treatment of parkinson's disease Flashcards
Cardinal features of Parkinson’s
Tremors
Rigidity
Akinesia/Bradykinesia
Idiopathic PD initial presentations
Asymmetric
Positive response to levodopa or apomorphine
Postural instability and falls not present
Less rapid progression
Autonomic dysfunction not present
Morbidity in PD
Unable to perform basic ADLs
Dysphagia
Falls due to postural imbalance
Pathology
Significant loss of dopaminergic neurons in the substantia niagra Age-related Environmental toxins Genetics - Predisposition to toxins/insults - Genetic abnormalities
Non-movement symptoms
Cognitive impairment
Sleep disorders
Psychiatric disorders
Autonomic dysfunction
Goal of treatment
Manage symptoms
Maintain function and autonomy
Non-pharmacological treatment
PT
OT
Speech and swallowing
Surgery
Levodopa
Most effective for bradykinesia and rigidity
Causes N/V, hypotension
Levodopa PK
A: proximal part in small intestines
Increased F with benserazide/carbidopa
Decreased absorption with high fat/protein meals
DOPA decarboxylase inhibitors
Do not cross BBB
75-100mg daily for saturation of dopa decarboxylase (1:1 action)
1:4 – Sinemet, Madopar
1:10 – Sinemet
Levodopa AE
N/V Orthostatic hypotension Drowsiness, sudden sleep onset Hallucinations, psychosis Dyskinesia within 3-5y
Levodopa DI
Pyridoxine (Vit B6) - cofactor for dopa decarboxylase Iron Protein Antidopaminergic drugs - Metoclopramide, prochlorperazine - 1st gen antipsychotics - Risperidone
Dopamine agonists MOA
Act on D2 receptors in the basal ganglia
Mimic action of dopamine
Dopamine agonists PK
Longer half-life and duration of action than levodopa
Ropinirole metabolised in liver to inactive metabolites, DA in hepatic impairment
Pramipexole excreted largely unchanged in urine, DA in renal impairment
Dopaminergic agonists AE
N/V Orthostatic hypotension Hallucinations Somnolence, daytime sleepiness Compulsive behaviours Fibrosis Valvular heart disease Leg edema