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28 Cards in this Set

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Question: Regarding the anticipated actions of levodopa, the PT would be informed that?

The prescribing physician will know that levodopa does?
GI distress, postural hypotension, and dyskinesias. Therapeutic benefits wont last forever.

L-dopa causes less peripheral toxicity but more CNS or behavioral SE when its conversion to dopamine is inhibited outside the CNS. L-dopa is a precursor of melanin and may activate malignant melanoma.
Question: Carbidopa is commonly used in the treatment of Parkinson's disease because it?
Inhibits L-amino acid decarboxylase.

Helps to decrease L-dopa dose and reduce peripheral SE of levodopa.
Question: A 72 year old PT with parkinsonism presents with swollen feet. They are red, tender, and very painful. These symptoms would abate within a few days if the PT were to stop taking?
Bromocriptine.

These are signs of erythromelalgia. More serious effects include pulmonary infiltrates and retroperiotoneal fibrosis; therefore, ergots are rarely used for Parkinson's disease.
Question: A PT with parkinsonism is treated with levodopa. He suffers from irregular, involuntary muscle jerks that affect the proximal muscles of the limbs. What is an accurate statement?
Dyskinesias occur in 80% of PTs taking levodopa.

Dopamine agonist will exacerbate dyskinesias.
Question: A PT with parkinsonism is being maintained on levodopa-carbidopa with adjunctive use of low doses of entacapone, but continues to have off-periods of alkinesia. The most appropriate drug to "rescue" the PT, but will only provide temporary relief is?
Apomorphine.

Note: pretreatment with antiemetic trimethobenzamide for 3 days is essential to prevent severe nausea.
Question: Concerning the drugs in parkinsonism, what is true?
Levodopa causes mydriasis and can precipitate an attack of acute glaucoma by increasing intraocular pressure.

Used cautiously with open-angle glaucoma and contraindicated in angle-closure glaucoma.
Question: Previously healthy 40 year old suffers from slowed mentation, lack of coordination, and brief writhing movements of her hands that are not rhythmic. In addition, she has delusions of being persecuted. The woman has no history of psychiatric or neurologic disorders. What is the most appropriate drug for treatment?
PT has Huntington's disease.

Use drugs that deplete dopamine (e.g., tetrabenazine, reserpine) or dopamine antagonists (e.g., haloperidol, perphenazine).
Question: In parkinsonian PTs who have prostatic hypertrophy or obstructive GI disease, great caution must be exercised in the use of this drug (or drugs form the same class).
Benztropine, a muscarinic antagonist. It may cause urinary retention and GI effects.

Contraindicated also angle-closure glaucoma.
Question: With respect to pramipexole, what is accurate?
Activates D3 in the striatum; effective when used as a monotherapy in mild cases; may cause postural hypotension; not an ergot derivative. Sometimes of value in PTs who have become refractory to L-dopa.
Describe the pathophysiology behind parkinsonism, and what is out of balance as a consequence?

What are the signs?
Degeneration of dopaminergic neurons in the nigrostriatal tract that normally inhibit the activity of striatal GABAergic neurons. This leads to excessive excitatory actions of cholinergic neurons on striatal GABAergic neurons. Therefore, dopamine and acetylcholine are out of balance in parkinsonism.

Signs: rigidity of skeletal muscles, akinesia (or bradykinesia), flat facies, tremor at rest.
What drugs can induce parkinsonism?
Antipsychotic drugs: block dopamine receptors.

Resperine: depletes brain dopamine.
What is the type of therapy involved in treating parkinsonism?
Increase dopamine in the brain (D2 receptor subtype) and decreasing muscarine cholinergic activity in the brain.
What is the MOA of L-dopa (levodopa)?

What drug is often given with L-dopa?
Passes the BBB, converted to dopamine via dopa decarboxylase.

Carbidopa, doesn't cross the BBB, but inhibits dopa decarboxylase found in the peripheral tissues; therefore, increasing the half-life of L-dopa.
What are the pharmacologic effects of levodopa?

