NSG 530 Exam 3 - Advanced Pathophysiology (2026/2027) - Wilkes University
NSG530 / NSG 530 EXAM 3 (LATEST ): ADVANCED
PATHOPHYSIOLOGY | QUESTIONS AND VERIFIED ANSWERS | 100% CORRECT |
GRADE A - WILKES
Wilkes University School of Nursing | NSG 530 Advanced Pathophysiology
Graduate Nursing Examination - Aligned with AACN Essentials of Master's Education (2026/2027 Edition)
Total Questions: 100 | Total Points: 100 | Cognitive Distribution: 20% Recall, 50% Application, 30% Analysis
Course: NSG 530 - Advanced Pathophysiology Exam: Exam 3 (Latest 2026/2027)
Institution: Wilkes University Grade Level: Graduate / Master's Level
Multiple Choice (4 options, single best
Format: Verified Answers: 100% Correct - Grade A
answer)
75% Scenario-Based, 25% Direct 15 Clinical Reasoning, 10
Question Mix: Special Inclusions:
Knowledge Lab/Diagnostic, 10 Mechanism
Examination Structure:
Section 1: Neurological Pathophysiology (20 Q) | Section 2: Musculoskeletal & Integumentary (15 Q) | Section 3:
Hematological & Oncological (15 Q) | Section 4: Immunological & Inflammatory (15 Q) | Section 5: Genetic &
Developmental (10 Q) | Section 6: Multisystem & Integrative (15 Q) | Section 7: Special Topics & Emerging Concepts (10
Q)
Section 1: Neurological Pathophysiology
Q1: A 68-year-old male presents to the ED with sudden onset of right-sided hemiparesis, expressive aphasia,
and right facial droop that began 90 minutes ago. CT scan shows no hemorrhage. His NIHSS score is 12. The
most likely underlying pathophysiological mechanism is:
A. Lacunar infarction due to lipohyalinosis of small penetrating arteries
B. Embolic occlusion of the left middle cerebral artery (MCA) from a cardiac or carotid source *[CORRECT]*
C. Rupture of a Charcot-Bouchard microaneurysm causing parenchymal hemorrhage
D. Venous sinus thrombosis with subsequent hemorrhagic conversion
Correct Answer: B
Rationale: Sudden focal neurologic deficits maximal at onset with CT-negative for hemorrhage strongly suggests acute
ischemic stroke. The left MCA distribution (right hemiparesis + expressive aphasia) is the classic embolic territory, with
cardiogenic or artery-to-artery embolism being the most common mechanism in this presentation. Lacunar infarcts (A)
present with pure motor or sensory deficits without cortical signs like aphasia. Charcot-Bouchard microaneurysms (C) cause
hypertensive intracerebral hemorrhage visible on CT. Venous sinus thrombosis (D) typically presents with headache,
seizures, and venous infarction.
Page 1 | NSG 530 - Wilkes University | 100 Questions, 100 Points
,NSG 530 Exam 3 - Advanced Pathophysiology (2026/2027) - Wilkes University
Q2: A 72-year-old female with a 20-year history of atrial fibrillation (non-adherent with anticoagulation)
develops acute left-sided weakness. Which hemodynamic mechanism in ischemic stroke pathophysiology
describes the penumbra zone surrounding the infarct core?
A. Irreversibly infarcted tissue with complete ATP depletion and mitochondrial failure
B. Tissue with restored blood flow and no metabolic compromise
C. Hypoperfused but potentially salvageable tissue with impaired but reversible neuronal function *[CORRECT]*
D. Tissue undergoing apoptotic cell death independent of perfusion
Correct Answer: C
Rationale: The ischemic penumbra is hypoperfused tissue surrounding the infarct core that is functionally impaired but
potentially salvageable if perfusion is restored. The core (A) represents irreversible infarction with complete ATP depletion
and ionic pump failure. Option B describes normal tissue. Option D is incorrect because penumbra viability is
perfusion-dependent - the rationale for time-critical reperfusion therapy (IV thrombolysis within 4.5 hours, mechanical
thrombectomy within 24 hours). This is fundamental NSG 530 content guiding acute stroke intervention.
Q3: Which laboratory or diagnostic finding is most specific for differentiating acute ischemic stroke from
hemorrhagic stroke in the emergency setting?
