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NUR 5461 Advanced Pathophysiology — Module 4 Concepts and
Alterations of the Neurologic System: Quiz Bank
Course: NUR 5461 Advanced Pathophysiology
Institution: William Paterson University — Department of
Nursing
Module: 4 of 7
Required Text: McCance, K. L., Huether, S. E., Brashers, V. L., &
Rote, N. S. (2019/2023). Pathophysiology: The biologic basis for
disease in adults and children (8th/9th ed.). Mosby Elsevier
Module 4 Overview: This module covers the structure and
function of the neurologic system and the pathophysiology of
neurologic alterations, including traumatic brain injury,
cerebrovascular disorders, spinal cord injury, neurodegenerative
diseases, seizures, pain, infections, and neuromuscular junction
disorders. Students must understand neurophysiology, cerebral
hemodynamics, the Monro-Kellie doctrine, excitotoxicity, and
the clinical manifestations of neurologic disease.
SECTION A: NEUROPHYSIOLOGY AND CELLULAR
NEUROBIOLOGY
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1. Which neurotransmitter is primarily responsible for inhibitory
signaling in the central nervous system?
A. Dopamine
B. Serotonin
C. Glutamate
D. Gamma-aminobutyric acid (GABA)
Answer: D
Rationale: GABA is the primary inhibitory neurotransmitter in
the CNS, hyperpolarizing neurons and reducing the likelihood of
action potential generation. Dopamine and serotonin are
modulatory neurotransmitters; glutamate is the primary
excitatory neurotransmitter. Acetylcholine is both excitatory and
inhibitory depending on receptor type.
2. In cerebral ischemia, neurons undergo excitotoxic death due
to excessive glutamate release. Which molecular event is most
directly responsible for acute neuronal injury?
A. Activation of metabotropic glutamate receptors
B. Overactivation of AMPA receptors causing sodium influx
C. Excessive calcium influx through NMDA receptors triggering
calpain and caspase activation
D. Desensitization of GABA-A receptors
Answer: C
Rationale: Excitotoxicity is primarily mediated by excessive
calcium entry through NMDA receptors. Calcium overload
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activates proteolytic enzymes (calpains) and caspases, leading
to cytoskeletal degradation and cell death. While AMPA
receptor overactivation contributes to sodium influx and early
depolarization, the calcium-mediated cascade through NMDA
receptors is the most direct mechanism of acute neuronal
injury.
3. A researcher identifies a mutation in a voltage-gated sodium
channel that impairs fast inactivation. Which
electrophysiological change is most likely?
A. Prolonged hyperpolarization following an action potential
B. Decreased amplitude of the action potential
C. Increased duration of the action potential due to persistent
sodium current
D. Faster repolarization due to enhanced potassium channel
opening
Answer: C
Rationale: Fast inactivation of sodium channels normally
terminates the sodium current rapidly after channel opening.
Impaired inactivation leads to a persistent sodium current that
prolongs depolarization, increasing action potential duration
and neuronal hyperexcitability. This mechanism is relevant to
certain epileptic channelopathies.
4. What is the primary function of astrocytes in the central
nervous system?
, https://www.stuvia.com/user/performance
A. Synaptic transmission and neurotransmitter release
B. Myelin production and insulation
C. Immune surveillance and microglial activation
D. Support, metabolic coupling, and ion homeostasis
Answer: D
Rationale: Astrocytes provide critical support to neurons
through metabolic coupling, buffering extracellular potassium,
regulating extracellular pH, and maintaining the blood-brain
barrier. Oligodendrocytes produce myelin; microglia provide
immune function; neurons handle synaptic transmission and
action potential generation.
5. Which structure is primarily responsible for the blood-brain
barrier?
A. Neuronal cell bodies
B. Tight junctions between capillary endothelial cells and
astrocyte foot processes
C. Oligodendrocyte myelin sheaths
D. Ependymal cells lining the ventricles
Answer: B
Rationale: The blood-brain barrier is formed by tight junctions
between capillary endothelial cells and astrocyte foot
processes, restricting passage of large or polar molecules while
allowing essential nutrients to cross. It protects the brain from
toxins, pathogens, and fluctuations in plasma composition.