What drug can inhibit on of the features associated with levodopa?
Dyskinesias is very common: choreoathetosis of the face and distal extremities. Also, chorea, ballismus, myoclonus, tics, tremor.

On-off phenomena

Note: COMT inhibitors can improve fluctuations in levodopa responses.

Behavioral: anxiety, agitation, confusion, delusions, psychosis (contraindicated in these PTs)

GI effects: emetic actions--dose dependent.

Postural hypotension, cardiac effects (arrhythmias, tachy)
What are the dopamine agonist that can be used for parkinsonism?
Bromocriptine: ergot alkaloid. Partial D2. Used for those who are refractory to or cannot tolerate L-dopa. Behavioral more common than newer dopamine agonist.

Pramipexole: non-ergot D3, smooth out fluctuation. SE: mental disturbances more common than levodopa.

Apomorphine:

Note: non-ergots are preferred. Ergot-related SE include erythromelaglia and pulmonary infiltrates.
What drug is given as a "rescue therapy" for parkinsonism?

What is necessary with this drug?
Apomorphine, a potent dopamine agonist give via injection for short temporary relief (1 - 2 h) of an "off-period" of akinesia.

Due to severe nausea, pretreatment for 3 days with s (eg., trimethobenzamide) is necessary.
What are two MAOIs used in parksinonism? MOA?
Selegiline and rasagilene are selective MAOI of type B, which prevents the metabolism of dopamine.

Selegiline: minimal efficacy when used alone, given with L-dopa.

Rasagiline: more potent, has been used as a monotherapy in early stages.
Issues dealing with selegiline?
Given with meperidine, results in mortality.

Implicated in serotonin syndrome when used with SSRIs.

SE of MAOIs type B result from enhance effect of L-dopa
What are two catechol-O-methyltransferase (COMT) inhibitors? MOA?
Entacapone and tolcapone

They inhibit COMT that converts levodopa to 3-O-methyldopa (3OMD). Increase 3OMD competes with levodopa for active transport into the CNS.

They help decrase fluctuations, and prolonging "on-time"
SE of COMT inhibitors?
Orange discoloration of the urine, sleep disturbances.

Tolcapone: hepatic failure<--must monitor liver function and obtain signed PT consent.
What antiviral can be used for parkinsonism? MOA, SE?
Amantadine, enhances release of dopamine from the nigra striatum.

Ataxia, dizziness, slurred speech. Livedo reticularis (netlike rash)

Note: binds to M2 surface protein on influenza A that blocks uncoating; also used for rubella.
What antimuscarinic drug is used for parkinsonism?
Benztropine: decreases actions of cholinergic neurons on cells in the striatum by blocking muscarinic receptors.

SE: antimuscarinic symptoms. Contraindicated in PTs with narrow-angle glaucoma.
DOC for essential tremor?
Propranolol.

Note: beta-blockers are used in caution with CHF, asthma, diabetes, hypoglycemia.
Pathophysiology behind Huntington's disease? Treatment?
GABA is diminished and dopaminergic functions are enhanced. Defective choline acetyltransferase (therefore, low acetylcholine).

Amine-depleting drugs: reserpine, tetrabenazine.

Dopamine receptor antagonist: haloperidol, perphenazine
Treatment of Tourette's syndrome?
Haloperidol and other dopamine D2 receptor blockers, including pimozide.
Drug-induced dyskinesias are treated by?
Lowering drug dosage, changing drug therapy, treating with muscarinic blockers. With acute dystonias, treat with benztropine, or diphenhydramine.

Note: L-dopa and bromocriptine are not useful since antipsychotic block dopamine receptors.

Tardive dyskinesias: older antipsychotic drugs, from denervation super-sensitivity. Irreversible.
DOC for Wilson's disease?

SE?
Penicillamine: copper chelator

Myasthenia, optic neuropathy, blood dyscrias.
DOC for restless leg syndrome?
Ropinirole: dopaminergic

Note: more common in pregnant women and in uremic and diabetic PTs.