A. Elevated serum lactate dehydrogenase (LDH)
B. Non-contrast head CT showing hyperdense vessel sign or hypodensity *[CORRECT]*
C. Elevated cerebrospinal fluid (CSF) protein without pleocytosis
D. Increased serum neuron-specific enolase (NSE)
Correct Answer: B
Rationale: Non-contrast head CT is the first-line diagnostic study in acute stroke and reliably distinguishes hemorrhagic
(hyperdense) from ischemic (hypodense or normal early) stroke within minutes. A hyperdense MCA sign indicates acute
thrombus. Serum biomarkers (LDH, NSE) lack sufficient sensitivity and specificity for clinical stroke differentiation. CSF
analysis is generally contraindicated in acute stroke and is not diagnostic for hemorrhage versus ischemia. AACN Essentials
emphasize rapid neuroimaging as standard of care for time-sensitive stroke intervention.
Q4: A 56-year-old male has a transient episode of left arm weakness and slurred speech lasting 15 minutes
with complete resolution. Vascular imaging reveals 70% stenosis of the right internal carotid artery. The
pathophysiological distinction between a TIA and ischemic stroke is:
A. TIA involves hemorrhagic events; stroke involves ischemic events
B. TIA symptoms resolve within 24 hours without evidence of infarction on imaging; stroke produces persistent deficits
with infarction *[CORRECT]*
C. TIA is caused by vasospasm; stroke is caused by thrombosis
D. TIA occurs only in posterior circulation; stroke occurs only in anterior circulation
Correct Answer: B
Rationale: The modern definition of TIA is a transient episode of neurologic dysfunction caused by focal brain, spinal cord,
or retinal ischemia without acute infarction on imaging. The traditional 24-hour time cutoff has been replaced by tissue-based
definition using MRI diffusion-weighted imaging. Distinguishing TIA from minor stroke requires imaging evidence (or
absence) of infarction. Options A, C, and D represent pathophysiological misconceptions - both TIA and stroke share similar
mechanisms (atherosclerosis, embolism, thrombosis), and TIA may occur in any vascular territory.
Page 2 | NSG 530 - Wilkes University | 100 Questions, 100 Points
,NSG 530 Exam 3 - Advanced Pathophysiology (2026/2027) - Wilkes University
Q5: A 78-year-old female with chronic hypertension presents with sudden severe headache, vomiting, and
rapid decline in consciousness. CT shows hemorrhage in the basal ganglia with intraventricular extension.
The primary pathophysiological mechanism of this hemorrhagic stroke is:
A. Rupture of a saccular (berry) aneurysm at the circle of Willis
B. Rupture of Charcot-Bouchard microaneurysms from chronic hypertensive vessel changes *[CORRECT]*
C. Arteriovenous malformation (AVM) rupture with venous bleeding
D. Cerebral amyloid angiopathy with lobar hemorrhage
Correct Answer: B
Rationale: Chronic hypertension causes lipohyalinosis and microaneurysm formation (Charcot-Bouchard) in small
penetrating arteries, particularly in the basal ganglia, thalamus, pons, and cerebellum. Rupture produces the classic
hypertensive intracerebral hemorrhage pattern. Saccular aneurysms (A) cause subarachnoid hemorrhage, not parenchymal
bleeds. AVMs (C) typically present in younger patients with seizures or hemorrhage. Cerebral amyloid angiopathy (D) causes
lobar (cortical) hemorrhages in elderly patients and is a less common cause than hypertension for deep ganglionic bleeds.
Q6: A 24-year-old male with history of epilepsy is brought to the ED after a seizure lasting 8 minutes without
recovery of consciousness. He has had three additional seizures in the past 30 minutes. The critical
pathophysiological consequence of status epilepticus that mandates emergent treatment is:
A. Permanent changes in GABA receptor sensitivity
B. Excitotoxic neuronal injury from sustained glutamate-mediated calcium influx *[CORRECT]*
C. Reversible alterations in sodium channel gating
D. Acute dopamine depletion in the substantia nigra
Correct Answer: B
Rationale: Status epilepticus (seizure >5 minutes or recurrent seizures without recovery) produces sustained neuronal
depolarization with massive glutamate release, NMDA/AMPA receptor activation, and intracellular calcium accumulation
causing excitotoxicity and neuronal necrosis, particularly in the hippocampus. This progresses to permanent brain injury and
systemic complications (lactic acidosis, hyperthermia, rhabdomyolysis). The longer the duration, the more refractory seizures
become due to GABA receptor internalization. Time-critical treatment with benzodiazepines is a foundational NSG 530
emergency concept.
