NURS 611 / NURS611 EXAM 3 (LATEST )
ADVANCED PATHOPHYSIOLOGY | QUESTIONS AND VERIFIED ANSWERS |
GRADED A - MARYVILLE
Maryville University | Graduate Nursing and Advanced Practice Education | Comprehensive Examination
Aligned with the NURS 611 Course Syllabus, the AACN Essentials of Master's Education in Nursing, and Advanced
Pathophysiology Competencies (2026/2027 Edition)
100 Questions | 7 Sections | Verified Answers with Detailed Rationales | Cognitive Levels: 20% Recall - 50% Application - 30%
Analysis | Format: 75% Scenario-Based - 25% Direct Knowledge
Section 1: Neurological Pathophysiology
Q1: A 68-year-old man is admitted 2 hours after the sudden onset of right-sided weakness and expressive aphasia.
CT angiography confirms an occlusion of the left middle cerebral artery, and the ischemic penumbra is identified
on perfusion imaging. Which pathophysiological mechanism is responsible for neuronal injury within this
penumbral zone?
A. Excessive adenosine accumulation causing premature neuronal apoptosis despite preserved perfusion
B. Demyelination of surviving axons triggered by oligodendrocyte apoptosis within the core infarct
C. Glutamate-mediated excitotoxicity in which NMDA receptor activation produces lethal calcium influx
into neurons *[CORRECT]*
D. Vasogenic edema from complete blood-brain barrier disruption that uniformly destroys all penumbral
neurons
Correct Answer: C
Rationale: In focal cerebral ischemia, depleted ATP disables the Na-K-ATPase pump, causing glutamate release and failed
reuptake; sustained NMDA receptor activation drives massive intracellular calcium influx, activating proteases, lipases, and
endonucleases that destroy neurons. This excitotoxic cascade is a core NURS 611 advanced pathophysiology concept and the
rationale for neuroprotection research. Adenosine is actually neuroprotective, demyelination is not the primary penumbral
mechanism, and BBB disruption with vasogenic edema is a later, secondary event rather than the initiating injury.
Q2: A 72-year-old woman experiences 25 minutes of left-arm weakness and word-finding difficulty that resolve
completely before emergency evaluation. Diffusion-weighted MRI shows no infarction. Based on advanced
pathophysiological principles, which statement correctly distinguishes a transient ischemic attack (TIA) from an
ischemic stroke?
A. In TIA, transient focal hypoperfusion resolves before tissue infarction occurs, leaving no permanent
neuronal death, whereas stroke produces completed infarction *[CORRECT]*
B. TIA results from hemorrhage into the subarachnoid space, while stroke results from embolic occlusion
only
C. TIA produces permanent laminar cortical necrosis, while stroke is limited to the gray-white matter
junction
D. TIA represents global hypoperfusion from systemic hypotension, while stroke reflects focal vascular
occlusion
Correct Answer: A
NURS 611 Advanced Pathophysiology | Maryville University 1
,NURS 611 EXAM 3 (LATEST ) - ADVANCED PATHOPHYSIOLOGY Questions and Verified Answers | Graded A
Rationale: The modern tissue-based definition holds that TIA is a brief episode of focal cerebral ischemia with full clinical
recovery and no infarction on imaging, reflecting restoration of perfusion through endogenous fibrinolysis or collateral flow
before the ischemic cascade completes. Stroke denotes tissue infarction with irreversible neuronal death. TIA is ischemic, not
hemorrhagic; it does not produce necrosis; and it is focal rather than global, consistent with NURS 611 cerebrovascular
pathophysiology content.
Q3: A 60-year-old man with poorly controlled chronic hypertension suddenly develops dense right hemiparesis
and progressive lethargy. Noncontrast CT reveals a deep intraparenchymal hemorrhage in the left basal ganglia.
Which pathophysiological mechanism most likely explains the location of this hemorrhage?
A. Rupture of a saccular aneurysm at the anterior communicating artery
B. Rupture of Charcot-Bouchard microaneurysms in small penetrating lenticulostriate arteries damaged by
chronic hypertension *[CORRECT]*
C. Venous sinus thrombosis producing hemorrhagic venous infarction in the deep white matter
D. Amyloid deposition in cortical and leptomeningeal vessels of the frontal and occipital lobes
Correct Answer: B
Rationale: Chronic hypertension causes lipohyalinosis and fibrinoid necrosis of small penetrating arteries, forming
Charcot-Bouchard microaneurysms that rupture most often in the basal ganglia, thalamus, pons, and cerebellum. Saccular
aneurysm rupture causes subarachnoid hemorrhage rather than deep intraparenchymal bleeding, cerebral amyloid angiopathy
produces lobar hemorrhages in the elderly, and venous thrombosis is a distinct entity. This vascular pathophysiology is
emphasized in the NURS 611 cerebrovascular unit.
