12.1 Neuropharmacology Flashcards

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1
Q

proportion of basal ganglia lost to give PD symptoms

A

> 50%

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2
Q

where do dopamingeric neurones project to?

A

caudate nucleus and putamen

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3
Q

abnormal protein in PD

A

alpha synuclein, misolds

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4
Q

why does dopamine reduce in PD, aside from less substantial nigra?

A

increased cell turnovers upregukate receptors so uses up remaining dopanine

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5
Q

describe the tremor of PD

A

asymmetric, low freq, pill rolling, at rest, goes away on touching somethign

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6
Q

describe the rigidity in PD

A

lead pipe: resistance constant throughout arc

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7
Q

describe the bradykinesia of PD

A

issue maintaining amplitude of movement
cant keep a rhythm

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8
Q

cog wheeling

A

jolting of joints throughout movement

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9
Q

describe the gait in PD

A

difficult to start/stop
forward flexed
unilateral
reduced arm swing
turn around as whole
reduced fluidity of movement

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10
Q

hallucinations in PD

A

frightening, aggressive

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11
Q

levodopa half life is 2 hours. consequences of this?

A

fluctuations in blood levels and symptoms

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12
Q

why is levodopa given with peripheral dopa decarboxylase inhibitor?

A

reduced dose
reduced side effects
more levodopa reaches brain

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13
Q

tablet formulations of levodopa

A

-standard
-controlled release
-dispersible non soluble

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14
Q

huntingtons chorea

A

hypo/hyperrelfexia, long term effect of too much levodopa

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15
Q

why cant COMT inhibitors be used alone? how to overcome?

A

no therapeutic effect
use with levodopa and dopa decarboxylase inhibitor

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16
Q

can dopamine receptor agonists be first line?

A

yes, if levodopa less good

17
Q

punding

A

rearranging stuff needlessly
repetitive compulsive activity

18
Q

why could people be quite susceptible to side effects of PD treatment?

A

elderly

19
Q

drug for PD patients with severe motor fluctuations

A

apomorphine s.c. bolus continuous infusion

20
Q

role of anticholinergics in PD

A

problematic tremor relief
NO EFFECT ON OTHER SYMTPOMS

21
Q

whos considered for surgery for PD?
what’s done?

A

dopamine responsive
but levodopa giving big side effects
no psychiatric illness
tried meds and increased doses

deep brain stimulation

22
Q

what’s MG?

A

fluctuating, fatiguable, weakness skeletal muscle

23
Q

what could happen in cholinergic crisis?

A

resp failure, aspiration, DVT

24
Q

action of pryidostigmine (AChE inhibitor)

A

prevents ACh breakdown in NMJ, so ACh more likely to engage with remaining receptors

25
Q

onset, peak, duration of pyridostigmine

A

30 mins
60-120
3-6 hours

26
Q

important dose timing for pyridostigmine

A

40 mins before food