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Pharmacology > !Drugs For Movement Disorders > Flashcards

!Drugs For Movement Disorders Flashcards

1
Q

Levodopa and combinations

A

Levodopa
Carbidopa
Levodopa and carbidopa

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2
Q

Dopamine receptor agonists

A

Apomorphine
Bromocriptine
Pramipexole
Ropinirole

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3
Q

Monoamine oxidase inhibitors

A

Rasagiline

Selegiline

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4
Q

Catechol-O-methyltransferase inhibitors

A

Entacapone

Tolcapone

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5
Q

Amantadine

A

Amantadine

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6
Q

Anticholinergic drugs

A 
Benztropine
Biperiden
Orophenadrine
Procyclidine
Trihexyohenidyl
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7
Q

Miscellaneous agents

A

Riluzole

Reserpine, tetrabenazine

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8
Q

What are the pathophysiological hallmarks of Parkinson’s disease

A

Loss of pigmented, dopaminergic neurons of the substantia nigra, with the appearance of intracellular inclusions known as Lewy bodies

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9
Q

Under normal conditions, dopaminergic neurons originating int he substantia nigra inhibit the GABAergic output from the ___ while cholinergic neurons exert an excitatory effect on GABAnrgic neurons

A

Striatum

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10
Q

The selective loss of dopaminergic neurons in patients with PD result in __ of GABAergic neurons and disturbed movement

A

Disinhibition

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11
Q

Based not he pathophysiology of PD, individuals with PD may be treated with what

A

Dopamine

Agonists and/or anticholinergic agents

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12
Q

Normal dopaminergic substantia nigra system

A

Neurons originating int he substantia nigra normally inhibit GABAergic output from he striatum whereas cholinergic neurons exert an excitatory effect

_lose dopamine in PD

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13
Q

Agents to treat dopamine

A

Levodopa

Dopamine receptor agonists

Monoamine oxidase inhibitors (MOA)

Catechol-O-methyltransferase COMT inhibitors

Apomorphine

Amantadine

Anticholinergic drugs

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14
Q

What is levodopa

A

Immediate metabolic precursor to dopamine

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15
Q

Levodopa enters the CNS via an ____. Does it cross the BBB

A

L amino acid transporter LAT

No

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16
Q

MOA levodopa

A

Agonist at dopamine receptors

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17
Q

What is the half life of levodopa. Why

A

1-2 hours

Rapidly absorbed from the small intestine with a peak plasma concentration usually between 1-2 hours after oral does

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18
Q

Only _% of administratered levodopa actually enters the brain unaltered (the remainder is metabolized extracerebreally, predominantly be decarboxyation to dopamine)

A

1-2%

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19
Q

Coadministration of levodopa with a __ __ ___ that does not cross the BBB (__) results in reduced peripheral metabolism, increased plasma levels, increased half life, and increased levodopa available for entry into the brain

A

DOPAMINE decarboxylase inhibitor

Carbidopa

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20
Q

Coadministation of levodopa with __ may reduce the daily requirements of levodopa by approximately 75%

A

Carbidopa

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21
Q

Clinical use for levodopa

A

Parkinsonian syndrome; does not stop the progression of PD but does lower mortality rate wen initiated early in the disease

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22
Q

The best results of levodopa are when

A

First few years..then wane off

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23
Q

Wearing off phenomenon

A

Can occur during long term treatment where each dose of levodopa effectively improves mobility for a period of time (1-2) hours but rigidity and akinesia return rapidly at the end of the dosing intercal; increasing the dose and frequency of administration can improve symptoms , but this is often limited by the development of dyskinesia (distortion or impairment of voluntary movement)

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24
Q

Does everyone respond to levodopa

A

1/3 yea
1/3 less
1/3 cant tolerate or do not respond at all

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25
Q

GI effects levodopa

A

If given without a peripheral decarboxylase inhibitor causes anorexia, nausea, and vomiting (due to activation of the chemoreceptor trigger zone) in 80% of patients; combo of levodopa/carbidopa causes less frequently and less troublesome GI side effects