Q4: A 45-year-old woman presents with the abrupt onset of the worst headache of her life, vomiting, and nuchal
rigidity. CT demonstrates diffuse blood in the basal cisterns, and angiography identifies a ruptured saccular
aneurysm of the posterior communicating artery. Which complication, occurring 4 to 10 days after the bleed,
poses the greatest risk of delayed cerebral ischemia?
A. Rebleeding from aneurysm re-rupture
B. Obstructive hydrocephalus from intraventricular extension
C. Hyponatremia from cerebral salt wasting
D. Cerebral vasospasm of arteries bathed in subarachnoid blood *[CORRECT]*
Correct Answer: D
Rationale: Blood breakdown products in the subarachnoid space provoke vasoconstriction and proliferative arteriopathy,
producing delayed cerebral vasospasm between days 4 and 10 that can cause infarction and is a leading cause of morbidity
after subarachnoid hemorrhage. Rebleeding and hydrocephalus are early complications, while hyponatremia worsens
outcomes but does not directly produce delayed focal ischemia. Recognition of vasospasm timing is a tested NURS 611
neurovascular pathophysiology concept.
Q5: A nursing student asks why a patient with a cortical lesion exhibits recurrent, abnormal synchronized
neuronal firing. Which mechanism best describes the fundamental pathophysiology of a seizure?
A. A paroxysmal depolarization shift in which neuronal membranes become hyperexcitable and excitatory
input overwhelms inhibitory GABAergic control *[CORRECT]*
B. Progressive loss of glutamatergic neurons with preserved GABAergic interneurons, producing net
inhibition
C. Excessive cholinergic activity in the reticular activating system causing diffuse cortical synchronization
D. Autoimmune destruction of voltage-gated sodium channels throughout the cerebral cortex
Correct Answer: A
NURS 611 Advanced Pathophysiology | Maryville University 2
,NURS 611 EXAM 3 (LATEST ) - ADVANCED PATHOPHYSIOLOGY Questions and Verified Answers | Graded A
Rationale: Seizures arise from an imbalance favoring excitation over inhibition: hyperexcitable neurons generate paroxysmal
depolarization shifts that recruit neighboring cells into synchronized high-frequency firing. Decreased GABA-mediated
inhibition, enhanced glutamatergic transmission, and altered ion channel function underlie this hyperexcitability, which is
foundational NURS 611 neurophysiology. The other options reverse the excitatory-inhibitory relationship or invoke
unsupported mechanisms.
Q6: A 22-year-old woman is brought to the emergency department in a generalized tonic-clonic seizure that has
continued for 8 minutes without stopping, and she does not regain consciousness between convulsions. Which
statement correctly characterizes her condition and its immediate management priority?
A. This is a typical generalized seizure that self-terminates; observation alone is appropriate
B. Status epilepticus is defined only after 30 minutes of continuous seizure activity, so treatment can wait
for imaging
C. This is status epilepticus, now defined as continuous seizure activity or recurrent seizures without
recovery lasting 5 minutes or longer, requiring immediate benzodiazepine therapy to abort neuronal injury
*[CORRECT]*
D. This represents psychogenic nonepileptic seizure; benzodiazepines are contraindicated
Correct Answer: C
Rationale: The operational definition of status epilepticus was shortened from 30 minutes to 5 minutes because seizures
rarely self-terminate beyond that point and delayed treatment predicts refractoriness and neuronal injury from excitotoxic
glutamate effects and metabolic demands. Benzodiazepines are first-line therapy because they enhance GABA-A receptor
activity. Waiting for imaging or assuming a psychogenic cause contradicts the urgency framework taught in NURS 611 and
AACN competency-based acute care content.
Q7: A 30-year-old man with focal epilepsy is prescribed a medication that enhances GABA-mediated chloride
channel opening. The APRN explains that this drug works by addressing which fundamental epileptogenic
mechanism?
