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Neuronal hyperpolarization due to potassium efflux
45%
135/297
Neuronal depolarization due to potassium influx
10%
30/297
Neuronal hyperpolarization due to sodium influx
11%
33/297
Neuronal depolarization due to sodium efflux
31/297
Neuronal hyperpolarization due to chloride influx
16%
47/297
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Somnolence, pupillary constriction, and respiratory depression are consistent with opioid toxicity, which was likely administered for pain control in this patient. Opiates cause neuron hyperpolarization due to potassium efflux. Morphine is a mu opioid agonist. Mu opioid receptors are G-protein coupled receptors that cause activation of potassium channels and lead to potassium efflux. The potassium efflux causes hyperpolarization (more negative), and reduces the excitability of the neuron, thus decreasing pain transmission. Patients who are opioid naive (often younger, previously healthy individuals who have never had surgery before) are more likely to experience the toxicities of opioid administration. Incorrect Answers: Answer 2: Morphine binding to its receptors leads to potassium efflux (flow out of the neuron), not influx (flow into the neuron). Answer 3-5: Morphine does not bind a receptor which directly affects the influx or efflux of sodium or chloride.
3.8
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