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Pharmacology > !Drugs For Movement Disorders > Flashcards

!Drugs For Movement Disorders Flashcards

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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
GI effects levodopa
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
26
CV effects levodopa
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
27
Dyskinesia levodopa
Can occur in 80% of patients. Choreoathetosis of the face and distal extremities is the most common presentation
28
Behavioral effects levodopa
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
29
Fluctuations in response and the on-off phenomenon with levodopa
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)
30
Subcutaneous injections of ___ may provide temporary benefit to those patients with severe off periods
Apomorphine
31
MOA and levodopa
Patients taking MOA inhibitors may experiencehypertensive crisis when combined with levodopa
32
Who is levodopa contraindicated in
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
33
___ __ ___ 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
Dopamine receptor agonists
34
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
Levodopa/carbidopa
35
What are the dopamine receptor agonists
Bromocriptine Pramipexole Ropinirole
36
Bromocriptine
Ergot alkaloid derivative that is a D2 agonist
37
What else can bromocriptine be used for besides parkinson
Endocrine disorders
38
Bioavailability of bromocriptine
28%(extensive first pass metabolism with cyp3A4) with peak plasma concentration usually attained within 1-3 hours; 15 hour half life
39
Pramipexole
Preferential affinity for D3 receptors
40
What else can pramipexole be used for besides PD
Primary restless leg syndrome
41
Pramipexole has a peak plasma concentration reached in _ hours with a half life of _ hours
2 | 8
42
Pramipexole excretion
Unchanged in the urine
43
Ropinirole
Preferential affinity for D2 receptors
44
What else can ropinirole be used for besides PD
RLS
45
Metabolism ropinirole
CYP450 metabolism (primarily CYP1A2)
46
Peak plasma concentration of ropinirole is reached in _ hours with a HL of _ hours
1-2 | 6
47
Adverse GI effects of dopamine receptor agonists
Anorexia, nausea, vomiting (reduced with meals), constipation, dyspepsia, and symptoms or reflux esophagitis
48
adverse CV effects of dopamine receptor agonist
Postural hypotension Digital vasospasm during long term treatment Presence of peripheral edema and cardiacarrhythmias may indicate the need to discontinue therapy
49
Adverse dyskinesia of dopamine agonists
Similar to those introduced by levodopa, reversed by reducing total dose
50
Mental disturbances of dopamine agonists
Confusion, hallucinations, delusions, other psychiatric reactions and more severe with then with levodopa and clear during withdrawal of medication
51
Contraindications dopamine agonist
History of psychotic illness Recent MI Active peptic ulcer Peripheral vascular disease (vasoconstriction effects)
52
What are the two forms of MAO inhibitors
MAO-A, MAO-B
53
MAO-A
Preferentially metabolizes NE and serotonin
54
MAO-B
Metabolizes phenylethyamine and benzylamine
55
__ and __ are metabolized equally by MAO-A and MAO-B
Dopamine | Tryptamine
56
Selegine
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
Bioavailability of selegiline
10% with peak plasma conc in an hour
58
Contraindication selegine
Patients taking meperidine, tricyclic antidepressants, or serotonin reuptake inhibitors (risk of serotonin syndrome)
59
Rasagiline
Irreversible inhibitor of MAO-B;more potent than selegine
60
What is rasagiline used for
Neuroprotective agent and for early symptomatic treatment of PD
61
Why avoid combination of levodopa and nonselective MAO inhibitor
May lead to hypertensive crisis (peripheral accumulation of NE)
62
Catechol-O-meethyltransferase COMT inhibitors
Metabolizes levodopa to 3-O-methyldopa, which competes with levodopa for transport across the intestinal mucosa and the BBB
63
What are some COMT inhibitors
Tolcapone and entacapone
64
Effect of COMT inhibitor
Prolong activity of levodopa by inhibiting its peripheral metabolism, which decreases clearance and increases bioavailability
65
Who takes COMT inhibitors