A. Excessive degradation of glutamate within the synaptic cleft
B. Impaired inhibitory neurotransmission due to deficient or dysfunctional GABAergic activity
*[CORRECT]*
C. Overactivity of the sodium-potassium pump causing neuronal hyperpolarization
D. Autoimmune damage to cerebellar Purkinje cells
Correct Answer: B
Rationale: Epilepsy reflects a chronic imbalance in which inhibitory GABAergic control is insufficient to restrain excitatory
glutamatergic networks; drugs that potentiate GABA-A chloride channel opening restore inhibition and raise the seizure
threshold. Enhancing GABA does not involve glutamate degradation, and neuronal hyperpolarization from pump overactivity
would be protective rather than epileptogenic. This mechanism-of-disease linkage is a hallmark of advanced pathophysiology
pharmacologic correlation taught in NURS 611.
NURS 611 Advanced Pathophysiology | Maryville University 3
, NURS 611 EXAM 3 (LATEST ) - ADVANCED PATHOPHYSIOLOGY Questions and Verified Answers | Graded A
Q8: A motorcyclist is thrown over the handlebars at high speed, strikes his helmeted head, and remains comatose
for 3 weeks. Initial CT shows no mass lesion, but MRI reveals axonal injury in the corpus callosum and
periventricular regions. Which mechanism best explains diffuse axonal injury (DAI) in severe traumatic brain
injury?
A. Direct cortical contusion at the site of skull impact producing localized axon rupture
B. Penetration of bone fragments severing fiber tracts at the injury site
C. Hemorrhagic necrosis of the temporal lobes from tentorial herniation
D. Shearing forces from rotational acceleration-deceleration that stretch and disrupt axons at the gray-white
matter interface *[CORRECT]*
Correct Answer: D
Rationale: DAI results from inertial rotational forces that create differential movement between brain regions of differing
density, mechanically shearing and stretching axons, particularly in the corpus callosum and parasagittal white matter, with
subsequent Wallerian-type degeneration. Coup-contrecoup contusions, penetrating injury, and herniation-related necrosis are
separate traumatic lesions. This distinction is central to the NURS 611 traumatic brain injury content aligned with AACN
Essentials master-level pathophysiology.
Q9: A patient with a severe head injury develops a systolic blood pressure of 200 mmHg with a widening pulse
pressure, heart rate of 44 beats per minute, and irregular respirations. Which pathophysiological process explains
this constellation of findings?
A. Compression of the medullary vasomotor and respiratory centers by brainstem distortion from severely
elevated intracranial pressure, producing the Cushing response *[CORRECT]*
B. Loss of sympathetic outflow from spinal shock above the T6 level
C. Reflex sinus bradycardia from increased vagal tone caused by meningeal irritation
D. Acute adrenal insufficiency producing hypotension and altered respirations
Correct Answer: A
Rationale: The Cushing triad of hypertension with widened pulse pressure, bradycardia, and irregular respirations is a late,
preterminal sign of markedly elevated intracranial pressure; brainstem distortion activates sympathetic vasomotor surges that
raise arterial pressure, and medullary compression triggers reflex bradycardia and irregular breathing. Spinal shock causes
hypotension, not hypertension, and neither vagal reflexes nor adrenal failure explain the full triad. Per the Monro-Kellie
doctrine reviewed in NURS 611, this finding demands immediate intervention.
Q10: A 6-year-old presents with fever, projectile vomiting, photophobia, and nuchal rigidity. Lumbar puncture
yields: opening pressure 280 mmH2O, glucose 25 mg/dL (blood glucose 110 mg/dL), protein 220 mg/dL, and
2,400 white blood cells/microliter with 92 percent neutrophils. These findings are most consistent with which
diagnosis?
