjacent tissues 
    • conga line- it starts with one abnormal cell (a group of cell) as the electrical charges are moving it grabs on to more cells (spread) 

    • starts with one hyper excitable and spreads
    • focus can be the result of congential defect, hypoxia, head trauma, tumor, meds...sometimes unknown genetics
  3. Seizure Threshold
    • The nervous system normally exhibits a basal level of excitable
    •  it is like when u reach your frustation
    • different levels
    • how much stimulation can ur brain take. 
    • every threshold is different

    in seizure disorders the threshold is low or mulitple areas are stimulated 

    when the degree of excitability exceeds a certain threshold (seizure threshold) abnormal discharges can occur in the CNS
  4. Who is at risk for seizure activity
    • developement- young/old
    • infections
    • medication- most meds lower the seizure threshold
    • trauma esp to the head
    • changes to the metabolic system- hypoglycemia, hypoatremia
    • any changes in the brain- vascular changes, neoplastic
  5. Outward manifestation of a seizure depends on (what u see)
    where seizures starts and where it goes too.

    • if it doesn't move it might be localized (one side local) and u will see someone hands twitching for example
    • generalize- effect both cerebral

    • tonic- increase tone
    • clonic- movement
  6. how do anticonvulsants work to decrease seizure activity?
    decrease discharge of neurons within the seizures (to stop hyper excitibility)

    suppress progation of seizure activity from the focus to the other areas of the brain- so doesnt stop hyper excitibility but it keeps it from spreading (pulling in other cells)

    end of seizure excitibility
  7. four basic mechanisms of action for antiseizure agents
    decreases Na reflux- decrease na into the cell

    decreases Ca reflux- into the cell

    Increase GABA- inhibitory nerve transmitter

    Decrease glucomate- if pt has high glucomate they have increase nerve damage can lead to cell death. we want to reduce glucomate to perserve neurons

    decrease neuron excitibility
  8. Goals of Antiseizure therapy
    reduce seizure activityto an extent that the individual can live a normal or near normal life (balance)

    ideal: elminate seizure activity but not possible

    manage side effects of anticonvulsants- CNS, headache dizziness, drowiness

    eliminate as much as u can so u can function
  9. Antiseizure choice for patients
    • type of seizure and manifestations, PMH
    • Pregnancy: most agents are category D (balance)

    • start at low dose and then titrate upwards
    • monitor drug levels as indicated
    • if seizure activity continues, may increase dosage or add another agent
    • always titrate off a med to prevent seizures with rapid withdrawl.
  10. Mg sulfate
    MOA: blocks neuronal transmission 

    • CI seizure disorder associated with pregnancy
    • decrease premature labor
    • replacement therapy for mag defiency

    • SE: Decrease DTR (with the hammer), hypotension, flushing (body), bradycardia
    • can progress to muscle weakness, flaccidity, resp arrest
    • vasodilate

    blocks nerve transmission
  11. Mg sulfate SE NI
    • Assess SE:
    • early s/s of high doses/toxicity thirst warmth, decrease dtr, sedation, muscle weakness, decrease urinary output assess BP/HR/DTR

    • Drugs levels Mg 1.3-2.1 mEq/L
    • careful administration, check dosage and concentration, infusion rates
    • antidot: calcium gluconate

    • CNS 
    • keep it simple
  12. hydantoins
    ex Dilantin (phenytoin)

    • MOA- decrease Na reflux decreases the spread of seizure activity
    • primarily works in the motor cortex
    • raises the seizure threshold
    • blocks nerve transmission

    CI: broad spectrum anticonvulsants (first choice), dysrhythmia (change rhythm), trigeminal neuralgia- pain associated with trigminal nerve
  13. Hydantoins Dilantin (phenytoin) SE
    at therapeutic levels few side effects

    • usually CNS (dose related)
    • correlation higher doses more CNS effects
    • normal drug level 10-20 mcg/ml
    • CNS- headaches

    as it increase servity of the symptoms increase
  14. hydantoins- dilantin (phenytoin) other SE
    gingival hyperplasia- overgrowth of gum usually seen in long term therapy and high doses

    Gi N/v/d

    skin rash


    • bone marrow depression esp at higher dose cell counts down, leukpenia, thrombocytenia, osteomalacia, osteoporosis (because it decreases calcium in the bones) at risk for fracture 
    • CV (IV)- hypotension, bradycardia, arrhythmia
    • phlebitis (IV)
  15. hydantoins dilantin (phenytoin) NI
    • multiple drug interaction, drug metabolizing enzymes
    • take with meals to decrease GI upset
    • avoid taking with milk or antacid- decreases aborption
    • can discolor urine 
    • oral care
    • assess CBC - decrease cell counts
    • narrow therapeutic range- small range
    • IV- Normal Saline mixed with dextrose will form crystals
    • admin with tube feeding- u have to stop g tube feeding because it tends to have calcium in it. Ca decrease absorption (stop hr before and one hour after)
    • dont abruptly withdraw the med
  16. Barbuturates
    Ex: Phenobarbital (luminal)