Q7: A 19-year-old college student presents with new-onset generalized tonic-clonic seizures. MRI reveals a
temporal lobe lesion. Which pathophysiological mechanism most commonly underlies new-onset epilepsy in
young adults?
A. Mesial temporal sclerosis with hippocampal neuronal loss *[CORRECT]*
B. Degeneration of the substantia nigra dopaminergic neurons
C. Demyelination of the corpus callosum
D. Neurofibrillary tangle formation in cortical neurons
Correct Answer: A
Rationale: Mesial temporal sclerosis (hippocampal sclerosis) is the most common cause of new-onset temporal lobe epilepsy
in young adults, characterized by neuronal loss and gliosis in the hippocampus, often following childhood febrile seizures.
Substantia nigra degeneration (B) causes Parkinson's disease, not epilepsy. Corpus callosum demyelination (C) occurs in
multiple sclerosis and is not a typical epilepsy substrate. Neurofibrillary tangles (D) are the hallmark of Alzheimer's disease,
presenting with dementia rather than new-onset seizures.
Page 3 | NSG 530 - Wilkes University | 100 Questions, 100 Points
, NSG 530 Exam 3 - Advanced Pathophysiology (2026/2027) - Wilkes University
Q8: A 32-year-old female is prescribed phenytoin for focal-onset seizures. Which laboratory value requires
ongoing monitoring to prevent medication toxicity in this patient?
A. Serum sodium and potassium
B. Complete blood count for neutropenia
C. Serum phenytoin level maintained at 10-20 mcg/mL with albumin-corrected free fraction *[CORRECT]*
D. Liver function tests for hepatotoxicity
Correct Answer: C
Rationale: Phenytoin has a narrow therapeutic window (10-20 mcg/mL total; 1-2 mcg/mL free) and exhibits nonlinear
(zero-order) kinetics near the therapeutic range. Because phenytoin is highly protein-bound, the free fraction must be
calculated in hypoalbuminemia or renal failure to avoid toxicity. Common toxic effects include nystagmus, ataxia, and
cognitive impairment. While CBC monitoring is reasonable for idiosyncratic reactions and LFTs for hepatotoxicity, serum
drug level monitoring is the principal safety requirement per AACN pharmacotherapy guidelines.
Q9: A 22-year-old male presents after a motor vehicle collision with loss of consciousness. GCS is 9. CT shows
a crescent-shaped extra-axial fluid collection crossing suture lines. The pathophysiology of this traumatic
brain injury complication is:
A. Tearing of bridging veins between the brain and dura with venous bleeding *[CORRECT]*
B. Rupture of the middle meningeal artery producing arterial bleeding
C. Tearing of cortical arteries with parenchymal hemorrhage
D. Diffuse axonal injury from rotational acceleration forces
Correct Answer: A
Rationale: A crescent-shaped, sutural-crossing extra-axial collection is a subdural hematoma, caused by tearing of bridging
veins between the brain and the dura. This is more common in elderly patients with cerebral atrophy. Rupture of the middle
meningeal artery (B) produces a lentiform (lens-shaped), sutural-bound epidural hematoma - a true neurosurgical
emergency. Parenchymal hemorrhage (C) appears as intracerebral blood. Diffuse axonal injury (D) is microscopic injury to
white matter tracts with often normal initial CT.
Q10: A patient with severe traumatic brain injury develops a unilateral fixed and dilated pupil, decerebrate
posturing, and bradycardia with hypertension (Cushing's triad). These findings indicate uncal herniation with
compression of which structure?
A. Contralateral cerebral peduncle and trochlear nerve
B. Ipsilateral oculomotor nerve (CN III) and cerebral peduncle *[CORRECT]*
C. Contralateral optic nerve and pituitary stalk
D. Bilateral abducens nerves and basilar artery
Correct Answer: B
Rationale: Uncal herniation compresses the ipsilateral oculomotor nerve (CN III) producing ipsilateral pupillary dilation
and ptosis, and compresses the ipsilateral cerebral peduncle producing contralateral hemiparesis. Cushing's triad
(hypertension, bradycardia, irregular respirations) reflects increased ICP from herniation. The contralateral peduncle (A)
may be compressed against the tentorium (Kernohan's notch), producing ipsilateral hemiparesis - a false localizing sign.
Optic nerve compression (C) is not a feature of uncal herniation. Bilateral CN VI palsy (D) is a non-localizing sign of
elevated ICP, not uncal herniation specifically.