A. Viral (aseptic) meningitis
B. Guillain-Barre syndrome
C. Acute bacterial meningitis *[CORRECT]*
D. Multiple sclerosis
Correct Answer: C
Rationale: Bacterial meningitis classically produces elevated opening pressure, marked neutrophilic pleocytosis, markedly
elevated protein from disrupted blood-brain barrier permeability, and low CSF glucose because bacteria and neutrophils
consume it and impair glucose transport. Viral meningitis shows lymphocytic predominance with normal glucose and
modestly elevated protein; Guillain-Barre shows elevated protein with normal cells; and multiple sclerosis shows oligoclonal
NURS 611 Advanced Pathophysiology | Maryville University 4
ADVANCED PATHOPHYSIOLOGY | QUESTIONS AND VERIFIED ANSWERS |
GRADED A - MARYVILLE
Maryville University | Graduate Nursing and Advanced Practice Education | Comprehensive Examination
Aligned with the NURS 611 Course Syllabus, the AACN Essentials of Master's Education in Nursing, and Advanced
Pathophysiology Competencies (2026/2027 Edition)
100 Questions | 7 Sections | Verified Answers with Detailed Rationales | Cognitive Levels: 20% Recall - 50% Application - 30%
Analysis | Format: 75% Scenario-Based - 25% Direct Knowledge
Section 1: Neurological Pathophysiology
Q1: A 68-year-old man is admitted 2 hours after the sudden onset of right-sided weakness and expressive aphasia.
CT angiography confirms an occlusion of the left middle cerebral artery, and the ischemic penumbra is identified
on perfusion imaging. Which pathophysiological mechanism is responsible for neuronal injury within this
penumbral zone?
A. Excessive adenosine accumulation causing premature neuronal apoptosis despite preserved perfusion
B. Demyelination of surviving axons triggered by oligodendrocyte apoptosis within the core infarct
C. Glutamate-mediated excitotoxicity in which NMDA receptor activation produces lethal calcium influx
into neurons *[CORRECT]*
D. Vasogenic edema from complete blood-brain barrier disruption that uniformly destroys all penumbral
neurons
Correct Answer: C
Rationale: In focal cerebral ischemia, depleted ATP disables the Na-K-ATPase pump, causing glutamate release and failed
reuptake; sustained NMDA receptor activation drives massive intracellular calcium influx, activating proteases, lipases, and
endonucleases that destroy neurons. This excitotoxic cascade is a core NURS 611 advanced pathophysiology concept and the
rationale for neuroprotection research. Adenosine is actually neuroprotective, demyelination is not the primary penumbral
mechanism, and BBB disruption with vasogenic edema is a later, secondary event rather than the initiating injury.
Q2: A 72-year-old woman experiences 25 minutes of left-arm weakness and word-finding difficulty that resolve
completely before emergency evaluation. Diffusion-weighted MRI shows no infarction. Based on advanced
pathophysiological principles, which statement correctly distinguishes a transient ischemic attack (TIA) from an
ischemic stroke?
A. In TIA, transient focal hypoperfusion resolves before tissue infarction occurs, leaving no permanent
neuronal death, whereas stroke produces completed infarction *[CORRECT]*
B. TIA results from hemorrhage into the subarachnoid space, while stroke results from embolic occlusion
only
C. TIA produces permanent laminar cortical necrosis, while stroke is limited to the gray-white matter
junction
D. TIA represents global hypoperfusion from systemic hypotension, while stroke reflects focal vascular
occlusion
Correct Answer: A
NURS 611 Advanced Pathophysiology | Maryville University 1
,NURS 611 EXAM 3 (LATEST ) - ADVANCED PATHOPHYSIOLOGY Questions and Verified Answers | Graded A
Rationale: The modern tissue-based definition holds that TIA is a brief episode of focal cerebral ischemia with full clinical
recovery and no infarction on imaging, reflecting restoration of perfusion through endogenous fibrinolysis or collateral flow
before the ischemic cascade completes. Stroke denotes tissue infarction with irreversible neuronal death. TIA is ischemic, not
hemorrhagic; it does not produce necrosis; and it is focal rather than global, consistent with NURS 611 cerebrovascular
pathophysiology content.
Q3: A 60-year-old man with poorly controlled chronic hypertension suddenly develops dense right hemiparesis
and progressive lethargy. Noncontrast CT reveals a deep intraparenchymal hemorrhage in the left basal ganglia.
Which pathophysiological mechanism most likely explains the location of this hemorrhage?
A. Rupture of a saccular aneurysm at the anterior communicating artery
B. Rupture of Charcot-Bouchard microaneurysms in small penetrating lenticulostriate arteries damaged by
chronic hypertension *[CORRECT]*
C. Venous sinus thrombosis producing hemorrhagic venous infarction in the deep white matter
D. Amyloid deposition in cortical and leptomeningeal vessels of the frontal and occipital lobes
Correct Answer: B
Rationale: Chronic hypertension causes lipohyalinosis and fibrinoid necrosis of small penetrating arteries, forming
Charcot-Bouchard microaneurysms that rupture most often in the basal ganglia, thalamus, pons, and cerebellum. Saccular
aneurysm rupture causes subarachnoid hemorrhage rather than deep intraparenchymal bleeding, cerebral amyloid angiopathy
produces lobar hemorrhages in the elderly, and venous thrombosis is a distinct entity. This vascular pathophysiology is
emphasized in the NURS 611 cerebrovascular unit.