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26
Q

CV effects levodopa

A

Postural hypotension (frequently asymptomatic) can occur but often dimishes with continuing treatment . Hypertensioncan occur when taking large doses of levodopaor levodopa in combination with nonselective monoamine oxidase inhibitors or sympathomimetics

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27
Q

Dyskinesia levodopa

A

Can occur in 80% of patients. Choreoathetosis of the face and distal extremities is the most common presentation

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28
Q

Behavioral effects levodopa

A

Depression, anxiety, agitation, insomnia, somnolence, confusion, delusions, hallucinations, nightmares, euphoria, ,other changes in mood or personality have been reported. Atypical antipsychotic agents (clozapine, olanzapine, quetiapine, risperidone) are able to help counteract behavioral complications

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29
Q

Fluctuations in response and the on-off phenomenon with levodopa

A

Can occur due to the timing of the dose (wearing off phenomenon,) or due to reasons unrelated to dose timing (on-off phenomenon). In the on-off phenomenon, off periods of marked akinesia alternate over the course of a few hours with on periods of improved mobility but often marked dyskinesia (exact mechanism is unknown)

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30
Q

Subcutaneous injections of ___ may provide temporary benefit to those patients with severe off periods

A

Apomorphine

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31
Q

MOA and levodopa

A

Patients taking MOA inhibitors may experiencehypertensive crisis when combined with levodopa

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32
Q

Who is levodopa contraindicated in

A

Psychotic patients, angle closure glaucoma(can be used in open), history of melanoma or suspicion of undiagnosed lesion(is a precursor of skin melanin); use with caution in patients with active peptic ulcer due to possibility of GI bleeding

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33
Q

___ __ ___ have a lower incidence of the response fluctuations and dyskinesia that occur with long term levodopa therapy, although patients who don’t respond well to levodopa generally don’t respond well to dopamine agonists

A

Dopamine receptor agonists

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34
Q

Dopamine receptor agonists can be administered in addition to __/__ and in patients who are taking levodopa and who have end of dose akinesia or on off phenomenon

A

Levodopa/carbidopa

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35
Q

What are the dopamine receptor agonists

A

Bromocriptine

Pramipexole

Ropinirole

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36
Q

Bromocriptine

A

Ergot alkaloid derivative that is a D2 agonist

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37
Q

What else can bromocriptine be used for besides parkinson

A

Endocrine disorders

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38
Q

Bioavailability of bromocriptine

A

28%(extensive first pass metabolism with cyp3A4) with peak plasma concentration usually attained within 1-3 hours; 15 hour half life

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39
Q

Pramipexole

A

Preferential affinity for D3 receptors

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40
Q

What else can pramipexole be used for besides PD

A

Primary restless leg syndrome

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41
Q

Pramipexole has a peak plasma concentration reached in _ hours with a half life of _ hours

A

2

8

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42
Q

Pramipexole excretion

A

Unchanged in the urine

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43
Q

Ropinirole

A

Preferential affinity for D2 receptors

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44
Q

What else can ropinirole be used for besides PD

A

RLS

45
Q

Metabolism ropinirole

A

CYP450 metabolism (primarily CYP1A2)

46
Q

Peak plasma concentration of ropinirole is reached in _ hours with a HL of _ hours

A

1-2

6

47
Q

Adverse GI effects of dopamine receptor agonists

A

Anorexia, nausea, vomiting (reduced with meals), constipation, dyspepsia, and symptoms or reflux esophagitis

48
Q

adverse CV effects of dopamine receptor agonist

A

Postural hypotension
Digital vasospasm during long term treatment
Presence of peripheral edema and cardiacarrhythmias may indicate the need to discontinue therapy