Page 4 | NSG 530 - Wilkes University | 100 Questions, 100 Points
NSG530 / NSG 530 EXAM 3 (LATEST ): ADVANCED
PATHOPHYSIOLOGY | QUESTIONS AND VERIFIED ANSWERS | 100% CORRECT |
GRADE A - WILKES
Wilkes University School of Nursing | NSG 530 Advanced Pathophysiology
Graduate Nursing Examination - Aligned with AACN Essentials of Master's Education (2026/2027 Edition)
Total Questions: 100 | Total Points: 100 | Cognitive Distribution: 20% Recall, 50% Application, 30% Analysis
Course: NSG 530 - Advanced Pathophysiology Exam: Exam 3 (Latest 2026/2027)
Institution: Wilkes University Grade Level: Graduate / Master's Level
Multiple Choice (4 options, single best
Format: Verified Answers: 100% Correct - Grade A
answer)
75% Scenario-Based, 25% Direct 15 Clinical Reasoning, 10
Question Mix: Special Inclusions:
Knowledge Lab/Diagnostic, 10 Mechanism
Examination Structure:
Section 1: Neurological Pathophysiology (20 Q) | Section 2: Musculoskeletal & Integumentary (15 Q) | Section 3:
Hematological & Oncological (15 Q) | Section 4: Immunological & Inflammatory (15 Q) | Section 5: Genetic &
Developmental (10 Q) | Section 6: Multisystem & Integrative (15 Q) | Section 7: Special Topics & Emerging Concepts (10
Q)
Section 1: Neurological Pathophysiology
Q1: A 68-year-old male presents to the ED with sudden onset of right-sided hemiparesis, expressive aphasia,
and right facial droop that began 90 minutes ago. CT scan shows no hemorrhage. His NIHSS score is 12. The
most likely underlying pathophysiological mechanism is:
A. Lacunar infarction due to lipohyalinosis of small penetrating arteries
B. Embolic occlusion of the left middle cerebral artery (MCA) from a cardiac or carotid source *[CORRECT]*
C. Rupture of a Charcot-Bouchard microaneurysm causing parenchymal hemorrhage
D. Venous sinus thrombosis with subsequent hemorrhagic conversion
Correct Answer: B
Rationale: Sudden focal neurologic deficits maximal at onset with CT-negative for hemorrhage strongly suggests acute
ischemic stroke. The left MCA distribution (right hemiparesis + expressive aphasia) is the classic embolic territory, with
cardiogenic or artery-to-artery embolism being the most common mechanism in this presentation. Lacunar infarcts (A)
present with pure motor or sensory deficits without cortical signs like aphasia. Charcot-Bouchard microaneurysms (C) cause
hypertensive intracerebral hemorrhage visible on CT. Venous sinus thrombosis (D) typically presents with headache,
seizures, and venous infarction.
Page 1 | NSG 530 - Wilkes University | 100 Questions, 100 Points
,NSG 530 Exam 3 - Advanced Pathophysiology (2026/2027) - Wilkes University
Q2: A 72-year-old female with a 20-year history of atrial fibrillation (non-adherent with anticoagulation)
develops acute left-sided weakness. Which hemodynamic mechanism in ischemic stroke pathophysiology
describes the penumbra zone surrounding the infarct core?
A. Irreversibly infarcted tissue with complete ATP depletion and mitochondrial failure
B. Tissue with restored blood flow and no metabolic compromise
C. Hypoperfused but potentially salvageable tissue with impaired but reversible neuronal function *[CORRECT]*
D. Tissue undergoing apoptotic cell death independent of perfusion
Correct Answer: C
Rationale: The ischemic penumbra is hypoperfused tissue surrounding the infarct core that is functionally impaired but
potentially salvageable if perfusion is restored. The core (A) represents irreversible infarction with complete ATP depletion
and ionic pump failure. Option B describes normal tissue. Option D is incorrect because penumbra viability is
perfusion-dependent - the rationale for time-critical reperfusion therapy (IV thrombolysis within 4.5 hours, mechanical
thrombectomy within 24 hours). This is fundamental NSG 530 content guiding acute stroke intervention.
Q3: Which laboratory or diagnostic finding is most specific for differentiating acute ischemic stroke from
hemorrhagic stroke in the emergency setting?
