Quiz 4 Flashcards
What is the autoimmune theory?
Attach on the CNS leading to a disruption of the BBB
Migration of T lymphocytes into the CNS
T-lymphocytes attack myelin
Results in demyelination
What is RRMS?
Relapsing-Remitting MS
What is the most common form of MS at diagnosis?
RRMS
What are RRMS exacerbations?
Clearly defined
What happens to neurologic function in RRMS?
Acute worsening
Is there remission from RRMS?
Periods of partial/complete
If a patient has RRMS, what other form may it develop into w.in 10 years?
SPMS
What is SPMS?
Secondary progressive MS
What happens to SPMS QOL during progression?
Steadily worsening +/- flare ups
Does SPMS have remission?
Minor recoveries
What is PPMS?
Primary progressive MS
How does disease progress in PPMS?
Slow but continuous worsening of their disease from the onset
Are there any relapses in PPMS?
No
What is the rate of progression in PPMS?
Varies over time
What is the least common MS?
PRMS
What is PRMS?
Progressive relapsing MS
How does PRMS progress?
Steadily worsening disease from the onset
Are there any relapses in PRMS?
Clear acute relapses +/- recovery
How does PRMS contrast to RRMS?
Periods between relapses are characterized by continuing disease progression
How do we treat acute exacerbations of MS?
HD methylprednisolone (500-1000mg/d) x 3-10 days
What are the 1a treatments for MS?
Interferon beta
Glatiramer
Dimethyl fumarate
What are the 1b treatments for MS?
Fingolimod
Teriflunomide
What are the 1c treatments for MS?
Natalizumab
Ocrelizumab
What are the 2nd line treatments for MS?
Mitoxantrone
Alemtuzumab
Daclizumab
What are the treatments of MS spasticity?
Baclofen
Tizanidine
Dalfampridine
What are the treatments of MS bladder sx?
Oxybutynin
Tolterodine
Dicyclomine
What are the treatments of MS sensory sx?
CBZ
Gaba
VPA
TCAs
What are the treatments of MS fatigue?
Amantadine
Modafinil
Methylphenidate
What is the pathophysiology of PD?
Loss/degeneration of dopamine neurons -> relative increase of cholinergic interneuron activity (tremors)
Development of Lewy Bodies
What are the cardinal features of PD?
Bradykinesia
Resting tremor
Muscle rigidity
Gait dysfunction, postural instability
What are SEs of levodopa therapy?
Abnormal involuntary movements (motor complications)
- Dyskinesia treatment
- Peak too high, must dose adjust
How do we treat dyskinesia d/t levodopa?
Smaller, more frequent doses of levodopa
Use sustained-release products
Amantadine 200-400mg QD
What is the “off” effect d/t in levodopa therapy?
End of dose deterioration
Motor sx of PD breakthrough
Trough
What is the management of the “off” effect?
Increase frequency of doses
Change to CR/ER formulation
When is CR/ER levodopa formula more effective?
For HS dose
What agents can be added to levodopa to get more steady dopamine effects?
DA, MAOI, COMT-i, or amantadine
If a PD patient is having a severe “off” effect, what can be given?
SQ apomorphine
What may cause drug resistant off periods
May be a result of delayed gastric emptying or absorption
What are ways we can manage drug resistant off periods?
Give on an empty stomach Crush/chew and take with a full glass of water Avoid CR formulation Switch to ODT Increase dose and/or frequency
How do we treat rapid on-off fluctuations?
Addition of DA, MAOI, COMT-i
Drug free period or drug holiday (rare)
How do we have nocturnal off state?
HS dose of DA
ER formulation of levodopa/dopamine agonist
What is the MOA of dimethyl fumarate?
Unknown
Thought to prevent damage of the brain and spinal cord through its antioxidant properties brought about by activation of the nuclear factor-like 2 pathway
What is the dose of dimethyl fumarate?
120mg twice daily for 7 days then increase to MD of 240mg twice daily
What is the BBW for dimethyl fumarate?
Increase risk of Progressive Multifocal Leukoencephalopathy (PML)
What are common AEs of dimethyl fumarate?
Flushing GI upset (ab pain, nausea, diarrhea), pruritus, rash, leukopenia
What do we monitor in dimethyl fumarate?
CBC at baseline then every 6-12 months
