Neuropharmacy Flashcards

1
Q

what are the stages of synaptic transmissoin

A

1 - synthesis and packing of neuro transmitter
2 - na actio protoensl reahces terminal
3 - activates voltage gated ca 2+ channels
4- triggers ca2+ dependent exocytosis of prepackaged vesicles of transmitters
5 - transmitters diffuse across the clef stand binds to the ionotrpic and or metablictopic recpotr to cause a post synaptic effect
6 - presynaptic repcots inhibit further release
7 - transmitter is inactive by uptake of glia or neurosn
8 - transmitter is metabolised within the cells

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2
Q

how do locan anethisc work

A

they block voltage gated na channesl, prveing activiation of the action portie working on cell

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3
Q

how does competive and non competice antagoists work

A

they work on the site of the ionotproc or metabolic recpot, stopping the transmitter form functions

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4
Q

how does spider vemon work

A

block voltage gagted ca 2+ channles

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5
Q

where do ca molueues move

A

into the cell

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6
Q

how does botlumim work

A

it blocks the rlase mahcine of neurotransmitters

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7
Q

how do ssris work

A

block the uptake of hte transmiter, meing more goes bakc into cells

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8
Q

how does benzodiapepieze work

A

they make the effect of the tranmsiter stronger on the receptor

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9
Q

where does dopamine distrobute to

A

brianstem
basal ganglia
limbic sytem and frontal cortex

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10
Q

what does dopamine control

A

vommiting
emotions
voluntary movemnet

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11
Q

what does parkinsons cause

A

degerneation of da cells in the sn
da defeciency in the basal ganglia

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12
Q

what chemicals can turn into the dopamine and cross bbb

A

tyroseins and dopa

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13
Q

what is the issue with having lots of dopa in periphery

A

nauesa
vommiting
psycois

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14
Q

why can tyrosine not be converted to dopaine in the rbain

A

as it becomes lost though degeneration

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15
Q

what is dopaine broken down to

A

homovanillic acid

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16
Q

signs of parkingons

A

change in posture
stiffness
tremor
slow movements

17
Q

what are da precurus exmales

18
Q

what drugs are da agonists ergots

A

bromocriptine
pergolide
cabergoline

19
Q

non ergot drugs

A

ropineiprole
pramipexole
rotigotine

20
Q

is the area postrema (vommiting cnetre ) in the perhiary or in brain

A

in the perhiphary

21
Q

example of da antagoinstis that do not cross bbb

A

domeridone

22
Q

risk of domperidone

A

qt prolongation

23
Q

what is dyskinesias

A

abnroal or involuntary movements , due to too mcu movement, due to excessive dopaimine

24
Q

what drugs cause dyskineiase

A

dopamingeric drugs

25
risk of long erm dopernargic anagisue use
pyscoiss dizines impulsibivty vmoitng
26
funcitno of noradrenalaine
reuptake blockers of antidepressants
27
serotonin 5ht role
ssris for depression tritants - selective 5hts for migraes
28
role of gaba
anti epilieptys durgs anti anxiety
29
funciton of maob and comt inhitors increase dopamine in the rbian
prevent brke down of dopaien by pathway, keeping its level higher in the brian
30
exmaples of maob inhibtors
selegiline, rasagiline, safinamide
31
examples of comt inhbitors
entacapone, opicapone
32
funciton of aaad inhibtors
prevent conerion of levodopa to topaine whihc is associated iwtht he nausea and vomiting symptons
33