Partial sz: - simple partial ( no loc, 20-60 sec) - complex partial ( impaired con, 45-90 sec) - secondarily generalized ( 1-3 min) Generalized seizure - tonic - clonic ( grand mal) - absence ( petit mal) - atonic ( loss of muscle tone) - myoclonic ( sudden muscle contraction ) - Statis epilepticus ( 15-30) - febrile

- reduce seizure to a level that allows the patient to live as normal a life as possible - balance the desire for complete seizure control with acceptable side effects

- Phenytoin ( Dilantin ) - Carbamazepine ( tegretol ) - Valproic Acid / sodium ( depakene, depakote) - Phenobarbital (luminal) - Ethosuximide (Zarontin)

Epilepsy Parkinsons ADHD Flashcards by Kaleigh Hunt

Type of sz

Partial sz:

simple partial ( no loc, 20-60 sec)
complex partial ( impaired con, 45-90 sec)
secondarily generalized ( 1-3 min)

Generalized seizure

tonic - clonic ( grand mal)
absence ( petit mal)
atonic ( loss of muscle tone)
myoclonic ( sudden muscle contraction )
Statis epilepticus ( 15-30)
febrile

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Seizure disorder

Excessive neuronal discharge occurs throughout all or part of the brain. The threshold is low

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Goals of treatment

reduce seizure to a level that allows the patient to live as normal a life as possible
balance the desire for complete seizure control with acceptable side effects

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MOA of anti-epileptic drugs

Modulation of voltage gated ion channels - surpresa CA + and NA + influx
Inhibition of sympathetic excitement ( antagonism of glutamate )
Enhancement of sympathetic excitement (potentiation of GABA)

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Drug evaluation

Antiepiléptic drug trial period
Doseage adjustment
Sz frequency chart

Monitor plasma drug levels
Promote patient adherence
Withdrawing ( wean and taper)

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Suicide risk

High risk drugs: topiramate, lamotrigine

Lower risk : valproic acid, carbamazepine

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Traditional AED

Phenytoin ( Dilantin )
Carbamazepine ( tegretol )
Valproic Acid / sodium ( depakene, depakote)
Phenobarbital (luminal)
Ethosuximide (Zarontin)

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Newer AED

Topamax
Nuerontin
Lamictal
Keppra

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Phenytoin ( Dilantin )

Use: partial and tonic-clonic sz, Epilepsy

MOA: inhibitor of sodium channels

Long half life

Therapeutic levels : 10-20 mcg/ml

Lots of Side effects and drug interactions

Pt education:

give with food, individualized
urine may turn pink, red, brown
avoid abrupt withdrawal

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Generalized adverse effects of antielpileptic drugs

Nystagmus, sedation, ataxia, diplopia, cognitive impairment , hepatotoxicity, pancreatitis, teratogenic effects

Gingival hyperplasia

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Valproic Acid ( depakene, depakote, depacon)

MAO: supresses high freq neuronal firing through blockade of sodium channel , suppresses calcium , may augment the inhibitory influence of GABA

Uses: sz, bipolar, mirgraine

Black box warning :Hepatotoxicity, pancreatitis, teratogenesis (use oral contraception)

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Tegretol ( carbamazepine)

Uses: epilepsy, bipolar, trigeminal neuralgias

MOA: supresses high freq neuronal discharge in and around sz foci ( making it local not all the brain)

Adverse: luekopenia, anemia, thrombocytopenia

Monitoring: 
Drug levels at 3,6,9 
Goal is 4-12 mcg/ml
Once in goal check ever 2 month
Check CBC 3-4 months

Check the HLA-B1502 and if absent may indicate increase in risk for Steven Johnson syndrome ( rash)

Watch for interaction with grapefruit juice

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Drug interactions generalized

Warfarin, oral contraceptives, grapefruit juice , isoniazid

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Phenobarbital

MOA: potentiates the effects of GABA, reduces sz without causing sedation, anticonvulsant

Uses: epilepsy, sedation, induction of sleep

Adverse: dependency

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Zarontin ( ethosuximide)

MOA: delaying calcium influx

Uses: to of absence sz

Monitoring: check levels 1-3 weeks after initiation

Range: 40-100mcg/ml

ADR’s: granulocytopenia

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Lamotrigine ( Lamictal )

Uses: adjunctive treatment of primary generalized tonic-clonic sz and partial sz in adults , bipolar,

In combo with : valproic acid and phenytoin

Adverse: black box ( Steven Johnson)

Pt edu: avoid alcohol, aviod OTC

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Gabapentin ( nuerontin)

MOA: binds to CA+ channel to reduce nuerotransmitter release

Uses: add on therapy for refractory partial sz, nueropathic onion

No routine monitoring

Serious adverse: leukopenia and thrombocytopenia

Keppra

MOA: unknown
Uses: adjunctive to of partial onset sz and myoclinic, generalized tonic -clonic sz
Children 4 older - adjunct partial sz
Children 6 older - primary generalized tonic clonic

