NURS 5315 UTA Exam 1 Questions and
Answers Latest (Verified Answers) | A+
Assured | 100% Correct
• Threshold -✓✓A certain threshold (usually around -55 mV) is reached
when a stimulus causes slight depolarization, triggering an action
potential.
• Depolarization -✓✓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 -✓✓At the peak of the action potential, the inactivation
gates of sodium channels close, stopping Na⁺ influx, while voltage-gated
potassium channels open.
• Repolarization -✓✓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 -✓✓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 -✓✓The sodium-potassium pump restores
the resting potential by transporting Na⁺ ions out and K⁺ ions back into
the neuron.
• Calcium Imbalance -✓✓Calcium imbalances can significantly affect
the action potential of neurons.
,• Hypercalcemia -✓✓High extracellular calcium levels can increase the
threshold required to initiate an action potential and enhance synaptic
release.
• Hypocalcemia -✓✓Low extracellular calcium reduces the threshold for
action potential initiation, increasing excitability and leading to
symptoms like muscle spasms.
• Potassium Imbalance -✓✓Potassium imbalances can also significantly
affect the action potential of neurons.
• Hyperkalemia -✓✓High potassium levels decrease the resting
membrane potential, bringing it closer to the threshold but can impair
action potential firing over time.
• Hypokalemia -✓✓Low potassium levels make the membrane potential
more negative, reducing excitability and making it harder for neurons to
fire action potentials.
• Muscle Weakness -✓✓Chronic depolarization from hyperkalemia can
lead to long-term paralysis or weakness due to inactivation of sodium
channels.
• Neuromuscular Effects of Hypocalcemia -✓✓Hypocalcemia can lead
to increased neuromuscular excitability, muscle cramps, and tingling
sensations.
• Muscle Weakness and Cramps from Hypokalemia -✓✓Hypokalemia
can lead to muscle weakness, cramps, and in severe cases, paralysis due
to reduced neuronal and muscular activity.
• Refractory Period -✓✓The period during hyperpolarization where the
neuron is less likely to fire another action potential.
, • Sodium-Potassium Pump -✓✓A mechanism that actively transports
Na⁺ ions out of the cell and K⁺ ions into the cell to maintain resting
potential.
• Neurotransmitter Release -✓✓Calcium is critical in neurotransmitter
release at synaptic terminals.
• Spontaneous Action Potentials -✓✓Low extracellular calcium can lead
to spontaneous action potentials due to increased excitability.
• Calcium Stabilization -✓✓Calcium stabilizes the membrane, making
neurons less excitable and requiring stronger stimuli to trigger action
potentials.
• Chronic Depolarization -✓✓A condition where persistent
depolarization can inactivate sodium channels, impairing action
potentials.
• Atrophy -✓✓Decrease in size and function
• Hypertrophy -✓✓Increase in size
• Hyperplasia -✓✓Increase in the number of cells; Size of organ
increases
• Metaplasia -✓✓One cell type replaced by another
• Dysplasia -✓✓Disorganized cellular growth
• Physiologic Atrophy -✓✓Example: Shrinkage of the thymus during
early development and aging.
Answers Latest (Verified Answers) | A+
Assured | 100% Correct
• Threshold -✓✓A certain threshold (usually around -55 mV) is reached
when a stimulus causes slight depolarization, triggering an action
potential.
• Depolarization -✓✓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 -✓✓At the peak of the action potential, the inactivation
gates of sodium channels close, stopping Na⁺ influx, while voltage-gated
potassium channels open.
• Repolarization -✓✓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 -✓✓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 -✓✓The sodium-potassium pump restores
the resting potential by transporting Na⁺ ions out and K⁺ ions back into
the neuron.
• Calcium Imbalance -✓✓Calcium imbalances can significantly affect
the action potential of neurons.
,• Hypercalcemia -✓✓High extracellular calcium levels can increase the
threshold required to initiate an action potential and enhance synaptic
release.
• Hypocalcemia -✓✓Low extracellular calcium reduces the threshold for
action potential initiation, increasing excitability and leading to
symptoms like muscle spasms.
• Potassium Imbalance -✓✓Potassium imbalances can also significantly
affect the action potential of neurons.
• Hyperkalemia -✓✓High potassium levels decrease the resting
membrane potential, bringing it closer to the threshold but can impair
action potential firing over time.
• Hypokalemia -✓✓Low potassium levels make the membrane potential
more negative, reducing excitability and making it harder for neurons to
fire action potentials.
• Muscle Weakness -✓✓Chronic depolarization from hyperkalemia can
lead to long-term paralysis or weakness due to inactivation of sodium
channels.
• Neuromuscular Effects of Hypocalcemia -✓✓Hypocalcemia can lead
to increased neuromuscular excitability, muscle cramps, and tingling
sensations.
• Muscle Weakness and Cramps from Hypokalemia -✓✓Hypokalemia
can lead to muscle weakness, cramps, and in severe cases, paralysis due
to reduced neuronal and muscular activity.
• Refractory Period -✓✓The period during hyperpolarization where the
neuron is less likely to fire another action potential.
, • Sodium-Potassium Pump -✓✓A mechanism that actively transports
Na⁺ ions out of the cell and K⁺ ions into the cell to maintain resting
potential.
• Neurotransmitter Release -✓✓Calcium is critical in neurotransmitter
release at synaptic terminals.
• Spontaneous Action Potentials -✓✓Low extracellular calcium can lead
to spontaneous action potentials due to increased excitability.
• Calcium Stabilization -✓✓Calcium stabilizes the membrane, making
neurons less excitable and requiring stronger stimuli to trigger action
potentials.
• Chronic Depolarization -✓✓A condition where persistent
depolarization can inactivate sodium channels, impairing action
potentials.
• Atrophy -✓✓Decrease in size and function
• Hypertrophy -✓✓Increase in size
• Hyperplasia -✓✓Increase in the number of cells; Size of organ
increases
• Metaplasia -✓✓One cell type replaced by another
• Dysplasia -✓✓Disorganized cellular growth
• Physiologic Atrophy -✓✓Example: Shrinkage of the thymus during
early development and aging.
