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Advanced pharmacology > Epilepsy Parkinsons ADHD > Flashcards

Epilepsy Parkinsons ADHD Flashcards

1
Q

Type of sz

A

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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2
Q

Seizure disorder

A

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

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3
Q

Goals of treatment

A
  • 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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4
Q

MOA of anti-epileptic drugs

A
  1. Modulation of voltage gated ion channels - surpresa CA + and NA + influx
  2. Inhibition of sympathetic excitement ( antagonism of glutamate )
  3. Enhancement of sympathetic excitement (potentiation of GABA)
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5
Q

Drug evaluation

A

Antiepiléptic drug trial period
Doseage adjustment
Sz frequency chart

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

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6
Q

Suicide risk

A

High risk drugs: topiramate, lamotrigine

Lower risk : valproic acid, carbamazepine

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7
Q

Traditional AED

A
  • Phenytoin ( Dilantin )
  • Carbamazepine ( tegretol )
  • Valproic Acid / sodium ( depakene, depakote)
  • Phenobarbital (luminal)
  • Ethosuximide (Zarontin)
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8
Q

Newer AED

A

Topamax
Nuerontin
Lamictal
Keppra

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9
Q

Phenytoin ( Dilantin )

A

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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10
Q

Generalized adverse effects of antielpileptic drugs

A

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

Gingival hyperplasia

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11
Q

Valproic Acid ( depakene, depakote, depacon)

A

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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12
Q

Tegretol ( carbamazepine)

A

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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13
Q

Drug interactions generalized

A

Warfarin, oral contraceptives, grapefruit juice , isoniazid

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14
Q

Phenobarbital

A

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

Uses: epilepsy, sedation, induction of sleep

Adverse: dependency

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15
Q

Zarontin ( ethosuximide)

A

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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16
Q

Lamotrigine ( Lamictal )

A

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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17
Q

Gabapentin ( nuerontin)

A

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

18
Q

Keppra

A

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

19
Q

Topamax ( topiramate)

A

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

20
Q

Management of status epilepticus

A

Continuous series of tonic -clonic sz
Medical emergency

Maintain ventilation, correct hypoglycemia, terminate sz,

  • IV benzos
  • once stopped initiate phenytoin and cerebyx
21
Q

AED’s and pregnancy ( agents)

A

Choose agent based on likelihood to become pregnant

Agents okay:

  • lacmictal
  • keppra
  • tegretol
  • tomapamax

Avoid:
Valproic Acid
Phenytoin
Phenobarbital

22
Q

Keys to AED and pregnancy

A

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

23
Q

Key points for AED

A

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

24
Q

Plasma drug levels

A

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)

25
Q

Key points ( withdrawing and suicide, generic)

A

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

26
Q

Parkinson’s goals

A

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

27
Q

Initial treat - Drug selection

A

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

28
Q

Levodopa

A

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

29
Q

Levodopa - weaning off

A

Three ways to minimize

  • shortening the dosing interval
  • giving a drug that prolongs levodopa plasma half life
  • giving a direct-acting dopamine agonist
30
Q

Levodopa - adverse effects

A

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

31
Q

Levodopa - Dyskinesias

A

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

32
Q

Carbidopa

A

Purpose: blacks peripheral dopa, increases amount of levodopa entering the brain

Effects: decreases peripheral adverse affect such as N/V, cardiac irritability and orthostatsis

33
Q

Levodopa - drug interactions / food interactions

A
  • antipsychotics, MAO-I, anticholinergic
  • meals with high protein content can reduce therapuetic responses
  • spread protein evenly throughout the day
34
Q

Levodopa / Carbidopa ( sinemet ) advantages

A

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
35
Q

Levodopa / Carbidopa - disadvantage

A

Carbidopa - no adverse effects on its own

Abnormal movements and psychiatric disturbances can occur soon and more intense than with levodopa alone

36
Q

COMT inhibitors

A

Tamar and Comtan
- must be given with levodopa

Effects: increases levodopa half-life and AUC

37
Q

Dopamine Agonist

A

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

38
Q

Monoamine Oxidase - B inhibitors

A

Selegiline, Rasagiline

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

39
Q

Centrally acting anticholinergic drugs: cogentin, artane

A

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)

40
Q

Amantadine ( symmetrel )

A

Dopaminergic agent

Responses diminish in 3-6 months

Not first line

41
Q

Pramipexole ( mirapex)

A

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

Advanced pharmacology (12 decks)

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