Parkinson's disease 4-6 Flashcards
parkinsons disease
-progressive neurodegenerative disease
-s/s: dyskinesia(tremors, rigidity, postural instability, slowed movements), flat affect, dementia, psychological disturb
two neurotransmitter for Parkinsons
-dopamine: inhibit release GABA
-ACh: excite neurons that release GABA
-in Parkinsons: not enough dopamine, too much ACh
–> give dopaminergic agents and antiACh agents
Levodopa
-MOA: dopamine replacement (PO)
-treatment of choice for more severe s/s
-always given with Carbidopa
-takes months for full effect
levodopa on/off phenomenon
-if use alone, long term use (5th year): tolerance builds, no more effect (loss can be sudden or gradual; happen any time)
-on:mobile
-off: unpredictable loss of immobility
TREAT:
=shorten dose interval: more doses
=add drug to prolong half life: Carbidopa or COMTi
=give direct acting dopamine agonist
d
levodopa adverse
-N/V (also dark sweat and urine)
+admin low doses
+NO give with food or high protein (bc competes with receptors in GI and decrease absorption)
-Cardiovascular: postural hypotn, dysrhtymias
-dyskinesia(head bobb, tics, involuntary jerks): within first year of txt
=reduce dose
= add dopamine releasing agent (Amantadine)
-EPS: acute dystonia, pseudoparkinsonism, akathasia, tardive dyskinesia
-psychosis and CNS effects: visual hallucinations, dreams and nightmares, paranoid –> reduce dose (treat with antipyschotic can be problematic)
-malignant melanoma: increase risk vice versa
Carbidopa
-MOA: no effect on its own –> give in combo with Levidopa (inhibits decarboxylation of Levodopa in intestine –> increase Levo available in brain = enhance Levodopa)
-also helps decrease adverse effects like N/V
Amantadine
-is a dopamine releaser (release it from its receptors)
-MOA: blocks dopamine reuptake
-best for managing dyskinesia due to Levodopa
-2-3 days response (response diminish within 3-6 months)
