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

A

levodopa

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
Q

risk of long erm dopernargic anagisue use

A

pyscoiss
dizines
impulsibivty
vmoitng

26
Q

funcitno of noradrenalaine

A

reuptake blockers of antidepressants

27
Q

serotonin 5ht role

A

ssris for depression
tritants - selective 5hts for migraes

28
Q

role of gaba

A

anti epilieptys durgs
anti anxiety

29
Q

funciton of maob and comt inhitors increase dopamine in the rbian

A

prevent brke down of dopaien by pathway, keeping its level higher in the brian

30
Q

exmaples of maob inhibtors

A

selegiline, rasagiline, safinamide

31
Q

examples of comt inhbitors

A

entacapone, opicapone

32
Q

funciton of aaad inhibtors

A

prevent conerion of levodopa to topaine whihc is associated iwtht he nausea and vomiting symptons

33
Q
A