How Does Lidocaine Achieve Its Effect On Sodium Channels

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Lidocaine is a sodium-channel blocker. How should this affect the activity of neurons? Will they more likely be more or less excitable after administration? Explain why this is by describing the ion channels involved in the generation of the action potential. (15 points)

Lidocaine will affect the activity of neurons by inhibiting the propagation of action potentials. Sodium channels (specifically voltage gated ones) are responsible for the initial rush of Na+ ions into the cell when a threshold potential is reached and these ions depolarize the cell. This rush of ions allows for an action potential to be reached. Once the cell is depolarized potassium floods into the cell to hyperpolarize it and allow for a refractory period during which another action potential cannot occur. That action potential allows for the continuation of the stimulus along to another neuron. Neurons will be a lot less excitable after administration as a result of this inhibition of sodium channels.
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How does lidocaine achieve these effects, given its effect on sodium channels? (15 points)

Two therapeutic uses for lidocaine are as an anaesthetic and as a treatment for ventricular arrhythmias. As an anaesthetic lidocaine is effective because it does block the transmission of neuronal impulses, numbing the area it is applied to or injected into. Ventricular arrhythmias are a result of electrical impulses to the heart that make the heart beat irregularly, and in the cases lidocaine would treat, too quickly as well. By treating that with lidocaine, which blocks action potentials, you decrease or entirely cease those signals that are causing arrhythmia.

What are the symptoms of stroke? Why should a lidocaine overdose mimic a stroke? (5