week 5- diseases Flashcards
Red flags for PD diagnosis
name something that would be decreased in the CSF of Parkinsons Its
Decreased HVA (hemovanillic acid- dopamine metabolite) in CSF
What is the Back hypothesis
GI sending toxins to the brain (vagus nerve innervates GI and it does bring stuff to the medulla brain starts in medulla (dorsal medulla CN X, XI) and makes its way up rostrally Can find lewy bodies to PD PTs early on,….smell lost first because olfactory neurons sensitive to toxins from the GI
what is the Parkinsons staging
starts in medulla (dorsal medulla CN X, XI) and makes its way up rostrally • Presymptomatic 1-2, symptomatic – 3-4 with lost dopamine, advanced 5-6 with dementia
what are the predisposing factors for Parkinsons disease
Age (incidence increases rapidly over 60y, mean age of dx 70.5y)
Males
Genetics: SNCA , LRRK2, GBA
Pesticide exposure
Europe, North American, South American have higher prevalence
what is the classical clinical presentation of parkinsons
Classic presentation TRAP – tremor, cogwheel rigidity, akinesia (bradykinesia, hypokinesia) and postural instability
May also see: masked faces, orthostatic hypotension, constipation prior to manifestation, festinating gait, freezing, micrographia, microphonia
clinically–> see less heel to toe tapping
what sign is always consistent for PD
Cogwheel rigidity classic for parkinsons
what is the Tx for PD
COMT –> MOA –> agonist –> L dopa
L-DOPA (levadopa) + carbidopa–>
Moderate to severe
DA agonists (e.g. pramipexole) –>
Can be used for moderate symptoms in <65 yo over levodopa b/c less likely to cause dyskinesias and once/day dosing
MAO-B inhibitors (e.g. rasagiline, selegiline)
Because dopamine can be converted into this
mild symptoms
COMT inhibitors (e.g. entacapone)
Because dopamine can be converted into this
Amantadine (antiviral)
(mech of action in PD is unknown. It may cause NE release; may block NMDA receptors)
Anticholinergics (mAChR antagonists)
where would you target a DBS for PD
rigidity and bradykinesia–> STN and GPI
tremor target thalamus
what is the mechanism of astrocyte modulation as a potential PD therapeutic
increase endocannabinoids and excite the direct pathway or inhibit the indirect
how do you distinguish between lewy body dementia and PD
PD- if dementia is more than a year after motor symptoms
How do you manage psychosis and hallucinations in PD PTs
1st: lower PD drugs (usually due to amantadine, MAO-Is, dopamine agonists or COMT….levodopa least likely to cause)
2nd: low-dose antipsychotic: quetiapine or Pimavanserin (only approved drug for PD psychosis)
what do PD PTs usually die of
malnutrition and aspiration pneumonia is the leading cause of death in PD
what is the prognosis of PD
80% severely disabled or dead within 10-14 years of diagnosis
From disease impairment to disability occurred between 3-7 years after the onset of PD
what are some associated conditions of PD
Akinetic crisis (stiffness, hyperthermia) - can occur as a result of unintended dopamine withdrawal in patients on dopamine therapy
parkinsonian tremor
characteristics
location
frequency
associated conditions
pathophysiology
postural tremor
characteristics
location
frequency
associated conditions
pathophysiology
Intentional/Cerebellar
characteristics
location
frequency
associated conditions
pathophysiology
ID some of the parkinsonisms
drug induced, supranuclear palsy, Multiple system atrophy, vascular, lewy body dementia, corticobasal degeneration