Q4: A 45-year-old woman presents with the abrupt onset of the worst headache of her life, vomiting, and nuchal
rigidity. CT demonstrates diffuse blood in the basal cisterns, and angiography identifies a ruptured saccular
aneurysm of the posterior communicating artery. Which complication, occurring 4 to 10 days after the bleed,
poses the greatest risk of delayed cerebral ischemia?
A. Rebleeding from aneurysm re-rupture
B. Obstructive hydrocephalus from intraventricular extension
C. Hyponatremia from cerebral salt wasting
D. Cerebral vasospasm of arteries bathed in subarachnoid blood *[CORRECT]*
Correct Answer: D
Rationale: Blood breakdown products in the subarachnoid space provoke vasoconstriction and proliferative arteriopathy,
producing delayed cerebral vasospasm between days 4 and 10 that can cause infarction and is a leading cause of morbidity
after subarachnoid hemorrhage. Rebleeding and hydrocephalus are early complications, while hyponatremia worsens
outcomes but does not directly produce delayed focal ischemia. Recognition of vasospasm timing is a tested NURS 611
neurovascular pathophysiology concept.
Q5: A nursing student asks why a patient with a cortical lesion exhibits recurrent, abnormal synchronized
neuronal firing. Which mechanism best describes the fundamental pathophysiology of a seizure?
A. A paroxysmal depolarization shift in which neuronal membranes become hyperexcitable and excitatory
input overwhelms inhibitory GABAergic control *[CORRECT]*
B. Progressive loss of glutamatergic neurons with preserved GABAergic interneurons, producing net
inhibition
C. Excessive cholinergic activity in the reticular activating system causing diffuse cortical synchronization
D. Autoimmune destruction of voltage-gated sodium channels throughout the cerebral cortex
Correct Answer: A
NURS 611 Advanced Pathophysiology | Maryville University 2
,NURS 611 EXAM 3 (LATEST ) - ADVANCED PATHOPHYSIOLOGY Questions and Verified Answers | Graded A
Rationale: Seizures arise from an imbalance favoring excitation over inhibition: hyperexcitable neurons generate paroxysmal
depolarization shifts that recruit neighboring cells into synchronized high-frequency firing. Decreased GABA-mediated
inhibition, enhanced glutamatergic transmission, and altered ion channel function underlie this hyperexcitability, which is
foundational NURS 611 neurophysiology. The other options reverse the excitatory-inhibitory relationship or invoke
unsupported mechanisms.
Q6: A 22-year-old woman is brought to the emergency department in a generalized tonic-clonic seizure that has
continued for 8 minutes without stopping, and she does not regain consciousness between convulsions. Which
statement correctly characterizes her condition and its immediate management priority?
A. This is a typical generalized seizure that self-terminates; observation alone is appropriate
B. Status epilepticus is defined only after 30 minutes of continuous seizure activity, so treatment can wait
for imaging
C. This is status epilepticus, now defined as continuous seizure activity or recurrent seizures without
recovery lasting 5 minutes or longer, requiring immediate benzodiazepine therapy to abort neuronal injury
*[CORRECT]*
D. This represents psychogenic nonepileptic seizure; benzodiazepines are contraindicated
Correct Answer: C
Rationale: The operational definition of status epilepticus was shortened from 30 minutes to 5 minutes because seizures
rarely self-terminate beyond that point and delayed treatment predicts refractoriness and neuronal injury from excitotoxic
glutamate effects and metabolic demands. Benzodiazepines are first-line therapy because they enhance GABA-A receptor
activity. Waiting for imaging or assuming a psychogenic cause contradicts the urgency framework taught in NURS 611 and
AACN competency-based acute care content.
Q7: A 30-year-old man with focal epilepsy is prescribed a medication that enhances GABA-mediated chloride
channel opening. The APRN explains that this drug works by addressing which fundamental epileptogenic
mechanism?