Does not use P450
Sz free from the first day of keppra

Topamax ( topiramate)

Uses: general and partial sz, mirgraines, off label uses

MOA: suppresses focal sz and spread by blocking sodium and calcium channels

PK: rapid absorption, peaks 2 hours

Well tolerated

Management of status epilepticus

Continuous series of tonic -clonic sz
Medical emergency

Maintain ventilation, correct hypoglycemia, terminate sz,

IV benzos
once stopped initiate phenytoin and cerebyx

AED’s and pregnancy ( agents)

Choose agent based on likelihood to become pregnant

Agents okay:

lacmictal
keppra
tegretol
tomapamax

Avoid:
Valproic Acid
Phenytoin
Phenobarbital

Keys to AED and pregnancy

Risk to fetus from uncontrolled sz > than risk from AED’s

Use lowest effect drug, one drug

Reduce neural tube defects by providing folic acid before conception and preg

Increased risk for bleeding ( give vit K during last week of preg and at birth

Key points for AED

May take several drugs

Pt can not drive on drug trial period

Drug should be not considered ineffective until sufficiently high dosage and for a reasonable amount of time

Plasma drug levels

Provide info to permit dosage adjustment

Monitoring drug adherence

Determine cause of loss of sz control

Identify cause of toxicity ( when taking more than one drug)

Key points ( withdrawing and suicide, generic)

Withdraw drugs slowly over 6 weeks If pt is taking 2 drugs they should be withdrawn sequentiality Suicide risk 1-24 week after starting meds CNS depression worsen by alcohol Fetal risk minimized by one drug for at the lowest effective dosage Generic drugs are not equivalent to trade drugs and switching is not recommended

Parkinson's goals

Ideal treatment that reverses neuronal degeneration or prevents further degeneration - currently doesnt exist The goal is to improve the patients ability to carry out ADL's

Initial treat - Drug selection

Mild symptoms - MAO-B - Selegiline More severe symptoms: levodopa ( combined with carbidopa) or dopamine agonist Management of motor fluctuations - " off times" - domaine agonists, COMT, MÃO-B

Levodopa

Only given in combo with carbidopa Cornerstone of PD, is more effective than dopamine agonists but long term use = disabling dyskinesias Rapidly absorbed from small intestine - food delays absorption, high protein food reduce therapeutic effects Well controlled for 2 yes and returns to pretreatment state at end of 5 yrs No direct effects of its own, is converted to dopamine its achieve form , it helps properly balanced between dopamine and Ach Check vitamin b6

Levodopa - weaning off

Three ways to minimize - shortening the dosing interval - giving a drug that prolongs levodopa plasma half life - giving a direct-acting dopamine agonist

Levodopa - adverse effects

N/v - give additional carbidopa Cardio, postural hypotension, increase intake of salt and water, psychosis, behavioral changes Can reduce levodopa but it will reduce beneficial effects

Levodopa - Dyskinesias

The med is given to alleviate movement disorder, but it also causes some movement disorders Dyskinesias can be managed in three ways - reduce dosage of levodopa - amantadine - surgery and ECT Darken swear and urine - watch skin assessment

Carbidopa

Purpose: blacks peripheral dopa, increases amount of levodopa entering the brain Effects: decreases peripheral adverse affect such as N/V, cardiac irritability and orthostatsis

Levodopa - drug interactions / food interactions

- antipsychotics, MAO-I, anticholinergic - meals with high protein content can reduce therapuetic responses - spread protein evenly throughout the day

Levodopa / Carbidopa ( sinemet ) advantages

Most effect therapy in PD Levodopa - goes across blood brain barrier Carbidopa - does not Carbidopa - enhances levodopa - the combination allows for decreased levodopa dosage which reduces cardio s/e and n/v

Levodopa / Carbidopa - disadvantage

Carbidopa - no adverse effects on its own Abnormal movements and psychiatric disturbances can occur soon and more intense than with levodopa alone

COMT inhibitors

Tamar and Comtan - must be given with levodopa Effects: increases levodopa half-life and AUC

Dopamine Agonist

Mirapex, parlodel, dostinex MOA: directly stimulates dopamine receptors, monotherapy or adjunct therapy with levodopa Ad: no metabolic conversion, longer half life Adverse:: possibility of patient falling asleep - mirapex

Monoamine Oxidase - B inhibitors

Selegiline, Rasagiline MAO: black metabolism of dopamine, extends duration of action of levodopa

Centrally acting anticholinergic drugs: cogentin, artane

Reduces tremor and possible rigidity Most appropriate for younger patients with mild symptoms Used as second line therapy for tremor Avoided in the elderly who are intolerant of CNS side effects ( hallucinations)

Amantadine ( symmetrel )

Dopaminergic agent Responses diminish in 3-6 months Not first line

Pramipexole ( mirapex)

DA receptor agonist Used as monotherapy in early stage PD Can improve motor performance Also used for restless leg syndrome