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NS II Exam II AP > Drugs- Movement Disorders (Kinder) > Flashcards

Drugs- Movement Disorders (Kinder) Flashcards

1
Q

parkinsonism tremor

A

tremor at rest

associated with rigidity and impairment of voluntary activity

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2
Q

postural tremor

A

tremor during maintenance of sustained posture

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3
Q

athetosis

A

c) Athetosis – abnormal movements which are slow and writhing.

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4
Q

tics

A

sudden, involuntary, coordinated abnormal movements; tend to occur repetitively, particularly about the face and head; can be suppressed voluntarily for short periods of time.

may be single, multiple; transient or chronic

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5
Q

what is Gilles de la Tourette’s

A

chronic multiple tics

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6
Q

4 main features of parkinson’s

A

rigidity, bradykinesia, tremor, and postural instability

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7
Q

what is the pathology in Parkinson’s

A

iii) Loss of dopaminergic neurons in substantia nigra results in disinhibition of GABAergic neurons and disturbed movement.

These neurons normally inhibit output of GABAergic cells in the corpus striatum, while cholinergic neurons (ACh) exert an excitatory effect on GABAergic neurons

this is in the indirect loop using D2

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8
Q

does dopamine cross the BBB?

A

no

If given peripherally, does not have any therapeutic effects in parkinsonism.

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9
Q

what is Levodopa

A

precursor of dopamine

does enter the brain via LAT (L-amino acid transporter)

once in the brain it is decarboxylated to dopamine

stimulates D2 receptors

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10
Q

when is the best time to take levodopa

A

30 - 60 min before meal

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11
Q

carbidopa

A

dopa decarboxylase inhibitor - reduces peripheral metabolism of levodopa
results in higher plasma levels, t1/2, and increased availability for CNS entry

reduces side effects of L-dopa

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12
Q

therapeutic use of Levodopa

A

i) Does not stop progression of Parkinson’s disease but may lower mortality with early initiation.
ii) Best results obtained in 1st few years of treatment.
iii) Benefits begin to diminish after 3-4 years of therapy (regardless of initial response).
(1) Daily dose may have to be decreased overtime to avoid ADRs at doses initially well-tolerated.
(2) Some may become less responsive to levodopa; perhaps due to loss of dopaminergic nigrostriatal nerve terminals.
iv) 1/3 of patients respond very well, 1/3 respond less well, and 1/3 are either unable to tolerate the medication or do not respond at all.

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13
Q

what are the ADR”s of levodopa

4 main areas

A

Gi- anorexia, nausea, vomiting

CV- postural hypotension

  • arrythmias- due to increased peripheral catecholamine formation
  • HTN –> when taking large doses of L-dopa or in combination with MAOI’s or sympathomimetics

Behaviorial
-depression, agitation, insomnia, somnolence, confusion, delusions/hallucinations, nightmares

Dyskinesia
-chorea of face and distal extremities

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14
Q

what is the on-off effect and wearing off effect of L-dopa therapy and what can happening with increased frequency as treatment continues

A

wearing off–> at then end of dose of L-dopa an akinesia can develop
there is improvement of mobility with L-dopa for a period of time (1-2 hours) but rigidity and akinesia return at the end of the dosing interval

on-off

  • (i) Off-periods of marked akinesia alternate over the course of few hours with on-periods of improved mobility but often marked dyskinesia.
    (ii) Exact mechanism unknown, most likely to occur in those who responded well initially.
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15
Q

what are 2 DDI’s of L-dopa

A

i) Pyridoxine (vitamin B6) – increases extracerebral metabolism; may prevent therapeutic effect unless peripheral decarboxylase inhibitor (carbidopa) also given.
ii) MAOIs – hypertension; do not give if taking MAOIs or within two weeks of MAOI discontinuation.