NUR 5461 Advanced Pathophysiology — Module 4 Concepts and
Alterations of the Neurologic System: Quiz Bank
Course: NUR 5461 Advanced Pathophysiology
Institution: William Paterson University — Department of
Nursing
Module: 4 of 7
Required Text: McCance, K. L., Huether, S. E., Brashers, V. L., &
Rote, N. S. (2019/2023). Pathophysiology: The biologic basis for
disease in adults and children (8th/9th ed.). Mosby Elsevier
Module 4 Overview: This module covers the structure and
function of the neurologic system and the pathophysiology of
neurologic alterations, including traumatic brain injury,
cerebrovascular disorders, spinal cord injury, neurodegenerative
diseases, seizures, pain, infections, and neuromuscular junction
disorders. Students must understand neurophysiology, cerebral
hemodynamics, the Monro-Kellie doctrine, excitotoxicity, and
the clinical manifestations of neurologic disease.
SECTION A: NEUROPHYSIOLOGY AND CELLULAR
NEUROBIOLOGY
,https://www.stuvia.com/user/performance
1. Which neurotransmitter is primarily responsible for inhibitory
signaling in the central nervous system?
A. Dopamine
B. Serotonin
C. Glutamate
D. Gamma-aminobutyric acid (GABA)
Answer: D
Rationale: GABA is the primary inhibitory neurotransmitter in
the CNS, hyperpolarizing neurons and reducing the likelihood of
action potential generation. Dopamine and serotonin are
modulatory neurotransmitters; glutamate is the primary
excitatory neurotransmitter. Acetylcholine is both excitatory and
inhibitory depending on receptor type.
2. In cerebral ischemia, neurons undergo excitotoxic death due
to excessive glutamate release. Which molecular event is most
directly responsible for acute neuronal injury?
A. Activation of metabotropic glutamate receptors
B. Overactivation of AMPA receptors causing sodium influx
C. Excessive calcium influx through NMDA receptors triggering
calpain and caspase activation
D. Desensitization of GABA-A receptors
Answer: C
Rationale: Excitotoxicity is primarily mediated by excessive
calcium entry through NMDA receptors. Calcium overload
,https://www.stuvia.com/user/performance
activates proteolytic enzymes (calpains) and caspases, leading
to cytoskeletal degradation and cell death. While AMPA
receptor overactivation contributes to sodium influx and early
depolarization, the calcium-mediated cascade through NMDA
receptors is the most direct mechanism of acute neuronal
injury.
3. A researcher identifies a mutation in a voltage-gated sodium
channel that impairs fast inactivation. Which
electrophysiological change is most likely?
A. Prolonged hyperpolarization following an action potential
B. Decreased amplitude of the action potential
C. Increased duration of the action potential due to persistent
sodium current
D. Faster repolarization due to enhanced potassium channel
opening
Answer: C
Rationale: Fast inactivation of sodium channels normally
terminates the sodium current rapidly after channel opening.
Impaired inactivation leads to a persistent sodium current that
prolongs depolarization, increasing action potential duration
and neuronal hyperexcitability. This mechanism is relevant to
certain epileptic channelopathies.
4. What is the primary function of astrocytes in the central
nervous system?
, https://www.stuvia.com/user/performance
A. Synaptic transmission and neurotransmitter release
B. Myelin production and insulation
C. Immune surveillance and microglial activation
D. Support, metabolic coupling, and ion homeostasis
Answer: D
Rationale: Astrocytes provide critical support to neurons
through metabolic coupling, buffering extracellular potassium,
regulating extracellular pH, and maintaining the blood-brain
barrier. Oligodendrocytes produce myelin; microglia provide
immune function; neurons handle synaptic transmission and
action potential generation.
5. Which structure is primarily responsible for the blood-brain
barrier?
A. Neuronal cell bodies
B. Tight junctions between capillary endothelial cells and
astrocyte foot processes
C. Oligodendrocyte myelin sheaths
D. Ependymal cells lining the ventricles
Answer: B
Rationale: The blood-brain barrier is formed by tight junctions
between capillary endothelial cells and astrocyte foot
processes, restricting passage of large or polar molecules while
allowing essential nutrients to cross. It protects the brain from
toxins, pathogens, and fluctuations in plasma composition.
