Parkinsons Flashcards
What are the classic Sx of PD
Resting tremor
Rigidity
Bradykinesia
What are other Sx of PD
Gait disturbance Micrographia Hypomimia (masked facies) Anosmia Depression Freezing Hypophonia
What is Atypical PD
Early speech and gait impairment
NO resting tremor
NOT relieved by L-dopa
What is Secondary PD
d/t drugs (dopamine blockers), stroke, tumor, infection, Wilson’s or Huntington disease
What is the theory behind PD
Gene mutation + toxic environmental factor
Who is PD most common in
Men
>60 y/o (increases w/ age, but can happen in younger too)
What are common RF for PD
1st degree relative has it
Pesticide exposure
high dairy consumption
+/- depression and constipation (RF or early Sx?)
What is “Parkinsonism”
Bradykinesia + Tremor and/or rigidity
PD is characterized pathologically by
Decrease in dopaminergic neurons in Substantia Nigra (causing paired masses of grey matter w/in white matter of cerebral hemispheres)
+/- Lewy Bodies (contain alpha synuclein proteins)
How do you diagnose PD
Clinically** Resting tremor + Asymmetry + Response to L-dopa
What other diagnostic tests can be done for PD
Brain MRI (r/o stroke) DaT scan/ PET/ advanced MRI (visualize dopamine system in brain)
What areas of the brain are involved in PD (dopamine)
Basal ganglia; Thalamus communicates with motor cortex
Dopamine involved in Direct and indirect pathways
When should you start treatment of PD
When Sx affect dominant hand
Sx interfere w/ ADL
bradykinesia/gait disturbances are severe
What is the gold standard for PD treatment
L-Dopa (most effective for bradykinesya, tremor, and rigidity)
Why isnt L-Dopa used first line
It loses effectiveness after a few years
Wearing off effect
Delayed on effect
peal-dose dyskinesia
What can you take with L-Dopa to increase BBB crossing
Carbidopa; a decarboxylase inhibitor
What is the real first line Tx to PD
Dopamine Agonists (Bromocri[tine and Pramipexole) used as monotherapy to delay eventual need for L-Dopa
What are S/E of Dopamine Agonists
Impulse control (gambling, sexual behavior, hallucinations, vivid dreams)
What are MAO-B inhibitors good for
reducing “off” time
They block central dopamine metabolism (Rasagaline, Selegiline)
What are COMT-Inhibitors good for
reducing “off” and prolonging “on” time
(tolcapone, entacapone)- prevent conversion of L-Dopa to inactive form
What are S/E of COMT inhibitors
N/V
Dyskinesia
discolored urine
Diarrhea
What are anti-cholinergics good for
Benztropine- used for tremors
Who is Amantadine used in
Young with mild PD
Older with severe dyskinesia
What is Amantadine
an antiviral (flu) that also increases dopamine release