A. Excessive degradation of glutamate within the synaptic cleft
B. Impaired inhibitory neurotransmission due to deficient or dysfunctional GABAergic activity
*[CORRECT]*
C. Overactivity of the sodium-potassium pump causing neuronal hyperpolarization
D. Autoimmune damage to cerebellar Purkinje cells
Correct Answer: B
Rationale: Epilepsy reflects a chronic imbalance in which inhibitory GABAergic control is insufficient to restrain excitatory
glutamatergic networks; drugs that potentiate GABA-A chloride channel opening restore inhibition and raise the seizure
threshold. Enhancing GABA does not involve glutamate degradation, and neuronal hyperpolarization from pump overactivity
would be protective rather than epileptogenic. This mechanism-of-disease linkage is a hallmark of advanced pathophysiology
pharmacologic correlation taught in NURS 611.
NURS 611 Advanced Pathophysiology | Maryville University 3
, NURS 611 EXAM 3 (LATEST ) - ADVANCED PATHOPHYSIOLOGY Questions and Verified Answers | Graded A
Q8: A motorcyclist is thrown over the handlebars at high speed, strikes his helmeted head, and remains comatose
for 3 weeks. Initial CT shows no mass lesion, but MRI reveals axonal injury in the corpus callosum and
periventricular regions. Which mechanism best explains diffuse axonal injury (DAI) in severe traumatic brain
injury?
A. Direct cortical contusion at the site of skull impact producing localized axon rupture
B. Penetration of bone fragments severing fiber tracts at the injury site
C. Hemorrhagic necrosis of the temporal lobes from tentorial herniation
D. Shearing forces from rotational acceleration-deceleration that stretch and disrupt axons at the gray-white
matter interface *[CORRECT]*
Correct Answer: D
Rationale: DAI results from inertial rotational forces that create differential movement between brain regions of differing
density, mechanically shearing and stretching axons, particularly in the corpus callosum and parasagittal white matter, with
subsequent Wallerian-type degeneration. Coup-contrecoup contusions, penetrating injury, and herniation-related necrosis are
separate traumatic lesions. This distinction is central to the NURS 611 traumatic brain injury content aligned with AACN
Essentials master-level pathophysiology.
Q9: A patient with a severe head injury develops a systolic blood pressure of 200 mmHg with a widening pulse
pressure, heart rate of 44 beats per minute, and irregular respirations. Which pathophysiological process explains
this constellation of findings?
A. Compression of the medullary vasomotor and respiratory centers by brainstem distortion from severely
elevated intracranial pressure, producing the Cushing response *[CORRECT]*
B. Loss of sympathetic outflow from spinal shock above the T6 level
C. Reflex sinus bradycardia from increased vagal tone caused by meningeal irritation
D. Acute adrenal insufficiency producing hypotension and altered respirations
Correct Answer: A
Rationale: The Cushing triad of hypertension with widened pulse pressure, bradycardia, and irregular respirations is a late,
preterminal sign of markedly elevated intracranial pressure; brainstem distortion activates sympathetic vasomotor surges that
raise arterial pressure, and medullary compression triggers reflex bradycardia and irregular breathing. Spinal shock causes
hypotension, not hypertension, and neither vagal reflexes nor adrenal failure explain the full triad. Per the Monro-Kellie
doctrine reviewed in NURS 611, this finding demands immediate intervention.
Q10: A 6-year-old presents with fever, projectile vomiting, photophobia, and nuchal rigidity. Lumbar puncture
yields: opening pressure 280 mmH2O, glucose 25 mg/dL (blood glucose 110 mg/dL), protein 220 mg/dL, and
2,400 white blood cells/microliter with 92 percent neutrophils. These findings are most consistent with which
diagnosis?
A. Viral (aseptic) meningitis
B. Guillain-Barre syndrome
C. Acute bacterial meningitis *[CORRECT]*
D. Multiple sclerosis
Correct Answer: C
Rationale: Bacterial meningitis classically produces elevated opening pressure, marked neutrophilic pleocytosis, markedly
elevated protein from disrupted blood-brain barrier permeability, and low CSF glucose because bacteria and neutrophils
consume it and impair glucose transport. Viral meningitis shows lymphocytic predominance with normal glucose and
modestly elevated protein; Guillain-Barre shows elevated protein with normal cells; and multiple sclerosis shows oligoclonal
NURS 611 Advanced Pathophysiology | Maryville University 4
