Question

Going Under the Knife: A Case on Membrane Structure and Function

Twenty-year-old Kevin groaned and clutched his abdomen as he lay on the emergency room gurney. He had just been diagnosed with acute appendicitis and was waiting to be taken to the operating room (OR). Although he desperately wanted the pain to stop, Kevin was terrified of having general anesthesia. He hoped his fear wasn’t obvious to his older brother Cole, who was finishing medical school and thought he knew everything.

“Hang in there,” Cole said, for what seemed like the eighteenth time. “I’m sure they’ll get you upstairs as soon as they can. They don’t want that thing to burst.”

Kevin grunted. “I know…but does that anesthesia staff work all the time? How can I not wake up when someone’s slicing my gut open?”

Cole assumed a professorial air, and Kevin wished he’d kept his mouth shut. However, Cole didn’t get a chance to say anything before an aide arrived to take Kevin to the OR.

In the OR, someone placed a mask over Kevin’s face and when he blinked, he suddenly found himself in a hospital room with Cole waiting in a chair by the bed. “Welcome back to consciousness, little brother. How’s your abdomen feel?”

Kevin frowned. “Not as bad as it did. So it’s over? How did I get here already?”

“You’ve been out for a few hours,” Cole chuckled and then launched into the wonders of general anesthesia. “Certain neurons have to depolarize and undergo an action potential to maintain consciousness, but some anesthetics can hyperpolarize them and produce unconsciousness. The anesthetic binds to and opens a certain kind of potassium channel, which increases the “leak” current of potassium. However, it doesn’t affect voltage-gated potassium channels. This inhibits the neurons, and therefore you aren’t conscious of the surgeons performing the procedure. Amazing!”

Kevin groaned again, but not from the pain this time. Cole was undoubtedly right but he sounded like a textbook. “I’m just glad the stuff worked. Now when can I go home?”

Short answer questions

1. Kevin is conscious when certain neurons in his brain are active—they depolarize and undergo action potentials. Describe the process of depolarization of a neuron to threshold.

2. What does Cole mean when he says that anesthesia “inhibits the neurons?”

3. If the anesthesia opens more potassium leak channels, why are Kevin’s neurons less likely to produce action potentials?

4. Suppose Kevin’s pre-op blood work indicates that his extracellular potassium concentration is much higher than usual. This condition is known as hyperkalemia and must be corrected before he can undergo surgery. One of the dangers of hyperkalemia is that it makes neurons and muscle cells more excitable. Why does elevated extracellular potassium have this effect?

Answer 1

1. Depolarization is a process by which cells undergo a change in membrane potential. Depolarization causes the rapid change in membrane potential from negative to positive state. In response to a stimulus, the voltage change causes the opening of voltage-gated sodium and calcium channels inside the cell membrane, because of which sodium ion enters the cell and potassium ions leaves the cell, this makes the membrane potential less negative or more positive, thus generating an action potential if threshold voltage is crossed.

2. Most of the local anasthetics work by moving into the cell and binding to the sodium channels, which blocks the influx of sodium ions into the cell because of which depolarization do not happen and stops generation of an action potential, this block stops nerve conductance and prevents further signals reaching the brain thereby he not able to perceive pain.

3. if more potassium ion leaks out of the cell, than it will alter the potential of cell membrane, it will make it more negative thereby causing hyperpolarization, this hyperpolarization will make it hard to generate an action potential.

4. In a condition of  hyperkalemia, the resting membrane potential is shifted to a less negative value, that is, from −90 mV to −80 mV, which in turn moves the resting membrane potential closer to the normal threshold potential of −75 mV, resulting in increased myocyte excitability