Alzheimer's and Parkinson's Medication Flashcards
Pathophysiology of Parkinson’s Dz
Progressive depletion of dopaminergic neurons in the substantia nigra of the basal ganglia
Functional increase in ACh occurs (causing the characteristic resting tremor)
Lewy bodies (protein aggregates) found post-portem in remaining DA cells in the SN
Percentage of dopamine lost by the time a patient presents w/ symptoms
70-80%
4 core clinical features of Parkinson’s
- Bradykinesia
- Resting Tremor
- Rigidity
- Postural Instability
What is needed to make the dx of Parkinson’s?
Bradykineasia and at least one of the following:
- -Resting tremor
- -Rigidity
- -Postural Instability
Bradykinesia + 1 = possible PK
Bradykinesia + 2= probably PK
Bradykinesia +2/3 +response to meds = PD
5 predictors of Parkinson’s disease progression (these make a worse prognosis)
- Older age at onset
- Rigidity as presenting symptom
- Male
- Presence of comorbidities
- Decreased response to dopamine
What are the two MAO-B inhibitors used to treat PD? Which is used 1st line?
Selegiline and Rasagiline
–>Rasagiline is 1st line
Is levodopa 1st line in a patient w/ PD?
You can begin levodopa tx 1st line in a PD pt who is older, has cognitive impairment, or has mod-severe functional impairment. Otherwise hold off on using this and use rasagiline 1st line
Why is Rasagiline used above Selegiline?
Rasagiline is neuroprotective so it has fewer adverse effects (Selegiline can cause insomnia, jitteriness, dyskinesias, orthostasis, and serotonin syndrome)
MOA of Amantadine (Symmetrel)
Unclear - Augmentation of dopamine release from presynaptic terminals and inhibition of dopamine reuptake. Might also inhibit NMDA (glutamate inhibition)
Place in therapy for Amantadine
Initiated early stages w/ mild symptoms of PD and it improves bradykinesia, rigidity, and tremors
Side effects of Amantadine:
Orthostatic hypotension confusion nightmares hallucinations nervousness irritability livedo reticularis
When would you give a Parkinson’s pt an anticholinergic agent?
If a patient presents early w/ resting tremor and has minimal bradykinesia or rigidity. Can be monotherapy or adjunct
In what types of patient’s with PD would you want to avoid anticholinergic agents?
Pt’s w/ cognitive deficits
BPH
Urinary issues
Glaucoma
**AKA - the elderly!
MOA of dopamine agonists
Direct stimulation of striatal dopamine receptors. Have longer half lives than LD so they produce more constant stimulation of dopamine receptors
Dopamine agonsts can delay the need for levodopa by _____ years in ____% of pts
4-5 years in 80% of patients
Important note about dosing of dopamine agonists.
START LOW AND GO SLOW
Effects will take 4-8 weeks to take effect
A patient who is currently taking LD wants to add a dopamine agonist. What needs to be done to either LD or DA?
LD needs to be decreased by 20-30%
Name the 4 dopamine agonists - non-ergot derivatives
- Pramipexole (Mirapex)
- Ropinirole (Requip)
- Rotigotine (Neupro)
- Apomorphine (Apokyn)
What is apomorphine (amokyn) used for?
“Rescue therapy” for “delayed on”/”no on”/ or “freezing episodes”
PRN tx of hypomobility in pts w/ advanced PD
If you want to start a pt on apomorphine what must you also do/prescribe?
Start trimethobenzamide 3 days prior to administering apomorphine and then continue trimethobenzamide for the 1st two months of treatment
Do not use apomorphine with _______ because the combination could result in severe hypotension
serotonin agonists (ondansetron)
What is the formulation of apomorphine?
SubQ - so pt may require someone else to inject it d/t hypomobility
NO ORAL DOSING!!
Why is carbidopa given with levodopa?
Levodopa is metabolized to dopamine by L-amino acid decarboxylase so that it cannot cross the BBB. Levodopa alone also causes significant N/V and the doses we require to get it into the substantia nigra.
Because of this problem, we give carbidopa which is a peripheral decarboxylase inhibitor used to increase LD’s bioavailability.
____ less LD dose required to achieve same effect when it is dosed with carbidopa.
80% less
