12.1 Neuropharmacology Flashcards
proportion of basal ganglia lost to give PD symptoms
> 50%
where do dopamingeric neurones project to?
caudate nucleus and putamen
abnormal protein in PD
alpha synuclein, misolds
why does dopamine reduce in PD, aside from less substantial nigra?
increased cell turnovers upregukate receptors so uses up remaining dopanine
describe the tremor of PD
asymmetric, low freq, pill rolling, at rest, goes away on touching somethign
describe the rigidity in PD
lead pipe: resistance constant throughout arc
describe the bradykinesia of PD
issue maintaining amplitude of movement
cant keep a rhythm
cog wheeling
jolting of joints throughout movement
describe the gait in PD
difficult to start/stop
forward flexed
unilateral
reduced arm swing
turn around as whole
reduced fluidity of movement
hallucinations in PD
frightening, aggressive
levodopa half life is 2 hours. consequences of this?
fluctuations in blood levels and symptoms
why is levodopa given with peripheral dopa decarboxylase inhibitor?
reduced dose
reduced side effects
more levodopa reaches brain
tablet formulations of levodopa
-standard
-controlled release
-dispersible non soluble
huntingtons chorea
hypo/hyperrelfexia, long term effect of too much levodopa
why cant COMT inhibitors be used alone? how to overcome?
no therapeutic effect
use with levodopa and dopa decarboxylase inhibitor
can dopamine receptor agonists be first line?
yes, if levodopa less good
punding
rearranging stuff needlessly
repetitive compulsive activity
why could people be quite susceptible to side effects of PD treatment?
elderly
drug for PD patients with severe motor fluctuations
apomorphine s.c. bolus continuous infusion
role of anticholinergics in PD
problematic tremor relief
NO EFFECT ON OTHER SYMTPOMS
whos considered for surgery for PD?
what’s done?
dopamine responsive
but levodopa giving big side effects
no psychiatric illness
tried meds and increased doses
deep brain stimulation
what’s MG?
fluctuating, fatiguable, weakness skeletal muscle
what could happen in cholinergic crisis?
resp failure, aspiration, DVT
action of pryidostigmine (AChE inhibitor)
prevents ACh breakdown in NMJ, so ACh more likely to engage with remaining receptors
onset, peak, duration of pyridostigmine
30 mins
60-120
3-6 hours
important dose timing for pyridostigmine
40 mins before food