49
Q

Adverse dyskinesia of dopamine agonists

A

Similar to those introduced by levodopa, reversed by reducing total dose

50
Q

Mental disturbances of dopamine agonists

A

Confusion, hallucinations, delusions, other psychiatric reactions and more severe with then with levodopa and clear during withdrawal of medication

51
Q

Contraindications dopamine agonist

A

History of psychotic illness
Recent MI
Active peptic ulcer
Peripheral vascular disease (vasoconstriction effects)

52
Q

What are the two forms of MAO inhibitors

A

MAO-A, MAO-B

53
Q

MAO-A

A

Preferentially metabolizes NE and serotonin

54
Q

MAO-B

A

Metabolizes phenylethyamine and benzylamine

55
Q

__ and __ are metabolized equally by MAO-A and MAO-B

A

Dopamine

Tryptamine

56
Q

Selegine

A

Selective irreversible MAO-B inhibitor (inhibitors MAOA at high doses)
This slows the breakdown of dopamine and prolongs the antiparkinsonian effects of levodopa;may reduce mild on off or wearing off phenomenon; adjunctive therapy in patients with declining or flucutuating response to levodopa

57
Q

Bioavailability of selegiline

A

10% with peak plasma conc in an hour

58
Q

Contraindication selegine

A

Patients taking meperidine, tricyclic antidepressants, or serotonin reuptake inhibitors (risk of serotonin syndrome)

59
Q

Rasagiline

A

Irreversible inhibitor of MAO-B;more potent than selegine

60
Q

What is rasagiline used for

A

Neuroprotective agent and for early symptomatic treatment of PD

61
Q

Why avoid combination of levodopa and nonselective MAO inhibitor

A

May lead to hypertensive crisis (peripheral accumulation of NE)

62
Q

Catechol-O-meethyltransferase COMT inhibitors

A

Metabolizes levodopa to 3-O-methyldopa, which competes with levodopa for transport across the intestinal mucosa and the BBB

63
Q

What are some COMT inhibitors

A

Tolcapone and entacapone

64
Q

Effect of COMT inhibitor

A

Prolong activity of levodopa by inhibiting its peripheral metabolism, which decreases clearance and increases bioavailability

65
Q

Who takes COMT inhibitors

A

Helpful in patients receiving levodopa who have developed response fluctuations

66
Q

Tolcapone

A

Central and peripheral active

67
Q

Entacapone

A

Peripheral acting

68
Q

__ causes an increase in liver enzyme levels and has been associated, rarely, with death from acute hepatic failure

A

Tolcapone

69
Q

Side effects COMT inhibitors

A

Often due to levodopa

Orange discoloration of the urine, diarrhea, abdominal pain and sleep disturbances

70
Q

Apomorphine

A

Dopamine agonist at dopamine D2 receptor

71
Q

Administration of apomorphine

A

Injection SQ for quick, temporary relief of off periods of akinesia in patients on dopaminergic therapy (clinical benefits in 10 min)

72
Q

Adverse effects apomorphine

A

Nausea (can treat with trimethobenzamide) dyskinesia, drowsiness, sweating, hypotension, and injection site bruising

73
Q

Amantadine

A

Antiviral agent whose MOA in Parkinsonism is unknown (may potentiation dopaminergic function by influencing synthesis, release, or reuptake of dopamine)

74
Q

HL amantadine

A

2-4 hours

75
Q

Peak plasma amantadine

A

1-4 hours

76
Q

Excretion amantadine

A

Unchanged in urine

77
Q

Adverse effects amantadine

A

Restlessness, depression, irritability, insomnia, agitation, excitement, hallucinations, and confusion (can all be mediated by discontinuation) as well as headaches, heart failure, postural hypotension, urinary retention and GI disturbances

78
Q

Amantadine may cause livedo reticularis. What is that

A

A vascular condition characterized by a purplish mottled discoloration of the skin usually on the legs

