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NS2 Test 3 > Drugs for Movement Disorders DSA > Flashcards

Drugs for Movement Disorders DSA Flashcards

1
Q

Patients with what experience tics?

A

Gilles de la Tourette syndrome

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2
Q

Parkinsons disease pathological hallmark

A
  • loss of dopaminergic neurons of substantia nigra

- lewy bodies–intracellular inclusions

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3
Q

dopaminergic neurons of SN–function

A
  • inhibit the GABAergic output from the striatum

- cholinergic neurons exert an excitatory effect on GABAergic neurons

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4
Q

treats Parkinson disease

A
  • levodopa
  • dopamine R agonist
  • MAO inhibitors
  • COMT inhibitors
  • Amorphine
  • Amantadine
  • Anticholinergic drugs
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5
Q

Levodopa MOA

Levodopa–coadmininistered with?

A

-precursor to dopamine; agonist at D Rs (mostly D2 R); absorbed from small intestine (peak plasma conc–1-2 hours after oral dose); 1-3% of levodopa enters the brain (the rest is metabolized extracerebrally by decarboxylation to dopamine)

  • carbidopa!
  • DOPA decarboxylase inhibitor that doesn’t cross the BBB–reduced peripheral metabolism, increased plasma levels, increased half life, increased levodopa for entry into brain
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6
Q

Levodopa clinical use

A
  • Parkinsonian syndrome
  • lowers mortality rate when initiated early
  • best results–first few years of treatment
  • 1/3 of patients respond very well, 1/3 respond less well, 1/3 unable to tolerate medication or doesn’t respond at all
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7
Q

Levodopa adverse effects–GI

A
  • in absence of carbidopa–anorexia, nausea, vomiting (80% of patients)
  • with carbidopa–less frequent side effects (20% of patients)
  • vomiting–act of chemo R trigger zone in brainstem
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8
Q

Levodopa adverse effects–CV

A
  • postural hypotension (asymptomatic frequently)
  • hypertension when taking large doses
  • increases in cardiac arrhythmias–rare–due to increased peripheral catecholamine synthesis
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9
Q

Levodopa adverse effects–dyskinesias

A
  • 80% of patients

- Choreoathetosis of face and distal extremities

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10
Q

Levodopa–adverse effects behavioral effects

A
  • ,amu changes in mood/personality

- atypical antipsychotic agents help counteract (clozapine, olanzapine, quetiapine, risperidone)

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11
Q

Levodopa–adverse effects–fluctutions in response; on-off phenomenon

A
  • wearing off phenomenon (due to dose timing)–less effective as time goes on?
  • on-off phenomenon–off periods of marked akinesia alternate of a few hours with on-periods of improved mobility but often marked dyskinesia
  • apomorphine–provide temporary benefit
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12
Q

Levodopa drug interactions

A

-monoamine oxidase A inhibitors–may experience hypertensive crisis when combined with levodopa

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13
Q

Levodopa–contraindications

A
  • psychotic patients
  • angle closure glaucoma
  • history of melanoma, skin lesions
  • active peptic ulcer (GI bleeding)
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14
Q

Dopamine R agonsits–used when?

A
  • in patients with PD–associated with lower incidence of response fluctuations and dyskinesias (that occur in long term levodopa therapy)
  • usually patients who dont respond well to levodopa, dont respond well to dopamine agonists
  • can be administered in addition to levodopa/carbidopa and in patients who are taking levodopa who have on-off phenomenon
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15
Q

Dopamine R agonits

A
  • Bromocriptine (D2)
  • Pramipexole (D3)
  • Ropinirole (D2)
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16
Q

Bromocriptine

A
  • D2 agonist
  • also approved for treatment of endocrine disorders
  • bioavailability 28% with peak plasma concentration attained
  • half-life–15 hrs
  • extensive first-pass metabolism (CYP3A4)
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17
Q

Prampipexole

A
  • D3 Receptors
  • also for treatment of RLS (restless leg syndrome)
  • peak plasma conc in 2 hours; half life of 8 hours
  • 90% excreted in urine (pts with renal insufficiency need dose adjustment)
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18
Q

Ropinirole

A
  • D2 Receptors
  • treats RLS
  • metabolized by CYP450 (CYP1A2)–coadmin with agents that are also metabolized by CYP1A2 may reduce the clearance of ropinirole
  • peak plasma concentration in 1-2 hours; half life of 6 hours
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19
Q

dopamine R agonists–adverse effects–GI

A

-anorexia, nausea, vomiting, constipation, dyspnea, reflux esophagitis

20
Q

dopamine R agonists–adverse effects–CV

A
  • -postural hypotension
  • -bromocriptine–digital vasospasm
  • -peripheral edema and cardiac arrhymias–may indicate need to discontinue therapy
21
Q

dopamine R agonists–adverse effects–dyskinesia

A
  • -similar to levodopa

- -reversed by reducing total dose

22
Q

dopamine R agonists–adverse effects–mental

A
  • -confusion, hallucinations, delusions, others
  • -move severe with dopamine agonists than levodopa
  • clear during withdrawl of medication
23
Q

contraindications to dopamine receptor agonists

A
  • psychotic illness, recent MI, active peptic ulcerartion

- bromocriptine–in patients with peripheral vascular disease (vasoconstricting effects)