A. Elevated serum lactate dehydrogenase (LDH)
B. Non-contrast head CT showing hyperdense vessel sign or hypodensity *[CORRECT]*
C. Elevated cerebrospinal fluid (CSF) protein without pleocytosis
D. Increased serum neuron-specific enolase (NSE)
Correct Answer: B
Rationale: Non-contrast head CT is the first-line diagnostic study in acute stroke and reliably distinguishes hemorrhagic
(hyperdense) from ischemic (hypodense or normal early) stroke within minutes. A hyperdense MCA sign indicates acute
thrombus. Serum biomarkers (LDH, NSE) lack sufficient sensitivity and specificity for clinical stroke differentiation. CSF
analysis is generally contraindicated in acute stroke and is not diagnostic for hemorrhage versus ischemia. AACN Essentials
emphasize rapid neuroimaging as standard of care for time-sensitive stroke intervention.
Q4: A 56-year-old male has a transient episode of left arm weakness and slurred speech lasting 15 minutes
with complete resolution. Vascular imaging reveals 70% stenosis of the right internal carotid artery. The
pathophysiological distinction between a TIA and ischemic stroke is:
A. TIA involves hemorrhagic events; stroke involves ischemic events
B. TIA symptoms resolve within 24 hours without evidence of infarction on imaging; stroke produces persistent deficits
with infarction *[CORRECT]*
C. TIA is caused by vasospasm; stroke is caused by thrombosis
D. TIA occurs only in posterior circulation; stroke occurs only in anterior circulation
Correct Answer: B
Rationale: The modern definition of TIA is a transient episode of neurologic dysfunction caused by focal brain, spinal cord,
or retinal ischemia without acute infarction on imaging. The traditional 24-hour time cutoff has been replaced by tissue-based
definition using MRI diffusion-weighted imaging. Distinguishing TIA from minor stroke requires imaging evidence (or
absence) of infarction. Options A, C, and D represent pathophysiological misconceptions - both TIA and stroke share similar
mechanisms (atherosclerosis, embolism, thrombosis), and TIA may occur in any vascular territory.
Page 2 | NSG 530 - Wilkes University | 100 Questions, 100 Points
,NSG 530 Exam 3 - Advanced Pathophysiology (2026/2027) - Wilkes University
Q5: A 78-year-old female with chronic hypertension presents with sudden severe headache, vomiting, and
rapid decline in consciousness. CT shows hemorrhage in the basal ganglia with intraventricular extension.
The primary pathophysiological mechanism of this hemorrhagic stroke is:
A. Rupture of a saccular (berry) aneurysm at the circle of Willis
B. Rupture of Charcot-Bouchard microaneurysms from chronic hypertensive vessel changes *[CORRECT]*
C. Arteriovenous malformation (AVM) rupture with venous bleeding
D. Cerebral amyloid angiopathy with lobar hemorrhage
Correct Answer: B
Rationale: Chronic hypertension causes lipohyalinosis and microaneurysm formation (Charcot-Bouchard) in small
penetrating arteries, particularly in the basal ganglia, thalamus, pons, and cerebellum. Rupture produces the classic
hypertensive intracerebral hemorrhage pattern. Saccular aneurysms (A) cause subarachnoid hemorrhage, not parenchymal
bleeds. AVMs (C) typically present in younger patients with seizures or hemorrhage. Cerebral amyloid angiopathy (D) causes
lobar (cortical) hemorrhages in elderly patients and is a less common cause than hypertension for deep ganglionic bleeds.
Q6: A 24-year-old male with history of epilepsy is brought to the ED after a seizure lasting 8 minutes without
recovery of consciousness. He has had three additional seizures in the past 30 minutes. The critical
pathophysiological consequence of status epilepticus that mandates emergent treatment is:
A. Permanent changes in GABA receptor sensitivity
B. Excitotoxic neuronal injury from sustained glutamate-mediated calcium influx *[CORRECT]*
C. Reversible alterations in sodium channel gating
D. Acute dopamine depletion in the substantia nigra
Correct Answer: B
Rationale: Status epilepticus (seizure >5 minutes or recurrent seizures without recovery) produces sustained neuronal
depolarization with massive glutamate release, NMDA/AMPA receptor activation, and intracellular calcium accumulation
causing excitotoxicity and neuronal necrosis, particularly in the hippocampus. This progresses to permanent brain injury and
systemic complications (lactic acidosis, hyperthermia, rhabdomyolysis). The longer the duration, the more refractory seizures
become due to GABA receptor internalization. Time-critical treatment with benzodiazepines is a foundational NSG 530
emergency concept.