79
Q

Contraindication amantadine

A

Caution in patients wth a history of seizures or heart failure

80
Q

Anticholinergic drugs

A

Centrally acting mAChR antagonists are available to treat patients with PD

81
Q

What can mAChR antagonists be used for

A

Improve tremor and rigidity but have little effect on bradykinesia

82
Q

Name some anticholinergic drugs

A

Benztropine, biperiden, orphenadrine, procyclidine, trihexyphenidyl

83
Q

How give anticholinergic drugs

A

Patientsare given a low dose of drug, which is titrated upwards in amount until benefit occurs or adverse effects limit use

84
Q

If one anticholinergic drug doesn’t work, what do u do

A

Try another one

85
Q

Adverse effects of anticholinergic drugs

A

Common peripheral anticholinergic effects (sedation, mental confusion, constipation, urinary retention, blurred vision)

86
Q

Tremor

A

B1 receptors have been implicated in some tremors
Or
Symptomatic tremor

87
Q

What do tremors respond to if caused by B1

A

Metoprolol and propranolol

88
Q

Symptomatic tremor

A

Controlled by the antiepileptic drug primidone in smaller doses than those used for seizures

89
Q

Topiramate and tremor

A

Serotonin receptor agonist

Effective for tremor

90
Q

Alprazolam(benzodiazepine) and intramuscular injections of Botox

A

Some patients help tremors

91
Q

Huntington

A

Imbalance of dopamine and GABAcauses overactivity of dopaminergic path

92
Q

Any therapy to slow Huntington depression

A

No

93
Q

What drugs alleviate chorea

A

Drugs that impair dopaminergic neurotransmission like

Reserpine, tetrabenazine, olanzapine, phenothiazines)

94
Q

What drugs exacerbate huntington

A

Drugs that activate dopaminergic signaling

95
Q

Tics

A

Pimozide, haloperidol, tetrabenzaine

Or

A adrenergic agents like clonidine, guanfacine

Or

Botox

96
Q

What do pimozide, haloperidol, and tetrabenzaine

A

Cause extrapyramidal syndromes, weight gain, sedation, irritability, and various phobias and are not always the first choice

97
Q

Clonidine and guanfacine

A

A adrenergic agents effective with tics with fewer effects; in some casese

98
Q

Botox tics

A

At a tic site will hep

99
Q

Restless leg syndrome

A

May resolve with correction of iron defiency anemia and often respond to dopamine agonists, levodopa, diazepam, clonazepam, or opiates; non ergot dopamine agonists pramipexoleand ropinirole and alpha 2 delta calcium channel ligands (gabapentin, pregaballin, both) are useful

100
Q

ALS

A

Riluzole is the only drug to have any impact on survival in ALS, which has been shown to prolong survival by a few months

101
Q

MOA riluzole

A

Inhibits glutamate release and blocks postsynaptic NMDA and kainite type glutamate receptors and inhibits voltage gate Na channels, though the precise mechanism in the treatment of ALS is unclear

102
Q

Major adverse effects ALS

A

Nausea and weakness

103
Q

Wilson disease drugs

A

Penicillamine
Potassium disulfide
Trientine

Zinc acetate and zinc sulfate

104
Q

Penicillamine MOA

A

Chelating agent that forms a stable complex with copper levels and a low copper diet (high copperfoods are calf liver, turnip greens, cashews, molasses, spinach)

105
Q

Penicillamine excretion

A

Kidney

106
Q

Adverse effects penicillamine

A

Nausea, vomiting, nephritis syndrome, myasthenia, optic neuropathy, and various blood disorders; after remission, patients may require maintenance dose

107
Q

Potassium disulfide

A

Reduces intestinal absorption of copper and can be described in addition to penicillamine

108
Q

Trientine

A

Chelating agent for Wilson

109
Q

Sinc acetate and zinc sulfate

A

Increase fecal excretion of copper by decreasing GI absorption

Pharmacology (52 decks)

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