NURS 5315 UTA TEST BANK 1 2026
COMPREHENSIVE QUESTIONS AND
ACCURATE SOLUTIONS VERIFIED
◉ Threshold. Answer: A certain threshold (usually around -55 mV) is
reached when a stimulus causes slight depolarization, triggering an
action potential.
◉ Depolarization. Answer: Voltage-gated sodium channels open
rapidly, allowing Na⁺ ions to rush into the cell, causing the membrane
potential to reach up to +30 mV.
◉ Peak Phase. Answer: At the peak of the action potential, the
inactivation gates of sodium channels close, stopping Na⁺ influx, while
voltage-gated potassium channels open.
◉ Repolarization. Answer: K⁺ ions flow out of the cell through opened
potassium channels, making the inside of the cell more negative and
returning towards resting potential.
◉ Hyperpolarization. Answer: The potassium channels are slow to
close, causing an overshoot where the membrane potential becomes
more negative than the resting potential.
,◉ Return to Resting Potential. Answer: The sodium-potassium pump
restores the resting potential by transporting Na⁺ ions out and K⁺ ions
back into the neuron.
◉ Calcium Imbalance. Answer: Calcium imbalances can significantly
affect the action potential of neurons.
◉ Hypercalcemia. Answer: High extracellular calcium levels can
increase the threshold required to initiate an action potential and
enhance synaptic release.
◉ Hypocalcemia. Answer: Low extracellular calcium reduces the
threshold for action potential initiation, increasing excitability and
leading to symptoms like muscle spasms.
◉ Potassium Imbalance. Answer: Potassium imbalances can also
significantly affect the action potential of neurons.
◉ Hyperkalemia. Answer: High potassium levels decrease the resting
membrane potential, bringing it closer to the threshold but can impair
action potential firing over time.
◉ Hypokalemia. Answer: Low potassium levels make the membrane
potential more negative, reducing excitability and making it harder for
neurons to fire action potentials.
, ◉ Muscle Weakness. Answer: Chronic depolarization from
hyperkalemia can lead to long-term paralysis or weakness due to
inactivation of sodium channels.
◉ Neuromuscular Effects of Hypocalcemia. Answer: Hypocalcemia can
lead to increased neuromuscular excitability, muscle cramps, and
tingling sensations.
◉ Muscle Weakness and Cramps from Hypokalemia. Answer:
Hypokalemia can lead to muscle weakness, cramps, and in severe
cases, paralysis due to reduced neuronal and muscular activity.
◉ Refractory Period. Answer: The period during hyperpolarization
where the neuron is less likely to fire another action potential.
◉ Sodium-Potassium Pump. Answer: A mechanism that actively
transports Na⁺ ions out of the cell and K⁺ ions into the cell to maintain
resting potential.
◉ Neurotransmitter Release. Answer: Calcium is critical in
neurotransmitter release at synaptic terminals.
◉ Spontaneous Action Potentials. Answer: Low extracellular calcium
can lead to spontaneous action potentials due to increased excitability.
COMPREHENSIVE QUESTIONS AND
ACCURATE SOLUTIONS VERIFIED
◉ Threshold. Answer: A certain threshold (usually around -55 mV) is
reached when a stimulus causes slight depolarization, triggering an
action potential.
◉ Depolarization. Answer: Voltage-gated sodium channels open
rapidly, allowing Na⁺ ions to rush into the cell, causing the membrane
potential to reach up to +30 mV.
◉ Peak Phase. Answer: At the peak of the action potential, the
inactivation gates of sodium channels close, stopping Na⁺ influx, while
voltage-gated potassium channels open.
◉ Repolarization. Answer: K⁺ ions flow out of the cell through opened
potassium channels, making the inside of the cell more negative and
returning towards resting potential.
◉ Hyperpolarization. Answer: The potassium channels are slow to
close, causing an overshoot where the membrane potential becomes
more negative than the resting potential.
,◉ Return to Resting Potential. Answer: The sodium-potassium pump
restores the resting potential by transporting Na⁺ ions out and K⁺ ions
back into the neuron.
◉ Calcium Imbalance. Answer: Calcium imbalances can significantly
affect the action potential of neurons.
◉ Hypercalcemia. Answer: High extracellular calcium levels can
increase the threshold required to initiate an action potential and
enhance synaptic release.
◉ Hypocalcemia. Answer: Low extracellular calcium reduces the
threshold for action potential initiation, increasing excitability and
leading to symptoms like muscle spasms.
◉ Potassium Imbalance. Answer: Potassium imbalances can also
significantly affect the action potential of neurons.
◉ Hyperkalemia. Answer: High potassium levels decrease the resting
membrane potential, bringing it closer to the threshold but can impair
action potential firing over time.
◉ Hypokalemia. Answer: Low potassium levels make the membrane
potential more negative, reducing excitability and making it harder for
neurons to fire action potentials.
, ◉ Muscle Weakness. Answer: Chronic depolarization from
hyperkalemia can lead to long-term paralysis or weakness due to
inactivation of sodium channels.
◉ Neuromuscular Effects of Hypocalcemia. Answer: Hypocalcemia can
lead to increased neuromuscular excitability, muscle cramps, and
tingling sensations.
◉ Muscle Weakness and Cramps from Hypokalemia. Answer:
Hypokalemia can lead to muscle weakness, cramps, and in severe
cases, paralysis due to reduced neuronal and muscular activity.
◉ Refractory Period. Answer: The period during hyperpolarization
where the neuron is less likely to fire another action potential.
◉ Sodium-Potassium Pump. Answer: A mechanism that actively
transports Na⁺ ions out of the cell and K⁺ ions into the cell to maintain
resting potential.
◉ Neurotransmitter Release. Answer: Calcium is critical in
neurotransmitter release at synaptic terminals.
◉ Spontaneous Action Potentials. Answer: Low extracellular calcium
can lead to spontaneous action potentials due to increased excitability.