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16
Q

what are MAOI’s

A

inhibit MAO (monoamine oxidase inhibitors)

MAO-A preferentially deaminates serotonin, melatonin, epinephrine, and norepinephrine. MAO-B preferentially deaminates phenethylamine and trace amines. Dopamine is equally deaminated by both types

inhibiting an MAO leads to increased availability of the substance (dopamine)

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17
Q

if a patient doesn’t repond well to L-dopa how will they respond to dopa agonist

A

not well

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18
Q

where is the site of action of dopamine agonists

A

dopamine postsynaptic receptor

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19
Q

bromocriptine

A

dopamine agonist D2

iii) Therapeutic use: additionally approved for treatment of endocrine disorders (e.g., hyperprolactinemia, prolactin secreting adenomas, acromegaly

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20
Q

pramipexole

A

Mirapex
dopamine agonist at D3

dose adjust in renal disease

iii) Therapeutic use: additionally approved for the treatment of moderate-to-severe, primary, restless legs syndrome (RLS).

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21
Q

Ropinirole

A

(requip)
dopamine agonist D2

ii) PK: metabolized by hepatic CYP450 enzymes (primarily CYP1A2); co-administration with agents that are also metabolized by CYP1A2 may reduce the clearance of ropinirole.

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22
Q

rotigotine

A

dopamine agonist

i) Approved for early Parkinson’s disease; may provide more continuous dopaminergic stimulation.
ii) May cause serious application site reactions.

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23
Q

apomoprhine

A

dopamine agonist

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24
Q

what are the ADR’s of Dopamine agonists

A

GI- n/v, anorexia

CV- postural hypotension (particularly at initiation)

Dyskinesia

Mental disturbance-(1) Disorders of impulse control (exaggeration of previous tendency or as new phenomenon) may lead to compulsive gambling, shopping, betting, sexual activity, and other behaviors.

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25
Q

what is a particular ADR of ergot derivatives (Bromocriptine)

A

painless digital vasospasm

pleural and retroperitoneal fibrosis have been reported with bromocriptine use

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26
Q

in pt’s taking pramipexole or ropinirole (non ergot derivatives dopamine agonists) what is a particular side effect

A

(2) Rarely, patients who are taking pramipexole or ropinirole may feel the uncontrollable tendency to fall asleep at inappropriate times.

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27
Q

what are the contraindications for taking dopamine agonists x4

A

history of psychotic illness

recent MI

active peptic ulcer disease

best avoided in PVD (ergots)

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28
Q

Rasagiline

Selegiline

A

Monoamine oxidase inhibitors (MAOI’s)

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29
Q

what does monoamine oxidase A metabolize

A

NE
serotonin
dopamine

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30
Q

what does monoamine oxidase B metaboilze

A

dopamine selectively

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31
Q

Selegiline
MOA
when should you take this drug

A

selective, irreversible inhibitor of MAO B at normal doses (+ MAOI A at higher doses). Decreases breakdown of dopamine.

take at breakfast and lunch = if taken later, may cause insomnia

32
Q

selegiline therapeutic use

A

ii) Therapeutic use: adjunct for those declining or experiencing fluctuating response to levodopa.
(1) Enhances and prolongs anti-parkinsonism effect of levodopa (thereby allowing levodopa dose to be reduced) and may reduce mild on-off or wearing-off phenomenon.

33
Q

Rasagiline

MOA

A

i) MOA: irreversible inhibitor of MAO-B; more potent than selegiline.

34
Q

therapeutic use of Rasagiline

A

ii) Therapeutic use: used as a neuro-protective agent and for early symptomatic treatment of Parkinson’s.

35
Q

what is an important DDI of monoamine oxidase inhibitors (MAOI’s)

A

d) DDIs: combined administration of levodopa and a nonselective MAO inhibitor must be avoided because it may lead to a hypertensive crisis (due to peripheral accumulation of norepinephrine).
i) Do not use in patients receiving meperidine, tramadol, methadone, propoxyphene, cyclobenzaprine, or St. John’s Wort. Best to avoid dextromethorphan and all over-the-counter cold preparations.

