Anti Parkinsons Flashcards
What is Parkinson’s disease
Degeneration of cell bodies which decrease dopamine transmission
What is the difference between Parkinson’s and parkinsonism
Parkinsonism is usually drug developed symptoms of Parkinson’s
What are the common symptoms of Parkinson’s
Muscle rigidity
Tremor
Uncontrollability of voluntary movement
Where is DA produced usually which then isn’t produced in Parkinson’s
Nigra substantia
What does the nigra substantia have their terminals to for DA transmission
Striatum
What is the nigra striatum system called
Nigro striatal pathway
What are the other 3 pathways other than the nigra striatal pathway
Mesocortical
Mesolimbic
Tuberoinfundibular
Why would decreased DA at the nigra substantia cause lower control of muscle
Because less DA would bind to D2 inhibitory receptors At the striatum
This usually stops firing to control voluntary movement
This causes firing down neurones to the spinal cord and causes uncontrollable voluntary control
How is dopamine synthesised
Via tyrosine
Tyrosine hydroxylase
L dopa
Dopa decarboxylase
Dopamine
Which enzyme is limiting in making dopamine
Tyrosine hydroxylase
Which protein transfers DA from cytosol to vesicles
VMAT
What enzyme would metabolise DA if not in vesicle
MAO
Explain the steps of dopamine metabolism
DA
MAO metabolises it into
DOPA L
Converted to DOPA C via aldehyde dehydrogenase
Converted to HVA via catechol - O - methyl transferase
At what point does DA become inactive
As DOPA L, C and HVA
What happens when DA binds to D2 inhibitory receptors
Inhibits adenylate cyclase
Or can open K channels stopping firing down striatum
What happens at D1 receptors
Usually stimulated adenylate cyclase (excitatory causing firing down striatum)
Until DA binds which causes decreased camp and decreased firing down striatum (inhibitory)
Which protein reuptake DA
DAT protein
Which molecule is added to treat Parkinson’s disease by increasing levels of DA (to stop firing)
Add L dopa intermediate
Why would L dopa be added instead of tyrosine to treat Parkinson’s
Because tyrosine hydroxylase is limiting
Which drug is given with L dopa to stop too much dopamine production
Carbidopa
It inhibits the rate of dopa decarboxylase
Why can’t DA be given instead of L dopa (3 reasons)
It’s polar so can’t cross membrane
Also would be metabolised quickly by MAO
Also causes sympathomimetic effects like tachycardia
Why would MAOI be used to increase DA
Less metabolised
More DA in the vesicles
More released
More inhibition of firing at D1 and 2
Why type of agonists would be given to treat Parkinson’s via increase in DA effects
D2 receptor agonists which also mimic DA inhibition of firing down the striatum
Why would L dopa not have anywhere to be stored in Parkinson’s
Neuronal body degeneration (less nigra substantia)
What is the negative effect of D2 agonists
They affect the other pathways like mesolimbic and mesocortical which causes psychosis
What is the word for drug induced parkinsonism
Iatrogenic Parkinsonism
Why would anti psychotics cause Parkinsonism
They block D2 pathways like the nigro striatal pathway
This would increase firing down striatal and cause Parkinson symptoms
