Pharm Test 3 Parkinson

Question 1

Bromocriptine

Answer 1

Ergot DA receptor agonist 2nd line treatment
MOA: D2 agonist
Actions: combined with levodopa
AE: GI and cardiovascular effects, Dyskinesia, mental disturbance, pulmonary infiltrates, pleural and retroperitoneal fibrosis, erythromelalgia
**Little response in pt’s who do not respond to levodopa

Question 2

Pramipexole
Ropinirole
Rotigotine
Apomorphine

Answer 2

NON Ergot DA Agonists 2nd line tx
Actions: Apom: rescue Tx for “off” episodes. Pram and ropi: Well tolerated, better AE profile, Initial treatment esp. in younger pt’s
AE: QT prolongation, Dyskinesia, Drowsiness, Sweating, Hypotension
AE Apom: emetogenic–>pretreat with trimethobenzamide
***Rotigo: once daily transdermal patch

Question 3

Selegiline

Rasagiline

Answer 3

MAO inhibitors. Reduce motor fluctuations in pt’s with advanced disease
MOA Seleg: irreversible and selective MAO-B inhibitor
MOA Rasag: MAO-B
Actions: Mainly used as an adjunct to levodopa; has little potential forcausing a hypertensive crisis
***Rasag may be used as monotherapy eearly in disease

Question 4

Tolcapone

Entacapone

Answer 4

COMT inhibitors. Reduces motor fluctuations in pt’s with advanced disease
MOA: decrease metabolism of levodopa and decrease plasma 3-o-methyldopa. Increase uptake of evodopa–>increases DA in the CNS
Actions: Tol: CNS and periphery, Ent: periphery and is preferred b/c it lacks hepatotoxicity.
AE of Tol: fulminating hepatic necrosis is sassociated with tolcapone
**Inhibition of dopa decarboxylase–>compensatory activation of COMT pathway leading to increased 3-o-methyldopa which competes with levodopa for transport across the BBB and intestinal mucosa

Question 5

Amantadine

Answer 5

Antiviral, less efficacious than L-dopa
MOA: increased synthesis, release, or re-uptake of DA from surviving neurons
Actions: Tolerance develops more readily, but there are fewer side effects.
AE: Restlessness, agitation, confusion, hallucinations, Acute toxic psychosis at high doses, peripheral edema (responds to diuretics), Livedo reticularis–> mottled purple discoloration of the skin in a lace like pattern (resolves when drug is discontinued)
**USe with caution in pt’s with history of seizures or heart failure

Question 6

Benztropine

Trihexyphenidyl

Answer 6

Antimuscarinic used as adjuvant therapy to control tremor and drooling

Actions: improve tremor and rigidity, but have little effect of bradykinesia
AE: mood changes, xerostomia, pupil dilation, confusion, hallucination, urinary retention and dry mouth
**Cannot be used in pt’swith glaucoma, BPH, pyloric stenosis

Question 7

Levodopa

Answer 7

Dopamine precursor. Must be combined with Carbidopa (decarboxylase inhibitor that does not cross BBB) *only 10% reaches the CNS when combined with carbidopa
Does not stop the progression of disease but can decrease mortality
MOA: crosses BBB and gets converted to Dopamine by dopa decarboxylase. restores dopamine levels in extrapyramidal cells
Actions/use: DOC for parkinson’s. Relief is only symptomatic and olny lasts as long as drug is in body. Wearing off rxn’s –>end of dose akinesia. On-Off phenomenon–>fluctuations in response that are unrelated to timing; pt’s may benefit from apomorphine
AE: N/V/hTN/arrhythmia, B6 increases in peripheral metabolism (cofactor for dopa decarboxylase), Hypertensive crisis, may exacerbate psychotic sxs. CI in angle closure glaucoma
**may be a decline in the 3-5th year of therapy due to dclining neurons.
**Antipsychotic drugs may produce parkinsonism