dopamine agonists and week 2 drugs

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  • Created by: hadar
  • Created on: 11-02-16 17:16
Bromocriptine- mechanism of action
blocking of the calcium channels on the membrane inhibits the uptake pump of dopamine and so more dopamine present in the synapse- increasing dopamine affect
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Bromocriptine- therapeutic affect
Stimulation of dopamine D2 receptors in the nigrostriatal pathway leads to improvements in coordinated muscle activity in those with movement disorders.
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Ropinirole- mechanism of action
blocking of the calcium channels on the membrane inhibits the uptake pump of dopamine and so more dopamine present in the synapse- increasing dopamine affect
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Ropinirole- therapeutic affect
Stimulation of dopamine D2 receptors in the nigrostriatal pathway leads to improvements in coordinated muscle activity in those with movement disorders.
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Nimodipine- mechanism of action
binds specifically to L-type voltage-gated calcium channels. And prevents calcium ions from entering the cell so the cell does not become depolarized, there is no excitation.
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Nimodipine- therapeutic affect
Nimodipine inhibits calcium ion transfer into these cells and thus inhibits contractions of vascular smooth muscle.
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Carbamazepine- mechanism of action
stabilizes the inactivated state of voltage-gated sodium channels, making fewer of these channels available to subsequently open. GABA receptor agonist
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Carbamazepine- therapeutic affect
decrease repetitive firing of neurons by reducing AP in excitatory neuron and increasing inhibitory neurons
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Lamotrigine
binds to the sodium channels on the pre-synaptic neuron and this results no sodium influx→ no action potential → glutamate cannot be released→ cannot bind to post synaptic sodium channel → no action potential in post synaptic membrane
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Lamotrigine
decrease repetitive firing of neurons by reducing AP in excitatory neuron
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Sodium valproate- mechanism of action
GABA agonist. binds to the sodium channels on the pre-synaptic neuron and this results no sodium influx→ no action potential → glutamate cannot be released→ cannot bind to post synaptic sodium channel → no action potential in post synaptic membrane
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Sodium valproate- therapeutic affect
by increasing the GABA concentration GABA effect is prolonged and will bind to chloride and potassium channels Influx of chloride and efflux of potassium leads to hyperpolarization and inhibition
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Phenytoin- mechanism of action
binds to the sodium channels on the pre-synaptic neuron and this results no sodium influx→ no action potential → glutamate cannot be released→ cannot bind to post synaptic sodium channel → no action potential in post synaptic membrane
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Phenytoin- therapeutic affect
decrease repetitive firing of neurons by reducing AP in excitatory neuron
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Zopiclone- mechanism of action
binding on the benzodiazepine receptor complex and modulation of the GABABZ receptor chloride channel macromolecular complex.(full agonist) enhancement of the inhibitory actions of GABA
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Zopiclone- therapeutic affect
to increase duration an quality of sleep increasing hypnotic properties of GABA
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Card 2

Front

Stimulation of dopamine D2 receptors in the nigrostriatal pathway leads to improvements in coordinated muscle activity in those with movement disorders.

Back

Bromocriptine- therapeutic affect

Card 3

Front

blocking of the calcium channels on the membrane inhibits the uptake pump of dopamine and so more dopamine present in the synapse- increasing dopamine affect

Back

Preview of the back of card 3

Card 4

Front

Stimulation of dopamine D2 receptors in the nigrostriatal pathway leads to improvements in coordinated muscle activity in those with movement disorders.

Back

Preview of the back of card 4

Card 5

Front

binds specifically to L-type voltage-gated calcium channels. And prevents calcium ions from entering the cell so the cell does not become depolarized, there is no excitation.

Back

Preview of the back of card 5
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