36
Q

Tolcapone

A

COMT inhibitor (catechol- o - methyltransferase ) ‘

both central and peripheral effects

37
Q

Entacapone

A

COMT inhibitor (catechol-o-methyltransferase)

peripheral effects only

38
Q

what is the MOA of COMT’s

A

b) Inhibition of dopa decarboxylase (carbidopa) is associated with compensatory activation of other pathways of levodopa metabolism – especially COMT, this increases levels of 3-O-methyldopa (3OMD).
i) 3OMD competes with levodopa for active carrier mechanisms that govern transport across intestinal mucosa and blood-brain barrier, which results in a poor therapeutic response.
b) MOA: prolong action of levodopa by diminishing peripheral metabolism (decreases clearance and increases bioavailability).

39
Q

what is the therapeutic use of COMT inhibitors

A

c) Therapeutic use: may be useful in patients who have developed response fluctuations.

40
Q

What is an unusual and dangerous ADR of tolcapone

A

e) Tolcapone may cause an increase in liver enzyme levels and has been associated, rarely, with death from acute hepatic failure (use in the USA requires signed patient consent). Entacapone generally preferred for these reasons.

41
Q

other ADR’s of COMT inhibitors

A

f) ADRs: relate to increased levodopa exposure; but also may cause diarrhea, abdominal pain, orthostatic hypotension, sleep disturbances, and orange discoloration of urine.

42
Q

what is apomorphine used for and what is its site of action

A

potent, non-ergot dopamine agonist; interacts with postsynaptic D2 receptors in caudate nucleus and putamen.

give subQ injection

starts working within 10 min

b) Therapeutic use: temporary relief (“rescue”) of off-periods of akinesia in patients on optimized dopaminergic therapy.

43
Q

with what drug can you pre-treat pt’s whom you are giving apomorphine

A

trimethobenzamide

this is an antiemetic

44
Q

amantadine

A

antiviral agent with relatively weak anti-parkinsonism properties (may increase dopa release and decrease reuptake)

45
Q

why is amantadine a good option instead of levodopa

A

it is less effacacious than levodopa BUT it may favorably impact bradykinesia, rigidity and tremor

help reduce iatrogenic dyskinesia in pt’s with advanced disease

46
Q

what are some ADR’s of amantadine and ONE particular ADR specific to amantadine

A

restlessness, depression, irritability, insomnia, agitation, excitement, hallucinations, and confusion (all can be reversed by stopping drug) as well as headache, heart failure, postural hypotension, urinary retention, and GI disturbances

Livedo reticularis –> purplish mottled discoloration of the skin

47
Q

in what pt’s must caution be taken when using amantadine

A

history of seizures or heart failure

48
Q

Benztropine

A

antimuscarinic

49
Q

biperiden

A

antimuscarinic

50
Q

orphenadrine

A

antimuscarinic

51
Q

procyclidine

A

antimuscarinic

52
Q

trihexyphenidyl

A

antimuscarinic

53
Q

what is the purpose of using antimuscarinics in parkinsons

A

curb excess choinergic activity (ACh) - since there is loss of dopamine there is more activity of the ACh

improves tremor and rigidity but has LITTLE EFFECT on bradykinesia

54
Q

what are the ADR’s of antimuscarinics

A

common peripheral antimuscarinic effects (sedation, mental confusion, constipation, urinary retention, blurred vision).

55
Q

what is your starting regimen in young patients with parkinson’s

A

-trial of

rasagiline - MAOI’s
amantadine - antiviral
antimuscarinic

56
Q

what is the most effective symptomatic treatment of motor disturbance in parkinson’s

A

carbidopa-levodopa

57
Q

what if a pt has a severe disease of Parkinson’s and long term complications of levoodopa. what therapy should you begin instead?