Q7: A 19-year-old college student presents with new-onset generalized tonic-clonic seizures. MRI reveals a
temporal lobe lesion. Which pathophysiological mechanism most commonly underlies new-onset epilepsy in
young adults?
A. Mesial temporal sclerosis with hippocampal neuronal loss *[CORRECT]*
B. Degeneration of the substantia nigra dopaminergic neurons
C. Demyelination of the corpus callosum
D. Neurofibrillary tangle formation in cortical neurons
Correct Answer: A
Rationale: Mesial temporal sclerosis (hippocampal sclerosis) is the most common cause of new-onset temporal lobe epilepsy
in young adults, characterized by neuronal loss and gliosis in the hippocampus, often following childhood febrile seizures.
Substantia nigra degeneration (B) causes Parkinson's disease, not epilepsy. Corpus callosum demyelination (C) occurs in
multiple sclerosis and is not a typical epilepsy substrate. Neurofibrillary tangles (D) are the hallmark of Alzheimer's disease,
presenting with dementia rather than new-onset seizures.
Page 3 | NSG 530 - Wilkes University | 100 Questions, 100 Points
, NSG 530 Exam 3 - Advanced Pathophysiology (2026/2027) - Wilkes University
Q8: A 32-year-old female is prescribed phenytoin for focal-onset seizures. Which laboratory value requires
ongoing monitoring to prevent medication toxicity in this patient?
A. Serum sodium and potassium
B. Complete blood count for neutropenia
C. Serum phenytoin level maintained at 10-20 mcg/mL with albumin-corrected free fraction *[CORRECT]*
D. Liver function tests for hepatotoxicity
Correct Answer: C
Rationale: Phenytoin has a narrow therapeutic window (10-20 mcg/mL total; 1-2 mcg/mL free) and exhibits nonlinear
(zero-order) kinetics near the therapeutic range. Because phenytoin is highly protein-bound, the free fraction must be
calculated in hypoalbuminemia or renal failure to avoid toxicity. Common toxic effects include nystagmus, ataxia, and
cognitive impairment. While CBC monitoring is reasonable for idiosyncratic reactions and LFTs for hepatotoxicity, serum
drug level monitoring is the principal safety requirement per AACN pharmacotherapy guidelines.
Q9: A 22-year-old male presents after a motor vehicle collision with loss of consciousness. GCS is 9. CT shows
a crescent-shaped extra-axial fluid collection crossing suture lines. The pathophysiology of this traumatic
brain injury complication is:
A. Tearing of bridging veins between the brain and dura with venous bleeding *[CORRECT]*
B. Rupture of the middle meningeal artery producing arterial bleeding
C. Tearing of cortical arteries with parenchymal hemorrhage
D. Diffuse axonal injury from rotational acceleration forces
Correct Answer: A
Rationale: A crescent-shaped, sutural-crossing extra-axial collection is a subdural hematoma, caused by tearing of bridging
veins between the brain and the dura. This is more common in elderly patients with cerebral atrophy. Rupture of the middle
meningeal artery (B) produces a lentiform (lens-shaped), sutural-bound epidural hematoma - a true neurosurgical
emergency. Parenchymal hemorrhage (C) appears as intracerebral blood. Diffuse axonal injury (D) is microscopic injury to
white matter tracts with often normal initial CT.
Q10: A patient with severe traumatic brain injury develops a unilateral fixed and dilated pupil, decerebrate
posturing, and bradycardia with hypertension (Cushing's triad). These findings indicate uncal herniation with
compression of which structure?
A. Contralateral cerebral peduncle and trochlear nerve
B. Ipsilateral oculomotor nerve (CN III) and cerebral peduncle *[CORRECT]*
C. Contralateral optic nerve and pituitary stalk
D. Bilateral abducens nerves and basilar artery
Correct Answer: B
Rationale: Uncal herniation compresses the ipsilateral oculomotor nerve (CN III) producing ipsilateral pupillary dilation
and ptosis, and compresses the ipsilateral cerebral peduncle producing contralateral hemiparesis. Cushing's triad
(hypertension, bradycardia, irregular respirations) reflects increased ICP from herniation. The contralateral peduncle (A)
may be compressed against the tentorium (Kernohan's notch), producing ipsilateral hemiparesis - a false localizing sign.
Optic nerve compression (C) is not a feature of uncal herniation. Bilateral CN VI palsy (D) is a non-localizing sign of
elevated ICP, not uncal herniation specifically.
Page 4 | NSG 530 - Wilkes University | 100 Questions, 100 Points