Helpful in patients receiving levodopa who have developed response fluctuations
66
Tolcapone
Central and peripheral active
67
Entacapone
Peripheral acting
68
__ causes an increase in liver enzyme levels and has been associated, rarely, with death from acute hepatic failure
Tolcapone
69
Side effects COMT inhibitors
Often due to levodopa Orange discoloration of the urine, diarrhea, abdominal pain and sleep disturbances
70
Apomorphine
Dopamine agonist at dopamine D2 receptor
71
Administration of apomorphine
Injection SQ for quick, temporary relief of off periods of akinesia in patients on dopaminergic therapy (clinical benefits in 10 min)
72
Adverse effects apomorphine
Nausea (can treat with trimethobenzamide) dyskinesia, drowsiness, sweating, hypotension, and injection site bruising
73
Amantadine
Antiviral agent whose MOA in Parkinsonism is unknown (may potentiation dopaminergic function by influencing synthesis, release, or reuptake of dopamine)
74
HL amantadine
2-4 hours
75
Peak plasma amantadine
1-4 hours
76
Excretion amantadine
Unchanged in urine
77
Adverse effects amantadine
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
Amantadine may cause livedo reticularis. What is that
A vascular condition characterized by a purplish mottled discoloration of the skin usually on the legs
79
Contraindication amantadine
Caution in patients wth a history of seizures or heart failure
80
Anticholinergic drugs
Centrally acting mAChR antagonists are available to treat patients with PD
81
What can mAChR antagonists be used for
Improve tremor and rigidity but have little effect on bradykinesia
82
Name some anticholinergic drugs
Benztropine, biperiden, orphenadrine, procyclidine, trihexyphenidyl
83
How give anticholinergic drugs
Patientsare given a low dose of drug, which is titrated upwards in amount until benefit occurs or adverse effects limit use
84
If one anticholinergic drug doesn’t work, what do u do
Try another one
85
Adverse effects of anticholinergic drugs
Common peripheral anticholinergic effects (sedation, mental confusion, constipation, urinary retention, blurred vision)
86
Tremor
B1 receptors have been implicated in some tremors Or Symptomatic tremor
87
What do tremors respond to if caused by B1
Metoprolol and propranolol
88
Symptomatic tremor
Controlled by the antiepileptic drug primidone in smaller doses than those used for seizures
89
Topiramate and tremor
Serotonin receptor agonist | Effective for tremor
90
Alprazolam(benzodiazepine) and intramuscular injections of Botox
Some patients help tremors
91
Huntington
Imbalance of dopamine and GABAcauses overactivity of dopaminergic path
92
Any therapy to slow Huntington depression
No
93
What drugs alleviate chorea
Drugs that impair dopaminergic neurotransmission like | Reserpine, tetrabenazine, olanzapine, phenothiazines)
94
What drugs exacerbate huntington
Drugs that activate dopaminergic signaling
95
Tics
Pimozide, haloperidol, tetrabenzaine Or A adrenergic agents like clonidine, guanfacine Or Botox
96
What do pimozide, haloperidol, and tetrabenzaine
Cause extrapyramidal syndromes, weight gain, sedation, irritability, and various phobias and are not always the first choice
97
Clonidine and guanfacine
A adrenergic agents effective with tics with fewer effects; in some casese
98
Botox tics
At a tic site will hep
99
Restless leg syndrome
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
ALS
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
MOA riluzole
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
Major adverse effects ALS
Nausea and weakness
103
Wilson disease drugs
Penicillamine Potassium disulfide Trientine Zinc acetate and zinc sulfate
104
Penicillamine MOA
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
Penicillamine excretion
Kidney
106
Adverse effects penicillamine
Nausea, vomiting, nephritis syndrome, myasthenia, optic neuropathy, and various blood disorders; after remission, patients may require maintenance dose
107
Potassium disulfide
Reduces intestinal absorption of copper and can be described in addition to penicillamine
108
Trientine
Chelating agent for Wilson
109
Sinc acetate and zinc sulfate
Increase fecal excretion of copper by decreasing GI absorption

Pharmacology (52 decks)

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