Neuro part 2 Flashcards
Long-term affects of dopamine replacement
Dyskinesia
Wearing-off phenomenon
On-off medication state
3 ways to treat Parkinson’s disease
Dopamine replacement therapy
- Dopamine agonist therapy
- Anticholinergic therapy
1st line for Parkinsons drug treatment
Levodopa-carbidopa (Sinemet)
Levodopa-carbidopa (Sinemet) MOA
Levodopa (l-dopa) MOA: precursor to dopamine that can cross BBB and be converted to have CNS action
Carbidopa MOA: stops breakdown of l-dopa to dopamine in periphery so more l-dopa crosses BBB
Levodopa-carbidopa (Sinemet) AE:
Problematic AE: motor disturbances
End of dose “wearing off” – stiffness and rigidity return
Due to short t½ of l-dopa and/or med nonadherence
“Delayed on” or “no on” – med is not having effect
Due to absorption issues
Freezing – sudden inhibition of lower-extremity function, “feel stuck to the floor”
Exacerbated by anxiety
“On” period dyskinesia- Usually due to peak drug levels causing increased dopamine response
don’t take with food/high protein food → decrease absorption
MAO-B Inhibitors MOA, AE
MOA: inhibit monoamine oxidase B (MAO B) which typically breaks down dopamine thus increasing dopamine levels in CNS
Risk of serotonin syndrome when combined with serotonergic meds
COMT Inhibitor MOA, AE
MOA: inhibits COMT which in turn decreases breakdown of l-dopa
AE >10%: involuntary movements, nausea
Amantadine
MOA: unknown; possible increases dopamine release or may have direct effect on dopamine neurons (different sources classify as dopamine replacement or dopamine therapy)
AE: anticholinergic AE, CNS effects (confusion, hallucinations, dizziness)
Usually in early disease management
ropinirole (Requip) MOA, AE
MOA: binds to and agonizes dopamine receptors
AE: nausea, drowsiness, dizziness, syncope
Monitor for light-headedness and postural hypotension (especially when start and ↑ dose)-especially with older patient, hallucinations, lower-extremity edema
Less common: impulsive behavior, sleep attacks
Parkinson’s Disease Drug Concerns
Timing of PT session with delivery of medications
Improved motor function seen within 1-1.5 hr of taking dopamine replacement medication
PT during “on-cycle” can enable improved patient participation/performance
Still important to treat patients during “off-cycle” – to see how much impaired their mobility is during that off cycle
Long-term medication use and disease progression
Levadopa dosage less effective over time
More “off” cycles as disease state progresses
symptoms of MS
weakness, fatigue, sensory loss, UMN signs,visual disturbance, autonomic dysfunction. All of these issues results in gait and balance deficits, memory problems, and disability
most common MS
Relapsing-Remitting type most common
Drugs to treat progression of MS
Interferon β
Glatiramer acetate
Sphingosine 1-Phosphate Receptor Modulator
Dimethyl fumarate
Monoclonal antibodies: natalizumab, ocrelizumab
Interferon β
MOA: has an impact on immune function
AE >50%: flu-like symptoms, injection site reaction
Monitor for: neuropsychiatric changes, drug-induced hypothyroidism, worsening cardiac function in HF
Glatiramer acetate
MOA: reduce autoimmune response to myelin by reducing T-cell response against myelin
Most common AE: injection site reaction (mass, pain, erythema, itching, lipoatrophy if not rotating site
Fingolimod (Gilenya)
blocks release of lymphocytes into CNS = ↓ inflammation
AE >15%: headache, ↑ LFTs (liver function test
Monitor: bradycardia (especially within 24 hours of first dose; usually return to baseline HR after 1 month therapy
Dimethyl fumarate
MOA: may have anti-inflammatory properties
AE: GI (N/V/D, abdominal pain in 12-18%) and flushing (up to 40%) usually improve with time
Monoclonal Antibodies
Overall MOA: ↓ inflammation in CNS
Monitor for infection (respiratory, skin, herpes-related) due to increased risk
What is PML?
serious risk associated natalizumab, ocrelizumab, dimethyl fumarate,
and SP1 Receptor modulators
Demyelinating CNS disorder
Refer if any suspicion of PML*
S/Sx: altered mental status (AMS), aphasia, ataxia, hemiparesis, hemiplegia, visual disturbance (double vision, partial blindness), seizure
MS drug concerns
FATIGUE: most common and disabling MS symptom
Patient may take additional medications to address fatigue
Disease-modifying drugs can have substantial adverse effects including flu-like symptoms to immunosuppression
AZD treatment
Blocking acetylcholinesterase
Medications targeting NMDA pathway
General Treatment Approach AZD
Mild:
Cholinesterase inhibitor
Moderate:
Cholinesterase inhibitor + memantine more likely to delay progression
Donepezil (Aricept)
Cholinesterase Inhibitors
MOA: inhibits acetylcholinesterase
Only modest improvements in cognition and activities of daily living
Weigh AE risk and cost vs. limited benefit
Duration of benefit: 3 to 24 months
AE: anticholinergic effects (DUMBELLS)
Taper if discontinuing, monitor for worsened cognitive function
Memantine (Namenda)
antagonizes NMDA receptor = stops excessive receptor activation by glutamate = decreases excitation and neuronal death
AE: monitor for falls, dizness
Who should not be taking with additonal AZD drugs?
Anticholinergic drugs
Some OTC antihistamines like diphenhydramine (Benadryl)
Inhaled anticholinergic drugs like tiotropium (Spiriva) for respiratory disorders
Some meds for overactive bladder like oxybutynin
Anticholinergic drugs for Parkinson Disease
Tricyclic antidepressants which are also used for neuropathic pain
AZD drugs PT concerns
Be aware of potential AE with meds
Cholinergic meds: GI issues (NVD) most common-
Memantine may cause dizziness, watch for falls
Communicate behavioral issues to healthcare providers
Timing of ph ysical therapy
Provide structure to reduce behavioral issues
Reduce behavioral issues related to sundowning
Utilize time of day when patient most alert