    • MOA: Potentiates  GABA
    • increases seizure Threshold
    • limits the spread of seizure activity

    reduce seizure activity without causing sedation
  17. Barbuturates CI
    CI: generalized seizures

    low margin of safety, high potential for dependence

    • assess risk of abuse, overdose
    • long actining- long half life (2-6 days)
  18. Barbuturates phenobarbital SE
    • Most common: CNS effects (sedation)
    • drowiness diszzines, sedation
    • paradoxical excitement (children)
    • most serious is resp depression
    • other effects GI VC (hypotension)
    • assess for hyperalgia- increase sensitivity to pain

    • dosage for antiseizure meds rarely cause resp depression 
    • related to dosage- CNS, resp (higher dose the high for these symptoms)
  19. Barbuturates phenobarbital NI
    • Multiple drug interaction
    • takes several weeks for oral doses to reach therapeutic levels
    • therapeutic range 10-25mcg/ml over 25 increase thr risk for CNS depressants and SE
    • cautious use with other CNS depressants
    • can increase post op pain
    • assess respiratory rate
    • withdrawl slowly- withdral s/s 8-12 later , CNS irritability
  20. Benzodiazepines

    • MOA: binds to GABA receptor (inhibiting neurotransmission) 
    • decrease the propagation of seizure activity (stops the spread)
    • raises the seizure threshold

    limited the amount of CNS depression produced
  21. Benzodiazepines (Valium) CI
    CI: used a adjuct (secondary treatment to another drug, long term treatment for seizures

    long term management

    • anti anxiety (b/c of stopping the neurotransmission
    • sedative agent
    • muscle relaxation- increase GAba slows transmission down and relaxes the muscles
    • treatment for alchohol withdraw
    • conscious sedation
  22. Benzodiazepines SE
    • Most common side effects- CNS
    • most common sedation
    • CV- hypotension
  23. Benzo vilium NI
    • safe assessment CNS effects
    • assess for withdrawl- can start from 1-10 and it may not start until a month last- anxiety attack
    • multiple drug interaction
    • tolerance can develop in a few months- so that means it doesn't work at that dosage anymore
    • monitor for overdose (CNS depression)
    • overdose- CV- hypotension, bradycardia
    • respiratory- slows down resp
    • IV Flumazeril (competitive Benzo antagonist)if u overdose u this...benzo antidote works within minutes
  24. Iminostilibenes
    Ex- Tegretol

    MOA- specific action unknown

    decreases high frequency neoronal discharges around focus 

    neuronal activity decreases
  25. Iminostilibenes CI
    second line therapy for seizures

    • trigeminal neurolgia- decreases pain
    • PTSD, bipolar, atypical psychoses (other uses)
  26. Iminostilibenes SE
    CNS- dose related drowiness, dizziness ataxia

    • bone marrow supression- anemia, thrombocytopenia, leukopenia
    • anticholinergic effects- dry mouth, constipation blurried vision, increase temp, 
    • urinary retention

    • long term use can lead to SIADH (Syndrome of inappropriate of ADH)
    • anti0direciteric hormone
    • more so increase ADH, increase retention and hyponatremia (confusion decrease Na)
    • drug makes u increase ur ADH--- dose related
  27. Iminostilibenes NI Tegretol
    • Assess safety (CNS effects)
    • with meals to decrease GI upset
    • assess CBC- bc decrease bone marrow
    • multiple drug interactions
    • therapeutic level: 4-12mcg/ml
  28. Misc agents
    • Valprioc Acid (depakote)
    • Gabapentin (neurotin)
    • Mg Sulfate
  29. Valproic Acid (depakote)
    • MOA: not clearly understood
    • decreases Na and Ca influx- decreases nerve transmission
    • imcreases GABA
    • end- decreases stimulation slow it down

    • adjuct therapy (with another agent)
    • broad spectrum- used for difference things

    prevention of migraine headaches, anxiety, panic attacks, and treatment of bipolar disorder
  30. Valproic Acid (depakote) Se
    • Most common SE and GI
    • nausea, vomiting and indigestion (GI most common)
    • desation
    • blood dyscrasias- - bone marrow suppresion anemia, thrombcy, 
    • high mortility- can cause liver function hepatotoxcity- fatal liver failure
    • - young childre, elder, pt with multiple anticonvulsant agent, liver problems,
  31. Valproic (Depakote) NI
    • Monitor LFTs, and CBC
    • contraindicated with liver disease- unless it is a last resort or undx)
    • admin wit meal to decrease gi upse
    • - do not chew extended  release: mouth sores
    • - do not mix with carbonated drinks
    • - open capsule and add with food
    • Therapeutic- 50-100mcg/ml
  32. Gabapentin (neurotonin)
    MOA: not fully understood- enhances GABA release, works on multiple sites

    • CI: broad spectrum anticonvulsant, often use as a an adjunct
    • other uses- chronic pain, bipolar, migraines, neurolgia, neuropathy (pain disorders)
  33. Gabapentin (neurotonin) SE NI
    SE CNS- drowiness, fatigue- decrease with use

    • NI
    • start with a low dose and titrate up
    • therapeutic effects- weeks 
    • few drug interactions
    • - antacids can decrease aborption
    • assess safety
  34. teaching pt
    • take meds as prescribed
    • do not abruptly stop- can cause seizure activity
    • monitor blood levels
    • safety precaution
    • - all antiseizures meds have a degree of CNS depression
    • newer drugs have CNS depression
    • pregnancy category D
    • beaware of drus that increase CNS depression
    • careful re IV dosages.titration/admin techniques
Card Set
Medication Therapy to Control Seizure Activity
Show Answers