24
Q

MAO–A and B metabolizes

A
  • A–NE and serotonin
  • B–phenylethlamine and benzylamine
  • dopamine and tryptamine–metabolized equally by A and B
25
Q

MAO inhibitors

A
  • Selegiline

- Rasagiline

26
Q

Selegiline

A
  • selective irreversible MAO-B inhibitor
  • slows breakdown of dopamine, prolongs the effects of levodopa
  • used as adjunctive therapy in patients with declining or fluctuating response to levodopa
  • 10% bioavailability, peak plasma concentration in 1 hour
27
Q

Selegiline–contraindications

A

–in patients taking meperidine, tricyclic antidepressants, serotonin reuptake inhibitors

28
Q

Rasagiline

A
  • irreversible MAO-B inhibitor–more potent than Selegiline
  • used as neuroprotective agent and for early symptomatic treatment for PD
  • combined administration of levodopa and a non-selective MAO inhibitor should be avoided–may lead to hypertensive crisis (accum of NE)
29
Q

COMT function

A

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

30
Q

COMT inhibitors

A
  • tolcapone, entacapone
  • prolong activity of levodopa by inhibiting its peripheral metabolism which decreases clearance and increases bioavailability
  • helpful in some patients receiving levodopa who have response fluctuations
  • tolcapone–central and peripheral effects
  • entacapone–peripheral effects
31
Q

COMT side effects

A
  • Tolcapone may cause increase in liver enzyme levels, associated rarely with death from acute hepatic failure
  • -orange discoloration of urine, diarrhea, abdominal pain, sleep disturbances
32
Q

Apomorphine–MOA

A
  • dopamine agonist–stimulate postsynaptic D2 receptors in caudate-putamen
  • subcutaneously–quick temporary relief of off-periods of akinesia
  • -nausea–pretreat with trimethobenzamide
  • *INJECTABLE
33
Q

Amantadine MOA

A
  • antiviral agent, MOA in parkonsinism is unknown
  • benefits may be short lived
  • may cause livedo reticularis, vascular condition of purplish mottled discoloration of skin, legs
  • use with caution in patients with seizure, heart failure
34
Q

anti-cholinergic drugs–used for?

A

centrally acting mACHR antagonists–can improve tremor

-benztropine, biperiden, orphenadrine, procyclidine, trihexyphenidyl

35
Q

tremor responds well to?

A
  • metoprolol and propanolol (B1 receptors implicated in some tremors)
  • Topirimate (serotonin R agonist)
  • Alprazolam (benzodiazepine)
  • botulinum toxin A (intramuscular injections)
36
Q

symptomatic tremor–controlled by?

A

primidone (antiepileptic drug)

37
Q

Huntington disease–imbalance in?

A
  • dopamine, Ach, GABA in basal ganglia
  • results in overactivity of dopaminergic nigrostriatal pathways
  • GABAergic neurons degenerate
38
Q

drugs that impair dopaminergic Nt often alleviate chorea

A
  • reserpine
  • tetrabenazine
  • block vesicular monoamine transporter and deplete cerebral dopamine stores
39
Q

HD–therapy for patients who are depressed

A
  • antidepressants
  • Fluoxetine–depression and irritability
  • carbamazepine–depression
40
Q

Tics–most effective pharmacologic approach

A
  • -neuroleptic antipsychotics–pimozide (but cause extrapyramidal syndromes, weight gain, sedation, phobias)
  • -alpha-adrenergic agents–clonidine, guanfacine
  • -botulinum toxin A
41
Q

restless leg syndrome–first line of treatment

A
  • -correction of coexisting iron-deficiency anemia
  • -dopamine agonists, levodopa, diazepam, clonazepam, opiates
  • -first line of treatment–non-ergot dopamine agonists–pramipexole and ropinirole
42
Q

ALS–drug, MOA

A
  • -Riluzole–prolongs survival by a few months

- -inhibits glutamate release, blocks postsynaptic NMDA-glutamate receptors, inhibits Nav channels

43
Q

Wilson disease–what is it?

A
  • autosomal recessive
  • reduced ceruloplasmin (major copper-carrying protein in blood)
  • increased conc of copper in brain and viscera
  • signs of hepatic and neurologic dysfunction
44
Q

Wilson disease–drugs

A
  • Penicillamine–chelating agents that forms a stable complex with copper and is excreted by kidney
  • -Potassium disulfide–reduces intestinal absorption of copper
45
Q

Wilson disease–other helpful agents

A
  • trientine (chelating agent)

- zinc acetate and zinc sulfate (increase fetal excretion of copper by decreasing GI absorption)

46
Q

Though not as effective, DA agonists

A

Do not require metabolic conversion to active product
Longer half life so less daily dosing needed
Initial therapy associated with fewer motor complications and delays need for levodopa
Provide benefit when used as mono therapy in 80% of pts in early stage diseaase
DA agonists is first line for pts 65

NS2 Test 3 (14 decks)

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