A

trial of COMT inhibitor (entacapone, tolcapone) or rasagiline

58
Q

Essential tremor treatment

x5

A

propanolol and metoprolol (beta 1 blockers)
useful in pt’s with concomitant pulmonary disease

primidone = barbituate (anti-epileptic drug)

Topiramate- anticonvulsant

Alprazolam- benzodiazepine

IM botulinum toxin A

59
Q

Huntington’s disease

A

i) Autosomal dominant inherited disorder caused by an abnormality in chromosome 4 and is characterized by progressive chorea and dementia that usually begin in adulthood.

chorea most likely develops b/c there is increased dopamine and decreased GABA and ACh

60
Q

what is the treatment of huntington’s

A

iii) Drugs that impair dopaminergic neurotransmission (see mechanisms below) often alleviate chorea, while drugs that activate dopaminergic signaling (levodopa) exacerbate it.
1) Reserpine and tetrabenazine- block the VMAT transporter and deplete cerebral dopamine stores

2) Dopamine receptor blocker
- Olanzapine
- perphenazine
- haloperidol

61
Q

Reserpine

A

VMAT blocker

leads to decrease in dopamine
for Huntington’s disease

62
Q

tetrabenazine

A

VMAT blocker

leads to decrease in dopa. used for huntington’s disease

63
Q

Haloperidol

A

dopamine receptor blocker used in the treatment of huntington’s

64
Q

olanzapine

A

dopamine receptor blocker used in the treatment of huntington’s

65
Q

perphenazine

A

dopamine receptor blocker used in the treatment of huntington’s

66
Q

`what is the treatment of tics

A

neuroleptic antipsychotics

  • tetrabenazine
  • haloperidol
  • pimozide

-alpha two agonist (clonidine)

67
Q

what are the treatment options for Restless leg syndrome

A

fix co-existing iron deficiency anemia

***1st line is pramipexole and ropinirole (non-ergot dopamine agonists)

dopamine agonits
levodopa
diazepam
clonazepam
opiates
68
Q

what is Wilson’s disease

A

i) Wilson’s disease, recessively inherited disorder of copper metabolism, characterized:
(1) Biochemically by: reduced serum copper and ceruloplasmin (major copper-carrying protein in the blood) concentrations.
(2) Pathologically by: markedly increased concentration of copper in the brain and viscera.
(3) Clinically by: signs of hepatic and neurologic dysfunction (e.g., tremor, choreiform movements, rigidity, hypokinesia, and dysarthria and dysphagia).

69
Q

what are the treatment options for Wilson’s disease

A

Penicillamine - chelating agent, forms a stable complex with copper

70
Q

what are the ADR’s of penicillamine

A

(b) ADRs: nausea, vomiting, nephrotic syndrome, myasthenia, optic neuropathy, and various blood disorders.

71
Q

potassium disulfide

A

reduces instestinal absorption of copper

can be prescribed in addition to penicillamine for wilsons disease

72
Q

trientine

A

chelating agent preferred by many b/c lesser drug reactions or neurologic worsening

used in WIlson’s disease

73
Q

what is the use of zinc acetate and zinc sulfate and how do they work

A

(increase fecal excretion of copper by decreasing gastrointestinal absorption).

74
Q

A 68 y/o female presents with recent diagnosis of Parkinson’s disease and is administered appropriate, first-line therapy. Shortly after beginning therapy, she begins to vomit.
This adverse effect is most likely associated with activation of which receptor?

A

D2 (dopamine)

Chemoreceptor trigger zone–> Located in brainstem but outside blood-brain barrier
CTZ monitors for toxic substances and relays info to emesis center to trigger nausea and vomiting

75
Q

preferred treatment in parkinson’s of pt’s <65 years old?

A

dopamine agonist

76
Q

preferred treatment in PD of pt’s >65

A

Levodopa

77
Q

it what pt’s are anticholinergic agents most useful

A

Useful if < 70 years old, with tremor without significant bradykinesia or gait disturbance

NS II Exam II AP (7 decks)

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