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23 Cards in this Set
- Front
- Back
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how are d1 and d2 proteins similar? how are d1 and d2 different? |
both are g protiens d1 is stimulatory and increases camp and pkc activity d2 is inhibitory and decreases camp |
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where are d1 recpetors found? where are d2 recpetors found? |
striatum and neocortex striatum, subtania nigra, pituaaitary glad |
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movement disorders occur in which part of the brain? reward mediate behaviors drug addiction, and adhd occur where in the brain? what area of the brain involves neurosecretory disorders? |
nigrostriatal mesolimibi/mesocrotical tuberoinfundibular tract |
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what affects dopaminerrgic stimulation? what exactly is the cause of parkinsons? what does the loss of dopamine trigger? |
d1 and d2 expression in striatial neurons state of DA defiency, direct pathway is reduced, indirect pathway is overactiving...leading to reduced movement increases in inhibitory signal to thalamus, decrease in excitatory signals to cortex |
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in parkinsons where exactly are the dopaminergic neurons lost? what are the 4 cardinal symptoms of PD? what 3 things are consider genetic predispostions to parkinsons? |
substantia nigra tremor, muscular rigidity, bradykinesia, postural instability oxidative stress, mitocondrial dysfunction, protien accumulation |
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what protiens are involved in protein accumulation? what proteins are involved in mitochonrial dysfuntions? what protiens are involved in oxidative stress? |
aplpha synuclein, sardarin, parkin. inclusion bodies pink1,parkin dj1, parkin |
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what is alpha synuclein found in? what gene codes for dardarin? what happens if it is mutated? what is the funciton of parkin? what happens if it is mutated? |
amyloid plagues, down syndrome brains, lewy bodies LRRK2, inclusion body formation adds ubiquinone to proteins for protesome destruction accumulation of toxic substrates via dysfuntion of ubiquitin protesome systme |
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why does MPTP cause parkinsons? what does the metabolite of MPTP cause? |
it is associated with an accumulation of an enviromental toxin creates MPP+ which inbhitis mitochondrial respiration, which impairns atps syntheses, causes free radicals, apoptosis, cell death |
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what does dopamine get metabolized by? into what products? what happens to these products if glutathione is present? what if FE is present? |
MAO into DOPAC and peroxide makes water makes free radicals |
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what is the oxidative metabolite of dopamine? what metabolizes this? what are the products? what are the causes of these products? |
6 hydroxydopamine metabolized by MAO to yield ROS and quinolinic products morphological changes to mitochondria and apoptosis |
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what two treatment strategies are utilized to treat PD? what drugs are the dopaminerigic agents? what drugs are the ergot dopamine agonists? |
enhance dopaminergic function and suppress cholinergin funciton levodopa, amantadine bromocriptine, apomorphine |
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what drugs are the non ergot dopamine agonists? what drugs are the COMT inhibitiors? what drugs are the anticholinergics? |
ropinirole, pramipexole entacapone, tolcapone benztropine, trihexyphenidyl |
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what 4 ways can you increase dopamine? |
add dopamine analogs inhibit dopamine metabolsim decrase re uptake stimulate healthy dopa neurons |
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what form of dopamine is active? what advatage does levodopa have over dopamine? what converts it to dopamine? |
trans alpha rotamer it is less basic, so it can easily cross the BBB aromtaic amino acid decarboxylase (AAADC) |
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does carbidopa cross the BBB? how does it work? |
it is charged, so doesnt cross the BBB inhbits AADC in the prephirey (no dopamine in the periphery) and allows conversion to dopamine in the CNS |
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what are the two parrellel dopaminergic pathways arising from the substantia nigra? what pathways does adminstration of dopa restore? |
d1 resotration of normal dopaminergic signaing of the dirct pathway d2 restoration of normal dopaminergic signaling of the indirect pathway both of these, relative decrease in inhibitory signals from thalamus and relative increase in excitary outflow from cortex |
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what vitamin is a cofactor in dopa decarboxylase? what is the MOA of bromocriptine? |
vitamin b6 binds D2 and activates teh indirect dopaminergic pathway (partial agonist at d1) |
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MOA of ropinirole/prmipexole? what are the metabolites of the MAO B inhibitors? what two benefits are MAOs supposed to have when you look at the mechanism? |
slective activity at D2 and D3 amphetamine and methamphetamine increases dopamine levels, prevents formation of DOPAC and free radicals |
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what is unique about the metaboism of rasaglinie? what population is rasagline better to use in? |
it is not metabolized to amphetmaine older patients since it is less likely to cause hallucinations or confusion as compared to selegine or dopamine agonists |
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what do COMT inbhitors prevent the metabolism of? what do these help manage? are these ever used as monotherapy? |
DOPAC (dihydroxyphenlacetic acid) wearing off phenomenon since they provide a longer levodopa duration and more receptor stimualtion no, only in combo with levodopa |
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what comt inhibitor causes liver failure? what are the three ways (MOA) amantadine works? |
tolcapone NMDA antagonist, inhbits dopamine reuptake (main function), stimulation of dopamine release |
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how do choliergic neurons affect dopaminergic neurons? what is the aim of anticholergin therapy? |
they oppose them, excess ach is associated with parkinsons resotre dopamine in basal ganglia, antagonize excitatory effect of choliergic neurons to restablish dopamine/ach balance |
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what enzyme breaks down acetylcholine? what are the products? are anticholergics better for tremor or bradykinsia? |
acetylcholinesterase choline and acetate tremor |
