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BAHS-504 PHARMACOLOGY EXAM 2 > ANTICONVULSANT AND ANTIPARKINSON DRUGS > Flashcards

ANTICONVULSANT AND ANTIPARKINSON DRUGS Flashcards

1
Q

definition:

a family of chronic neurobiological disorders caused by development of a persistently low seizure threshold and characterized by periodic, pnpredictable seizures

A

epilepsy

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2
Q

what is the prevalence of epilepsy by age 20? by age 80?

A

1% by age 20

3% by age 80

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3
Q

how is epilepsy managed?

A

70% – currently available anticonvulsants

20% – surgery

10% – intractable

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4
Q

define the principles of epilepsy pharmacotherapy

A
  1. drug tx is symptomatic
  2. most anticonvulsants have low therapeutic index
  3. pharmacokinetics are important
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5
Q

definition:

Na channels, Ca2+ channels, SV2A, GABAA receptors, GABA transporters, GABA transaminase, K+ channel openers, and AMPA receptor antagonists

A

molecular targets of antiepileptic drugs

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6
Q

what is the 1st mechanism of AED (antiepileptic drug) activation?

name two AEDs that produce this effect

A

enhance Na channel inactivation

  1. carbamazepine (tegratol)
  2. topiramate (topomax)
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7
Q

name the AED:

P450 inducer (1/2 life shortens from 36hr to 8-12hr with chronic tx)

common adverse reactions: diplopia, ataxia, drowsiness

also used for neuropathic pain and bipolar disorder

A

carbamazepine (tegratol)

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8
Q

name the AED:

D-fructose analog

multiple mechanisms of action (block Na channels, increases affinity of GABA for its receptors, blocks AMPA-type glutamate receptors)

T1/2 = 21hr; mostly excreted unchanged in the liver

broad spectrum anticonvulsant, widely used

common adverse reactions: sleepiness, dizziness, balance issues, often resolve over time

also used for migraine prophylaxis

A

topiramate (topomax)

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9
Q

what is the 2nd mechanism of action of AEDs?

name the AED that produces this effect.

A

block Ca channels

ethosuximide (zarontin)

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10
Q

name the AED:

drug of choice for absence epilepsy

t-type Ca channels not involved in transmitter release

no plasma protein binding

T1/2 = 40-60hr with renal excretion

A

ethosuximide (zarontin)

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11
Q

what is the 3rd mechanism of action of AEDs?

name two drugs that produces this effect

A

enhance GABAergic inhibition

valproate (depakote)

tiagabine

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12
Q

name the AED:

broad-spectrum anticonvulsant

divalproex Na – sustained release form

hepatotoxicity – contraindicated in hepatic disease, children < 2yo

mixed mechanism: also blocks Na channels

also used for bipolar disorder, migraine prophylaxis

A

valproate (depakote)

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13
Q

AED interactions:

carbamezepine, phenytoin, phenobarbital

A

induce metabolism of other drugs

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14
Q

AED interactions:

valproate, felbamate

A

inhibit metabolism of other drugs

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15
Q

AED interactions:

valproate, phenytoin

A

highly protein bound

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16
Q

what is the consequence of administration of carbamazepine, ethosuximide, cloazepam, lamotrigine, topiramate, or tiagabine in the presence of a mutation of the 3A4*1B P450 isoform?

A

decreased clearance, increased toxicity

17
Q

what are the factors that produce fetal anomalies in 4-6% of pregnancies by epileptic mothers? (3)

A
  1. drug effects
  2. consequence of the mother’s underlying diseases
  3. consequence of maternal seizures
18
Q

T/F:

all anticonvulsant drugs carry some teratogenic risk

A

TRUE

19
Q

what can be taken to reduce the teratogenic risk of anticonvulsant therapy?

A

folate (≥ 1mg/day)

20
Q

definition: basal ganglia disorders

degeneration of dopaminergic neurons in substantia nigra pars compacta

A

parkinsonism

21
Q

definition: basal ganglia disorders

degeneration of cholinergic and GABAergic stratal neurons

A

Huntington’s disease

22
Q

definition: basal ganglia disorders

damage to one subthalamic nucleus (often due to vascular accident)

A

Ballism

23
Q

definition: basal ganglia disorders

iatrogenic disorder due to long term treatment with antipsychotics

A

tardive dyskinesia

24
Q

definition:

resting tremor, (cogwheel) rigidity, bradykinesia, (later) stooped posture

A

motor symptoms of parkinson’s disease

25
Q

what is the mean onset age of parkinson’s disease?

A

60yr

26
Q

parkinson’s disease was the first disease of the brain demonstrated to have __________________

A

a molecular basis

27
Q

what is the proximal cause of parkinsonism?

A

degeneration of > 40% of the nigral dopaminergic neurons

28
Q

describe the primary therapy for parkinson’s disease

A

replace the lost dopamine (L-DOPA, carbidopa)

29
Q

what are the short-term side effects of dopamine replacement therapy?

A

nausea, cardiac arrythmias

30
Q

what are the lont-term side effects of L-DOPA therapy?

A

dyskinesias, “end-of-dose” deterioration, “on-off” effect

hallucinations, delirium, depression, sleep disturbances (clozapine – can blunt psychotic effects)

31
Q

describe the secondary therapy for parkinson’s disease

A

directly activate dopamine receptors in striatum

32
Q

what is the prototype secondary parkinson’s disease drug therapy that is a D2 agonist, has >90% first pass metabolism and a 3hr 1/2 life?

A

bromocryptine (parlodel)

33
Q

what secondary parkinson’s disease drug therapy has a 66 1/2 hour half life, and is take 2X/week PO?

A

cabergoline

34
Q

what sencondary parkinson’s disease drug therapy is often used initially, or in combination with L-DOPA, causes fewer dyskinesias than L-DOPA, but may cause nausea, mental confusion, and hallucinations?

A

ropinirole

35
Q

describe the third therapy for parkinson’s disease

A

scavenge free radicals & inhibit MAO-B

36
Q

what is the prototype third parkinson’s disease drug therapy that is metabolized to methamphetamine (stimulates DA release), and who’s interaction with tricyclic antidepressants and SSRIs leads to serotonin syndrome (hyperthermia, hypertension, rigidity)

A

selegiline (eldepryl)

37
Q

definition:

caused by triplet repeat expansion (poly-Q) of huntingtin, displays autosomal dominant inheritance, results in the death of GABAergic and cholinergic striatal neurons

A

Huntington’s disease

38
Q

what is the huntington’s disease drug therapy approve in 2008, that is a VMAT2 inhibitor that depletes dopamine, reduces dyskinesias but not cognitive decline or mood issues

A

tetrabenazine

39
Q
A

BAHS-504 PHARMACOLOGY EXAM 2 (6 decks)

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